LAUSR

In the present issue of the European Journal of Nuclear Medicine and Molecular Imaging, Sciagrà and coworkers report an investigation of the mechanisms underlying a decrease in left ventricular (LV) ejection fraction during dipyridamoleinduced coronary vasodilation in a group of patients with hypertrophic cardiomyopathy (HCM) [1]. As a major finding, transient LV dysfunction did not identify patients with more severe impairment in coronary flow reserve and maximal blood flow. Rather, it was associated with stress-induced development of a transmural gradient in myocardial perfusion characterized by a relative reduction in maximal flow capacity in the subendocardial layers. In several aspects, this study extends the notion that selective coronary vasodilation can induce myocardial ischaemia causing true subendocardial hypoperfusion even in the absence of both changes in myocardial oxygen need and significant obstructions in major coronary arteries. Concurrently, it confirms that the ability to delineate the transmural extent of perfusional, metabolic or contractile impairment might be a prerequisite for a deeper understanding of the pathophysiological mechanisms underlying a variety of cardiac disorders. For obvious reasons, this issue represents a specific challenge for cardiac imaging. In the setting of nuclear medicine, many studies have actually shown a relative subendocardial underperfusion under different physiological conditions. However, an accurate description of transmural flow distribution is still challenging for virtually all imaging modalities because cardiac contraction cyclically modifies the shape and thickness of the LVmyocardiumwhile respiratory activity periodically shifts the heart position throughout the time needed to measure myocardial tracer concentration. Below, we briefly discuss how these basic features of cardiac physiology affect radionuclide imaging of transmural perfusion gradient.