trandolapril and Atrial-Fibrillation

Atrial fibrillation is very common in the United States. After a search of Medline, EMBASE, and CINAHL, 4 trials evaluating inhibitors of the renin-angiotensin system were identified for prevention of new-onset atrial fibrillation, facilitation of electrical cardioversion of atrial fibrillation, and prevention of atrial fibrillation recurrence after electrical cardioversion. A meta-analysis was performed using a random-effects model. Use of an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB) was associated with a reduction in new-onset atrial fibrillation (OR [95% CI] = 0.51 [0.36-0.72]), a lower failure rate of electrical cardioversion of atrial fibrillation (0.47 [0.24-0.92]), and a lower rate of recurrence of atrial fibrillation after electrical cardioversion (0.39 [0.20-0.75]). With the exception of the new-onset atrial fibrillation analysis, these findings were not associated with statistical heterogeneity. These hypothesis-generating data suggest that inhibitors of the renin-angiotensin system may provide benefit across the spectrum of atrial fibrillation.

Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Atrial Fibrillation; Combined Modality Therapy; Electric Countershock; Enalapril; Humans; Indoles; Losartan; Randomized Controlled Trials as Topic; Renin-Angiotensin System; Secondary Prevention; Tetrazoles; Valine; Valsartan

Atrial fibrillation (AF) is a common complication in patients with acute myocardial infarction and is associated with an increase in the risk of death. The excess mortality associated with AF complicating acute myocardial infarction has not been studied in detail. Observations indicate that AF facilitates induction of ventricular arrhythmias, which may increase the risk of sudden cardiovascular death (SCD). A close examination of the mode of death could potentially provide useful knowledge to guide further investigations and treatments.. We analysed the relation between AF/atrial flutter (AFL) and modes of death in 5983 consecutive patients discharged alive after an acute myocardial infarction screened in the TRAndolapril Cardiac Evaluation registry. This cohort of patients with an enzyme-verified acute myocardial infarction was admitted to 27 centres in 1990-92. Survival status was obtained 2 years after screening of the last patient. An independent endpoint committee assessed the modes of death. Left ventricular ejection fraction was determined in all the screened patients and information about presence or absence of AF/AFL was prospectively collected. Sustained or paroxysmal AF/AFL was observed in 1149 patients (19%) during hospitalization. During follow-up, 1659 patients (34%) died: 482 (50%) patients with AF/AFL and 1177 (30%) patients without AF/AFL, P<0.001. SCD occurred in 536, non-SCD occurred in 725, and 398 died of non-cardiovascular causes (includes 142 unclassifiable cases). The adjusted risk ratio of AF/AFL for total mortality was 1.33 (95% CI: 1.19-1.49; P<0.0001) and the risk ratio for SCD was 1.31 (95% CI: 1.07-1.60; P<0.009). The adjusted risk ratio of AF/AFL for non-SCD was 1.43 (95% CI: 1.21-1.70; P<0.0001).. The excess mortality observed in patients with AF/AFL following acute myocardial infarction is due to a significant increase in both SCD and non-SCD.

Topics: Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Atrial Fibrillation; Atrial Flutter; Cause of Death; Cohort Studies; Death, Sudden, Cardiac; Female; Humans; Indoles; Male; Middle Aged; Myocardial Infarction; Sweden

Studies have suggested that ACE inhibitors have an antiarrhythmic effect on ventricular arrhythmias. Whether they have an effect on atrial fibrillation is unknown.. We investigated the effect of ACE inhibition with trandolapril on the incidence of atrial fibrillation in patients with reduced left ventricular function secondary to acute myocardial infarction. The patients in this study were those who qualified for inclusion into the TRAndolapril Cardiac Evaluation (TRACE) study, a randomized double-blind placebo-controlled study and who had sinus rhythm on the ECG obtained at randomization. Patients who fulfilled the criteria for inclusion were randomized to treatment with the ACE inhibitor trandolapril or placebo and were followed up for 2 to 4 years. Development and time to occurrence of atrial fibrillation in one 12-lead ECG recorded at the outpatient visits was the primary end point of this investigation. Of the 1749 patients included in the TRACE study, 1577 had sinus rhythm on the ECG recorded at randomization. Of these patients, 790 were randomized to trandolapril treatment and 787 to placebo treatment. The groups differed only slightly with respect to baseline characteristics. A total of 64 patients developed atrial fibrillation during the 2- to 4-year follow-up period. Significantly more patients developed atrial fibrillation in the placebo group than in the trandolapril group, 5.3% (n=42) versus 2.8% (n=22), respectively, P<0.05. Cox multivariable regression analysis, adjusting for important baseline characteristics, revealed that trandolapril treatment significantly reduced the risk of developing atrial fibrillation (RR, 0.45; 95% CI, 0.26 to 0.76; P<0.01).. The results from the present study demonstrate that trandolapril treatment reduces the incidence of atrial fibrillation in patients with left ventricular dysfunction after acute myocardial infarction.

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Atrial Fibrillation; Electrocardiography; Female; Follow-Up Studies; Humans; Incidence; Indoles; Male; Myocardial Infarction; Ventricular Dysfunction, Left

The development of atrial fibrillation ablation has revolutionized the field of antiarrhythmic treatment by reducing the recurrence of atrial fibrillation (AF) significantly in patients with paroxysmal atrium fibrillation (PAF). However, the effect of ablation on the patients with persistent atrial fibrillation (PeAF) is not as good as it on PAF. Although doctors have created a series of ablation strategy, they still cannot treat PeAF effectively. This phenomenon is caused by structural remodeling and electrical remodeling of atrium during the long period of AF. Many experimental have demonstrated remodeling of atrium correlated with high level of angiotensin in atrial tissue, and blockade of renin-angiotensin system (RAS) through angiotensin-converting-enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) can reverse atrial remodeling. Clinical studies also confirmed that blockade of RAS can prevent AF effectively. Thus, for the object of treating PeAF effectively, we can combine the circumferential pulmonary vein isolation with blockade of RAS treatment, this combined strategy eliminate the trigger (pulmonary vein potential ) of AF and reverse the atrial remodeling, may be have a good effect on PeAF.

Topics: Angiotensin-Converting Enzyme Inhibitors; Atrial Fibrillation; Humans; Indoles; Models, Biological; Pulmonary Veins; Renin-Angiotensin System