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The sudden development of a harsh apical systolic murmur in a patient with a recent myocardial infarct is usually considered to indicate rupture of a papillary muscle or perforation of the interventricular septum.1,2 the differential diagnosis of a loud precordial systolic murmur of sudden onset may be difficult and to describe a syndrome whereby such a murmur may occur secondary to mechanical dysfunction of a papillary muscle. ILLUSTRATIVE PATIENTS PATIENT 1. —An 85-year-old white male, previously in good health, was admitted to hospital with severe crushing substernal pain which he had had for several hours. His blood pressure was 135/75 mm Hg, and his pulse rate was 88 per minute and regular. The lungs were clear on auscultation. The heart was not enlarged, and there were no murmurs or gallop sounds. The electrocardiogram on admission showed an acute anteroseptal myocardial infarct. The serum glutamic oxaloacetic transaminase (SGOT) was 165

It has been known for some time that patients with polycythemia vera are predisposed to angina pectoris and myocardial infarction.1 A recent study described a group of patients with angina pectoris or acute myocardial infarction, or both, who had moderate erythrocytosis but in whom hematologic studies failed to demonstrate any evidence of polycythemia vera.2 Reduction of the hematocrit by phlebotomy decreased the frequency of anginal attacks in some patients. In an effort to learn the relationship of hematocrit to myocardial infarction the hematocrit levels of 100 men and 120 women with acute myocardial infarction were compared with those of age-matched subjects without clinical evidence of coronary artery disease.3,4 It was found that the hematocrit levels for the men and women with acute myocardial infarction were significantly higher than those for the control subjects (Fig. 1).The purpose of this paper is to present evidence that phlebotomy may

Continuous and simultaneous pressures were recorded from the pulmonary artery, small pulmonary vein (1.5–2.0 mm in diameter), large pulmonary vein and left atrium in 7 intact dogs lightly anesthetized with urethane. Pressures within the pulmonary artery and left atrium remained relatively constant whereas pressure in the small pulmonary vein varied widely. Pressure in the large pulmonary vein fluctuated over a narrower range than did the pressure in the small pulmonary veins. At times the pressure in the large pulmonary vein changed without a corresponding change in left atrial pressure, It is suggested that the pulmonary venous blood reservoir behaves in a manner similar to the systemic venous blood reservoir and that pressure variations reflect spontaneous adjustments in volume of the reservoir. The findings also support the concept of a “throttle valve” action of the pulmonary veins.