Myocardial infarction usually seen in middle-aged, male smokers presenting with central chest pain radiating to the left arm, with ST-segment elevation, elevated troponin levels and coagulative necrosis.
Description
Myocardial infarction (MI), colloquially known as a heart attack, is a medical condition resulting from insufficient blood flow to a part of the heart, leading to myocardial necrosis. The lack of oxygenated blood is usually due to a blockage in a coronary artery, typically from atherosclerosis. It is one of the most common causes of death globally, with a high burden of morbidity.
Pathogenesis
The pathogenesis of myocardial infarction is largely linked to atherosclerosis, a condition in which plaques comprising lipids, inflammatory cells, and fibrous tissue accumulate in the arterial walls, particularly in coronary arteries. Rupture or erosion of these plaques can trigger platelet aggregation and thrombus formation, causing partial or complete occlusion of the coronary artery, and hence myocardial ischaemia and infarction.
Subtypes
Myocardial infarctions are commonly classified into two types based on ECG findings:
- ST-elevation myocardial infarction (STEMI): Characterised by ST-segment elevation due to complete occlusion of a coronary artery.
- Non-ST elevation myocardial infarction (NSTEMI): Characterised by ST-segment depression or T-wave inversion due to partial occlusion of a coronary artery.
Epidemiology, Risk Factors & Associations
- Male gender and advanced age increase the risk.
- Lifestyle factors including smoking, lack of physical activity, poor diet.
- Medical conditions such as diabetes, hypertension, hyperlipidaemia.
Clinical Features
- Classic presentation includes severe central chest pain, radiating to the left arm or jaw, associated with sweating and dyspnoea.
- Some individuals, particularly diabetics and the elderly, may have a ‘silent’ myocardial infarction, with no recognised chest pain.
Complications
Early Complications (within the first few days to a week)
- Arrhythmias: The most common early complication, occurring in about 90% of patients, primarily within the first 10 hours following the MI. These can include ventricular tachycardia, ventricular fibrillation, atrial fibrillation, and heart block.
- Heart Failure/Cardiogenic Shock: Heart failure can occur in about 22% of patients within the first 24 hours following an MI, usually as a result of significant left ventricular dysfunction. Cardiogenic shock, a severe form of heart failure, occurs in approximately 7% of patients and carries a high mortality rate.
- Myocardial Rupture: Although rare (1-3% of cases), rupture of the ventricular free wall, ventricular septum, or papillary muscle can occur within the first 3-5 days after an MI, often leading to sudden death.
Late Complications (after the first week to years)
- Postinfarction Cardiomyopathy: Also known as ischemic cardiomyopathy, it is a common late complication and can lead to chronic heart failure.
- Ventricular Aneurysm: Occurs in about 10-15% of patients, usually within the first 2 weeks to several months after the MI. This can lead to ventricular arrhythmias or thrombus formation with subsequent embolisation.
- Dressler Syndrome: A form of pericarditis occurring weeks to months after MI, affecting around 1-3% of patients.
Reperfusion Injury – Reperfusion injury can occur upon re-establishment of the coronary blood flow. It can lead to arrhythmias, myocardial stunning (temporary loss of contractile function), and microvascular obstruction.
Pathological Features
Histopathology
- Macroscopic: Early changes are not visible. By 12-24 hours, the infarcted myocardium may appear dark mottled.
- Microscopic: Timeline of changes – Coagulative necrosis with loss of nuclei and striations (4-12 hours), neutrophilic infiltrate (1-3 days), phagocytosis with early granulation tissue (4-7 days), mature granulation tissue with neovascularisation (1-3 weeks), and finally scar formation (>1 month).
Serology
- Elevation in cardiac biomarkers, most notably cardiac troponin I or T.
Biochemistry
- Other markers include creatine kinase-MB (CK-MB) and myoglobin, but these are less specific.
Radiological Features
General Features
- Radiologic imaging is not typically the first-line diagnostic tool for MI, but it can provide supportive evidence and assess complications.
XR
- Chest X-ray may show signs of pulmonary oedema in the case of left ventricular failure secondary to MI.
CT
- Non-contrast: Can assess for complications, such as ventricular aneurysm.
- C+ Arterial: Cardiac CT angiography can visualise coronary artery occlusions or stenosis.
MRI
- T1: In the acute and subacute stages, T1-weighted imaging shows hyperintense signal due to oedema and haemorrhage.
- T2: T2-weighted imaging shows hyperintense signal due to oedema.
- T1 Gad+: Late gadolinium enhancement (LGE) allows for visualisation of myocardial scarring.
US
- B-mode: Echocardiography can assess ventricular function and identify regional wall motion abnormalities.
- Colour Doppler: Can identify valvular regurgitation secondary to papillary muscle dysfunction.
Diagnosis
Diagnosis of myocardial infarction is typically made based on clinical presentation, ECG changes, and elevated cardiac biomarkers.
Differential Diagnosis
- Angina pectoris: This is chest pain due to transient myocardial ischaemia, but without myocardial necrosis.
- Acute pericarditis: This can cause chest pain and ECG changes, but cardiac biomarkers are typically not elevated.
- Pulmonary embolism: Can cause chest pain and dyspnoea. ECG may show right heart strain.
Management
Management includes immediate reperfusion therapy, either via thrombolysis or percutaneous coronary intervention (PCI), along with antiplatelet agents, beta-blockers, ACE inhibitors, and statins.