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Previous studies have demonstrated that infarct volume and global sympathetic denervation predict total appropriate implantable cardiac defibrillator (ICD) therapies. Nevertheless, this composite endpoint overestimates the much lower frequency of sudden death. We hypothesized that different substrates could distinguish patients with sudden cardiac arrest or equivalent (SCAE, arrhythmic death or ICD discharge for fast VT >240 bpm or ventricular fibrillation) from those with ICD shocks for slow VT (≤ 240 bpm).
The NIH sponsored PAREPET trial (Prediction of ARrhythmic Events with Positron Emission Tomography) enrolled 204 subjects with ischemic cardiomyopathy eligible for an ICD for the primary prevention of SCA. Denervated, viable denervated, infarcted and hibernating myocardium were quantified as % LV with PET (with 11C-hydroxyephedrine, 13N-ammonia and 18F-2-deoxyglucose). The primary endpoint was SCAE.
SCAE (n = 33) or ICD shock for slow VT (n = 20) occurred in 26% of patients at 4.1 years. The 53 patients with arrhythmic events had a lower ejection fraction (EF, 24 ± 8 vs. 28 ± 9%, p = 0.001) and greater infarct volume (22 ± 8 vs. 19 ± 9%, p = 0.08) than those without arrhythmic events. Nevertheless, neither parameter could distinguish SCAE from slow VT (EF 24 ± 8 vs. 23 ± 9%, p = 0.52; Infarct 22 ± 7 vs. 22 ± 9%, p = 0.96; respectively). In contrast, sympathetic denervation was significantly greater in those with SCAE than those with slow VT (33 ± 10 vs. 26 ± 9%, p = 0.03), reflecting a much larger volume of viable denervated myocardium (10 ± 6 vs. 6 ± 4%, p = 0.02). Furthermore, volume of denervated myocardium in the slow VT group was no different than those without arrhythmic events (26 ± 11%, p = 0.87 vs. slow VT). Hibernating myocardium was similar in all groups, averaging 3% of the LV.
These data indicate that infarct volume does not distinguish patients with SCAE from those with slow VT. In contrast, greater volumes of denervated and viable denervated myocardium predict SCAE, but not slow VT. This is consistent with a different substrate for slow VT, and suggests that slow VT may not be an appropriate surrogate endpoint for SCAE.
West, Room 3001
Sunday, March 10, 2013, 11:15 a.m.-11:30 a.m.
Session Title: Nuclear Cardiology and PET: Pushing the Boundaries
Abstract Category: 21. Imaging: Nuclear
Presentation Number: 926-5
- 2013 American College of Cardiology Foundation