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INTEREST in the management of patients with coronary artery disease has focused on subgroups of patients defined by arteriographic findings. In the Veterans Administration Cooperative Study, the first subgroup with significantly improved survival when managed surgically and followed for 2-3 years was that of patients with disease of the left main coronary artery.1 Other reports, including the only other randomized controlled study,2 confirmed this finding.Patients with left main disease are not a homogeneous group.3'4 Those with more severe stenosis or with an abnormality of left ventricular (LV) function were reported to have a worse prognosis.4 In coronary heart disease patients without left main disease, a benefit from surgery has also been reported in subgroups based on clinical criteria alone.5 In this report, we examine the effects of bypass surgery on survival and on the incidence of myocardial infarction (MI) in angiographically and clinically defined subgroups of patients with left main coronary artery disease. tients who had a significant stenosis (at least 50% reduction of the luminal diameter) of the left main coronary artery. The coronary arteriograms were reviewed to confirm the presence of a significant left main lesion and to assess the degree of stenosis. MIs that occurred after randomization were identified in accordance with definitions used by the Coronary Drug Project8 and by Hultgren et al.9 (appendix A). ECGs and autopsy protocols, as well as most left ventriculograms, were reviewed centrally (appendix B).In

In five men with a history of susceptibility to high-altitude pulmonary edema (HAPE), hemodynamics and pulmonary gas exchange were measured at sea level, and again 24 hours following ascent to an altitude of 3,100 m. At sea level, all findings were essentially normal including a mean pulmonary arterial pressure [See Equation in PDF File] of 13.8 ± 1.9 mm Hg. None of the subjects developed clinically detectable pulmonary edema at altitude. Wedge pressures and cardiac output remained normal. [See Equation in PDF File] increased remarkably, being 38.8 ± 10.3 mm Hg at rest and 53.2 ± 11.6 mm Hg during moderate exercise. Acute relief of hypoxia only partially relieved this pulmonary hypertension. Arterial blood gases were normal at sea level. In spite of hyperventilation at altitude, arterial O 2 pressure was only 50.8 ± 6.1 torr at rest and fell to 41.4 ± 3.3 torr during exercise due to a widening of the alveolar-arterial O 2 pressure difference to 28.0 ± 6.8 torr. Hence, these men susceptible to HAPE developed excessive pulmonary hypertension and impaired pulmonary O 2 exchange without detectable pulmonary edema following ascent to high altitude. The increase in pulmonary vascular resistance is only partially explained by hypoxic pulmonary vasoconstriction.

Cardiac catheterization studies have been performed in four patients during acute pulmonary edema at an elevation of 12,300 feet in the central Peruvian Andes. Pulmonary hypertension, low cardiac output, arterial unsaturation, and low normal pulmonary artery wedge pressures were observed. Oxygen breathing was accompanied by a prompt, marked fall in pulmonary artery pressure and a slight rise in wedge pressure, indicating the presence of anoxic pulmonary arteriolar constriction. In one patient, pulmonary artery wedge pressures were not elevated during added hypoxia nor during exercise. The blood pressure response to the Valsalva maneuver was normal. Similar studies were carried out in four subjects after recovery from pulmonary edema. One 9-year-old boy had persisting pulmonary hypertension. None had evidence of underlying cardiac disease. An abnormal rise in pulmonary artery pressure during induced hypoxia was observed in three of four patients. It is concluded that pulmonary edema at high altitude is a unique form of pulmonary edema produced by hypoxia under certain conditions of exposure at high altitude. Severe pulmonary hypertension due to anoxic pulmonary arteriolar constriction is present. There is no evidence that pulmonary venous constriction and cardiac failure are causative mechanisms.

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