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PubMed1981

Risk factor and sex differences in single versus multiple vessel coronary artery disease.

We analyzed 305 patients with either single or multiple vessel disease, as demonstrated by coronary arteriography, to determine risk factor and sex differences. Women accounted for more than one fourth of the patients with single vessel disease (group A), but for only one seventh of the individuals with multiple vessel disease (group B). Group A patients were younger and had fewer risk factors, and fewer abnormalities on chest roentgenogram, ECG, and stress test than those in group B. The better reported prognosis for patients with single (versus multiple) vessel coronary artery disease may be due to (1) slightly younger age, (2) greater representation by women, (3) fewer functional abnormalities as assessed by noninvasive tests, and (4) a lower incidence of cardiac risk factors. The presence of hypertension and diabetes seemed most likely to defeat the biologic advantage enjoyed by women over men in resistance to the development of atherosclerotic heart disease.

Adult↗
PubMed1994

[Membrane-physiologic reaction of arteriosclerotic coronary vessels to hypoxia in man].

Human coronary arteries were taken from heart transplant patients. Arteriosclerotic arteries were more depolarized and constricted over the whole PO2 range between 535 and 0 mmHg. During oxygen deficiency, control preparations showed a maximal hyperpolarization of delta V = 10.9 mV and a maximal relaxation of delta T = 0.466 g. Arteriosclerotic arteries, however, became hyperpolarized by merely delta V = 7.1 mV and relaxed by delta T = 0.258 g. In normal coronary arteries, indomethacin reduced the hypoxic hyperpolarization and dilatation at 30 mmHg PO2 by about 51%. The reduction was 26% in arteriosclerotic vessels. The complete removal of the endothelium caused a 49% (74%) restriction of dilatory vascular reactivity. The relationship was quite similar for a carbogen Krebs solution. The hyperpolarizing and dilatory contribution by prostacyclin was 32% in normal and 12% in arteriosclerotic coronary arteries. The remainder could be attributed to the basal release of the endothelial dilator endothelium-derived hyperpolarizing factor (EDHF). Thus it may be concluded that in arteriosclerotic blood vessels, prostacyclin (PGI2) synthesis and release are predominantly diminished. Finally, we found that the ratio PGI2/EDHF in the voltage and tension changes strongly shifted to the PGI2 side with a declining oxygen concentration. This is true for normal and arteriosclerotic vessels. In accordance with the activation curve for vascular smooth muscle, the hyperpolarization leads to relaxation via a closure of Ca2+ channels. Hyperpolarization of 2.5 mV reduces the tension developed by one-half. Minimal changes in cell polarization cause large changes in tissue perfusion.

Animals↗