Predictive value of pre-procedural QTc interval for in-hospital major adverse cardiovascular events following primary percutaneous coronary intervention in acute myocardial infarction.

BACKGROUND: The relationship between pre-procedural corrected QT (QTc) interval and in-hospital major adverse cardiovascular events (MACE) following primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) remains incompletely understood. This study evaluated the predictive value of pre-procedural QTc for in-hospital MACE.

METHODS: This single-center retrospective cohort study consecutively enrolled AMI patients undergoing primary PCI. QTc intervals were manually measured from pre-procedural 12-lead electrocardiograms using the Bazett formula, with a prespecified sensitivity analysis using the Fridericia formula. Missing data sensitivity analyses (complete-case BNP model and multiple imputation, m = 20) confirmed that BNP adjustment did not alter the QTc effect. No formal sample size calculation was performed; findings are exploratory. The primary endpoint was in-hospital MACE (composite of ventricular arrhythmias, cardiogenic shock, acute heart failure, and bleeding complications). Logistic regression and receiver operating characteristic (ROC) analyses were performed.Among 123 patients (mean age 55.3 ± 11.9 years; 91.1% male), 53 (43.1%) experienced MACE. Prolonged QTc (>440 ms) was associated with MACE in univariate analysis (OR = 3.01, 95% CI: 1.41-6.39, P = 0.004). After multivariate adjustment, reduced LVEF (OR = 0.76 per 5%, P = 0.019) and elevated baseline heart rate (OR = 1.57 per 10 bpm, P = 0.023) were independent predictors; continuous QTc was not (OR = 1.03 per 10 ms, P = 0.605). The model AUC was 0.767 (optimism-corrected AUC = 0.782; optimism = -0.014). Adding QTc to conventional risk factors yielded negligible incremental AUC (Δ = 0.001, P = 0.888). A numerically high MACE rate was observed in the small subgroup with both LVEF <40% and QTc >440 ms (9/11, 81.8%; 95% CI: 48.2%-97.7%), but the LVEF-QTc interaction was not statistically significant (P = 0.941), precluding any conclusion of synergistic risk. A prespecified sensitivity analysis excluding isolated bleeding events (cardiovascular MACE = 40/123, 32.5%) confirmed that LVEF remained independently predictive (OR = 0.73, P = 0.008) while QTc showed no independent association (P = 0.915) and no incremental value (ΔAUC = 0.000, P = 0.772). A further sensitivity analysis using the Fridericia formula abolished the univariate QTc-MACE association (OR = 1.23, P = 0.615 vs. OR = 3.01, P = 0.004 with Bazett), indicating that Bazett overcorrection at high heart rates contributed substantially to the apparent univariate signal. BNP adjustment (complete-case and multiple imputation) did not change the QTc coefficient (>1% variation), indicating no residual BNP confounding.

CONCLUSIONS: Pre-procedural QTc prolongation is associated with in-hospital MACE but is not an independent predictor after adjustment for conventional risk factors, with limited incremental value (ΔAUC = 0.001). A numerically high MACE rate was noted among patients with both reduced LVEF and prolonged QTc, but this observation derives from only 11 patients with a nonsignificant interaction term (P = 0.941); it should be regarded as exploratory and requires validation in larger prospective studies.