Cardiology Flashcards

Question

Thiazide like diuretics

Answer 1

chlortalidone (12.5 – 25.0 mg once daily) or indapamide (1.5 mg modified release or 2.5 mg once daily reduce calculi formation

Answer 2

The pathology of mitral stenosis involves progressive thickening, fibrosis, and calcification of the valve leaflets, leading to a smaller valve opening and increased resistance to blood flow.

Answer 3

ischemic heart disease, dilated or hypertrophic cardiomyopathy, and myocarditis. heart failure, mitral or tricuspid regurgitation, or volume overload rapid ventricular filling in early diastole. It is a low-pitched sound that occurs after the second heart sound (S2). While S3 can be normal in children and young adults

Answer 4

In congestive cardiac failure, there is pathophysiological activation of the renin angiotensin aldosterone system due to reduced renal perfusion pressure, which is identified within the nephron by the juxtaglomerular apparatus. This leads to elevated levels of these hormones. Serum cortisol levels are not usually significantly elevated in congestive cardiac failure. Atrial natriuretic peptide would be elevated in congestive cardiac failure in response to increased atrial blood volume and atrial wall stretch

Answer 5

Fluid Overload: Dyspnea, Edemalegs and ankles, abdomen (ascites), Jugular Venous Pressure (JVP)(Kussmaul's sign), Abdominal Swelling- Hepatomegaly (enlarged liver) and ascites (fluid buildup in the abdomen), Decreased Cardiac Output: Fatigue, Exercise Intolerance, Palpitations Pericardial Knock, Diastolic Apex Beat: A palpable precordial impulse that persists throughout diastole., Abnormal S3 Signs of Chronic Illness: Muscle wasting and other signs of chronic disease. order of prevailance : Jugular venous pulse rise>Hepatomegaly>Edema>Ascites Causes : often idiopathic, cardiovascular surgery, radiation therapy, and tuberculosis, rheumatoid arthritis or lupus. pathophysiologic hallmarks: Non-compliant pericardium, Elevated and equalized diastolic pressures, Respiratory-related ventricular interdependence, Dissociation of intrathoracic and intracardiac pressures ECG - low QRS voltages, flattened or inverted T-waves, and in advanced cases, atrial fibrillation diagnosis - Cardiac Catheterization - Pressure Equalization, Right Ventricular Systolic Pressure Mean Right Atrial Pressure, Narrow Pulse Pressure Ventricular Interdependence

Answer 6

Mild hyperoxaemia (while breathing room air) and respiratory alkalosis associated with sudden onset of dyspnoea and tachypnoea supranormal PO2

Answer 7

microdeletion on chromosome 7 mild to moderate intellectual disability, distinctive facial features, and cardiovascular problems not usually inherited, if a person with Williams syndrome has children, there's a 50% chance of passing on the genetic change. difficulty with visual-spatial tasks but excel in areas like language and rote memorization. ue to elastin deficiency - Supravalvar Aortic Stenosis (SVAS): Narrowing of the aorta above the aortic valve, a common finding in WS. Peripheral Pulmonary Artery Stenosis (PPS): Narrowing of the arteries that carry blood to the lungs, another frequent abnormality. Coronary Artery Disease: Narrowing or blockage of the arteries that supply blood to the heart muscle. Hypertension: High blood pressure, often associated with vascular stiffness. Other Stenoses: Narrowing of other blood vessels in the bod Increased Risk

Answer 8

The commonest cause is vascular claudication. The confounder here is the history of myocardial infarction, indicating a high risk for macrovascular disease. Clinical examination confirms that feet pulses rule out a vascular cause of claudication. The correct answer is spinal stenosis, which can mimic vascular claudication. Nerve pressure is dynamic and hence symptoms resolve with rest. For the same reason, neurological examination can be normal. Osteoarthritis, peripheral neuropathy and venous insufficiency do not cause claudication.

Answer 9

Anacrotic pulse: a low-volume pulse seen in patients with aortic stenosis. Collapsing pulse: a finding in patients with moderate-to-severe aortic regurgitation. Pulsus alternans: usually found in severe left ventricular dysfunction as a result of cardiomyopathy, coronary artery disease, systemic hypertension, and aortic stenosis. Pulsus bisferiens: a finding in patients with moderate-to-severe aortic regurgitation; also occurs in patients with combined aortic stenosis and regurgitation. Pulsus paradoxus: this is the only sign that would fit with the clinical scenario of a patient who is likely to have tamponade. Hyperdynamic Pulse: High-output states (anemia, thyrotoxicosis). Radio-Radial Delay: Subclavian artery stenosis (e.g., atherosclerosis). Pulse Pressure (Systolic – Diastolic BP): Wide: Aortic regurgitation, hyperthyroidism Narrow: Cardiogenic shock, aortic stenosis Radial-Femoral Delay (Coarctation of aorta) Asymmetric Pulses (Takayasu arteritis, aortic dissection) Absent Pedal Pulses (PAD, thromboembolism)

Answer 10

Class IA (disopyramide phosphate, quinidine sulfate), Class IC (flecainide acetate, propafenone hydrochloride) and Class III (amiodarone, dofetilide, dronedarone, sotalol hydrochloride) drugs reduce recurrence of atrial fibrillation. Amiodarone and propafenone are superior to sotalol in maintaining long-term normal sinus rhythm in patients with atrial fibrillation. Amiodarone is superior to propafenone. All but amiodarone and propafenone increases pro-arrhythmia.

Answer 11

B-type natriuretic peptide is released from myocytes in the cardiac ventricles in response to stretch-associated high ventricular filling pressures.

Answer 12

This question is testing knowledge on the medical management of heart failure. The patient has an acute presentation of heart failure, likely biventricular systolic dysfunction (also known as congestive cardiac failure), given the presentation of left- (breathlessness) and right- (peripheral oedema) sided symptoms and the history of alcohol misuse and high BP. He is started on treatment with a beta-adrenoceptor blocker and ACE inhibitor for morbidity and mortality benefit and then a diuretic for symptom control. The question is then, following investigations, what additional therapy would be indicated and therefore offer additional benefit. The patient is in sinus rhythm at 60 beats/min, so digoxin, which should be offered third line in worsening or severe heart failure (not second line as in this case), is not indicated. Eplerenone is the correct answer, as an aldosterone antagonist should be offered second line in patients with moderate to severe heart failure. The patient's BP is not given, nor is any intolerance to the ACE inhibitor suggested, so offering an arterial dilator (hydralazine) or a venodilator (isosorbide mononitrate), which are often given in combination, particularly in African–Caribbean patients, as first or second line, is not indicated. Even though a left ventricular ejection fraction of less than 35% is an indication for ivabradine, it is not indicated because the patient's heart rate is not above 75 beats/min, it is not following 4 weeks after starting first- and second-line treatments, and the patient does not have ischaemic heart disease or require an additional antianginal.

Answer 13

DP (adenosine diphosphate) is a molecule that plays a key role in platelet aggregation. When platelets are activated, they release ADP, which binds to the ADP receptor (P2Y12 receptor) on other platelets, causing them to aggregate and form a clot. ADP receptor inhibitors block this interaction, preventing platelets from aggregating and reducing the risk of clot formation.

Answer 14

an inflammatory condition affecting the heart muscle, often triggered by a viral infection. It can lead to symptoms like chest pain, shortness of breath, and irregular heart rhythms. While many people recover completely with treatment, severe cases can result in complications like heart failure or arrhythmias.

Answer 15

edication combining an angiotensin receptor blocker (ARB) and a neprilysin inhibitor (ARNI), plays a crucial role in treating heart failure with reduced ejection fraction (HFrEF). It helps reduce the risk of hospitalization for heart failure, cardiovascular death, and overall mortality in patients with HFrEF.

Answer 16

First-line (start ASAP, titrate to max tolerated doses): ACE inhibitor (e.g., lisinopril) or ARB (if ACE-intolerant). Beta-blocker (bisoprolol, carvedilol, or nebivolol). Mineralocorticoid receptor antagonist (MRA) (e.g., spironolactone) if still symptomatic. Additional therapies if persistent symptoms or worsening: SGLT2 inhibitors (dapagliflozin or empagliflozin) – now recommended early in HFrEF. ARNI (sacubitril/valsartan) – replace ACEi/ARB if still symptomatic on optimal therapy. Ivabradine (if HR ≥75 bpm on max beta-blocker). Diuretics (e.g., furosemide) for fluid overload. Avoid: NSAIDs, glitazones, non-dihydropyridine CCBs. Diagnosis Symptoms: Breathlessness, fatigue, ankle swelling. Tests: NT-proBNP (≥400 pg/mL → refer for echocardiography within 6 weeks; 125–400 pg/mL → consider other causes). Echocardiography to confirm HF and classify type: HFrEF (LVEF ≤40%), HFmrEF (LVEF 41–49%), HFpEF (LVEF ≥50%). SGLT2 inhibitors now recommended early in HFrEF. ARNI preferred over ACEi in select patients.

Answer 17

Inferior MI-related heart blocks are often transient and can resolve with reperfusion. Moreover, pacemaker insertion can be a complex procedure with potential risks in the context of acute MI. Permanent pacemaker implantation is generally reserved for cases where the heart block is persistent and causing symptoms or hemodynamic instability, or when other treatments have failed.

Answer 18

A. Wells Score (Simplified) Clinical signs of DVT (e.g., swelling, pain): +3 PE is the most likely diagnosis: +3 Heart rate >100 bpm: +1.5 Immobilization/surgery in past 4 weeks: +1.5 Previous DVT/PE: +1.5 Hemoptysis: +1 Malignancy (active or treated <6 months): +1 Interpretation: ≤4 points: Low/intermediate probability. >4 points: High probability. B. Revised Geneva Score (Alternative) No need to judge "most likely diagnosis." 2. Rule-Out Pathways A. Low/Intermediate Probability (Wells ≤4) D-dimer test (high-sensitivity assay): Negative D-dimer (below cutoff) + low/intermediate probability → PE excluded. Positive D-dimer → proceed to imaging (CTPA or V/Q scan). PERC Rule (for very low risk patients only): If all 8 PERC criteria are negative, PE is ruled out without D-dimer: Age <50, HR <100, SpO₂ ≥95%, no unilateral leg swelling, no hemoptysis, no recent trauma/surgery, no prior DVT/PE, no estrogen use. B. High Probability (Wells >4) Skip D-dimer (high false-negative rate) → proceed directly to CTPA. 3. Imaging Choices CTPA (1st line for most patients). V/Q scan if contraindications to CTPA (e.g., pregnancy, renal failure). Leg ultrasound if DVT symptoms (may avoid lung imaging if positive). 4. Special Populations Pregnancy: CTPA preferred over V/Q (lower fetal radiation). Renal impairment: Consider V/Q scan or low-dose CTPA.

Answer 19

caused by an extra electrical pathway in the heart that allows electrical signals to bypass the normal conduction pathway. This accessory pathway, a bundle of heart muscle tissue, connects the atria (upper chambers) to the ventricles (lower chambers). The presence of this pathway can lead to rapid heart rates (tachycardia) and other irregular heart rhythms. 1. Normal Electrical Conduction: In a healthy heart, electrical signals travel from the atria to the ventricles through the atrioventricular (AV) node, which slows down the signals briefly to allow the atria to contract and pump blood into the ventricles. 2. WPW and the Accessory Pathway: In WPW syndrome, the electrical signal can also travel through the accessory pathway, which bypasses the AV node. This causes the ventricles to contract before the AV node can slow down the signal, potentially leading to a rapid heart rate. 3. Re-entry and Tachycardia: The accessory pathway can also facilitate re-entry, where electrical signals travel in a circular path, causing a rapid, sustained heart rate

Answer 20

Types of ASDs: Secundum ASD: The most common type, occurring in the middle of the atrial septum. Primum ASD: Less common, occurring in the lower part of the septum, often associated with other heart defects. Sinus venosus ASD: Occurs near the superior vena cava. Patent Foramen Ovale (PFO): A small opening between the atria that usually closes after birth, but sometimes remains open. occurs when there's a hole in the wall separating the heart's two upper chambers (atria). This allows oxygen-rich blood to flow from the left atrium to the right atrium, and then to the lungs, causing an increase in blood flow to the lungs.

Answer 21

Aortic Area: Second right intercostal space, near the sternum. Pulmonary Area: Second left intercostal space, near the sternum. Erb's Point: Third intercostal space, left sternal border. Tricuspid Area: Fourth intercostal space, left sternal border. Mitral Area: Fifth intercostal space, mid-clavicular line.

Answer 22

S3 Gallop (Ventricular Gallop): This occurs during early diastole, after S2, and is caused by the rapid filling of the ventricles, particularly a non-compliant ventricle. It sounds like "Ken-tuc-ky" (S1 S2 S3). S4 Gallop (Atrial Gallop): This occurs late in diastole, just before S1, and is caused by the atria contracting against a stiff ventricle. It sounds like "Bel-ub-dub" (S4 S1 S2).

Answer 23

ction (MI), often leading to severe mitral regurgitation and requiring urgent surgical intervention occurs within a week of the MI, particularly following inferior wall MI, and can also be caused by infective endocarditis Findings: Mitral or tricuspid regurgitation, flail leaflet or bi-leaflet prolapse, ruptured papillary muscle head with detachment, and mobile masses attached to the chordae tendineae. Transesophageal echocardiography (TEE): May be more helpful than transthoracic in visualizing the ruptured muscle head

Answer 24

a nuclear medicine test that assesses how well your heart pumps blood. It's also known as radionuclide ventriculography or cardiac blood pool scan. The scan uses a small amount of radioactive substance (tracer) that is injected into a vein, Diagnose heart problems: MUGA scans help diagnose conditions like coronary artery disease, valvular heart disease, and heart failure. Assess heart function: It can assess how well the heart is functioning, especially after procedures like surgery or during chemotherapy. Monitor treatment: MUGA scans can be used to monitor the effectiveness of treatments for heart conditions.

Answer 25

Step 1: ECG Assessment Type 1 pattern (spontaneous or drug-induced) + clinical criteria → diagnosis confirmed. Type 2/3 → proceed to drug challenge if clinical suspicion is high. Step 2: Clinical Criteria (At Least 1 Required) Documented VF/polymorphic VT. Family history of sudden cardiac death (<45 years). Syncope suggestive of arrhythmia. Nocturnal agonal respirations. Step 3: Drug Challenge (If ECG is Non-Diagnostic) Administer sodium channel blocker (ajmaline/flecainide/procainamide) under monitored conditions. Positive test: Conversion to Type 1 pattern. Step 4: Genetic Testing (Optional) SCN5A mutation found in ~20% of cases, but not required for diagnosis. Management (Based on Risk) Symptomatic patients (VF/syncope): ICD implantation (Class I recommendation). Asymptomatic with Type 1 ECG: Risk-stratify (EPS controversial; consider ICD if high-risk features). Avoid: Sodium channel blockers, tricyclic antidepressants, fever (aggravates ECG changes).

Answer 26

The CHA₂DS₂-VASc score is used to assess the risk of stroke or systemic embolism in patients with non-valvular atrial fibrillation (AF) and guide anticoagulation therapy. Scoring System Risk Factor Points Congestive heart failure (or LVEF ≤40%) 1 Hypertension (BP ≥140/90 mmHg or treated) 1 Age ≥75 years 2 Diabetes mellitus 1 Stroke/TIA/thromboembolism (prior history) 2 Vascular disease (MI, PAD, aortic plaque) 1 Age 65–74 years 1 Sex category (Female) 1 Maximum Score = 9 NOACs (DOACs) (e.g., apixaban, rivaroxaban, dabigatran, edoxaban) are preferred over warfarin in most cases.

Answer 27

1. Major Criteria A. Blood Culture Evidence Typical microorganisms in ≥2 separate cultures: Viridans streptococci, Streptococcus bovis, HACEK group (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella). Staphylococcus aureus or enterococci (without a primary focus). Persistently positive blood cultures (≥2 samples >12 hours apart, or all 3/3 with ≥1 hour between draws). B. Imaging Evidence Echocardiographic findings: Vegetation (oscillating mass on valve/implants). Abscess/pseudoaneurysm. New valvular regurgitation (worsening murmur). 2. Minor Criteria Predisposition (heart condition or IV drug use). Fever (>38°C). Vascular phenomena (septic emboli, Janeway lesions). Immunologic phenomena (Osler nodes, Roth spots, glomerulonephritis). Microbiological evidence (positive blood culture not meeting major criteria or serology for Coxiella burnetii).

Answer 28

a treatment for heart failure that uses a specialized pacemaker or defibrillator to synchronize the heart's pumping action A. CRT-P (Pacemaker) or CRT-D (Defibrillator) in HFrEF B. CRT in Atrial Fibrillation (AF) CRT may be considered in AF patients with LVEF ≤35% and QRS ≥130ms if: Ventricular rate controlled (allowing ≥95% biventricular pacing). AV nodal ablation may be needed to ensure pacing. C. CRT in Mild HF (NYHA I) LVEF ≤30% + LBBB + QRS ≥150ms (Class IIb, weak evidence). 2. Contraindications QRS <130ms (No benefit, may worsen outcomes). Non-cardiac conditions with life expectancy <1 year. Asymptomatic HF without pacing indication. 3. CRT-P vs. CRT-D Choice CRT-D preferred if: Primary prevention of sudden cardiac death (LVEF ≤35%, expected survival >1 year). Ischemic cardiomyopathy (higher arrhythmia risk). CRT-P may suffice in: Non-ischemic cardiomyopathy with low arrhythmia risk. Older patients with multiple comorbidities. 4. Response Predictors Best responders: LBBB, QRS ≥150ms, female sex, non-ischemic etiology. Poor responders: Non-LBBB, QRS 130-149ms, ischemic cardiomyopathy, RV dysfunction.

Answer 29

Viridans Streptococci (VGS): These are a major cause of infective endocarditis, particularly in native valve endocarditis. Specific species within the VGS group that have been linked to endocarditis include S. mitis, S. sanguinis, S. mutans, and S. gordonii. Streptococcus bovis: This species, also known as Streptococcus gallolyticus, is another significant cause, especially in Europe. It is often associated with gastrointestinal cancers. Other Streptococci: In addition to VGS and S. bovis, other streptococcal species like S. pneumoniae and S. pyogenes can also be involved in infective endocarditis, though less commonly. Beta-Hemolytic Streptococci (BHS): While less common than VGS and S. bovis, BHS IE can be aggressive and have a high mortality rate.

Answer 30

1. Stable Angina Treatment Overview First-line antianginal medications Beta-blockers (e.g., bisoprolol, metoprolol) – preferred in post-MI patients. Calcium channel blockers (e.g., amlodipine, diltiazem) – preferred in vasospastic angina or if beta-blockers contraindicated. Long-acting nitrates (e.g., isosorbide mononitrate) – used as add-on therapy. 1st line dose is optimized before second drug added Second-line options: Ivabradine (if HR >70 bpm on beta-blockers). Ranolazine (especially in microvascular angina). Nicorandil (K+ channel activator with nitrate-like effects). 2. Nitrate Use in Stable Angina A. Types of Nitrates Short-acting (for acute relief): Sublingual nitroglycerin (GTN) spray/tablets (onset: 1–3 min). Long-acting (prophylaxis): Isosorbide dinitrate (ISDN) – 2–3x daily dosing. Isosorbide mononitrate (ISMN) – once/twice daily (due to longer half-life). B. Mechanism of Action Nitrates → converted to NO → vasodilation → ↓ preload (venous) & afterload (arterial) → ↓ myocardial O₂ demand.

Answer 31

A. Why Does Tolerance Develop? Depletion of sulfhydryl groups needed for NO generation. Neurohormonal counter-regulation (↑ sympathetic activity, RAAS activation). B. How to Prevent Tolerance Nitrate-Free Interval (8–12 hrs/day) ISMN: Give once daily (e.g., morning) or staggered dosing (e.g., 8 AM & 2 PM). Avoid 24-hour nitrate patches (tolerance develops in 12–24 hrs). Combination with Hydralazine Hydralazine provides sulfhydryl donors, reducing tolerance. ACE Inhibitors/ARBs May blunt RAAS activation caused by nitrates. Avoid High Doses Lower doses may delay tolerance. C. Clinical Signs of Tolerance Reduced symptom relief despite same nitrate dose. Rebound angina during nitrate-free periods (rare). 4. Practical Tips for Nitrate Use Acute attacks: Use GTN spray/tablets (repeat every 5 mins × 3; call EMS if no relief). Chronic prophylaxis: Use ISMN once daily (e.g., 8 AM) or patch with daytime removal. Avoid PDE-5 inhibitors (sildenafil, tadalafil) → risk of severe hypotension.

Answer 32

Paroxysmal AFib: These episodes are intermittent, lasting less than a week, and often resolve spontaneously without treatment. While these episodes may come and go, individuals with paroxysmal AFib still have an increased risk of stroke. Persistent AFib: This type lasts longer than a week and may require treatment to either slow the heart rate or restore a normal rhythm (cardioversion). Long-standing Persistent AFib: This type continues for more than a year and can be more challenging to treat, potentially requiring specialized interventions. Permanent AFib: This is a long-term AFib that has not responded to attempts to restore a normal rhythm and may be managed with rate control medications and anticoagulation.

Answer 33

DES Mechanism: DES are coated with a drug, like paclitaxel or sirolimus, that is released into the surrounding tissue and inhibits the growth of new cells, preventing the artery from re-narrowing. Benefits: Lower risk of restenosis compared to BMS. May reduce the need for repeat procedures to keep the artery open. Drawbacks: Slightly higher risk of stent thrombosis compared to BMS. Requires longer duration of dual antiplatelet therapy (anti-clotting medication) compared to BMS. Potential for long-term side effects from the drug. Bare Metal Stents (BMS): Mechanism: BMS are simple metal mesh tubes that are placed in the artery to hold it open. Benefits: Lower cost compared to DES. Shorter duration of dual antiplatelet therapy required compared to DES. Lower risk of stent thrombosis compared to DES. Drawbacks: Higher risk of restenosis compared to DES. May require repeat procedures to keep the artery open.

Answer 34

interfering with the body's ability to produce vitamin K-dependent clotting factors 1. Standard INR Targets for Cardiac Conditions Condition Target INR Key Notes Atrial Fibrillation (Non-Valvular) 2.0–3.0 NOACs preferred, but warfarin used if contraindicated. Atrial Fibrillation (Valvular) 2.5–3.5 Higher INR for mechanical valves or mitral stenosis. Mechanical Heart Valves 2.5–3.5 Mitral valves often need higher INR (e.g., 3.0–3.5). Bioprosthetic Valves 2.0–3.0 (first 3–6 months) Often switched to aspirin afterward. Venous Thromboembolism (VTE) 2.0–3.0 Short-term (3–6 months) or long-term if recurrent. LV Thrombus (Post-MI) 2.0–3.0 Typically for 3–6 months (with imaging follow-up). Antiphospholipid Syndrome (APS) 2.5–3.5 Warfarin preferred over NOACs (higher throm

Answer 35

2. Warfarin Dosing Principles Initiation: Start with 5 mg daily (lower doses for elderly/frail). Adjust based on INR. Maintenance: Usually 2–10 mg/day (high interpatient variability). Monitoring: Check INR every 1–2 weeks once stable (goal TTR >70%). More frequent checks if dose changes, illness, or new medications. 3. Special Considerations Bridging with Heparin/LMWH: Needed for high-risk patients (e.g., mechanical valves) before surgery. Drug Interactions: ↑ INR: Amiodarone, antibiotics (e.g., ciprofloxacin), antifungals. ↓ INR: Rifampin, phenytoin, St. John’s wort. Diet: Consistent vitamin K intake (avoid sudden changes in leafy greens). 4. When to Choose Warfarin Over NOACs Mechanical heart valves (NOACs contraindicated). Severe renal failure (CrCl <15–30 mL/min). Antiphospholipid syndrome (higher thrombosis risk with NOACs).

Answer 36

High in vitamin K: Green leafy vegetables (like spinach, kale, lettuce, and broccoli), liver, chickpeas, egg yolks, certain cheeses (mature and blue), avocados, and olive oil. Grapefruit: Some studies suggest grapefruit juice may increase INR in some patients. Green tea: May lower INR in large quantities. Cranberry and pomegranate juice: May increase INR. Alcohol: Can affect anticoagulant control, so moderation is advised. Mango: May increase the anticoagulant effect of warfarin.

Answer 37

1. Diagnosis & Severity Assessment Echocardiography (TTE first, ±TEE if unclear): Severe MS: Valve area ≤1.5 cm² (or ≤1.0 cm² in very severe cases). Mean gradient ≥10 mmHg or PASP >50 mmHg. Symptoms: Dyspnea (NYHA II-IV), fatigue, AF, hemoptysis. 2. Medical Management (All Patients) Therapy Indication Diuretics (furosemide) Fluid overload (pulmonary congestion). Beta-blockers/CCBs (e.g., bisoprolol, diltiazem) Control heart rate (esp. in AF). Anticoagulation (warfarin) AF or prior embolic event (INR 2.0–3.0). Penicillin prophylaxis Rheumatic fever history (per UK guidelines). Avoid: ACEi/ARBs (no proven benefit in pure MS). 3. Intervention Criteria Scenario Recommended Intervention Symptomatic severe MS (NYHA II-IV) + favorable valve morphology Percutaneous mitral commissurotomy (PMC) (Class I). Symptomatic severe MS + contraindication to PMC Surgical mitral valve replacement (MVR) (Class I). Asymptomatic severe MS + high-risk features (PASP >50 mmHg, AF, thromboembolism) Consider PMC (Class IIa).

Answer 38

Key Notes: PMC preferred if: No left atrial thrombus, minimal calcification, no significant MR. Surgery if: Heavy calcification, subvalvular fusion, or concomitant MR. 4. Post-Intervention Follow-Up Annual echocardiography (monitor re-stenosis after PMC). Lifelong anticoagulation if: Post-PMC with AF. Mechanical valve replacement (INR 2.5–3.5). 5. Special Cases Pregnancy: PMC if severe symptoms (avoid surgery). Asymptomatic MS: Monitor yearly; intervene if PA pressure rises.

Answer 39

Symptoms of Mitral Stenosis: Shortness of breath, Fatigue, Swollen ankles and feet Heart palpitations, Dizziness or fainting, Coughing up blood (hemoptysis), Chest pain or discomfort, Orthopnea, Paroxysmal nocturnal dyspnea, Fluid buildup in the lungs, Irregular heart rhythms (arrhythmias), Hoarseness, Ascites (abdominal swelling), Hepatomegaly (enlarged liver)

Answer 40

Primary Causes: Heart Failure, Kidney Failure, Pulmonary Embolism Secondary Causes: Left Ventricular Hypertrophy, Right Ventricular Overload, Ischemia, Tachycardia, Hypoxemia Age: increase with age, especially after 70. Sepsis, Diabetes, Liver Cirrhosis, COPD Other Factors: Medications: Some medications, like ACE inhibitors, beta-blockers, and diuretics, can lower BNP and NT-proBNP levels. Stress, Obesity

Answer 41

Cardiac Syndrome X (CSX), which is now also known as Microvascular Angina.

Answer 42

1. Mechanisms of QT Prolongation Drugs prolong the QT interval by disrupting cardiac repolarization, primarily via: Blockade of hERG potassium channels (↓ IKr current → delayed repolarization). Altered sodium/calcium channel activity (less common). High-Risk Drug Classes: Class Examples Antiarrhythmics Amiodarone, sotalol, dofetilide, quinidine Antipsychotics Haloperidol, ziprasidone, quetiapine Antidepressants Citalopram, escitalopram, TCAs Antibiotics Macrolides (azithromycin, clarithromycin), fluoroquinolones (levofloxacin, moxifloxacin) Antiemetics Ondansetron, domperidone Others Methadone, pentamidine, chloroquine 2. Risk Factors for Torsades de Pointes (TdP) Electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia). Bradycardia (↑ QT interval duration). Female sex (higher baseline QT). Genetic predisposition (e.g., congenital LQTS). Polypharmacy (CYP3A4 inhibitors ↑ drug levels). 3. Clinical Management A. Prevention Baseline ECG before starting high-risk drugs (repeat after dose changes). Correct electrolytes: Maintain K⁺ >4.0 mmol/L, Mg²⁺ >2.0 mg/dL. Avoid combinations that prolong QT (e.g., SSRI + antipsychotic). Dose adjustment in renal/hepatic impairment. B. Acute Management of TdP Immediate actions: Stop offending drug. IV magnesium sulfate (1–2 g bolus, even if Mg²⁺ normal). Correct hypokalemia (target K⁺ ≥4.5 mmol/L). If unstable (syncope/VF): DC cardioversion. Temporary pacing (if bradycardia-dependent TdP). C. Long-Term Strategies Switch to low-risk alternatives (e.g., olanzapine instead of haloperidol). Consider ECG monitoring for high-risk patients.

Answer 43

A. Stanford Classification (Most clinically relevant) Type Description Management Type A Involves ascending aorta (regardless of distal extension). Emergency surgery (risk of rupture, tamponade, stroke). Type B Involves descending aorta only (distal to left subclavian artery). Medical therapy first (surgery only for complications). B. DeBakey Classification (Anatomic) Type I: Ascending + descending aorta. Type II: Ascending aorta only. Type III: Descending aorta only (IIIa: limited; IIIb: extends to abdomen). 3. Diagnostic Workup A. Imaging (Choose fastest available) CT angiography (CTA) – Gold standard (sensitivity/specificity >95%). Transesophageal echo (TEE) – Useful intraoperatively or if CTA contraindicated. MRI – For stable, chronic dissections (rarely used acutely). B. Labs D-dimer (elevated but nonspecific; negative result helps rule out). CBC, troponin (exclude MI), creatinine (contrast risk). 4. Management A. Type A Dissection Immediate surgical repair (graft replacement ± aortic valve repair). Blood pressure control pre-op: Target SBP <120 mmHg, HR <60 bpm. First-line: IV beta-blocker (e.g., esmolol, labetalol). Add vasodilator (e.g., nitroprusside) if needed. B. Type B Dissection Medical management unless complications: IV beta-blockers + vasodilators (same targets as Type A). Surgery/TEVAR (thoracic endovascular repair) for: Malperfusion (renal, mesenteric, limb ischemia). Refractory pain/hypertension. Aneurysmal expansion (>5.5 cm). 5. Complications Rupture (tamponade, hemothorax). Organ malperfusion (mesenteric ischemia, renal failure). Chronic aneurysm formation.

Answer 44

Family History of Sudden Cardiac Death (FHSD): Syncope: Non-Sustained Ventricular Tachycardia (NSVT): Left Ventricular Outflow Tract Obstruction (LVOTO): Maximum Left Ventricular Wall Thickness (MLVWT): Myocardial Fibrosis (LGE): NYHA Functional Class: Diastolic Dysfunction: Left Ventricular Ejection Fraction: Genotype:

Answer 45

Modified Duke Criteria for PVE Major Criteria: Vegetation/abscess on echocardiography (TEE preferred over TTE). Blood cultures positive for typical organisms (S. aureus, S. epidermidis, Enterococci, HACEK group). Minor Criteria: Fever, vascular phenomena, new regurgitation. Imaging: TEE (sensitivity >90% for PVE). FDG-PET/CT (if TEE inconclusive; detects paravalvular infection). 2. Empirical Antibiotic Therapy (Start after blood cultures, adjust based on results) Suspected Pathogen Empirical Regimen Early PVE (<1 yr post-op) Vancomycin + Gentamicin + Rifampin (cover S. aureus & coagulase-negative staph). Late PVE (>1 yr post-op) Ampicillin-sulbactam + Gentamicin (cover Enterococci, Streptococci). Culture-negative PVE Vancomycin + Ceftriaxone + Gentamicin (broad coverage). Key Adjustments: MRSA risk? → Continue vancomycin. HACEK organisms? → Ceftriaxone alone. 3. Pathogen-Specific Therapy Organism Preferred Regimen Duration MSSA (Methicillin-sensitive S. aureus) Nafcillin/Oxacillin + Rifampin + Gentamicin (first 2 weeks). 6 weeks MRSA Vancomycin + Rifampin + Gentamicin. 6 weeks Coagulase-negative staph Vancomycin + Rifampin + Gentamicin. 6 weeks Enterococci Ampicillin + Ceftriaxone (if aminoglycoside-resistant). 6 weeks HACEK Ceftriaxone. 3. Pathogen-Specific Therapy Organism Preferred Regimen Duration MSSA (Methicillin-sensitive S. aureus) Nafcillin/Oxacillin + Rifampin + Gentamicin (first 2 weeks). 6 weeks MRSA Vancomycin + Rifampin + Gentamicin. 6 weeks Coagulase-negative staph Vancomycin + Rifampin + Gentamicin. 6 weeks Enterococci Ampicillin + Ceftriaxone (if aminoglycoside-resistant). 6 weeks HACEK Ceftriaxone. 4 weeks Notes: Rifampin is critical for biofilm penetration (start after bacteremia clears). Gentamicin is used for synergy (limit to 2 weeks due to nephrotoxicity). 4. Indications for Surgery Heart failure (acute valve dysfunction causing pulmonary edema/shock). Uncontrolled infection (abscess, fistula, persistent fever >10 days). Fungal endocarditis (Candida, Aspergillus). Recurrent emboli (large vegetations >10 mm). Valve dehiscence/paravalvular leak. Surgical Options: Valve replacement (mechanical/bioprosthetic). Homograft (for aortic root abscess). 5. Adjunctive Therapy Anticoagulation: Mechanical valves: Continue warfarin (INR 2.5–3.5). Bioprosthetic valves: Hold if CNS emboli (risk of hemorrhage). Follow-up: Repeat blood cultures until sterile. Echocardiography post-treatment (assess for relapse).

Answer 46

Aortic Regurgitation (AR) Management (NICE NG208) 1. Diagnosis & Assessment TTE (Transthoracic Echo) is first-line for diagnosis and severity grading. Severe AR criteria: VC width ≥6 mm (vena contracta). Regurgitant volume ≥60 mL/beat or RF ≥50%. ERO ≥0.30 cm² (effective regurgitant orifice). Diastolic flow reversal in descending aorta (Doppler). Exercise testing if symptoms are equivocal. Cardiac MRI if echo is inconclusive. 2. Medical Management No proven medical therapy to slow progression in chronic AR. Treat hypertension (if present) with dihydropyridine CCBs (e.g., amlodipine) or ACEi/ARBs (avoid beta-blockers unless for another indication). Vasodilators (e.g., nifedipine) may be used short-term in acute severe AR (bridge to surgery). 3. Indications for Surgery (ESC/NICE-Aligned) A. Symptomatic Severe AR (NYHA II-IV) → Class I (Urgent AVR). B. Asymptomatic Severe AR + Any of: LV systolic dysfunction (LVEF ≤50%) → Class I. LV dilation (LVESD >50 mm or LVEDD >65 mm) → Class IIa. Undergoing other cardiac surgery (e.g., CABG) → Class I. Acute Severe AR (e.g., aortic dissection, endocarditis) → Emergency surgery. 4. Surgical Options Aortic Valve Replacement (AVR): Mechanical valve (young patients, no contraindication to warfarin). Bioprosthetic valve (older patients, avoid anticoagulation). Valve repair (selected cases, e.g., bicuspid valve with repairable cusps). 5. Follow-Up Asymptomatic mild/moderate AR: Echo every 3–5 years. Severe AR (no surgery): Echo every 6–12 months. Post-AVR: Lifelong surveillance (risk of prosthetic valve complications).

Answer 47

Causes: Primary Valve Disease: Degeneration or calcification of the valve leaflets, congenital defects (like a bicuspid valve), endocarditis (infection of the valve), or rheumatic fever. Aortic Root Dilation: Enlargement of the aorta, which can prevent the valve leaflets from closing properly. This can be caused by conditions like Marfan syndrome or other connective tissue disorders. Other Causes: Trauma to the aorta, high blood pressure, or certain inflammatory diseases can also contribute to aortic regurgitation. Presentation: Chronic AR: May be asymptomatic for years, with initial symptoms including palpitations, uncomfortable awareness of the heart pounding, or shortness of breath with exertion. Acute AR: Presents as a medical emergency, with symptoms including sudden shortness of breath, rapidly developing heart failure, chest pain, and potentially cardiovascular collapse.

Answer 48

antiarrhythmic action is connected to its ability to block K+, Na+, and Ca2+ channels while noncompetitively blocking α- and β-adrenergic receptors of the heart, thus prolonging the action potential and effective refractive period of atrial cells, atrioventricular junctions, and ventricles of the heart, Amiodarone: Indications & Contraindications A. Arrhythmia Management Life-threatening ventricular arrhythmias: Recurrent ventricular fibrillation (VF) or hemodynamically unstable ventricular tachycardia (VT). Secondary prevention in high-risk patients (e.g., post-MI, cardiomyopathy). Atrial fibrillation (AF) & flutter: Rate/rhythm control when other agents fail (off-label in some countries but widely used). Post-cardiac surgery AF prophylaxis (short-term use). B. Other Uses Stable monomorphic VT (if other drugs ineffective). Bridge to ICD implantation in high-risk patients. 2. Contraindications Absolute Contraindications: Severe sinus node dysfunction or 2nd/3rd-degree AV block (without pacemaker). Hypersensitivity to amiodarone/iodine (risk of anaphylaxis). Pregnancy (2nd & 3rd trimesters) → Risk of neonatal hypothyroidism/goiter. Severe hepatic impairment (risk of hepatotoxicity). Relative Contraindications (Use with Caution): Pulmonary fibrosis or interstitial lung disease (amiodarone can worsen). Thyroid dysfunction (hypo-/hyperthyroidism). Bradycardia (HR <50 bpm). Concurrent QT-prolonging drugs (↑ risk of Torsades de Pointes). 3. Key Monitoring Requirements Baseline tests before initiation: Thyroid function (TSH, T3/T4). LFTs (ALT/AST, bilirubin). CXR/PFTs (if lung disease suspected). ECG (QT interval, HR). Follow-up: Thyroid/LFTs every 6 months. Annual CXR (if long-term use). 4. Adverse Effects Organ System Side Effects Cardiac Bradycardia, QT prolongation (rare TdP). Pulmonary Fibrosis (dose-dependent, fatal in 10%). Thyroid Hypothyroidism (6%) or hyperthyroidism (3%). Hepatic Elevated LFTs, hepatitis (monitor ALT/AST). Dermatologic Photosensitivity, blue-gray skin discoloration. Ocular Corneal microdeposits (vision halos). 5. Drug Interactions CYP3A4 inhibitors (e.g., verapamil, grapefruit juice) → ↑ Amiodarone toxicity. Warfarin → ↑ INR (↓ warfarin dose by 30–50%). Digoxin → ↑ Digoxin levels (↓ dose by 50%). Simvastatin → ↑ Risk of myopathy (avoid >20 mg/day).

Answer 49

blocking both alpha-1 and beta-adrenergic receptors, leading to a decrease in blood pressure. Specifically, it blocks beta-1 receptors in the heart, slowing the heart rate and reducing the force of contraction, and also blocks alpha-1 receptors in blood vessels, causing them to relax and widen, which further lowers blood pressure.

Answer 50

1. Mechanism of Action Mixed alpha-1 (α₁) and non-selective beta (β₁/β₂) blocker: Beta-blockade (↓ heart rate, contractility). Alpha-blockade (vasodilation → ↓ blood pressure). 2. Approved Indications Hypertensive emergencies (IV form). Chronic hypertension (oral form). Pregnancy-induced hypertension/preeclampsia (preferred due to safety profile). Acute aortic dissection (combined with vasodilators like nitroprusside). 3. Dosing Guidelines Formulation Dosage Notes IV Labetalol 20 mg bolus, then 20–80 mg every 10 min (max 300 mg in 24h). Used in hypertensive crisis (target BP reduction by 25% within 1h). Oral Labetalol 100–400 mg twice daily (max 2.4 g/day). Titrate gradually in chronic hypertension. 4. Contraindications Acute decompensated heart failure (↓ cardiac output risk). Severe bradycardia/AV block (without pacemaker). Asthma/severe COPD (non-selective β-blockade worsens bronchospasm). Cardiogenic shock. 5. Adverse Effects Hypotension (especially with IV use). Bronchospasm (caution in asthma). Masked hypoglycemia in diabetics. Fatigue, dizziness, scalp tingling (α-blockade effect). 6. Key Monitoring BP & heart rate (avoid excessive bradycardia). Lung auscultation (wheezing in COPD/asthma). Glucose monitoring in diabetics. 7. Comparison to Other Beta-Blockers Feature Labetalol Metoprolol Carvedilol Selectivity Non-selective (β + α₁) β₁-selective Non-selective (β + α₁) Vasodilation Yes (α₁-blockade) No Yes (α₁-blockade) Pregnancy Use Preferred Avoid Avoid

Answer 51

1. Mechanism of Action Non-dihydropyridine calcium channel blocker (CCB): Blocks L-type calcium channels in cardiac myocytes and vascular smooth muscle. Primary effects: ↓ AV node conduction (antiarrhythmic). Coronary/systemic vasodilation (antihypertensive, antianginal). 2. Approved Indications A. Cardiovascular Atrial fibrillation/flutter (rate control). Hypertension (oral, chronic management). Chronic stable angina (vasospastic or effort-induced). PSVT (paroxysmal supraventricular tachycardia). B. Off-Label Uses Migraine prophylaxis. Esophageal spasm. 3. Dosing Guidelines Formulation Indication Dosage Notes IV Diltiazem AF/flutter (acute rate control) 0.25 mg/kg bolus, then 5–15 mg/hr infusion. Avoid in HFrEF or hypotension. Oral Immediate-Release (IR) HTN, angina 30–120 mg TID. Short-acting; used for titration. Oral Extended-Release (ER) HTN, chronic AF 120–360 mg once daily. Preferred for maintenance. 4. Contraindications Heart failure with reduced EF (HFrEF) (may worsen systolic function). Severe bradycardia/2nd/3rd-degree AV block (without pacemaker). Hypotension (SBP <90 mmHg). Concurrent IV beta-blockers (↑ risk of cardiogenic shock). 5. Adverse Effects Cardiac: Bradycardia, AV block, peripheral edema. GI: Constipation (common with non-DHP CCBs). CNS: Dizziness, headache. Hypotension (especially with IV use). 6. Drug Interactions Beta-blockers (↑ risk of bradycardia/AV block). CYP3A4 inhibitors (e.g., clarithromycin, grapefruit juice) → ↑ diltiazem levels. Simvastatin (max dose 20 mg/day with diltiazem). Digoxin (↑ digoxin levels by 20–50%). 7. Monitoring ECG (PR interval prolongation, bradycardia). BP (avoid excessive hypotension). Symptoms of HF (dyspnea, edema) in at-risk patients. 8. Comparison to Other CCBs Feature Diltiazem Verapamil Amlodipine AV Node Effect ↓ Conduction ↓ Conduction No effect Vasodilation Moderate Moderate Strong HF Safety Avoid in HFrEF Avoid in HFrEF Safe

Answer 52

1. Mechanism of Action Class IV antiarrhythmic (non-dihydropyridine calcium channel blocker). Blocks L-type calcium channels in: Cardiac myocytes (↓ SA/AV node conduction → negative chronotropy/dromotropy). Vascular smooth muscle (mild vasodilation). 2. Approved Indications A. Cardiovascular Atrial fibrillation/flutter (rate control). PSVT (paroxysmal supraventricular tachycardia). Hypertension (oral, chronic management). Vasospastic/stable angina. B. Off-Label Uses Cluster headache prophylaxis. Hypertrophic cardiomyopathy (symptom relief). 3. Dosing Guidelines Formulation Indication Dosage Key Notes IV Verapamil Acute PSVT 2.5–5 mg bolus (repeat ×1 after 15–30 min if needed). Avoid in WPW + AF (risk of VF). Oral IR HTN, angina 80–120 mg TID. Short-acting; titrate carefully. Oral SR/ER Chronic HTN/AF 120–480 mg once daily. Preferred for maintenance. 4. Contraindications Absolute: Severe HF (HFrEF) (may precipitate cardiogenic shock). 2nd/3rd-degree AV block (without pacemaker). Sick sinus syndrome. Concurrent IV beta-blockers (↑ risk of asystole). WPW + AF (↑ ventricular rate → VF risk). broad complex tachicardia Relative: Hypotension (SBP <90 mmHg). Liver cirrhosis (↓ metabolism). 5. Adverse Effects Cardiac: Bradycardia, AV block, heart failure exacerbation. GI: Constipation (up to 40% of patients). CNS: Dizziness, headache. Peripheral edema (less common than with dihydropyridines). 6. Drug Interactions Digoxin: ↑ Digoxin levels by 50–75% (↓ digoxin dose). Beta-blockers: ↑ Risk of bradycardia/AV block (avoid concurrent IV use). CYP3A4 inhibitors (e.g., erythromycin, grapefruit juice) → ↑ verapamil toxicity. Statins: Limit simvastatin to ≤20 mg/day (↑ myopathy risk). 7. Monitoring ECG (PR interval prolongation, bradycardia). BP (especially with IV use). Symptoms of HF (weight gain, dyspnea). LFTs (with chronic use in liver disease). 8. Comparison to Other CCBs Feature Verapamil Diltiazem Amlodipine AV Node Effect Strong ↓ Moderate ↓ None Vasodilation Mild Moderate Strong HF Safety Contraindicated in HFrEF Avoid in HFrEF Safe Constipation Risk High Moderate Low 9. Clinical Pearls IV verapamil is first-line for PSVT (unless contraindicated). Avoid in WPW + AF (use procainamide/ibutilide instead). For HTN, ER formulations improve adherence.

Answer 53

1. Key Features Congenital accessory pathway (AP): Bypasses AV node → pre-excitation on ECG. ECG Hallmarks: Short PR interval (<120 ms). Delta wave (slurred QRS upstroke). Wide QRS (fusion of normal and AP conduction). Tachyarrhythmias: Orthodromic AVRT (narrow QRS, most common). Antidromic AVRT (wide QRS, mimics VT). Atrial fibrillation (AF) with rapid AP conduction → life-threatening risk of VF. 2. Acute Management of Tachycardia Arrhythmia Treatment Avoid Stable orthodromic AVRT Adenosine (6–12 mg IV). Verapamil (if uncertain diagnosis). Unstable (hypotension/CHF) Synchronized cardioversion (50–100 J). — AF with WPW (wide QRS, irregular) Procainamide or Ibutilide. AV nodal blockers (adenosine, verapamil, beta-blockers, digoxin) → may ↑ ventricular rate → VF. 3. Long-Term Management Catheter ablation (first-line for symptomatic WPW): Success rate >95%; low complication risk. Indications: Symptomatic arrhythmias (AVRT, AF). Asymptomatic with high-risk features (AP refractory period <250 ms, AF with rapid conduction). Drug therapy (if ablation deferred): Flecainide, Propafenone (slow AP conduction). Sotalol/Amiodarone (second-line). 4. Risk Stratification High-risk markers: Intermittent pre-excitation loss (suggests long AP refractory period). AP refractory period >250 ms on EP study. Asymptomatic WPW: Exercise testing: Sudden delta wave loss suggests lower risk. EP study recommended if high-risk profession (e.g., pilot). 5. Special Considerations Pregnancy: Avoid flecainide/procainamide (use beta-blockers or ablation pre-pregnancy). Children: Higher spontaneous AP regression rate; ablation often deferred.

Answer 54

a skin condition characterized by a mottled, reddish-blue or purplish net-like pattern on the skin, often appearing on the legs and arms. Primary livedo reticularis: This is often a benign condition triggered by cold exposure, tobacco use, or emotional stress. Secondary livedo reticularis: This is linked to various underlying medical conditions, including connective tissue disorders (like lupus), thrombophilia (increased risk of blood clots), vasculitis (inflammation of blood vessels), endocrine disorders, and certain medications. Symptoms: A mottled, net-like discoloration of the skin, often reddish-blue or purplish. The pattern may appear on the legs, arms, or other areas of the body. Numbness or tingling in the affected areas, especially in cold temperatures, may occur. In some cases, ulcers or nodules may develop.

Answer 55

A. Antiphospholipid Syndrome (APS) Strong association: LR is present in 25% of APS patients and 70% of APS with systemic lupus erythematosus (SLE)12. Mechanism: Autoantibodies cause hypercoagulability, leading to microthrombosis in skin vessels and systemic arterial/venous thrombosis (e.g., stroke, myocardial infarction)57. Cardiac risks: Valvular disease (Libman-Sacks endocarditis), coronary artery thrombosis, and pulmonary embolism B. Cholesterol Embolization Syndrome Cause: Plaque rupture in aortic atherosclerosis releases cholesterol crystals, obstructing small vessels Triggers: Cardiac catheterization, aortic surgery, or anticoagulant use. Systemic signs: Acute kidney failure, blue toe syndrome, and LR (due to cutaneous ischemia. C. Infective Endocarditis Septic emboli from infected heart valves can occlude cutaneous vessels, causing retiform purpura or LR. Key pathogens: Staphylococcus aureus, Streptococcus viridans. D. Sneddon Syndrome Triad: LR + stroke + hypertension Pathology: Non-inflammatory arteriopathy affecting medium-sized vessels (brain and skin) Cardiac link: Associated with valvular abnormalities (e.g., mitral regurgitation) and thrombotic events E. Vasculitis (e.g., Polyarteritis Nodosa) Medium-vessel vasculitis can cause LR via vascular inflammation and thrombosis Cardiac complications: Coronary artery vasculitis, cardiomyopathy 2. Diagnostic Workup for Cardiac-Related LR Key Tests Blood tests: Antiphospholipid antibodies (lupus anticoagulant, anti-β2-glycoprotein I) Inflammatory markers (ESR, CRP) for vasculitis8. Cryoglobulins, complement levels Imaging: Echocardiography (valvular abnormalities, vegetations)4. CT/MRI angiography (aortic plaque, vasculitis)8. Skin biopsy: Deep biopsy may show vascular occlusion (e.g., cholesterol clefts, thrombus) 3. Management APS: Anticoagulation (warfarin with INR 2–3) Cholesterol emboli: Statins, avoid anticoagulants (may worsen embolization) Vasculitis: Immunosuppressants (e.g., glucocorticoids, cyclophosphamide) Endocarditis: IV antibiotics ± valve surgery 4. Prognosis Benign LR (e.g., cutis marmorata) resolves with warmin. Secondary LR carries risks of thromboembolism, organ ischemia, or stroke

Answer 56

1. Indications for PCI (NICE CG172 & NG185) A. Stable Coronary Artery Disease (SCAD) PCI recommended for: ✅ Symptomatic angina refractory to optimal medical therapy. ✅ Objective evidence of ischemia (e.g., positive stress test, FFR ≤0.80). Not routinely recommended for: ❌ Asymptomatic patients without proven ischemia. ❌ Low-risk lesions (FFR >0.80). B. Acute Coronary Syndromes (ACS) a) ST-Elevation Myocardial Infarction (STEMI) Primary PCI is the preferred reperfusion strategy (if available within 120 mins of diagnosis). If PCI unavailable within 120 mins → thrombolysis + urgent transfer for PCI. b) Non-ST-Elevation ACS (NSTEMI/unstable angina) Early PCI (within 72 hrs) recommended for: ✅ High-risk features (elevated troponin, GRACE score >140, dynamic ECG changes). ✅ Refractory symptoms. 2. PCI Techniques & Stents (NICE TA668 & TA669) A. Stent Types Drug-eluting stents (DES) preferred over bare-metal stents (BMS) in most cases. Bioresorbable scaffolds (e.g., Absorb) not recommended due to higher thrombosis risk. B. Adjunctive Therapies Dual antiplatelet therapy (DAPT) post-PCI: Minimum 6 months for stable CAD. 12 months for ACS (consider longer in high-risk cases). 3. Non-Invasive Testing Pre- & Post-PCI (NICE NG185) A. Pre-PCI Assessment First-line: Coronary CT angiography (CCTA) if low-to-intermediate CAD probability. Inconclusive CCTA? → Stress imaging (MRI/PET/SPECT) or invasive angiography. B. Post-PCI Monitoring Routine non-invasive testing not needed if asymptomatic. If symptoms recur: Repeat CCTA or functional ischemia testing. 4. When to Choose PCI vs. CABG (NICE NG185) Scenario PCI Preferred CABG Preferred 1-vessel disease Yes (if ischemia present) No Multivessel disease If SYNTAX score ≤22 If SYNTAX score ≥23 Left main disease If SYNTAX score ≤32 If SYNTAX score ≥33 5. Cost-Effectiveness (NICE TA Assessment) PCI is cost-effective for: Symptomatic angina with ischemia. STEMI (vs. thrombolysis). Not cost-effective for: Low-risk stable CAD without symptoms. 6. Key NICE Recommendations Summary ✔ PCI is first-line for STEMI (if timely access). ✔ DES over BMS in most cases. ✔ CCTA first for stable CAD diagnosis before invasive angiography. ✔ DAPT duration depends on clinical scenario (6–12+ months).

Answer 57

an angiotensin-converting enzyme (ACE) inhibitor. It works by blocking a substance in the body that causes blood vessels to tighten. As a result, ramipril relaxes the blood vessels. This lowers blood pressure and increases the supply of blood and oxygen to the heart Ramipril works by: Inhibiting ACE, preventing the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to: Vasodilation, reducing blood pressure. Decreased aldosterone secretion, reducing sodium and water retention. Increasing bradykinin levels (due to ACE inhibition), which contributes to vasodilation but may also cause side effects like a dry cough Pharmacokinetics Absorption: ~50-60% bioavailability; absorption is slowed by food but not reduced 36. Metabolism: Converted in the liver to its active form, ramiprilat (6x more potent than ramipril) 56. Half-life: Ramiprilat has a triphasic elimination: Initial phase: 2–4 hours (distribution). Intermediate phase: 9–18 hours (free drug clearance). Terminal phase: >50 hours (ACE-bound drug clearance). Excretion: Primarily renal (60%) and fecal (40%) Contraindications Pregnancy (risk of fetal harm, especially in 2nd/3rd trimester) History of ACE inhibitor-induced angioedema Concomitant use with aliskiren (in diabetics or renal impairment) or sacubitril/valsartan Drug Interactions NSAIDs (e.g., ibuprofen): Reduce antihypertensive effect and increase kidney risk Diuretics: Increase risk of hypotension Potassium supplements/K+-sparing diuretics: Risk of hyperkalemia Key Considerations Monitor: Blood pressure, renal function, potassium levels Pregnancy: Switch to safer alternatives (e.g., methyldopa) if planning pregnancy Black Box Warning: Fetal toxicity if used during pregnancy

Answer 58

a persistent opening between the two major blood vessels leading from the heart Treatment Options: Medication: Medications like indomethacin or ibuprofen can help close the PDA by reducing prostaglandin production, which keeps the ductus open. Catheter-Based Procedures: A long, thin tube (catheter) can be inserted into a blood vessel and guided to the PDA, where a device can be placed to close it. Surgical Closure:

Answer 59

general requirements Blood Pressure Limit: Must be ≤180/100 mmHg (persistent readings above this disqualify until controlled) Ejection Fraction (EF): Must be ≥40% for HGV licensing post-cardiac events Exercise Tolerance Test (ETT): Required for angina, heart attacks, or coronary interventions (must complete 9 minutes on a treadmill) 2. Restrictions by Cardiac Condition A. Angina Must notify DVLA (form VOCH1 Driving ban if symptoms occur: At rest With emotion While driving Relicensing possible after 6 weeks symptom-free + passing ETT B. Heart Attack (Acute Coronary Syndrome, ACS) Immediate driving ban (minimum 6 weeks) Additional requirements: EF ≥40% (confirmed by echocardiogram). Successful Exercise ECG (9-minute treadmill test) If treated with PCI (stent): May resume after 6 weeks if stable. C. Coronary Artery Bypass Graft (CABG) Ban for 3 months post-surgery Relicensing requires: EF ≥40%. Successful ETT D. Arrhythmias (Including Atrial Fibrillation) Must notify DVLA if symptomatic (dizziness, fainting) Ban until controlled for 3 months (with EF ≥40%) Catheter ablation: 2-week ban for simple ablations. 3-month ban for VT ablation E. Pacemakers & ICDs Pacemaker: 6-week ban post-implant (must notify DVLA) Implantable Cardioverter Defibrillator (ICD): Permanent ban for HGV driving (regardless of reason for implant) F. Heart Failure EF must be ≥40% to retain HGV licence If EF <40%, licence revoked until improvement

Answer 60

third-degree atrioventricular (AV) block, is diagnosed on an electrocardiogram (ECG) by the complete absence of conduction between the atria and ventricles ECG is characterized by: Independent atrial and ventricular activity. More P waves than QRS complexes. Variable PR interval. Regular P-P and R-R intervals. Narrow or wide QRS complexes depending on the location of the block with slower ventricular rates and AV dissociation (atria and ventricles beating independently), the intensity of S1 can be diminished or become variable. If the escape rhythm originates below the AV node, the QRS complex will be wider, and the heart rate slower, potentially leading to more pronounced variations in S1

Answer 61

the most common type of primary cardiac tumor, and it's a benign tumor that typically develops in the left atrium of the heart. gelatinous and pedunculated, often grow from the septum (the wall separating the left and right atria) and can interfere with heart function. The main complications associated with atrial myxomas include mitral valve obstruction, embolization (tumor fragments traveling in the bloodstream), and constitutional symptoms like fever and fatigue.

Answer 62

1. DAPT (ticagrelor + aspirin) for 12 months is the gold standard 2. Beta-blockers and ACEIs/ARBs improve survival, especially in LV dysfunction 610. - Indicated for all STEMI patients unless contraindicated (e.g., severe bradycardia, cardiogenic shock, asthma) - Duration: Lifelong in heart failure; otherwise, ≥12 months 3. High-intensity statins are mandatory for secondary prevention - Goal: LDL <1.8 mmol/L (<70 mg/dL), Lifelong therapy with periodic lipid monitoring 4. MRAs benefit high-risk patients with reduced LVEF - Eplerenone or spironolactone for patients with LVEF ≤40% + heart failure or diabetes, Monitor potassium (risk of hyperkalemia, especially with ACEIs/ARBs) Lifestyle modifications (smoking cessation, exercise, Mediterranean diet) are equally critical Additional Considerations SGLT2 Inhibitors (e.g., empagliflozin): Consider in STEMI patients with heart failure or diabetes to reduce hospitalization Anticoagulants: Reserved for atrial fibrillation or LV thrombus (warfarin or DOACs)

Answer 63

Immediate Assessment & Reperfusion Therapy Eligibility for reperfusion: Assess immediately for primary PCI or fibrinolysis, regardless of age, sex, or ethnicity Primary PCI preferred: If presentation is within 12 hours of symptom onset and PCI can be delivered within 120 minutes of when fibrinolysis could have been given Radial access is preferred over femoral for angiography/PCI Fibrinolysis alternative: Offer if PCI cannot be delivered within 120 minutes of eligibility Follow with ECG at 60–90 mins; if reperfusion fails, proceed to emergency angiography Pharmacological Management Aspirin: 300 mg loading dose ASAP unless contraindicated Dual Antiplatelet Therapy (DAPT) for PCI: Prasugrel + aspirin (first-line unless high bleeding risk or on anticoagulants) Clopidogrel + aspirin if on anticoagulants or aged ≥75 with bleeding risk Antithrombin therapy during PCI: Unfractionated heparin + bailout GPIIb/IIIa inhibitors (radial access) Bivalirudin considered for femoral access Revascularization Strategies Complete revascularization: Recommended for multivessel disease without cardiogenic shock (preferably during index admission) Culprit-only PCI: Preferred for cardiogenic shock patients Drug-eluting stents (DES): First choice if stenting is indicated

Answer 64

a type of pulse waveform characterized by two distinct peaks during systole, separated by a small dip Characteristics of a Bisferiens Pulse: Two systolic peaks, Mid-systolic dip, Best felt in peripheral arteries, Associated with aortic valve disease Common Causes of a Bisferiens Pulse: Severe aortic regurgitation: A major cause, where the aortic valve leaks blood back into the heart during diastole, leading to the second pulse peak. Combined aortic stenosis and regurgitation: Aortic stenosis (narrowing of the valve) can also contribute to the double pulse. Hypertrophic cardiomyopathy: A condition where the heart muscle thickens, potentially causing outflow obstruction and a bisferiens pulse.

Answer 65

Hypothermia is defined as a core body temperature of < 35 °C [degrees centigrade]: Mild hypothermia is 32-35 °C Moderate hypothermia is 29-32 °C Severe hypothermia is < 29 °C Bradyarrhythmias (see below) Osborne Waves (= J waves) Prolonged PR, QRS and QT intervals Shivering artefact Ventricular ectopics Cardiac arrest due to VT, VF or asystole Bradycardia is a common finding in hypothermia Sinus bradycardia (may be marked) Atrial fibrillation with slow ventricular response Slow junctional rhythms Varying degrees of AV block (1st-3rd)

Answer 66

Negative Vasodilator Response: A negative vasodilator response in PH, particularly idiopathic pulmonary arterial hypertension (IPAH), indicates that the pulmonary vasculature is not responsive to the effects of vasodilators, such as calcium channel blockers (CCBs oral phosphodiesterase-5 (PDE5) inhibitors or endothelin receptor antagonists (ERAs), or considered for other therapies like intravenous prostacyclin or lung transplant

Answer 67

a combination of medications, and potentially a procedure like percutaneous coronary intervention (PCI). Pain Relief: Morphine or fentanyl for pain control, and nitroglycerin for angina. Antiplatelet Therapy: Aspirin and often a second antiplatelet agent like clopidogrel, ticagrelor, or prasugrel. The choice depends on the patient's risk of bleeding and the planned intervention. Anticoagulation: Antithrombin therapy with fondaparinux or heparin is usually given, unless immediate coronary angiography is planned or there's a high bleeding risk. Oxygen:

Answer 68

1. Immediate Management A. Anti-Ischemic Therapy Oxygen: Administer only if SpO₂ <90% or signs of respiratory distress (avoid routine use) Nitroglycerin: Sublingual or IV for persistent chest pain (avoid in hypotension or right ventricular infarction) Morphine: Reserved for refractory pain (use cautiously due to association with worse outcomes) B. Antiplatelet Therapy Aspirin: 162–325 mg chewed at diagnosis (non-enteric coated for faster absorption) P2Y12 Inhibitors: First-line: Ticagrelor (180 mg LD, 90 mg BD) or Prasugrel (60 mg LD, 10 mg daily) if PCI planned (avoid prasugrel in prior stroke/TIA) Clopidogrel (600 mg LD, 75 mg daily) if high bleeding risk or contraindications to ticagrelor/prasugrel. GP IIb/IIIa Inhibitors: Restricted to high-risk PCI with thrombotic complications (e.g., no-reflow) C. Anticoagulation Enoxaparin (preferred) or unfractionated heparin (UFH) for early invasive strategy Bivalirudin: Alternative for PCI, especially in high bleeding risk 2. Invasive vs. Conservative Strategy A. Early Invasive Strategy (Within 24–48 Hours) Indications: GRACE score >140, dynamic ST changes, or elevated troponin Hemodynamic instability or refractory angina Radial Access: Preferred over femoral to reduce bleeding Intracoronary Imaging: Class I recommendation for IVUS/OCT in complex lesions (e.g., left main disease) B. Ischemia-Guided Therapy Reserved for low-risk patients (GRACE score ≤140, no ECG changes) Includes stress testing or CT angiography (CCTA) for diagnosis

Answer 69

Definite Infective Endocarditis Pathologic confirmation: Microorganisms identified in vegetations, cardiac tissue, or emboli (via culture, PCR, or histopathology) OR histologic evidence of active endocarditis (e.g., vegetations with inflammation) **Clinical confirmation:** 2 major criteria - OR 1 major + 3 minor criteria - OR 5 minor criteria Possible Infective Endocarditis - - 1 major + 1 minor criterion - OR 3 minor criteria Rejected Diagnosis - Firm alternate diagnosis (e.g., sepsis, non-infective thrombotic endocarditis) - OR resolution of symptoms with <4 days of antibiotics - OR no pathologic evidence at surgery/autopsy Major Criteria A, B, C A. Microbiological Positive blood cultures for typical IE organisms: ≥2 separate sets for S. aureus, viridans streptococci, HACEK group, Enterococcus faecalis ≥3 sets for atypical organisms (e.g., Corynebacterium, Candida) Serologic/PCR evidence of Coxiella burnetii (Q fever), Bartonella spp., or Tropheryma whipplei B. Imaging Echocardiography or cardiac CT showing: Vegetations, abscess, perforation, fistula, or prosthetic valve dehiscence New valvular regurgitation (worsening of preexisting insufficiency is insufficient) 18F-FDG PET/CT: Abnormal metabolic activity in prosthetic valves (>3 months post-implant) or CIED leads C. Surgical Direct visualization of IE during cardiac surgery 3. Minor Criteria - 6 1. Predisposing conditions: Prosthetic valve, congenital heart disease, IV drug use, prior IE, CIEDs 2. Fever >38°C (100.4°F) 4. 3. Vascular phenomena: Septic emboli, Janeway lesions, conjunctival hemorrhages, mycotic aneurysm 4. Immunologic phenomena: Glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor 5. Microbiologic evidence (not meeting major criteria): Single positive blood culture for typical IE organisms 6. FDG-PET/CT (within 3 months of prosthetic valve implantation)

Answer 70

A. Dual Antiplatelet Therapy (DAPT) Duration: 12 months (default) with aspirin + ticagrelor/prasugrel Shorten to 3–6 months if high bleeding risk (e.g., PRECISE-DAPT score ≥25) De-escalation: Switch to clopidogrel after 1 month if tolerated B. Lipid Management High-intensity statin (e.g., atorvastatin 80 mg) for all patients Add non-statin agents (ezetimibe, PCSK9 inhibitors) if LDL ≥70 mg/dL despite statins C. Other Key Therapies Beta-blockers: Start within 24 hours unless contraindicated (e.g., cardiogenic shock) ACEi/ARBs: Indicated for LVEF ≤40%, hypertension, or diabetes MRAs (eplerenone/spironolactone): For LVEF ≤40% + heart failure symptoms Special Populations Chronic Kidney Disease: Reduce enoxaparin/UFH doses; avoid prasugrel Atrial Fibrillation: Use NOAC + clopidogrel (avoid triple therapy beyond 1 week) Cancer Patients: Individualize antiplatelet duration based on bleeding/ischemic risk

Answer 71

1. Mechanical Valves Composition Made of carbon-coated titanium or pyrolytic carbon (e.g., St. Jude Medical, On-X). Advantages Durability: Lasts 20–30+ years (lifelong in most patients). Lower reoperation risk: Ideal for younger patients (<50–60 years). Disadvantages Mandatory lifelong anticoagulation: Warfarin (INR 2.5–3.5 for mitral, 2.0–3.0 for aortic). Direct oral anticoagulants (DOACs) contraindicated (risk of valve thrombosis). Bleeding risk: Annual risk of major bleeding (1–2%) and thromboembolism (0.5–2%). Valve noise: Audible clicking in some patients. Best For Patients <50–60 years without high bleeding risk. Those already on anticoagulation (e.g., for atrial fibrillation). 2. Bioprosthetic Valves Composition Animal tissue (porcine/bovine pericardium) or human homografts. Advantages No long-term anticoagulation: Aspirin/clopidogrel suffices after 3–6 months of warfarin (if no other indications). Lower bleeding risk: Avoids warfarin-related complications. Silent operation: No audible valve sounds. Disadvantages Structural valve deterioration (SVD): 10–15 years lifespan (shorter in younger patients). Higher reoperation risk (20–30% at 15 years). Early degeneration risk: Accelerated in <50-year-olds, dialysis patients, or hypercalcemia. Best For Patients >65–70 years (ESC: >60 for aortic, >65 for mitral). Those with high bleeding risk or contraindications to anticoagulation. Young patients wanting pregnancy (temporary anticoagulation possible).

Answer 72

A. Causes Degenerative calcific AS (most common in elderly): Age-related thickening/calcification of a trileaflet valve (50–70% of cases) Risk factors: Hypertension, dyslipidemia, diabetes, CKD, smoking Congenital bicuspid aortic valve (30–40% of cases): Presents earlier (ages 50–70) due to accelerated calcification Associated with aortic dilation/dissection Rheumatic AS (rare in developed countries): Commissural fusion + mitral valve involvement 2. Pathophysiology Mechanical obstruction → Increased LV pressure → Concentric hypertrophy (compensatory phase). Over time: LV diastolic dysfunction (stiffness) → Pulmonary hypertension. Myocardial ischemia (O₂ demand-supply mismatch) → Angina. Low cardiac output → Syncope, fatigue Heyde syndrome: GI bleeding due to acquired von Willebrand factor deficiency 3. Symptoms & Signs Classic Triad (SAD): Syncope (exertional, due to fixed CO + vasodilation). Angina (LV hypertrophy + coronary compression). Dyspnea (heart failure) Physical Exam: Pulsus parvus et tardus (weak, delayed carotid pulse). Crescendo-decrescendo ejection murmur (louder at R 2nd ICS, radiates to carotids). Gallavardin phenomenon: High-pitched murmur at apex mimicking MR 4. Diagnosis Echocardiography (Gold Standard) Severity Peak Velocity (m/s) Mean Gradient (mmHg) Valve Area (cm²) Mild 2.0–2.9 <20 >1.5 Moderate 3.0–3.9 20–40 1.0–1.5 Severe ≥4.0 ≥40 <1.0 Very Severe ≥5.0 ≥60 <0.6 Low-flow, low-gradient AS: AVA <1 cm² but gradient <40 mmHg (assess with dobutamine stress echo or CT calcium scoring) Additional Tests: Cardiac CT: Aortic valve calcium score (>2000 AU in men, >1300 AU in women suggests severe AS) Exercise testing: Contraindicated in symptomatic AS but useful in unmasking symptoms in asymptomatic patients 5. Treatment A. Medical Therapy No pharmacotherapy slows progression Hypertension management: ACEi/ARBs cautiously in severe AS B. Definitive Treatment: Valve Replacement Indications for Intervention : Symptomatic severe AS (Class I). Asymptomatic severe AS + LVEF <50% (Class I). Asymptomatic severe AS + abnormal exercise test (e.g., hypotension). Options: Surgical AVR (SAVR): Preferred for low-risk patients (<75 years, no comorbidities). Mechanical valves: Lifelong anticoagulation (warfarin). Bioprosthetic valves: Avoid anticoagulation but limited durability (10–15 years) Transcatheter AVR (TAVI): Preferred for high-risk/prohibitive surgical risk (STS score >8%, age >80). Expanding to intermediate-risk patients with comparable outcomes to SAVR 6. Prognosis Asymptomatic severe AS: 5-year survival ~50% Symptomatic severe AS: 2-year mortality >50% without intervention Post-AVR survival matches age-matched controls

Answer 73

Atrial flutter (AFL) is a macroreentrant atrial tachycardia characterized by organized, rapid atrial contractions (typically 250–350 bpm) with variable ventricular response. A. Mechanism Reentry circuit: Most commonly involves the cavotricuspid isthmus (CTI) in the right atrium (typical AFL). Atypical AFL: Non-CTI circuits (e.g., scar-related post-ablation or post-cardiac surgery). B. Types Type Circuit Location ECG Features Typical AFL Cavotricuspid isthmus Sawtooth P-waves (inferior leads II/III/aVF), atrial rate ~300 bpm Atypical AFL Left atrium/scar-related Variable P-wave morphology, irregular atrial rate 2. Clinical Presentation Symptoms: Palpitations, fatigue, dyspnea, chest pain, or syncope (if 1:1 conduction). Asymptomatic: Common in controlled ventricular rates (e.g., 2:1 or 4:1 block). Complications: Thromboembolism (stroke risk similar to AF). Tachycardia-induced cardiomyopathy (if untreated). 3. Diagnosis A. ECG Findings Classic sawtooth "F-waves" (best seen in II/III/aVF). Regular atrial rate ~300 bpm with fixed or variable AV block (e.g., 2:1, 4:1). QRS typically narrow (unless pre-existing BBB). B. Additional Workup Transesophageal echocardiogram (TEE): If thrombus suspected before cardioversion. Holter monitor: For paroxysmal AFL. Electrophysiology study (EPS): For definitive diagnosis/ablation planning. 4. Acute Management A. Rate Control First-line: Beta-blockers (metoprolol) or non-DHP CCBs (diltiazem). Avoid AV nodal blockers if pre-excitation (WPW) present (risk of VF). B. Rhythm Control Electrical cardioversion (synchronized 50–100J): Preferred for unstable patients (e.g., hypotension, HF). Pharmacologic cardioversion: Ibutilide (most effective, but QT prolongation risk). Dofetilide (requires monitored initiation). C. Anticoagulation Same stroke risk as AF → Use CHA₂DS₂-VASc score to guide therapy. If cardioversion planned: ≥48h duration or unknown: Anticoagulate × 3 weeks pre/post or rule out thrombus via TEE. NOACs preferred over warfarin (ESC 2024). 5. Long-Term Management A. Catheter Ablation (First-line for recurrent AFL) Typical AFL: CTI ablation (success rate >95%). Atypical AFL: Requires 3D mapping (success rate ~70–80%). B. Antiarrhythmics Second-line if ablation contraindicated: Class III (sotalol, dofetilide) or Class IC (flecainide, propafenone) + AV nodal blocker. C. Anticoagulation Permanent anticoagulation if CHA₂DS₂-VASc ≥2 (same as AF).

Answer 74

a selective If channel inhibitor used primarily for heart rate reduction in conditions like chronic heart failure (HF) and stable angina pectoris. 2. Approved Indications A. Chronic Heart Failure (HFrEF) FDA/ESC indications: Symptomatic HF (NYHA II-IV) with LVEF ≤35%. Sinus rhythm + resting HR ≥70 bpm, despite maximal beta-blocker therapy (or if beta-blockers are contraindicated) Reduces HF hospitalizations by 26% (SHIFT trial) B. Stable Angina Pectoris Alternative for patients intolerant to beta-blockers or with inadequate HR control (HR ≥70 bpm) Non-inferior to atenolol/amlodipine in improving exercise tolerance (INITIATIVE trial) 3. Pharmacokinetics Bioavailability: ~40% (increased by 20–30% with food) Metabolism: Hepatic (CYP3A4) → active metabolite N-desmethyl ivabradine Half-life: 2–11 hours (dosed twice daily). Excretion: Urine (4% unchanged) + feces 5. Adverse Effects Common (≥1%) Serious (Rare) Phosphenes (14.5%) Symptomatic bradycardia Bradycardia (5%) Atrial fibrillation (↑24% risk vs placebo) Dizziness/Headache AV block (if predisposed) Blurred Vision QT prolongation (uncorrected) 6. Key Clinical Trials Trial Population Outcome SHIFT (2010) HFrEF (HR ≥70 bpm) ↓26% HF hospitalizations BEAUTIFUL CAD + LV dysfunction ↓MI in HR >70 bpm subgroup SIGNIFY Stable CAD (no HF) No mortality benefit; ↑AF risk 7. Contraindications & Interactions Absolute: Sick sinus syndrome, severe hepatic impairment, CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin) Relative: Concomitant verapamil/diltiazem (↑bradycardia risk) Grapefruit juice (↑ivabradine levels) 6.

Answer 75

Statins are HMG-CoA reductase inhibitors, the first-line treatment for lowering LDL cholesterol and reducing cardiovascular (CV) risk. They are widely used for primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD). Mechanism of Action Inhibit HMG-CoA reductase, blocking cholesterol synthesis in the liver. Increase LDL receptor expression → enhanced LDL clearance from blood. Have pleiotropic effects (anti-inflammatory, plaque stabilization). Indications for Statin Therapy Primary Prevention High-risk individuals (10-year ASCVD risk ≥10%) Diabetes (type 2 with risk factors, or type 1 with complications) Chronic kidney disease (CKD) (eGFR <60 mL/min) Familial hypercholesterolemia (FH) Secondary Prevention Established ASCVD (CAD, stroke/TIA, PAD) Post-revascularization (PCI, CABG) 3. Types of Statins & Potency Statin LDL Reduction Dosing Notes Atorvastatin ~50-60% 10-80 mg OD First-line, long half-life Rosuvastatin ~50-65% 5-40 mg OD Strongest potency Simvastatin ~30-50% 10-40 mg OD Avoid >20 mg with amlodipine Pravastatin ~20-30% 10-40 mg OD Fewer drug interactions Fluvastatin ~20-30% 20-80 mg OD Less potent 4. NICE & ESC/EAS Guidelines (2023-2024) NICE (UK) Recommendations Primary prevention: Offer atorvastatin 20 mg if QRISK2 ≥10%. Secondary prevention: Atorvastatin 80 mg (unless contraindicated). Diabetes: Consider if QRISK ≥10% or CKD. ESC/EAS (European) Guidelines Very high-risk (ASCVD, FH, diabetes + organ damage): LDL-C target <1.4 mmol/L (<55 mg/dL). High-risk: LDL-C <1.8 mmol/L (<70 mg/dL). Use high-intensity statins first (atorva/rosuva), add ezetimibe or PCSK9i if needed. 5. Side Effects & Monitoring Common Side Effects Myalgia (~5-10%, rarely severe) Elevated liver enzymes (ALT >3× ULN in ~1%) Increased blood sugar (small diabetes risk) Rare but Serious Rhabdomyolysis (CK >10× ULN + myoglobinuria) Hepatotoxicity (discontinue if ALT >3× ULN) Monitoring Baseline LFTs & CK (before starting). Repeat LFTs at 3 months, then annually. Check LDL-C at 3 months (adjust dose if needed). 6. Drug Interactions Avoid with CYP3A4 inhibitors (e.g., clarithromycin, azoles, grapefruit juice) → ↑ statin toxicity. Gemfibrozil (↑ myopathy risk). Amiodarone, verapamil, diltiazem (↑ simvastatin toxicity). 7. Alternatives if Statin-Intolerant Ezetimibe (monotherapy or combo). PCSK9 inhibitors (alirocumab, evolocumab). Bempedoic acid (newer, less myopathy risk).

Answer 76

cause hypokalemia (low potassium levels) primarily through two mechanisms: increasing sodium delivery to the distal tubule, which stimulates potassium secretion, and stimulating the renin-angiotensin-aldosterone system, leading to increased aldosterone levels, which also promotes potassium excretion. 1. Increased Sodium Delivery to the Distal Tubule: Thiazide diuretics block the sodium-chloride transporter in the distal convoluted tubule, leading to a higher concentration of sodium in the tubular fluid reaching the distal tubule. This increased sodium delivery to the distal tubule acts as a stimulus for the sodium-potassium exchange pump, leading to an increased excretion of potassium in the urine. 2. Renin-Angiotensin-Aldosterone System (RAAS) Activation: Thiazide diuretics can reduce blood volume and blood pressure, which activates the RAAS. This activation leads to increased aldosterone secretion. Aldosterone promotes sodium reabsorption and potassium excretion in the collecting duct of the nephron, further contributing to potassium loss and hypokalemia. 3. Other Contributing Factors: Lowered Luminal Calcium Concentration: Thiazides can lower the luminal calcium concentration in the distal tubules, which can activate epithelial sodium channels and promote potassium secretion, Flow-Sensitive Maxi-K Channels: Thiazides can also enhance potassium secretion by activating flow-sensitive maxi-K channels, which are distinct from the K secretory channels described above

Answer 77

A C X V Y. It stands for: A wave (atrial contraction), C wave (ventricular contraction), X descent (atrial relaxation), V wave (atrial venous filling), and Y descent (atrial emptying). Here's a more detailed breakdown: A wave: Represents the peak of atrial contraction, which pushes blood into the ventricles. C wave: Corresponds to the bulging of the tricuspid valve during ventricular contraction. X descent: Marks the rapid descent of the waveform as the atria relax. V wave: Reflects the maximum filling of the atria with venous blood. Y descent: Indicates the opening of the tricuspid valve and the emptying of the atria into the ventricles.

Answer 78

Statin-induced myopathy is a spectrum of muscle-related adverse effects caused by statins, ranging from mild myalgia to life-threatening rhabdomyolysis. It is the most common reason for statin discontinuation, affecting 5–30% of patients in clinical practice, though severe cases are rare 2. 1. Types of Statin-Induced Myopathy Statin-associated muscle symptoms (SAMS) are classified by severity: Myalgia: Muscle pain, stiffness, or weakness without significant creatine kinase (CK) elevation (<3× ULN). Myositis: Muscle inflammation with CK 3–10× ULN Rhabdomyolysis: Severe muscle breakdown with CK >10× ULN, myoglobinuria, and risk of acute kidney injury (incidence: ~1 in 100,000) 2. Mechanisms of Myopathy The exact cause is multifactorial, but proposed mechanisms include: Mitochondrial dysfunction: Statins reduce coenzyme Q10 (ubiquinone), impairing energy production Calcium dysregulation: Statins disrupt sarcoplasmic reticulum calcium release, leading to muscle injury Isoprenoid depletion: Reduced geranylgeranyl pyrophosphate (GGPP) and farnesyl pyrophosphate (FPP) disrupt muscle cell signaling Autoimmune myositis: Rarely, statins trigger anti-HMG-CoA reductase antibodies, causing necrotizing autoimmune myopathy (NAM) 3. Risk Factors Patient-Related Demographics: Older age (>80), female sex, low BMI Comorbidities: Hypothyroidism, diabetes, CKD, liver disease Lifestyle: Heavy alcohol use, vigorous exercise, grapefruit juice (inhibits CYP3A4) Drug-Related High-dose statins (e.g., simvastatin 80 mg) Drug interactions: CYP3A4 inhibitors (e.g., macrolides, antifungals, amiodarone), fibrates (especially gemfibrozil) 4. Diagnosis Clinical evaluation: Symmetrical proximal muscle pain (thighs, shoulders) Lab tests: CK levels (if >10× ULN, rule out rhabdomyolysis) Myoglobinuria (dark urine) in severe cases Anti-HMG-CoA reductase antibodies (if NAM suspected) Dechallenge/rechallenge: Symptoms resolve after stopping statins and recur upon reintroduction 5. Management Mild to Moderate SAMS Statin switch: Replace with lower-dose rosuvastatin or pravastatin (less myotoxic) Alternate-day dosing: Effective for statins with long half-lives (e.g., atorvastatin, rosuvastatin) Coenzyme Q10 supplementation: Evidence is mixed, but may help some patients Severe SAMS (Rhabdomyolysis or NAM) Immediate statin discontinuation IV hydration for rhabdomyolysis to prevent renal failure Immunosuppressants (e.g., corticosteroids, IVIG) for NAM Non-Statin Alternatives Ezetimibe: Lowers LDL by 15–20% PCSK9 inhibitors (e.g., alirocumab, evolocumab): For high-risk patients Bempedoic acid: Less myotoxic (activated only in the liver) 6. Prevention Avoid high-risk combinations (e.g., simvastatin + gemfibrozil) Monitor CK in high-risk patients (baseline + symptomatic) Encourage moderate exercise: Paradoxically, light exercise may reduce statin myopathy risk

Answer 79

Stent Thrombosis: This is a serious complication where a blood clot forms within the stent, potentially blocking blood flow and leading to a heart attack. Acute Thrombosis: Occurs within the first 24 hours after stent placement. Subacute Thrombosis: Happens between 24 hours and one month after placement. Late Stent Thrombosis: Develops between one and twelve months after placement. Very Late Stent Thrombosis: Occurs after one year of stent placement. Restenosis: This refers to the re-narrowing or blockage of the artery where the stent was placed. It can occur within the first three to twelve months after stenting. Pathology of Early Complications: Early complications like thrombosis involve platelet and fibrin deposition, often near areas of strut injury or incomplete endothelial coverage. Pathology of Late Complications: Late complications like delayed healing, neoatherosclerosis, and late stent thrombosis are linked to factors like persistent fibrin, inflammatory cell infiltration, and incomplete endothelialization.

Answer 80

Chronic Inflammation: Long-term exposure to irritants This inflammation involves various cells, including neutrophils, macrophages, and lymphocytes, which release inflammatory mediators. The inflammatory process leads to increased mucus production, airway thickening, and damage to the lung tissue. 2. Airway Remodeling and Narrowing: 3. Emphysema (Alveolar Destruction): 4. Reduced Gas Exchange: 5. Systemic Effects: Spirometry (Gold Standard) Post-bronchodilator FEV₁/FVC <0.7 confirms persistent airflow obstruction Severity staging (GOLD criteria): GOLD 1 (Mild): FEV₁ ≥80% predicted GOLD 2 (Moderate): 50%≤ FEV₁ <80% GOLD 3 (Severe): 30%≤ FEV₁ <50% GOLD 4 (Very severe): FEV₁ <30% Additional Tests CXR/CT: Hyperinflation, flattened diaphragms, bullae (emphysema) ABG: Assess for hypoxemia/hypercapnia (late disease) α₁-antitrypsin testing (if early-onset/family history) 4. Management (GOLD 2024 Guidelines) A. Non-Pharmacologic Smoking cessation (most effective intervention) Pulmonary rehabilitation (improves symptoms/exercise capacity) Vaccinations (Influenza, pneumococcal, COVID-19) Long-term oxygen (if PaO₂ ≤55 mmHg or ≤59 mmHg + cor pulmonale) B. Pharmacologic Therapy Drug Class Examples Role SABA Salbutamol PRN relief LAMA Tiotropium 1st-line maintenance LABA Salmeterol Combined with LAMA/LABA+ICS ICS Fluticasone For frequent exacerbations + high eosinophils PDE4 Inhibitor Roflumilast Severe COPD + chronic bronchitis Stepwise Approach: Group A (Few symptoms, low exacerbation risk): LAMA or LABA Group B (More symptoms, low risk): LAMA + LABA Group E (Frequent exacerbations): Eosinophils ≥300/μL: LAMA + LABA + ICS Eosinophils <300/μL: LAMA + LABA C. Exacerbation Management Acute bronchodilators (nebulized SABA + SAMA) Oral corticosteroids (prednisone 40mg ×5 days) Antibiotics (if purulent sputum; amoxicillin-clavulanate, doxycycline) NIV for acute hypercapnic respiratory failure 5. Complications Chronic respiratory failure → cor pulmonale Pneumothorax (ruptured bullae) Lung cancer (↑ risk in smokers) Depression/anxiety (common in advanced disease)

Answer 81

1. Lung Function: FEV1 The primary marker of COPD progression is the decline in FEV1 over time. FEV1/FVC Ratio: A ratio of less than 0.7 indicates airflow limitation. GOLD Stages: stage representing a different level of airflow obstruction and severity. 2. Patient-Reported Outcomes (PROs): Saint George's Respiratory Questionnaire (SGRQ): COPD Assessment Test (CAT): Another PRO measure that assesses the impact of COPD on daily life and well-being. 3. Exacerbations: Exacerbation Frequency: Exacerbation Severity: 4. Functional Measures: 6-Minute Walk Test (6MWD): Dyspnea: 5. Biomarkers: C-reactive protein (CRP) and Fibrinogen: Inflammatory Cytokines (IL-6, IL-8, TNF-α): Other potential biomarkers: 6. Imaging Markers: CT Emphysema Index: Bronchiectasis: The presence of widened airways on CT scans, which can indicate disease progression. Coronary Artery Calcification (CAC): 7. Clinical Signs and Symptoms: Chronic and progressive dyspnea, Chronic cough and sputum production, Wheezing and chest tightness, Increased fatigue and reduced exercise tolerance, Frequent or prolonged exacerbations Peak expiratory flow rate for mortality prediction

Answer 82

2. Pharmacotherapy for HFrEF (Reduced EF ≤40%) Core Drugs (Proven Mortality Benefit): ARNI (Sacubitril/Valsartan) First-line over ACEi/ARB (PARADIGM-HF trial). Start if stable on low-dose ACEi/ARB. Beta-Blockers (Bisoprolol, Carvedilol, Metoprolol succinate) Titrate to max tolerated dose. MRA (Spironolactone, Eplerenone) If EF ≤35% + symptoms (monitor K⁺/creatinine). SGLT2i (Dapagliflozin, Empagliflozin) Add regardless of diabetes (DAPA-HF, EMPEROR-Reduced). Add-On Therapies: Ivabradine: If HR >70 bpm on max beta-blocker. Hydralazine/ISDN: Black patients or intolerant to ACEi/ARB/ARNI. Diuretics (Loop diuretics, e.g., furosemide): For volume overload. 3. HFpEF (Preserved EF ≥50%) SGLT2i (Empagliflozin/Dapagliflozin) – 1st-line (EMPEROR-Preserved, DELIVER). Diuretics for congestion. Control comorbidities (HTN, AF, DM, obesity). Avoid routine use of beta-blockers/ACEi unless other indications. 4. Advanced HF Therapies CRT (if EF ≤35%, LBBB, QRS ≥150 ms). ICD (primary prevention if EF ≤35% despite 3 months of optimal meds). LVAD (bridge to transplant or destination therapy). Heart transplant (refractory HF). 5. Monitoring & Follow-Up BNP/NT-proBNP for prognosis/guiding therapy. Echo (repeat if clinical change). Telemonitoring (reduce readmissions). 6. Acute Decompensated HF Diuresis (IV furosemide ± thiazide for resistance). Vasodilators (Nitroglycerin/Nitroprusside if BP >110 mmHg). Inotropes (Dobutamine/Milrinone) if cardiogenic shock.

Answer 83

Clinical Assessment: Evaluate symptoms (e.g., intermittent claudication, critical limb ischemia), examine pulses, and check for ulcers or non-healing wounds Ankle-Brachial Pressure Index (ABI): Diagnostic if <0.90 Caution in diabetes: ABI may be falsely elevated; consider toe-brachial index or imaging if suspicion persists 2. Secondary Prevention Cardiovascular Risk Management: Statins: LDL goal <1.8 mmol/L Antihypertensives: ACE inhibitors/ARBs preferred (target BP <140/90 mmHg) Antiplatelets: Aspirin or clopidogrel for secondary prevention Lifestyle Modifications: Smoking cessation, weight management, and exercise 3. Management of Intermittent Claudication First-Line: Supervised exercise program: 2 hours/week for 3 months, encouraging exercise to maximal pain Second-Line: Naftidrofuryl oxalate: Consider if exercise fails and patient declines revascularization. Review after 3–6 months; discontinue if no benefit Revascularization: Angioplasty: Offered if exercise and medical therapy fail, and imaging confirms suitability Stents: Reserved for complete aorto-iliac occlusions (not stenosis) 4. Critical Limb Ischemia (CLI) Management Multidisciplinary Team Assessment: Essential before treatment decisions Revascularization: Angioplasty or bypass surgery: Choice depends on comorbidities, disease pattern, and patient preference Vein grafts preferred for infra-inguinal bypass Pain Management: Opioids (weak or strong) + adjuncts (e.g., laxatives) Refer to pain specialists if refractory 5. Follow-Up & Advanced Therapies Imaging: Duplex ultrasound first-line for revascularization planning; MRA/CTA if further detail needed Amputation: Last resort after revascularization options exhausted

Answer 84

1. Genetic Cause Microdeletion of ~26–28 genes (including ELN [elastin], LIMK1, GTF2IRD1, and GTF2I). ELN haploinsufficiency → vascular and connective tissue abnormalities. 2. Clinical Presentation Category Features Facial Dysmorphism - "Elfin" facies (short nose, wide mouth, full lips, stellate iris pattern) - Periorbital fullness, small jaw (micrognathia) Cardiovascular - Supravalvular aortic stenosis (SVAS, ~75%) - Peripheral pulmonary stenosis - Hypertension (due to vascular stiffness) Neurodevelopmental - Mild-to-moderate intellectual disability (IQ 50–70) - Strong verbal skills but poor visuospatial abilities (e.g., difficulty drawing) - Hypersociability (indiscriminate friendliness, lack of stranger anxiety) Growth & Endocrine - Prenatal/postnatal growth retardation - Hypercalcemia (infantile hypercalcemia, resolves with age) Other Features - Hoarse voice - Joint laxity, hernias - ADHD, anxiety, phobias (e.g., loud noises) Diagnosis Clinical suspicion (based on facial features + SVAS + developmental delay). Genetic testing (FISH, chromosomal microarray, or MLPA to detect 7q11.23 deletion). Management Issue Intervention Cardiovascular - Echo monitoring for SVAS - BP management - Surgery if severe stenosis Hypercalcemia - Low-calcium diet (infants) - Hydration, avoid vitamin D excess Developmental - Early speech/occupational therapy - Special education support Behavioral - Social skills training - Anxiety/ADHD management (behavioral therapy ± meds) Prognosis Life expectancy is near-normal if cardiac complications are managed. Adults often require support for independent living due to cognitive/behavioral challenges. Key Clinical Pearls "ELF" mnemonic for Williams syndrome: Elfin facies Learning disability (with strong language skills) Friendly personality

Answer 85

Congenital Heart Disease (CHD) Pulmonary Valve Stenosis (PVS): Most prevalent (40–70% of NS patients) Valve leaflets are often dysplastic (thickened/fused), reducing success rates of balloon valvuloplasty (65% require reintervention) Severity: Mild (60%, non-progressive), moderate (10%), or severe (30%, often needing surgery) Septal Defects: Atrial Septal Defect (ASD): 30–50% of cases, often with PVS Ventricular Septal Defect (VSD) and Atrioventricular Septal Defect (AVSD): Less common but associated with PTPN11 mutations Other CHD: Aortic coarctation (9%), mitral valve anomalies (6%), Tetralogy of Fallot (rare) B. Hypertrophic Cardiomyopathy (HCM) Occurs in 10–20% of NS patients, often infant-onset (more severe than non-syndromic HCM) Genotype links: RAF1 and RIT1 mutations: Strongly associated with HCM PTPN11 mutations: Rarely cause HCM but linked to PVS/ASD

Answer 86

Atrioventricular Septal Defect (AVSD) – ~40–45% Also called "Endocardial Cushion Defect" Complete AVSD (most common in DS): Single common AV valve + large ASD + VSD Leads to left-to-right shunting → pulmonary hypertension Partial AVSD (primum ASD + cleft mitral valve) Symptoms: Heart failure (tachypnea, poor feeding, failure to thrive) Recurrent lung infections Treatment: Surgical repair in infancy (before pulmonary hypertension worsens). 2. Ventricular Septal Defect (VSD) – ~30–35% Perimembranous VSD most common Small VSDs may close spontaneously; large ones require surgery. 3. Atrial Septal Defect (ASD) – ~10–15% Secundum ASD most frequent May be asymptomatic initially but can lead to right heart enlargement. 4. Patent Ductus Arteriosus (PDA) – ~5–10% Failure of ductus arteriosus to close after birth Can cause heart failure if large; treated with indomethacin or surgery. 5. Tetralogy of Fallot (TOF) – ~5% Less common in DS than in general CHD population Classic four features: VSD, overriding aorta, pulmonary stenosis, RV hypertrophy 6. Isolated Mitral Valve Abnormalities Cleft mitral valve (often with partial AVSD) May cause mitral regurgitation.

Answer 87

First-Degree AV Block Definition: PR interval > 200 ms (5 small ECG boxes) Every P wave is followed by a QRS, but conduction is delayed. Causes: Normal variant (athletes) Medications (beta-blockers, calcium channel blockers) Ischemia, myocarditis Symptoms: Usually asymptomatic (no treatment needed). Second-Degree AV Block A. Mobitz I (Wenckebach) Definition: Progressive PR prolongation until a P wave is not followed by QRS (dropped beat). "Longer, longer, longer, DROP!" Causes: Increased vagal tone (common in athletes) Inferior MI (RCA occlusion) Drugs (digoxin, beta-blockers) Symptoms: Often asymptomatic, but can cause dizziness. Mobitz II Definition: Sudden dropped QRS without prior PR prolongation. PR interval remains constant before the block. Causes: Anterior MI (LAD occlusion) Severe conduction system disease Symptoms: High risk of progressing to 3rd-degree block! May cause syncope, Stokes-Adams attacks. 1st Degree & Mobitz I: Observe unless symptomatic. Mobitz II & 3rd Degree: Permanent pacemaker required. Acute MI-related blocks: Inferior MI → Mobitz I (often resolves). Anterior MI → Mobitz II/3rd degree (bad prognosis, needs pacing).

Answer 88

Autosomal dominant (most common) with incomplete penetrance. Mutations in desmosomal genes: PKP2 (most common, ~40% of cases) DSP, DSG2, DSC2, JUP Recessive form (Naxos disease, with woolly hair & palmoplantar keratoderma). 2. Pathophysiology Desmosomal protein dysfunction → cardiomyocyte detachment → fibrofatty infiltration (mainly RV, but LV can be involved). Arrhythmias due to re-entry circuits in scarred tissue. ECG Findings - Epsilon wave (terminal notch in QRS, V1–V3) - T-wave inversions (V1–V3) - Ventricular tachycardia (LBBB morphology) Imaging - CMR (gold standard): RV dilatation/dysfunction, fatty infiltration - Echo: RV hypokinesis, aneurysms

Answer 89

Key Features of Takayasu Arteritis Demographics & Epidemiology Predominantly affects young women (typically under 50), with a female-to-male ratio of up to 9:1 in some populations. More common in individuals of Asian, Mexican, and Mediterranean descent Incidence is estimated at 1–3 cases per million per year, making it a rare disease Pathophysiology A granulomatous inflammatory process leads to thickening of arterial walls, fibrosis, and eventual stenosis or aneurysm formation Autoimmune mechanisms involving T-cell-mediated immunity (CD4+/CD8+ T cells) and cytokines (e.g., TNF-α, IL-6) play a role Symptoms Early phase (inflammatory): Fever, fatigue, weight loss, muscle aches, and malaise Late phase (vascular occlusion): Limb claudication (pain with activity) Absent or weak pulses (especially in arms) Blood pressure discrepancies between arms Hypertension (due to renal artery stenosis) Neurological symptoms (stroke, dizziness) from carotid or vertebral artery involvement Diagnosis Clinical suspicion in young patients with unexplained hypertension, vascular bruits, or pulse deficits. Imaging: CTA (Computed Tomography Angiography) is the gold standard for assessing vessel wall thickening and stenosis PET/CT detects metabolic activity in inflamed arteries, useful for early diagnosis and monitoring MRI/MRA avoids radiation and is useful for long-term follow-up Lab tests: Elevated CRP and ESR (though not always present) Treatment First-line: High-dose corticosteroids (e.g., prednisone 0.5–1 mg/kg/day) to induce remission Steroid-sparing agents: Conventional DMARDs (methotrexate, azathioprine, mycophenolate) Biologics (anti-TNF agents like infliximab/adalimumab, or IL-6 inhibitors like tocilizumab) for refractory cases Surgical/Endovascular intervention: Required for severe stenosis/aneurysms (e.g., bypass grafting, stenting) High restenosis rates with angioplasty alone Prognosis & Complications Chronic, relapsing disease with high rates of vascular complications (stroke, heart failure, renal failure). Relapse risk factors: Male sex, high CRP, and initial high disease activity (ITAS.A score ≥12) Long-term monitoring (imaging + labs) is essential Special Considerations Pediatric TAK: Similar features but may have delayed diagnosis; methotrexate is commonly used 3. Pregnancy: Requires careful management due to medication risks 7. Cardiac involvement: Aortic regurgitation, coronary artery disease, and myocarditis can occur 9.

Answer 90

1. Acute Coronary Syndromes (ACS) ST-Elevation Myocardial Infarction (STEMI) Immediate aspirin: A 300 mg loading dose should be given unless contraindicated (e.g., allergy) Dual Antiplatelet Therapy (DAPT) for PCI: Prasugrel + aspirin (preferred for primary PCI in patients <75 years without high bleeding risk) Clopidogrel + aspirin if oral anticoagulants are already used or in high-bleeding-risk patients Ticagrelor + aspirin as an alternative, especially for non-PCI-managed STEMI Fibrinolysis: Use if PCI cannot be delivered within 120 minutes, followed by antithrombin therapy (e.g., heparin) Non-ST-Elevation ACS (NSTEMI/Unstable Angina) Aspirin + fondaparinux (unless immediate PCI is planned) DAPT duration: 12 months with ticagrelor/prasugrel for ACS patients post-PCI Consider shorter durations (1–3 months) in high-bleeding-risk patients with modern drug-eluting stents 2. Secondary Prevention Post-MI Lifelong aspirin (75 mg daily) unless contraindicated DAPT duration: 12 months post-ACS (ticagrelor/prasugrel preferred over clopidogrel) 6 months for stable coronary artery disease Statins: High-intensity statins (e.g., atorvastatin 80 mg) are recommended alongside antiplatelets 3. Stroke and Transient Ischemic Attack (TIA) Acute phase: Aspirin 160–300 mg immediately after hemorrhage exclusion Short-term DAPT (21–30 days): Clopidogrel + aspirin for high-risk TIA/minor stroke (NIHSS ≤3) Long-term: Clopidogrel monotherapy (preferred) or aspirin/dipyridamole Avoid prolonged DAPT (>21 days) due to bleeding risks 4. Special Populations & Considerations High bleeding risk (HBR): Use clopidogrel over prasugrel/ticagrelor; consider proton pump inhibitors Renal impairment: Fondaparinux preferred; avoid prasugrel in severe CKD Perioperative management: Continue aspirin in most surgeries; stop P2Y12 inhibitors (e.g., clopidogrel) 3–7 days pre-op if bleeding risk is high