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Updated: Mar 13, 2026
In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Effect of Diffuse Subendocardial Hypoperfusion on Left Ventricular Cavity Size by 13N-Ammonia Perfusion PET in
Hulya Yalçin1, Ines Valenta2, Fatih Yalçin1
1Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
Insights
Transient left ventricular (LV) cavity dilation in hypertrophic cardiomyopathy (HC) is linked to subendocardial hypoperfusion. This study reveals microvascular dysfunction contributes to HC-related LV dilation, impacting myocardial blood flow and ejection fraction.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Nuclear Cardiology
Background:
- Transient left ventricular (LV) cavity dilation is frequently observed in patients with hypertrophic cardiomyopathy (HC) during vasodilator stress testing with positron emission tomography (PET).
- This phenomenon often occurs in the absence of obstructive epicardial coronary artery disease, suggesting an alternative underlying mechanism.
Purpose of the Study:
- To investigate the hypothesis that vasodilator-induced subendocardial hypoperfusion, stemming from microvascular dysfunction, is the cause of transient LV cavity dilation in HC.
- To quantify myocardial blood flow (MBF) and LV ejection fraction (LVEF) in HC patients with and without LV cavity dilation.
Main Methods:
- 104 patients with HC and no significant coronary artery disease underwent 13NH3-PET to assess global, subepicardial, and subendocardial MBF, along with LVEF.
- Patients were categorized into two groups based on the presence (LVvolume_stress/LVvolume_rest >1.13) or absence of LV cavity dilation.
Main Results:
- 52% of HC patients exhibited transient LV cavity dilation.
- Patients with LV cavity dilation showed higher LV mass, stress LV outflow tract gradient, mitral E/E', late gadolinium enhancement, and ischemic ST-T changes.
- LV cavity dilation was associated with lower stress-LVEF, reduced subendocardial MBF, increased perfusion abnormalities, and diminished stress-transmural perfusion gradients, indicating subendocardial hypoperfusion.
Conclusions:
- Diffuse subendocardial hypoperfusion and myocardial ischemia, driven by microvascular dysfunction, are key contributors to the development of transient LV cavity dilation in hypertrophic cardiomyopathy.
- The findings highlight the role of microvascular dysfunction in the pathophysiology of HC and its impact on LV remodeling and function.
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, using 13NH3-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.
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