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Higher incidence of vasodilator-induced left ventricular cavity dilation by PET when compared to treadmill
Dai-Yin Lu1,2,3, Hulya Yalçin1, Sanjay Sivalokanathan1
1Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, MD, USA.
Insights
Transient left ventricular cavity dilation (LVCD) during vasodilator stress in hypertrophic cardiomyopathy (HCM) patients, detected by PET, indicates significant microvascular dysfunction. However, this dilation is not consistently observed with echocardiography during exercise stress.
Area of Science:
- Cardiology
- Medical Imaging
- Cardiovascular Physiology
Background:
- Transient left ventricular cavity dilation (LVCD) induced by vasodilators via positron emission tomography (PET) is linked to microvascular dysfunction in hypertrophic cardiomyopathy (HCM).
- The study investigates whether HCM patients exhibiting PET-detected LVCD during vasodilator stress also show echocardiography-detected LVCD (ECHO-LVCD) during exercise stress.
Purpose of the Study:
- To compare left ventricular cavity dilation (LVCD) in hypertrophic cardiomyopathy (HCM) patients using positron emission tomography (PET) during vasodilator stress versus echocardiography (ECHO) during exercise stress.
- To assess the relationship between PET-detected LVCD and echocardiographic parameters of cardiac function and microvascular dysfunction in HCM.
Main Methods:
- Retrospective analysis of 108 HCM patients who underwent both perfusion-PET and exercise-ECHO.
- Head-to-head comparison of left ventricular (LV) volumes and ejection fraction (LVEF) at rest and stress (vasodilator for PET, post-exercise for ECHO).
- Definition of PET-LVCD (stress/rest LV volume ratio > 1.13) and ECHO-LVCD (stress/rest LV end-systolic volume ratio > 1.17); assessment of myocardial blood flow (MBF), myocardial flow reserve (MFR) by PET, and global longitudinal strain (GLS) by ECHO.
Main Results:
- PET-LVCD was present in 51% of HCM patients; only one patient showed ECHO-LVCD, who also had PET-LVCD.
- The PET-LVCD group exhibited lower PET-LVEF during vasodilator stress, higher LV mass, worse resting and stress GLS, and lower MFR.
- Ischemic ST-T changes were more frequent during vasodilator stress in the PET-LVCD group (42% vs 17%), but similar during exercise stress (30% in both groups).
Conclusions:
- PET-detected LVCD in HCM signifies a more severe myopathy and pronounced microvascular dysfunction.
- Discrepancies in LVCD detection between PET and ECHO may stem from differing physiological responses to exercise versus vasodilators and variations in stress-imaging acquisition timing.
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.
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