Acute coronary syndrome Flashcards
What is the definition of STEMI?
Clinical syndrome defined by characteristic symptoms of myocardia ischemia in association with persistent ECG changes and subsequent release of biomarkers of myocardial necrosis
- new ST elevation at the J point in at least 2 contiguous leads of >2mm in men or >1.5mm in women in leads V2- V3
- and/ or of >1mm in other contiguous chest leads or limb leads
Acute, often complete occlusion of a coronary artery, typically by a ruptured atherosclerotic plaque
Contiguous leads
- Anterior: V1-V4
- Lateral: V5, V6, Lead I, aVL
- Inferior: Leads II, III, aVF
- R Sided Leads: V4R – V6R
- Posterior Leads: 15-Lead ECG
What are the ECG changes in STEMI?
[Within minutes]
Hyperacute T waves
- T waves more prominent, symmetrical and pointed
- most evident in anterior chest leads
- usually present only for 5- 30 minutes from onset
ST segment changes
- ST segment straightens, followed by loss of ST, T wave angle
- T wave becomes broad and ST segment elevates, loss of normal concavity
- Segment tends to become convex upwards
- ST segment and T wave fuse to form single monomorphic deflection “tomb stones”
Reciprocal ST segment depression
• ST segment depression in leads remote from site of acute infarct
• Very useful if in doubt about clinical significance of ST elevation
[Hours- days]
Pathological Q waves
- loss of R wave height
- due to loss of viable myocardium beneath recording electrode
- may develop within 1-2 hours from onset of symptoms
- usually take 12- 24 hours
[Days]
Resolution of changes in ST segment
• ST segment elevation diminishes and T waves invert
• T wave inversion may persist for many months; may be permanent
What is DeWinter T waves?
Seen in 2% of LAD occlusions, in young pt who have hypercholesterolaemia
- Upsloping ST depression (> 1mm at J-point) in the precordial leads V2-6, leads I & II
- Peaked anterior T waves, with the ascending limb of the T wave commencing below the isoelectric baseline
Differentiate from HyperK b/c latter does not have preceding ST depression
What is the most sensitive lead for right ventricular infarction?
Most sensitive lead: V4R
• ST segment elevation in RV infarct may be short lived
Right Ventricular Infarction
• Associated with 40% of __________
• May also complicate some anterior infarctions
• Rarely occurs as an isolated phenomenon
• Do right sided chest leads for __________ immediately
• Most sensitive lead: _______
• ST segment elevation in RV infarct may be short lived
• Patients with RV infarction are very preload sensitive due to ____________
• ________ are contraindicated: Can develop severe hypotension in response to nitrates and other preload reducing agents
• Hypotension in RV infarct is treated with __________
inferior infarctions;
ALL inferior STEMI ;
V4R;
poor RV contractility;
Nitrates;
fluid loading
Posterior MI
• Occurs in 15-20% of STEMIs in context of an ____________
• Posterior extension implies _____________
• Increased risk of _____________
• Isolated posterior MI less
common (3-11%)
• Do __________ to confirm presence of ST elevations
Look at leads V1-3 (which face the endocardial surface of posterior wall of LV) for clues: • Tall, broad R waves • Dominant R wave (R/S > 1) in V2 • Horizontal \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ • \_\_\_\_\_\_\_ T waves
inferior or lateral infarct:
larger area of myocardial damage;
LV dysfunction and death
leads V7-9;
ST depression;
Upright
What is Wellen’s syndrome?
• Pattern of T wave changes associated with critical, _________________
Criteria
• ___________________ in V2-3
• Isoelectric or minimally elevated ST segment
• No ______________
• History of _________
• Presence of ECG pattern even in __________
• ____________ serum cardiac markers
Proximal LAD artery stenosis
Deeply inverted or biphasic T waves;
precordial Q waves
angina;
pain free state;
Normal or minimally elevated
What is the Diamond and Forrester classification of angina to determine whether chest pain is cardiac in origin?
Typical angina (Definite)
- Substernal chest discomfort with a characteristic quality & duration: Central crushing / squeezing chest pain >20min, Radiation down the left arm / L shoulder or Jaw
- Worse w/ exertion or emotional stress
- Relieved by rest or GTN (Glyceryl Trinitrate)
Atypical angina (Probable): Meets 2 of the above characteristics
Non-cardiac chest pain
- Meets one or none of the typical anginal characteristics
What is the difference between stable and unstable angina?
Stable angina: Chest pain characteristics unchanged over the preceding 60 days (>2 months)
Unstable angina
- Resting angina
- New-onset angina (<2 months)
- Prior angina increasing in severity, duration and frequency
What is Prinzmetal’s Angina?
- Due to coronary artery vasospasm
- Presents with angina at rest, usually in early morning hours
- Patients are generally younger with few CVS risk factors
- Treat with GTN and CCB
What are the different types of MI based on aetiology?
- Type 1: Plaque Rupture
- Type 2: PE, anemia, arrhythmia, HTN, HypoTN, Sepsis, Tachycardia
- Type 3 = sudden cardiac death before ECG can be done to understand Dx (can any cause)
- Type 4a = MI in patients with percutaneous coronary intervention (aka angioplasty)
- Type 4b = MI in patients with thrombosis within stent
- Type 5 = MI in patients with CABG
What are the risk factors for ACS?
Age & male gender
- Ethnic origin
- Family Hx of premature CAD (premature = <55 for males, <65 for females)
- This is due to cardioprotective hormones in females
Modifiable
- Smoking (increases risk by 50%)
- Hypertension & hyperlipidemia
- Diabetes
- Obesity & metabolic syndrome
- Sedentary lifestyle
- Psychological stresses
What is the approach to acute coronary syndrome?
1) Take history and physical examinations
2) Do initial investigations + ECG findings + Cardiac Enzymes
3) TIMI Scoring for STEMI / NSTEMI / UA
4) Medication w/ AAABS (DAPT, ACE-I, Anticoagulation, Beta Blockers, Statins)
+/- Nitrates, +/- Morphine, +/- Oxygen
- Remove ACE-I and BB if hypotensive from cardiogenic shock
- Nitrates are C/I in R Sided AMI
- Morphine only given if severe pain
- Oxygen only given if desaturating
- Note: A stands for Aspirin -> think DAPT
5) Coronary Angiogram to elucidate level of clot + severity of occlusion
6) Revascularization Therapy
7) Discharge advice + Meds
i. e. DAPT for 1-year, lifelong Aspirin, BB, ACE-I, Statins
- Control Risk Factors and Metabolic Co-morbids
- Lifestyle Management
What are the symptoms of unstable angina?
Features of Typical angina
- Substernal chest discomfort with a characteristic quality & duration
- Central crushing / squeezing chest pain >20min
- Radiation down the left arm / L shoulder or Jaw
- Worse w/ exertion or emotional stress
- Relieved by rest or GTN (Glyceryl Trinitrate)
Associated w/: N&V, Diaphoresis, Palpitations, Dyspnoea
Atypical presentation in elderly & diabetics (due to peripheral neuropathy):
- syncope, pulmonary oedema
- epigastric pain, vomiting, confusion, diabetic
- hyperglycaemic states
- Numbness in the arm (instead of pain),
- Cough (esp in patients w/ DM)
R Sided AMI can lead to BRADYCARDIA / Heart Blocks instead of Tachycardia
- Due to SA node dysfunction / AV blocks
- Such nodal dysfunction are transient and due to edema not ischaemia
Complications – to ask in history + look out for in PE
- Syncope
- Features of Heart Failure: Pedal Edema, Dyspnoea, Orthopnoea, PND
What are the ECG changes found in NSTEMI i.e. Sub-endocardial ischemia Ischaemia, <100% CA Occlusion? What sort of monitoring is required?
Classical Findings: T wave inversion OR ST depression
HOWEVER: Any non-STEMI changes (incl. Normal ECG) w/ ↑ Cardiac Enzymes = NSTEMI!
SERIAL ECG & CARDIAC MARKERS for NSTEMI w/o intervention or UNSTABLE ANGINA
- q8h (every 8 hours) for 1 day, then daily
- In the event that NSTEMI / UA converts into a STEMI!
What are the other initial investigations in acute coronary syndrome
[Cardiac Enzymes – look at both ABSOLUTE value & TRENDING]
Cardiac troponin I – most sensitive and specific
- ↑ within 4 hrs from onset of chest pain
- Peak at 24-48 hrs
- Decrease to baseline over 5-14 days
Creatine kinase Muscle-Brain subtype (CKMB)
- 1st to rise & peak – rises within 2 hours
- CKMB – peaks at 24hours, lasts 3 days
- Levels twice the upper limit consider abnormal
- Useful for evaluation of re-infarction (esp if pt may have had 2 MIs within 14 days, because troponins take 10-14 days to decrease after a cardiac event)
Blood Tests
- FBC, Renal panel, Glucose, Lipids
- FBC will see a slightly raised TW
- Renal panel b/c of contrast used in CA Angiogram
CXR – to screen for Heart Failure (if suspected)
- Cardiomegaly
- Pulmonary oedema
- Widened mediastinum (aortic rupture)
What are the goals of therapy in ACS?
Rapid initiation of therapy to limit myocardial damage and minimize complications
And we do that by
1) Restoring normal coronary blood flow
2) Decreasing myocardial oxygen consumption.
What is medical therapy for immediate stabilisation of STEMI?
[Antithrombotic therapies]
1) DAPT (Aspirin + Plavix [Clopidogrel] / Ticagrelor)
- Comprises: PO Aspirin (300mg loading dose then 100mg om)
- AND a P2Y12 Inhibitor: PO Plavix ie Clopidogrel (300mg loading dose then 75mg om) OR PO Ticagrelor (180mg Loading Dose then 90mg BD)
2) Anticoagulation: Unfractionated Heparin and Low Molecular weight Heparin
[Anti- ischemic therapies]
3) Beta Blockers – remove if Hypotensive (Cardiogenic Shock)
- Cardioselective BB: 1st dose Atenolol 5mg IV, followed by oral
- C/I: ABCD – Asthma, COPD, Heart Block, Decompensated HF
4) Nitrates: C/I in RV Infarct as RV STEMI is Preload.
• Recall: Nitrates = Venodilator; Hydralazine = Arteriodilator
5) Ca Channel Blockers
[Adjunctive therapies]
6) ACE-Inhibitors – remove if Hypotensive (Cardiogenic Shock)
7) Statins – should be started ASAP as it has mortality benefit
[Other anti anginals]
- Ivabradine
- Trimetazidine
[Others]
8) IV Morphine: ONLY if severe pain, as opioids can limit drug absorption. No longer routinely used! For pain / anxiety relief; given w/ Maxalon (Metoclopramide) for N&V
9) Oxygen: ONLY if desaturated, as excessive O2 can limit drug absorption
How do you decide on rapid reperfusion therapy for STEMI?
If admitted within 12 hours of onset of symptoms – PCI is GOLD STANDARD
If admitted >12 hours of onset – Consider Thrombolysis
Also consider thrombolysis 1st if PCI cannot be done within 30min of admission
After all:
- Door to needle time (Thrombolysis) = 30min
- Door to balloon time (PCI) = 90 min
If Left Main Stem Disease / Double or Triple Vessel Disease – CABG
Percutaneous Coronary Intervention (PCI)
- indications
- complications
- choice of anticoagulation and PY12 inhibitor
Indications
- Single vessel disease
- Admitted within 12 hours of S&S
Complications: 1% risk of stroke, recurrent infarction, bleeding or death
2 Types of stents available
1) Bare Metal Stent
• The rupture recovers and grow over the stent
• Hence may be Cx by in-stent re-narrowing of the CA
2) Drug Eluting Stent – i.e. Stent coated with antiproliferative agents
• Coated with anti-proliferative medication such as chemo drugs
• Reduces the rate of healing that area – reduced fibrous tissue deposition & prevents in stent-narrowing
• HOWEVER, b/c it heals slowly 🡪 vessel is not reendothelialised 🡪 may cause ACUTE stent thrombosis 🡪 hence pt needs adhere to 1Yr DAPT
P2Y12 inhibitor: ticagrelor (180mg) or prasugrel (60mg)
Anticoagulation therapy: LMWH Clexane ie Enoxaparin (1mg/kg bd, or om if GFR <30)
Thrombolysis
- indications
- contraindications
- choice of anticoagulation and PY12 inhibitor
Indications
• If patient has contraindications to PCI
• OR PCI cannot be done within 30 min of onset
• OR pt presents >12 hours of symptoms
Absolute contraindications: • Recent ischemic stroke (3 months) 🡪 risk hemorrhagic conversion • Previous intracranial hemorrhage • Current intracranial neoplasm • Suspected aortic dissection • Active bleeding
Relative contraindications: • States that increase risk of bleeds - Poorly controlled hypertension - Recent internal bleeding (4 weeks) - PUD (active) – risk bleeds - Recent surgery (3 weeks) - Current use of anticoagulants • Pregnancy
P2Y12 inhibitor: clopidogrel (300mg)
Anticoagulation therapy: LMWH Clexane ie
Enoxaparin
- Patient low risk of bleeding: enoxaparin
- Patient high risk of bleeding: fondaparinux
- Continue up to 8 days or until discharge
What are the complications of STEMI?
Arrhythmia
1) Tachycardia
2) Bradycardia
Myocardial rupture
1) LV free wall
2) papillary muscle –> MR
3) ventricular septum –> VSD
Shock/ CHF
Post infarction angina
Recurrent MI
Thromboembolism
Pericarditis
Dressler’s syndrome
What is dressler’s syndrome?
Dressler’s syndrome = Pericarditis 2’ to heart /pericardial injury from AMI
Presentation
- S&S of pericarditis: fever, pleuritic pain, worse on lying, radiates to trapezius
- May be complicated by pericardial effusion, +/- pericardial friction rub
- Usually occurs 2-3 weeks after MI, can also be delayed for a few months
ECG: Widespread saddle-shaped ST elevation w/ ST depression in aVR
Pathophysiology: Believed to be caused by autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of MI
Management: High dose aspirin, Supportive Mx
What are the preparing for discharge medical therapy?
1) Duel anti-platelet Therapy: for 1 yr followed by lifelong Aspirin
- Aspirin 75mg/day (indefinitely)
- Clopidogrel 75mg/day (at least 1 year for drug eluting stent)
2) ACE I or ARB e.g. lisinopril
- Reduces remodeling (even w/o HF this is beneficial)
- ARBs if pt cannot tolerate ACE-I (eg: angioedema due to excessive bradykinin)
3) Beta blockers (Cardioselective)
- Reduces remodeling (even w/o HF this is beneficial)
- Metoprolol 25-50 mg BD
- Atenolol 50-100 mg daily
4) Statin
- Atorvastatin 40-80mg daily
- Check LFT & CK prior to giving statins
5) Calcium channel blockers (given to patients intolerable to beta-blockers)
- Dihydropiridines (selective vasodilators) - Amlodipine (3rd gen), Nifedipine (1st gen)
6) GTN
- High-intensity statins have been shown to effectively control cardiovascular risk factors
- Has plaque stabilizing effects, reduces mortality and recurrent MI
7) Control of Risk factors + Lifestyle Modification
- Smoking cessation
- Glycemic control
- Hypertension treatment
- HLD management
- Diet/exercise
What is the approach to managing a NSTEMI patient?
Secure ABCs and manage symptomatically
Calculate TIMI score to prognosticate + whether PCI is EMERGENTLY indicated
- Look for high risk features where PCI is EMERGENTLY indicated
• Hemodynamic instability or shock
• Persistent angina despite medical therapy
• New/ persistent mitral regurgitation/new VSD
• Ventricular arrhythmia
• Severe LV dysfunction or heart failure
Otherwise, intermediate-risk and low-risk NSTEMI are indicated for EARLY PCI within 3 days of presentation
What is the conservative strategy in managing a NSTEMI?
Medical therapy – i.e. AAABS +/- MON • DAPT • Anticoagulation • ACE-I • BB • Statins • +/- Nitrates, Oxygen, Morphine
SERIAL ECG & CARDIAC MARKERS to monitor for STEMI conversion
NSTEMI with low / intermediate risk 🡪 early PCI in 3 days’ time
Cardiac stress test or other ischemia testing (within 72hours) 🡪 positive results 🡪 early invasive strategy
What is the early invasive strategy in managing a NSTEMI?
NSTEMI high risk with features of heart failure etc 🡪 urgent PCI on admission!
ABCs & Ix 🡪 NAABS +/ MON 🡪 Coronary angiography 🡪 PCI i.e. exactly the same workflow as per STEMI
Note: thrombolysis is NOT administered for UA/NSTEMI
What is the management of chronic stable angina?
4 main medications: Statins, Aspirin, ACE-I, Beta Blockers
General measures
- Goals: to reduce myocardial oxygen demand and/or increase oxygen supply
- Lifestyle modification (diet, exercise)
- Treatment of risk factors: Statins, antihypertensives, etc.
1) Single antiplatelet therapy (first-line therapy)
- Aspirin 75mg daily, often taken with omeprazole
- Clopidogrel 75mg daily - when ASA absolutely contraindicated (active peptic ulcer disease)
2) β-blockers (first-line therapy: decrease overall mortality)
- Increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)
- Cardioselective agents preferred (e.g. metoprolol, atenolol) to avoid peripheral effects (inhibition of vasodilation and bronchodilation via β2 receptors)
- Avoid intrinsic sympathomimetics (e.g. acebutolol) which increase demand
- Contraindicated in patients with asthma, severe LV dysfunction, bradycardia, coronary artery spasm
3) ACE inhibitors (not used to treat symptomatic angina)
- Angina patients tend to have risk factors for CV disease which warrant use of an ACEI (e.g. hypertension, diabetes, proteinuric renal disease, previous MI with LV dysfunction)
- Benefit in all patients at high risk for CV disease (concomitant DM, renal dysfunction or LV systolic dysfunction)
- Angiotensin II receptor blockers (ARBs) can be used when ACEI contraindicated (e.g. hypersensitivity, angioedema)
4) Nitrates (symptomatic control, no clear impact on survival)
- Decrease preload (venous dilatation) and afterload (arteriolar dilatation), and increase coronary perfusion
- Maintain daily nitrate-free intervals to prevent tolerance (tachyphylaxis)
5) Calcium channel blockers (CCBs, second-line or combination)
- Dihydropyridines e.g. nifedipine, amlodipine 5-10mg
- Increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload)
- Caution: verapamil/diltiazem combined with β-blockers may cause symptomatic sinus bradycardia or AV block
6) Invasive strategies: Revascularization
Glyceryl Trinitrate
- Mechanism
- Side effects
- Onset
- Peak action
- Duration
MOA
- Vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins.
- Reduces cardiac oxygen demand by decreasing preload(left ventricular end-diastolic pressure)
- Reduce afterload modestly
- Dilate coronary arteries and improve collateral flow to ischemic regions
Side effects: hypotension, reflex tachycardia
Onset of action: Sublingual tablet: 1 to 3 minutes
Peak effect: Sublingual tablet: 5 minutes;
Duration: Sublingual tablet: At least 25 minutes
Ticagrelor
- Mechanism
- Side effects
- Onset
- Peak action
- Duration
MOA
- Belongs to a novel chemical class, cyclopentyltriazolopyrimidine
- An oral reversibly binding noncompetitive inhibitor of the P2Y12 receptor (adenosine diphosphate (ADP) P2Y12receptor) on the platelet surface which prevents ADP-mediated activation of the GPIIb/IIIa receptor complex thereby reducing platelet aggregation
Side effects: bleeding, shortness of breath
Onset of inhibition of platelet aggregation:180 mg loading dose: ~41% within 30 minutes
Peak effect: 88% at 2 hours post administration
Duration of IPA: 2 to 8 hours
What are Thienopyridines and what drugs fall under that class?
What are the side effects and C/Is of these drugs?
A class of drugs that irreversibly inhibit the binding of ADP to the P2Y12 receptor.
Include – Prasugrel (3rd Gen), Clopidogrel (2nd gen), Ticlopidine (1st gen)
Ticlopidine can cause – neutropenia (occurs in first 3mths), liver abnormalities and thrombotic thrombocytopenic purpura (TTP), making it less safe than Clopidogrel.
Clopidogrel has less major GI bleeding than aspirin.
Clopidogrel is a prodrug that requires metabolic activation by hepatic cytochrome P450. (CYP2C19 allele associated with increased rates of ischemic events and stent thrombosis post PCI)
Prasugrel-mediated inhibition of platelet aggregation is approx.5-9x more potent than that of Clopidogrel achieving greater platelet inhibition with an onset of action within 1hr BUT has increased bleeding risk and contraindicated in patients with previous stroke, weight less than 60kg and age > 75yrs.
Morphine
- Mechanism
- Side effects
- Onset
- Peak action
- Duration
Binds to opioid receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression
Side effects: Drowsiness, vomiting, constipation, respiratory depression, potential for abuse
Onset: Oral (immediate release): ~30 minutes; IV: 5 to 10 minutes
Duration for Pain relief: Immediate-release formulations: 4 hours
Heparin
- MOA
- Advantages
- Disadvantages
MOA
a) Binds to antithrombin which increases the potency of that plasma protein in the inactivation of clot-forming thrombin.
b) Inhibits coagulation factor Xa, slowing thrombin formation and thereby further impeding clot development.
- Include: Unfractionated Heparin and Low Molecular weight Heparin.
- LMWH preferentially inhibits factor Xa (note Fondaparinux, an alternative factor Xa inhibitor
Advantages
- greater bioavailability
- lower risk of heparin induced thrombocytopenia
- easier dosing: does not require monitoring of PTT
Disadvantages
- slightly delayed onset of action (e.g. 20-30min) rather than instantaneous
- longer duration of action, making it more difficult to rapidly stop therapy
- less easily inactivated with protamine sulfate
- prolonged half life in patients with renal failure, especially with LMWH.
Fibrinolytic terapy
- Class of drugs
- MOA
- Potential issues
- C/Is
Alteplase, Reteplase, Tenecteplase (Streptokinase)
Mechanism: Stimulates the natural fibrinolytic system, transforming inactive precursor plasminogen into the active protease plasmin which then lyses fibrin clots
Potential issues: Plasmin can degrade other proteins including fibrinogen and result in bleeding
Contraindications: PUD, Bleeding disorders, Recent stroke, Recent surgery
What is the MOA of Glycoprotein IIb/IIIa Receptor Antagonists? What drugs do they include and what significant adverse effects are there?
MOA
- Class of drugs which inhibit one of the platelet integrin adhesion receptors (GPIIb/IIIa)
- Block final platelet activation and cross-linking by fibrinogen and vWF
Include – Abciximab, Tirofiban, Eptifibatide (PCI)
Significant adverse effects include thrombocytopenia (hence need to monitor platelet counts on FBC)
Given IV or intracoronary during PCI
Bisoprolol
- MOA
- Onset of Action
- Side effects
Selective inhibitor of beta1-adrenergic receptors competitively block beta1-receptors, with little or no effect on beta2-receptors at doses ≤20 mg
- Cardioinhibitors, by reducing heart rate, contractility, and arterial pressure, reduce the work of the heart and the oxygen demand of the heart.
- Relieve a patient ofanginal painthat is caused by a reduction in the oxygen supply/demand ratio due to coronary artery disease.
- Ability to inhibit subsequent cardiac remodeling.
Onset of action: 1 to 2 hours
Side Effects: Bradycardia, hypotension, fatigue
Calcium channel blockers
- MOA
- Drugs included
- indications
- C/Is
- effects
MOA
- bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes).
- CCBs cause vascular smooth muscle relaxation (vasodilation)
- Decrease contractility (negative inotropy)
- Decrease heart rate (negative chronotropy)
- Decrease conduction velocity (negative dromotropy)
Dihydropyridines (selective vasodilators, potential reflex increase in HR, myocardial contractility and O2 dd): Amlodipine, Nifidipine, Nicardipine
Non dihydropyridines (equipotent for cardiac tissue and vasculature): verapamil, dilitiazem
Calcium channel blockers primarily serve as adjunctive therapy in patients with ongoing or recurrent symptoms of ischemia despite optimal therapy with beta blockers (with or without nitrates), in patients who are unable to tolerate adequate doses of one or both of these agents, or in patients with rapid atrial fibrillation when beta blockers are contraindicated.
In certain patients they may be harmful
- HF
- left ventricular dysfunction
- atrioventricular block.
ACE-I and ARBs
- MOA
MOA
- Improvement in the oxygensupply /demandratio of the myocardium by reversing angiotensin II-induced vasoconstriction and inotropic activity, Improvement in endothelial function
- Attenuation of ventricular remodeling and ventricular dilation, which are factors for arrhythmogenesis
Lisinopril
- Onset of action
- duration
- Side effects
Onset of action: 1 hour
Peak effect:
- Hypotensive: Oral: ~6 hours
Side effects: cough, hypotension, elevated potassium and creatinine
Artovastatin
- Onset of action
- MOA
- Side effects
Onset of action: Initial changes: 3 to 5 days; Maximal reduction in plasma cholesterol and triglycerides: 2 weeks
MOA: results in plaque stabilization, reversal of endothelial dysfunction, inhibition of monocyte recruitment, decreased thrombogenicity, and a reduction in inflammation
Side effects: arthralgia, myalgia, GI, increased serum transaminases
Ivabradine
- MOA
- Drug interactions
- Indications
- Side effects
MOA
- Selective sinus node inhibitor
- Inhibits the funny channel (If) receptor in a current-dependent fashion. If current is an inward Na+/K+ current that activates pacemaker cells of the SA node
- Slows the heart rate by delaying depolarisation and sinus node activation
Ivabradine is a substrate of the CYP450 system and is not an inhibitor of this system. Diltiazem and verapamil, erythromycin and retroviral agents are also metabolised by CYP450 and therefore should not be used with ivabradine.
Indicated in chronic stable angina, heart failure
Side effects
- Blurring of vision
- No QT prolongation
- No negative inotropic properties
- Improvements in exercise tolerance and prevention of exercise-induced ischaemia
Trimetazine
- MOA
- Side effects
MOA
- Myocardial cells derive their energy via fatty acid and glucose metabolism. During ischemia the fatty acid pathway predominates. However, this pathway requires more oxygen than the glucose pathway
- CPT -1 inhibitor and also acts in inhibition of the enzyme long-chain 3-ketoacyl coenzyme A thiolase (LC 3- KAT)
- No significant negative inotropic or vasodilator properties either at rest or during dynamic exercise
Side effects
- Extrapyramidal and parkinsonian symptoms
- Restless leg syndrome.
- Use is limited in severe renal impairment.
Left main coronary artery disease (or equivalent)
• Widespread _______________
• Most prominent in _________________
• ST elevation in aVR ≥ 1mm
• ST elevation in aVR ≥ _____
• In context of symptoms of ischaemia
• Indicates ____________/ ___________/ _______________
• Patients may benefit from _________________
horizontal ST depression;
leads I, II and V4-6;
V1;
severe left main coronary artery / proximal LAD / severe triple vessel disease
early coronary angiography and intervention
What is the modified Sgarbossa criteria?
- ≥ 1 lead with ≥1 mm of concordant ST elevation -> 5 points
- ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression -> 3 points
- ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave -> 2 points
- Score ≥3 (concordance) was found to be highly specific (95%) for diagnosis of AMI
What is the modified Sgarbossa criterria?
- ≥ 1 lead with ≥1 mm of concordant ST elevation
- ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression
- ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave
- Score ≥3 (concordance) was found to be highly specific (95%) for diagnosis of AMI
What is the STEMI equivalents?
Conventional STEMI: elevation of ST segment at J point
De Winter syndrome: J point depression and upsloping ST depression in V1- V6 that continues into tall positive symmetrical T waves often with 1-2mm ST elevation in aVR
Posterior STEMI: ST depression in V1-V3
Wellens sign A: Biphasic anterior T waves
Wellens sign B: Deeply inverted anterior T waves, not always accompanied by chest pain
Hyperacute T waves: tall, often asymmetrical broad based anterior T waves often associated with reciprocral ST depression
Sgarboss criterion
NSTE-ACS
• 2 patterns of ECG associated with NSTEACS
- ST segment depression
- T wave flattening or inversion
• Dynamic changes are strongly suggestive of myocardial ischemia
• ST depression can be upsloping, down-sloping
or horizontal
• _________________ indicates myocardial ischemia
• ______________ more specific and conveys worse prognosis
• ___________________ non-specific for myocardial ischemia
Horizontal or down-sloping ≥ 0.5mm at J point in ≥ 2 contiguous leads;
ST depression ≥ 1mm;
Upsloping ST depression
