Acute Right Ventricular Dilatation in Response to Ischemia Significantly Impairs Left Ventricular Systolic Performance
Male
Cardiotonic Agents
Swine
Systole
Heart Ventricles
Myocardial Ischemia
Reproducibility of Results
Pilot Projects
Myocardial Contraction
Ventricular Dysfunction, Left
03 medical and health sciences
0302 clinical medicine
Dobutamine
Pericardiectomy
Animals
Female
Cardiac Output
Pericardium
Echocardiography, Transesophageal
Dilatation, Pathologic
DOI:
10.1161/01.cir.100.7.761
Publication Date:
2012-06-12T00:42:29Z
AUTHORS (6)
ABSTRACT
Background
—Right ventricular (RV) dilatation that occurs as a consequence of RV infarction is thought to produce hemodynamic instability by reducing left ventricular (LV) preload and compliance. We hypothesized that these geometric changes may also adversely affect LV systolic performance.
Methods and Results
—Twelve 40-kg pigs were studied. Integrated conductance catheters and micromanometers were placed in both the LV and RV to allow simultaneous recordings of pressure and volume and derivation of indices of contractile function. RV ischemia was induced by balloon occlusion of the proximal right coronary artery (RCA) under 3 conditions: 1) with the pericardium intact, 2) with the pericardium intact and inotropic support, and 3) with the pericardium wide open. With an intact pericardium, RCA occlusion produced a decrease in LV end-diastolic volume associated with a marked decline in the contractile function. With the pericardium open, the same ischemic insult resulted in both LV and RV dilatation, which produced a significantly smaller negative effect on cardiac output (
P
=0.03), LV systolic pressure (
P
=0.02), LV preload-recruitable stroke work (
P
<0.01), and LV end-systolic pressure-volume relations (
P
<0.01). Similarly, administration of dobutamine during RCA occlusion decreased the ventricular volume changes and produced a relative improvement in LV contractile performance.
Conclusions
—The hemodynamic compromise seen in association with acute RV dilatation within an intact pericardium is partly attributable to impaired LV systolic performance and cannot be wholly ascribed to changes in LV preload or compliance.
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