June 22, 2018

Absence of late gadolinium enhancement on cardiac magnetic resonance imaging in ventricular fibrillation and nonischemic cardiomyopathy

Structured PICO

Does the presence of late gadolinium enhancement on CMR correlate with ventricular fibrillation risk in patients with nonischemic cardiomyopathy?

Population

87 consecutively resuscitated ventricular fibrillation (VF) survivors undergoing contrast-enhanced 1.5T CMR, divided into nonischemic cardiomyopathy (NICM) (n=22), LV dilatation with normal LVEF (n=40), and normal LV size and LVEF (n=25). Exclusions: coronary artery disease, hypertrophic cardiomyopathy, amyloid, sarcoid, arrhythmogenic right ventricular cardiomyopathy, channelopathy, and preexisting ICD. Comparison groups included 277 NICM patients without prior VT/VF and 37 NICM patients with sustained monomorphic ventricular tachycardia (SMVT).

Intervention

Contrast-enhanced 1.5T cardiac magnetic resonance (CMR) imaging to identify late gadolinium enhancement (LGE)

Comparator

NICM patients without prior VT/VF and NICM patients with SMVT

Outcome

Incidence of late gadolinium enhancement (LGE) on CMRsurrogate

Most ventricular fibrillation survivors with nonischemic cardiomyopathy do not exhibit late gadolinium enhancement on CMR, indicating that the absence of LGE does not guarantee a benign prognosis regarding sudden cardiac death.

Abstract

INTRODUCTION: Cardiac magnetic resonance (CMR)-identified late gadolinium enhancement (LGE), representing regional fibrosis, is often used to predict ventricular arrhythmia risk in nonischemic cardiomyopathy (NICM). However, LGE is more closely correlated with sustained monomorphic ventricular tachycardia (SMVT) than ventricular fibrillation (VF). We characterized CMR findings of ventricular LGE in VF survivors. METHODS: We examined consecutively resuscitated VF survivors undergoing contrast-enhanced 1.5T CMR between 9/2007 and 7/2016. We excluded coronary artery disease, hypertrophic cardiomyopathy, amyloid, sarcoid, arrhythmogenic right ventricular cardiomyopathy, and channelopathy. Preexisting implantable cardioverter-defibrillator (ICD) was a CMR contraindication. VF patients were divided into three groups: (1) NICM, (2) left ventricular (LV) dilatation with normal LV ejection fraction (LVEF), and (3) normal LV size and LVEF. Two groups of NICM patients with and without SMVT were examined for comparison. RESULTS: We analyzed 87 VF patients, and found that LGE was seen in 8/22 (36%) with NICM (LVEF 38 ± 11%, LV end-diastolic volume index LVEDVI 134 ± 68 mL/BSA), 11/40 (28%) with LV dilatation and normal LVEF (LVEDVI 103 ± 17 mL/BSA), 4/25 (16%) with normal LV size and LVEF. Incidence of LGE in NICM patients without prior ventricular tachycardia/VF (LVEF 36 ± 12%, LVEDVI 141 ± 46 mL/body surface area BSA) was 117/277 and was not lower than those with VF and NICM (42% vs 36%; P = 0.59). By contrast, 22/37 NICM patients with SMVT (LVEF 42 ± 11%, LVEDVI 123 ± 48 mL/BSA) were LGE-positive (59% NICM-SMVT vs 36% NICM-VF; P = 0.04). CONCLUSION: Most VF survivors with a diagnosis of NICM did not have LGE on CMR and would not have met primary prevention ICD criteria based on LVEF. Absence of LGE may not portend a benign prognosis in NICM. Novel strategies for determining SCD risk in this cohort are required.

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