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Biomedical subjects

SK Sharma

Publications and source records attributed to SK Sharma.

At least 19 recordsLinked to original sources
PubMed1999

Prevention of Vascular Apoptosis in Myocardial Infarction by Losartan.

BACKGROUND: Previous studies have demonstrated the occurrence of apoptosis in cardiomyocytes in different types of cardiovascular diseases. This report provides the first evidence for the presence of vascular apoptosis in myocardial infarction induced in rats by occluding the coronary artery for 7 weeks. METHODS AND RESULTS: Apoptosis was characterized by DNA fragmentation, upregulation of caspase-3, downregulation of poly (ADP-ribose) polymerase (PARP), increased c-fos mRNA expression and caspase-3/PARP ratio in aortic vascular smooth muscle cells. The results show apoptotic changes in 10-25% of the aortic vascular cells after myocardial infarction; these alterations were prevented after treating the 3-week operated animals with an angiotensin II receptor antagonist, losartan (25 mg/kg/day; intraperitoneal) for 4 weeks. Cultured rat aortic smooth muscle cells exposed to 10 nmol/L angiotensin II for 48 hours also exhibited apoptotic changes, which were inhibited by 10 nmol/L losartan. CONCLUSIONS: These results suggest that vascular apoptosis occurs in myocardial infarction, and this may be due to an increase in the circulating levels of angiotensin II.

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PubMed1998

Early Changes in Minimal Luminal Diameter After Balloon Angioplasty and Directional Coronary Atherectomy.

Early elastic recoil has been implicated in the pathophysiology of restenosis after balloon coronary angioplasty (PTCA). Directional atherectomy (DCA) may significantly attenuate this vessel wall reaction by altering the vessel wall architecture, specifically by removing or injuring the medial smooth muscle cells. We compared the magnitude of early changes in minimal lumen diameter (MLD) after DCA followed by adjunctive PTCA (group I) in comparison to PTCA alone (group II). In two groups of 30 lesions, matched for vessel size and location, group I cases showed significantly less recoil than group II cases, as assessed by routinely performed 15 minute post-procedure angiograms: mean changes in post-procedure MLD +0.06mm (increase) vs. -0.31mm (decrease) respectively, p = 0.02. In a histopathologic substudy of the DCA treated patients, those without early recoil had significantly higher incidence of media removal compared to patients with recoil (50% vs. 7%, p = 0.03). Therefore, early changes in MLD, presumably related to elastic recoil, are less with DCA and adjunct PTCA in comparison to PTCA alone. Attenuation of early recoil may be an additional mechanism accounting for the acute lumen gain achieved with this technique.

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PubMed1997

Thrombin Generation and Activity During Coronary Angioplasty: Influence of Angiographic Lesion Morphology.

OBJECTIVE: To investigate the relationships between coronary atherosclerotic plaque injury, lesion morphology, and activation of the coagulation cascade. BACKGROUND: Balloon angioplasty of coronary lesions may result in intracoronary thrombin generation and activity. It is unknown whether the angiographic morphology of the lesion prior to intervention, an indicator of the presence of thrombus in the lesion, is a determinant of the degree of coagulation cascade activation. METHODS AND RESULTS: Biochemical markers of thrombin generation (prothrombin fragment F1+2) and thrombin activity (fibrinopeptide A; FPA) were measured in coronary blood before, 1 and 10 minutes after percutaneous transluminal coronary angioplasty (PTCA) in 24 patients with an angiographically complex lesion morphology and 24 patients with an angiographically simple lesion morphology. Using previously defined criteria, 18 of the 48 patients (38%) demonstrated a significant rise in coronary plasma F1+2; 8 of these 18 (44%) had simple and 10 of 18 (55%) had complex angiographic lesion morphologies (p=NS). With respect to thrombin activity, 15 of the 48 patients (31%) demonstrated a significant rise in coronary plasma FPA; 7 of these 15 patients (47%) had a simple lesion morphology and 8 (53%) had a complex morphology (p=NS). When analyzed as a group, patients with complex lesion morphologies demonstrated a small elevation in coronary plasma levels of FPA 10 minutes post-PTCA (median 3.2 ng/ml, 95% CI 2.4Ð5.8 ng/ml) in comparison to the levels measured proximal to the lesion pre-PTCA (median 2.1 ng/ml, 95% CI 1.6Ð3.5 ng/ml; p=0.05). In contrast, in the group of patients with simple lesion morphologies, the plasma FPA levels proximal to the lesion pre-PTCA (median 2.1 ng/ml, 95% CI 1.5 to 3.9 ng/ml) were similar to those measured 10 minutes after the procedure (median 2.0 ng/ml, 95% CI 1.5 to 6.3 ng/ml; p=NS). CONCLUSIONS: In comparison to patients with angiographically complex lesions, patients with angiographically simple lesions demonstrate a similar incidence (~33%) of elevated coronary plasma thrombin generation (F1+2) and activity (FPA) after PTCA. As a group, patients with angiographically complex lesions (irregular borders, overhanging edges, filling defects) demonstrate a slightly greater increase in thrombin activity in comparison to patients with simple lesion morphologies. Percutaneous coronary interventions of lesions with a wide variety of angiographic morphologies are prone to result in activation of the coagulation cascade.

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