This study was designed to examine the importance of the underlying cardiac pathology on outcome of cardiac resynchronization therapy (CRT), hypothesizing that myocardial infarction scar and other noncontractile segments represent limitations to the ability to resynchronize cardiac contraction in patients with congestive heart failure associated with dilated cardiomyopathy. From October 1999 to April 2002, 158 patients (mean age 65 years, 121 men) were included in a single center, longitudinal, comparative study. All patients had dilated cardiomyopathy and indications for CRT with a mean QRS duration of 174 ms. The patient population was divided into a coronary artery disease (CAD) group that included patients with significant CAD, and no indication, or a contraindication for revascularization, and a non-CAD group that included patients with nonischemic dilated cardiomypopathy. Follow-up data were collected at 3, 6, and 12 months, and yearly thereafter. The median follow-up was 11.2 months. In the CAD group, the LVEF increased from 0.29 to 0.34 (P < 0.0001), the 6-minute walk test distance increased from 310 to 463 m (P < 0.0001), and the percentage of patients in NYHA functional Class III-IV decreased from 83% to 23% (P = 0.04). In the non-CAD group, LVEF increased from 29% to 42% (P < 0.0001), the 6-minute walk test distance increased from 332 to 471 m (P < 0.0001), and the percentage of patients in NYHA functional Class III-IV decreased from 79% to 5%, (P < 0.0001). Comparison of the two groups showed that patients in the non-CAD group had a significantly greater increase in LVEF (P = 0.007) and decrease in NYHA class (P < 0.05). Patients with CAD or non-CAD significantly improved clinically during CRT. Non-CAD patients had a greater increase in LVEF and decrease in NYHA functional class than patients with CAD.

Heart failure patients with ventricular conduction disturbance and permanent AF treated with CRT showed large and sustained long-term (up to 4 year) improvements of left ventricular function and functional capacity, similar to patients in SR, only if AVJ ablation was performed.

Short-term hemodynamic studies consistently report greater effects of cardiac resynchronization therapy (CRT) in patients stimulated from a LV lateral coronary sinus tributary (CST) compared to a septal site. The aim of the study was to compare the long-term efficacy of CRT when performed from different LV stimulation sites. From October 1999 to April 2002, 158 patients (mean age 65 years, mean LVEF 0.29, mean QRS width 174 ms) underwent successful CRT, from the anterior (A) CST in 21 patients, the anterolateral (AL) CST in 37 patients, the lateral (L) CST in 57 patients, the posterolateral (PL) CST in 40 patients, and the middle cardiac vein (MCV) CST in 3 patients. NYHA functional class, 6-minute walk test, and echocardiographic measurements were examined at baseline, and at 3, 6, and 12 months. Comparisons were made among all pacing sites or between lateral and septal sites by grouping AL + L + PL CST as lateral site (134 patients, 85%) and A + MC CST as septal site (24 patients, 15%). In patients stimulated from lateral sites, LVEF increased from 0.30 to 0.39 (P < 0.0001), 6-minute walk test from 323 to 458 m (P < 0.0001), and the proportion of NYHA Class III-IV patients decreased from 82% to 10% (P < 0.0001). In patients stimulated from septal sites, LVEF increased from 0.28 to 0.41 (P < 0.0001), 6-minute walk test from 314 to 494 m (P < 0.0001), and the proportion of NYHA Class III-IV patients decreased from 75% to 23% (P < 0.0001). A significant improvement in cardiac function and increase in exercise capacity were observed over time regardless of the LV stimulation sites, either considered singly or grouped as lateral versus septal sites.

The flecainide test is widely used in Brugada syndrome. However, its reproducibility and safety remain ill-defined. This study included 22 patients (18 men, mean age 34 years). Mutations in the SCN5A gene were found in eight patients. Two patients had aborted sudden cardiac death, 8 had syncope/presyncope, and 12 were asymptomatic. The ECG was diagnostic in 19 patients and suggestive in 3. At baseline, 21 of 22 patients underwent a flecainide test (2 mg/kg IV bolus over 10 minutes). In 21 of 21 patients the test was diagnostic or amplified the typical ECG pattern. At the end of drug infusion, sustained VT lasting 7-10 minutes developed in two patients. A second flecainide test was performed within 2 months in 20 patients. The test was not repeated in the two patients with prior development of VT. The flecainide test was diagnostic in 20 of 20 patients. Sustained VT occurred in one patient and recurrent VF in another. The reproducibility of the flecainide test was 100%. In 4 (18%) of 22 patients major VAs were documented after the end of flecainide infusion. VA occurred in 3 (43%) of 7 patients with, versus 1 (7%) 15 without SCN5A gene mutation (P < 0.05). No diagnostic ECG changes or arrhythmias developed in 25 control patients without structural heart disease who underwent the same study protocol. This study shows a high flecainide reproducibility, supporting its diagnostic value in Brugada syndrome. However, the occurrence of major VA, significantly higher in patients with documented SCN5A gene mutation, including in asymptomatic patients, mandates the performance under appropriate medical supervision. Whether a slower rate of drug infusion can lower the risk of VA induction, while maintaining the sensitivity of the test should be explored.

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