Diagnosis of AMI/ ACS

Diagnosis of AMI/ ACS: Both CK-MB and troponin levels rise 4-6 hours after infarction. Troponins are more sensitive and specific for the diagnosis of AMI than CK-MB. CK-MB is useful to diagnose re-infarctions happening within 10-15 days of previous AMI as troponin levels take about 10-12 days to come back to baseline. Fresh ECGs will also help in diagnosing re-infarctions. Serum myoglobin level rises the earliest in AMI, but it is non-specific. Serum LDH levels start to rise after 24 hours, peak in 3-6 days and normalize in 14 days. LDH 1 is cardiac specific. Ratio of LDH1:LDH 2 > 1 is seen in AMI. Levels of brain natriuretic peptide or BNP and proBNP rise a few hours after AMI. Elevated levels of C-reactive protein (CRP), IL6 and serum amyloid A (SAA) have been found to correlate positively with impending plaque rupture and AMI in patients with CAD. Echo will show regional wall motion abnormalities.

Differential diagnosis of ACS

STEMI

• ST elevation of more than 0.1 mV
• New LBBB
• T wave inversion
• Hyperacute T waves
• Reciprocal ST depression
• Presence of Q wave
• Elevated cardiac biomarkers

NSTEMI

• No Q wave
• ST depression
• T wave inversion
• Elevated cardiac biomarkers

Unstable Angina

• No Q wave
• ST depression
• T wave inversion
• Normal cardiac biomarkers

Correlation between ECG changes and corresponding vessel involved

Posterior wall MI: It is seen in CAD involving the posterior descending artery, also called posterior interventricular artery. It can branch off from the RCA (right dominant circulation, most common), left circumflex (left dominant) or both (co-dominant). Hence, posterior wall MI may accompany inferior wall or lateral wall MI.

Right ventricular MI (RVMI): It may accompany inferior wall MI. Diuretics and nitrates are contraindicated in right ventricular MI. Fluids and reperfusion are the cornerstone of treatment. Arrhythmias, syncope and cardiogenic shock are common in RWMI. The typical triad observed on physical examination is hypotension, jugular vein distention and clear lungs. Tricuspid regurgitation, Kussmaul’s sign and pulsus paradoxus may occur. LV ejection fraction is normal. ECG shows ST elevation in leads II,III and aVF with disproportionate ST segment elevation in lead III than in lead II. Right sided chest leads, V1R to V6R, will show ST elevation.

Cocaine and AMI: Cocaine use can cause AMI by inhibition of uptake of catecholamines, coronary vasoconstriction, alpha adrenergic receptor activation, increased endothelin 1 production, decreased nitric oxide production, platelet activation and thrombus formation. Patients are typically younger and do not have classic CAD. Both STEMI and NSTEMI can occur. Treatment is as for AMI, beta blockers should be used with caution though.

III) Complications of myocardial infarction

i) Sudden cardiac death: It is defined as death occurring within one hour of the onset of symptoms. It is most commonly from ventricular fibrillation. Risk factors are male gender, smoking, long QT syndrome, age>40 years, atrial fibrillation, presence of LVH and hypertension.

ii) Arrhythmias: They can happen due to ischemia of the SA node or conducting system. Sinus bradycardia, VPCs, AF, VF, ventricular tachycardia, LBBB or RBBB and heart blocks can occur. Heart block and sinus bradycardia are more common in IWMI.

iii) Cardiogenic shock: Cardiogenic shock is defined as a systolic blood pressure of less than 90 mmHg for at least 30 minutes, which is secondary to myocardial dysfunction. It is unresponsive to fluids but improves with inotropic support. It is seen more commonly in anterior wall STEMI. Left ventricular dysfunction is the most frequent cause of cardiogenic shock.

iv) Heart failure: It may involve the left or right ventricle or be bi-ventricular.

v) Rupture: It is a rare complication, occurring on days 3-7 after an AMI. It is often fatal. Ventricular free wall rupture is seen in anterior wall AMI with LAD involvement. It leads to cardiac tamponade, hemopericardium, or rupture can be through interventricular septum or papillary muscle. The latter two scenarios will present with new onset systolic murmurs.

vi) Mural thrombosis and embolism: Mural thrombi are often associated with large anterior wall AMI. They can embolize to the brain (causing stroke) and other organs.

vii) Aneurysm formation: It typically forms around 4-8 weeks after an AMI. It is seen in the left ventricle and consists of a thin fibrous, collagen rich wall. Aneurysmal tissue is non-contractile and can cause arrhythmias. It is a common site for mural thrombus formation.

viii) Pericarditis: Transient, fibrinous pericarditis with effusion may be seen in transmural AMI.

ix) Post-myocardial infarction syndrome or Dressler’s syndrome: It is an autoimmune pericarditis that develops as a reaction to pericardial antigens, 6-8 weeks after AMI. Patients present with fever, malaise, pleuritic chest pain that is worse on inspiration and in supine position, improves on leaning forward, and the presence of pericardial friction rub. It is treated with NSAIDs or corticosteroids. Rarely cardiac tamponade can occur.