This report describes the clinical, angiographic, and hemodynamic findings in nine patients who manifested nonatheromatous' ischemic heart disease induced by chronic industrial exposure to nitroglycerin and subsequent withdrawal. They represent nearly 5% incidence in the group of 200 workers with similar exposure. One patient died suddenly, and the disease was commonly without premonitory symptoms. Of the eight survivors, five were studied and none showed evidence of significant organic obstructive disease. However, in one studied during the withdrawal state, coronary and digital arteriospasm was demonstrated, and was readily reversed by nitroglycerin. Survivors exhibited exercise symptomatology and hemodynamic impairment similar to other patients with myocardial dysfunction from ischemic heart disease. Complete left bundle-branch block with late sudden death occurred in one, and chronic recurrent atrial fibrillation is present in a second.An attractive hypothesis suggests that chronic vasodilatation evokes homeostatic vasoconstriction, the latter persisting during the withdrawal period with cardiac ischemia. A more detailed study of the vasodilator action of organic nitrate and the homeostatic reaction is warranted. In addition, the effect of chronic administration of potent, longacting organic nitrate-based drugs should be examined in the light of this industrial experience.Additional Indexing Words: Industrial medicine Compensatory vasoconstriction Chronic vasodilator therapy Coronary artery spasm T HE ACUTE vasodilatory effects of nitroglycerin form the basis for the symptomatic therapy of angina pectoris. Daily

No abstract

A patient with chronic fibrous mediastinitis presented with bronchial, superior vena caval, and pulmonary venous obstruction, pulmonary hypertension, and pulmonary fibrosis. Pulmonary venous obstruction was confirmed at surgery and explains the hemodynamic findings of elevated pulmonary artery and pulmonary wedge pressures despite low left atrial pressure. Pulmonary function studies showed marked alterations in ventilation-distribution, diffusion, work of breathing, and fixed airway resistance. It is concluded that the pulmonary arterial hypertension was due, in large part, to the pulmonary venous hypertension caused by pulmonary venous obstruction. Unsuccessful surgical intervention has been followed by 10 months of observation during which aldosterone inhibition together with use of chlorothiazide has prevented recurrence of heart failure and pleural effusion. The relationship between the physiological abnormalities and the patient's symptoms is discussed along with the possible relationship between pulmonary venous obstruction and pulmonary fibrosis.

No abstract