Right Ventricular Free Wall Thickness Research Articles

Estimation of Right Ventricular Free-Wall Mass Using Two-Dimensional Echocardiography

Echocardiographic methods based on geometric models have long been in use for estimating left ventricular mass, but there is currently no similar method for estimating right ventricular (RV) free-wall mass. We hypothesized that a one-quarter prolate ellipsoid model could be used with two-dimensional echocardiography to approximate RV mass. Over a 2-year period 39 patients who had both a complete cardiac magnetic resonance imaging (MRI) scan and an echocardiogram within 2 weeks of each other were retrospectively analyzed. MRI-derived RV mass was used as the standard for comparison. Echocardiographic RV mass was estimated using three equations based on the geometric model. Linear regression analysis was performed to determine the correction factors used in the final formulae. The formula with the lowest standard error of the estimate was then prospectively analyzed for accuracy using a separate group of 88 subjects. The most accurate echocardiographic equation derived was RV mass = 5.84 (apical four-chamber RV cavity planar area) (RV free-wall thickness) + 1. Compared to MRI-RV mass the correlation coefficient was 0.97 and the standard error of the estimate was 16.8%. The positive and negative predictive values for diagnosing RV hypertrophy were 95% and 88%, respectively. We conclude that RV free-wall mass can be estimated by two-dimensional echocardiography using a one-quarter prolate ellipsoid shell model.

Sustained pulmonary hypertension and right ventricular hypertrophy after chronic hypoxia in mice with congenital deficiency of nitric oxide synthase 3.

Chronic hypoxia induces pulmonary hypertension and right ventricular (RV) hypertrophy. Nitric oxide (NO) has been proposed to modulate the pulmonary vascular response to hypoxia. We investigated the effects of congenital deficiency of endothelial NO synthase (NOS3) on the pulmonary vascular responses to breathing 11% oxygen for 3-6 wk. After 3 wk of hypoxia, RV systolic pressure was greater in NOS3-deficient than in wild-type mice (35+/-2 vs 28+/-1 mmHg, x+/-SE, P < 0.001). Pulmonary artery pressure (PPA) and incremental total pulmonary vascular resistance (RPI) were greater in NOS3-deficient than in wild-type mice (PPA 22+/-1 vs 19+/-1 mmHg, P < 0.05 and RPI 92+/-11 vs 55+/-5 mmHg.min.gram.ml-1, P < 0.05). Morphometry revealed that the proportion of muscularized small pulmonary vessels was almost fourfold greater in NOS3-deficient mice than in wild-type mice. After 6 wk of hypoxia, the increase of RV free wall thickness, measured by transesophageal echocardiography, and of RV weight/body weight ratio were more marked in NOS3-deficient mice than in wild-type mice (RV wall thickness 0.67+/-0.05 vs 0.48+/-0.02 mm, P < 0.01 and RV weight/body weight ratio 2.1+/-0.2 vs 1.6+/-0.1 mg. gram-1, P < 0.05). RV hypertrophy produced by chronic hypoxia was prevented by breathing 20 parts per million NO in both genotypes of mice. These results suggest that congenital NOS3 deficiency enhances hypoxic pulmonary vascular remodeling and hypertension, and RV hypertrophy, and that NO production by NOS3 is vital to counterbalance pulmonary vasoconstriction caused by chronic hypoxic stress.

Disparate structural effects on left and right ventricles by angiotensin-converting enzyme inhibitors and calcium antagonists in essential hypertension

Reduced left ventricular (LV) mass and wall thicknesses with angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists occur in essential hypertension. Experimental studies have shown that reduction in LV mass is related to hemodynamic as well as nonhemodynamic factors that may influence LV and also right ventricular (RV) structure. Sixty-eight patients with essential hypertension were studied echocardiographically 4 to 8 weeks after antihypertensive therapy was initiated. LV dimensions and wall thicknesses, as well as RV free wall thickness, were measured using 2-dimensionally guided techniques. Patients were divided in 2 groups: those receiving either ACE inhibitors or calcium antagonists. This short-term therapeutic period produced similar hemodynamic changes and reductions in LV mass in both groups. In these 2 groups of patients, we found opposite effects in RV free wall thickness. Thus, RV wall thickness increased from 0.44 ± 0.02 to 0.56 ± 0.02 cm (p <0.01) after therapy in the calcium antagonist group, whereas no change was found in the ACE inhibitor group (0.36 ± 0.04 vs 0.34 ± 0.04). These structural changes suggest that ACE inhibitors and calcium antagonists produce dissimilar effects on cardiac cell growth and growth reversal, which may be mediated through different nonhemodynamic effects after short-term therapy.

Coronary blood flow and distribution in right ventricular hypertrophy

Myocardial blood flow and distribution in animals with righ ventricular (RV) hypertrophy have not been studied extensively in the experimental laboratory. This study was carried out to investigate whether or not ischemia can be induced in the hypertrophied right ventricle. Ten adult foxhounds underwent banding of the pulmonary artery. One year later coronary flow and distribution were studied by use of radioactive microspheres. Myocardial oxygen supply and demand were estimated by planimetry of aortic and RV pressure tracings. Data were obtained in the control state, during atrial pacing to a heart rate of 200 +/- 4 beats/min (mean +/- SD), during aorta-right atrial shunting to reduce mean aortic pressure to 60 +/- 6mm Hg, and during aortic constriction to produce a mean aortic pressure of 145 +/- 8mm Hg. RV weight/body weight ratio was 2.2 +/- 0.2 gm/kg(normal, 1.3 +/- 0.1 gm/kg) (p less than 0.001). RV free wall thickness was 11.3 +2- 0.7 mm (normal, 6.7 +/- 0.4 mm) (p less than 0.001). At rest, RV oxygen supply/demand ration was 4.7, and the RV subendocardial/subepicardial (Endo/Epi) flow ratio was 0.93. During atrial pacing, RV supply/demand was 54% of control (p less than 0.01), RV Endo/Epi ratio was 1.00 (p less than 0.05), and right coronary artery (RCA) resistance was 59% of control (p less than 0.01). Aorto-right atrial shunting resulted in an RV supply/demand ratio of 31% of control (p less than 0.01), RV Endo/Epi ratio of 0.95, and RCA resistance of 45% of control (p less than 0.01). During aortic constriction, RV supply/demand ratio was 132% of control (p less than 0.05), RV Endo/Epi ratio was 0.92, and RCA resistance was 146% of control (p less than 0.01). Phasic RCA flowmeter tracings demonstrated an increased proportion of diastolic flow in the study animals as compared to normal animals. In conclusion, myocardial blood flow and distribution in the hypertrophied right ventricle remained normal at rest and during hemodynamic stress. Compensatory mechanisms which maintain normal flow and distribution may include changes in RCA resistance and phasic flow patterns. Under the imposed conditions, RV ischemia and failure did not occur.