PeerJ · 2024
Single-cell transcriptome reveals the heterogeneity of malignant ductal cells and the prognostic value of REG4 and SPINK1 in primary pancreatic ductal adenocarcinoma.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Orlando M P, Bonanno M A, Russo F Y, Ralli M, Turchetta R, Passali F M, Minni A, Greco A, De Vincentiis M, Tattoli M
Аннотация
OBJECTIVES: To determine the factors (clinical, biochemical, angiographic, and echocardiographic) which predict left ventricular (LV) dysfunction in Takayasu's arteritis (TAK). TAK causes inflammation of the aorta and its large branches. Systemic hypertension, aortic valvular disease, and coronary artery involvement are probable contributors to LV dysfunction in some patients. In other patients, inflammation and resulting myocarditis play an essential role. However, the prevalence and relative contribution of such predictors of LV dysfunction in TAK patients is unknown.
METHODS: We enrolled 87 patients with angiographically confirmed TAK in the study after proper informed consent. A complete clinical, biochemical, and echocardiographic evaluation of all the cases was done. We defined LV systolic dysfunction as an ejection fraction below 50% and diastolic dysfunction by ASE 2016 criteria into grades I, II, and III.
RESULTS: We evaluated 87 consecutive angiographically proven TAK patients. The incidence of LV systolic and diastolic dysfunction in our study was 19.5% (17/87) and 100% (87/87), respectively. All the patients with LV dysfunction (n=17, 100%) had an ITAS 2010 score of more than two suggestive of active disease. In 15 (88%) out of 17 patients with LV systolic dysfunction, we could identify a significant haemodynamic cause of LV dysfunction (untreated hypertension HTN, descending thoracic or abdominal aorta stenosis, renal artery stenosis, coronary stenosis, significant valvular regurgitation). In the rest 2 cases, no important haemodynamic factor was present, and here LV dysfunction was probably because of myocarditis and its sequalae.
CONCLUSIONS: This study represents the largest cohort of TAK patients to estimate LV systolic and diastolic dysfunction. We have found LV systolic and diastolic dysfunction multifactorial, with hemodynamic and inflammatory factors contributing to its pathophysiology.
METHODS: We enrolled 87 patients with angiographically confirmed TAK in the study after proper informed consent. A complete clinical, biochemical, and echocardiographic evaluation of all the cases was done. We defined LV systolic dysfunction as an ejection fraction below 50% and diastolic dysfunction by ASE 2016 criteria into grades I, II, and III.
RESULTS: We evaluated 87 consecutive angiographically proven TAK patients. The incidence of LV systolic and diastolic dysfunction in our study was 19.5% (17/87) and 100% (87/87), respectively. All the patients with LV dysfunction (n=17, 100%) had an ITAS 2010 score of more than two suggestive of active disease. In 15 (88%) out of 17 patients with LV systolic dysfunction, we could identify a significant haemodynamic cause of LV dysfunction (untreated hypertension HTN, descending thoracic or abdominal aorta stenosis, renal artery stenosis, coronary stenosis, significant valvular regurgitation). In the rest 2 cases, no important haemodynamic factor was present, and here LV dysfunction was probably because of myocarditis and its sequalae.
CONCLUSIONS: This study represents the largest cohort of TAK patients to estimate LV systolic and diastolic dysfunction. We have found LV systolic and diastolic dysfunction multifactorial, with hemodynamic and inflammatory factors contributing to its pathophysiology.