[Clinical studies of the hemodynamics of coronary circulation using the methods of selective administration of xenon-133 into the coronary vessels].
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We disrupted the FOG-2 gene in mice to define its requirement in vivo. FOG-2(-/-) embryos die at midgestation with a cardiac defect characterized by a thin ventricular myocardium, common atrioventricular canal, and the tetralogy of Fallot malformation. Remarkably, coronary vasculature is absent in FOG-2(-/-) hearts. Despite formation of an intact epicardial layer and expression of epicardium-specific genes, markers of cardiac vessel development (ICAM-2 and FLK-1) are not detected, indicative of failure to activate their expression and/or to initiate the epithelial to mesenchymal transformation of epicardial cells. Transgenic reexpression of FOG-2 in cardiomyocytes rescues the FOG-2(-/-) vascular phenotype, demonstrating that FOG-2 function in myocardium is required and sufficient for coronary vessel development. Our findings provide the molecular inroad into the induction of coronary vasculature by myocardium in the developing heart.
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A macroscopic pathological assessment of the coronary arteries of a pig's heart, in which stent implantation and intra-vascular ultrasound and thermography pullbacks were performed, shows that during percutaneous coronary catheterization and intervention, one of the major vessel traumas occurs in the very proximal part of the coronary arteries, where the guiding catheter tip is manipulated to adequately engage the vessels.
Management of patients with concomitant coronary and aorto-iliac atherosclerosis is controversial. It is universally accepted that coronary artery surgery should precede aorto-iliac reconstruction. The technique described consists of an ascending aorta to bifemoral graft. This technique allows combined surgery of the coronary arteries and to the lower limbs without opening the peritoneum.
OBJECTIVE: We examined the morphological changes induced by repeated endothelial denudation in coronary artery (CA), as well as functional changes in the endothelium-dependent and smooth muscle responses to various vasoactive agents during the process of intimal thickening. METHODS: We observed vascular responses in denuded and non-denuded portions of pig CA while being fed a normal diet (n = 11, N group) or 2% cholesterol diet (n = 25, C group) to intracoronary acetylcholine (ACh), 5-hydroxytryptamine (5-HT), substance P (SP), and isosorbide dinitrate (ISDN) with and without the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v.) over a period of 8 weeks. Balloon endothelial denudation of the left anterior descending CA was carried out every 2 weeks. RESULTS: In N group, maximum vasoconstriction was obtained with ACh 2 weeks after the first denudation [26 +/- 5% vs. 1 +/- 1% pre-denudation, p < 0.05]. L-NAME did not affect ACh-induced CA diameter changes. Thereafter, the response to ACh was attenuated by repeated denudation in N groups. However, the degree of 5-HT-induced CA narrowing at the denuded portion increased from 7 +/- 4% (0 week) to 88 +/- 8% (8 weeks) (p < 0.05). The changes resulted in severe myocardial ischaemia, and suggested that endothelium-dependent vasodilation was progressively attenuated while hyperreactivity of vascular smooth muscle simultaneously increased. Vasodilation induced by SP was attenuated somewhat, but ISDN-induced vasodilation was preserved. Although mild hypercholesterolaemia was induced in C group, the vascular responses to these vasoactive agents did not differ from those of N group. CONCLUSIONS: Repeated CA endothelial injury and regeneration induce the change of morphology and vascular reactivity in the denuded portion regardless of atherogenic diet. This study strongly suggests that intimal thickening caused by repeated endothelial injury and regeneration induces specific vascular responses to vasoactive agents. Moreover, it is also suggested that during the progression of intimal thickening, increased vascular smooth muscle contraction and decreased endothelium-dependent dilation appear in a stimulus-dependent manner, often leading to severe coronary vasoconstriction accompanied with definitive ECG ST change.
UNLABELLED: The diameter changes of angiographically normal epicardial coronary arteries were studied in 25 patients in correlation to nifedipine plasma levels. In group 1 (15 patients) 20 mg of s.l. nifedipine were administered. Measurements of the coronary lumen size (automated contour detection system, accuracy 0.12 mm) and detection of plasma levels (gas-chromatography) were done before and 10, 20 and 30 min after drug administration. According to the slope of nifedipine plasma levels, patients were divided into group 1 A (n = 4) and 1 B (n = 11). Plasma levels in both groups were: at 10 min, 27.8 +/- 9.8 and 13.5 +/- 4.5 ng/ml resp.; P less than 0.05; at 20 min, 54.0 +/- 11.7 and 21.7 +/- 6.6 ng/ml resp.; P less than 0.001; at 30 min, 79.1 +/- 9.3 and 28 +/- 9.8 ng/ml resp.; P less than 0.001. The corresponding diameter changes in A and B were: 7.3 +/- 5.1%/.-5.6 +/- 9.0% resp.; P less than 0.01; 11.4 +/- 4.1% and -4.5 +/- 11.3% resp.; P less than 0.01; 14.5 +/- 5.9% and 0.5 +/- 13.6% resp.; P less than 0.05. In group 2 (10 patients) 1 mg nifedipine was administered intravenously within 4 min. Measurements were done at 1 min intervals during infusion as well as 7 and 15 min after beginning and compared to a placebo group (n = 10). Peak plasma levels amounted to 16.7 +/- 5.7 ng/ml after 7 min. The maximum coronary dilation was reached after 4 min (verum 5.0 +/- 6.8%; placebo 3.2 +/- 3.6%). Significant differences between both groups were observed after 7 min (verum 4.1 +/- 5.3%; placebo -3.1 +/- 5.8%, P less than 0.05) and 15 min (verum 1.2 +/- 3.2%; placebo -6.2 +/- 8.4%; P less than 0.05). CONCLUSION: based on significantly different plasma levels following sublingual application of 20 mg nifedipine a classification of patients into "early-" and "late-coronary-responders" could be established. After intravenous infusion of 1 mg nifedipine peak plasma levels were much lower than after sublingual application of 20 mg and coronary diameters showed only a mild increase.
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