Pressure Overload Of Right Ventricle Research Articles

Biventricular systolic function in young lambs subject to chronic systemic right ventricular pressure overload.

In various clinical situations of congenital heart disease, the right ventricle (RV) is subject to a chronic systemic pressure overload which affects biventricular function and may progress to the development of RV failure. Young lambs (2-3 wk old) underwent adjustable pulmonary artery banding (PAB) at systemic (aortic) level for 8 wk. Biventricular function was determined by using load-independent indexes of global ventricular contractile performance by the end-systolic pressure-volume relationship (ESPVR) using the conductance catheter at baseline and during dobutamine infusion. PAB resulted in a significant fivefold increase in RV end-systolic pressure (12-64 mmHg) and a doubling of the RV-to-left ventricular (LV) wall thickness ratio (P < 0.01). RV global contractile performance increased significantly, as indicated by an increased slope of the ESPVR. Compared with age-matched control lambs, cardiac output decreased from 2.6 to 1.6 l/min (P < 0.05) whereas heart rates were equal. In contrast with RV volume, LV volume decreased significantly after PAB (P < 0.01), whereas the LV-ESPVR slope was unchanged. In the PAB group, the RV, but not the LV, showed a reduced response to dobutamine. We concluded that chronic RV pressure overload for 8 wk results in diminished pump function despite compensatory increased RV global contractile performance.

Impaired Left Ventricular Filling Due to Right Ventricular Pressure Overload in Primary Pulmonary Hypertension: Noninvasive Monitoring Using MRI

To analyze the effect of primary pulmonary hypertension (PPH) on cardiac function using MRI. In 12 patients (9 women; age range, 30 to 56 years), the diagnosis of PPH had been established by catheterization (mean +/- SD pulmonary artery pressure [PAP] was 56 +/- 8 mm Hg). With breath-hold cine MRI, a series of short-axis images was acquired covering the whole left ventricle (LV) and right ventricle (RV). The curvature, defined as 1 divided by the radius of curvature in centimeters, was calculated for the septum and the LV free wall in early diastole. Leftward ventricular septal bowing (LVSB) is denoted by a negative curvature. For the LV and the RV, the end-diastolic volume (EDV), stroke volume (SV), and volumetric filling rate were calculated. The control subjects were all healthy (n = 14; 11 women; age range, 20 to 57 years). In the patients, LVSB was quantified in early diastole by the septal curvature of - 0.14 +/- 0.07 cm(-1), and the septal to free-wall curvature ratio of - 0.42 +/- 0.21. LV EDV and LV SV correlated negatively with diastolic PAP (p = 0.004 and p = 0.04, respectively). In patients vs control subjects, RV SV was reduced (52 +/- 12 mL vs 82 +/- 11 mL, p < 0.0001); LV peak filling rate was smaller (2.2 +/- 0.7 EDV/s vs 3.3 +/- 0.5 EDV/s, p < 0.001); LV EDV was smaller (81 +/- 23 mL vs 117 +/- 19 mL, p = 0.001); and LV SV was smaller (49 +/- 18 mL vs 83 +/- 13 mL, p < 0.0001). In PPH, RV pressure overload leads to LVSB and reduced RV output. By decreased blood delivery, LV filling is reduced, which results in decreased LV SV by the Frank-Starling mechanism.

In vivo 31P-NMR spectroscopy of right ventricle in pigs.

The energy metabolism of the right ventricle (RV) in vivo has been largely unexplored. The goal of this study was to develop and implement techniques for in vivo 31P nuclear magnetic resonance (NMR) spectroscopy of the RV free wall. A two-turn, crossover-design elliptical surface coil was constructed to provide high sensitivity across the thin RV wall but minimal sensitivity in the blood-filled RV cavity. In 36 open-chest, anesthetized pigs, 31P spectroscopy of the RV free wall was performed with this coil at a field strength of 2 Tesla. Spectra were obtained from 800 acquisitions in 24 min with an average signal-to-noise ratio of 13.2 for phosphocreatine (PCr). The PCr-to-ATP (PCr/ATP) ratio of porcine RV was 1.42 +/- 0.05 (mean +/- SE), uncorrected for saturation at a repetition time of 1.8 s. With the use of literature values of the time constant of longitudinal relaxation (T1) to correct for partial saturation, the RV PCr/ATP was estimated to lie between 1.7 and 2.3. Decreased RV PCr/ATP was observed during RV ischemia and pressure overload. Thus in vivo 31P spectroscopy of the RV is readily accomplished with an appropriate surface coil and can provide new information about RV energy metabolism.

Right ventricular performance after monocrotaline-induced pulmonary hypertension

Chronic pulmonary hypertension leads to a compensatory hypertrophy of the right ventricle (RV). Performance of the hypertrophied heart has been shown to vary depending on the type and severity of the overload, the species, age, and sex of the animal in which the hypertrophy is induced and the ventricle to which the overload is applied (left ventricle vs. right ventricle). In this study we employed two novel approaches to examine the performance of the hypertrophied right ventricle in male Sprague-Dawley rats. First, monocrotaline (MCT), a pyrrolizidine alkaloid isolated from the plant Crotalaria spectabilis, was used to noninvasively induce chronic pulmonary hypertension, RV pressure overload, and RV hypertrophy. After 5 wk the RV-to-(left ventricle + septum) ratio was increased by 94% over control. The volume of isolated right ventricular myocytes from MCT-treated rats was increased due primarily to an increase in cell cross-sectional area. Second, a stable, isolated, working heart preparation, normally used to study left ventricular function, was modified to study right ventricular function. In vitro ventricular performance of severely hypertrophied hearts was elevated compared with control hearts at all preloads. Significant elevations in positive and negative maximum pressure development (dP/dtmax) suggested that both the rate of pressure development and the rate of relaxation were enhanced. Coronary flow and RV-diastolic pressure were similar in the MCT and control group. Thus RV hypertrophy caused by a chronic pressure overload induced by MCT resulted in enhanced ventricular performance with no evidence of failure.