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At least 631 records · Page 35Linked to original sources
PubMed1996

[Angiographic study of stenosis and calcification of coronary vessels in long-term dialysis patients: examination of risk factors for coronary calcification].

Coronary atherosclerosis and calcification score were assessed angiographically in 30 uremic patients receiving dialysis (8 patients with diabetes mellitus [DM dialysis group] and 22 patients without DM [non-DM dialysis group] who were suspected of having coronary artery disease because of their clinical symptoms and electrocardiographic findings. Thirty non-uremic subjects (11 with DM and 19 without DM) served as controls. Twelve dialysis patients (40%) did not have significant coronary artery disease, and the rate of significant coronary artery disease in dialysis patients overall was less than that in the control subjects. The calcification score of dialysis patients was significantly higher than that of the control patients (P < 0.0001), and also scores of the non-DM dialysis group and the DM dialysis group were higher than those of each group of control subjects. The scores were significantly correlated with the duration of dialysis in uremic patients as a group (r = 0.52; P < 0.01) and the non-DM dialysis group (r = 0.70; P < 0.01), but were not correlated with the duration of dialysis in the DM dialysis group. The scores were correlated with serum phosphate concentration, but not with serum calcium concentration, calcium phosphate product, alkaline phosphatase levels total cholesterol or age. Calcification scores were extremely high (> 21) in six uremic patients who had high serum c-terminal parathyroid hormone concentrations. These findings indicate that serum phosphate concentration, serum c-terminal parathyroid hormone concentration, and the duration of dialysis are closely associated with coronary calcification in long-term dialysis patients.

Adult↗
PubMed1996

Coronary and systemic hemodynamic effects of sustained inhibition of nitric oxide synthesis in conscious dogs. Evidence for cross talk between nitric oxide and cyclooxygenase in coronary vessels.

Sustained inhibition of NO synthesis (N omega-nitro-L-arginine [L-NNA], 20 mg.kg-1.d-1, 7 days) was investigated at rest and during exercise in conscious dogs. At rest, L-NNA did not alter mean arterial blood pressure but markedly increased total peripheral resistance (+73 +/- 14%, P < .01). Exaggerated hypertension was observed during exercise (+132 +/- 5 mm Hg after L-NNA versus +113 +/- 5 mm Hg before L-NNA, P < .01). L-NNA decreased the resting coronary artery diameter by 6 +/- 1% and suppressed its exercise-induced dilation but had no effect on coronary blood flow and resistance. L-NNA decreased flow repayment volumes during reactive hyperemia, but corresponding flow debt volumes remained unchanged. The cyclooxygenase inhibitor diclofenac (10 mg/kg) had no effect on reactive hyperemia parameters before L-NNA but reduced flow repayment volumes, durations, and corresponding debt-to-repayment ratios in L-NNA-treated dogs (all P < .05). In vitro, indomethacin blunted the residual relaxation to bradykinin of large coronary arteries taken from L-NNA-treated, but not from control, dogs. Bradykinin-induced increase in 6-ketoprostaglandin F1 alpha production was greater in coronary arteries taken from L-NNA-treated dogs (+ 179 +/- 41 pg/mm2) than from control dogs (+ 66 +/- 18 pg/mm2) (P < .05). These results indicate that (1) NO is of major importance in the control of systemic but not coronary resistance vessels at rest and during exercise, and (2) after L-NNA, the cyclooxygenase pathway is involved in myocardial reactive hyperemia and in the residual relaxation to bradykinin of isolated coronary arteries. Thus, in conscious dogs, the cyclooxygenase pathway might act as a protective mechanism of the coronary circulation when endothelial nitric oxide synthesis is altered.

Acetylcholine↗
PubMed1993

Prospective evaluation of thallium-201 reinjection in single-vessel coronary patients undergoing coronary bypass surgery.

Twenty-two patients with single-vessel left anterior descending coronary artery disease were investigated by means of dipyridamole stress thallium-201 myocardial perfusion scintigraphy, using single photon emission tomography (SPET), 1 week before and 2-5 weeks after coronary bypass surgery. The dose of dipyridamole was 0.56 mg/kg, and the injected activity of 201Tl was 74 MBq. Before surgery, and after completion of the redistribution study, a further 37 MBq of 201Tl was injected. Ten minutes and 1 h later, repeated SPET imaging were performed. SPET images were evaluated both subjectively and semiquantitatively, using a five-grade segmental defect score system, with higher scores for more severe perfusion defects. Before surgery, the 3-h redistribution images revealed complete or partial persistence of the perfusion defects in all patients. On the images taken 10 min after reinjection, these defects were completely filled in four cases, and partially filled in ten cases. Further positive changes were observed on the 1-h post-reinjection images in four cases. Three of the 1-h post-reinjection images exhibited a paradox redistribution. The stress images after surgery corresponded well to the 201Tl distribution on the preoperative 1-h post-reinjection images in 11 cases. The average of the segmental defect severity scores was 17.0 after stress, 10.1 at rest, 7.1 10 min after reinjection and 6.4 1 h after reinjection. After surgery, the average of both the post-stress and the 3-h redistribution scores was 3.1.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Bypass↗
PubMed1988

The differential effects of alpha 2-adrenergic stimulation on the myocardium and coronary vessels in the isolated rat heart.

The differential effects of alpha 2-adrenoceptor stimulation on myocardial contractility and coronary circulation were examined in the isolated perfused rat heart. We studied 20 Sprague-Dawley rats of similar age (26-28 weeks) and body weight (500-550 gm). Myocardial contractility (LV +dp/dt and developed pressure, LVP) and coronary flow resistance (CFR) were tested in the isolated isovolumic hearts using Langendorff preparation at a constant perfusion rate (2.5 ml/min/100 g BW) of Krebs-Henseleit bicarbonate solution. Group I (N-7) received B-HT 920 (specific alpha 2-adrenergic agonist, 0.6 to 58 micrograms/min), Group II (N-7) received B-HT 920+Yohimbine (300 nM in the perfusate). Group III (N-6) received vehicle only. Baseline LVP, LV +dP/dt and CFR were not significantly different among the 3 groups. During drug or vehicle administration, LVP and LV +dP/dt remained unchanged in all the groups. Coronary flow resistance increased in a dose-response fashion with a maximum increase of 22.7 +/- 3.6 (SE) mmHg/ml/min/g LV in Group I, and 10.5 +/- 2.0 mmHg/ml/min/g LV in Group II (p less than 0.02). We conclude that in the Sprague-Dawley rat heart, the physiologic effects of alpha 2-adrenoceptors are predominant in the coronary circulation but not in the myocardium itself possibly because of absence of post-synaptic alpha 2-adrenergic receptors in the rat myocardium.

Adrenergic alpha-Agonists↗
PubMed1996

[Simultaneous operations of the carotid bifurcation and coronary vessels in moderate systemic hypothermia].

Comorbidity of coronary heart disease and carotid stenosis raises the question of surgical stratification. A simultaneous approach of carotid endarterectomy and coronary revascularization, both under conditions of moderate hypothermic extracorporeal circulation, was applied in 48 patients. Considering the complexity of the procedures required the 30-day mortality (2.1%) and perioperative incidence of permanent stroke (2.1%) or myocardial infarction (0%) appeared to be comparably low.

Aged↗
PubMed1991

[Alinidine in multi-vessel coronary disease: reduction of stress-induced ischemic reaction].

Ten patients suffering from an angiographically documented coronary two- or three-vessel disease were examined to evaluate the effects of the specific bradycardiac agent alinidine during a bicycle stress test. Hemodynamic and electrocardiographic parameters were compared before and after an intravenous application of 30 mg of the substance. The alinidine plasma levels 30 min after the injection were 160.6 +/- 22.5 ng/ml) (mean +/- SEM). Alinidine significantly (p less than 0.05) reduced the resting levels of heart rate (8.5%), double product (10.3%), myocardial oxygen consumption (9.1%), and cardiac output (9.0%). During exercise, significantly less ST-segment depression (p less than 0.001) in the EKG was observed after alinidine application in nine out of 10 patients, and the rise of pulmonary artery pressure was significantly reduced (34.7 vs 38.1 mm Hg, mean p less than 0.05). However, alinidine had no effect on the maximum heart rate at the end of exercise. We, therefore, assume that the substance has additional anti-ischemic properties.

Adult↗