CardiomyopathyEffect of Diffuse Subendocardial Hypoperfusion on Left Ventricular Cavity Size by 13N-Ammonia Perfusion PET in Patients With Hypertrophic Cardiomyopathy
Section snippets
Methods
This study was approved by the Institutional Review Board at the Johns Hopkins University. We included patients with HC (n = 104) evaluated at the Johns Hopkins Hypertrophic Cardiomyopathy Clinic who underwent cardiac rest-stress 13N ammonia PET/computed tomography (CT) from 2009 to 2013. All patients fulfilled the standard diagnostic criteria of HC, namely presence of unexplained left ventricular hypertrophy with maximum wall thickness ≥15 mm and septal/posterior wall ratio >1.3 in the absence
Results
This study included 104 patients with a clinical diagnosis of HC. Patients with HC were divided into 2 groups, based on the presence or absence of transient PET-LV cavity dilation after vasodilator stress (Figure 1). Demographic characteristics, LVEF, and LV volumes were similar in the 2 groups, but patients with HC with PET-LV cavity dilation had greater degree of LV hypertrophy, diastolic dysfunction, higher stress-left ventricular outflow tract (LVOT) gradients, and greater amounts of
Discussion
The main result of our study is that vasodilator-induced subendocardial hypoperfusion and myocardial ischemia resulting from microvascular dysfunction contribute to development of transient PET-LV cavity dilation in patients with HC.
Transient LV cavity dilation and reduction in LVEF are frequently observed by nuclear imaging and echocardiography after vasodilator/dobutamine infusion and exercise,19 in patients with severe, extensive CAD. In contrast, most patients with HC lack obstructive
Acknowledgment
The authors would like to acknowledge help from Dr. Junaid Afzal, MS, Dr. Dhananjay Vaidya, PhD, and the Image Response Assessment Team (NIH P30CA006973).
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2023, JACC: Cardiovascular ImagingCitation Excerpt :High prevalence of subclinical reduced subendocardial perfusion during dipyridamole PET is the pathophysiologic fluid dynamic manifestation of widespread coronary atherosclerosis without flow limiting stenosis as reported for intracoronary intravascular ultrasound, by longitudinal pull back FFR of diffuse CAD6 or reduced FFR in patients with no significant angiographic stenosis excluded from the FAME trials7. Although reduced subendocardial perfusion is reported for severe LVH in small studies of aortic stenosis and hypertrophic cardiomyopathy,1-3 in our large cohort of routine PET for CAD, LVH did not contribute importantly to reduced subendocardial perfusion. Quantitative invasive or noninvasive physiologic metrics are not widely measured and are performed with diverse protocols or methodologies with variable measures of severity and criteria for intervention.
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This study was supported by the John Taylor Babbit (JTB) Foundation.
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