Factors determining programmed stimulation responses and long-term arrhythmic outcome in survivors of ventricular fibrillation with ischemic heart disease

The clinical and angiographic features of 38 patients with ischemic heart disease and nonacute infarction pre-hospital ventricular fibrillation (VF) were examined as a function of their drug-free programmed electrical stimulation (PES) responses. Twenty-two patients (58%) had inducible ventricular tachycardia (VT) at drug-free PES (group I) and 16 patients (42%) did not (group II). Group I had more patients with: (1) remote infarction (22 of 22 vs 2 of 16; p < 0.01; (2) history of congestive failure (16 of 22 vs 0 of 16; p < 0.01); (3) prior cardiac arrest (11 of 22 vs 0 of 16; p < 0.01); (4) left ventricular (LV) ejection fraction < 40% (19 of 22 vs 1 of 16; p < 0.01); and (5) akinetic or dyskinetic LV wall motion (22 of 22 vs 2 of 16; p < 0.001). Group II had more patients with: (1) LV segments at “ischemic jeopardy” (16 of 16 vs 14 of 22; p < 0.01) and (2) factors suggestive of ischemia at the onset of VF (13 of 16 vs 1 of 22; p < 0.001). Inducible VT (IVT) was suppressed in 16 of the 20 group I patients surviving hospitalization while four were discharged with persistence of IVT despite therapy. At 27 ± 15 months, all four with persistent IVT had a recurrence of their arrhythmia. In the 16 group II patients, therapy was limited to antilschemic measures: coronary bypass in 12, propranolol in 3, and angioplasty in one. At 38 ± 9 months, no group II patient has had a recurrence of his arrhythmia. In patients with coronary disease and nonacute infarction VF: (1) absence of IVT at drug-free PES is a common finding; (2) patients free of IVT typically have features that implicate acute ischemia in the pathogenesis of VF; and (3) the outcome of such patients is excellent when antilschemic therapy is empioyed. IVT at drug-free PES is typically limited to patients with markers of LV dysfunction. Arrhythmogenesis in the inducible patient appears to derive from a state of chronic electrical instability caused by prior myocardial infarction.