Putthapiban, Prapaipan

Gastrointestinal bleeding (GIB) especially from arteriovenous malformations (AVM) remains one of the devastating complications following continuous-flow left ventricular device (CF-LVAD) implantation. Blockade of angiotensin II pathway using angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB) was reported to mitigate the risk of GIB and AVM-related GIB by suppressing angiogenesis. We performed a systematic review and meta-analysis to evaluate the association between ACEI/ARB treatment and GIB in CF-LVAD population. Comprehensive literature search was performed through December 2019. We included studies reporting risk of GIB and/or AVM-related GIB events in LVAD patients who received ACEI/ARB with those who did not. Data from each study were combined using the random-effects to calculate odd ratios and 95% confidence intervals. Three retrospective cohort studies were included in this meta-analysis involving 619 LVADs patients (467 patients receiving ACEI/ARB). The use of ACEI/ARB was statistically associated with decreased incidence of overall GIB (pooled OR 0.35, 95% CI 0.22–0.56, I 2 = 0.0%, p < 0.001). There was a non-significant trend toward lower risk for AVM-related GIB in patients who received ACEI/ARB (pooled OR 0.46, 95% CI 0.19–1.07, I 2 = 51%, p = 0.07). Larger studies with specific definitions of ACEI/ARB use and GIB are warranted to accurately determine the potential non-hemodynamic benefits of ACEI/ARB in CF-LVAD patients.

AbstractIntroductionBrugada syndrome (BrS) is associated with ventricular arrhythmia leading to sudden cardiac death. Risk stratification is challenging, as major arrhythmic events (MAEs) are rare. We assessed the utility of drug challenge testing in BrS by a systematic review and meta‐analysis.Methods and ResultsWe comprehensively searched the databases of MEDLINE and EMBASE from inception to May 2019. Included studies compared the incidence of MAE between spontaneous and drug challenge–induced Type 1. Mixed‐effects Poisson regression was used to calculate the incidence rate ratio (IRR). Eighteen studies from 2006 to 2018 were included (4099 patients, mean follow‐up: 4.5 years). Pooled annual incidences of MAE in spontaneous, drug challenge induced (regardless of symptoms), asymptomatic drug challenge induced, and symptomatic drug challenge–induced Type 1 were 23.8 (95% confidence interval [CI]: 19.8–27.8), 6.5 (95% CI: 3.9–9.1), 2.1 (95% CI: −0.3 to 4.4), and 19.6 (95% CI: 9.9–29.3) per 1000 person‐years, respectively. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type 1 was not statistically different (IRR = 1.0; 95% CI: 0.6–1.7).ConclusionsThe incidence of MAE in drug challenge–induced Type 1 in asymptomatic patients is low. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type 1 was similar.

Introduction: Brugada syndrome is associated with ventricular arrhythmia leading to sudden cardiac death. Risk stratification is challenging, as major arrhythmic events (MAE) are rare. We assessed the utility of drug challenge testing in Brugada syndrome by a systematic review and meta-analysis. Methods and results: We comprehensively searched the databases of MEDLINE and EMBASE from inception to May 2019. Included studies compared the incidence of MAE between spontaneous and drug challenge induced Type-1. Data were combined using the random-effects, generic inverse variance method, to calculate pooled incidence and odds ratio (OR). Mixed-effects Poisson regression was used to calculated incidence rate ratio (IRR). Eighteen studies from 2006 to 2018 were included (4,099 patients, mean follow-up 4.5 years). Pooled annual incidences of MAE in spontaneous, drug challenge induced (regardless of symptoms), asymptomatic drug challenge induced, and symptomatic drug challenge induced Type-1 were 23.8 (95% confidence interval [CI]: 19.8-27.8), 6.5 (95% CI: 3.9-9.1), 2.1 (95% CI: -0.3-4.4), and 19.6 (95% CI: 9.9-29.3) per 1,000 person-years respectively. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type-1 was not statistically different (IRR=1.0, 95%CI: 0.6-1.7). The presence of ventricular tachyarrhythmia during drug challenge testing was a predictor of MAE (OR=3.73, 95% CI: 1.77-7.86, p=0.001). Conclusions: The incidence of MAE in drug challenge induced Type-1 in asymptomatic patients is low. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type-1 was similar. Ventricular tachyarrhythmia during drug challenge testing could be a useful risk marker for MAE in Brugada syndrome.