Of 43 consecutive black patients (42 male) with sarcoidosis, 12 (28%) complained of chest pain that met the clinical criteria for typical (four patients) or atypical (eight patients) angina pectoris. These patients underwent cardiopulmonary assessment, which included exercise and redistribution thallium-201 scans and, ifindicated, coronary angiography. Nine control patients with sarcoidosis matched for age and duration of disease, but without chest pain, were also studied by thallium-201 scintigraphy. Six of the 12 patients with chest pain had thallium scans indicative of myocardial ischaemia, but all had normal coronary angiograms; no patient from the control group had evidence of ischaemia on the thallium scan. Four additional patients with chest pain and one from the control group had other (non-specific) abnormalities on the thallium scan, so that scans were abnormal in 10 of the 12 patients with sarcoidosis who had chest pain. Most patients with anginal chest pain reported partial or complete relief of symptoms with nitrates. Anginal chest pain appears to be common in black male patients with sarcoidosis, is associated with abnormal myocardial perfusion scans, and may result from myocardial sarcoidosis.
To determine how often acute lateral myocardial infarcts may be electrocardiographically "silent," a new approach was utilized in which subjects were selected by admission thallium scintigraphy. Thirty-one patients with their first infarction were identified with moderate to severe perfusion defects of the lateral and posterolateral walls, persistent over 7 days and associated with severe wall motion abnormalities. Patients with involvement of the anterior, septal or "inferior" regions were not included. In nine patients, the perfusion defect extended to the anterolateral wall: all developed ST elevation and Q waves in at least one of the "lateral" leads (I, aVL or V6) but none showed changes in the "inferior" leads (II, III or aVF). In the other 22 patients, the perfusion defect was limited to the lateral and posterolateral walls: only 12 showed ST elevations (inferior leads only in 7, lateral leads only in 2, both leads in 3) and only 9 developed Q waves (inferior in all). In 8 of these 22 patients, the infarct was silent in the sense that no ST segment elevation or Q waves were seen, although ST depressions or T wave inversions, or both, in all but one patient were compatible with subendocardial infarction. The results indicate that the standard electrocardiogram is insensitive to changes in the lateral and posterolateral regions. Additional diagnostic studies are needed for proper localization and sizing of acute myocardial infarcts.
Summary: Exercise testing has changed dramatically in scope over the past 50 years. While initially used to assess functional capacity, it is now also utilized to detect the presence and severity of coronary artery disease (CAD), to evaluate postmyocardial infarction patients at risk for future cardiac events, to screen certain asymptomatic populations for CAD, and to evaluate dysrhythmias, peripheral vascular disease, and lung disease. Dynamic exercise in continuous multistage protocols is most popularly employed because of the more easily measured workload. The safety of exercise testing, its contraindications and termination end points are summarized. The sensitivity of exercise testing ranges between 60 and 70% while specificity has been reported between 85 and 90%. Both sensitivity and specificity are enhanced through use of radionuclide exercise thallium imaging and ventricular angiography .
Summary: Diltiazem, a calcium-channel blocker, is an effective antianginal agent, particularly in treating the vasospastic type of angina pectoris. This drug has recently been released for use in the United States. Noncardiac untoward effects of diltiazem are few. We describe a case of mania with psychotic features that occurred while a patient was on diltiazern.Key words: coronary heart disease, diltiazem, mania Case ReportA 56-year-old man with chronic stable angina was seen because of chest pain at rest and increasing chest pain on exertion. Coronary angiography had revealed an 80% proximal lesion of a small nondominant right coronary artery. His medications included propranolol and nitrates. Following administration of diltiazem 30 mg q.i.d., his chest pain disappeared. There was no personal or family history of psychiatric disorders. After one week on diltiazem, changes in his mental status were noted including initability and increased level of activity. After being on the diltiazem for approximately 8 weeks, he was admitted to the psychiatric ward with symptoms and signs that met DSM-III criteria for diagnosis of mania. These symptoms and signs included labile mood, pressure of speech, restlessness, hyperactivity (riding a bike 12 miles a day), paranoid ideations, delusions of granduer, and threatening behavior. However, in the absence of personal or family history of mental disorders and a relatively late age of onset, the possibility of an organic affective syndrome was considered. Due to coincident temporal sequence of symptoms and diltiazem therapy, the decision was made to withhold the diltiazem and observe the patient without adding psychotropic medications. Symptoms of paranoid ideations, hyperactivity, grandiosity, and pressure of speech cleared during the first 48 h of admission. Lability of mood, restlessness, and threatening behavior returned to baseline within 7 days.
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