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PubMed1983

Sustained hemodynamic and clinical effects of a new cardiotonic agent, WIN 47203, in patients with severe congestive heart failure.

The hemodynamic and clinical effects of WIN 47203, a newly synthesized noncatecholamine, nonglycosidic inotropic agent, were studied in 11 patients with severe chronic congestive heart failure. Intravenous WIN 47203 increased cardiac index from 1.93 +/- 0.36 to 2.87 +/- 0.45 l/min/m2 (p less than 0.001) and reduced pulmonary capillary wedge pressure from 27.0 +/- 8.4 to 16.3 +/- 6.1 mm Hg (p less than 0.001). Mean systemic arterial pressure decreased from 75.2 +/- 6.7 to 72.4 +/- 6.3 mm Hg (p less than 0.01) and systemic vascular resistance from 1591 +/- 397 to 1071 +/- 293 dyn-sec-cm5 (p less than 0.001); heart rate was unchanged. Oral WIN 47203 produced similar hemodynamic improvement. Hemodynamic monitoring of six consecutive doses did not demonstrate evidence for attenuation of effectiveness. Chronic therapy with WIN 47203 produced substantial symptomatic improvement and increased maximal oxygen uptake at 1 week. Patients were further improved after 4 weeks of WIN 47203, and maximal oxygen uptake increased from 9.0 +/- 1.9 to 11.6 +/- 2.5 ml/kg/min (p less than 0.01 vs control). No overt clinical or laboratory manifestations of toxicity were observed. Withdrawal of WIN 47203 in two patients in whom clinical benefit was not sustained resulted in clinical and hemodynamic deterioration, which was reversed by reinstitution of the drug. Therefore, this study demonstrates the acute and sustained cardiotonic efficacy of WIN 47203 in man. If long-term administration remains well tolerated and without side effects, this drug appears to be very promising for treatment of chronic severe congestive heart failure.

Administration, Oral↗
PubMed1983

The neurohumoral and hemodynamic response to orthostatic tilt in patients with congestive heart failure.

Thirty-five patients with varying degrees of congestive heart failure were subjected to 60 degrees upright tilt. Eight of the patients with normal resting hemodynamics had elevated resting plasma norepinephrine levels (PNE) (p less than 0.001), but their response to upright tilt was similar to that in normal subjects: All had increases in heart rate, plasma norepinephrine (from 263 +/- 32 to 483 +/- 78 pg/mg, p less than 0.02) and plasma renin activity (from 4.8 +/- 0.9 to 13.7 +/- 7.6 ng/ml/hour, p less than 0.05). In 27 patients with high resting pulmonary wedge pressure and low cardiac index, resting PNE was higher (668 +/- 71 ng/ml), but PNE, plasma renin activity and heart rate did not increase significantly during tilt despite a fall in pulmonary capillary wedge pressure and cardiac index. In 18 of these patients, PNE rose during tilt, whereas in nine it did not change or fell; the resting hemodynamics and the hemodynamic response to tilt were not significantly different in these two groups. These data suggest that an abnormality of mechanoreceptor or baroreceptor function is common in patients with CHF. This abnormality corresponds in part to the severity of the resting hemodynamic abnormality, but among patients with severe CHF, the reflex neurohumoral abnormality may provide independent information about the severity of the disease.

Adult↗
PubMed1985

Hemodynamic findings at rest and during mild supine exercise in adults with isolated, uncomplicated ventricular septal defects.

Fifty-two patients with isolated congenital ventricular septal defects (VSDs), studied for the first time at age 10 or older, were restudied an average of 16 years later (range 4 to 21). The study protocol included a symptom-limited bicycle ergometer test, M mode echocardiographic examination, and hemodynamic studies at rest and during mild supine exercise. Of the 52, 17 had been operated on an average of 19 years earlier (range 11 to 21) (group 1) and 35 with smaller defects were not operated on (group 2). Although more pronounced findings were made in group 1, a similar pattern was observed in group 2: In most subjects in both groups a subnormal working capacity was observed. A subnormal left ventricular fractional shortening and circumferential shortening velocity was noted in a high proportion at echocardiography. A number of hemodynamic aberrations were observed in a high proportion of patients during exercise but not at rest. Thus a subnormal increase in left and right ventricular cardiac output was found in addition to pathologic increase in right and left ventricular end-diastolic, pulmonary arterial, and pulmonary capillary wedge pressures. In group 1, elevated pulmonary arterial pressures before operation and/or small residual VSDs were associated with a poor hemodynamic outcome. In neither group could significant correlations be observed between hemodynamic aberrations, shunt size, and/or age. Among patients who underwent surgery, the earlier surgical trauma might have contributed to the functional aberrations, but in group 2 the only likely explanation for the findings seems to be the VSD itself. Possibly a long-standing VSD--found unnecessary to repair according to commonly accepted criteria--may lead to disturbed systolic function and increase in compliance of both ventricles via a chronic pressure and volume overload.

Adult↗
PubMed1988

Potentiation of the hemodynamic effects of acutely administered nitroglycerin by methionine.

It is believed that nitroglycerin causes vasodilatation by interacting with sulfhydryl groups present in vascular smooth muscle. This study was performed to assess whether methionine, an amino acid capable of increasing sulfhydryl availability, would potentiate the hemodynamic effects of nitroglycerin. Nitroglycerin was initially infused in incremental doses from 1 to 50 micrograms/min in all patients to determine the dose required to reduce mean arterial pressure by 10% and pulmonary capillary wedge pressure by 30%. After a washout period, 10 patients received 5 g methionine i.v. and five patients received an equal volume of 5% dextrose in water (control). Nitroglycerin dose titration was then repeated. Methionine alone induced no hemodynamic effects, but after methionine infusion, there was a significant reduction in the nitroglycerin infusion rate required to reach each hemodynamic endpoint (p less than 0.01). In the control group, there was no significant change in responsiveness to nitroglycerin between infusions. Thus, methionine potentiates the hemodynamic effects of acutely administered intravenous nitroglycerin.

Analysis of Variance↗
PubMed1989

Increased beta-receptor density and improved hemodynamic response to catecholamine stimulation during long-term metoprolol therapy in heart failure from dilated cardiomyopathy.

Severe heart failure is associated with a reduction in myocardial beta-adrenergic receptor density and an impaired contractile response to catecholamine stimulation. Metoprolol was administered during a 6-month period to 14 patients with dilated cardiomyopathy to examine its effects on these abnormalities. The mean daily dose of metoprolol for the group was 105 mg (range, 75-150 mg). Myocardial beta-receptor density, resting hemodynamic output, and peak left ventricular dP/dt response to dobutamine infusions were compared in 9, 14, and 7 patients, respectively, before and after 6 months of metoprolol therapy while the patients were on therapy. The second hemodynamic study was performed 1-2 hours after the morning dose of metoprolol had been given. Myocardial beta-receptor density increased from 39 +/- 7 to 80 +/- 12 fmol/mg (p less than 0.05). Resting hemodynamic output showed a rise in stroke work index from 27 +/- 4 to 43 +/- 3 g/m/m2, p less than 0.05, and ejection fraction rose from 0.26 +/- 0.03 to 0.39 +/- 0.03 after 6 months of metoprolol therapy, p less than 0.05. Before metoprolol therapy, dobutamine caused a 21 +/- 4% increase in peak positive left ventricular dP/dt; during metoprolol therapy, the same dobutamine infusion rate increased peak positive dP/dt by 74 +/- 18% (p less than 0.05). Thus, long-term metoprolol therapy is associated with an increase in myocardial beta-receptor density, significant improvement in resting hemodynamic output, and improved contractile response to catecholamine stimulation. These changes indicate a restoration of beta-adrenergic sensitivity associated with metoprolol therapy, possibly related to the observed up-regulation of beta-adrenergic receptors.

Cardiomyopathy, Dilated↗
PubMed1989

Captopril restores hemodynamic responsiveness to atrial natriuretic peptide in rats with heart failure.

Atrial natriuretic peptide levels are elevated in heart failure. However, the hemodynamic responses to exogenous atrial natriuretic peptide infusion in heart failure are blunted. To determine if captopril can restore hemodynamic responsiveness to atrial natriuretic peptide infusion in rats with heart failure, studies were performed in a rat model of heart failure after coronary artery ligation. Rats with heart failure received either captopril (2 g/l drinking water) or placebo for 4 weeks and then were treated with an infusion of atrial natriuretic peptide (0.3 microgram/kg/min). Captopril treatment alone improved hemodynamics. Left ventricular end-diastolic pressure, mean aortic pressure, and mean circulatory filling pressure decreased from 22 +/- 2 to 14 +/- 1, from 106 +/- 4 to 76 +/- 3, and from 10.5 +/- 0.6 to 8.8 +/- 0.4 mm Hg, respectively. Heart rate, right atrial pressure, and hematocrit were unchanged. Total blood volume decreased from 66.0 +/- 1.0 to 60.0 +/- 1.0 ml/kg; venous compliance increased from 2.1 +/- 0.1 to 2.7 +/- 0.1 ml/kg/mm Hg. Atrial natriuretic peptide alone had minimal hemodynamic effects on rats with heart failure. There was no change in right atrial pressure, mean aortic pressure, left ventricular end-diastolic pressure, mean circulatory filling pressure, and total blood volume. However, atrial natriuretic peptide infusion increased venous compliance from 2.1 +/- 0.1 to 2.4 +/- 0.1 ml/kg/mm Hg. Heart rate and hematocrit increased from 323 +/- 5 to 359 +/- 8 beats/min and from 48 +/- 1% to 51 +/- 1%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Comparative hemodynamic effects of procainamide, tocainide, and encainide in severe chronic heart failure.

Many of the newer antiarrhythmic agents are said to cause minimal myocardial depression, but their hemodynamic effects have not been invasively evaluated and compared in patients with severe chronic heart failure. In a randomized, crossover study, the hemodynamic responses to single oral doses of procainamide (750 mg), tocainide (600 mg), and encainide (50 mg) given to 21 patients with severe chronic heart failure were compared. Cardiac performance decreased with all three drugs, but the magnitude of deterioration differed among the three agents. Stroke volume index decreased with procainamide (-5 +/- 1 ml/m2, p less than 0.001), tocainide (-7 +/- 1 ml/m2, p less than 0.001), and encainide (-8 +/- 1 ml/m2, p less than 0.001), but the decline was significantly greater with encainide than with procainamide (p less than 0.05). Similarly, left ventricular filling pressure increased with tocainide and encainide (+4 +/- 1 and +5 +/- 2 mm Hg, respectively; both p less than 0.05), but not with procainamide; the increase was significantly greater with tocainide and encainide than with procainamide (p less than 0.001). These deleterious hemodynamic effects were accompanied by worsening symptoms of heart failure in six patients with encainide and seven patients with tocainide but in only two patients with procainamide. Serum levels for all drugs were in the therapeutic range. In conclusion, although the three type I antiarrhythmic agents tested may all adversely affect left ventricular function in patients with heart failure, encainide and tocainide are more likely than procainamide to cause hemodynamic and clinical deterioration.

Aged↗
PubMed1990

Determinants of hemodynamic compromise with severe right ventricular infarction.

To elucidate determinants of hemodynamic compromise in patients with acute right ventricular (RV) infarction, we studied 16 patients with hemodynamically severe RV infarction by right heart catheterization and two-dimensional ultrasound. Severe RV systolic dysfunction, evident by ultrasound in all patients as RV dilatation and depressed RV free wall motion, was associated with a broad sluggish RV waveform, diminished peak RV systolic pressure (27.6 +/- 4.5 mm Hg), and depressed RV stroke work (4.6 +/- 2.4 g.m/m2). Paradoxical septal motion was consistently noted. In some cases, the septum bulged into the right ventricle in a pistonlike fashion and appeared to mediate systolic ventricular interaction through which left ventricular septal contraction contributed to RV pressure generation. RV diastolic dysfunction was indicated by elevated RV end-diastolic pressures (13.7 +/- 2.7 mm Hg), RV "dip and plateau," equalization of diastolic filling pressures, and reversal of diastolic septal curvature toward the volume-deprived left ventricle. A prominent right atrial (RA) X and blunted Y descent, indicative of impairment of RV filling throughout diastole, were confirmed in all patients by their relation to RV systolic events. Patients manifested one of two distinct RA waveform morphologies differentiated by A wave amplitude and associated with disparate clinical courses. In eight patients, an RA W pattern was evident, characterized by augmented A waves; eight others manifested an M pattern constituted by depressed A waves. Compared with those with an M pattern, patients with a W pattern had higher peak RV pressures (29.6 +/- 3.8 versus 25.5 +/- 4.3 mm Hg, p less than 0.05), better cardiac output (3.4 +/- 0.3 versus 2.9 +/- 0.7 l/min, p less than 0.05), more favorable response to volume and inotropes, and less frequently required emergency revascularization for refractory shock (none versus five for those with an M pattern). Patients with a W pattern were more severely compromised if atrioventricular dyssynchrony developed and were more dramatically improved by restoration of physiological rhythm. Angiography in patients with depressed A waves demonstrated more proximal coronary obstruction leading to ischemic compromise of RA function, whereas in those with augmented A waves, the culprit lesion was proximal to the RV but distal to the RA branches. These results indicate that hemodynamic compromise in patients with RV infarction is exacerbated by decreased preload reserve that is dependent on atrial systole. The amplitude of the RA A wave, an indication of the status of RA function, is an important determinant of RV performance and hemodynamic compromise.

Blood Pressure↗
PubMed1993

Acute effect of percutaneous transvenous mitral commissurotomy on ventilatory and hemodynamic responses to exercise. Pathophysiological basis for early symptomatic improvement.

BACKGROUND: Improvement of exertional dyspnea occurs immediately after percutaneous transvenous mitral commissurotomy (PTMC), but the pathophysiological basis for this early symptomatic improvement has not been elucidated. METHODS AND RESULTS: Exercise hemodynamic measurement and exercise ventilatory measurement with arterial blood gas analysis were performed in 21 patients aged 50.4 +/- 9.5 years (mean +/- SD) with symptomatic mitral stenosis before and a few days after PTMC. Exercise ventilatory measurement were also performed in 14 normal control subjects aged 48.9 +/- 4.9 years. After PTMC, mitral valve area increased (from 1.0 +/- 0.3 to 1.7 +/- 0.3 cm2, P < .001), mean mitral gradient (from 12.2 +/- 5.2 to 5.2 +/- 2.2 mm Hg, P < .001), and mean left atrial pressure (from 18.7 +/- 6.1 to 12.1 +/- 4.0 mm Hg, P < .001) decreased. All patients experienced significant symptomatic improvement soon after PTMC. Comparison of hemodynamic parameters at the same ergometer work rate showed a significant decrease in pulmonary artery systolic pressure (from 77 +/- 18 to 67 +/- 14 mm Hg, P < .001) and diastolic pressure (from 36 +/- 10 to 28 +/- 7 mm Hg, P < .001) and a significant increase in cardiac output (from 6.4 +/- 1.4 to 8.1 +/- 1.9 L/min, P < .001). Despite the improvement in exercise hemodynamics and symptoms, exercise capacity determined by peak oxygen uptake (from 18.0 +/- 2.9 to 18.6 +/- 3.1 mL.kg-1 x min-1) and anaerobic threshold (from 11.7 +/- 2.4 to 12.0 +/- 2.4 mL.kg-1 x min-1) remained unchanged. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output, decreased significantly from 37.2 +/- 6.7 to 33.9 +/- 5.8 (P < .001), but remained significantly higher than that in the normal subjects (27.9 +/- 3.6, P < .01). The ratio of total dead space to tidal volume and total dead space per breath during exercise decreased significantly after PTMC (P < .05). The change in excessive exercise ventilation after PTMC was correlated with the change in dead space to tidal volume ratio (r = .59). CONCLUSIONS: Significant relief of exertional dyspnea immediately after PTMC is not accompanied by an improvement in exercise capacity. A decrease in excessive ventilation due to a decrease in physiological dead space resulting from hemodynamic improvement partly contributes to the early relief of symptoms after PTMC. However, lung compliance, which was not measured in the present study, may have changed after PTMC. This change may also contribute to the symptomatic improvement.

Anaerobic Threshold↗
PubMed1994

Arterial baroreflex control of renal hemodynamics in humans.

BACKGROUND: Control of renal hemodynamics by the arterial baroreflex has never been proved in humans. Apart from the physiological viewpoint, this issue is relevant because altered baroreflex function has been implicated in the pathogenesis of human hypertension. METHODS AND RESULTS: Renal function studies were performed in seated healthy volunteers (n = 12; age range, 20 to 34 years) during sustained neck suction at -60 mm Hg, aiming to selectively activate the carotid sinus arterial baroreceptors. Two protocols were followed. One group of 6 volunteers taking a 20 mmol/d sodium diet underwent 90 minutes of neck suction. Compared with a time-control study, neck suction decreased arterial pressure and heart rate; increased glomerular filtration rate (inulin clearance) from 104 +/- 6 to 114 +/- 8 mL/min (P < .01), renal plasma flow (para-aminohippurate clearance) from 616 +/- 52 to 665 +/- 42 mL/min (P < .01), and renal blood flow (from 1120 +/- 95 to 1209 +/- 77 mL/min, P < .01); and decreased renal vascular resistance (from 86 +/- 8 to 76 +/- 6 mm Hg.min.L-1, P < .01). Neck suction had no effect on plasma renin activity, aldosterone, atrial natriuretic peptide, catecholamines, and renal sodium excretion. The other 6 volunteers took a normal sodium diet and underwent sustained neck suction for 60 minutes. In this group, no effects on renal hemodynamics could be discerned, despite a modest decrease in blood pressure and heart rate. CONCLUSIONS: These data show, for the first time, that the arterial baroreflex is involved in the control of renal hemodynamics in humans. However, basal arterial baroreflex control of renal hemodynamics is probably low, and arterial baroreflex activation with subsequent renal vasorelaxation may be found only in conditions in which basal arterial baroreflex control of kidney function is significant, as is presumably the case in seated sodium-restricted subjects.

Adult↗
PubMed1995

Postoperative course and hemodynamic profile after the arterial switch operation in neonates and infants. A comparison of low-flow cardiopulmonary bypass and circulatory arrest.

BACKGROUND: The neurological morbidity associated with prolonged periods of circulatory arrest has led some cardiac surgical teams to promote continuous low-flow cardiopulmonary bypass as an alternative strategy. The nonneurological postoperative effects of both techniques have been previously studied only in a limited fashion. METHODS AND RESULTS: We compared the hemodynamic profile (cardiac index and systemic and pulmonary vascular resistances), intraoperative and postoperative fluid balance, and perioperative course after deep hypothermia and support consisting predominantly of total circulatory arrest or low-flow cardiopulmonary bypass in a randomized, single-center trial. Eligibility criteria included a diagnosis of transposition of the great arteries and a planned arterial switch operation before the age of 3 months. Of the 171 patients, 129 (66 assigned to circulatory arrest and 63 to low-flow bypass) had an intact ventricular septum and 42 (21 assigned to circulatory arrest and 21 to low-flow bypass) had an associated ventricular septal defect. There were 3 (1.8%) hospital deaths. Patients assigned to low-flow bypass had significantly greater weight gain and positive fluid balance compared with patients assigned to circulatory arrest. Despite the increased weight gain in the infants assigned to low-flow bypass, the duration of mechanical ventilation, stay in the intensive care unit, and hospital stay were similar in both groups. Hemodynamic measurements were made in 122 patients. During the first postoperative night, the cardiac index decreased (32.1 +/- 15.4%, mean +/- SD), while pulmonary and systemic vascular resistance increased. The measured cardiac index was < 2.0 L.min-1.m-2 in 23.8% of the patients, with the lowest measurement typically occurring 9 to 12 hours after surgery. Perfusion strategy assignment was not associated with postoperative hemodynamics or other nonneurological postoperative events. CONCLUSIONS: After heart surgery in neonates and infants, both low-flow bypass and circulatory arrest perfusion strategies have comparable effects on the nonneurological postoperative course and hemodynamic profile.

Cardiopulmonary Bypass↗
PubMed1995

Hemodynamic characteristics of neonates following first stage palliation for hypoplastic left heart syndrome.

BACKGROUND: It is widely held that the postoperative course of patients with hypoplastic left heart syndrome (HLHS) after stage 1 palliation is characterized by hemodynamic instability, which in part may be due to excessive pulmonary blood flow. Hence, avoidance of alkalosis and the use of minimally oxygen-enriched inspiratory gas are thought by many to be important, although there is little pertinent published data. This study was undertaken to characterize the postoperative course and to determine whether the FIO2 and blood pH are related to indices of hemodynamic stability in these infants. METHODS AND RESULTS: The postoperative course of 25 consecutive infants undergoing first stage palliation for HLHS were retrospectively reviewed and the following data were obtained: arterial pressure, arterial blood gas measurements, the inotropic agents used, and multiple respiratory parameters. There was one operative death, and 2 patients died within 2 days, but 22 were extubated (mean, 5.2 +/- 4.1 days after surgery). Hospital mortality was 24%. Mean pH was > or = 7.51 for the first 9 hours after surgery and was > or = 7.45 for the entire period. The mean FIO2 was > or = 50% for the first 18 hours. The PaO2 was appropriate (37 +/- 6 mm Hg at 1 hour after surgery, increasing to 45 +/- 5 mm Hg by hour 73). Only modest inotropic support was needed to maintain appropriate blood pressure. CONCLUSIONS: These data suggest that neither alkalosis nor relatively high inspired oxygen necessarily cause hemodynamic instability in these patients. To what extent these results are generalizable is unclear, but they suggest that there is nothing inherent with HLHS that mandates postoperative hemodynamic instability or unacceptable mortality.

Arteries↗
PubMed1996

Comparative hemodynamic, left ventricular functional, and antiadrenergic effects of chronic treatment with metoprolol versus carvedilol in the failing heart.

BACKGROUND: The basic pharmacology of the third-generation beta-blocking agent carvedilol differs considerably from second-generation compounds such as metoprolol. Moreover, carvedilol may produce different, ie, more favorable, clinical effects in chronic heart failure. For these reasons, we compared the effects of carvedilol and metoprolol on adrenergic activity, receptor expression, degree of clinical beta-blockade, hemodynamics, and left ventricular function in patients with mild or moderate chronic heart failure. METHODS AND RESULTS: The effects of carvedilol versus metoprolol were compared in two concurrent placebo-controlled trials with carvedilol or metoprolol that had common substudies focused on adrenergic, hemodynamic, and left ventricular functional measurements. All subjects in the substudies had chronic heart failure resulting from idiopathic dilated cardiomyopathy. Carvedilol at 50 to 100 mg/d produced reductions in exercise heart rate that were similar to metoprolol at 125 to 150 mg/d, indicating comparable degrees of beta-blockade. Compared with metoprolol, carvedilol was associated with greater improvement in New York Heart Association functional class. Although there were no significant differences in hemodynamic effects between the carvedilol and metoprolol active-treatment groups, carvedilol tended to produce relatively greater improvements in left ventricular ejection fraction, stroke volume, and stroke work compared with changes in the respective placebo groups. Carvedilol selectively lowered coronary sinus norepinephrine levels, an index of cardiac adrenergic activity, whereas metoprolol did not lower coronary sinus norepinephrine and actually increased central venous norepinephrine levels. Finally, metoprolol was associated with an increase in cardiac beta-receptor density, whereas carvedilol did not change cardiac beta-receptor expression. CONCLUSIONS: The third-generation beta-blocking agent carvedilol has substantially different effects on left ventricular function, hemodynamics, adrenergic activity, and beta-receptor expression than dose the second-generation compound metoprolol. Some or all of these differences may explain the apparent differences in clinical results between the two compounds.

Adrenergic beta-Antagonists↗
PubMed1996

Simultaneous coronary pressure and flow velocity measurements in humans. Feasibility, reproducibility, and hemodynamic dependence of coronary flow velocity reserve, hyperemic flow versus pressure slope index, and fractional flow reserve.

BACKGROUND: To assess coronary lesion severity in the catheterization laboratory, several guide wire-based methods have been proposed. The purpose of the present study was to compare the feasibility and the reproducibility of coronary flow velocity reserve (CFVR), instantaneous hyperemic diastolic velocity-pressure slope index (IHDVPS), and pressure-derived myocardial fractional flow reserve (FFRmyo). METHODS AND RESULTS: From distal coronary pressure and flow velocity signals (0.014-in guide wires), CFVR, IHDVPS, and FFRmyo were computed in 15 stenoses (13 patients) under the four following pairs of conditions: (1) twice under baseline conditions; (2) during atrial pacing at 80 and 110 bpm; (3) before and during intravenous infusion of nitroprusside; and (4) before and during intravenous infusion of dobutamine. A total of 104 measurements were obtained. Both CFVR and FFRmyo could be calculated in all cases. IHDVPS could be calculated in only 79% of cases. The mean value of CFVR did not change between the two baseline measurements and during infusion of nitroprusside but decreased from 1.85 +/- 0.41 to 1.66 +/- 0.45 (P < .05) during atrial pacing and from 1.90 +/- 0.50 to 1.41 +/- 0.28 (P < .05) during dobutamine infusion. The mean values of IHDVPS and FFRmyo remained similar, whichever the changes in hemodynamic conditions. The coefficient of variation between two consecutive measurements was significantly lower for FFRmyo (4.2%) than for CFVR (17.7%) and for IHDVPS (24.7%). CONCLUSIONS: CFVR is easy to measure but sensitive to hemodynamic changes. IHDVPS can be measured only in < 80% of cases and is highly variable even without changes in hemodynamic conditions. FFRmyo is easy to measure and almost independent of hemodynamic changes.

Aged↗
PubMed1997

Association between thrombolytic treatment and the prognosis of hemodynamically stable patients with major pulmonary embolism: results of a multicenter registry.

BACKGROUND: Thrombolytic treatment has been shown to accelerate resolution of major pulmonary embolism and lead to a rapid improvement of right-side hemodynamics. However, the association between these favorable effects and the clinical outcome of patients who have no severe hemodynamic compromise at presentation remains unknown. METHODS AND RESULTS: The present multicenter registry included 719 consecutive patients with major pulmonary embolism according to clinical, echocardiographic, scintigraphic, and cardiac catheterization criteria. Symptom onset was acute (<48 hours) in 63% of patients. All patients were hemodynamically stable (ie, without evidence of cardiogenic shock) at presentation. Primary thrombolytic treatment (within 24 hours of diagnosis) was given to 169 patients (23.5%), whereas the remaining 550 patients were initially treated with heparin alone. Overall 30-day mortality was significantly lower in the patients who received thrombolytic agents (4.7 versus 11.1%, P=.016). Clinical factors associated with a higher death rate were syncope (P=.012), arterial hypotension (P=.021), history of congestive heart failure (P=.013), and chronic pulmonary disease (P=.032). However, only primary thrombolysis was found by multivariate analysis to be an independent predictor of survival (odds ratio for in-hospital death, 0.46; 95% confidence interval, 0.21 to 1.00). Patients who underwent early thrombolytic treatment had a reduced rate of recurrent pulmonary embolism (7.7 versus 18.7%, P<.001) but also a higher frequency of major bleeding episodes (21.9% versus 7.8%, P<.001). Cerebral bleeding occurred in 2 patients in each treatment group, and 1 patient in each group died of a bleeding complication. CONCLUSIONS: The results of our study suggest that thrombolysis may favorably affect the clinical outcome of hemodynamically stable patients with major pulmonary embolism.

Adolescent↗
PubMed1997

Disturbed intracoronary hemodynamics in myocardial bridging: early normalization by intracoronary stent placement.

BACKGROUND: The purpose of this study was to evaluate the hemodynamic mechanisms leading to myocardial ischemia in patients with myocardial bridging. Myocardial bridging is known to induce angina and even severe myocardial ischemia. METHODS AND RESULTS: In 12 symptomatic patients with myocardial bridges, quantitative coronary angiography was performed to obtain systolic/diastolic vessel diameters within the bridged segments. Coronary flow velocities, flow reserve, and pressures were determined with a 0.014-in Doppler and a 0.014-in pressure microtransducer. In 3 symptomatic patients, coronary stents were implanted and hemodynamic measurements were repeated immediately and after 7 weeks. An in vitro validation of the pressure measurements was performed. Angiography revealed a systolic diameter reduction of 80.6+/-9.2% and a persistent diastolic reduction of 35.3+/-11% within the bridged segment. Diastolic flow velocities (cm/s) were increased (31.5+/-14.3 within versus 17.3+/-5.7 proximal and 15.2+/-6.3 distal, P<.001). Coronary flow reserve distal to the bridge was 2.5+/-0.5. There was an increased peak systolic pressure within the bridged segment (171+/-48 versus 113+/-10 mm Hg proximal, P<.001). Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, the intracoronary peak systolic pressure, and clinical symptoms. Coronary flow reserve improved to 3.8+/-0.3. CONCLUSIONS: Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.

Adult↗
PubMedDate not supplied

Early impairment of renal hemodynamic reserve in patients with asymptomatic heart failure is restored by angiotensin II antagonism.

BACKGROUND: The early/asymptomatic stages of heart failure (HF) are characterized by sodium retention secondary to derangement of sodium reabsorption at the proximal nephron level. Because this phenomenon is reversed by ACE inhibition, abnormalities of renal sodium handling may depend on intrarenal changes of angiotensin II (AII)/nitric oxide (NO) levels. Renal hemodynamic reserve (ie, the glomerular vasodilatory response to amino acid infusion) has been proposed as a reliable test to assess in vivo AII/NO balance. METHODS AND RESULTS: In this study, the effects of 6 weeks of treatment with 5 mg/d of enalapril or with 50 mg/d of losartan on systemic hemodynamics and renal function were assessed, at baseline and after amino acid infusion (AA), in patients with mild HF (NYHA class I) and in healthy volunteers. Untreated HF patients showed a basal renal function comparable to that of healthy subjects. After AA, glomerular filtration rate and renal plasma flow significantly increased in healthy subjects (+29.0% and +30.4%, respectively), whereas no vasodilatory response was observed in HF. Although they did not affect basal renal hemodynamics, both enalapril and losartan restored a normal response to AA in HF patients. Blood pressure and heart rate were comparable in HF subjects and healthy subjects at baseline and were not modified by either treatment. Left ventricular ejection fraction was depressed in HF but did not change after either drug. Urinary excretions of cGMP and nitrate (indexes of NO activity in the kidney), comparable in healthy subjects and in HF patients, were unchanged by either enalapril or losartan and did not correlate with renal reserve. CONCLUSIONS: (1) Renal functional reserve is absent in patients with early/asymptomatic HF and normal renal function and (2) both enalapril and losartan restore a normal vasodilatory response to AA in these patients without affecting basal systemic and renal hemodynamics. These data suggest a major role of AII in the development of early abnormalities in patients with HF.

Adult↗
PubMed2002

Hemodynamic and humoral effects of vasopeptidase inhibition in canine hypertension.

Vasopeptidase inhibitors are potent new antihypertensive agents. The dual inhibition of ACE and neutral endopeptidase may result in synergistic humoral effects with unique hemodynamic actions. We investigated the hemodynamic and neurohumoral effects of vasopeptidase inhibition in conscious dogs made hypertensive by bilateral renal wrapping and subsequently instrumented for long-term assessment of left ventricular pressure and volume (n=8). Intravenous vasopeptidase inhibition (omapatrilat, 30 micromol/kg over 10 minutes) reduced peak left ventricular pressure (171+/-6 versus 130+/-6 mm Hg immediately after infusion, P<0.01) through arterial vasodilation (arterial elastance, 9.8+/-0.8 to 5.8+/-1.6 mm Hg/mL, P<0.01) and preload reduction (left ventricular end-diastolic volume, 51.1+/-6.8 to 46.0+/-6.9 mL, P<0.01). At 60 minutes, preload decreased further (40.5+/-5.9 mL, P<0.01 versus baseline). Vasopeptidase inhibition increased plasma levels of adrenomedullin (41.2+/-9.6 versus 72.3+/-15 pg/mL, P<0.01), whereas levels of the natriuretic peptides and cGMP were unchanged. Similar hemodynamic and humoral effects were observed with long-term therapy. Neither an equimolar dose of an ACE inhibitor (fosinopril) nor exogenous adrenomedullin had as potent of a hypotensive effect, and neither reduced preload. In summary, the potent short-term and long-term hypotensive effects of vasopeptidase inhibition were prominently mediated by preload reduction, an effect not reproduced by ACE inhibition nor adrenomedullin augmentation and not associated with enhanced natriuretic peptide levels. Combined arterial vasodilation and preload reduction may confer additional potency as well as unique cardioprotective effects. Synergistic effects on humoral and probably endothelial vasodilatory factors appear to be important in mediating the unique hemodynamic profile of vasopeptidase inhibition in this form of experimental hypertension.

Adrenomedullin↗