Acute coronary syndromes clinical presentation

Patients with acute coronary syndromes such as acute myocardial infarction and unstable angina remain at risk for recurrent myocardial ischemia despite therapy with antiplatelet agents and heparin. Although first clinical trials indicate a possible use of oral direct TIs for the prevention of cardiovascular events in patients after acute myocardial infarction, the presently available data are still limited and it has not... 

Overdose is common amongst users (up to 22% of heavy users report losing consciousness). The desired euphoria and excitement turns to acute fear, with psychotic symptoms, convulsions, hypertension, haemorrhagic storke, tachycardia, arrhythmias, hyperthermia coronary vasospasm (sufficient to present as the acute coronary syndrome with chest pain and myocardial infarction) may occur, and acute left ventricular dysfunction. Treatment is chosen according to the clinical picture (and the known mode of action), from amongst, e.g. haloperidol (rather than chlorpromazine) for mental disturbance diazepam for convulsions a vasodilator, e.g. a calcium channel blocker, for hypertension glyceryl trinitrate for myocardial ischaemia (but not a p-... 

This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features - arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve -, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein Ilb/IIIa antagonism. 

Generally, the clinical presentation of myocardial ischaemia is the characteristic pain known as angina pectoris or some equivalents (e.g. dyspnoea), although sometimes ischaemia may be silent (see Silent ischaemia , p. 302). If the anginal pain is new or if it has increased with respect to previous discomfort (crescendo angina), this constitutes the clinical condition called acute coronary syndrome (ACS), which may evolve into myocardial infarction (MI) (see Section Acute coronary syndrome , p. 209). If the angina pain appears with exercise... 

The term acute coronary syndrome (ACS) encompasses all the clinical situations with acute myocardial ischaemia expressed by chest pain, discomfort or equivalent, which appears suddenly at rest (de novo) or has increased with regard to prior anginal (in crescendo angina). All this leads the patient to seek urgent medical care. However, occasionally the patient may underestimate the symptoms or the physician may not interpret them properly. In addition, the ACS may occur with no anginal pain, or the pain may be atypical or may present other... 

Peripheral arterial occlusion can be the initial manifestation of cardiac or systemic disease. At times, patients with chronic stable claudication may experience abrupt shortening of the distance at which claudication occurs, and this may be the only symptomatic evidence of an acute arterial occlusion either by embolization of by thrombus formation on a pre-existing arterial stenosis. The situation is not chronic and stable any more, but acute and unstable. As ischemia becomes more severe, the patient with chronic peripheral arterial disease develops ischemic pain at rest. The pathophysiologic mechanisms and the clinical presentation parallel the evolution of chronic stable angina pectoris to unstable angina and acute coronary syndromes. 

A comparison of these two diseases in respect to the clinical symptoms may seem impossible at first sight. However, a few details of the syndromes in both diseases may be mentioned. The most evident symptom of toxemia of pregnancy, the elevated blood pressure, is not seen in coronary sclerosis or, at least, not to such an extent. However, according to Brown et oi. (1957), the blood pressure in coronary disease, before infarction has occurred, is slightly raised on an average, compared with that in healthy men of the same age. After the recovery from the acute phase of an infarction, the blood pressure becomes fixed at a lower level than that in the healthy controls. A regulating system to supply the tissues with blood as well as possible is certainly present and substances released from the ischemic and injured tissues must play a role. 

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