ABSTRACT
Lipoprotein (a) [Lp(a)] is an independent risk factor for cardiovascular disease. There are currently limited therapeutic options to lower Lp(a) levels. L-Carnitine has been reported to reduce Lp(a) levels. The aim of this study was to compare the effect of L-carnitine/simvastatin co-administration with that of simvastatin monotherapy on Lp(a) levels in subjects with mixed hyperlipidemia and elevated Lp(a) concentration. Subjects with levels of low-density lipoprotein cholesterol (LDL-C) >160 mg/dL, triacylglycerol (TAG) >150 mg/dL and Lp(a) >20 mg/dL were included in this study. Subjects were randomly allocated to receive L-carnitine 2 g/day plus simvastatin 20 mg/day (N = 29) or placebo plus simvastatin 20 mg/day (N = 29) for a total of 12 weeks. Lp(a) was significantly reduced in the L-carnitine/simvastatin group [-19.4%, from 52 (20-171) to 42 (15-102) mg/dL; p = 0.01], but not in the placebo/simvastatin group [-6.7%, from 56 (26-108) to 52 (27-93) mg/dL, p = NS versus baseline and p = 0.016 for the comparison between groups]. Similar significant reductions in total cholesterol, LDL-C, apolipoprotein (apo) B and TAG were observed in both groups. Co-administration of L-carnitine with simvastatin was associated with a significant, albeit modest, reduction in Lp(a) compared with simvastatin monotherapy in subjects with mixed hyperlipidemia and elevated baseline Lp(a) levels.
Subject(s)
Cardiovascular Diseases/prevention & control , Carnitine/administration & dosage , Hyperlipoproteinemia Type V/drug therapy , Lipoprotein(a)/metabolism , Simvastatin/administration & dosage , Adult , Apolipoprotein B-100/metabolism , Cardiovascular Diseases/metabolism , Carnitine/pharmacology , Cholesterol/blood , Double-Blind Method , Drug Therapy, Combination , Female , Humans , Hyperlipoproteinemia Type V/metabolism , Male , Middle Aged , Prospective Studies , Simvastatin/pharmacology , Treatment Outcome , Triglycerides/metabolism , Young AdultABSTRACT
In a substantial number of patients, AF recurs after successful electrical cardioversion. The purpose of this study was to investigate if the atrial arrhythmias recorded immediately after cardioversion are associated with the risk of recurrence of the arrhythmia and to compare the prognostic significance of this parameter with that of other established risk factors. In a series of 71 patients, the risk factors for recurrence of AF during the first year after successful electrical cardioversion were analyzed. A new parameter that was investigated was the frequency of atrial premature beats and the presence of runs of supraventricular tachycardia in the Holter recording started immediately after the cardioversion. Age, left atrial size, left ventricular systolic function, duration of the arrhythmia before cardioversion, underlying cardiac disease, or medication taken were not found to be predictive of recurrence of the arrhythmia. However, the natural logarithm of the number of atrial premature complexes per hour of the Holter recording in the 37 patients in whom AF recurred was higher compared to that of the 34 patients who maintained sinus rhythm (P < 0.0005). The same was true if only the first 6 hours of the recording were analyzed (P < 0.0005). There was a trend for more frequent arrhythmia recurrence if runs of supraventricular tachycardia were present. The finding of > 10 atrial premature complexes per hour in the recording had a relative risk of 2.57 (1.51-4.37), a positive predictive accuracy of 76.5%, and a negative predictive accuracy of 70.3% for subsequent arrhythmia recurrence. We can conclude that frequent (> 10/hour) atrial premature complexes in the Holter recording after electrical cardioversion for AF is a significant risk factor for recurrence of the arrhythmia.
