Affiliation: | 1 Cardiovascular Research Laboratory, Department of Biomedical Engineering, Rutgers University, Piscataway, NJ 08855-0909, USA 2 Noninvasive Laboratory, Division of Cardiology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, NY 10467, USA |
Abstract: | The degree of left ventricular hypertrophy is generally thought to reflect the severity of aortic stenosis. However, the compounded influence of arterial system load is poorly understood. We developed a computer model to investigate the effects of aortic valve stenosis in combination with various systemic arterial parameters in the development of left ventricular hypertrophy. Data show that an increased peripheral resistance and/or aortic valve resistance, results in an increase in left ventricular wall thickness and mass, while peak systolic wall stress remains constant. Changing arterial compliance to above normal level would not induce significant changes in wall thickness, while reduction in arterial compliance below normal would cause an increase in ventricular wall thickness. When a double load is imposed on the left ventricle by way of a stenotic valve and an increased arterial afterload, a greater and an aggregated increase in wall thickness results, hastening the hypertrophic process. |