Differences in electrophysiological substrate in patients with coronary artery disease and cardiac arrest or ventricular tachycardia. Insights from endocardial mapping and signal-averaged electrocardiography.

BACKGROUND

Many studies have combined patients with hemodynamically well-tolerated ventricular tachycardia (VT) and those with cardiac arrest (CA) as a single, homogenous group. Recent studies suggest that these two groups have different electrophysiological substrates and responses to therapy. Most of these studies, however, enrolled patients with a variety of cardiac diagnoses.

METHODS AND RESULTS

We used signal-averaged electrocardiography (SAECG) and endocardial catheter mapping to define the electrophysiological substrate in patients with coronary artery disease and VT or CA and correlate the results of the two methods. We also examined the usefulness of SAECG in CA patients to differentiate those with inducible arrhythmias from those who are noninducible. VT patients were more likely to have had a prior myocardial infarction (p = 0.0005) and to have inducible arrhythmias (p = 0.0001) than were CA patients. The induced arrhythmias in patients who presented with VT was VT in more than 90% of cases, whereas in CA patients, polymorphic ventricular tachycardia (PMVT) accounted for one third of induced arrhythmias. Mean filtered QRS duration was longer (135 versus 120 msec) and the terminal QRS voltage was smaller (20 versus 34 microV) in VT than in CA patients (p less than 0.01). Sixty-three percent of CA patients and 87% of VT patients had abnormal SAECG (p = 0.001). VT patients had more extensive endocardial abnormalities and more abnormal (53% versus 40%, p = 0.002), fractionated (8% versus 3%, p = 0.02), late (17% versus 8%, p = 0.0003), and late abnormal or fractionated (14% versus 4%, p = 0.0001) sites than CA patients. VT patients had a greater duration of the longest electrogram (129 versus 109 msec, p = 0.0006) and total endocardial activation time (68 versus 54 msec, p = 0.009). Among CA patients, those with induced VT had more extensive substrate than did those with induced PMVT and were similar to VT patients with induced VT. Among CA patients, the trend for more patients with inducible VT (77%) or PMVT (55%) than noninducible patients (47%) to have an abnormal SAECG did not reach statistical significance (p = 0.14). The positive and negative predictive values of an abnormal SAECG were 77% and 44%, respectively.

CONCLUSIONS

VT patients have more extensive endocardial substrate than CA patients, which translates into greater and more frequent SAECG abnormalities. Among CA patients, there are significant differences in substrate between patients with induced VT and those with induced PMVT. SAECG is not useful in differentiating CA patients who have inducible VT or PMVT from those who do not.