An echocardiographic study of right and left ventricular adaptation to physical exercise in elite female orienteers. (1/804)

BACKGROUND: A considerable body of echocardiographic studies has described how athletic training induces morphological adaptation of the left ventricle in male endurance athletes, but only a few studies have described left ventricular adaptation in female endurance athletes. In contrast to changes in the left ventricle far less attention has been directed towards right ventricular changes due to extensive physical exercise. The purpose of this study was to obtain normal values and to determine if there are any differences in right and left ventricular cavity and wall dimensions between female orienteers and females with a mainly sedentary lifestyle. METHODS: Echocardiography was performed in 42 highly trained elite female orienteers and 32 healthy female students with a predominantly sedentary lifestyle. The 74 females had no history of cardiac disease, a normal electrocardiogram and showed no echocardiographic abnormalities. M-mode and two-dimensional measurements of the right and left ventricular cavity and wall were obtained in elite orienteers and sedentary females. For the right ventricle and wall, multiple cross-sections were used and measurements were obtained from the right ventricular inflow and outflow tract. RESULTS: The left ventricular end-diastolic cavity dimension and the left ventricular wall thickness were significantly greater in the athletes compared with the sedentary controls. The right ventricular inflow tract measurements were all significantly greater in the orienteers compared with the controls but the right ventricular outflow tract measurements were comparable in the study groups. The right ventricular wall thickness, calculated as the mean of three different wall measurements was an average of 13% greater in the athletes compared with the sedentary controls. CONCLUSION: This study suggests symmetrical cardiac enlargement with a concomitant increase in both the right and left ventricular wall, probably reflecting the increased haemodynamic loading in the female athletes.  (+info)

Role of endothelin in deterioration of heart failure due to cardiomyopathy in hamsters: increase in endothelin-1 production in the heart and beneficial effect of endothelin-A receptor antagonist on survival and cardiac function. (2/804)

BACKGROUND: We previously reported that chronic endothelin (ET) receptor blockade ameliorated the survival rate and cardiac hemodynamics in rats with chronic heart failure (CHF) due to myocardial infarction. However, it remains unclear whether ET-1 is involved in the pathophysiology of cardiomyopathy, which is one of the major causes of CHF. Accordingly, we investigated the production of ET-1 in the heart and the effect of chronic ETA receptor blockade on survival rate and cardiac function in the Bio 14.6 hamster, which is an idiopathic model of CHF caused by cardiomyopathy. METHODS AND RESULTS: We used 52-week-old Bio 14.6 cardiomyopathic hamsters and age-matched F1b normal hamsters. The expression of preproET-1 mRNA and the ET-1 level in the hearts were markedly higher in the cardiomyopathic hamsters than in the normal hamsters. The cardiomyopathic hamsters showed severe CHF, illustrated by lower left ventricular (LV) +dP/dt/Pmax and right ventricular (RV) +dP/dt/Pmax and by higher LV end-diastolic pressure (EDP), RVEDP, and central venous pressure compared with the normal hamsters. Long-term (9 weeks) treatment with an ETA antagonist (TA-0201, 1.3 mg. kg-1. d-1) markedly increased survival of cardiomyopathic hamsters (untreated, 16%; TA-0201-treated, 65.2%; P<0.001). After 6 weeks of treatment, LV +dP/dt/Pmax and RV +dP/dt/Pmax were significantly higher and LVEDP and RVEDP were lower in the TA-0201-treated group than in the untreated group, suggesting that chronic TA-0201 treatment effectively prevented deterioration of cardiac dysfunction. CONCLUSIONS: In the cardiomyopathic hamsters with CHF, the production of ET-1 in the heart was markedly increased, and chronic ETA receptor blockade greatly ameliorated survival and cardiac dysfunction. These results suggest that ET-1 plays an important role in the deterioration of CHF caused by cardiomyopathy, and ETA antagonists may exert therapeutic effects in CHF due to cardiomyopathy.  (+info)

Hemodynamic effects of direct biventricular compression studied in isovolumic and ejecting isolated canine hearts. (3/804)

BACKGROUND: Biventricular direct cardiac compression (DCC) can potentially support the failing heart without the complications associated with a blood/device interface. The effect of uniform DCC on left and right ventricular performance was evaluated in 7 isolated canine heart preparations. METHODS AND RESULTS: A computer-controlled afterload system either constrained the isolated heart to contract isovolumically or simulated hemodynamic properties of physiological ejection. Biventricular DCC was provided by a chamber surrounding the heart that allowed adjustment of the compression pressure, onset time, and duration. Through a series of ventricular preloads, the effect of DCC on the end-systolic pressure-volume relationship (ESPVR) was evaluated under isovolumic and ejecting conditions. Under both conditions, DCC shifted the ESPVR of the left and right ventricles upward by an amount approximately equal to the compression pressure. The augmentation of end-systolic pressure for each initial preload tested, however, was less under ejecting conditions, because reductions in end-systolic and end-diastolic volumes occurred with ejection. Nevertheless, the net effect was to increase stroke volume. Measurement of M&f1;O2 demonstrated that at a given ventricular volume, M&f1;O2 did not change with DCC; however, peak ventricular pressure increased substantially, so that the effective pressure-volume area increased. CONCLUSIONS: Biventricular DCC can augment end-systolic pressure with no added costs of M&f1;O2. Under ejecting conditions, this augmentation of ventricular contracting ability manifests as increases in stroke volume. Thus, DCC represents a feasible alternative form of ventricular assist, and devices that support the heart in this manner should be further explored.  (+info)

Reduced heart rate variability following repair of tetralogy of Fallot. (4/804)

OBJECTIVE: To examine autonomic function as assessed by heart rate variability in patients 10 or more years after repair of tetralogy of Fallot, and to relate this to cardiac structure, function, and electrocardiographic indices. METHODS: Heart rate variability was measured by standard time domain techniques on a 24 hour Holter ECG in 28 patients, aged 12 to 34 years (mean 19.5), who had undergone repair of tetralogy of Fallot at least 10 years previously. Echocardiography was performed to assess left ventricular size and function, right ventricular size and pressure, and any proximal pulmonary arterial stenosis. Right ventricular function was evaluated by radionuclide scan. QRS duration, QT interval, and QT dispersion were measured on a standard 12 lead ECG. Measurements of heart rate variability were compared with values from 28 age matched healthy controls (mean age 19.9 years). Interrelations between variables were assessed using Pearson correlation coefficients and stepwise regression analysis. RESULTS: Heart rate variability was reduced, compared with values for age matched normal controls, in 12 of the 28 patients. Reduced heart rate variability was associated with increased age, increased right ventricular size and pressure, and widening of the QRS complex. CONCLUSIONS: Reduced heart rate variability is a feature following repair of tetralogy of Fallot. It is associated with increasing age, impaired right ventricular haemodynamics, and widening of the QRS complex. Under these circumstances, reduced heart rate variability may be a marker for deteriorating right ventricular function. Increased QRS duration has been identified as a risk factor for sudden death following repair of tetralogy of Fallot, and impaired cardiac autonomic control may be one of the mechanisms involved.  (+info)

Effects of amiodarone on cardiac electrophysiology in right ventricular rapid pacing-induced heart failure dogs. (5/804)

AIM: To study the effects of amiodarone (Ami) on cardiac electrophysiologic properties and ventricular fibrillation threshold (VFT) in right ventricular rapid pacing-induced congestive heart failure (CHF) dogs. METHODS: Dogs (n = 25) were randomly allocated into 3 groups: A) control group; B) CHF group induced by right ventricular rapid pacing (4 pulses.s-1) for 4-5 wk; C) CHF models p Ami 300 mg.d-1 for 4-5 wk. The electrophysiologic parameters and VFT were evaluated by electric stimulation and monophasic action potential (MAP) recording. RESULTS: In CHF models, ventricular MAP duration (MAPD90), ventricular late repolarization duration (VLRD), and intra-ventricular conduction time (IVCT) were prolonged by 43%, 318%, and 19%, respectively; the ratio of ventricular effective refractory period (VERP) to MAPD90 (VERP/ MAPD90) and VFT were decreased by 13% and 48% respectively; the dispersion of ventricular recovery time (RT-D) was increased by 185%. In CHF models, Ami had no effects on ventricular MAPD90, but increased VERP/ MAPD90, IVCT, and VFT by 15%, 10%, and 67%, respectively, shortened VLRD by 87%; and decreased RT-D by 87%. Ami had no significant influences on the hemodynamic parameters of the CHF dogs. CONCLUSION: Ami normalizes the cardiac electrophysiologic properties in CHF dogs.  (+info)

Increased stress right ventricular activity on dual isotope perfusion SPECT: a sign of multivessel and/or left main coronary artery disease. (6/804)

OBJECTIVES: This study sought to determine the anatomic and physiologic correlates of increased right ventricular (RV) activity on exercise single-photon emission computed tomography (SPECT) perfusion imaging in patients with coronary artery disease (CAD). BACKGROUND: Because SPECT perfusion imaging delineates relative myocardial blood flow, patients with global left ventricular (LV) hypoperfusion but normal RV perfusion may have increased relative RV tracer uptake as an indicator of multivessel CAD. METHODS: Rest thallium-201 and exercise 99mTc-sestamibi or 99mTc-tetrofosmin SPECT perfusion images were analyzed for peak RV and LV activity (RV:LV index) in 315 patients, including 240 patients with documented CAD, 39 patients with no significant CAD on arteriography, and a "normalcy" group of 36 patients with a low pre- and posttest probability of CAD. RESULTS: Resting RV:LV perfusion index ranged from 0.32 to 0.34 in each group, increasing to 0.36 with exercise in control and normalcy groups. CAD patients with the highest exercise RV:LV were those with severe left main CAD (or "left main equivalent"), with a lesser degree of proximal right CAD (0.51, n = 14, p < 0.001 vs. other groups). An exercise RV:LV >0.42 with a exercise:rest ratio >1.2 was present in 93% patients with this pattern of CAD, but was absent in 97% of the normalcy group, 92% of patients without significant angiographic CAD, and 100% of patients with proximal right CAD tighter than stenoses in the left system. CONCLUSIONS: Increased RV:LV activity exercise may occur in patients with acute RV strain, but is otherwise an indicator of exercise-induced RV:LV perfusion imbalance associated with severe CAD, particularly high-grade left main with less severe proximal right CAD.  (+info)

Relative contributions of endothelial, inducible, and neuronal NOS to tone in the murine pulmonary circulation. (7/804)

Nitric oxide plays an important role in modulating pulmonary vascular tone. All three isoforms of nitric oxide synthase (NOS), neuronal (nNOS, NOS I), inducible (iNOS, NOS II), and endothelial (eNOS, NOS III), are expressed in the lung. Recent reports have suggested an important role for eNOS in the modulation of pulmonary vascular tone chronically; however, the relative contribution of the three isoforms to acute modulation of pulmonary vascular tone is uncertain. We therefore tested the effect of targeted disruption of each isoform on pulmonary vascular reactivity in transgenic mice. Isolated perfused mouse lungs were used to evaluate the effect of selective loss of pulmonary nNOS, iNOS, and eNOS with respect to hypoxic pulmonary vasoconstriction (HPV) and endothelium-dependent and -independent vasodilation. eNOS null mice had augmented HPV (225 +/- 65% control, P < 0.02, mean +/- SE) and absent endothelium-dependent vasodilation, whereas endothelium-independent vasodilation was preserved. HPV was minimally elevated in iNOS null mice and normal in nNOS null mice. Both nNOS and iNOS null mice had normal endothelium-dependent vasodilation. In wild-type lungs, nonselective NOS inhibition doubled HPV, whereas selective iNOS inhibition had no detectable effect. In intact, lightly sedated mice, right ventricular systolic pressure was elevated in eNOS-deficient (42.3 +/- 1.2 mmHg, P < 0.001) and, to a lesser extent, in iNOS-deficient (37.2 +/- 0.8 mmHg, P < 0.001) mice, whereas it was normal in nNOS-deficient mice (30.9 +/- 0.7 mmHg, P = not significant) compared with wild-type controls (31.3 +/- 0.7 mmHg). We conclude that in the normal murine pulmonary circulation 1) nNOS does not modulate tone, 2) eNOS-derived nitric oxide is the principle mediator of endothelium-dependent vasodilation in the pulmonary circulation, and 3) both eNOS and iNOS play a role in modulating basal tone chronically.  (+info)

Right ventricular diastolic function in patients with hypertrophic cardiomyopathy--an invasive study. (8/804)

To assess diastolic function of the right ventricle (RV) in patients with hypertrophic cardiomyopathy (HCM), biplane RV angiograms and RV pressures were analyzed in 19 HCM patients and in 13 normal subjects. RV and left ventricle (LV) pressures were measured using catheter-tip manometers. RV volumes were obtained from frame-by-frame tracings of angiograms. Ventricular relaxation was assessed by the time constant of isovolumic pressure decay (T). The peak filling rate (PFR) and the time to PFR (TPFR) were used as parameters of early diastolic filling, and the right atrial contribution to RV filling (%AF) was used as a parameter of late diastolic filling. The T for the RV was significantly prolonged in HCM patients. However, there was no significant correlation between the T for the RV and LV, nor did the T for the RV correlate with the RV ejection fraction or interventricular septal wall thickness. The TPFR, but not PFR, was significantly greater in HCM patients, and the %AF tended to be increased in HCM, but not significantly. The RV diastolic pressure-volume relations in the HCM patients shifted upward. In conclusion, impaired isovolumic relaxation and delayed diastolic filling and decreased diastolic distensibility are present in the RV of HCM patients.  (+info)