Ischemic heart disease electrocardiogram

Cardiovascular Effects. Information regarding cardiovascular effects in humans after inhalation exposure to chromium and its compounds is limited. In a survey of a facility engaged in chromate production in Italy, where exposure concentrations were 0.01 mg chromium(VI)/m3, electrocardiograms were recorded for 22 of the 65 workers who worked in the production of dichromate and chromium trioxide for at least 1 year. No abnormalities were found (Sassi 1956). An extensive survey to determine the health status of chromate workers in seven U.S. chromate production plants found no association between heart disease or effects on blood pressure and exposure to chromates. Various manufacturing processes in the plants resulted in exposure of workers to chromite ore (mean time-weighted concentration of 0-0.89 mg chromium(ni)/m3) water-soluble chromium(VI) compounds (0.005-0.17 mg chromium(VI)/m3) and acid-soluble/water-insoluble chromium compounds (including basic chromium sulfate), which may or may not entirely represent trivalent chromium (0-0.47 mg chromium/m3) (PHS 1953). No excess deaths were observed from cardiovascular diseases and ischemic heart disease in a cohort of 4,227 stainless steel production workers from 1968 to 1984 when compared to expected deaths based on national rates and matched for age, sex, and calender time (Moulin et al. 1993). No measurements of exposure were provided. In a cohort of 3,408 individuals who had worked in 4 facilities that produced chromium compounds from chromite ore in northern New Jersey sometime between 1937 and 1971, where the exposure durations of workers ranged from <1 to >20 years, and no increases in atherosclerotic heart disease were evident (Rosenman and Stanbury 1996). The proportionate mortality ratios for white and black men were 97 (confidence limits 88-107) and 90 (confidence limits 72-111), respectively. 

The cardiotoxicity of fluorouracil was first identified in 1975 (38). Of 140 patients treated with intravenous 5-fluorouracil, 4 developed ischemic chest pain within 18 hours of either the second or third dose. In three of these patients the pain recurred after subsequent doses. Predose electrocardiograms in two cases were normal. None of the four patients had a history of ischemic heart disease, although all had received left ventricular irradiation (39). 

Rapid peripheral intravenous injection of concentrated ionic contrast media produces a brief rise in systemic arterial pressure followed by a prolonged fall the diastolic pressure decreases more than the systolic pressure and the heart slows the pulse contour changes, and the venous pressure rises the arterial hypotension is more marked if injection is rapid. The electrocardiogram can show flattening, splitting, or T-wave inversion tachycardia is probably compensatory, as are the concomitant increases in venous pressure and pulmonary arterial pressure. Hypotension associated with a vasovagal reaction probably explained four deaths from acute coronary insufficiency (two each with iodoalphionic acid and iopa-noic acid) in patients with ischemic heart disease. 

Either planar or tomographic imaging is performed for diagnosis of ischemic heart disease and myocardial infarction. Both may be performed electrocardiogram (ECG)-gated. 

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