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Summary:Because thromboembolic pathogenesis in mechanical prosthetic valves (MP) might involve selective MP platelet consumption with consequent reduced platelet survival, it has been suggested that lowered platelet half-life (TI 1 2 ) detection provides identification of postoperative thrombotic risk. Porcine heterografts (PH) possess less thromboembolic hazards than MP; thus, comparative evaluation of PH versus MP platelet Tl/2 is germane to the test's thrombotic predictive value, yet platelet kinetics in PH require elucidation. Accordingly, 5khromium platelet Tl/2 was determined in 16 patients with substituted valves (10 PH and 6 MP). Average platelet Tl/2 in PH (2.9f0.6 d) was similar (p>0.05) to MP (3.2f0.6 d), and both were considerably lower (pC0.05) than platelet TI^ in normal subjects (NL, 5.1 f0.5 d). Furthermore, platelet T , p was below the lowest NL platelet T i p (4.0 d) in seven PH and three MP patients. Thus, frequency and extent of decreased platelet survival in PH are common and equal to MP. These results indicate that platelet half-life does not afford thromboembolic predict-* This work was supported in part by Program Project grant HL-14780 from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, and by California chapters of the American Heart Association, Dallas, Texas, USA.This work was presented in part at the 52nd Scientific Sessions of the American Heart Association, November 14, 1979, Anaheim, California, USA. ability in patients with mechanical valves and, instead, favors prosthetic-induced physical trauma causing abnormal platelet survival.

Although morphine sulfate and aminophylline are commonly employed in the management of acute pulmonary edema of diverse etiologies including idiopathic hypertrophic subaortic stenosis (IHSS), the effects of morphine and aminophylline on left ventricular (LV) outflow obstruction in IHSS are unknown. Thus to determine the actions of morphine and aminophylline in IHSS, seven patients with IHSS (mean peak resting systolic gradient 16 mmHg, mean Valsalva provoked gradient 87 mmHg) received 5 mg morphine intravenously and simultaneous LV and brachial arterial pressures were continously monitored and cardiac outputs obtained. On return to control hemodynamics, 250 mg aminophylline was infused in three patients and hemodynamics repeated. Peak increase in gradient with morphine occurred in 5 min in each patient and average maximal gradient was 48 mmHg (p<0.001). Peak LV systolic pressure increased 158 to 182 mmHg (p<0.05); LV end‐diastolic pressure declined 12 to 8 mmHg (p<0.005); cardiac index decreased 3.18 to 2.89 l/min/m2 (p<0.005); while heart rate and total systemic vascular resistance were unchanged (p>0.05). Aminophylline increased peak gradient to 57 mmHg; lowered LV end‐diastolic pressure by 2 mmHg; decreased total systemic vascular resistance 1610 to 1120 dyne s · cm−5; while cardiac index was unchanged. Therefore morphine and aminophylline can rapidly increase LV outflow obstruction to marked extents in IHSS. These data indicate morphine worsens subaortic stenosis by decrease in LV preload through systemic venodilation, whereas aminophylline increases intraventricular gradient predominantly by peripheral arterial dilation. Thus morphine and aminophylline should be avoided, or used cautiously in low doses, in management of acute pulmonary edema in IHSS.