Corrected QT (QTc) is an important electrocardiographic (ECG) interval. Physicians rely on automated QTc provided by ECG machines while the manual method is the recommended method. We sought to assess the prevalence and predictors of false positive QTc prolongation by the automated measurement.

Consecutive ECGs were retrieved from the ECG database at King Khaled University Hospital. Manual QT was measured by a trained physician using the tangent method and was corrected for heart rate and QRS duration. Automated QTc measurement was recorded by the ECG machine. "Long QT (LQT)" was defined as QTc≥470 ms for males and ≥480 for females. False positive LQT was defined as LQT by automated QTc but not manual QTc. Pre-determined factors were included in a multivariate logistic regression to assess predictors of false positive LQT. A total of 567 ECGs were included in this study. Automated QTc was longer than manual QTc (440 ms [±35] vs. 417 ms [±35], respectively) which resulted in a high negative predictive value (NPV) (99%) and a low positive predictive value (PPV) (32%). Male gender and abnormal rhythm were found to be independently associated with false positive LQT (OR = 1.9 [95% 1.1-3.5], p = 0.03 and OR = 3.1 [95% 1.2-8.3], p = 0.02; respectively).

Automated QTc measurement is unreliable for detecting long QT, necessitating manual verification and further research to enhance its accuracy.

The relationships between heart rates (HR) and corresponding PR intervals (PR) were studied in 12 healthy young subjects during rest, standing and graduated treadmill exercise to heart rates of 160 to 170 beats min-1 and during the infusion of isoprenaline to heart rates of 100 to 110 beats min-1. During exercise, PR diminished with increasing HR. Over the range of HR from 60 to 160 beats min-1 all 12 individual subjects exhibited negative linear correlations between HR and PR described by the equation: PR (ms) = -0.351 HR (beats min-1) + 176.7 for composite data. During isoprenaline infusion the PR interval also diminished with increasing heart rate. Over the range of HR from 60 to 110 beats min-1, 11 of the 12 subjects exhibited negative linear correlations between HR and PR described by the equation: PR (ms) = -0.582 HR (beats min-1) + 186.5 for composite data. The exercise model was used to study the indirect (or rate-dependent) effects and the direct actions on atrioventricular conduction of beta-adrenoceptor blocking drugs and calcium channel antagonists, alone and in combination, in three groups of healthy subjects. Control and placebo observations on HR and PR at rest, standing and during exercise in these additional subjects also exhibited individual inverse linear relationships between HR and PR. Following the administration of beta-adrenoceptor blockers, PR were prolonged more than expected at the HR observed. Rate-adjusted PR prolongation during exercise exceeded standing which exceeded resting, indicating greater beta-adrenoceptor blockade in atrioventricular nodal tissue than in sinoatrial nodal tissue at each level of activity.(ABSTRACT TRUNCATED AT 250 WORDS)