Hibernating substrate of ventricular tachycardia: a three-dimensional metabolic and electro-anatomic assessment

Hibernating myocardium (HM) is associated with sudden cardiac death (SCD). Little is known about the electrophysiological properties of HM and the basis of its association with SCD. We aimed to electrophysiologically characterize HM in patients with ventricular tachycardia (VT).

Endocardial voltage mapping, metabolic ¹⁸FDG-positron emission tomography (PET) and perfusion ⁸²Rb, ²⁰¹Tl, or ^99mTc scans were performed in 61 ischemic heart disease patients with VT. Hibernating areas were identified which was followed by three-dimensional PET reconstructions and integration with voltage maps to allow hybrid metabolic-electro-anatomic assessment of the arrhythmogenic substrate.

Of 61 patients with ischemic heart disease and refractory VT, 7 were found to have hibernating myocardium (13%). A total of 303 voltage points were obtained within hibernating myocardium (8.2 points per 10 cm²) and displayed abnormal voltage in 48.5 and 78.3% of bipolar and unipolar recordings, respectively, with significant heterogeneity of bipolar (p < 0.0001) and unipolar voltage measurements (p = 0.0004). Hibernating areas in 6 of 7 patients contained all three categories of bipolar voltage-defined scar (<0.5 mV), border zone (0.5-1.5 mV), and normal myocardium (>1.5 mV). The characteristics of local electrograms were also assessed and found abnormal in most recordings (76.6, 10.2% fractionated, 5.3% isolated potentials). Exit sites of clinical VTs were determined in 6 patients, of which 3 were located within hibernating myocardium.

Hibernating myocardium displays abnormal and heterogeneous electrical properties and seems to contribute to the substrate of VT. These observations may underlie the vulnerability to reentry and SCD in patients with hypoperfused yet viable myocardium.