Myocardial Infarction

Definition

Etiology and risk factors

• Coronary atherosclerosis with plaque rupture or plaque erosion, followed by platelet aggregation and thrombus formation.

• Coronary vasospasm, for example cocaine-induced or Prinzmetal angina
• Coronary embolism, such as in atrial fibrillation or infective endocarditis
• Coronary dissection
• Severe anemia, shock, sepsis, tachyarrhythmia, or severe hypertension causing oxygen supply-demand mismatch
• Small-vessel disease, vasculitis, or sickle-cell disease

• Non-modifiable: increasing age, male sex, family history of premature coronary artery disease
• Modifiable: smoking, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle, unhealthy diet, and psychosocial stress.

Pathogenesis

1. An atherosclerotic plaque in a coronary artery ruptures, erodes, or hemorrhages.
2. Subendothelial collagen and lipid-rich necrotic material are exposed.
3. Platelets adhere, become activated, and aggregate. They release ADP, thromboxane A2, and serotonin, which amplify platelet aggregation and vasospasm.
4. Tissue factor activates the coagulation cascade.
5. A thrombus forms and may completely occlude the coronary artery.
6. Ischemia causes loss of contractility within seconds to minutes. Persistent ischemia causes irreversible myocyte necrosis, beginning in the subendocardium and progressing outward as a wavefront.
7. The extent of infarction depends on site of occlusion, duration of occlusion, collateral circulation, and myocardial oxygen demand.

Types of MI

• Usually caused by complete and persistent coronary artery occlusion.
• ECG shows ST-segment elevation in contiguous leads or a new equivalent ischemic pattern.
• Requires immediate reperfusion therapy.

• Usually due to subtotal or transient coronary occlusion.
• Troponin is elevated, but there is no persistent ST-segment elevation.
• ECG may show ST depression, T-wave inversion, or may be initially normal.

• Spontaneous MI due to atherosclerotic plaque rupture/erosion and acute coronary thrombosis.

• MI due to mismatch between myocardial oxygen supply and demand, without acute plaque rupture necessarily.

• Occurs in association with PCI, CABG, or stent thrombosis.

Clinical features

• Severe, crushing, constricting retrosternal chest pain lasting more than 20 minutes
• Radiation to left arm, shoulder, neck, jaw, back, or epigastrium
• Pain is usually not fully relieved by rest or sublingual nitrates
• Sweating, pallor, anxiety, nausea, vomiting, dyspnea, and palpitations

• Dyspnea
• Syncope
• Unexplained fatigue
• Epigastric discomfort
• Silent MI, especially in diabetes

• Tachycardia or bradycardia
• Hypotension
• Cool clammy skin
• Fourth heart sound
• Basal crepitations and raised JVP in heart failure
• New systolic murmur in papillary muscle dysfunction or ventricular septal rupture

Diagnosis

1. ECG

• STEMI: ST elevation in anatomically contiguous leads
• NSTEMI/unstable ischemia: ST depression and/or T-wave inversion may occur
• Development of pathological Q waves suggests myocardial necrosis

2. Cardiac biomarkers

• High-sensitivity cardiac troponin I or T is the preferred test.
• A dynamic rise and/or fall supports acute myocardial injury.
• CK-MB may assist in suspected reinfarction because it returns to baseline earlier than troponin.

3. Echocardiography

• Regional wall-motion abnormality
• Reduced left ventricular ejection fraction
• Mechanical complications, such as acute mitral regurgitation or ventricular septal rupture

4. Coronary angiography

5. Additional tests

• Complete blood count, blood glucose, renal function, electrolytes, lipid profile
• Chest radiograph if heart failure or another diagnosis is suspected

Management

Initial management

• Rest and cardiac monitoring
• Oxygen only if hypoxemic, in respiratory distress, or shock
• Aspirin, unless contraindicated
• A P2Y12 inhibitor in appropriate patients
• Anticoagulation
• Nitrates for persistent ischemic pain if blood pressure permits
• Analgesia for severe pain
• Treat arrhythmias, pulmonary edema, hypotension, or cardiogenic shock promptly

Reperfusion therapy

• Primary PCI is preferred when it can be performed rapidly.
• If timely PCI is unavailable and there are no contraindications, fibrinolytic therapy may be considered in eligible patients with recent symptom onset, followed by transfer for angiography/PCI.

• Fibrinolysis is not indicated.
• Management is based on risk stratification, antithrombotic therapy, and an early invasive strategy for high-risk patients.

Drugs for secondary prevention

• Dual antiplatelet therapy for the indicated duration after ACS/PCI
• High-intensity statin
• Beta-blocker, particularly with left ventricular dysfunction, arrhythmia, or ongoing angina
• ACE inhibitor or ARB, particularly in anterior MI, hypertension, diabetes, chronic kidney disease, or reduced LVEF
• Mineralocorticoid receptor antagonist when LVEF is reduced with heart failure or diabetes, provided renal function and potassium allow

Complications

Early complications

1. Arrhythmias: ventricular tachycardia, ventricular fibrillation, atrial fibrillation, sinus bradycardia, and heart block
2. Acute left ventricular failure and pulmonary edema
3. Cardiogenic shock
4. Pericarditis: usually within days after transmural MI
5. Right ventricular infarction: can cause hypotension with raised JVP and clear lungs

Mechanical complications

• Papillary muscle rupture: acute severe mitral regurgitation and pulmonary edema
• Ventricular septal rupture: harsh pansystolic murmur with acute heart failure/shock
• Free-wall rupture: hemopericardium and cardiac tamponade, often rapidly fatal

Late complications

• Ventricular aneurysm
• Mural thrombus with systemic embolism
• Chronic heart failure
• Recurrent MI
• Post-MI pericarditis, also called Dressler syndrome
• Persistent ventricular arrhythmias and sudden cardiac death

Prevention and rehabilitation

• Complete smoking cessation
• Control of hypertension, diabetes, and dyslipidemia
• Regular exercise and cardiac rehabilitation
• Weight management and a heart-healthy diet
• Adherence to antiplatelet, statin, and other prescribed therapy
• Psychological support and return-to-work counseling

Conclusion

1. Specimen collection and transport
   Blood, urine, sputum, stool, pus, CSF, throat swab, etc. Correct timing, aseptic collection, proper container, and rapid transport are essential.
2. Direct examination of specimens
   Microscopy using Gram stain, acid-fast stain, wet mount, and special stains to demonstrate organisms and inflammatory cells.
3. Culture methods
   Inoculation on appropriate media such as blood agar, MacConkey agar, chocolate agar, and selective/enrichment media, followed by incubation.
4. Identification of bacteria
   Colony morphology, haemolysis, pigment, motility, biochemical reactions, antigen detection, automated identification, MALDI-TOF, and molecular tests.
5. Antimicrobial susceptibility testing
   Kirby-Bauer disc diffusion, MIC determination, E-test, automated susceptibility systems, and detection of resistance mechanisms.
6. Serology and antigen detection
   Detection of bacterial antigen or antibody in selected infections.
7. Molecular diagnosis
   PCR, nucleic-acid amplification tests, sequencing, and rapid multiplex assays.
8. Blood culture and culture-negative infection work-up
   Especially important in septicemia, endocarditis, and enteric fever.