Risk of sudden cardiac arrest and ventricular arrhythmia with sulfonylureas: An experience with conceptual replication in two independent populations.

Sulfonylureas are commonly used to treat type 2 diabetes mellitus. Despite awareness of their effects on cardiac physiology, a knowledge gap exists regarding their effects on cardiovascular events in real-world populations. Prior studies reported sulfonylurea-associated cardiovascular death but not serious arrhythmogenic endpoints like sudden cardiac arrest (SCA) or ventricular arrhythmia (VA). We assessed the comparative real-world risk of SCA/VA among users of second-generation sulfonylureas: glimepiride, glyburide, and glipizide. We conducted two incident user cohort studies using five-state Medicaid claims (1999-2012) and Optum Clinformatics commercial claims (2000-2016). Outcomes were SCA/VA events precipitating hospital presentation. We used Cox proportional hazards models, adjusted for high-dimensional propensity scores, to generate adjusted hazard ratios (aHR). We identified 624,406 and 491,940 sulfonylurea users, and 714 and 385 SCA/VA events, in Medicaid and Optum, respectively. Dataset-specific associations with SCA/VA for both glimepiride and glyburide (vs. glipizide) were on opposite sides of and could not exclude the null (glimepiride: aHRMedicaid 1.17, 95% CI 0.96-1.42; aHROptum 0.84, 0.65-1.08; glyburide: aHRMedicaid 0.87, 0.74-1.03; aHROptum 1.11, 0.86-1.42). Database differences in data availability, populations, and documentation completeness may have contributed to the incongruous results. Emphasis should be placed on assessing potential causes of discrepancies between conflicting studies evaluating the same research question.

Ventricular fibrillation with intracoronary adenosine during fractional flow reserve assessment.

Fractional flow reserve (FFR) measurement provides useful hemodynamic assessment of intermediate coronary stenoses affecting long term outcomes. While the gold standard remains intravenous adenosine, intracoronary (IC) bolus administration of adenosine is routinely used in clinical practice because of its ease of use and lower dose providing comparative hyperemia with the most common side effect being a transient atrioventricular block. A 62year old male underwent left heart catheterization after ruling in for non-ST elevation myocardial infarction (NSTEMI). Presenting electrocardiogram (ECG) showed an old left bundle branch block and T-wave inversions in lateral leads (QTc 494ms) with no significant electrolyte abnormalities. Coronary angiography revealed an intermediate lesion in mid left anterior descending coronary artery. FFR assessment with IC adenosine (24µg/mL of normal saline) was performed inducing ventricular fibrillation (VF). He was successfully defibrillated with a single 200J shock and no further arrhythmias were noticed during rest of his hospital stay.

Ventricular fibrillation induction and diffuse abnormal ST-segment response to ajmaline in a patient with apparent pre-existing dynamic right bundle branch block.

OBJECTIVE: ST-segment elevation in the right precordial electrocardiography (ECG) leads in Brugada syndrome (BS) can be unmasked by class I anti-arrhythmic drugs (sodium channel blockers) administration. It is still debated whether this ECG pattern is better explained by abnormal repolarization or ventricular conduction and depolarization. Conduction diseases can conceal type 1 BS-like ECG in standard V1-V3 leads. ECG alterations were found also in alternative leads. The role of electrophysiology study (EPS) in sudden cardiac death risk stratification remains controversial, and could depend on the phenotypic expression of the cardiac sodium channels disease. CASE REPORT: We describe unmasked diffuse J-point and ST-segment anomalies in peripheral and precordial ECG leads and ventricular fibrillation (VF) induction by EPS after ajmaline administration in a patient with pre-existing atypical right bundle branch block (RBBB) concealing subtle anomalies in standard V1-V3 leads. RBBB was influenced by the underlying BS-like ECG associating repolarization anomaly and pre-existing conduction disease. EPS induced VF when RBBB was associated with BS-like ECG, and failed to induce VF when RBBB was present alone. CONCLUSIONS: BS phenotype heterogeneity requires further studies to improve the knowledge of its pathophysiological mechanisms associated with conduction diseases in order to better identify an individual therapy and prognostic stratification.