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J Thorac Cardiovasc Surg 2002;124:964-972
© 2002 The American Association for Thoracic Surgery


Cardiopulmonary Support and Physiology (CSP)

Right ventricular diastolic relaxation in conscious dog models of pressure overload, volume overload, and ischemia

Ares D. Pasipoularides, MD, PhD, Ming Shu, PhD, Ashish Shah, MD, Donald D. Glower, MD

From the Department of Surgery, Division of Cardiothoracic Surgery, and the Duke Center for Emerging Cardiovascular Technologies, Duke University, Durham, NC.

This work was supported in part by National Heart, Lung, and Blood Institute grant R01 HL-50446 (Dr Pasipoularides) and the Duke/NSF ERC for Emerging Cardiovascular Technologies.

Received for publication Nov 6, 2001. Revisions requested Feb 5, 2002; revisions received April 4, 2002. Accepted for publication May 28, 2002. Address for reprints: Donald D. Glower, MD, Division of Cardiac and Thoracic Surgery, PO Box 3851, Medical Center, Duke University, Durham, NC 27710 (E-mail: glowe001{at}mc.duke.edu).

Objective: Limitations in clinical understanding of right ventricular relaxation can be attributed to the paucity of information from basic studies in animal models of right ventricular disease. This study examined, in the conscious state, right ventricular relaxation dynamics under normal conditions (n = 15) and in subacute (2-5 weeks) canine models of right ventricular pressure overload (n = 6), volume overload (n = 7), and free wall ischemia (n = 7).
Methods: Right-heart micromanometric measurements were obtained by using multisensor catheters. A new algorithm was developed to obtain representative ensemble averages of hemodynamic waveform data sets. Right ventricular relaxation was analyzed by using an exponential model with 3 parameters: P0, {tau}, and Pb. Significant changes versus control values were determined by means of analysis of variance and the Student unpaired t test with Bonferroni's adjustment.
Results: In the state of pressure overload, right ventricular pressure decay exhibits an increased P0 (56.2 ± 19.1 vs 13.1 ± 5.1 mm Hg [mean ± SD]) and prolonged {tau} (57.1 ± 2.8 vs 27.8 ± 3.9 ms); there is also a decreased Pb (-7.9 ± 1.5 vs 0.28 ± 1.8 mm Hg). The only significant change in volume overload is an increased asymptote, Pb (5.3 ± 2.9 mm Hg). In right ventricular ischemia, prolongation of {tau} (41.4 ± 13.0 ms) and decreased Pb (-1.95 ± 1.1 mm Hg) attain high significance.
Conclusions: Distinctive abnormalities in right ventricular relaxation dynamics accompany pressure overload, volume overload, and ischemia and may contribute to clinical right ventricular dysfunction.




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