Myocardial Infarction

MYOCARDIAL INFARCTION  
Myocardial infarction (MI) is almost always due to the formation of occlusive thrombus at the site of rupture or erosion of an atheromatous plaque in a coronary artery (Fig. 18.59, p. 579). The thrombus often undergoes spontaneous lysis over the course of the next few days, although by this time irreversible myocardial damage has occurred. Without treatment the infarct-related artery remains permanently occluded in 30% of patients. The process of infarction progresses over several hours and therefore most patients present when it is still possible to salvage myocardium and improve outcome (Fig. 18.71).  
CLINICAL FEATURES  
Pain is the cardinal symptom of MI, but breathlessness, vomiting, and collapse or syncope are common features (Box 18.70). The pain occurs in the same sites as angina but is usually more severe and lasts longer; it is often described as a tightness, heaviness or constriction in the chest. At its worst, the pain is one of the most severe which can be experienced and the patient's expression and pallor may vividly convey the seriousness of the situation.  
Most patients are breathless and in some this is the only symptom. Indeed, some myocardial infarcts pass unrecognised. Painless or 'silent' myocardial infarction is particularly common in older or diabetic patients. If syncope occurs, it is usually due to an arrhythmia or profound hypotension. Vomiting and sinus bradycardia are often due to vagal stimulation and are particularly common in patients with inferior MI. Nausea and vomiting may also be caused or aggravated by opiates given for pain relief. Sometimes infarction occurs in the absence of physical signs.  
Sudden death, from ventricular fibrillation or asystole, may occur immediately, and many deaths occur within the first hour. If the patient survives this most critical stage, the liability to dangerous arrhythmias remains, but diminishes as each hour goes by. Thus, it is vital that patients know not to delay...