ABSTRACT
Heart failure [HF] is a common cardiovascular condition whose incidence and prevalence are increasing. Being a common reason for urgent hospital admission, it is a major cause of morbidity and mortality for the patients. In the developed countries coronary artery disease remains the leading cause of HF, whereas, in the underdeveloped countries, rheumatic heart disease leading to valvular lesion still remains the commonest causes of HF admission. The current study was designed to evaluate the clinical profile and medications prescribed reflecting the extent to which evidence based medicine is being practiced at our community. Clinical profile and prescribed medications of patients with diagnosis of HF who were admitted in the cardiology department of College of Medical Sciences and Teaching Hospital [CMS-TH], Bharatpur, Nepal, April 2010 to May 2012, were analyzed. A total of 255 patients presented with HF during the studied period were included. Coronary artery disease, rheumatic heart disease, dilated cardiomyopathy, hypertensive heart failure, cor-pulmonale, and congenital heart disease leading to HF were found in 93 [36.5%], 65 [25.5%], 37 [14.5%], 22 [8.6%], 31 [12.2%],and 7 [2.7%] patients respectively. The commonest presenting symptom was shortness of breath [81%] and the commonest sign was bilateral basal crepitations [68%]. From all patients, 89%, 64%, 51%, 16%, 48%, and 32% received loop diuretics, angiotensin-converting enzyme inhibitor, digoxin, angiotensin receptor blocker, spironolactone, and beta-blocking agents respectively. Coronary artery disease leading to HF was the commonest cause of HF admission in our centre. Despite current guidelines suggesting the use of beta-blocking agent in patients with HF, only 32% of our patients received this class of medications. Thus, many patients were not being managed fully in accordance with the evidence-based guidelines
Subject(s)
Humans , Male , Female , Practice Guidelines as Topic , Adrenergic beta-Antagonists , Evidence-Based Practice , Heart Failure/diagnosis , Heart Failure/etiology , Retrospective StudiesABSTRACT
To observe the effects of simvastatin on nuclear factor kappaB (NF-kappaB)-DNA binding activity and on the expression of monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group (LC), high-cholesterol group (HC), high-cholesterol+simvastatin group (HC+S) and then were fed for 12 weeks. At the end of the experiment, standard enzymatic assays, electrophoretic mobility shiftassay (EMSA), immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-kappaB-DNA binding activity, MCP-1 protein expression, intima thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-kappaB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC+S groups were significantly lower than those in the HC group (P0.05), but the NF-kappaB-DNA binding activity, the expression of MCP-1 protein and the intima thickness and plaque area of aorta in the HC+S group were significantly decreased as compared to the LC group (P<0.05). This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NF-kappaB-DNA binding activity and by reducing the expression of MCP-1 protein.
ABSTRACT
To observe the effects of simvastatin on nuclear factor kappaB (NF-κB)-DNA binding activity and on the expression of monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects.Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group (LC), highcholesterol group (HC), high-cholesterol+ simvastatin group (HC+S) and then were fed for 12weeks. At the end of theexperiment, standard enzymatic assays, electrophoretic mobility shift assay (EMSA), immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-κB-DNA binding activity, MCP-1 protein expression, intima thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-κB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC+S groups were significantly lower than those in the HC group (P＜0.05). There was no significant difference in the serum lipids between the LC and HC+S groups (P＞0.05), but the NF-κB-DNA binding activity, the expression of MCP-1 protein and the intima thickness and plaque area of aorta in the HC+S group were significantly decreased as compared to the LC group (P＜0.05). This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NFκB-DNA binding activity and by reducing the expression of MCP-1 protein.
ABSTRACT
Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion [I/R] injury. Inhibition of Fas expression prevents I/R induced apoptosis. However, the influence of atorvastatin on Fas expression in I/R injury was not studied. Therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis and Fas expression following acute I/R in vivo. Thirty Wistar rats were selected and divided into three groups [n = 10]: acute ischemia-reperfusion [I/R] group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. Apoptosis of the cardiomyocytes was observed under electron microscopy and determined by optic microscopy with TUNEL [terminal deoxynucleotidyl transferase [TdT]-mediated dUTP nick end-labeling] staining. To detect the expression of Fas in the cardiomyocytes, immunohistochemistry method was used. Image analysis system was used to quantitatively estimate the positive metric substances of immunohistochemistry through the mean optic density. Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and weren't observed in the sham-operated group. Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression