Stress-induced QTc-interval shortening as an ancillary marker of ischemia in patients with complete left bundle branch block.

BACKGROUND: In patients with left bundle branch block (LBBB), ischemia-induced repolarization changes associated with QTc-interval shortening may be recorded during coronary angioplasty. We aimed to assess whether these repolarization changes may be predictive of severe coronary artery disease in patients with LBBB. METHODS: Fifty noninfarcted LBBB patients underwent dipyridamole stress test and coronary angiography for chest pain. To localize the site of ischemia, we considered four groups of conventional ECG leads (V1-V2-V3; V4-V5-V6; aVL-I; III-aVF-II), exploring the anteroseptal, lateral, high-lateral, and inferior left ventricular walls. ST-T changes and QTc intervals were estimated at rest and peak stress, lead by lead, in each group of leads and the fractional percentage difference between rest-stress QTc intervals ([DELTA]QTc) was calculated. A [DELTA]QTc greater than -10% was used to define significant QTc-interval shortening. Coronary stenosis of more than 70% and more than 90% were considered 'significant' and 'severe'. RESULTS: According to dipyridamole stress test response, two groups were identified: group I (35 patients) with dipyridamole-induced ischemia and group II (15 patients) without dipyridamole-induced ischemia. The wall motion score index at peak stress (compared with resting wall motion score index) was significantly higher in group I (1.98 +/- 0.13 vs. 1.28 +/- 0.08, P < 0.0001) than in group II (1.36 +/- 0.18 vs. 1.25 +/- 0.08, P = 0.296). The patients of group I showed a significant QTc-interval shortening ([DELTA]QTc = -16.9 +/- 3.9%), whereas this did not happen in patients of group II ([DELTA]QTc = +8.8 +/- 2.4%, P < 0.0001). The patients of group I also had a more severe stenosis in the vessel related to the stress-induced dyssynergic area (I = 90.5 +/- 9.5 vs. II = 34.3 +/- 31.1%; P < 0.0001). CONCLUSION: In patients with LBBB, stress-induced pseudonormalization pattern, associated with QTc-interval shortening, allows the identification of cardiac areas supplied by severely stenosed coronary arteries.

Assessing the pattern of ST-segment depression during subendocardial ischemia using a computer simulation of the ventricular electrogram.

UNLABELLED: The primary aim of the study was to write a simple educational personal computer (PC)-based program able to simulate normal and pathological electrogram (EG) to analyze the ST-segment and T-wave patterns during subendocardial ischemia. BACKGROUND: The EG waveforms are know to depend on the properties of transmembrane action potentials (APs) of atrial and ventricular myocytes, the spread of excitation, and the characteristics of the volume conductor. Transmembrane AP is an electromotive generator that plays a central role, and it is the principal responsible for the potential differences that are recorded as an EG. The EG can be considered as the algebric sum of 2 transmembrane APs, that is, the AP of the underlying endocardial region minus the AP of the underlying epicardial region. METHODS: Using an educational PC software (Microsoft Excel), a normal EG was simulated reproducing planimetrically, point-by-point, normal transmembrane APs recorded from the epicardial and endocardial regions in normal animals. The shape and the voltage of the APs were then modified to closely mimic human APs. To simulate typical subendocardial ischemia, we changed the subendocardial AP according to experimental and clinical observations. RESULTS: The reconstruction of EG by the algebric subtraction (endocardial minus epicardial) APs was possible. The EG, mirroring typical subendocardial ischemia, was simulated without changing the epicardial AP. The EG simulating typical subendocardial ischemia showed a horizontal pattern of ST segment depression. In our model modification of the subendocardial AP combined with "unnatural" changes of the phase 3 of the subendocardial AP produced a downsloping pattern of ST-segment depression. CONCLUSION: The derivated EG waveform obtained with our PC program properly describe the algebric sum of endocardial and epicardial APs. In our opinion, this method represents a useful tool for the study of the AP changes. The simulated ST-depression morphology during subendocardial ischemia appears to be essentially "horizontal" and not downsloping. On the basis of our simplified theoretical model, we propose that ischemia-induced downsloping ST depression should be considered a reciprocal EG change and a manifestation of transmural ischemia in the wall opposite the exploring electrode.