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PubMed1988

Hemodynamic significance of internal carotid artery disease.

Neurologic symptoms in the region of an internal carotid artery stenosis are considered to be embolic in most instances. Only in a subgroup has carotid occlusive disease with impairment of the collateral supply, caused a state of hemodynamic failure with marked reduction of perfusion pressure. Though unproven, it is reasonable to assume that without surgical intervention, the risk is higher than average for patients with hemodynamic failure. Equally, should there be any postoperative improvement of cerebral blood flow or neurologic deficits, it should be looked for in this group. Thus, it is necessary to distinguish those with low perfusion pressure from the population of patients with carotid artery disease. Preoperative clinical evaluation and direct visualization of the carotid bifurcation should be supplemented by indirect physiological tests which allow assessment of collateral perfusion. Examination of periorbital flow direction or oculoplethysmography could be used as a screening procedure. Negative tests most certainly rule out any severe pressure gradient across the stenosis, irrespective of the luminal reduction. A positive result, on the other hand, should be further quantified since most indirect tests become positive at relatively small pressure gradients. Studies of cerebral blood flow at rest and during cerebral vasodilation makes it possible to identify patients with severe reduction of cerebral perfusion pressure. Such hemodynamic failure of one hemisphere may be identified in most cases by a conventional non-invasive xenon-133 technique and stationary detectors. Smaller focal regions of hypoperfusion may be identified by computer emission tomography, either by the detection of single-photon emission or by paired detection of annihilation photons. Endarterectomy does improve cerebral hemodynamics in terms of increased flow through the reconstructed vessel and elimination of pressure gradients. The cerebral blood flow, though remains unchanged in the majority of patients, at least when measured at baseline. Only in those patients with a reduction in perfusion pressure can a significant improvement in baseline flow occur. Flow reserve determined by cerebral vasodilation, however, will improve in most patients with hemodynamic failure. In addition, some patients in the low-pressure group develop marked, but temporary, hyperperfusion after reconstruction of very high grade carotid stenosis. This is considered a result of chronic low perfusion pressure with subsequent loss of autoregulation, and autoregulatory control is first regained after some days.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiography↗
PubMed2005

The impact of intralesional interferon alpha-2b injection therapy on penile hemodynamics in men with Peyronie's disease.

INTRODUCTION: Penile duplex Doppler ultrasound (PDDU) is currently the preferred method for the functional evaluation of penile hemodynamics. PDDU may be used to monitor objectively changes in penile vascular parameters in men who undergo treatment for Peyronie's disease (PD), including intralesional interferon alpha-2b (IFN alpha-2b). AIM: To investigate the impact of intralesional IFN alpha-2b therapy for PD on penile hemodynamics by using PDDU and to assess the objective role of PDDU in monitoring treatment outcomes. MATERIALS AND METHODS: Thirty-nine patients (20 in the placebo and 19 in the IFN alpha-2b treatment arm) were enrolled in this prospective, placebo-controlled, parallel study. Patients received either 10 mL saline or 5 x 10(6) units of IFN alpha-2b intralesional injections every other week for a total of six injections. Patients in each group were evaluated at baseline and after completion of treatment regarding changes in penile hemodynamic parameters, penile curvature, plaque size and density, pain on erection, and erectile function. Specific published criteria were used for PDDU measurements. Outcomes were statistically compared between each group by using Mann-Whitney U and chi-square tests. RESULTS: The mean age of the patients and the duration of PD were similar in both groups. The improvement in penile blood flow was significantly greater in IFN alpha-2b-treated patients than those in the placebo group. The number with the nonvascular classification increased significantly in the IFN alpha-2b arm from 31.5% to 57.8%. Additionally, improvements in penile curvature, plaque size and density, and pain on erection were better in the IFN alpha-2b group compared with the control. No significant improvement was observed in the erectile function domain in either group. CONCLUSION: This study reveals that intralesional IFN alpha-2b injections have a significant benefit on penile hemodynamic parameters. Moreover, intralesional IFN alpha-2b is an effective, minimally invasive treatment for PD, and PDDU is a useful adjunct to monitor objectively changes in penile vascular parameters. interferon alpha-2b injection therapy on penile hemodynamics in men with Peyronie's disease.

Adult↗
PubMed2001

The effect of proximal artery flow on the hemodynamics at the distal anastomosis of a vascular bypass graft: computational study.

The formation of distal anastomotic intimal hyperplasia (IH), one common mode of bypass graft failure, has been shown to occur in the areas of disturbed flow particular to this site. The nature of theflow in the segment of artery proximal to the distal anastomosis varies from case to case depending on the clinical situation presented. A partial stenosis of a bypassed arterial segment may allow residual prograde flow through the proximal artery entering the distal anastomosis of the graft. A complete stenosis may allow for zero flow in the proximal artery segment or retrograde flow due to the presence of small collateral vessels upstream. Although a number of investigations on the hemodynamics at the distal anastomosis of an end-to-side bypass graft have been conducted, there has not been a uniform treatment of the proximal artery flow condition. As a result, direct comparison of results from study to study may not be appropriate. The purpose of this work was to perform a three-dimensional computational investigation to study the effect of the proximal artery flow condition (i.e., prograde, zero, and retrograde flow) on the hemodynamics at the distal end-to-side anastomosis. We used the finite volume method to solve the full Navier-Stokes equations for steady flow through an idealized geometry of the distal anastomosis. We calculated the flow field and local wall shear stress (WSS) and WSS gradient (WSSG) everywhere in the domain. We also calculated the severity parameter (SP), a quantification of hemodynamic variation, at the anastomosis. Our model showed a marked difference in both the magnitude and spatial distribution of WSS and WSSG. For example, the maximum WSS magnitude on the floor of the artery proximal to the anastomosis for the prograde and zero flow cases is 1.8 and 3.9 dynes/cm2, respectively, while it is increased to 10.3 dynes/cm2 in the retrograde flow case. Similarly, the maximum value of WSSG magnitude on thefloor of the artery proximal to the anastomosis for the prograde flow case is 4.9 dynes/cm3, while it is increased to 13.6 and 24.2 dynes/cm3, respectively, in the zero and retrograde flow cases. The value of SP is highest for the retrograde flow case (13.7 dynes/cm3) and 8.1 and 12.1 percent lower than this for the prograde (12.6 dynes/cm3) and zero (12.0 dynes/cm3) flow cases, respectively. Our model results suggest that the flow condition in the proximal artery is an important determinant of the hemodynamics at the distal anastomosis of end-to-side vascular bypass grafts. Because hemodynamic forces affect the response of vascular endothelial cells, the flow situation in the proximal artery may affect IH formation and, therefore, long-term graft patency. Since surgeons have some control over the flow condition in the proximal artery, results from this study could help determine which flow condition is clinically optimal.

Anastomosis, Surgical↗
PubMed2005

Hemodynamic signals correlate tightly with synchronized gamma oscillations.

Functional imaging methods monitor neural activity by measuring hemodynamic signals. These are more closely related to local field potentials (LFPs) than to action potentials. We simultaneously recorded electrical and hemodynamic responses in the cat visual cortex. Increasing stimulus strength enhanced spiking activity, high-frequency LFP oscillations, and hemodynamic responses. With constant stimulus intensity, the hemodynamic response fluctuated; these fluctuations were only loosely related to action potential frequency but tightly correlated to the power of LFP oscillations in the gamma range. These oscillations increase with the synchrony of synaptic events, which suggests a close correlation between hemodynamic responses and neuronal synchronization.

Action Potentials↗
PubMed1995

Role of endogenous endothelin in normal hemodynamic status of anesthetized dogs.

Endothelin (ET) is a potent vasoconstrictor that may be involved in a number of cardiovascular disorders, although its role in normal hemodynamics remains unclear. Twenty-two anesthetized open-chest dogs were instrumented for measurement of systemic and pulmonary hemodynamics, cardiac output, coronary blood flow, and cardiac contractility. Big ET induced peripheral and coronary vasoconstriction, which occurred before significant elevations in plasma ET and which was nearly completely blocked by bosentan, a new nonpeptidic mixed (ETA and ETB) ET receptor antagonist. Bosentan also prevented the peripheral dilatation caused by the specific ETB receptor agonist, sarafotoxin S6c, but did not prevent the peripheral vasoconstriction induced by angiotensin II. Bosentan alone had no significant hemodynamic effect in the normal anesthetized dog, although it did induce a reactive increase in the plasma level of ET-1 and ET-3. This study demonstrates that, despite blocking both ETA and ETB receptors, bosentan alone had no hemodynamic effect, suggesting that ET does not play a major role in the normal hemodynamic status of anesthetized dogs.

Analysis of Variance↗
PubMed1997

Systemic hemodynamic determinants of blood pressure in women: age, physical activity, and hormone replacement.

We tested the hypothesis that the age-related changes in systemic hemodynamic determinants of arterial blood pressure in healthy women are related to physical activity and hormone replacement status. We studied 66 healthy, normotensive premenopausal (21-35 yr) and postmenopausal (50-72 yr) sedentary and endurance-trained women under supine resting conditions. Mean blood pressure was 7 mmHg higher in sedentary post- compared with premenopausal women, which was associated with an 11-mmHg higher systolic blood pressure, a 25% lower stroke volume and cardiac output, and a 50% higher systemic vascular resistance (all P < 0.05). Absolute (ml) levels of total blood volume did not differ across age, but resting oxygen consumption was approximately 35% lower in the postmenopausal women (P < 0.05). The elevations in mean and systolic blood pressures with age were similar in endurance-trained runners, but, in contrast to the sedentary women, the elevations were not associated with significant age-related differences in cardiac output, stroke volume, or oxygen consumption, and only a modest (15%) increase in systemic vascular resistance (P = 0.06). Postmenopausal swimmers demonstrated the same systemic hemodynamic profile as that of postmenopausal runners, indicating a nonspecific influence of the endurance-trained state. Blood pressure and its systemic hemodynamic determinants did not differ in postmenopausal users compared with those of nonusers of hormone replacement therapy. Resting oxygen consumption was the strongest physiological correlate of cardiac output in the overall population (r = 0.65, P < 0.001). We conclude that 1) the increases in arterial blood pressure at rest with age in healthy normotensive women are not obviously related to habitual physical activity status; 2) the systemic hemodynamic determinants of the age-related elevations in blood pressure are fundamentally different in sedentary vs. active women, possibly due, in part, to an absence of decline in resting oxygen consumption in the latter; and 3) systemic hemodynamics at rest are not different in healthy normotensive postmenopausal users vs. nonusers of estrogen-based hormone replacement.

Adult↗
PubMed1998

Hemodilution mediates changes in renal hemodynamics after acute volume expansion in rats.

The present study examined the factors responsible for triggering renal hemodynamic adjustments during acute volume expansion. The renal hemodynamic effects of graded volume expansion with 0.9% saline (Sal; 1, 2, and 4% of body wt), 7% BSA solution (0.35, 0.70, and 1.4% body wt), or whole blood from a donor rat (WBL; 0.35, 0.70, and 1.4% body wt) were compared in rats anesthetized with pentobarbital sodium. Neural influences on the kidney were eliminated by vagus nerves, baro/chemoreceptor afferents, and renal nerves section, and renal perfusion pressure was controlled at constant level (approximately 120 mmHg) throughout the experiments. In Sal- and BSA-expanded rats, renal blood flow (RBF) increased (Sal: 15, 40, 71%; BSA 17, 49, 107%) and renal vascular resistance (RVR) decreased in parallel with the degree of volume expansion (RVR: Sal 17, 31, 44%; and BSA: 15, 35, 54%). Renal hemodynamics remained unaltered after expansion with WBL. In rats expanded with Sal or BSA, correction of the fall of hematocrit restored RBF and RVR to control levels. Interference with tubuloglomerular feedback by uretheral obstruction had no effect on the decrease in RVR with Sal or BSA. Inhibition of the vascular tone by intrarenal papaverine infusion also did not alter the renal hemodynamic response to volume expansion with Sal or BSA. These findings suggest that the changes in renal hemodynamics after acute expansion are likely mediated by changes in rheologic properties of the blood rather than by changes in active vascular tone.

Animals↗
PubMed1995

Renal hemodynamics and blood flow autoregulation during acute cyclooxygenase inhibition in male rats.

After the acute inhibition of prostanoid synthesis, adjustments of renal hemodynamics may not be characterized immediately. Therefore, time-related effects of indomethacin on hemodynamics and renal blood flow (RBF) autoregulation were studied in anesthetized euvolemic male rats injected intravenously with vehicle, indomethacin (3, 4, or 5 mg/kg body wt), or meclofenamate (4 or 5 mg/kg body wt). Hemodynamics and RBF autoregulation were not influenced by vehicle injection, nor by time (n = 6). In contrast, mean arterial pressure (MAP) decreased significantly from 117 +/- 4 to 103 +/- 3 mmHg, and RBF progressively and significantly increased from 8.00 +/- 0.34 to 9.17 +/- 0.50 ml/min in the 3 mg/kg body wt indomethacin group (n = 8). Treatment with the higher doses of indomethacin (n = 9) or meclofenamate (n = 6) did not change RBF, while MAP decreased by 15 mmHg. A time-dependent significant enhancement of RBF autoregulatory efficiency was found in the drug-treated rats. Changes in renal function and reductions of prostanoid excretion in urine, of plasma renin activity, or serum aldosterone were similar in the nonsteroidal antiinflammatory drug groups. In conclusion, our findings demonstrate important time-related adjustments of renal hemodynamics in male rats treated with indomethacin, especially with the lower dose (3 mg/kg body wt iv). The factor(s) responsible for the hemodynamic changes remains unknown.

Aldosterone↗
PubMed1982

Hemodynamic responses to methoxamine in exercise-conditioned and aorta-constricted rats.

Hemodynamic responses to methoxamine hydrochloride (Vasoxyl) were determined in rats conditioned by a moderate treadmill exercise program and in rats subjected to 5 wk of abdominal aortic constriction. Rats of comparable age served as controls. Initial hemodynamic values for control rats were as follows: left ventricular pressure, 124 +/- 4 Torr and cardiac index, 145 +/- 8 ml . min-1 . kg-1. Although minor variations were noted, initial hemodynamic values for exercise-conditioned rats were within the normal range, and no left ventricular hypertrophy was present. Aorta-constricted rats exhibited a 50% increase in left ventricular weight and significant differences in left ventricular pressure (173 +/- 9 Torr) and cardiac index (117 +/- 10 ml . min-1 . kg-1). Sequentially increasing doses of methoxamine were infused to elevate myocardial preload and afterload. When compared with control rats, exercise-conditioned animals were better able to maintain cardiac index at comparable increases in either mean arterial or left ventricular end-diastolic pressures. In contrast, aorta-constricted rats demonstrated profound reductions in hemodynamic functions in response to methoxamine infusion. Directionally divergent hemodynamic results occur in exercise-conditioned and aorta-constricted animals when subjected to identical cardiovascular stresses.

Animals↗
PubMed1983

Pulmonary hemodynamics and gas exchange properties during progressive edema.

In this investigation we have studied the effect of increments of pulmonary edema on pulmonary hemodynamics, and physiological and hemodynamic shunt in an isolated lung preparation. Hemodynamic shunt was defined by the slope of the relationship between pulmonary arterial and airway pressures; when the slope decreases, there is a greater degree of shunt. Cardiovascular changes were analyzed using a Starling resistor model of the pulmonary circulation where the effective downstream pressure to flow as seen from the pulmonary artery exceeds the pulmonary venous outflow pressure. This effective downstream pressure is referred to as the critical pressure (Pc), and at low lung inflation the locus of this critical pressure is in extra-alveolar vessels. With 3-4 h of progressive edema to an average of 185% initial lobe weight we found a progressive rise in pulmonary arterial pressure (Ppa) from 12.1 to 21.5 cmH2O. About one-third of this increase in Ppa resulted from an increased Pc and the remainder resulted from an increased resistance upstream from the locus of Pc. These results are consistent with the hypothesis that the interstitial accumulation of fluid creates enough of an increase in interstitial pressure to compress extra-alveolar vessels. There was no significant correlation between the amount of edema and the measured physiologic shunt, but the hemodynamic shunt showed a highly significant correlation. The hemodynamic shunt theoretically measures the extent of obstructed airways and may be a useful index of the degree of pulmonary edema.

Animals↗
PubMed1983

Endogenous prostaglandin E2 metabolite levels, renin-angiotensin system and catecholamines versus acute hemodynamic response to captopril in chronic congestive heart failure.

Hemodynamic and hormonal responses to captopril were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25-mg dose, stroke volume (SV) increased from 53 +/- 7 to 63 +/- 9 ml (p less than 0.05), while pulmonary wedge pressure (PWP) decreased from 20 +/- 2 to 14 +/- 2 mm Hg (p less than 0.01). The hemodynamic changes were associated with increases in plasma renin activity (PRA; p less than 0.05) and in plasma levels of a novel bicyclo-prostaglandin E2 metabolite (bicyclo-PGE-m; p less than 0.01), whereas norepinephrine (NE) showed a falling tendency. In general, basal hemodynamic and basal hormonal levels did not correlate. Captopril-induced changes in mean artery pressure (MAP) and mean pulmonary artery pressure (mPAP) were positively correlated to pre-captopril PRA (r = 0.74, p less than 0.01; r = 0.64, p less than 0.05) and to changes in PRA (r = 0.85, p less than 0.01; r = 0.80, p less than 0.01) with a similar trend for angiotensin II (AII); decreases of systemic vascular resistance were more pronounced in patients with higher control NE levels (r = 0.62, p less than 0.05), the reduction of NE levels being highest in patients with higher basal concentrations (p less than 0.001); the captopril-induced decreases of mPAP and PWP were inversely related to basal bicyclo-PGE-m levels (r = 0.60, p less than 0.05; r = 0.61, p less than 0.05), and changes in mPAP were closely related to basal ratios of AII/bicyclo-PGE-m (r = 0.67, p less than 0.01). Thus, captopril exerts its acute beneficial hemodynamic effect by inhibiting the generation of AII, associated with toning down of sympathetic stimulation and increased production of vasodilating prostaglandins, such as PGE2. The relation between AII and PGE2-counteracting substances-might determine the hemodynamic response to captopril in the patients.

Adult↗
PubMed1988

Relationships between anaerobic threshold and exercise hemodynamic pattern in patients with previous myocardial infarction.

UNLABELLED: In 78 male class I and II NYHA patients with previous myocardial infarction, the relationships between ventilatory anaerobic threshold levels and hemodynamic patterns during a maximal symptom-limited stress test in the supine position were studied. Among the 36 patients with abnormal exercise wedge values, 11 showed an anaerobic threshold (AT) less than 35% of the maximal predicted VO2(mpVO2) (group A) and 23 showed an AT of 36-50% mpVO2 (group B). In 2 patients, the AT was greater than 50% mpVO2. Among the 42 patients with normal exercise wedge pressure, 13 showed an AT of 36-50% mpVO2 (group C), whereas in 29 patients, the AT was greater than 50% mpVO2 (group D). The mean value of AT in group A was significantly lower than in group B (8.6 +/- 0.7 vs. 11.7 +/- 0.5 ml/kg.min; p less than 0.05). No difference was found in the mean of the AT between groups B and C, while the mean value of AT in group D was significantly higher than in group C (16.9 +/- 0.4 vs. 12.9 +/- 0.6 ml/kg.min; p less than 0.005). No significant differences between groups C and D were found in the invasive and noninvasive parameters considered. Groups C and D were statistically different from groups A and B for pulmonary capillary pressures, total pulmonary resistances, stroke indexes, heart rates, arteriovenous O2 differences, total systemic resistances and lactate concentrations. Total pulmonary resistances and heart rates were statistically higher and stroke indexes were statistically lower in group A than in group B. IN CONCLUSION: (1) patients with normal exercise wedge values show a higher AT than patients with abnormal exercise wedge values. (2) Patients with normal exercise hemodynamic patterns classified according to their AT show no difference in hemodynamics; in these patients the level of AT seems to be related to peripheral determinants. (3) Patients with abnormal exercise hemodynamic patterns classified according to their AT level show different hemodynamics and different responses in ventricular function; in these patients the level of AT seems to be related to the cardiac impairment.

Adult↗
PubMed1982

Hemodynamic differences between supine and upright exercise in patients with congestive heart failure.

Although the differences in hemodynamic responses to supine and upright exercise have been studied in normal subjects and in patients with angina pectoris, no such comparison has been made in patients with congestive heart failure. Many investigators measure exercise hemodynamics in heart failure patients to assess the effect of vasodilator and inotropic drugs. Both modes of exercise have been used and have often yielded differing results. We compared the hemodynamic response to supine and upright exercise in 14 patients with stable, New York Heart Association class III chronic heart failure. During upright exercise, peak heart rate was higher (124 +/- 15 vs 115 +/- 18 beats/min, p less than 0.025) and peak mean arterial pressure was lower (102 +/- 15 vs 95 +/- 17 mm Hg, p less than 0.25), yielding similar double products. Although the peak left ventricular filling pressure was slightly lower during upright exercise (40 +/- 7 vs 35 +/- 10 mm Hg, p less than 0.05), the maximum cardiac and stroke indexes were not significantly different (3.6 +/- 0.8 vs 3.4 +/- 0.8 l/min/m2 and 30 +/- 8 vs 30 +/- 6 ml/m2, upright vs supine exercise). In contrast to these relatively similar hemodynamic responses, exercise capacity was significantly greater during upright exercise (peak work load 336 +/- 84 vs 293 +/- 73 kpm/min, p less than 0.1; maximum oxygen consumption 12.1 +/- 2.4 vs 9.8 +/- 1.9 ml/min/kg, p less than 0.001). We conclude that either exercise method may be used to assess the hemodynamic effects of drugs, but that exercise capacity should be measured in the upright position.

Aged↗
PubMed1985

Inotropic therapy for refractory congestive heart failure with oral fenoximone (MDL-17,043): poor long-term results despite early hemodynamic and clinical improvement.

Thirteen male patients with NYHA class IV congestive heart failure refractory to conventional therapy were treated with oral fenoximone, a new imidazole compound with inotropic and vasodilator effects, for a mean duration of 11 weeks (range 2 to 34). On initial hemodynamic evaluation, the effects of oral fenoximone were comparable to those of the intravenous form and included a significant (p = .0001) increase in cardiac index (mean +/- SD) (1.7 +/- 0.4 to 3.0 +/- 0.7 liters/min/m2) and a significant (p = .0001) but modest decrease in pulmonary capillary wedge pressure (27 +/- 6 to 23 +/- 6 mm Hg), with only minor overall changes in heart rate and arterial blood pressure. Symptomatic improvement by at least one NYHA class was observed in all patients during the first week of therapy with fenoximone; however, severe and symptomatic congestive heart failure recurred in seven patients within an average of 8 weeks after initiation of therapy, resulting in death in all seven. Of the remaining six patients, two died suddenly at home within 3 weeks of initiation of therapy, one died from ventricular fibrillation in the hospital 7 weeks after initiation of therapy, and two died from noncardiac causes. One patient is currently alive with NYHA class II heart failure 21 weeks after the initiation of therapy. Partial or complete attenuation of hemodynamic efficacy of oral fenoximone during long-term administration was demonstrated during repeat hemodynamic evaluation in six of eight patients. We conclude that despite short-term hemodynamic and clinical benefits, oral fenoximone therapy in patients with NYHA class IV congestive heart failure does not produce sustained clinical or hemodynamic benefit and is associated with a high mortality.

Administration, Oral↗
PubMed1985

Long-term hemodynamic follow-up of cardiac transplant patients treated with cyclosporine and prednisone.

To evaluate the long-term hemodynamic results in cardiac transplant patients treated with cyclosporine and prednisone, 19 patients were studied by cardiac catheterization and endomyocardial biopsy 13 +/- 3 months after transplantation. Immunosuppression consisted of 6 +/- 4 mg/kg/day cyclosporine and 20 +/- 8 mg/day prednisone. Eighteen patients were asymptomatic but had developed postoperative systemic hypertension (17 on antihypertensive therapy). These patients were compared with a normotensive control group of 18 patients without cardiovascular disease. Significant differences were found in heart rate; right atrial, pulmonary arterial, pulmonary arterial wedge, systemic arterial, and left ventricular end-diastolic pressures; cardiac index and stroke volume index; systemic and pulmonary vascular resistance; and end-diastolic volume index and left ventricular ejection fraction. The most frequent hemodynamic abnormalities included an elevated arterial pressure in 10 patients (56%), an elevated left ventricular end-diastolic pressure in six patients (33%), and a reduced ejection fraction in five patients (28%). Hemodynamic abnormalities tended to resolve or improve in the five patients restudied 2 years after transplantation. There was no significant relationship between fibrosis or inflammation on endomyocardial biopsy and hemodynamic abnormalities. We conclude that mild-to-moderate hemodynamic abnormalities are common in asymptomatic cardiac transplant patients receiving cyclosporine and prednisone.

Adult↗
PubMed1996

Effects of brain natriuretic peptide on exercise hemodynamics and neurohormones in isolated diastolic heart failure.

BACKGROUND: Experimental models suggest that brain natriuretic peptide (BNP) can modify left ventricular diastolic performance. The aim of this study was to evaluate the effects of BNP on resting and exercise hemodynamics and neurohormones in patients with isolated diastolic heart failure. METHODS AND RESULTS: Six patients with isolated diastolic heart failure were studied. After baseline hemodynamic measurements were obtained with use of thermistor-tipped pulmonary artery catheters, patients were randomized to receive infusion of BNP or placebo in a single-blind, crossover study. Hemodynamic and neurohormonal parameters were measured at rest after 30 minutes of infusion and during incremental supine bicycle exercise. BNP did not significantly affect resting hemodynamics but attenuated the rise in both pulmonary capillary wedge pressure (placebo, 23 +/- 2 mm Hg; BNP, 16 +/- 2 mm Hg; P < .01) and mean pulmonary artery pressure (placebo, 34 +/- 3 mm Hg; BNP, 29 +/- 3 mm Hg; P < .05) during exercise without affecting changes in heart rate, systemic blood pressure, or stroke volume. In response to BNP, there was significant suppression of plasma aldosterone concentration (placebo, 551 +/- 107 pmol/L; BNP, 381 +/- 56 pmol/L; P < .05). CONCLUSIONS: BNP infusion causes beneficial hemodynamic and neurohormonal effects during exercise in patients with isolated diastolic heart failure.

Aged↗
PubMed1996

Coupling of hemodynamic measurements with oxygen consumption during exercise does not improve risk stratification in patients with heart failure.

BACKGROUND: Measurement of peak Vo2 has become an accepted method to select patients for cardiac transplantation. Some investigators have suggested that the addition of exercise hemodynamic measurements can further enhance risk stratification because these measurements may identify patients with a noncardiac limitation to exercise. METHODS AND RESULTS: Accordingly, we performed maximal bicycle exercise with respiratory gas analysis and hemodynamic measurements in 65 patients (47 men, 18 women) 53 +/- 10 years old (mean +/- SD) who underwent a transplant evaluation at Columbia Presbyterian Medical Center. Skeletal muscle oxygenation of the vastus lateralis during exercise was assessed with near-infrared spectroscopy. Exercise hemodynamic, ventilatory, and muscle oxygenation measurements were obtained in all patients. For each subject, a linear correlation was derived between Vo2 and pulmonary artery saturation (PA Sao2). The slope of this relationship and a theoretical Vo2max at a PA Sao2 of 0% (Vo2 intercept) was derived. Baseline measurements were left ventricular ejection fraction, 22 +/- 9%; pulmonary capillary wedge pressure (PCWP), 16 +/- 10 mm Hg; cardiac index (CI), 2.1 +/- 0.5 L. min-1. m-2; and PA Sao2, 53 +/- 8%. The cardiac output response to exercise was categorized as normal or abnormal by comparison to the linear equation of peak Vo2 versus peak cardiac output as described by Higginbotham. Exercise measurements were peak Vo2, 12.1 +/- 3.0 mL.kg-1.min-1; Vo2 intercept, 19.1 +/- 5.5 mL. kg-1.min-1; PCWP, 31 +/- 11 mm Hg; CI, 3.8 +/- 1.3 L.min-1.m-2; and PA Sao2, 27 +/- 9%. Only 6% of patients exhibited a normal cardiac output response to exercise. Multivariate analysis was performed with peak Vo2, Vo2 intercept, skeletal muscle oxygenation at end exercise, and peak exercise hemodynamic variables. Only left ventricular stroke work and left ventricular stroke work index were shown to be predictive of survival. CONCLUSIONS: Addition of exercise hemodynamic measurements to noninvasive metabolic stress testing minimally improves risk prognostication in patients with severe heart failure.

Adult↗
PubMed2006

Emergence of novel genetic effects on blood pressure and hemodynamics in adolescence: the Georgia Cardiovascular Twin Study.

Multiple longitudinal studies have demonstrated reasonable stability of blood pressure (BP) levels and hemodynamics throughout childhood and adolescence and into adulthood. Part of this stability might be caused by genetic factors that are expressed steadily over time. We aimed to determine the relative contributions of genetic and environmental factors to the stability of BP and underlying hemodynamic characteristics between ages 14 and 18 years. In addition, potential ethnic differences were examined. To this end, resting levels of BP and impedance-derived hemodynamic variables were measured twice in >500 pairs of European American (EA) and African American (AA) twins, with an intervening period of 4.1 years. Structural equation modeling of the twin data on BP and underlying hemodynamic variables (adjusted for age, sex, and body mass index) showed that heritabilities were moderate to high (25% to 64%) and relatively stable over time. These genetic influences accounted for 60% to 100% of the phenotypic tracking correlations (range 0.39 to 0.62). Emergence of novel genetic influences accounted for a significant part of the variance (17% to 33%) at the second measurement occasion. There were significant ethnic differences for BP, with nonshared environmental influences becoming larger over time in AAs compared with EAs for both systolic and diastolic BP. In summary, novel genetic effects emerge during development into adulthood and explain a considerable part of the variation in BP and hemodynamics. Environmental influences become more important with age in AAs compared with EAs for both systolic and diastolic BP. Future elucidation of these environmental factors may help explain ethnic differences in hypertension risk.

Adolescent↗