Myocardial infarction (MI) is the ischemic myocardial necrosis usually resulting from abrupt reduction in coronary blood flow to a segment of myocardium. It is an evolving process that occurs over several hours.
In over 90% of patients with acute MI, an acute thrombus (often associated with plaque rupture) occludes the artery that supplies the damaged area. Other reasons include increased demand in a vulnerable area, and – more rarely – a primary coronary vasospasm (Prinzmetal's), anomalous coronary arteries or embolus.
With a classic presentation, patients report more than 15-30 minutes of crushing chest pain, dyspnea, diaphoresis, nausea with or without vomiting, or lightheadedness. Other presentations include pain in other locations, syncope, cardiac arrest, ventricular tachycardia or ventricular fibrillation, bradydysrrythmias (e.g., bradycardia), shock or malaise (especially in the elderly).
Various enzyme markers are used to try to diagnose myocardial infarction. Troponin is the most sensitive and specific for myocardial injury, but it can be elevated by contusion, myocarditis, or stretching from pulmonary embolization and arrhythmias. Troponin T levels are also elevated in renal failure.
Physical examination may be normal, especially in uncomplicated infarcts. Pulse and heart rate can be normal, increased, or decreased. Inferior MI often has bradycardic symptoms due to the parasympathetic response, whereas an anterior MI often shows tachycardic symptoms due to sympathetic stimulation. Blood pressure may also be normal, elevated, or low, and mild fever is common, though tremendously non-specific.
Extra heart sounds (S3 or S4) may be heard, as well as heart murmurs.
When assessing a patient for myocardial infarction, the blood pressure should always be checked in both arms. Also, heart failure and congestion should be evaluated, as well as jugular venous distention and pulmonary crackles.
An ST elevation is indicative of an in-progress infarct caused by a complete occlusion. After necrosis occurs, the elevation disappears, and a Q wave may appear. If there is a partial occlusion, there may be as ST depression or inverted T wave.
The ultimate goal of management, however, is to reperfuse the heart. The maximum effect happens within one hour, and there is less benefit as time passes, with no real benefit after 24 hours.
Complications of acute myocardial infarction can be broken down into mechanical and electrical. 20-30% of patients who have had an acute myocardial infarction will have post-MI ischemia, which confers an increased risk of reinfarction or death.
Mechanically, the papillary muscles of the mitral valves may break.
The Killip classification is one way of assessing the prognosis of a patient with an MI, though this system's usefulness is disputed. In essence, however, it says that people with no real symptoms of MI will have a good prognosis, and that the prognosis decreases as the patient has more symptoms.