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At least 883 records · Page 49Linked to original sources
PubMed1985

A cooperative multicenter study of captopril in congestive heart failure: hemodynamic effects and long-term response.

The acute hemodynamic effects, long-term clinical efficacy, and safety of the oral angiotensin-converting enzyme inhibitor, captopril, were assessed in a multicenter cooperative study of 124 patients with heart failure resistant to digitalis and diuretics. The cardiac status of most patients was deteriorating prior to the study. Favorable acute hemodynamic effects consistently occurred with captopril. Maximal mean percentage increases in cardiac index, stroke index, and stroke work index were, respectively, 35%, 44%, and 34%. Systemic and pulmonary vascular resistances were each decreased by approximately 40%, as were the filling pressures of the right and left heart. Infusion of nitroprusside in some of the same patients to an end point of a pulmonary capillary wedge pressure of 12 to 18 mm Hg (equivalent to that after captopril) revealed no significant difference in the effect of either drug on the other hemodynamic parameters. Recatheterization after 8 weeks of captopril therapy revealed sustained hemodynamic changes. Significant and sustained improvements in clinical status were observed in most patients as measured by changes in New York Heart Association (NYHA) functional classification and exercise tolerance times. Seventy-nine percent of patients for whom there were adequate NYHA class data improved. Twenty percent remained unchanged and 1% deteriorated. Those patients who had both pretreatment and post-treatment exercise stress testing exhibited a highly significant mean increase in exercise tolerance times of 34% (317 +/- 32 seconds pretreatment to 425 +/- 34 seconds, final measurement). There was no evidence of tachyphylaxis over an 18-month period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Detrimental arrhythmogenic and sustained beneficial hemodynamic effects of oral salbutamol in patients with chronic congestive heart failure.

The long-term efficacy and potential side effects of oral sympathomimetic amines in the treatment of advanced congestive heart failure remain controversial. We studied the acute and chronic hemodynamic and arrhythmogenic effects of the beta-2 agonist, salbutamol, 6 mg by mouth four times/day, in 20 patients with NYHA classes III to IV congestive heart failure. Acutely, salbutamol increased the cardiac index (1.9 to 2.3 L/min/m2, p less than 0.01) and heart rate (92 to 97 bpm, p less than 0.01) while it decreased pulmonary capillary wedge pressure (35 to 31 mm Hg, p less than 0.01). Salbutamol increased the number of patients having episodes of ventricular tachycardia from two to six and increased the number of episodes of ventricular tachycardia from 2 to 27. Once salbutamol was discontinued, no further episodes of ventricular tachycardia occurred in these six patients. Six patients did not have long-term hemodynamic studies because of serious arrhythmias and two died. In the 12 patients who had long-term studies, the initial beneficial hemodynamic effects of salbutamol were maintained. Thus, although salbutamol may have beneficial long-term hemodynamic effects, it may cause serious arrhythmias in patients predisposed to develop arrhythmias.

Aged↗
PubMed1985

Immediate central hemodynamic effects of five different beta-adrenoceptor-blocking agents, acebutolol, atenolol, pindolol, practolol, and propranolol, in patients with ischemic heart disease.

The hemodynamic effects of acebutolol were studied in six patients with ischemic heart disease. The changes in heart rate, cardiac output, and arterial blood pressure were determined after intravenous administration of six increasing doses of acebutolol to a cumulative dose of 0.64 mg/kg. After the sixth dose of acebutolol, cardiac output and heart rate were reduced 15% and 8%, respectively. Pulmonary artery pressure was increased by 4 mm Hg. Arterial blood pressure was not changed significantly. The effects of graded doses of acebutolol on heart rate and cardiac output were compared with earlier obtained results after atenolol (0.19 mg/kg), pindolol (0.025 mg/kg), practolol (0.64 mg/kg), and propranolol (0.19 mg/kg). The effects of increasing doses of acebutolol and practolol were very similar and significantly different from the effects of the other three drugs in spite having been administered at equipotent doses. The hemodynamic effects of acebutolol support the hypothesis that the hemodynamic response to beta-adrenoceptor antagonist drugs at rest is determined primarily by the degree of intrinsic sympathomimetic activity, whereas beta-1 selectivity does not modify the central hemodynamic response.

Acebutolol↗
PubMed1986

Relative effects of propranolol and timolol on ventricular fibrillation threshold and hemodynamics in the dog.

The relationship between the antifibrillatory and hemodynamic effects of propranolol and timolol was tested in 32 dogs divided into three groups. In closed-chest animals (group 1), the maximal increase of the ventricular fibrillation threshold (VFT) from the control state was 67.3 +/- 22.6% (n = 5, p less than 0.01) for propranolol and 95.8 +/- 18.8% (n = 9, p less than 0.005) for timolol. These effects were paralleled by a decrease in the cardiac index of 34.7 +/- 10.2% (p less than 0.05) and 32.5 +/- 9.4% (p less than 0.02) for propranolol and timolol, respectively. The mean systemic arterial pressure (SAP) also decreased by 25.0 +/- 8.8% (p less than 0.05) and 19.2 +/- 5.1% (p less than 0.01). In open-chest animals (group 2), timolol increased the VFT by 86.6 +/- 27% (n = 5, p less than 0.05) and decreased the cardiac index by 57.3 +/- 6.3% (p less than 0.005) and the mean SAP by 28.5 +/- 2.9% (p less than 0.02). In open-chest animals with stabilized peripheral hemodynamics (group 3), VFT increased by 354 +/- 130% (p less than 0.05) and 437 +/- 144% (p less than 0.05) after the maximal administered doses of propranolol (n = 6) and timolol (n = 7), respectively. These results suggest that the electrophysiologic and hemodynamic effects of beta blockade are parallel and interdependent, with the hemodynamic deterioration markedly blunting the beneficial electrophysiologic effects.

Animals↗
PubMed1986

Amiodarone and N-desethylamiodarone concentrations in plasma, red blood cells, and myocardium after a single oral dose: relation to hemodynamic effects in surgical patients.

In an attempt to assess their respective values for purposes of drug monitoring, plasma, red blood cell, atrial, and ventricular concentrations of amiodarone and N-desethylamiodarone (NDA) were measured, in 50 surgical patients, after a single oral dose (30 mg/kg); hemodynamic changes were assessed also. Amiodarone concentration was lower in red blood cells than in plasma and in myocardium. A relationship was found between the red blood cell concentration and plasma or myocardial concentrations of amiodarone (r = 0.79 and r = 0.68, p less than 0.00001). Hemodynamic studies were available in 17 treated patients and 13 control subjects before and at the time of surgery. In control subjects, hemodynamics did not change with time and general anesthesia. Oral amiodarone decreased the cardiac index (p less than 0.05) and heart rate (p less than 0.001) without significant changes in arterial pressure, systemic vascular resistance, or stroke volume index. The increase in capillary wedge pressure was related to amiodarone or NDA plasma, myocardial, and red blood cell concentrations (for amiodarone: r = 0.61, p = 0.006; r = 0.69, p less than 0.001; and r = 0.53, p = 0.02, respectively). We concluded that oral amiodarone impairs hemodynamics and that measurement of the amiodarone plasma concentration rather than the red blood cell concentration is the easiest method of monitoring the drug. However, establishment of the clinical utility of drug monitoring during chronic administration of amiodarone needs further investigation.

Administration, Oral↗
PubMed1987

Natural history of pulmonary hemodynamics in primary pulmonary hypertension.

To study the relationship between the hemodynamic characteristics and prognosis in PPH, we analyzed the data on patients whose prognosis was well documented from the time of hemodynamic monitoring. Our subjects were 87 patients obtained from a nationwide survey in Japan. PCWPs were obtained in 44 patients and COs were measured in 59 patients. The average age was 33 years (range 14 to 69). Patients were followed prospectively for up to 100 months and were categorized based on the survival period from the time of catheterization. Hemodynamic variables that showed significant differences or prognostic trends were RVedp, pulmonary artery diastolic pressure, PCWP, CI, PVR, and PVR/SVR ratio. The CI correlated with the number of survival months (r = 0.583; p less than 0.01). The hemodynamic state of patients who died suddenly within 1 year from the time of catheterization was no different from those who died of clinical right-sided heart failure. The partial pressure of oxygen of arterial blood was the only variable discriminating sudden deaths from right-sided heart failure deaths (54 +/- 2 vs 66 +/- 4 mm Hg; p less than 0.05). The results of this study indicate that the major determinant of prognosis is right ventricular function and that the CI might be used as a prognostic indicator. In addition, sudden death is more likely to occur in patients with severe hypoxia.

Adolescent↗
PubMed1987

The hemodynamic effects of ventricular pacing with and without atrioventricular synchrony in patients with normal and diminished left ventricular function.

The relative hemodynamic effects of heart rate, inotropic state, and atrioventricular (AV) synchrony during ventricular pacing were evaluated in 10 patients with normal left ventricular ejection fraction (LVEF) (0.66 +/- 0.07, mean S.D.) and in eight patients with a diminished LVEF (0.34 +/- 0.18). Hemodynamics were measured at AV intervals of 130, 0, and -130 msec during ventricular pacing at a baseline rate that was 10 pulses/min greater than the resting heart rate, at 130 pulses/min alone, and at 130 pulses/min during continuous intravenous infusion of dobutamine. During baseline ventricular pacing and during ventricular pacing at 130 pulses/min with and without dobutamine, both groups of patients had a significant decrease in cardiac index, stroke volume index, and stroke work index when the AV pacing interval was decreased from 130 to 0 msec. The observed decrease in these three hemodynamic variables was similar when patients with diminished LVEF were compared to patients with normal LVEF. No further significant decrease in cardiac index, stroke volume index, and stroke work index occurred in either group when the AV interval was changed from 0 to -130 msec during baseline ventricular pacing or during ventricular pacing at 130 with and without dobutamine. Beneficial hemodynamic effects occur during ventricular pacing when AV synchrony is maintained at resting heart rates and during increases in heart rate and inotropic state in patients with normal and diminished LVEF.

Adult↗
PubMed1988

Intravenous fenoldopam in heart failure: comparing the hemodynamic effects of dopamine1 receptor agonism with nitroprusside.

Dopamine1 receptors mediate hemodynamic effects that may be beneficial in patients with congestive heart failure. We infused the selective dopamine1 receptor agonist, fenoldopam mesylate (SKF 82526 J), to evaluate hemodynamic and neurohumoral changes during continuous intravenous infusion in patients with congestive heart failure and compared them with the effects of nitroprusside, a traditional vasodilator that works by a distinctly different mechanism. In 15 patients with a mean radionuclide ejection fraction of 17%, the agents were infused in a random-ordered, double-blinded, crossover, active drug-controlled protocol after optimal dosing was determined during a titration period. Hemodynamic changes were induced in minutes with both drugs during a mean (+/- standard deviation) infusion dose of 1.45 +/- 1.66 micrograms/kg/min for fenoldopam and 2.99 +/- 1.59 micrograms/kg/min for nitroprusside. At 1 hour, mean blood pressure decreased and cardiac index rose with both drugs, and the effect lasted throughout the 6-hour infusion period. Nitroprusside, but not fenoldopam, reduced right heart filling pressures (including mean pulmonary capillary wedge, mean right atrial, and mean pulmonary artery pressures) during the infusion period. Both drugs caused significant reduction in systemic vascular and pulmonary arteriolar resistances. No significant change occurred in plasma norepinephrine levels. Fenoldopam ameliorates some of the adverse hemodynamic changes that occur during heart failure but does not reduce right heart filling pressures as does nitroprusside. Because of fenoldopam's unique characteristics, it may benefit certain patients with heart failure.

Adult↗
PubMed1991

Comparative hemodynamic effects of mexiletine and quinidine in patients with severe left ventricular dysfunction.

Mexiletine and quinidine are often administered to patients with severe congestive heart failure, but their hemodynamic effects have not been adequately studied in these individuals. In a randomized, crossover study, the hemodynamic responses to single oral doses of quinidine (600 mg) and mexiletine (400 mg) were compared in 20 patients with marked left ventricular dysfunction. Quinidine predominantly caused vasodilation, with mean arterial, left ventricular filling, and right atrial pressures all decreasing (-7 +/- 2, -2.3 +/- 1.0, and -1.1 +/- 0.5 mm Hg, respectively) and the systemic vascular resistance also declining (-308 +/- 84 dynes.sec.cm5). In contrast, the systemic vascular resistance increased (314 +/- 84 dynes.sec.cm-5) and the mean arterial, left ventricular filling, and right atrial pressures also increased (+2 +/- 2, +6.1 +/- 1.8, and +1.8 +/- 0.6 mm Hg, respectively) after mexiletine. Cardiac performance declined with mexiletine (cardiac and stroke work indexes decreasing -0.3 +/- 0.1 L/min/m2 and -5 +/- 1 gm.m/m2, respectively), but there was no significant change in cardiac or stroke work indexes with quinidine (+0.1 L/min/m2 and -0.3 +/- 0.9 gm.m/m2, respectively). The response to the two agents significantly differed for all parameters measured (p less than 0.005). These hemodynamic changes were accompanied by clinical effects. Mexiletine induced increased dyspnea in five patients and quinidine led to symptomatic hypotension in two patients. Plasma concentrations of mexiletine and serum concentrations of quinidine were within or below the therapeutic range in all patients. In conclusion, mexiletine and quinidine exert different hemodynamic effects when given to patients with severe congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Effects of a twenty-four-hour milrinone infusion in patients with severe heart failure and cardiogenic shock as a function of the hemodynamic initial condition.

The systemic and pulmonary arterial hemodynamics of 40 patients with severe congestive heart failure were determined during a 24-hour infusion of milrinone (0.5 micrograms/kg/min) after a loading dose of 50 micrograms/kg. A subgroup (n = 18) with severe cardiac pump dysfunction and three patients in cardiogenic shock were analyzed separately; their hemodynamic response was compared with that of the total group (n = 40). After 15 minutes of intravenous therapy with milrinone, the total group (n = 40) showed an increase of 65% in cardiac index; in the subgroup (n = 18) cardiac index increased by 94% after 15 minutes and by 106% after 30 minutes. Likewise, pulmonary capillary wedge pressure decreased after 30 minutes in both the total group (n = 40) and the subgroup (n = 18). The heart rate showed an overall tendency to decrease. The systolic blood pressure tended upward and remained statistically unchanged in the total group, whereas in the subgroup in which pressure was initially low, there was an increase in the systolic pressure after 1 hour and a further increase after 24 hours. Mean arterial pressure also rose in this subgroup. The early improvement in all measured hemodynamic parameters was sustained throughout the 24-hour infusion period. Development of tolerance was not observed, nor were any clinically symptomatic side effects or symptomatic arrhythmias. Thus intravenous milrinone is a safe medication for the rapid and prolonged improvement in hemodynamics, specifically in patients with severely restricted cardiac pumping function.

Adult↗
PubMed1975

Variability of hemodynamic responses to acute digitalization in chronic cardiac failure due to cardiomyopathy and coronary artery disease.

Eight patients with chronic congestive heart failure (four with cardiomyopathy and four with ischemic heart disease) underwent hemodynamic studies during acute administration of digoxin, given intravenously in two 0-5 mg doses 2 hours apart. Observations were made before administration of digitalis (control period) and serially therafter for 4 hours after the first dose. Resting mean cardiac index and pulmonary arterial wedge pressure were as follows: 2.0 liters/min per m2 and 23 mm Hg (control period); 2.1 and 24 (at 1 hour); 2.0 and 23 (at 2 hours); 2.7 and 19 (at 3 hours); and 2.3 and 20 (at 4 hours). Exercise responses of mean cardiac index and pulmonary arterial wedge pressure in five patients were: 3.1 liters/min per m2 and 36 mm Hg (control period); 3.2 and 33 (at 1 hour); 3.2 and 28 (at 2 hours); 3.1 and 27 (at.3 hours); and 3.4 and 31 (at 4 hours). The pulmonary arterial wedge pressure remained elevated during exercise in all cases. Arrhythmias were seen in five patients after administration of 0.5 mg of digoxin. Hemodynamic improvement at 4 hours involving both reduced filling pressure and increased blood flow was observed in only two patients at rest and in one additional patient during exercise. Acute deterioration of cardiac function (elevated pulmonary arterial wedge pressure of decreased cardiac index) occurred 30 minutes after administration of digoxin in four patients, concomitantly with increased systemic resistance. In six patients, a peak hemodynamic effect appeared 1 to 1 1/2 hours after administration of digoxin, with partial or total loss of initial benefit by 2 and 4 hours. In previously performed studies observations have seldom exceeded 1 hour; the results of this 4 hour study suggest that, in patients with cardiomyopathy or coronary artery disease and chronic congestive heart failure, acute digitalization does not necessarily lead to consistent, marked or lasting hemodynamic improvement. Thus, current concepts of the use of digitalis is such patients may require revision.

Adult↗
PubMed1984

Sustained beneficial hemodynamic responses to large doses of transdermal nitroglycerin in congestive heart failure and comparison with intravenous nitroglycerin.

The hemodynamic effects of a new transdermal preparation of nitroglycerin were evaluated in 9 patients with chronic congestive heart failure (CHF). A graded infusion of nitroglycerin was administered initially to establish the dose-response relation for nitroglycerin and estimate the dose of topical nitroglycerin to be applied. Significant hemodynamic improvement was observed 0.5 to 1.0 hour after the cutaneous application of the nitroglycerin-impregnated polymer. The peak effect occurred at 6 hours, with the left ventricular filling pressure decreasing from 24 +/- 2 to 18 +/- 1 mm Hg (mean +/- standard error of the mean) (p less than 0.01) and the cardiac index increasing from 2.0 +/- 0.2 to 2.6 +/- 0.2 liters/min/m2 (p less than 0.01). The systemic vascular resistance decreased from 1,860 +/- 198 to 1,531 +/- 162 dynes s cm-5 (p less than 0.01). Heart rate and mean arterial pressure were unchanged. Significant hemodynamic benefit was observed for 24 hours, and no rebound deterioration occurred upon withdrawal of the drug. The average dose of transdermal nitroglycerin applied was 51 +/- 6 cm2 (1.7 +/- 0.2 mg/kg; 6 of the 9 patients received 64 cm2). Thus, topical application of a new nitroglycerin-impregnated polymer induces an improvement in cardiac performance that is sustained for 24 hours in patients with chronic CHF. However, substantial doses of the drug may be required to produce a satisfactory hemodynamic response in most patients with CHF.

Adult↗
PubMed1985

Assessment of hemodynamic status in the intensive care unit immediately after closure of ventricular septal defect.

Hemodynamic values measured 12 to 24 hours postoperatively in the intensive care unit (ICU) were compared with those measured at a later cardiac catheterization in 68 patients after closure of ventricular septal defect (VSD). A pulmonary arterial (PA) saturation of more than 80% or a pulmonary to systemic blood flow ratio (Qp:Qs) greater than 1.5 in the ICU were sensitive indicators for identifying patients at risk of having a hemodynamically significant residual left-to-right shunt (Qp:Qs greater than 1.5) at catheterization. Measurement of PA pressure in the ICU was a useful predictor of PA pressure at catheterization. In the absence of factors known to alter PA pressure, measurement of PA pressure in the ICU overestimates what it will be at a subsequent cardiac catheterization. Early assessment of hemodynamics after closure of VSD is useful in identifying patients at risk of having hemodynamically significant residual VSD and those who may have persistent PA hypertension.

Adolescent↗
PubMed1985

Hemodynamic and metabolic effects of diltiazem during coronary sinus pacing with particular reference to left ventricular ejection fraction.

To determine the systemic and coronary hemodynamic effects of diltiazem at rest and during pacing, 14 patients with stable angina pectoris undergoing coronary angiography were studied before and after 0.165 mg/kg (n = 7) and 0.25 mg/kg (n = 7) of intravenously administered diltiazem. Hemodynamic variables, metabolic measurements and left ventricular (LV) ejection fraction (EF) were obtained at rest and during coronary sinus (CS) pacing before and during diltiazem administration. Lactate production during control pacing turned into extraction after diltiazem (p less than 0.05). At rest, systemic resistance was reduced by 21% (p greater than 0.01) and mean arterial pressure by 12% (p less than 0.01); cardiac index increased from 2.4 +/- 0.4 to 2.6 +/- 0.4 liters/min/m2 (p less than 0.01), with no significant change in heart rate. The mean pulmonary artery pressure increased from 17 +/- 2 to 19 +/- 3 mm Hg (p less than 0.01), but other hemodynamic variables were not affected. Diltiazem given during pacing reduced the mean aortic pressure (from 112 +/- 15 to 104 +/- 15 mm Hg, p less than 0.05), but other hemodynamic variables were not affected significantly. LVEF decreased 16%, from 0.63 +/- 0.9 to 0.53 +/- 0.8 with CS pacing (p less than 0.01); when the pacing was performed after diltiazem administration the 8% decrease in LVEF from 0.64 +/- 0.09 to 0.59 +/- 13 was less marked (p less than 0.01). Diltiazem had no significant effect on LVEF at rest. The overall data suggest that the ischemic manifestations of CS pacing are attenuated by diltiazem in doses of the drug that exert no significant depressant effect on LV function in patients with coronary artery disease.

Adult↗
PubMed1985

Clinical and hemodynamic experience with enalapril in congestive heart failure.

The renin-angiotension system is activated in many patients with congestive heart failure (CHF), resulting in angiotensin-mediated vasoconstriction and aldosterone-mediated sodium and water retention. To evaluate the effectiveness of enalapril, a new converting enzyme inhibitor, enalapril was administered to patients either orally or intravenously in a single dose, and hemodynamic and hormonal responses were measured. Patients were then placed on oral enalapril therapy for 1 month, and treadmill exercise duration and invasive hemodynamics were compared with baseline pretreatment data. With single-dose administration, both oral and intravenous enalapril reduced systemic vascular resistance and increased cardiac output. However, the effects of oral enalapril were not manifest for 3 to 4 hours, because oral enalapril is a pro-drug form that requires hepatic deesterification. In contrast, intravenous enalapril resulted in significant hemodynamic and hormonal changes 15 to 30 minutes after administration. During long-term therapy, enalapril was associated with improved symptomatology, increase of treadmill exercise duration and sustained hemodynamic improvement. Enalapril was effective therapy for chronic CHF. Optimal short-term response may require coadministration of both intravenous and oral preparations of enalapril; however, the magnitude of the short-term response was comparable for both preparations. Long-term therapy is most effective when the drug is administered as a twice-daily regimen.

Administration, Oral↗
PubMed1985

Hemodynamic and hormonal effects of high-dose transdermal nitroglycerin in patients with chronic congestive heart failure.

The hemodynamic effect of a large dose of nitroglycerin (NTG) (90 mg) given transdermally using a reservoir system was studied in 10 patients with severe, long-standing congestive heart failure. Serial hemodynamic measurements over 24 hours revealed a mild decrease in mean pulmonary artery wedge pressure. However, the change from baseline was significant only at 2 hours (19 +/- 9 vs 27 +/- 6 mm Hg). Mean right atrial pressure fell 1 hour after initiation of therapy, from 12 +/- 7 to 8 +/- 5 mm Hg. However, the change from control was not statistically significant. No significant changes were noted in heart rate, mean blood pressure, cardiac index, and systemic and pulmonary vascular resistance. Individual analysis of the effect of transdermal NTG on pulmonary artery wedge pressure demonstrated at 20% or greater reduction in 8 of 10 patients. However, persistent effect (longer than 8 hours) was seen in only 4 patients. Removal of NTG patches at 24 hours did not result in hemodynamic rebound. Serum catecholamine levels and renin concentration did not change 2 hours and 24 hours after initiation of NTG therapy or after removal of NTG patches. Thus, a large dose (90 mg) of transdermal NTG using a reservoir system results in mild and mostly statistically insignificant hemodynamic effect in patients with chronic severe congestive heart failure. Although a reduction in pulmonary artery wedge pressure is seen in most patients, rapid attenuation of this response is found in many patients and the effect only rarely lasts for 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1986

Hemodynamic changes after meals and placebo treatment in chronic congestive heart failure.

To determine whether significant spontaneous hemodynamic changes occur without therapeutic intervention, 15 patients with stable heart failure underwent right-sided cardiac catheterization and were observed without active treatment during an 8-hour period. Significant changes that mimic those seen during treatment with vasodilating medications were found. Increases were seen in heart rate (minimum 82 +/- 19 beats/min, maximum 88 +/- 18 beats/min, p less than 0.05) and cardiac index (minimum 2.14 +/- 0.45 liters/min/m2, maximum 2.42 +/- 0.79 liters/min/m2, p less than 0.05). Decreases were observed in pulmonary artery wedge pressure (maximum 24 +/- 7 mm Hg, minimum 21 +/- 7 mm Hg, p less than 0.05) and systemic vascular resistance (maximum 1,600 +/- 280 dynes-s-cm5, minimum 1,390 +/- 310 dynes-s-cm-5, p less than 0.05). Except for the decrease in pulmonary artery wedge pressure, all hemodynamic changes appeared to be related to eating. In addition, a statistically significant postprandial decrease in mean blood pressure (before meal 85 +/- 12 mm Hg, after meal 78 +/- 11 mm Hg, p less than 0.05) was seen. These data reinforce the need for caution in interpreting small hemodynamic changes, even if statistically significant, and they indicate the desirability of including placebo groups or phases in drug studies and of performing hemodynamic measurements the postabsorptive state.

Adult↗
PubMed1987

Use of invasive ergometric exercise to assess the hemodynamic response to nicardipine.

The calcium antagonists are potent vasodilators. This physiologic property suggests that these agents have a potential role in the treatment of patients with hypertension and congestive heart failure. Although the clinical response to calcium antagonism in hypertension is promising, the response in patients with congestive heart failure is less than hoped for; this is due to the fact that this class of agents may induce a hemodynamically important degree of negative inotropic effect. To test the hemodynamic response to nicardipine, a second-generation dihydropyridine, the hemodynamic response to maximal ergometric exercise was evaluated in a group of patients with moderate to severe chronic congestive heart failure. One week of nicardipine therapy was associated with a significant reversal of vasoconstriction at rest and during peak exercise with a secondary increase of cardiac index, and a decrease in pulmonary wedge pressure. The reversal of vasoconstriction was associated with a decrease in mean arterial pressure, with no change in the heart rate. There was no change in oxygen consumption or carbon dioxide production; however, there was a decrease in arteriovenous oxygen difference, consistent with a reduction of oxygen extraction. This short-term study identified the potent vasodilator properties of nicardipine in patients with chronic congestive heart failure; a hemodynamically significant negative inotropic effect could not be identified. Although the use of calcium antagonists for the treatment of congestive heart failure may have a limited role, this study nonetheless suggests that nicardipine may have a favorable vasodilator effect without an overt negative inotropic effect. This would be of considerable advantage in the treatment of hypertension, when compared with beta-adrenergic blocking agents.

Adult↗