Measures Of Right Ventricular Function Research Articles

Quantification of right ventricular function with magnetic resonance imaging in children with normal hearts and with congenital heart disease

In clinical treatment of children with congenital heart disease (CHD) assessment of right ventricular (RV) function is important. Available imaging techniques have been of limited value because of technical factors and the complex geometry of the right ventricle. To validate magnetic resonance (MR) imaging measurements of RV function in children, gradient echo MR imaging of both ventricles and MR flow mapping of great vessel and tricuspid flow was performed in 20 children with CHD affecting the right ventricle and in 22 healthy children ranging in age from 5 to 16 years. Close correlation between RV versus LV stroke volumes ( r = 0.96) and RV stroke volume versus great artery ( r = 0.97) or tricuspid flow ( r = 0.97) was observed with small interobserver and intraobserver variability. Results of healthy children were end-diastolic volume: 70 ± 9 ml/m 2, end-systolic volume: 21 ± 5 ml/m 2, and ejection fraction: 70% ± 4%. In the patient groups clinically important differences were noted. We conclude that MR imaging provides accurate noninvasive measurements of RV function in healthy children and patients with (operated) CHD.

Effects of aortic constriction during experimental acute right ventricular pressure loading. Further insights into diastolic and systolic ventricular interaction.

Acute right ventricular (RV) hypertension may result in hemodynamic collapse. The associated reduction in left ventricular (LV) end-diastolic volume is thought to result from reduced RV output (secondary to RV ischemia) and adverse direct ventricular interaction. Aortic constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an increased coronary perfusion pressure. We hypothesized that altered ventricular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction. We instrumented nine dogs with ultrasonic dimension crystals to measure RV segment length, septum-to-RV free wall and septum-to-LV free wall diameters, and LV anterioposterior diameter. Catheter-tipped manometers were used to measure LV and RV pressures. Pericardial pressure was measured with flat, liquid-containing balloon transducers. Inflatable cuff constrictors were placed on the pulmonary artery (PA) and aorta, and a flow probe was placed on the PA. The right coronary artery (RCA) was perfused independently by a roller pump calibrated for flow. During moderate PA constriction, while RCA pressure was maintained at control level, RCA flow did not change significantly (15.8 +/- 6.2 to 16.9 +/- 11.5 mL/min) and was similar during severe PA constriction (18.6 +/- 9.8 mL/min). During severe PA constriction, RV stroke volume decreased from a control value of 10.3 +/- 4.9 to 2.3 +/- 1.4 mL/beat (P < .05). When aortic constriction was added while RCA pressure was maintained at control level, there was an increase in RV stroke volume to 4.5 +/- 2.0 mL/beat (P < .05) with no associated change in RCA flow (17.8 +/- 9.5 mL/min). However, pressure-dimension loops clearly demonstrated changes in diastolic and systolic ventricular interaction; with aortic constriction, there was a large increase in the transeptal pressure gradient associated with a rightward septal shift. During either isolated severe PA constriction or simultaneous severe PA and aortic constriction, RCA flow was increased until RCA pressure was approximately equal to that in the aorta. This produced an increase in RCA flow of 50% (P < .05); however, this increase in coronary flow was ineffective in improving any measure of RV function. In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.

Production and reversibility of right ventricular hypertrophy and right heart failure in dogs

Combined heart-lung transplantation has been used for end-stage primary pulmonary hypertension. Experience with single-lung transplantation for other conditions suggested that associated severe right ventricular dysfunction resulting from increased afterload would recover after placement of a satisfactory lung allograft. Early experience with the application of single-lung transplantation for pulmonary hypertension supports this contention. We devised a reversible canine model of chronic progressive pressure-overloaded right heart failure by pulmonary artery banding to study the echocardiographic, hemodynamic, and pathological reversibility of the failing right heart. Clinical right heart failure was defined as the development of ascites and pleural effusions. Right heart failure developed in 23 dogs 67 to 348 days after banding, and they were divided into two groups to determine its early and long-term effects. Group 1 dogs (n = 11) were either sacrificed immediately after the onset of right heart failure (n = 5) or unbanded (n = 6); group 2 dogs (n = 12) were maintained in right heart failure for 3 months and then either sacrificed (n = 6) or unbanded. Unbanded dogs in both groups were observed for 4 additional months before sacrifice. A control group of 6 normal dogs was sacrificed for pathological comparisons. After unbanding, the right ventricular systolic pressure fell from 97 ± 17 mm Hg (group 1) and 88 ± 31 mm Hg (group 2) to 44 ± 11 mm Hg and 47 ± 13 mm Hg, respectively. Despite this persistent gradient across the pulmonary artery, echocardiographic and hemodynamic measures of right ventricular function returned to normal, albeit more slowly in the group 2 dogs. Pathologic examination revealed incomplete regression of hypertrophy and persistent mild fibrosis in both groups. There was no difference in the degree of recovery between the acute and chronic failure groups. These results suggest that reduction of pulmonary afterload permits right ventricular recovery and supports the application of lung transplantation in patients with severe pulmonary hypertension.

Development and Modulation of Experimental Right Ventricular Hypertrophy in Rats

Two models of right ventricular (RV) hypertrophy in rats have been created and characterized: chronic myocardial infarction and pulmonary artery stenosis. A Millar ultraminiature catheter pressure transducer designed specifically for right heart catheterization was used for the measurement of RV function in closed-chest, anesthetized rats. Four weeks after coronary artery ligation, left ventricular (LV) function was depressed as evidenced by the reduction of LV systolic pressure (LVSP), the maximal rate of rise in LV pressure (LV dp/dtmax), cardiac output, and by the elevation of LV end-diastolic pressure (LVEDP). There was an increase in RVSP and an elevation in RV dp/dtmax as well as an increase in the RV weight/body weight ratio. Myocytes isolated from the RV 4 weeks after coronary artery ligation had a greater volume and cross-sectional area. In addition, 14 days after pulmonary artery stenosis, there also was an elevation in RVSP and in RV dp/dtmax. In this model, the effect of angiotensin-converting enzyme (ACE) inhibition with ramipril (1 mg/kg daily) was examined. The increase in RVSP from 35 +/- 2 to 61 +/- 4 mm Hg after pulmonary artery stenosis was not influenced by ramipril (63 +/- 4 mm Hg), neither was the elevation of RV weight. However, the increase in cell volume and cross-sectional area of myocytes isolated from the RV was less pronounced in the ramipril-treated group (+27% compared with +58% in untreated animals). Thus, ACE inhibition with ramipril altered the hypertrophic response at the cellular level.

Right ventricular pump dysfunction with acute experimental septic shock

Right ventricular (RV) function has been poorly characterized at the onset of acute bacterial septic shock. Using a volumetric thermodilution catheter, previously validated in our laboratory, we serially measured RV function in a porcine model of acute septic shock. Six pigs (21.3 ± 0.9 kg) were instrumented and Pseudomonas aeruginosa (3.4 × 10 8 cfu/ml, 0.3 ml/20 kg/min) was infused. RV ejection fraction, RV volumes, cardiac output, arterial pressure, central venous pressure, and pulmonary arterial pressure were measured at baseline and at 30, 60, 120, and 240 min after starting the bacterial infusion. RV ejection fraction and stroke volume were decreased at 30 min compared to baseline (21 ± 5 vs 43 ± 5% and 14 ± 3 vs 23 ± 3 ml, respectively; P < 0.05) and remained depressed throughout the experiment. Mean arterial pressure was significantly reduced at 60, 120, and 240 min compared to baseline ( P < 0.05). There was a significant increase in pulmonary vascular resistance (1771 ± 493 vs 301 ± 99 dyn-sec-cm −5 at 30 min; P < 0.05) and RV stroke work (5.7 ± 1.1 vs 2.3 ± 0.3 gm-m/beat at 30 min; P < 0.05) while no significant change in RV endiastolic volume or central venous pressure was observed. Thus, a decrease in RV pump performance was associated with an increase in afterload and no change in preload. These results suggest that severe RV pump dysfunction occurs early in acute septic shock. This was manifested by significant reductions in RV ejection fraction and increased in stroke work. This study demonstrated that thermodilution methods can successfully be used to follow changes in RV performance in the setting of acute septic shock. Serial measurements of RV function may be useful for assessing RV failure during clinical septic shock.

Radionuclide measurement of right ventricular function in atrial septal defect, ventricular septal defect and complete transposition of the great arteries

Right ventricular (RV) function was assessed in 80 patients with congenital heart disease by first-pass and gated equilibrium radionuclide angiography. In 30 patients with a ventricular septal defect (VSD) the mean RV ejection fraction (± standard deviation) was 64 ± 7%. In 30 patients with a secundum atrial septal defect it was 61 ± 9% and in 20 patients with surgically corrected complete transposition of the great arteries it was 49 ± 13%. These values are in close agreement with values established with cineangiography for similar groups of patients. The mean ejection fraction in the group with transposition of the great arteries was significantly less than in the group with VSD (p < 0.001). Phase analysis of the equilibrium studies showed that there was delayed RV contraction in many patients in the absence of conduction abnormalities. This delay was significantly greater in patients with atrial septal defect than in those with VSD (p < 0.05). There was a strong correlation between size of left-to-right shunt and phase delay in patients with VSD (r = −0.72). Thus, first-pass gated radionuclide angiography provides a valid measurement of RV ejection fraction, and delayed RV contraction on phase analysis may be a sensitive index of early RV dysfunction.

Evaluation of right ventricular function in patients with idiopathic dilated and ischemic cardiomyopathy by equilibrium radionuclide ventriculography.

We performed equilibrium radionuclide ventriculography in 12 patients with idiopathic dilated cardiomyopathy, 11 patients with ischemic cardiomyopathy and 11 normal subjects to determine whether measurements of right ventricular function could be used to distinguish dilated cardiomyopathy from ischemic cardiomyopathy. The left ventricular ejection fraction in patients with dilated cardiomyopathy (26 +/- 8%, mean +/- SD) or ischemic cardiomyopathy (32 +/- 5%) was significantly lower than in normals (69 +/- 6%, p less than 0.001). The right ventricular ejection fraction (RVEF) in normals was 57 +/- 7%. RVEF was decreased in 11 of 12 patients with dilated cardiomyopathy and the mean value (32 +/- 10%) was significantly lower than that in patients with ischemic cardiomyopathy (56 +/- 7%, p less than 0.001), none of whom had decreased RVEF. Our data show that right ventricular dysfunction commonly exists in patients with dilated cardiomyopathy but not in patients with ischemic cardiomyopathy. This finding may be useful in the differentiation between dilated and ischemic cardiomyopathy.

Assessment of cardiac performance with quantitative radionuclide angiocardiography: Right ventricular ejection fraction with reference to findings in chronic obstructive pulmonary disease

A reproducible noninvasive technique for measuring right ventricular ejection fraction was developed using first pass quantitative radionuclide angiocardiography. Studies were obtained in the anterior position with a computerized multicrystal scintillation camera with high count rate capabilities. Right ventricular ejection fraction was calculated on a beat to beat basis from the high frequency components of the background-corrected right ventricular time-activity curve. In 50 normal adults, right ventricular ejection fraction averaged 55 percent (range of 45 to 65 percent). This radionuclide measure of right ventricular function was reproducible, with minimal inter- and intraobserver variability and was sensitive to changes in inotropic state induced with isoproterenol. In 36 patients with chronic obstructive pulmonary disease, right ventricular ejection fraction ranged from 19 to 71 percent. All 10 patients with cor pulmonale, as well as 9 additional patients, had an abnormal right ventricular ejection fraction. Arterial oxygen tension and forced expiratory volume were depressed significantly more in patients with abnormal right ventricular ejection fraction than in subjects with normal right ventricular function. There was no relation between abnormalities in right and left ventricular ejection fraction.