Estimated read time is 5 minutes, 4 seconds
Acute Myocardial Infarction (AMI) also known as a heart attack is caused by the complete or partial occlusion of a coronary artery and requires prompt hospitalization and extensive care management. It is part of a spectrum of conditions that result from myocardial ischemia known as an acute coronary syndrome. Get more details on acute coronary syndrome here.
Acute MI includes both non-ST segment elevation myocardial infarction in short NSTEMI and ST-segment elevation myocardial infarction - STEMI.
Causes of Acute Myocardial Infarction are due to:
Severe pre-existing coronary artery disease (coronary atheroma),
Prinzmetal angina or drug-induced vasoconstriction,
Reduced O2 content (e.g. In Hypoxia or anemia).
Decreased coronary perfusion pressure (CPP=DAP-LVEDP) caused by hypotension or raised LV wall tension (hypertrophy or dilation).
Vasodilator drugs causing coronary steal,
Heart valve disease (particularly aortic stenosis).
Sustained tachycardia, arrhythmias (also reduce diastolic time),
Sympathetic stimulation (e.g. pain, agitation, or inadequate sedation),
Hyperdynamic states (e.g. pregnancy, hyperthyroidism, sepsis, inotropes including beta-agonists, calcium e.t.c.
The 3 acute coronary syndromes are:
ST-segment elevation myocardial infarction aka transmural MI is myocardial necrosis with electrocardiogram changes indicating ST-segment elevation not quickly reversed by nitroglycerin.
This is characterized by elevated troponin I or troponin T and Creatinine kinase. In practice, the ST elevation alone is sufficient to treat because the troponins take time to rise.
Non–ST-segment elevation myocardial infarction also known as subendocardial MI is myocardial necrosis that is evidenced by elevation of cardiac markers in the blood specifically troponin I or troponin T and CK.
There is no acute ST-segment elevation. Electrocardiogram changes such as an ST-segment depression or T-wave inversion may be present.
Unstable angina is characterized by prolonged, severe angina, usually at rest, possibly with ECG changes.
NSTEMI and unstable angina are often grouped together as non-ST elevation ACS (NSTEACS)
Based on the causative mechanism, myocardial infarction can be classified into five types:
Type 1: This is the commonest type. It occurs due to a primary coronary event such as atherosclerotic plaque rupture, fissuring, coronary dissection or erosion. It is also referred to as a spontaneous myocardial infarction.
Type 2: This occurs due to an imbalance in myocardial oxygen supply and demands. This can be a case of ischemia because of an increased oxygen demand like in hypertension or due to decreased oxygen supply like in an embolism, coronary artery spasm, hypotension(reduced blood pressure), arrhythmia, anemia or tachycardia (increased heart rate). It usually happens during surgery or illness.
Type 3: This type is related to sudden cardiac death with ischaemic features on an electrocardiogram, angiography, or autopsy but before troponin could be checked.
Type 4a: This is a myocardial infarction that is associated with percutaneous coronary intervention whereby there are signs and symptoms of myocardial infarction with cTn values more than 5 × 99th percentile upper reference limit.
Type 4b: This type is associated with a documented stent thrombosis
Type 5: It is a myocardial Infarction associated with coronary artery bypass grafting (CABG) with features of myocardial infarction with cTn values >10 × 99th percentile upper reference limit.
The patient with either STEMI or NSTEMI will present with similar symptoms:
Chest pain is usually the first symptom. It is deep, substernal or retrosternal/epigastric crushing severe pain. The pain radiates to the jaw, neck and down the inner part of the left arm and shoulders lasting at least 20 minutes to 7 hours.
It is accompanied by dyspnea, sweating, nausea, and vomiting, feeling of impending doom,
The pain is relieved little or only temporarily by rest or nitroglycerin.
Difficulty in ventilating (Dyspnea) and weakness may be the presenting complains in patients with left ventricular failure, pulmonary edema, shock, or with arrhythmia (Tachycardia or bradycardia, palpitations, ventricular arrhythmias),
some patients present with syncope,
Patients with a right ventricular infarction may present with an elevated right ventricular filling pressure, distended jugular veins clear lung fields, and hypotension.
Patients may have pallor, cool, and diaphoretic skin. Some may present with peripheral or central cyanosis.
In cases of hypotension, Pulse may be thready with variable low blood pressure, although many patients initially have some degree of hypertension during pain.
On auscultation, heart sounds are usually somewhat distant; a 4th heart sound is almost universally present in these patients. There may be a soft systolic blowing apical murmur that indicates a papillary muscle dysfunction.
Chest x-ray to rule out other causes and check for heart failure.
Urea and electrolytes,
Blood Glucose levels,
Magnesium, Calcium, Phosphate levels.
Serial 12 lead Electrocardiogram shows ST-segment depression/elevation or T-wave elevation/inversion.
For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more contiguous leads subtending the damaged area
Serial Serum cardiac markers / Cardiac enzymes particularly Troponin I and T (12 hours post-onset of chest pain) kinase (CK) – MB and isoforms, Myoglobin and other non-specific markers.
Immediate coronary angiography (unless fibrinolytics are given) for patients with STEMI.
Coronary angiography most often combines diagnosis with percutaneous coronary intervention. When possible, emergency coronary angiography and PCI are done as soon as possible after the onset of acute myocardial infarction.
Imaging – Echocardiogram (Ischemic section of the myocardium may be dyskinetic),
Treatment of acute myocardial infarction is the use of antiplatelet drugs, anticoagulants, nitrates, beta-blockers, statins, and reperfusion therapy.
Management is divided into;