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Ann Thorac Surg 2003;75:178-183
© 2003 The Society of Thoracic Surgeons

Original article: cardiovascular

Smooth muscle cell hypertrophy of renal cortex arteries with chronic continuous flow left ventricular assist

Shin’ichiro Kihara, MD, PhDa*, Kenneth N. Litwak, DVM, PhDa, Larry Nichols, MDb, Philip Litwak, DVM, PhDa, Marina V. Kameneva, PhDa, Zhongjun Wu, PhDa, Robert L. Kormos, MDa, Bartley P. Griffith, MDc

a Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
b Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
c Department of Surgery, University of Maryland, Baltimore, Maryland, USA

Accepted for publication July 23, 2002.

* Address reprint requests to Dr Kihara, McGowan Institute for Regenerative Medicine, University of Pittsburgh, 3025 E Carson St, Pittsburgh, PA 15203, USA.
e-mail: kiharas{at}msx.upmc.edu

BACKGROUND: Pathophysiology of long-term continuous flow left ventricular assist is not well described. With many of these devices becoming available, it is important to examine for possible pathologic effects. In this study we examined the relationship between diminished pulsatility and pathologic changes in renal cortical arteries.

METHODS: Twenty-nine calves were implanted with various continuous flow left ventricular assist systems in a left ventricle-descending thoracic aorta bypass configuration. Pulsatility was quantified by pulse pressure and pulsatility index. Pathologic changes of the renal cortex arteries were described and evaluated by medial thickness, medial/vascular cross-sectional area ratio, and smooth muscle cell count, to quantify hypertrophy or hyperplasia. Seven calves, which underwent a sham-implant, were used as controls.

RESULTS: Systolic arterial pressure, pulse pressure, and pulsatility index were significantly lower and diastolic pressure was significantly higher than before implant in pump-implanted animals. Twenty-three of 29 pump-implanted calves (79.3%) had medial smooth muscle cell hypertrophy in renal cortex arteries, whereas none of sham-implanted calves had any abnormal lesions. When the pump-implanted calves were grouped according to the presence of smooth muscle cell hypertrophy, there was a clear trend toward lower pump flow rate in calves with lesions. Renal function was within the normal range in all calves.

CONCLUSIONS: There appears to be a relationship between smooth muscle cell hypertrophy in renal cortex arteries and continuous flow left ventricular assist. Furthermore, although the pathologic changes are likely multifactorial, these lesions appear to be related to lower pump assist rates.




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