Dai-Yin Lu1,2,3, Hulya Yalçin1, Sanjay Sivalokanathan1, Gabriela V Greenland1,4, Nestor Vasquez1, Fatih Yalçin1, Min Zhao5, Ines Valenta5, Peter Ganz4, Miguel Hernandez Pampaloni6, Stefan Zimmerman5, Thomas H Schindler5, Theodore P Abraham1,4, M Roselle Abraham7,8. 1. Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, MD, USA. 2. Division of Cardiology, Taipei Veterans General Hospital, Taipei, Taiwan. 3. Institute of Public Health, National Yang-Ming University, Taipei, Taiwan. 4. Division of Cardiology, University of California San Francisco, 555 Mission Bay Blvd South, Smith Cardiovascular Research Building, 452K, San Francisco, CA, 94158, USA. 5. Department of Radiology and Radiological Sciences, Johns Hopkins University, Baltimore, MD, USA. 6. Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, USA. 7. Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, MD, USA. Roselle.Abraham@ucsf.edu. 8. Division of Cardiology, University of California San Francisco, 555 Mission Bay Blvd South, Smith Cardiovascular Research Building, 452K, San Francisco, CA, 94158, USA. Roselle.Abraham@ucsf.edu.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Authors: L Belardinelli; J C Shryock; S Snowdy; Y Zhang; A Monopoli; G Lozza; E Ongini; R A Olsson; D M Dennis Journal: J Pharmacol Exp Ther Date: 1998-03 Impact factor: 4.030
Authors: Y Choi; S C Huang; R A Hawkins; W G Kuhle; M Dahlbom; C K Hoh; J Czernin; M E Phelps; H R Schelbert Journal: J Nucl Med Date: 1993-03 Impact factor: 10.057
Authors: Min Zhao; Min Liu; Jeffrey P Leal; Benjamin M W Tsui; Dean F Wong; Martin G Pomper; Yun Zhou Journal: PLoS One Date: 2019-03-20 Impact factor: 3.240