Acute hemodynamic and antiischemic effects of intravenous amiodarone

The acute hemodynamic and antiischemic properties of amiodarone were investigated in 16 patients with more than 70% diameter reduction of a left coronary artery. Two successive atrial pacing stress tests (APST I and II) were performed, with an interval of 40 minutes in between, and amiodarone, 5 mg/kg/5 min, was infused 30 minutes after APST I. Hemodynamic changes during amiodarone administration consisted of a 20% decrease in left ventricular (LV) systolic pressure, a 13% decrease in systemic vascular resistance and an 18% decrease in stroke work. Coronary vascular resistance was reduced 19% and coronary sinus flow increased 23%. Despite a secondary 14% increase in heart rate, contractility decreased 21%, accompanied by a 45% increase in LV end-diastolic pressure, which persisted until APST II. Although most hemodynamic changes were observed only during the infusion, contractility and LV systolic pressure were still diminished at the beginning of APST II and remained so during pacing, resulting in a reduction in myocardial oxygen demand compared to APST I. Although overall myocardial oxygen consumption and coronary flow were equal during both pacing tests, amiodarone significantly reduced pacing-induced myocardial ischemia. Lactate metabolism remained normal during APST II (lactate extraction 12 +/- 3% vs -28 +/- 8% (APST I) at maximal pacing rates [p less than 0.05]), while ST-segment depression, LV end-diastolic pressure postpacing and angina were also significantly reduced during APST II. Thus, in humans, intravenous amiodarone reduces vascular resistance and contractility and inhibits pacing-induced myocardial ischemia, presumably by reducing myocardial oxygen demand.     

Acute intravenous and long-term oral hemodynamic effects of encainide

The short- and long-term hemodynamic effects of encainide, a new class IC antiarrhythmic agent, were studied in 25 patients (mean age 61 +/- 11) with complex symptomatic ventricular arrhythmia and left ventricular dysfunction. Ninety-two percent had previous myocardial infarction and 8% had dilated cardiomyopathy. Seventy-five percent had congestive heart failure, class III or IV, according to the New York Heart Association. All patients underwent a nuclear ventriculogram performed at least 3 days after discontinuing previous antiarrhythmic drugs. Nuclear ventriculograms were repeated 1 to 6 weeks later while the patients were receiving therapeutic doses of encainide ranging from 75 to 300 [corrected] mg/day. Nuclear ventriculograms were also repeated after 6 months or 1 year of encainide therapy in 16 of these patients. Encainide did not have significant effects on heart rate, blood pressure, left ventricular ejection fraction, systolic or end-diastolic volumes. None of the patients showed a worsening of congestive heart failure during encainide therapy. These results compare favorably with those of other class I antiarrhythmic agents. A review of published reports on the hemodynamic effects of intravenous encainide shows it to have a mild but statistically significant dose-related depressant effect on cardiac function. This effect, however, appears to be no different from that of other newer class I agents.     

乌拉地尔对心力衰竭患者的血液动力学效应

乌拉地尔是α１受体阻滞剂，可用于心力衰竭治疗。本组观察了１１例缺血性心脏病心力衰竭患者静脉滴注乌拉地尔２～１２μｇｋｇ－１／ｍｉｎ的血液动力学效应。结果表明：乌拉地尔可降低总外周阻力、肺毛细血管楔压、肺血管阻力、肺动脉压，增加心排血量、心脏指数、左室作功指数，而心率、平均动脉压与用药前比较无明显统计学差异。因此，结果提示，静脉滴注乌拉地尔对缺血性心脏病所致心力衰竭有良好的血流动力学效应。     

Acute hemodynamic effects of adriamycin

Several authors reported about acute haemodynamic effects of ADM years ago. We studied this problem in five patients in the invasive and noninvasive way and thus obtained the most important haemodynamic parameters. Acute haemodynamic effects in the meaning of a negative inotropy and vasodilatation are confirmed. The usual intravenous injection does not avoid the decrease of important haemodynamic parameters (SV, SWI, CI) even though injected over ten minutes. Possible infarction and complications during the injection may be the result of decrease of perfusion pressure in the meaning of a "steal phenomenon".     

Acute hemodynamic effects of celiprolol

Beta-adrenoceptor blockade is an effective treatment for ischemic heart disease and hypertension, but the more widespread use of beta antagonists is limited by their bronchoconstrictor, vasoconstrictor and negative inotropic properties. Celiprolol has been shown in preclinical studies to be a beta 1-selective antagonist with bronchosparing and vasodilating properties, but without any cardiodepressant effect. This has been confirmed by clinical studies undertaken to date. The aim of the present study was to examine the acute effects of intravenous celiprolol on the cardiac hemodynamics of patients pretreated with oral atenolol.     

静脉滴注L-精氨酸对充血性心力衰竭患者的急性血流动力学效应

目的：评价充血性心力衰竭患静脉滴注L－精氨酸（L－arg）的急性血流动力学效应,探讨L－arg治疗心力衰竭的机制。方法：36例心力衰竭患（心功能Ⅳ级1例,Ⅲ级24例,Ⅱ1级11例）,以20％L－arg100ml加入5％葡萄糖溶液100ml,1h内恒速静脉滴注,每日1次,连续7d。记录用药后心率、血压变化,并对其中11例患（心功能Ⅲ级8例,Ⅱ级3例）采用有创检查观察血流动力学效应,同时测定用药后血液和尿液一氧化氮（NO）。结果：静脉滴注L－arg5min收缩压、舒张压、收缩压与心率乘积均有显降低（P＜0．05）,最大效应时间10－60min,心率无变化。血流动力学检查结果表明,静脉滴注L－arg可使平均动脉压和体循环阻力、肺动脉压、肺毛细血管嵌压、肺血管阻力显降低（P＜0．05－0．01）,心指数和左心室作功指数显增加（P＜0．01）。用药后尿液NO显升高。结论：心力衰竭患静脉滴注L－arg增加了体内NO,血流动力学明显改善。     

Acute hemodynamic study of intravenous nicardipine in arterial hypertension

The acute hemodynamic effects of intravenous Nicardipine (N), a new calcium antagonist, were studied in 8 patients with moderate essential hypertension. The forearm arterial blood flow (ABF) was measured using plethysmography before and after N infusion: 1st step was obtained after infusion of 1 mg during 5 min then 1 mg during 25 min; a second step was obtained after the infusion of the same dose during the same time; thus a cumulative dosage of 4 mg was infused over a total duration of 60 mn. Systolic (SBP), diastolic (DBP) mean (MBP) blood pressure and heart rate (HR) were measured every minute using a non invasive device (Dinamap). Systemic vascular resistances (SVR) were calculated. Plasma concentration of N was determined at the beginning, in the middle and at the end of each step. Results are as follows: (table; see text) A 33% decrease in SVR was observed at the 2nd step whereas MBP decreased by 15% only. The date confirm the potent vasodilatory effect of intravenous N at low dosage; the BP alteration was moderate in relation to an increase in local blood flow. These results indicate that Nicardipine could be useful as part of the treatment of chronic arteriopathy and Raynaud disease.     

Antihypertensive and hemodynamic effects of calcium channel blockade with isradipine after acute exercise.

In a randomized, double-blind, placebo-controlled, crossover study with two 4-week treatment periods, we investigated the effects of calcium channel blockade with 5 mg slow release oral isradipine on postexercise blood pressure and systemic hemodynamics (echocardiography) in ten hypertensive patients. The results show that the combination of exercise and isradipine treatment exerts additive antihypertensive effects in hypertensive patients after exercise. The antihypertensive effect of prior exercise with placebo was related to a significant fall in total peripheral resistance. After exercise during isradipine treatment, total peripheral resistance was lower than with placebo. Thus, isradipine exerts an additional antihypertensive effect during the postexercise period, which appears to be mediated by a further reduction of total peripheral resistance.     

Coronary and systemic hemodynamic effects of intravenous nisoldipine

Systemic and coronary hemodynamic effects of the new dihydropyridine calcium antagonist nisoldipine were studied over a 30-minute period in 12 patients with angina pectoris. Previously instituted β-blocker therapy was continued. Nisoldipine was administered in an intravenous bolus of 6 μg/kg over 3 minutes. Heart rate increased as mean aortic pressure and systemic vascular resistance decreased in all patients. Cardiac output increased significantly, from 5.8 ± 0.3 to 7.9 ± 0.5 liters/min, 10 minutes after nisoldipine infusion. These trends were maintained over the 30-minute observation period. Coronary sinus blood flow increased from 103 ± 11 to 139 ± 13 ml/min immediately after nisoldipine, but had returned to the control level by 30 minutes, as had the reduction in coronary vascular resistance. Myocardial oxygen consumption and heart rate-systolic blood pressure product did not change significantly. Nisoldipine is a potent peripheral and coronary vasodilator free of major myocardial depressant effects after acute intravenous administration. The systemic vasodilatory effects appear to outlast the coronary effects over 30 minutes.     

Acute hemodynamic and electrophysiologic effects and safety of high-dose intravenous diltiazem in patients receiving metoprolol.

The anti-ischemic efficacy of diltiazem may improve with increments in dosage and with additional beta-blocking therapy. However, the combined administration could lead to adverse effects through amplification of negative inotropic and chronotropic properties. To evaluate hemodynamic tolerability and safety of high-dose intravenous diltiazem in patients with coronary artery disease receiving long-term metoprolol treatment, 9 such patients were studied for 30 minutes after onset of intravenous diltiazem administration (0.5 mg/kg for 5 minutes, followed by 15 mg/hour). Diltiazem plasma levels peaked at 5 minutes (641 +/- 74 micrograms/liter), decreasing to 177 micrograms/liter at 30 minutes. Average metoprolol levels (43 +/- 12 micrograms/liter) did not change. Diltiazem immediately decreased systemic vascular resistance, left ventricular systolic and mean aortic pressures (29, 21 and 20%, respectively, at 5 minutes), and they remained significantly reduced at 30 minutes. Heart rate initially increased by 11% during the bolus infusion (p < 0.05). Concomitantly, contractility indexes Vmax and Vce40, measured at fixed heart rates, also increased significantly by 11%. Both heart rate and contractility indexes returned to baseline levels thereafter. Cardiac output increased by 10% (p = not significant), stroke index remained unchanged, but stroke work decreased significantly by 20%. Also, the tension-time index was significantly reduced (23%). Diltiazem induced moderate negative lusitropic effects, the first derivative of negative left ventricular pressure decline decreased by 12% and Tau 2 lengthened by 13%. Concomitantly, left ventricular filling pressure increased from 19 +/- 2 to 23 +/- 3 mm Hg, but only at 5 and 15 minutes. PQ, QRS and QTc intervals were not affected.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute hemodynamic and arrhythmogenic effects of high-dose intravenous salbutamol in patients with chronic left ventricular dysfunction

The short-term hemodynamic and possible arrhythmogenic effects of intravenous salbutamol at a dose of 30 or 60 micrograms/min were evaluated in 14 patients with severe chronic left ventricular dysfunction using equilibrium radionuclide angiocardiography and electrocardiographic monitoring. Salbutamol infusions at a dose of 30 micrograms/min did not cause significant hemodynamic changes; however, at a dose of 60 micrograms/min there was a significant increase in stroke volume, cardiac output, and left ventricular ejection fraction. Heart rate increased significantly while systemic peripheral resistance decreased significantly. Two patients developed ventricular premature beats and another two supraventricular tachycardia, but none were associated with adverse consequences. Thus, high-dose intravenous salbutamol is effective and safe, and may be used in the acute management of patients with poor left ventricular function.     

Acute hemodynamic effects of intravenous nicardipine in patients treated chronically with propranolol for coronary artery disease

Intravenous nicardipine, 5 mg, was infused over 5 minutes in 2 comparable groups of 8 patients with chronic coronary artery disease but no clinical signs of heart failure. Eight patients had received no previous treatment and served as a control group; 8 other patients had received long-term treatment with large doses of propranolol. The hemodynamic responses to nifedipine were similar in the 2 groups, but was greater in patients taking propranolol. At 10 minutes, systemic vascular resistance decreased by 47% in patients taking propranolol and by 39% in the control group; mean aortic pressures decreased by 25% and 10%; heart rate increased by 23% and 19%; and cardiac index increased by 45% in both groups. At 20 minutes, left ventricular end-systolic volume index decreased by 20% in patients taking propranolol and 15% in the control patients; angiographic stroke index increased by 19% and 8%; left ventricular ejection fraction increased by 22% and 11%; and mean circumferential fiber velocity increased by 46% and 32%. Intravenous nicardipine infusion (5 mg) did not induce negative inotropic effects in patients with chronic coronary heart disease, and no evidence of congestive heart failure was seen, even in patients receiving large doses of propranolol. Nicardipine counteracted the potential deleterious effects of propranolol; increased peripheral vascular resistance and left ventricular stroke work and decreased cardiac output.     

法舒地尔对先天性心脏病重度肺动脉高压的急性肺血管反应

目的:比较成人先天性心脏病(CHD)相关性重度肺动脉高压(PAH)患者,对雾化吸入伊洛前列素(万他维)与静脉泵入法舒地尔的急性肺血管扩张效应,以评价法舒地尔在CHD相关性重度PAH的急性肺血管反应。方法:回顾性分析161例进行急性肺血管扩张试验的成人CHD相关性重度PAH患者,其中万他维组126例,法舒地尔组35例,比较两组用药前后血流动力学参数变化。结果:万他维组与法舒地尔组用药后肺动脉平均压、肺小动脉阻力、肺总阻力、肺循环阻力与体循环阻力比值、平均肺动脉压力与体循环压力比值均显著降低,且肺循环血流量/体循环血流量比值(Qp/Qs)显著增加,差异均有统计学意义(P<0.05)。用药前后,万他维组右心房压(P=0.056)无明显变化,而法舒地尔组(P<0.01)明显降低。两组患者动脉氧饱和度(Sa O2)、体循环血压、心脏指数(CI)及体循环阻力等差异均无统计学意义。结论:静脉使用法舒地尔可明显降低肺动脉压及肺血管阻力,显著增加Qp/Qs,而CI、体循环血压及Sa O2无变化;法舒地尔可能成为CHD相关性PAH的另一种安全有效的治疗药物。     

Acute hemodynamic effects of enhanced external counterpulsation

Introduction
In the United States, there are about 17.6 million patients suffer from symptomatic coronary artery disease （CAD）, affecting 7.9% of adults ≥ 20 years of age.1 An estimated 10.2 million patients have angina, and 500,000 patients will develop new angina pectoris each year. 1 A subset of angina patients are categorized as refractory when symptoms continue despite optimal medical therapy and revascularization.Routine daily activities become impossible without experiencing chest pain in this patient population.2     

Acute hemodynamic effects of molsidomine in man

Molsidomine was administered sub-lingually to two groups of five patients. One group had normal left ventricular function and the other had abnormal left ventricular function. Molsidomine was found to induce a decrease in the left ventricular filling pressure and volume and an increase in ventricular distensibility. It helps reduce the pre-load on the ventricle and parietal rigidity. It also reduces systemic blood pressure and resistance as well as the parietal pressure and the total systolic load opposing ejection. It helps reduce the post-load and the metabolic requirements of the myocardium. It does not have any depressant action on the myocardium, even when the ventricular function was initially abnormal. The action of the molecule is apparent between the 20th and the 30th minute and is maximal at the 40th minute, which was the limit of the experiment. The tolerance of the product was excellent in these ten subjects.     

Short-term hemodynamic effects of intravenous propionyl-L-carnitine in anesthetized dogs

The effects of intravenous administration of propionyl-L-carnitine (PLC) were investigated in anesthetized dogs instrumented for the analysis of general hemodynamic and electrocardiographic data, peripheral blood flows, coronary blood flow and oxygen consumption, urine flow, and renal function. PLC was administered in bolus (20, 60, and 200 mg/kg) or by infusion (20 mg/kg/min ^* 15 min or 30 mg/kg/min ^* 10 min). In some cases also L-carnitine (LC) and L-carnitine + propionate (LC + P) were administered in doses equimolar to those of PLC. PLC elicited dose-dependent, short-lasting enhancements of cardiac output, both in open-and close-chest conditions. Arterial blood pressure, heart rate, and contractility varied slightly and unpredictably; the substance did not elicit electrocardiographic effects. These responses were not changed by alpha- or beta-adrenergic blockade, nor by the administration of a calcium antagonist, but they were abolished or reversed by the combination of such blocking interventions. Mesenteric and iliac blood flows were increased by both PLC and LC; LC + P increased these, and in addition increased renal blood flow. A strong diuresis obtained with PLC, LC, and LC + P was due to osmotic clearance following the administration of hyperosmotic solutions. PLC elicited coronary vasodilation with reduced oxygen extraction; this effect lasted longer than the general hemodynamic effects and was not seen with LC. All the cardiovascular actions of PLC can be attributed to its pharmacologic properties, rather than to its role as a metabolic intermediate.     

Acute hemodynamic effects of nitroglycerin in pulmonary hypertension

Therapy of pulmonary hypertension is limited by the low potency and adverse effects of current pulmonary vasodilators. The hemodynamic effects of nitroglycerin in human pulmonary hypertension are not known. We administered nitroglycerin to nine patients with chronic pulmonary hypertension. Nitroglycerin increased cardiac index 40% (p less than 0.01), increased stroke volume 40% (p less than 0.01), decreased pulmonary vascular resistance 40% (p less than 0.01), and decreased mean pulmonary artery pressure 15% (p less than 0.01). Pulmonary vascular resistance decreased more than 25% in eight of the nine patients. In four patients the effects of intravenous nitroglycerin were reproduced by topical nitroglycerin preparations; cardiac index increased 50%, stroke volume increased 48%, pulmonary vascular resistance decreased 43%, and mean pulmonary artery pressure decreased 19%. Five of six patients treated with long-acting nitrates had substantial improvement of their symptoms. We conclude that therapy with nitroglycerin can be effective in patients with severe pulmonary hypertension.     

Acute hemodynamic effects of intravenous bolus injection of isosorbide dinitrate in aged patients with congestive heart failure]

In order to investigate whether intravenous bolus injection of isosorbide dinitrate (ISDN) is a safe and efficient therapy in aged patients with congestive heart failure, we studied acute hemodynamic effects in 11 patients. Peak effects on preload were observed after 5 to 10 minutes of bolus injection and unloading effects continued effectively for 60 minutes. At peak effect, pulmonary systolic pressure decreased from 50.2 +/- 2.6 to 36.2 +/- 2.6 mmHg (-28.5%, p less than 0.01) and pulmonary end diastolic pressure decreased from 25.0 +/- 2.2 to 18.5 +/- 2.1 mmHg (-26.0%, p less than 0.01). Mean pulmonary artery wedge pressure decreased from 23.4 +/- 2.2 to 16.0 +/- 2.1 mmHg (-31.6%, p less than 0.01). Mean right atrial pressure decreased from 10.5 +/- 1.8 to 7.4 +/- 2.0 mmHg (-29.5%, p less than 0.01). Blood pressure, heart rate, cardiac index, systemic and pulmonary vascular resistance showed no significant changes. Thus, intravenous bolus injection of ISDN showed a potent vasodilator effects on preload, and may be a safe and useful treatment for aged patients with acute congestive heart failure.     

Acute hemodynamic changes during intravenous dipyridamole thallium imaging early after infarction

In order to determine the safety and hemodynamic effects of intravenous dipyridamole infusion for thallium-201 scinitigraphy in patients with acute ischemic syndromes, 10 patients with recent uncomplicated myocardial infarction (7 +/- 2 days pre-test) had central pressures and cardiac output values measured serially in a coronary care unit during and after the administration of dipyridamole (0.56 mg/kg over 4 minutes) and following aminophylline reversal (50 to 150 mg intravenously) of dipyridamole effect. Cardiac medications were not discontinued. Double product did not change significantly (8522 +/- 1811 versus 9044 +/- 1701; p = NS). Serious ischemic events did not occur, although 20% of patients had noncardiac side effects and 30% developed greater than or equal to 1 mm ST segment depression with associated angina in one-third of these cases. The peripheral blood pressure and heart rate response did not predict the occurrence of myocardial ischemia. Dipyridamole significantly reduced systemic vascular resistance (1218 +/- 302 to 739 +/- 166 dyne/sec-1/cm-5; p less than 0.05) and increased cardiac index (3.1 +/- 0.7 to 4.7 +/- 1.0 L/min/m2; p less than 0.05) within approximately 10 minutes, in association with a significant increase in pulmonary capillary wedge pressure (13 +/- 5 to 17 +/- 6 mm Hg; p less than 0.05). Three patients developed silent new "V" waves in their pulmonary capillary wedge pressure tracing, associated with anterior thallium redistribution. All three patients with newly elevated wedge pressures (greater than 15 mm Hg) had both thallium-201 redistribution and multivessel coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)