摘要:

Hydralazine was administered acutely to 12 patients who had pulmonary arterial hypertension of unknown cause. All of the patients were studied at rest and nine during exercise. On the basis of hydralazine response at rest, the patients were divided in two groups. In six patients (group A), pulmonary arteriolar resistance (Rp) decreased from 8.4 ± 1.4 to 4.8 ± 1.4 U/in(p< 0.001), cardiac index (CI) increased from 3.47 i 0.3 to 5.86 ± 0.5 1/min/m'(p< 0.005) and systemic resistance (Rs) decreased from 25 4 to 14 ± 2 U/mi(p< 0.01). The Rp/Rs ratio did not change significantly after hydralazine (0.32 ± 0.03 vs 0.33 ± 0.07, NS). In the other six patients (group B), Rs decreased from 25 ± 2 to 17.0 ± 1 U/mi(p< 0.01), but the other variables did not change significantly. Our results suggest that the pulmonary vasodilatory effect of hydralazine caused a marked reduction in right ventricular afterload in group A. In group B, a marked systemic vasodilatory effect occurred and right ventricular afterload was not reduced. On the basis of the previous hemodynamic response, only group A patients were treated with oral hydralazine (50 mg every 6 hours). Hemodynamic measurements were repeated 48 hours after hydralazine, both at rest and during exercise, as well as 8 months later in five of the six patients in whom the beneficial hemodynamic effects persisted. These data suggest that hydralazine can reduce Rp in selected patients (pulmonary arterial pressure < 60 mm Hg, Rp < 15 U/Miand Rp/Rs ratio < 0.7) with pulmonary hypertension of unknown cause.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Verapamil has been used clinically as an antiarrhythmic and antianginal agent. However, the intrinsic negative inotropic properties of verapamil could preclude its use in patients with coronary artery disease concurrently receiving β-adrenergic blocking agents. To investigate this possibility, 20 patients with coronary artery disease and normal left ventricular function receiving chronic propranolol therapy were given i.v. verapamil (0.025, 0.05, or 0.1 mg/kg over 2 minutes, followed by 0.005 mg/kg/min infusion) and the hemodynamic and angiographic effects were studied. The mean (± SD) plasma verapamil concentration at the time the hemodynamic effects were being measured was 122 ± 51 ng/ml for the 10 patients who received low doses (0.025 or 0.05 mg/kg) and 214 ± 108 ng/ml for the 10 patients who received high doses (0.1 mg/kg). Verapamil reduced mean arterial pressure by 22% (p< 0.001), systemic vascular resistance by 24% (p< 0.001), mean pulmonary artery pressure by 16% (p< 0.01), and pulmonary vascular resistance by 23% (p< 0.001) in all 20 patients. Concomitant increases in cardiac index, mean velocity of circumferential fiber shortening, and ejection fraction (due to the unloading effect of verapamil) were not observed. These results were not significantly different between the two dosage levels.The combined negative inotropic effects of verapamil and propranolol are of negligible importance; however, the lack of improvement in the indexes of the left ventricular function suggests some myocardial interaction of these two drugs, which may be of concern in cardiac patients with evidence of depressed myocardial performance.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The administration of verapamil to patients receiving, β-adrenergic blocking drugs is reported to produce adverse circulatory reactions, but a systematic investigation of this potential drug interaction has not been performed in man. We administered 40-, 80- and 120-mg doses of verapamil orally to 15 patients with angina pectoris who were receiving high doses of propranolol or metoprolol. Verapamil produced dose-dependent decreases in cardiac performance: with 120 mg, cardiac index decreased by 0.38 I/min/m2, stroke volume index decreased by 2.8 ml/beat/m2and heart rate decreased by 6 beats/min, associated with increases in pulmonary capillary wedge (2.2 mm Hg) and mean right atrial pressures (1.7 mm Hg) (allp< 0.01); two patients had marked, but asymptomatic, hypotensive reactions. In contrast, repeat administration of 120-mg doses of verapamil 24–30 hours after withdrawal of A blockade produced no significant cardiodepressant effects despite significantly higher plasma levels of verapamil than during propranolol therapy (383.1 vs 205.1 ng/ml,p< 0.01). In conclusion, verapamil produces significant negative inotropic and chronotropic effects in patients treated with 3-adrenergic antagonists; combination therapy should therefore be used with caution in patients with angina pectoris.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

In 14 patients with chronic heart failure, changes in coronary hemodynamics, myocardial metabolism and left ventricular function were evaluated after administration of captopril, prazosin and hydralazine. Eleven patients received captopril in incremental doses (6.25–150 mg) until the arterial pressure decreased by 10 mm Hg; 11 patients received prazosin (5 mg) and 10 patients received hydralazine (100 mg). The control hemodynamics and metabolic variables before each drug trial were similar. All three vasodilators increased cardiac index (captopril 19%,p< 0.001; prazosin 29%,p< 0.001; hydralazine 36%,p< 0.001), and decreased the pulmonary capillary wedge pressure (captopril 24 ± 6 to 17 ± 6 mm Hg,p< 0.001; prazosin 20 ± 7 to 13 ± 6 mm Hg,p< 0.001; hydralazine 19 ± 8 to 16 + 7 mm Hg,p< 0.025), indicating improved left ventricular function with all three agents. The average rate-pressure product decreased after captopril and prazosin by 27% and 14%, respectively, but only captopril decreased the myocardial oxygen consumption significantly (19%,p< 0.025). There was myocardial lactate production, indicating ischemia, in one patient with captopril, two patients with prazosin and two patients with hydralazine.These results suggest that only captopril consistently improves left ventricular function at a decreased metabolic cost. Despite improved hemodynamics and left ventricular function, metabolic function can deteriorate during vasodilator therapy in some patients with chronic ischemic heart failure.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

High levels of, β-adrenergic stimulation accompany strenuous exercise, but the possibility that β-adrenergic blockade might prevent exercise conditioning has not been adequately investigated. We studied normal, sedentary men, ages 21–35 years, before and after 5 weeks of intensive aerobic conditioning. On a double-blind protocol, eight received placebo and nine propranolol throughout the conditioning period. A high level of, β-adrenergic blockade was documented in all subjects receiving propranolol; individual mean plasma propranolol concentrations were 100–292 ng/ml. Both groups trained at comparable intensities. Graded maximal treadmill tests were performed before starting drugs or training, and were repeated 3–5 days after completing the conditioning period, when, β-adrenergic blockade was no longer present. In subjects who received placebo, training increased exercise duration (16.4 ± 1.3 to 21.2 ± 1.5 minutes [± SEMI,p< 0.01) and maximal oxygen uptake (43.6 ± 2.9 to 52.7 ± 3.2 ml/kg/min,p< 0.05). Subjects who received propranolol had only modest improvement in exercise duration (16.0 ± 0.6 to 17.3 i 0.9 minutes,p< 0.05), and no significant change in maximal oxygen uptake (40.4 ± 1.4 to 40.9 i 0.9 ml/kg/min). With training, diastolic pressure at maximal exercise decreased in subjects who received placebo (63 ± 3 to 48 ± 3 mm Hg,p< 0.05) but was unchanged in subjects who received propranolol. Training did not alter maximal heart rate in either group. Thus, high levels of f3-adrenergic blockade markedly attenuated aerobic conditioning in these normal subjects. We conclude that, β-adrenergic stimulation is essential in exercise conditioning.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

Forty patients (35 men and five women) who experienced hypotension during maximal symptom-limited exercise test were retested after a 12 ± 4-month interval. Mean age was 53.5 years. All patients had multiple-vessel disease. Seventeen patients underwent coronary artery bypass surgery because of disabling angina, and 23 patients without disabling angina continued under medical management. At entry, there were no significant differences in age, left ventricular function or exercise performance between the medical and surgical groups.At follow-up, the surgical group showed an average increase in the exercise duration of 2.2 ± 1.7 minutes (p< 0.001), maximal heart rate of 17 ± 15 beats/min (p< 0.001), maximal systolic blood pressure of 26 ± 23 mm Hg (p< 0.001) and maximal rate-pressure product of 60 ± 41 (p< 0.001). These measurements did not change significantly in the medically managed group.Exercise-induced hypotension is apparently caused by ischemic left ventricular dysfunction, since in the majority of patients, it is reversible after successful revascularization. This observation is supported by the lack of improvement in a comparable group of patients managed without surgery.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

When a decrease in left ventricular isovolumic pressure is considered as an exponential, the rate of relaxation can be defined by a time constant (T). Previously, T has been calculated from the slope of In (pressure) against time, but this method is valid only when the asymptote of the exponential is zero. In this study two estimates of T were made: Tinfrom the slope of In (pressure) against time, and TEXPby a method of exponential analysis that also estimated the asymptote. These techniques were applied to measurements of left ventricular pressure made at increasing pacing rates in three groups of patients catheterized for chest pain: group 1 (n = 9) - normal coronary arteriograms; group 2 (n = 9) - coronary artery disease (CAD) but no angina or lactate production during pacing; and group 3 (n = 9) - CAD and angina during pacing. Tjnwas always shorter than TEXP, and in groups 1 and 2 TEXPwas dependent on heart rate, whereas Tinwas not. The asymptote was negative, and increased toward zero during pacing in groups 1 and 2. The difference between TEXPand Tin could be related to the value of the asymptote. In 18 of 20 beats tested, pressures calculated from TEXPand the asymptote were in closer agreement with measured pressures than were the pressures predicted by Tin. Despite their different values, TEXPand Tineach distinguished between the three groups. Although the choice of an exponential model is arbitrary, isovolumic pressure decrease approximates to a single expontial; but this study suggests that both T and the asymptote are variable.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID

摘要:

The normal human left ventricular response to large variations in preload was studied in 12 young men. M-mode echocardiograms were recorded at supine rest and compared with studies obtained during head-down tilt (HDT) at 5° and during progressive lower body negative pressure (LBNP) to −40 mm Hg.During HDT, end-diastolic volume (EDV) increased 23% (p< 0.001), stroke volume (SV) increased 35% (p< 0.001) and ejection fraction (EF) increased 10% (p< 0.05). Heart rate (HR) decreased by 5 beats/min (p< 0.025). During LBNP, EDV decreased 28% (p< 0.001), end-systolic volume (ESV) decreased 21% (p< 0.001) and SV decreased 33% (p< 0.001). LBNP was accompanied by a minor increase in HR (9 beats/min,p< 0.001) and a small increase in systolic blood pressure (11 mm Hg,p< 0.01). Comparisons between measurements obtained during HDT and LBNP showed significant differences in EDV, ESV, SV, EF, HR and diastolic blood pressure. The mean velocity of circumferential fiber shortening was unchanged. The combined data from the control studies and the interventions defined the normal left ventricular function curve as an exponential function where SV = 0.36 EDVY'' ml (r= 0.93,p< 0.001), which was not significantly different from the linear regression SV = 0.6 EDV + 0.57 (r= 0.92,p< 0.001).Our data indicate that the mean velocity of circumferential fiber shortening is an index of contractile state that is independent of preload, whereas other echocardiographic measurements are significantly altered by large changes in preload.

ISSN:0009-7322    

出版商:OVID    

年代:1982

数据来源: OVID