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R D Page

Publications and source records attributed to R D Page.

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Determinants of maximal right ventricular function.

After heart transplantation, right ventricular failure can occur because of increased afterload. Previous studies have suggested that the maximal pressure the right ventricle can develop is determined primarily by right ventricular perfusion pressure. However, the interaction of the left ventricle and the pericardium as functional co-determinants of maximal right ventricular function is unknown. This study was undertaken to determine the interaction of the pericardium, left ventricular pressure, and right coronary artery perfusion pressure as potential determinants of maximal right ventricular function. In an acute canine preparation, with progressive pulmonary artery constriction, maximal generated right ventricular pressure was determined over a range of left ventricular systolic pressures. Additional groups of dogs were studied with the right coronary artery cannulated and were maintained at constant perfusion pressure. In all preparations, the maximal pressure the right ventricle could generate was linearly related to left ventricular systolic pressure. Having a closed pericardium markedly enhanced this effect; some effect was present with an open pericardium, although the magnitude of the influence of left ventricular pressure on maximal right ventricular pressure was much less. Maintaining constancy of right coronary artery perfusion pressure, either at high or low values, did not alter these findings nor did it alter the influence of the pericardium. These results suggest that right ventricular perfusion may not be the sole determinant of maximal right ventricular function. Furthermore, with the pericardium open, such as in the posttransplantation state, the left ventricular contribution to maximal right ventricular function may be diminished, increasing vulnerability for right ventricular failure caused by increased afterload.

Animals↗

Allograft diastolic dysfunction and chronotropic incompetence limit cardiac output response to exercise two to six years after heart transplantation.

BACKGROUND: Because prolonged survival of heart transplant recipients is expected with the current immunosuppressive treatment, the functional capacity of these long-term survivors is of interest. Previous exercise studies showed no objective improvement in exercise tolerance several years after transplantation, but the extent to which chronotropic incompetence and allograft diastolic dysfunction observed early after transplantation may improve over time has not been defined. METHODS: Thirteen untrained heart transplant recipients without symptoms, between 27 and 70 months after transplantation, and 13 age-matched sedentary normal controls underwent maximal upright bicycle exercise testing with simultaneous hemodynamic, radionuclide, and expired gas measurements. RESULTS: Systolic function as measured by ejection fraction was supranormal at rest in the transplant group and normalized with exercise. Despite their maximal exercise effort, transplant recipients had a 60% reduction in their exercise capacity compared with nontransplant recipients. Peak oxygen consumption was similarly reduced by 52%. Cardiac output response to exercise was 43% lower in the transplant group because of a 78% reduction in heart rate reserve and an 18% reduction in maximal stroke volume. Ventricular volumes were similarly reduced after transplantation, but filling pressures remained normal, indicating allograft diastolic dysfunction. Despite the significantly reduced maximal cardiac output, maximal arteriovenous oxygen difference was 25% lower in the transplant recipients, suggesting a peripheral deficit in oxygen handling. CONCLUSIONS: Therefore, patients, 2 to 6 years after transplantation, continue to have a significant reduction in exercise tolerance as a result of a combination of severe chronotropic incompetence, limited stroke volume reserve caused by a reduced ventricular size and allograft diastolic dysfunction, and an abnormality in peripheral oxygen delivery or use. Efforts aimed at improving these factors may further enhance the functional capacity of these long-term survivors of heart transplantation.

Cardiac Output↗