Cardiovascular disease coronary angiography

Coronary vasoconstriction is a potential risk of all triptans, but the risk is minimal in the absence of coronary artery disease or uncontrolled hypertension. Chest tightness and pain are reported in up to 15% of patients taking sumatriptan and are presumed to be due to vasoconstriction of the coronary arteries. Myocardial infarction has been reported and as a consequence sumatriptan should not be used in patients with cardiovascular disease (11). Intravenous sumatriptan causes some coronary vasoconstriction during diagnostic angiography. Myocardial infarction occurred in a patient who had received sumatriptan 6 mg subcutaneously, but the causal association was not clear. 

The block of middle fibers of LBB has to be included in the differential diagnosis of prominent R wave in VI (see Table 5.5). To make this diagnosis in patients with ischemic heart disease the involvement (ischaemia or necrosis) of lateral wall has to be rule out (coronary angiography and/or cardiovascular magnetic resonance-CMR-) (Fig. 5.64). In the case of lateral MI a positive T wave in VI is seen, and in case of block of middle fibers the T wave in VI is usually negative. 

A 38-year-old man with a family history of cardiovascular and cerebrovascular disease makes an appointment for a routine physical examination with a physician he has not seen before. He explains that his father died young of a heart attack and that two paternal uncles have suffered strokes in their late 40s. Physical examination reveals yellowish lumps on his eyelids (xanthelasmas, which are often associated with a lipid disorder) and a resting blood pressure of 186/95 mm Hg. There is some excess visceral fat, and his body mass index calculates to 26.5. Total serum cholesterol (476 mg/dL) and triglycerides (288 mg/dL) are elevated and subsequent angiography reveals atherosclerotic restrictions of at least two coronary arteries. 

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. 

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