Features and outcome of no-reflow after percutaneous coronary intervention.

No-reflow is an uncommon complication that may occur after revascularization of patients with acute myocardial infarction, after interventions in saphenous vein bypass grafts, and after the use of some new interventional devices. However, the clinical impact of no-reflow after coronary intervention is unknown. Accordingly, this study examined the incidence, clinical presentation, angiographic characteristics, and outcome of no-reflow after percutaneous coronary intervention. No-reflow was defined as an acute reduction in antegrade flow (< or = 1, as defined by the Thrombolysis in Myocardial Infarction [TIMI] trial) not attributable to abrupt closure, high-grade stenosis, or spasm of the original target lesion. Among 10,676 coronary interventions performed between October 1988 and June 1993, no-reflow occurred in 66 patients (0.6%). These patients were compared with a subgroup of 500 consecutive patients who did not exhibit no-reflow. The incidence of no-reflow was 30 of 9,431 (0.3%) for percutaneous transluminal coronary angioplasty, 1 of 317 (0.3%) for excimer laser, 8 of 104 (7.7%) for Rotablator (Heart Technologies, Bellevue, Washington), 21 of 469 (4.5%) for extraction atherectomy, and 6 of 355 (1.7%) for directional atherectomy. Compared with those without no-reflow, patients with no-reflow experienced a 10-fold higher incidence of in-hospital death (15%) and acute myocardial infarction (31%). Correlates of in-hospital mortality included acute myocardial infarction on presentation (p = 0.006) and final flow < 3 (as defined by the TIMI trial) at completion of the procedure (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamics of mitral stenosis: a review.

This review discusses the latest developments in the hemodynamics of mitral stenosis. English-language journal articles, reviews, and textbooks from the clinical, physiology, and engineering literature related to mitral valve stenosis were identified and reviewed. The main conclusions are: (1) the hemodynamics of mitral stenosis are determined by the complex anatomical and pathophysiologic features of the valve apparatus, (2) the properties of the left ventricle, atrium, and pulmonary vasculature also have a major impact on the hemodynamic significance and the clinical syndrome of mitral stenosis, (3) the valve and the cardiac chambers have a functional reserve that become exhausted as the stenosis worsens and/or the compensatory mechanisms of the chambers fail, and (4) a careful approach to data acquisition and analysis will lead to an accurate assessment of the hemodynamics of mitral stenosis before and after therapeutic interventions.

Inhibition of radiogenic mammary carcinoma in rats by estriol or tamoxifen.

Mammary carcinomas have been induced by 3.5 Gy whole-body gamma radiation administered at age 40 to 50 days to virgin female Sprague-Dawley rats. In 142 irradiated controls carcinoma incidence averaged 7.8% in survivors observed less than 300 days and 38.3% of those surviving longer (P less than 0.001 by t test). Mammary cancer promotion was inhibited by two methods: estriol (E3) 638 micrograms/month (2.2 microns/mo) subcutaneously for natural life span begun 2 weeks after exposure reduced cancer incidence from 76% in controls to 48% after 331 to 449 mean days observation until neoplasia was palpable (P less than 0.02 by chi-square analysis). Uterine weights were similar in control and treated groups, and were 15% to 18% greater than uteri of nonirradiated controls from other simultaneous experiments. Six monthly 638-micrograms doses of 17 alpha ethinyl estriol (EE3) reduced tumors from 88% in controls to 64% (P less than 0.05 by chi-square analysis) and delayed cancer onset (P less than 0.01-0.04 by life table analysis). Ethinyl estradiol (EE2) after 6 months' treatment similarly delayed mammary tumor development reducing incidence to 75% (NS), with a six-fold increase in nonmammary epithelial malignant tumors. Estriol administration begun between 3 days before to 5 days after radiation did not alter mammary cancer incidence in six experiments. Monthly implantation of 2.5 mg tamoxifen (4.44 microns/mo) started 2 weeks after radiation reduced mammary cancer incidence from 83% to 14% after 307 to 314 days' observation (P less than 0.001 by chi-square analysis). Treated rats had atrophic ovaries and uteri consistent with blockade of endogenous estradiol activity. Short-term parenteral E3 or EE3 therapy using 10 to 30 micrograms/kg/day (35-100 microns/kg/day) rapidly differentiated virgin rat mammary glands without impairment of subsequent estrus cycles and offers an alternative to castration or life-long antiestrogen therapy for reduction of risk of radiogenic mammary carcinoma.