Increased Risk of Heart Failure in Elderly Patients Treated with Beta-Blockers After AV Node Ablation.

INTRODUCTION: Controversy exists regarding the indication of beta-blockers (BB) in different scenarios in patients with cardiovascular disease. We sought to evaluate the effect of BB on survival and heart failure (HF) hospitalizations in a sample of pacemaker-dependent patients after AV node ablation to control ventricular rate for atrial tachyarrhythmias. METHODS: A retrospective study including consecutive patients that underwent AV node ablation was conducted in a single center between 2011 and 2019. The study's primary endpoints were the incidence of all-cause mortality, first HF hospitalization and the cumulative incidence of subsequent hospitalizations for HF. Competing risk analyses were employed. RESULTS: A total of 111 patients with a mean age of 73.9 years were included in the study. After a median follow-up of 45.5 months, 43 patients had died (38.7%) and 31 had been hospitalized for HF (27.9%). The recurrent HF hospitalization rate was 74/1000 patients/year. Patients treated with BB had a non-significant trend to higher mortality rates and a higher risk of recurrent HF hospitalizations (incidence rate ratio 2.23, 95% confidence interval 1.12-4.44; p = 0.023). CONCLUSION: After an AV node ablation, the use of BB is associated with an increased risk of HF hospitalizations in a cohort of elderly patients.

Lessons learned in attempting catheter-based interatrial electrical disconnection for nonpharmacologic rate control of atrial fibrillation or flutter.

PURPOSE: Ablation of atrioventricular (AV) conduction and pacemaker implantation is the therapy of last resort for symptomatic atrial tachyarrythmias when rhythm and rate control fail, but is far from ideal. To evaluate whether interatrial electrical disconnection as a result of catheter ablation is feasible and of potential clinical utility as a means of non-pharmacological heart rate control. METHODS: Eleven patients with medically refractory atrial fibrillation or left atrial flutter and symptomatic rapid ventricular response were included. The ablation strategy consisted primarily of right atrial ablation of the interatrial electrical connections, which were located by electroanatomical activation maps performed during coronary sinus stimulation. Successive activation maps were performed as each connection was blocked. If the procedure was considered unsuccessful AV nodal ablation was performed. RESULTS: The coronary sinus ostium was earliest in 10/11 and could be ablated in 5/10 patients. Interatrial conduction block was only achieved in one patient (9.1%). An unexpected AV nodal modulation with an increase in the Wenckebach cycle length (> 50 ms) occurred in 8/11 patients. These patients remained without pacemaker implantation and only 1/8 required AV nodal ablation during the 1-year follow-up. Quality of life questionnaires indicated significant improvement in patients with AV nodal modulation. CONCLUSION: Interatrial electrical disconnection by right atrial catheter ablation is a not feasible with present day technology. The extensive right atrial septal ablation performed resulted in significant AV nodal modulation in most patients, which persisted and resulted in improvement in quality of life.

[Minimum salvaged myocardium after rescue percutaneous coronary intervention: quantification by cardiac magnetic resonance]. / Miocardio rescatado tras angioplastia coronaria de rescate: cuantificación mediante resonancia magnética cardiaca.

INTRODUCTION AND OBJECTIVES: When fibrinolysis fails in patients with ST elevation myocardial infarction, they are referred for a rescue percutaneous coronary intervention (PCI). However, there is still no evidence of how much myocardium potentially at risk we can actually salvage after rescue PCI. METHODS: Fifty consecutive patients. Cardiac magnetic resonance was performed within 6 days. Myocardial necrosis was defined by the extent of abnormal late enhancement, myocardium at risk by extent of edema, and the amount of salvaged myocardium by the difference between myocardium at risk and myocardial necrosis. Finally, myocardial salvage index (MSI) resulted from the fraction (area-at-risk minus infarct-size)/area-at-risk. RESULTS: The mean time elapsed between pain onset and fibrinolitic agent administration was 176 ± 113 min; time lysis-rescue=PCI 209 ± 122 min; time pain onset-PCI = 390 ± 152 min. The area at risk was 37% ± 13% and infarct size 34.5% ± 13%. Salvaged myocardium was 3% ± 4% and MSI 9 ± 8. Salvaged myocardium and MSI were similar between patients with the artery open on arrival at the catheterization lab (Thrombolysis in Myocardial Infarction [TIMI] 3) and those with TIMI flow ≤ 2 (3.3% ± 3.6% and 8.2 ± 6.9 in TIMI 0-2 vs 3.0% ± 3.7% and 10.8 ± 10.9 in TIMI 3; P=.80 and 0.31, respectively). No significant difference was observed between patients who went through rescue PCI within a shorter time and those with longer delay times. CONCLUSIONS: The myocardial salvage after rescue PCI quantified by cardiac magnetic resonance is very small. The long delay times between pain onset and the opening of the infarct-related artery with PCI are most probably the reason for such a minimal effect of rescue PCI.