Angina pectoris clinical presentation

Nesto RW, Waxman S, Mittleman MA, et al. Angioscopy of culprit coronary lesions in unstable angina pectoris and correlation of clinical presentation with plaque morphology. Am J Cardiol 1998 81 225-228. 

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... 

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 similarly interesting case is that of a 68 year old male patient who was first seen in 1958 with symptoms of marked myocardial ischemia and electrocardiographic evidence of an old inferior myocardial infarction. Insulin dependent diabetes melli-tus had been present since 1932. In spite of diabetic control with diet and insulin in this subject, lipemia (approximately 2 gm neutral fat per 100 ml plasma) persisted and abdominal colics recurred. With heparin and later Depot-Thrombocid his neutral lipids ranged between 300—500 mg per 100 ml and clinical symptoms (angina pectoris and episodes of abdominal pain) improved considerably. An additional feature in this patient was gout with uric acid levels above 9 mg per 100 ml and attacks of acute gouty arthritis on several occasions between 1958 and 1959. 

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