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J Thorac Cardiovasc Surg 2002;124:768-774
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Inelastic vascular prosthesis for proximal aorta increases pulsatile arterial load and causes left ventricular hypertrophy in dogs

From the Departments of Cardiovascular Surgery^a and Cardiology,^b Faculty of Medicine, Kyushu University, Fukuoka, Japan.

This work was partly supported by grant 60570645 from the Ministry of Education, Science and Culture, Japan.

Received for publication Oct 18, 2001. Revisions requested Jan 2, 2002; revisions received Jan 15, 2002. Accepted for Feb 16, publication 2002. Address for reprints: Shigeki Morita, MD, Department of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan (E-mail: morita{at}heart.med.kyushu-u.ac.jp).

Objectives: Elastic property of the proximal aorta plays an important role in reducing pulsatile load to the ventricle. When a stiff vascular prosthesis is used for the proximal aorta, the pulsatile load increases. We designed this study to elucidate whether the increase in pulsatile load caused left ventricular hypertrophy.
Methods: We created an ascending aorta-abdominal aorta bypass in 9 dogs with a noncompliant vascular prosthesis. The aortic arch proximal to the left subclavian artery was occluded to direct blood flow into the bypass. Closed chest studies were performed after a median of 139 days (range 45-588) days. We assessed the pulsatile load of the ventricle by calculating characteristic impedance from pressure and flow velocity in the ascending aorta. The left ventricle was weighed, normalized with body weight, and compared with the control group, which had sham operations (7 dogs).
Results: Characteristic impedance of the bypassed dogs was 175% higher than the control (0.146 ± 0.056 vs 0.053 ± 0.014 mm Hg · s · mL^-1, P = .009), which resulted in wider pulse pressure (57 ± 11 vs 25 ± 11 mm Hg, P < .001). No difference was found in arterial resistance, cardiac output, or systolic blood pressure. Left ventricular weight normalized by body weight was significantly heavier in the bypass group (5.61 ± 0.75 vs 4.15 ± 0.62 g/kg, P = .001).
Conclusion: Since there was no increase in arterial resistance, we conclude that the increase in pulsatile load was the cause of left ventricular hypertrophy. A stiff vascular prosthesis used for the proximal aorta may cause left ventricular hypertrophy.

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