Kumiko Hirata

BACKGROUND: Thrombotic microangiopathy (TMA) syndromes include thrombotic thrombocytopenic purpura (TTP) and haemolytic uremic syndrome, and contribute to myocardial infarction and multiple organ failure. Although coronary microvascular dysfunction (CMD) is the key for understanding the pathophysiology of cardiac involvement in TMA, there is limited knowledge on the recovery from CMD in patients with TMA. CASE SUMMARY: An 80-year-old woman was brought to the emergency department due to worsening back pain, dyspnoea on exertion, jaundice, and fever. Although she had typical TTP symptoms and elevated cardiac troponin level, ADAMTS13 activity was preserved (34%), leading to the diagnosis of TMA with myocardial infarction. She underwent plasma exchange and was administered aspirin and prednisolone. Magnetic resonance imaging revealed iliopsoas abscess, which is a possible aetiologic factor of sepsis-related TTP. She had impaired coronary flow reserve (CFR) with angiographically non-obstructive epicardial coronary arteries. Improved CFR was observed on follow-up, suggesting existence of transient CMD caused by TMA. After treatment of the iliopsoas abscess with antibiotics for 3 months, she was discharged without any adverse complications. DISCUSSION: Coronary microvascular dysfunction is an underlying mechanism of myocardial infarction, with or without epicardial obstructive coronary artery stenosis. TMA is characterized by pathological lesions caused by endothelial cell damage in small terminal arteries and capillaries, with complete or partial occlusion caused by platelet and hyaline thrombi. CMD and its recovery are keys for understanding the natural history of cardiac involvement in TMA. In vivo evaluations of CMD can provide mechanistic insights into the cardiac involvement in TMA.

BACKGROUND: This study aimed to investigate the association between the extent and severity of coronary atherosclerosis, epicardial adipose tissue (EAT) accumulation, and left ventricular (LV) global longitudinal strain (GLS) in patients with preserved LV ejection fraction (LVEF) and without LV regional wall motion abnormalities. METHODS: This study included 169 preserved LVEF patients without LV wall motion abnormalities who underwent coronary computed tomography (CT) angiography for the assessment of suspected coronary artery disease (CAD). The segment stenosis score (SSS) and segment involvement score (SIS) were calculated to evaluate CAD extent. The EAT volume was defined as CT attenuation values ranging from -250 to -30 HU within the pericardial sac. LVGLS was measured using echocardiography to assess subclinical LV dysfunction. RESULTS: All patients had preserved LVEF of ≥50%, and the mean LVGLS was -18.7% (-20.5% to -16.9%). Mean SSS and SIS were 2.0 (0-5) and 4.0 (0-36), respectively, while mean EAT volume was 116.1 mL (22.9-282.5 mL). Multivariate analysis using linear regression model demonstrated that LVEF (β, -17.0; 95% CI, -20.9 - -13.1), LV mass index (β, 0.03; 95% CI, 0.01-0.06), and EAT volume (β, 0.010; 95% CI, 0.0020-0.0195) were independently associated with LVGLS; however, obstructive CAD was not. The multivariate models demonstrated that SSS (Î, 0.12; 95% CI, 0.05-0.18) and SIS (Î, 0.27; 95% CI, 0.10-0.44) were correlated with deterioration of LVGLS, independent of other parameters. CONCLUSION: This study demonstrates that EAT volume and CAD extent are associated with the deterioration of LVGLS in this population.

BACKGROUND: Wide-volume scanning with 320-row multidetector computed tomography coronary angiography (CTCA-WVS) enables the assessment of the aortic arch plaque (AAP) morphology and coronary arteries without requiring additional contrast volume. This study aimed to investigate the prevalence of AAPs and their association with coronary artery disease (CAD) and major adverse cardiovascular events (MACEs) in patients who underwent CTCA-WVS. METHODS: This study included 204 patients without known CAD (mean age, 65 years; 53% men) who underwent CTCA-WVS. We evaluated the presence of aortic plaques in the ascending aorta, aortic arch, and thoracic descending aorta using CTCA-WVS. Large aortic plaques were defined as plaques of at least 4 mm in thickness. A complex aortic plaque was defined as a plaque with ulceration or protrusion. MACEs were defined as composite events of cardiovascular (CV) death, nonfatal myocardial infarction, and ischemic stroke. RESULTS: AAPs and large/complex AAPs were identified in 51% ( n = 105) and 18% ( n = 36) of the study patients, respectively. The prevalence of AAPs with large/complex morphology increased with CAD severity (2.1% in no CAD, 12% in nonobstructive CAD, and 39% in obstructive CAD). The univariate Cox hazard model demonstrated that the predictors associated with MACEs were diabetes, obstructive CAD, and large/complex AAPs. Independent factors associated with large/complex AAPs were male sex [odds ratio (OR), 2.90; P = 0.025], stroke history (OR, 3.48; P = 0.026), obstructive CAD (OR, 3.35; P = 0.011), and thoracic aortic calcification (OR, 1.77; P = 0.005). CONCLUSION: CTCA-WVS provides a comprehensive assessment of coronary atherosclerosis and thoracic aortic plaques in patients with CAD, which may improve the stratification of patients at risk for CV events.