摘要:

No Abstract.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

No Abstract.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

No Abstract.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

No Abstract.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

No Abstract.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTThe potent platelet inhibitory and vasodilator properties of prostacyclin suggest that levels of this substance may be of relevance to drug action and pathologic processes in the coronary vascular bed. Attempts to estimate the coronary secretion rate of prostacyclin have relied on measurements of metabolites obtained via cardiac catheter, usually as an adjunct to coronary angiography. To test the hypothesis that such procedures might themselves perturb endogenous biosynthesis of prostacyclin we used mass spectrometry to measure plasma levels of 6-keto-prostaglandin (PG) F,, across the coronary vascular bed, as well as to assess the excretion of a major urinary metabolite, 2,3-dinor-6-keto-PGF,, (PGI-M), in patients undergoing cardiac catheterization. PGI-M excretion increased variably from a median 100 to 205 pg/mg creatinine (p < .01) during catheterization with angiography and remained elevated 2 to 4 hr after initiation of the procedure. However, cardiac catheterization without angiography also stimulated metabolite excretion, perhaps reflecting catheter-induced vascular trauma. The direct effect of radiocontrast media on vascular release of prostacyclin was indicated by increased PGI-M excretion in healthy volunteers administered intravenous radiocontrast and by studies of the canine coronary artery and jugular vein in vitro. Measurement of plasma 6-keto-PGF, after left heart catheterization showed that levels in aortic (21 +- 8 pg/ml) and coronary sinus (14 ± 2 pg/ml) blood were increased compared with peripheral venous levels (c 4 + 1 pg/ml) determined before this procedure. The aortic and coronary sinus concentrations of 6-keto-PGF,, both increased markedly in one of the five patients after injection of radiocontrast but an aortic coronary sinus gradient of 6-keto- PGF, was undetectable before or after angiography. These results indicate that cardiac catheterization and angiography are associated with an increase in prostacyclin formation in vivo.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTIn major prospective studies it has been reported that high heart rate at rest predicts the development of coronary heart disease (CHD) or cardiovascular disease (CVD) in men, but the mechanisms producing these relationships are unknown. Since lipoprotein levels contribute strongly to the risk of CHD and CVD, we examined the relationship of resting heart rate to plasma concentrations of high-density (HDL), low-density (LDL), and very low-density (VLDL) lipoproteins, apolipoprotein (apo) A-I and A-IL, and serum concentrations of lipoprotein subfractions in 81 men to determine if atherogenic lipoproteins could potentially induce the reported association of heart rate with development ofCHD or CVD. The significant (p .05) Spearman's correlations for resting heart rate vs HDL2 mass (rs = - .24), HDL3 mass (r, = - .40), HDL cholesterol (rs = - .36), apo A-I (rs = - .29), triglycerides (r, = .31), VLDL cholesterol (r, = .24), VLDL mass (rs = .27), and LDL mass of SO 0-7 subfraction (rs = .30) lend support to our hypothesis of lipoprotein-induced relationships of CHD with heart rate. The correlations for resting heart rate vs triglycerides, HDL cholesterol, HDL3 mass, VLDL mass, and LDL mass of SO 0-7 subfraction remain significant when adjusted for adiposity, age, smoking habits, diet, and physical fitness as measured by maximum aerobic power (V0M max) or submaximal heart rate during a graded exercise test.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

NO ABSTRACT

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTThe effects of verapamil on junctional and sinoatrial activity were studied in eight patients with third-degree atrioventricular block and stable junctional rhythms. After intravenous infusion of verapamil three steady-state levels were reached as follows: 34 ± 16 (SS1), 68 ± 30 (SS2), and 129 ± 54 (SS3) ng/ml. At each steady-state level, spontaneous sinus and junctional cycle lengths, QT intervals, junctional recovery times after ventricular pacing, blood pressure, and circulating catecholamine concentrations were measured. These measurements were compared with observations made during an identical protocol (except for the exclusion of verapamil infusions) on a control day. No significant changes were detected in the spontaneous sinus or junctional cycle length, junctional recovery times at a fixed pacing cycle length, blood pressure, or circulating catecholamine concentrations during the control day. In response to verapamil, the mean junctional cycle length decreased from abaseline value of 1320 + 239 to 1254 ± 210, 1199 + 214, 1069 + 151, and 1069 ± 151 msec at SS1, SS2, and SS3 (p < .01). Sinus cycle length (msec) was unaffected or slightly lengthened from 749 + 165 at baseline to 821 ± 222 at SS,, 831 ± 222 at SS2, and 817 + 175 at SS3 (NS). Mean blood pressure, circulating catecholamine concentrations, and corrected QT intervals were also unchanged by verapamil. Verapamil enhanced junctional pacemaker activity in patients with third-degree atrioventricular block, suggesting that (1) these rhythms originate in cells that are not suppressed by the slowchannel antagonism of verapamil and (2) the acceleration of junctional activity seen in response to verapamil reflects a verapamil effect rather than toxicity.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

ABSTRACTWe studied the exercise ejection fraction response in 56 patients with chronic aortic insufficiency. All had left ventricular dilatation but preserved resting ejection fraction and minimal or no symptoms. The exercise ejection fraction increased by 0.05 units or greater in 18 (32%) patients (group I), remained within 0.05 units of the resting value in 18 (32%) patients (group 11), and fell by 0.05 units or greater in 20 (36%) patients (group III). There were no significant differences among the groups in left ventricular end-diastolic dimension, end-systolic dimension, or fractional shortening by echocardiography or in resting left ventricular volumes and ejection fraction by radionuclide angiography. Left ventricular end-systolic wall stress was significantly higher in group III than in either group I or group 11(89 + 20 vs 70 + 18 and 69 ± 17 X 103 dyne/cm2; p < .005). At peak exercise there were no differences among groups in systolic blood pressure. However, end-systolic volume increased from 65 ± 28 to 77 + 36 mI/m2 in group 111 and fell from 50 ± 21 to 28 + 18 ml/i2 in group I during exercise. Thus, at peak exercise end-systolic volume was nearly three times greater in group 111 than in group I. Although stress could not be determined directly during exercise, the directional changes in its determinants suggest that it also would have been higher in group Ill patients. A highly significant inverse correlation was present between the ejection fraction response and the change in end-systolic volume (r = -.87, p < .0001). Exercise capacity was significantly lower in group 111 than in groups I and 1I. These data demonstrate that patients with chronic aortic insufficiency whose ejection fraction falls during exercise have elevated resting left ventricular systolic wall stress, suggesting that left ventricular hypertrophy has not been adequate. Although these patients have a normal resting ejection fraction, left ventricular systolic pump performance cannot be sustained during exercise when wall stress rises further.

ISSN:0009-7322    

出版商:OVID    

年代:1985

数据来源: OVID