Cardio Flashcards
Acute Coronary Syndrome - Definition
A spectrum of acute myocardial ischaemia and/or infarction.
There are 3 types:
- STEMI
- NSTEMI
- Unstable Angina
Unstable Angina - Definition & Presentations
Myocardial ischaemia at rest/on minimal excursion in the absence of acute cardiomyocyte injury/necrosis.
–> Poor blood flow through coronary artery/ies
Characterised by:
- Prolonged angina at rest >20 mins
- New onset of severe Angina
- Angina that is increasing in frequency, lasting longer, or lower in threshold
- Angina that occurs after a recent episode of Myocardial Infarction
(Does not cover pregnant women)
Presentations:
- Chest pain
- Marked sweating
- Epigastric pain
- Dyspnoea (SOB)
- Syncope (fainting)
Unstable Angina - Aetiology & Risk Factors
Underlying cause in almost all patients: Coronary Artery Disease
Most common cause: Coronary artery narrowing by a thrombus that develops on a disrupted atherosclerotic plaque, it is usually non-occlusive
Risk Factors:
(risk factors for cardiovascular diseases –> Things that will cause plaque formation)
- Diabetes Mellitus
- Hyperlipidaemia
- Hypertension
- Metabolic syndrome
- Smoking
- Obesity/inactivity
- Advanced age
Unstable Angina - Epidemiology
Cardiovascular Disease (CVD) is the leading cause of deaths globally for men and women
Unstable Angina - Differentials
1) Stable angina –> Pain only occurs on exertion/emotional distress. It doesn’t worsen over time and is relieved by nitrates & rest
2) Vasospastic angina –> Usually occurs w/out provocation and resolves spontaneously or with rapid-acting nitrates. Most episodes happen in the early morning.
Calcium channel blockers supress symptoms, beta-blockers do not
3) NSTEMI –> Can be undistinguishable
4) STEMI –> Can be undistinguishable
5) CHF (Congestive Heart Failure) –> SOB, orthopnoea, tachycardia & peripheral oedema are usually predominant.
Chest pain may occur if coronary perfusion is poor
Unstable Angina - Investigations
1st line:
- ECG
- High-sensitivity troponin –> Rule out acute MI
- CXR
- FBC
–> Check for secondary causes (i.e. anaemia is common for unstable angina and associated with increased mortality)
–>Check for thrombocytopenia as treatment of unstable angina increases risk of bleeding
- Urea, electrolytes and creatinine –> measure renal function
- LFT –> check Liver in bleeding risk assessment before starting anticoagulant
- Blood glucose
- CRP –> rule other causes
Consider:
- Echocardiography
- Invasive coronary angiography
- Functional (stress) testing
- Coronary computed tomography angiography
Unstable Angina - Management
Acute - suspected/confirmed unstable angina:
1st line:
- Aspirin (unless significant bleeding risk) - Single loading dose
–> aspirin: 300 mg orally (chewed or dispersed in water) as a loading dose, followed by 75-100 mg once daily thereafter
- P2Y12 inhibitor (not recommended if invasive coronary angiography is planned w/in 24/hrs) –> prevents blood clots
–> clopidogrel: 300 mg orally as a loading dose, followed by 75 mg once daily thereafter - Manage hyperglycaemia if needed
consider:
- Glyceryl trinitrate –> glyceryl trinitrate translingual: 400-800 micrograms administered under the tongue via aerosol spray as a single dose, may repeat every 5 minutes if required, maximum 3 dose
- Morphine –> morphine sulfate: 2.5 to 10 mg intravenously initially, followed by 2.5 to 10 mg if required (at a rate of 1-2 mg/minute)
- Anti-emetic (stops vomiting & nausea) –> ondansetron: 4-8 mg intravenously as a single dose
- Referral for invasive coronary angiography
Ongoing Unstable Angina:
1st line:
- Start/increase anti-anginal medication –> Beta-blocker (bisoprolol)
- Short-acting Nitrate - Glyceryl trinitrate (glyceryl trinitrate translingual: 400-800 micrograms administered under the tongue via aerosol spray as a single dose, may repeat every 5 minutes if required, maximum 3 dose) –> immediate relief to symptoms
- Continue Aspirin indefinitely unless the patient has a sensitivity –> aspirin: 75-100 mg once daily thereafter
consider:
- ACE inhibitor/ angiotensin II receptor antagonist –> if reduced left ventricular ejection fraction/diabetes/CKD –> ramipril: 2.5 mg orally twice daily for 3 days, increase gradually according to response, maximum 10 mg/day
- Statin –> reduce cholesterol risk –> atorvastatin: 40-80 mg orally once daily
- Aldosterone antagonist –> if reduced left ventricular ejection fraction –> spironolactone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day
Unstable Angina - Prognosis & Complications
A year on there is a 10% mortality rate
Adverse prognostic markers:
- Chest pain at rest
- Comorbidities
- Signs of Left ventricular failure
- ST depression
- Elderly
Complications:
- Complication of treatment - bleeding = high
–>
- Complication of treatment - thrombocytopenia = high
- Ventricular arrythmias = high
- CHF = medium
NSTEMI - Definition & Presentations
An acute ischaemic event causing myocyte necrosis, with an ECG showing no ST elevation
–> Partial/incomplete blocking of a coronary artery
Presentations:
- Chest pain
- Marked Sweating
- Cardiogenic shock
- Nausea & vomiting
- Arrhythmias
- Heart murmur
- Epigastric pain
NSTEMI - Aetiology & Risk Factors
Usually due to a transient/incomplete occlusion of a coronary artery, depriving the myocardium of Oxygen
i.e. embolism
–> severe progressive atherosclerosis
–> recreational drug use
–> arterial inflammation
Risk Factors:
- Atherosclerosis (Hx of Angina, MI, Stroke, tec…)
- Diabetes
- Smoking
- Family Hx
- Age >65
- Hypertension
- Obesity/Physical inactivity
- Cocaine use
- CKD
- Sleep Apnoea –> Sever/untreated obstructive sleep apnoea associated with 17% increased cardiovascular risk
NSTEMI - Epidemiology
NSTEMI occurs more frequently than STEMI
Cardiovascular Disease (CVD) is the leading cause of deaths globally for men and women
NSTEMI - Differentials
1) STEMI –> Clinical presentation may not differentiate
2) Unstable Angina –> Clinical presentation may not differentiate
3) Aortic dissection
–> Pain described as ‘tearing back pain’
–> Often occurs in patients w/ collagen vascular disease (i.e. Marfan syndrome)
4) Pulmonary Embolism
–> Often present w/ dyspnoea, pleuritic chest pain, cough or haemoptysis
–> Hypoxia may be present
–> Lower limbs should be examined for DVT
5) Peptic Ulcer
–> Pain is often described as burning epigastric pain that occurs hrs after meals or with hunger
–> Often wakes the patient up at night
–> Is relieved w/ food and antacids
–> May be a previous Hx of Reflux or medicines that can cause Peptic Ulcers
6) Acute Pericarditis
–> Pain is relieved by sitting forwards
–> Friction rub or distant heart sounds may be heard on auscultation
–> Look for Hx of recent cardiac procedure, Renal failure or a preceding illness
NSTEMI - Investigations
1st line:
-ECG
- High-sensitivity Troponin –> would be elevated
- CXR
- FBC
- Urea, electrolytes and creatinine
- LFTs
- Blood glucose
- CRP
consider:
- Echocardiography
- Invasive coronary angiography
NSTEMI - Management
Acute first line:
- Refer for immediate invasive coronary angiography and/or revascularisation
- Aspirin, single loading dose (unless high bleeding risk or hypersensitivity) –> aspirin: 300 mg orally (chewed or dispersed in water) as a loading dose, followed by 75-100 mg once daily thereafter
–> consider P2Y12 inhibitor,, usually used however the use of this must be balanced between the risk of bleeding and the risk of clots.
(Aspirin and P2Y12 inhibitors together = dual antiplatelet therapy)
–> clopidogrel: 300 mg orally as a loading dose, followed by 75 mg once daily thereafter
consider:
-Oxygen -> only if sats <90%
- Glyceryl trinitrate -> pain relief –> glyceryl trinitrate translingual: 400-800 micrograms administered under the tongue via aerosol spray as a single dose, may repeat every 5 minutes if required, maximum 3 dose
- Morphine -> pain relief –> morphine sulfate: 2.5 to 10 mg intravenously initially, followed by 2.5 to 10 mg if required (at a rate of 1-2 mg/minute)
- Anti-emetic -> When giving morphine –> ondansetron: 4-8 mg intravenously as a single dose
Post-stabilisation first line:
- Continue dual antiplatelet therapy
+ Start/continue beta blocker –> bisoprolol: 1.25 mg orally once daily initially for 1 week, increase gradually according to response, maximum 10 mg/day
+ Start/continue ACE inhibitor –> ramipril: 2.5 mg orally twice daily for 3 days, increase gradually according to response, maximum 10 mg/day
+ Statin –> atorvastatin: 40-80 mg orally once daily
+ Possible cardiac rehabilitation
consider:
- Aldosterone antagonist -> if reduced LVEF –> spironolactone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day
NSTEMI - Prognosis & Complications
High risk of morbidity and death in the future
predictors of poor prognosis:
-Ventricular arrythmias
- LV dysfunction
Complications (many due to LV failure/fibrillation/arrythmias):
- Cardiac arrythmias = medium chance
- Acute heart failure = low chance
- Cardiogenic shock = low chance
- Venous thromboembolism = low chance
- Ventricular rupture/aneurysm = low chance
STEMI - Definition & Presentations
Myocardial cell death that occurs due to a prolonged mismatch between perfusion and demand, usually caused by a complete occlusion of a coronary artery
Marked ST elevation on ECG that is persistent and new/increased
Presentations:
- Severe chest pain
- Dyspnoea
- Pallor
- Diaphoresis (sweating)
- Nausea/vomiting
- Dizziness
- Anxiety/distress
- Palpitations
STEMI - Aetiology & Risk Factors
Typically a thrombosis/embolism leading to complete occlusion of a coronary artery –> Resulting from Atherosclerosis
Usually a consequence of coronary artery disease
Can be due to coronary spasm or spontaneous coronary/aortic dissection
Risk Factors:
- Smoking
- Hypertension
- Diabetes
- Obesity/Inactivity
- Metabolic Syndrome
- Renal insufficiency
- Family Hx
- Male sex
- Age >50
- Cocaine use
STEMI - Epidemiology
Ischaemic Heart Death = most common cause of death globally
STEMI incidence has been decreasing
STEMI patients often younger than NSTEMI patients
STEMIs more common in men
STEMI - Differentials
1) Unstable angina –> Clinical presentation may not differentiate
2) NSTEMI –> Clinical presentation may not differentiate
3) Aortic dissection –> ‘Tearing’ chest pain between shoulder blades. Peripheral pulses may be unequal or absent distally
4) Pulmonary Embolism –> acute stabbing sharp pleuritic pain (pain on breathing), SOB, Hx of clotting disorders or long period of immobilisation
5)Pneumothorax
–> Sudden onset pleuritic chest pain and SOB
–> Tachycardia, hypotension and cyanosis
–> Hx of COPD or recent chest trauma would support this
STEMI - Investingations
1st line:
- ECG
- Coronary angiography
- Urea, electrolytes & creatinine
- Cardiac Troponin
- FBC –> check for anaemia, will influence dual anti-platelet therapies given
- Glucose –> hyperglycaemia is common
- CRP
- Serum lipids –> not useful for the acute attack but helps inform patient’s risk factor for future Cardiac events
Consider:
- ABG
- CXR
- point-of-care transthoracic echocardiogram
STEMI - Management
1st line for Acute STEMI:
- Aspirin –> aspirin: 300 mg orally (chewed or dispersed in water) as a loading dose, followed by 75-100 mg once daily thereafter
- Assess eligibility for Coronary reperfusion therapy ASAP
- Analgesia –> morphine sulfate: 2.5 to 10 mg intravenously initially, followed by 2.5 to 10 mg if required (at a rate of 1-2 mg/minute)
- Anti-emetic –> ondansetron: 4-8 mg intravenously as a single dose
consider:
- Oxygen if sats <90%
- Intravenous nitrate –> Sublingual Glyceryl trinitrate can sometimes cause spontaneous relief from a STEMI, suggesting coronary spasm w/ or w/out associated MI
–> Consider only if there is persistent chest pain after sublingual chest pain or sustained hypertension
Ongoing STEMI:
- Continue dual antiplatelet therapy
–> aspirin: 75-100 mg once daily thereafter & clopidogrel: 75 mg orally once daily
-Start/continue beta-blocker –> bisoprolol: 1.25 mg orally once daily initially for 1 week, increase gradually according to response, maximum 10 mg/day
-Start/continue ACE inhibitor –> ramipril: 2.5 mg orally twice daily for 3 days, increase gradually according to response, maximum 10 mg/day
- Statin –> atorvastatin: 40-80 mg orally once daily
Consider:
-Aldosterone antagonist –> spironolactone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day
- Cardiac rehabilitation –>
Changes to diet
Reduction of alcohol consumption
Smoking cessation
Weight management
Physical exercise.
STEMI - Prognosis & Complications
Faster a STEMI is treated from onset of symptoms the better the diagnosis
Prognosis is improved by early reperfusion
Predictors for worse prognosis:
- High Troponin levels
- Major bleeding
Complications:
- CHF = high chance (decreased LV function)
- Ventricular Arrythmias = high chance
- Recurrent Ischaemia & Infarction = high chance (further plaque rupture from Atherosclerosis)
- Depression = high chance
- Recurrent chest pain = medium chance
- Sinus bradycardia, first-degree heart block & type 1 second degree heart block = medium chance
- Complete heart block w/ anterior MI = medium chance
Anaemia - Definition & Presentations
Anaemia is a haemoglobin (Hb) level two standard deviations below the mean for the age and sex of the patient
Hb <11 g/dL in children under 5 years and in pregnant women
Hb <11.5 g/dL in children aged 5 to 11 years
Hb <12 g/dL in children aged 12 to 14 years and in women (aged over 15 years)
Hb <13 g/dL in men (aged over 15 years)
General Presentations:
- Fatigue/Weakness
- Pale skin
- SOB
- Dizziness/Light-headedness
- Headaches
- Cold peripherals
- Brittle nails & Pale nail beds
- Arrhythmia/palpitations
- Sometimes craving for unusual things (i.e. clay or starch) if due to iron deficiency
- Restless Legs Syndrome
- Jaundice if haemolytic
Presentations can vary depending on the cause
Many anaemic patients with no acute or active bleeding are asymptomatic
Anaemia - Aetiology & Types + Risk Factors
Risk Factors:
- Extremes of age
- Female sex
- Lactation
- Pregnancy
Types:
- Nutrient deficiency (vit. B12/Folate/General malnutrition)
- Bone marrow disease
- Blood loss
- Anaemia of chronic disease
- Toxin exposure
- Haemolytic anaemia (Autoimmune/Infections/Uraemic syndrome)
- Genetic Disorders (Thalassaemias/Sickle cell anaemia/Hereditary spherocytosis/Glucose-6-phosphate dehydrogenase (G6PD) deficiency)
- Macrovascular disease
- Pregnancy
- Thermal burns
- Cardiovascular problems are the biggest cause of individuals being intolerant to anaemia and showing symptoms
Anaemia - Investigations
- FBC -> Hb levels, reticulocyte levels, haematocrit (vol% of RBC in blood), MCV
- Prothrombin time/activated partial prothrombin time -> coagulation problems?
- Abdominal ultrasound scan -> Intestinal bleeding as cause?
- Faecal occult blood testing
- Joint x-rays -> Long-bone fractures can be a significant source of bleeding
- Hx -> Recent trauma? Diet changes indicating insufficiency? Any chronic diseases?
General algorithm:
Microcytic anaemia (MCV <80)
-> Check serum iron
–> Low iron & ferritin + high TIBC (total iron binding capacity) = Iron deficiency anaemia
–> Low/Normal iron & Ferritin w/ low TIBC = possibly chronic disease w/ iron deficiency
–> Mentzer Index (MCV/RBC) <13 = Thalassaemia
Normocytic anaemia (MCV 80-100)
-> Check Reticulocyte count
–> Hypoproliferative (<2%) = Leukaemias, Aplastic anaemia, Pure red cell aplasia, marrow failure syndromes
–> Hyperproliferative (>2%) = Haemorrhage, Haemolytic anaemias
Macrocytic anaemia (MCV >100)
-> Check Megalocytes & Segmented neutrophils on peripheral smear
–> Present (Megaloblastic) = Vitamin B12 and/or Folate deficiency, Drug induced
–> Absent (Non-megaloblastic) = Alcohol abuse, Myelodysplastic syndrome, Liver disease, Congenital bone marrow failure syndromes
Anaemia - Management
Addressing Underlying Causes:
Dietary Changes:
–> If the anaemia is due to a nutritional deficiency (such as iron, vitamin B12, or folate deficiency), dietary changes and supplementation may be recommended.
Vitamin and Mineral Supplements:
–> Vitamin B12 and Folate: Anaemia caused by vitamin B12 or folate deficiency may require vitamin B12 injections or folate supplements.
–> Vitamin C: Vitamin C supplements might be recommended alongside iron supplements to improve iron absorption.
Treating Chronic Diseases:
–> Anaemia related to chronic conditions, such as chronic kidney disease or inflammatory disorders, often requires managing the underlying disease to improve red blood cell production.
Stopping Blood Loss:
–> If anaemia is caused by chronic bleeding (e.g., gastrointestinal bleeding), the source of the bleeding needs to be identified and treated, which may involve medications, endoscopy, or surgery.
Iron Supplementation:
–> Iron Tablets: For iron-deficiency anaemia, iron supplements in the form of tablets or syrups may be prescribed to increase iron levels. It is often advised to take vitamin C alongside iron supplements to enhance absorption.
–> Intravenous Iron: In severe cases or when oral iron supplements are not well-tolerated or effective, iron may be given intravenously.
Erythropoiesis-Stimulating Agents (ESAs):
–> For anaemia associated with chronic kidney disease or cancer, erythropoiesis-stimulating agents can be prescribed to stimulate the production of red blood cells.
Blood Transfusions:
–> In severe cases of anaemia, especially if it causes significant symptoms or complications, blood transfusions may be necessary to rapidly increase haemoglobin levels.
Lifestyle Advice:
–> Lifestyle changes might be recommended, such as reducing alcohol consumption and quitting smoking, as these habits can contribute to anaemia.
Aortic regurgitation - Definition & Presentations
Aortic regurgitation (AR) is the diastolic (at rest) leakage of blood from the aorta into the left ventricle
It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root
Presentations:
- It can remain asymptomatic for decades before patients present with irreversible myocardial damage
- diastolic murmur -> The severity of the AR correlates well with the duration of murmur
- dyspnoea/orthopnoea/paroxysmal nocturnal dyspnoea/ tachypnoea
- fatigue
- weakness
- pallor
- collapsing (water hammer or Corrigan’s) pulse
- urine output <30 mL/hour -> Cardiogenic shock
Aortic regurgitation - Aetiology & Risk Factors
AR can be caused by primary disease of the aortic valve leaflets or dilation of the aortic root:
- In developing countries rheumatic heart disease is the most common cause
- In developed countries congenital bicuspid aortic valve and aortic root dilation account for most of the cases
- Causes of aortic root dilation include Marfan’s syndrome, related connective tissue diseases, and aortitis secondary to syphilis
- Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of blood
- Aortic root dissection is a cause of acute AR
Aortic regurgitation - Differentials
1) Mitral regurgitation
-> CXR: pulmonary oedema, enlarged left atrium and left ventricle, and mitral valve calcification
-> The classical murmur of MR is pansystolic at the apex radiating to the axilla
2) Mitral stenosis
-> CXR: pulmonary oedema, enlarged left atrium, and mitral valve calcification
-> Distinguishing features are a malar flush, low volume pulse, a tapping and undisplaced apex beat, and loud S1 with an opening snap
3) Aortic stenosis
-> CXR: left ventricular hypertrophy (LVH), calcified aortic valve
-> Characteristic signs are a slow rising pulse, heaving but undisplaced apex bear, left ventricular heave, and an ejection systolic murmur that radiates towards the carotids
4) Pulmonary regurgitation
-> CXR: may show dilation of main pulmonary artery with right ventricular dilation
-> Diamond-shaped diastolic murmur best heard in the second and third left intercostal spaces & increases w/ inspiration
Aortic regurgitation - Investigations
1) ECG -> Provides only supportive evidence. Echocardiography is required to confirm the presence of AR
2) CXR -> may show cardiomegaly
3) Echocardiogram -> Most important
4) M-mode and 2-dimensional imaging -> Two-dimensional echocardiography
5) Colour flow Doppler -> detection and quantification of regurgitant flow
6) Pulsed wave Doppler -> detection and quantification of holodiastolic flow reversal
7) Continuous wave Doppler
Aortic regurgitation - Management
Acute:
- Inotropes + vasodilators + urgent aortic valve replacement/repair
-> dobutamine: 0.5 micrograms/kg/min intravenously initially, titrate to effect, maximum 20 micrograms/kg/min
-> nitroprusside: 0.3 to 0.5 micrograms/kg/min intravenously, titrate to effect, maximum 10 micrograms/kg/mins
1) Valve replacement/repair is first line and should be done ASAP
2) As Prosthetic valve patients are at high risk for thromboembolism they need antithrombotic therapy
Chronic:
- Asymptomatic with normal left ventricular (LV) function do not require treatment and can be reassured
- If they are getting surgery for other cardiac diseases they can get a valve replacement/repair at the same time
- If LVEF <55% and/or LVESD >50mm/symptomatic, they become eligible for surgery
Aortic regurgitation - Prognosis & Complications
The outcome and prognosis of patients depends on the magnitude of left ventricular (LV) function and symptoms
5-year survival in patients with normal LV function has been reported as 96% whereas that in patients with reduced LV function is 62%
Patients who have an immediate reduction in LV dilatation following surgery are more likely to have short- and long-term improvements in the ejection fraction
The EF is unlikely to improve in patients who do not have an improvement in EF within the first 6 months of surgery
Complications:
- 4% chance of operative mortality
- Heart Failure
- Arrythmias
- Infective endocarditis -> complication in patients with underlying structural valvular defects, but unusual in AR
Aortic stenosis - Definition & Presentations
AS represents obstruction of blood flow across the aortic valve due to pathological narrowing
It is a progressive disease that presents after a decades-long subclinical period
Presentations:
- exertional dyspnoea -> One of most common symptoms
- fatigue -> One of most common symptoms
- chest pain
- exertional syncope
- ejection systolic murmur
- S2 diminished and single
Aortic stenosis - Aetiology & Risk Factors
Calcification and fibrosis of normal trileaflet valves is the most common cause of AS in adults
- Calcific aortic disease represents a spectrum ranging from aortic sclerosis (defined as leaflet thickening without obstruction) to severe AS
Risk Factors:
- smoking
- hypertension
- low-density lipoprotein (LDL)-cholesterol
- elevated C-reactive protein
- elevated lipoprotein
- age >60 years
- congenitally bicuspid aortic valve
- rheumatic heart disease
- chronic kidney disease
Aortic stenosis - Differentials
1) Aortic sclerosis
-> Transthoracic Doppler echo will demonstrate no significant pressure gradient (<5 mmHg) across the aortic valve with aortic sclerosis
2) Ischaemic heart disease
-> In ischaemic heart disease, common ECG findings include Q waves in contiguous leads, and the echocardiogram often shows segments of the myocardium with abnormal systolic thickening or wall motion abnormalities
-> In AS, Q waves are absent in the ECG; regional wall motion abnormalities are absent on the echocardiogram
3) Hypertrophic cardiomyopathy
-> Typical echocardiography findings include asymmetrical hypertrophy with the septal wall most prominently affected. Dynamic obstruction is observed at the sub valvular level, and calcification of the valve is often absent, especially in younger patients
Aortic stenosis - Investigations
1) Transthoracic echocardiogram (including Doppler) -> best test for the initial diagnosis and subsequent evaluation of AS
-> elevated aortic pressure gradient; measurement of valve area and left ventricular ejection function
2) ECG -> may demonstrate left ventricular hypertrophy and absent Q waves, atrioventricular block, hemiblock, or bundle branch block
3) CXR -> may be normal; may show pulmonary congestion or other lung pathology
Aortic stenosis - Management
Acute if clinically unstable:
1) Balloon valvuloplasty -> Re-stenosis rates are high at 6 months, more of an immediate measure
Once stable but symptomatic:
1) surgical aortic valve replacement
2) long-term infective endocarditis antibiotic prophylaxis -> Due to prostatic valve
+ Consider Long-term anticoagulation -> Anticoagulation with a vitamin K antagonist
(DOACs NOT recommended for a mechanical valve)
1) transcatheter aortic valve implantation -> If >80 or if life expectancy <10 years
Aortic stenosis - Prognosis & Complications
It is important to note that the rate of progression is extremely variable and so the recommended follow-up periods may vary between individuals
The onset of symptoms is a significant milestone and portends a poor prognosis, with an average survival of only 2 to 3 years without surgery
Surgical replacement of the aortic valve is extremely effective therapy - Surgical replacement of the aortic valve is extremely effective therapy
Complications:
1) Acute heart failure
-> occurs when the afterload burden created by the AS limits the ability of the left ventricle to pump blood to the body
2) Sudden cardiac death in symptomatic patients
-> Ventricular arrhythmia
-> Very rare but a significant concern in symptomatic patients