Kamal Nasser

Baylor College of Medicine, Houston, TX, United States

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Publications (3)21.76 Total impact

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    ABSTRACT: We sought to assess the role of regional diastolic function by Doppler echocardiography in predicting myocardial viability. Sixteen dogs underwent left anterior descending coronary artery (n = 8) or circumflex (n = 8) occlusion. All animals were imaged at baseline and 1-8 wk postinfarction (post-MI). In 10 dogs, invasive hemodynamic monitoring with a conductance catheter placed in the left ventricle (LV) was performed at the above time points. Dobutamine was infused at 1-8 wk post-MI to determine LV contractile reserve. Histomorphological analysis was performed to determine the presence of viable myocardium and changes in interstitial matrix. Post-MI, diastolic strain rate measurements (in radial and longitudinal planes) decreased significantly in the distribution of the diseased artery (P < 0.01) and on multiple regression analysis were determined by time constant of LV relaxation, end-diastolic pressure, regional stiffness, and the ratio of cellular infiltration to collagen deposition in the interstitial matrix. Among several indexes, diastolic strain rate during dobutamine infusion readily identified segments with >20% transmural infarction and related best to the extent of interstitial fibrosis (r = -0.86, P < 0.01). In an animal model of healing canine infarcts, diastolic strain rate by Doppler echocardiography appears to be a promising novel index of myocardial viability.
    AJP Heart and Circulatory Physiology 02/2006; 290(2):H724-31. · 4.01 Impact Factor
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    ABSTRACT: Angiogenesis is a critical process in healing of myocardial infarcts, leading to the formation of highly vascular granulation tissue. However, effective cardiac repair depends on mechanisms that inhibit the angiogenic process after a mature scar is formed, preventing inappropriate expansion of the fibrotic process. Using a canine model of reperfused myocardial infarction, we demonstrated that maturation of the infarct leads to the formation of neovessels, with a thick muscular coat, that demonstrate distinct morphological characteristics. Many of these "neoarterioles" lack a defined internal elastic lamina and demonstrate irregular deposits of extracellular matrix in the media. Vascular mural cells in healing infarcts undergo phenotypic changes, showing minimal expression of desmin during the proliferative phase (1 hr occlusion/7 days reperfusion) but in the mature scar (8 weeks reperfusion) acquire a phenotype similar to that of vascular smooth muscle cells in control areas. Non-muscle myosin heavy chains A and B are induced in infarct endothelial cells and myofibroblasts, respectively, but are not expressed in neovascular mural cells. Recruitment of a muscular coat and formation of neoarterioles in mature scars may inhibit endothelial cell proliferation and vascular sprouting, stabilizing the infarct vasculature.
    Journal of Histochemistry and Cytochemistry 09/2004; 52(8):1019-29. · 2.40 Impact Factor
  • Journal of the American College of Cardiology 03/2004; 43(5). · 15.34 Impact Factor