Myocardial Infraction 

Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with MI, many events are either "silent" or are clinically unrecognized, evidencing that patients, families, and health care providers often do not recognize symptoms of a MI. The appearance of cardiac markers in the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis.

Cardiac markers help to categorize MI, which is considered part of a spectrum referred to as acute coronary syndrome that includes ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina. This categorization is valuable because patients with ischemic discomfort may or may not have ST-segment elevations on their electrocardiogram. Those without ST elevations may ultimately be diagnosed with NSTEMI or with unstable angina based on the presence or absence of cardiac enzymes. Additionally, therapeutic decisions, such as administering an intravenous thrombolytic or performing percutaneous coronary intervention (PCI), are often made based on this categorization

Pathophysiology

The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality.

Nonatherosclerotic causes of MI include coronary vasospasm as seen in variant (Prinzmetal) angina and in patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve; occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of oxygen supply and demand, such as acute anemia from GI bleeding. MI induced by chest trauma has also been reported, usually following severe chest trauma such as motor vehicle accidents and sports injuries.

History

The history is critical in making the diagnosis of MI and sometimes may provide the only clues that lead to the diagnosis in the initial phases of the patient presentation.

  • Chest pain, usually across the anterior precordium is typically described as tightness, pressure, or squeezing.
  • Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is more frequently affected; however, a patient may experience pain in both arms.
  • Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor ventricular compliance in the setting of acute ischemia. Dyspnea may be the patient's anginal equivalent, and, in an elderly person or a patient with diabetes, it may be the only complaint.
  • Nausea, abdominal pain, or both often are present in infarcts involving the inferior or posterior wall.
  • Anxiety
  • Lightheadedness with or without syncope
  • Cough
  • Nausea with or without vomiting
  • Diaphoresis
  • Wheezing
  • Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
  • As many as half of MIs are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. A high index of suspicion should be maintained for MI especially when evaluating women, patients with diabetes, older patients, patients with dementia, and those with a history of heart failure. Patients with a permanent pacemaker in place may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.

Physical

The physical examination can often be unremarkable.

  • Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic.
  • Hypertension may precipitate MI, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics.
  • Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of MI usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct.
  • Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.
  • Rales may represent congestive heart failure.
  • Neck vein distention may represent pump failure. With right ventricular failure, cannon jugular venous a waves may be noted.
  • Third heart sound (S3) may be present.
  • A fourth heart sound is a common finding in patients with poor ventricular compliance that is due to preexisting heart disease or hypertension.
  • Dysrhythmias may present as an irregular heartbeat or pulse.
  • Low-grade fever is not uncommon.

Causes

The most frequent cause of MI is rupture of an atherosclerotic plaque within a coronary artery with subsequent arterial spasm and thrombus formation.

Other causes include the following:

  • Coronary artery vasospasm
  • Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)
  • Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts due to pulmonary disease usually occur when demand on the myocardium dramatically increases relative to the available blood supply.)
  • Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
  • Cocaine, amphetamines, and ephedrine
  • Arteritis
  • Coronary anomalies, including aneurysms of the coronary arteries
  • Increased afterload or inotropic effects, which increase the demand on the myocardium
  • Aortic dissection, with retrograde involvement of the coronary arteries
  • Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis (see Myocardial Infarction in Childhood).

Risk factors for atherosclerotic plaque formation include the following:

  • Age
  • Male gender
  • Smoking
  • Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders
  • Diabetes mellitus
  • Poorly controlled hypertension
  • Type A personality
  • Family history
  • Sedentary lifestyle