BACKGROUND: Left ventricular assist devices (LVADs) have been used as a bridge to cardiac transplantation and as destination therapy in patients with advanced heart failure. The period after LVAD support is associated with ventricular arrhythmias (VAs) despite ventricular unloading and such VAs can have a detrimental effect on survival. Despite the increasing use of LVAD, little is known regarding post-LVAD VAs at the molecular level and in vivo. METHODS: Forty-two patients who received LVAD over a 24-month period were evaluated and grouped on the basis of the presence or absence of VAs during LVAD support. We completed a comparative microarray analyses between six patients who developed ventricular tachycardia (VT) or ventricular fibrillation (VF) after LVAD support and six patients who did not develop VAs after LVAD. RESULTS: VAs occurred in 15 patients (35.7%) during LVAD support at a median post-LVAD day of 25.2. VAs were strongly associated with nonusage of a beta-blocker post-LVAD (odds ratio of 7.04, P-value = 0.001). Analysis of a subset of patients who had VT or VF after LVAD placement showed a decrease in the expression of connexin 43 (0.48 +/- 0.07), Na+/K+-ATPase (0.60 +/- 0.05), and voltage-gated K+ channel Kv4.3 (0.42 +/- 0.04), and an increase in Na+/Ca2+ exchanger (2.2 +/- 0.4) and the structural genes: Titin (2.1 +/- 0.2), laminin (1.7 +/- 0.4), calsequestrin (1.8 +/- 0.5), skeletal muscle isoform of troponin T (5.1 +/- 0.9), and skeletal muscle isoform of troponin I (3.9 +/- 0.7). CONCLUSION: After LVAD, the increased risk of VAs is strongly associated with nonusage of beta-blocker postoperatively.
BACKGROUND: Left ventricular assist devices (LVADs) have been used as a bridge to cardiac transplantation and as destination therapy in patients with advanced heart failure. The period after LVAD support is associated with ventricular arrhythmias (VAs) despite ventricular unloading and such VAs can have a detrimental effect on survival. Despite the increasing use of LVAD, little is known regarding post-LVADVAs at the molecular level and in vivo. METHODS: Forty-two patients who received LVAD over a 24-month period were evaluated and grouped on the basis of the presence or absence of VAs during LVAD support. We completed a comparative microarray analyses between six patients who developed ventricular tachycardia (VT) or ventricular fibrillation (VF) after LVAD support and six patients who did not develop VAs after LVAD. RESULTS:VAs occurred in 15 patients (35.7%) during LVAD support at a median post-LVAD day of 25.2. VAs were strongly associated with nonusage of a beta-blocker post-LVAD (odds ratio of 7.04, P-value = 0.001). Analysis of a subset of patients who had VT or VF after LVAD placement showed a decrease in the expression of connexin 43 (0.48 +/- 0.07), Na+/K+-ATPase (0.60 +/- 0.05), and voltage-gated K+ channel Kv4.3 (0.42 +/- 0.04), and an increase in Na+/Ca2+ exchanger (2.2 +/- 0.4) and the structural genes: Titin (2.1 +/- 0.2), laminin (1.7 +/- 0.4), calsequestrin (1.8 +/- 0.5), skeletal muscle isoform of troponin T (5.1 +/- 0.9), and skeletal muscle isoform of troponin I (3.9 +/- 0.7). CONCLUSION: After LVAD, the increased risk of VAs is strongly associated with nonusage of beta-blocker postoperatively.
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