Reduction of left ventricular hypertrophy by sirolimus in kidney transplant recipients: a nonrandomized clinical trial

Persistence of left ventricular hypertrophy [LVH] in renal transplant recipients is associated with unfavorable outcomes. Calcineurin-inhibitor [CNI] nephrotoxicity is a major cause of morbidity and mortality after kidney transplantation. In this study we compared sirolimus [SRL] with calcineurin-inhibitor as primary immunosuppressants for the attenuation of left ventricular hypertrophy in renal transplantation recipients. In this prospective cohort study done in Shariati Hospital in 2010, we evaluated the effects of sirolimus and CNI on LVH of 55 renal transplant recipients. The cases [19] received sirolimus while the controls [36] received CNI while being matched for age and duration of transplantation. Data regarding blood pressure [BP], hemoglobin, serum creatinine, uric acid and lipid concentrations were assessed and changes in left ventricular [LV] mass were evaluated by echocardiography over a one-year follow-up. Left ventricular mass significantly decreased [P=0.0001] in the SRL group but blood pressure did not differ between the two groups. LV mass and LV mass index both decreased significantly [P<0.05] but the difference was not associated with changes in BP. The difference in interventricular septal thickness at end diastole [IVSD] and posterior wall diameter [PWD] were significant [P<0.05] in the SRL group but the difference in end diastolic diameter [EDD] was not significant. Conversion from CNI to SRL-based immunosuppressive therapy in RTRs is safe and SRL may decrease LVH. SRL seems to be safe and improve renal function without cardiac compromise in kidney transplant recipients

role of serum lipoprotien[a] in increasing the risk of thrombus formation in patients with atrial fibrillation

Atrial fibrillation [AF] is prevalent among cardiac patients; and as the risk of thromboembolism is high in this arrhythmia, discrimination of the effective risk factors in producing left atrial [LA] thrombosis is clinically important. The molecular structure of lipoprotein[a] [Lp[a]] is very similar to plasminogen, so it can be hypothesized that the high level of Lp[a] is a compromising factor for the prevention of fibrinolysis [thrombogenesis]. This case-control study was conducted in patients with chronic AF. Most of the subjects had mitral stenosis. LA thrombosis was confirmed by transthoracic and transesophageal echocardiography. The study group consisted of 50 chronic AF patients mostly with mitral stenosis. Half the patients had LA thrombosis [patient group or P] and the other half did not [control group or C]. The mean age of the control group [C] and patient group [P] was 45 +/- 11 y and 57 +/- 9 y, respectively. There was no significant correlation between sex and LA gradient and existence of LA thrombus. LA size was 49 +/- 5 mm [C] and 56 +/- 9 mm [P], respectively. Left atrial blood velocity was 12 +/- 2 cm/sec [C] and 5 +/- 3 cm/sec [P], and Lp[a] concentration was 30 +/- 6.7 mg / dl [C] and 55 +/- 2.75 mg / dl [P]. There was a significant correlation [p<0.001] between age, LA blood velocity, LA size, and serum concentration of Lp[a], which was confirmed by t-test. There has been a great deal of research into the classic risk factors of LA thrombosis in chronic AF, but the study on the effect of Lp[a], which is an atherosclerosis risk factor, on the formation of LA thrombosis is almost new. According to the results of the present study, Lp[a] should be measured in all chronic AF patients. We can assume that lowering Lp[a] serum level may decrease the risk of LA thrombosis in chronic AF patients