Higher incidence of vasodilator-induced left ventricular cavity dilation by PET when compared to treadmill exercise-ECHO in hypertrophic cardiomyopathy

• Published in: Journal of nuclear cardiology 2020-12, Vol.27 (6), p.2031-2043
• Main Authors: Lu, Dai-Yin, Yalçin, Hulya, Sivalokanathan, Sanjay, Greenland, Gabriela V., Vasquez, Nestor, Yalçin, Fatih, Zhao, Min, Valenta, Ines, Ganz, Peter, Pampaloni, Miguel Hernandez, Zimmerman, Stefan, Schindler, Thomas H., Abraham, Theodore P., Abraham, M. Roselle
• Format: Article
• Language: English
• Subjects: Adult; Aged; Cardiology; Cardiomyopathy; Cardiomyopathy, Hypertrophic - diagnostic imaging; Cardiomyopathy, Hypertrophic - epidemiology; echocardiography; Echocardiography - methods; Ejection fraction; Exercise; Exercise Test - methods; Female; Genotype; Heart Ventricles; Humans; Hypertrophic cardiomyopathy; Hypertrophy, Left Ventricular - complications; Imaging; Incidence; left ventricular cavity dilation; Male; Medicine; Medicine & Public Health; Microcirculation; Middle Aged; Muscular Diseases; Myocardial Ischemia; Nuclear Medicine; Original Article; Patients; positron emission tomography; Positron Emission Tomography Computed Tomography - methods; Positron-Emission Tomography - methods; Radiology; Registries; Retrospective Studies; strain; Vasodilator Agents - adverse effects
• ISSN: 1071-3581; 1532-6551
• DOI: 10.1007/s12350-018-01521-x

Vasodilator-induced transient left ventricular cavity dilation (LVCD) by positron emission tomography (PET) is associated with microvascular dysfunction in hypertrophic cardiomyopathy (HCM). Here we assessed whether HCM patients who develop LVCD by PET during vasodilator stress also develop LV cavity dilation by echocardiography (ECHO-LVCD) following exercise stress. A retrospective analysis of cardiac function and myocardial blood flow (MBF) was conducted in 108 HCM patients who underwent perfusion-PET and exercise-ECHO as part of their clinical evaluation. We performed a head-to-head comparison of LV volumes and ejection fraction (LVEF) at rest and stress (during vasodilator stress, post-exercise), in 108 HCM patients. A ratio > 1.13 of stress to rest LV volumes was used to define PET-LVCD, and a ratio > 1.17 of stress to rest LVESV was used to define ECHO-LVCD. Patients were divided into 2 groups based on the presence/absence of PET-LVCD. MBF and myocardial flow reserve were quantified by PET, and global longitudinal strain (GLS) was assessed by ECHO at rest/stress in the two groups. PET-LVCD was observed in 51% (n = 55) of HCM patients, but only one patient had evidence of ECHO-LVCD (ratio = 1.36)—this patient also had evidence of PET-LVCD (ratio = 1.20). The PET-LVCD group had lower PET-LVEF during vasodilator stress, but ECHO-LVEF increased in both groups post-exercise. The PET-LVCD group demonstrated higher LV mass, worse GLS at rest/stress, and lower myocardial flow reserve. Incidence of ischemic ST-T changes was higher in the PET-LVCD group during vasodilator stress (42 vs 17%), but similar (30%) in the two groups during exercise. PET-LVCD reflects greater degree of myopathy and microvascular dysfunction in HCM. Differences in the cardiac effects of exercise and vasodilators and timing of stress-image acquisition could underlie discordance in ischemic EKG changes and LVCD by ECHO and PET, in HCM.