Effects of thrombolysis on vectorcardiographic indices of ventricular repolarization: correlation with ST-segment resolution.

To investigate the effects of thrombolysis on vectorcardiographic (VCG) descriptors of ventricular repolarization in association with ST-segment resolution, 70 consecutively recruited patients with acute myocardial infarction underwent digital 12-lead electrocardiograms (ECGs) before and at 3 hours after thrombolysis. The alterations in the VCG descriptors spatial T amplitude and spatial QRS-T angle from the pre- to the post-thrombolysis ECG, as well as the ST-segment resolution, were calculated. Angiography revealed patency of the infarct-related coronary artery after thrombolysis in 52 (74%) patients (group A) and occlusion in 18 (26%) (group B). The spatial T amplitude was highly significantly reduced after thrombolysis in group A (P<.0001), but only marginally reduced in group B (P=.016). The spatial QRS-T angle was also significantly, although only marginally, reduced after thrombolysis in group A (P=.019), whereas it was not changed after thrombolysis in group B (P=.868). An ST-segment resolution of 60% and a 25% reduction in the spatial T amplitude after thrombolysis were able to identify patency of the infarct-related coronary artery with sensitivities of 90% and 77% and specificities of 94% and 74%, respectively. Both VCG descriptors were significantly affected by thrombolysis in patients with acute myocardial infarction, but constituted only moderate markers of thrombolysis efficacy, as evidenced by the presence of patency in the infarct-related coronary artery, compared with the ST-segment resolution.

Ibutilide-induced alterations in electrocardiographic and spatial vectorcardiographic descriptors of ventricular repolarization.

BACKGROUND: Ibutilide is used for the pharmacologic cardioversion of atrial fibrillation (AF) or flutter (AFl). Ibutilide-induced QT interval prolongation has been demonstrated previously. However, its effects on vectorcardiographic (VCG) descriptors of ventricular repolarization (VR) have not been studied so far. HYPOTHESIS: To evaluate the effects of ibutilide on electrocardiographic (ECG) and VCG descriptors of VR, one or two repeated 10-min infusions of 1 mg of ibutilide were given in 50 consecutively recruited patients (36 women, mean age 69.4 +/- 9.3 years) with AF or AFl of recent onset. METHODS: The maximum and the minimum QT intervals, QT dispersion, the rate-corrected QT maximum, and the spatial VCG descriptors, spatial T amplitude, and spatial QRS-T angle were calculated before (baseline ECG) and 30 min after the start of ibutilide infusion (postinfusion ECG). RESULTS: After ibutilide infusion, 40 (80%) patients were cardioverted to sinus rhythm (Group 1), while in the remaining 10 (Group 2) AF or AFl persisted. In both study groups, temporal measures of VR were significantly increased from baseline to the postinfusion ECG. In Group 1, spatial T amplitude and spatial QRS-T angle did not differ between those two ECGs, while in Group 2 spatial T amplitude was significantly increased (p = 0.005) and spatial QRS-T angle was significantly decreased (p = 0.002) post infusion compared with baseline ECG. CONCLUSIONS: While temporal measures of VR are significantly affected in all patients who receive ibutilide infusion for AF or AFl cardioversion, spatial VCG descriptors of VR are significantly altered only in those patients who fail to respond to the drug. A dose-related effect of ibutilide on the different aspects of VR should be suspected.

Exercise-induced prolongation of the infarct-related Q-waves as a marker of myocardial viability in the infarcted area.

OBJECTIVE: It is known that exercise-induced ischemia in patients with coronary artery disease (CAD) may produce QRS prolongation in the surface electrocardiogram (ECG). To investigate the presence of exercise-induced Q-wave prolongation in patients with single-vessel CAD and Q-wave myocardial infarction (MI), in association with the presence of reversible perfusion defects during thallium scintigraphy in the infarcted area. METHODS: 107 consecutive patients (89 males, mean age 56+/-8 years) were evaluated. All patients underwent coronary arteriography, maximal treadmill exercise testing and thallium-201 scintigraphy. Q-wave duration was measured both before exercise testing and during maximal heart rate from 12-lead ECGs recorded with a paper speed of 50 mm/s. RESULTS: Only 57 out of the 107 studied patients showed reversible perfusion defects in the infarcted area during thallium scintigraphy. Q-wave duration was significantly increased from the resting to the stress ECG (DeltaQ-wave duration) in patients with reversible perfusion defects in the infarcted areas (10+/-13 ms), but not in patients with fixed defects in the infarcted zone (-2.0+/-5 ms, p<0.01). The sensitivities and the specificities of Q-wave prolongation, ST segment elevation, and the combination of ST segment elevation with ST segment depression in the reciprocal leads for the detection of myocardial viability in the infarcted area were 82%, 48%, 29% and 88%, 50%, and 90%, respectively. CONCLUSIONS: Exercise-induced Q-wave prolongation is demonstrated in those patients with single-vessel CAD and a recent MI who show reversible perfusion defects in thallium scintigraphy. Exercise-induced Q-wave prolongation was found to be a sensitive and specific ECG marker for the detection of myocardial viability in the infarcted area.