Impact of pericoronary adipose tissue inflammation on left ventricular hypertrophy and regional physiological indices in stable coronary artery disease patients with preserved systolic function

Systemic low-grade inflammation has been shown to be associated with left ventricular hypertrophy (LVH). However, the relationship between pericoronary adipose tissue attenuation (PCATA) and both LVH and regional physiological indices remains unknown. This study aimed to evaluate the association of PCATA with LVH and regional physiological indices in stable coronary artery disease (CAD) patients with preserved systolic function. A total of 114 CAD patients who underwent coronary CT angiography (CTA) and invasive physiological tests showing ischemia due to a single de novo lesion were included in the study. On proximal 40-mm segments of all three major coronary vessels on CTA, PCATA was assessed by the crude analysis of the mean CT attenuation value [− 190 to − 30 Hounsfield units [HU)] and the culprit vessel PCATA was used for the analysis. Regional physiological indices were invasively obtained by pressure–temperature sensor-tipped wire. The patients were divided into three groups by culprit vessel PCATA tertiles, and clinical, CTA-derived, and physiological indices were compared. Univariable and multivariable analyses were further performed to determine the predictors of LVH. Angiographic stenosis severity, culprit lesion locations, culprit vessel fractional flow reserve, coronary flow reserve, index of microcirculatory resistance, total and target vessel coronary calcium score, and biomarkers including high-sensitivity C-reactive protein were not different among the groups. The left ventricular (LV) mass, LV mass index (LVMI), and LV mass at risk were all significantly different in the three groups with the greatest values in the highest tertile group (all, P < 0.05). On multivariable analysis, male gender, NT-proBNP, and PCATA were independent predictors of LVMI. Culprit vessel PCATA was significantly associated with LVMI, but not with regional physiology in CAD patients with functionally significant lesions and preserved systolic function. Our results may offer insight into the pathophysiological mechanisms linking pericoronary inflammation and LVH to worse prognosis.