• Myocardial infarction

موضوع: • Myocardial infarction الخميس مايو 08, 2008 12:49 am

Definition

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 and physicians 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

CLINICAL
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
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

Lab Studies
Troponin is the preferred biomarker for diagnosis.
Troponins have the greatest sensitivity and specificity in detecting MI. The test result is both diagnostic as well as prognostic of outcome.
Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.
For early detection of myocardial necrosis, sensitivity of this laboratory test is superior to that of the creatine kinase-MB (CK-MB). Troponin I is detectable in serum 3-6 hours after an AMI and its level remains elevated for 14 days.
Troponin is also the optimum biomarker for the evaluation of patients with MI who have coexistent skeletal muscle injury.
Creatine kinase–MB level
CK-MB levels begin to rise within 4 hours after injury, peak at 18-24 hours, and subside over 3-4 days. A level within the reference range does not exclude myocardial necrosis.
Occasionally, very small infarcts can be missed by CK-MB; therefore, a troponin level should be measured for patients suspected of having had MI who have negative serial CK-MBs.
Myoglobin levels
Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as 2 hours after MI. Myoglobin levels rise early in the course of MI.
The marker has high sensitivity but poor specificity. When performed in conjunction with other studies, it may be useful for the early detection of MI.
Complete blood count
CBC is indicated if anemia is suspected as a precipitant. Transfusion with packed red blood cells may be indicated.
Leukocytosis may be observed within several hours after an AMI. It peaks in 2-4 days and returns to levels within the reference range within 1 week.
Chemistry profile
Potassium and magnesium levels should be monitored and corrected.
Creatinine levels must be considered before using an angiotensin-converting enzyme (ACE) inhibitor.
C-reactive protein (CRP) is a marker of acute inflammation. Patients without biochemical evidence of myocardial necrosis but with elevated CRP level are at increased risk of a subsequent ischemic event.
Erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for weeks.
Serum lactate dehydrogenase (LDH) level rises above the reference range within 24 hours of MI, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.

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