Systolic apical filling in a patient with progressive apical hypertrophic cardiomyopathy and giant negative T waves.

A relatively asymptomatic 58-year-old non-hypertensive male developed changes of remarkable apical hypertrophic cardiomyopathy associated with deep negative T-wave change and marked ventricular dyssynergy without apparent precipitating cause over a nine-year period.

Pulmonary hypertension secondary to thrombocytosis in a patient with myeloid metaplasia.

A 72-year-old physician with myeloid metaplasia developed marked thrombocytosis, pulmonary hypertension, and right heart failure following splenectomy. No cause for the pulmonary hypertension could be found. The pulmonary hypertension and right heart failure returned to normal when hydroxyurea therapy corrected the thrombocythemia. It is concluded that thrombocytosis may cause pulmonary hypertension, mediated by pulmonary capillary obstruction from cellular components, involving platelet aggregation, microthrombosis, and stasis, and possible vasoconstrictor effects.

Regional pulmonary function in supine patients with mitral valve disease.

Supine tidal volume regional ventilation and perfusion images obtained in the posterior and lateral projections demonstrated several alterations in patients with mitral valve disease. Reversal of the gravitational perfusion gradient correlated with pulmonary venous and arterial hypertension; the supine studies reliably distinguished normal subjects from mitral patients. The reversed gradient was from posterior-base to anterior-apex. Focal defects were common and contributed to the reversed gradient in 50% of patients. Perfusion defects larger than those of ventilation, simulating emboli, occurred in 32%, particularly in the middle lobe and superior segment areas. Relative hypoventilation of the left lung was seen in 44% of these patients.