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  • purchase TC-I 2000 Effect of atorvastatin in modulation

    2019-06-19

    Effect of atorvastatin in modulation and protection of cardiomyocyte ischemia and inflammatory phenomena (identified as a decline in perioperative CRP, hs-cTnT, and CPK-MB levels) [15,25–27] was not confirmed in the PROFACE trial. Because of no significant differences in the clinical preoperative or intraoperative variables between the treatment groups, we observed that preoperative characteristics of purchase TC-I 2000 valve surgery population could lead to a different physiological response to atorvastatin administration. Although not significant, diabetic patients were more frequently randomized to the atorvastatin group. Association between diabetes, inflammation, and pharmacological response variability following administration of atorvastatin in diabetic patients [28] could explain atorvastatin failure in decreasing serum CRP levels in this group. However, no significant differences in the CRP values were observed on comparing the diabetic patients randomized to the atorvastatin or control group. The percentage of diabetic patients in our study was significantly lower than that in previous studies including CABG patients, in whom peak CRP levels were significantly lower than those observed in the PROFACE trial [9,15,21]. In our study population, the lack of effectiveness of atorvastatin in reducing inflammatory biomarkers was significantly related to heart valve disease and preoperative variables, such as old age [29], increased preoperative left atrial volume index, and preoperative pulmonary hypertension, associated with increased circulating CRP levels [15,30,31]. Such a conclusion may also be applied to myocardial damage biomarkers, such as Hs-cTnT and CPK-MB, that increased proportional to the degree of surgical trauma, and were higher in patients undergoing heart valve procedure than in those undergoing CABG procedures. Atrial remodeling was infrequent in patients with isolated coronary disease and this might explain the more effective protection against POAF observed in this group. This hypothesis was confirmed after analyzing the clinical features of the ARMYDA-3 trial population. In this group of patients, arterial hypertension and diastolic dysfunction were the most significant risk factors for POAF [9]. AEI, the elongation of which is correlated with POAF [30,32], was not significantly modified in PROFACE patients. AEI length was shorter in patients of the PROFACE trial than that in CABG patients of previous trials (probably because beta-blockers were excluded), and it was not modified by atorvastatin therapy. Prophylactic atorvastatin effect in atrial remodeling observed in CABG patients is probably minimized due to a summative effect of advanced age, atrial dilatation, diastolic dysfunction, and pulmonary hypertension, evidenced in both the groups of patients in PROFACE trial. Left ventricular diastolic dysfunction and increased left atrial volume were associated with higher prevalence of POAF [33,34]. Neurohumoral expression in both phenomena correlated with the serum levels of proBNP [30,31]. The proBNP levels in patients with valvular AF increased proportional to the progression of heart valve disease [33,34]. In patients with aortic stenosis, a high preoperative serum proBNP level was associated with poor surgical prognosis [35]. The purpose of preoperative statin therapy in patients with valve disease was to regulate remodeling of myocardial hypertrophy, limit isoprenoid production, and consequently, reduce serum proBNP levels [7]. Proportional to the type of patients included in our clinical trial, the median value of preoperative proBNP was, at least, twice the normal reference values. The significantly higher values of proBNP observed in the atorvastatin group at 24h disappeared when the patients requiring higher inotropic support (>10mcg/kg/min) during this period were excluded from the analysis. The rise in proBNP level was due to a certain grade of postoperative ventricular dysfunction. In the analyzed population, increase in the proBNP level was more related to heart valve disease progression and grade of ventricular dysfunction than to atrial enlargement leading to POAF. This would explain the ineffectiveness of atorvastatin in POAF prevention and the conflicting results with previous studies about the influence of atorvastatin in reducing N-terminal-proBNP in patients affected by dilated cardiomyopathy [31,35].