D G Blanchard1, H C Dittrich. 1. Department of Internal Medicine, University of California, School of Medicine.
Abstract
BACKGROUND: The pericardium both limits cardiac distension and accentuates ventricular interdependence. Although this effect appears minimal under normal circumstances, the pericardium markedly restricts acute cardiac enlargement. Animal studies have demonstrated gradual pericardial adaptation and expansion in chronic volume overload and cardiomegaly, but the pericardial response in humans with cardiac hypertrophy and enlargement has not been examined fully. To investigate this further, 14 patients with right ventricular hypertrophy and cardiomegaly secondary to chronic pulmonary thromboembolic disease and severe pulmonary hypertension were studied during pulmonary thromboendarterectomy. METHODS AND RESULTS: Simultaneous intraoperative transesophageal Doppler echocardiography and direct biventricular hemodynamic measurements were performed at steady state immediately before and after pericardiotomy. All hemodynamic variables showed no significant change before and after pericardiotomy, including heart rate (76 +/- 16 versus 75 +/- 15 beats per minute), mean pulmonary arterial pressure (46.3 +/- 11.1 versus 45.5 +/- 11.7 mm Hg), cardiac index (1.8 +/- 0.5 versus 2.0 +/- 0.6 l/min/m2), left ventricular end-diastolic pressure (5.9 +/- 5.7 versus 7.1 +/- 5.0 mm Hg), and right ventricular end-diastolic pressure (7.9 +/- 6.6 versus 8.0 +/- 6.7 mm Hg). Similarly, there were no significant changes in all Doppler echocardiographic parameters, including right ventricular end-diastolic area (23.2 +/- 5.7 versus 22.6 +/- 5.4 cm2), left ventricular end-diastolic area (15.3 +/- 5.9 versus 15.5 +/- 4.4 cm2), the position of the interventricular septum, and the Doppler-derived mitral inflow measures of diastolic function. CONCLUSIONS: The pericardium appears to have little influence on the marked cardiac and septal deformations seen in patients with chronic, severe right ventricular pressure overload and cardiomegaly. This study confirms that the human pericardium is capable of adapting over time to changes in cardiac size and geometry.
BACKGROUND: The pericardium both limits cardiac distension and accentuates ventricular interdependence. Although this effect appears minimal under normal circumstances, the pericardium markedly restricts acute cardiac enlargement. Animal studies have demonstrated gradual pericardial adaptation and expansion in chronic volume overload and cardiomegaly, but the pericardial response in humans with cardiac hypertrophy and enlargement has not been examined fully. To investigate this further, 14 patients with right ventricular hypertrophy and cardiomegaly secondary to chronic pulmonary thromboembolic disease and severe pulmonary hypertension were studied during pulmonary thromboendarterectomy. METHODS AND RESULTS: Simultaneous intraoperative transesophageal Doppler echocardiography and direct biventricular hemodynamic measurements were performed at steady state immediately before and after pericardiotomy. All hemodynamic variables showed no significant change before and after pericardiotomy, including heart rate (76 +/- 16 versus 75 +/- 15 beats per minute), mean pulmonary arterial pressure (46.3 +/- 11.1 versus 45.5 +/- 11.7 mm Hg), cardiac index (1.8 +/- 0.5 versus 2.0 +/- 0.6 l/min/m2), left ventricular end-diastolic pressure (5.9 +/- 5.7 versus 7.1 +/- 5.0 mm Hg), and right ventricular end-diastolic pressure (7.9 +/- 6.6 versus 8.0 +/- 6.7 mm Hg). Similarly, there were no significant changes in all Doppler echocardiographic parameters, including right ventricular end-diastolic area (23.2 +/- 5.7 versus 22.6 +/- 5.4 cm2), left ventricular end-diastolic area (15.3 +/- 5.9 versus 15.5 +/- 4.4 cm2), the position of the interventricular septum, and the Doppler-derived mitral inflow measures of diastolic function. CONCLUSIONS: The pericardium appears to have little influence on the marked cardiac and septal deformations seen in patients with chronic, severe right ventricular pressure overload and cardiomegaly. This study confirms that the human pericardium is capable of adapting over time to changes in cardiac size and geometry.