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 for diagnosing re-infarction occurring within 10-15 days of a previous AMI, because troponin levels take about 10-12 days to return to baseline. Fresh ECGs also help in diagnosing re-infarction. Serum myoglobin 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. A ratio of LDH1:LDH2 > 1 is seen in AMI. Levels of brain natriuretic peptide (BNP) and proBNP rise a few hours after AMI. Elevated levels of C-reactive protein (CRP), IL6, and serum amyloid A (SAA) correlate positively with impending plaque rupture and AMI in patients with CAD. Echo will show regional wall motion abnormalities.
| Vessel involved | Leads showing primary changes | Type of infarct |
| LAD | V1-4 | Anterior |
| Proximal LAD | V1-2 | Anteroseptal |
| Mid LAD or Circumflex | I, aVL, V5-6 | Anterolateral |
| Left main or LMCA | ST elevation in aVR; ST depression in I,II, V4-6//Global convex ST elevation | Extensive anterior, global, diffuse |
| Left circumflex | I,aVL | Lateral |
| Right coronary | II,III,aVF | Inferior |
| Posterior descending artery | Tall R wave and ST depression in V1-V2; ST elevation, Q waves in posterior leads V7-9 | Posterior |
Posterior wall MI: This is seen in CAD involving the posterior descending artery (also called the posterior interventricular artery). It can branch off from the RCA (right-dominant circulation, most common), the left circumflex (left-dominant), or both (co-dominant). Because of this, posterior wall MI may accompany inferior wall or lateral wall MI.
Right ventricular MI (RVMI): This 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 RVMI. The typical triad 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 compared with lead II. Right-sided chest leads (V1R to V6R) will show ST elevation.
Cocaine and AMI: Cocaine use can cause AMI through inhibition of catecholamine uptake, 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.
III) Complications of myocardial infarction
i) Sudden cardiac death: This is defined as death occurring within one hour of the onset of symptoms. It is most commonly due to ventricular fibrillation. Risk factors include male gender, smoking, long QT syndrome, age > 40 years, atrial fibrillation, presence of LVH, and hypertension.
ii) Arrhythmias: These can occur due to ischemia of the SA node or the 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, 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: This may involve the left or right ventricle, or it may be bi-ventricular.
v) Rupture: This is a rare complication, occurring on days 3-7 after an AMI, and it is often fatal. Ventricular free wall rupture is seen in anterior wall AMI with LAD involvement. It can lead to cardiac tamponade and hemopericardium. Rupture can also occur through the interventricular septum or papillary muscle; these two scenarios 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: This 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: This 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 the 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.
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