title: Effect of Diffuse Subendocardial Hypoperfusion on Left Ventricular Cavity Size by13N-Ammonia Perfusion PET in Patients With Hypertrophic Cardiomyopathy.
abstract: Vasodilator-induced transient left ventricular (LV) cavity dilation by positron emission tomography (PET) is common in patients with hypertrophic cardiomyopathy (HC). Because most patients with PET-LV cavity dilation lack obstructive epicardial coronary artery disease, we hypothesized that vasodilator-induced subendocardial hypoperfusion resulting from microvascular dysfunction underlies this result. To test this hypothesis, we quantified myocardial blood flow (MBF) (subepicardial, subendocardial, and global MBF) and left ventricular ejection fraction (LVEF) in 104 patients with HC without significant coronary artery disease, using13NH3-PET. Patients with HC were divided into 2 groups, based on the presence/absence of LV cavity dilation (LVvolumestress/LVvolumerest>1.13). Transient PET-LV cavity dilation was evident in 52% of patients with HC. LV mass, stress left ventricular outflow tract gradient, mitral E/E', late gadolinium enhancement, and prevalence of ischemic ST-T changes after vasodilator were significantly higher in patients with HC with LV cavity dilation. Baseline LVEF was similar in the 2 groups, but LV cavity dilation+patients had lower stress-LVEF (43 ± 11 vs 53 ± 10; p <0.001), lower stress-MBF in the subendocardial region (1.6 ± 0.7 vs 2.3 ± 1.0 ml/min/g; p <0.001), and greater regional perfusion abnormalities (summed difference score: 7.0 ± 6.1 vs 3.9 ± 4.3; p = 0.004). The transmural perfusion gradient, an indicator of subendocardial perfusion, was similar at rest in the 2 groups. Notably, LV cavity dilation+patients had lower stress-transmural perfusion gradients (0.85 ± 0.22, LV cavity dilation+vs 1.09 ± 0.39, LV cavity dilation-; p <0.001), indicating vasodilator-induced subendocardial hypoperfusion. The stress-transmural perfusion gradient, global myocardial flow reserve, and stress-LVEF were associated with LV cavity dilation. In conclusion, diffuse subendocardial hypoperfusion and myocardial ischemia resulting from microvascular dysfunction contribute to development of transient LV cavity dilation in HC.
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Hulya
authors: H
authors: Yalçin
authors: Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
authors: Ines
authors: I
authors: Valenta
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Fatih
authors: F
authors: Yalçin
authors: Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
authors: Celia
authors: C
authors: Corona-Villalobos
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Nestor
authors: N
authors: Vasquez
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Joshua
authors: J
authors: Ra
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Nagehan
authors: N
authors: Kucukler
authors: Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
authors: Abdel
authors: A
authors: Tahari
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Iraklis
authors: I
authors: Pozios
authors: Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
authors: Yun
authors: Y
authors: Zhou
authors: Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
authors: Martin
authors: M
authors: Pomper
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
authors: Theodore P
authors: TP
authors: Abraham
authors: Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
authors: Thomas H
authors: TH
authors: Schindler
authors: Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland. Electronic address: mabraha3@jhmi.edu.
authors: M Roselle
authors: MR
authors: Abraham
mesh_terms: D000328:Adult; D000368:Aged; D000641:Ammonia; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging* / Q000503:physiopathology; D003326:Coronary Circulation; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging* / Q000503:physiopathology; D055414:Myocardial Perfusion Imaging; D009590:Nitrogen Radioisotopes; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals; D013318:Stroke Volume
chemical_list: D009590:Nitrogen Radioisotopes; D019275:Radiopharmaceuticals; D000641:Ammonia