دورية أكاديمية

Right Ventricle Response to Major Lung Resection (the RIVER Study).

التفاصيل البيبلوغرافية
العنوان: Right Ventricle Response to Major Lung Resection (the RIVER Study).
المؤلفون: Giustiniano, Enrico, Nisi, Fulvio, Piccioni, Federico, Gambino, Francesco, Aceto, Romina, Lungu, Ramona, Carrara, Alfonso, Neganov, Maxim, Cecconi, Maurizio
المصدر: Journal of Cardiovascular Echography; Apr-Jun2023, Vol. 33 Issue 2, p76-82, 7p
مستخلص: Backgrounds: Major lung resection is associated with high postoperative morbidity and mortality, especially due to cardiorespiratory complications. Right ventricle (RV) ejection, pulmonary artery (PA) pressure, and tone are tightly coupled. Since the RV is exquisitely sensitive to changes in afterload, an acute increase in RV outflow resistance (i.e., acute pulmonary embolism [PE]) will cause acute RV dilatation and, a reduction of left ventricle compliance too, rapidly spiraling to acute cardiogenic shock and death. We investigated the changing in RV performance after major lung resection. Materials and Methods: We carried out transthoracic echocardiography (TTE) aiming at searching for the incidence of early RV systolic dysfunction (defined as tricuspid annulus plane systolic excursion [TAPSE] <17 cm, S'-tissue Doppler imaging <10 cm/s) and estimate the RV-PA coupling by the TAPSE/pulmonary artery pressures (PAPs) ratio after major lung resection. The TTE has been performed before and immediately after surgery. Results: After the end of the operation the echocardiographic parameters of the RV function worsened. TAPSE decreased from 24 (21 ÷ 28) to 18 (16 ÷ 22) mm (P = 0.015) and PAPs increased from 26 (25 ÷ 30) to 30 (25 ÷ 39) mmHg (P = 0.013). TAPSE/PAPs ratio decreased from 0.85 (0.80 ÷ 0.90) to 0.64 (0.54 ÷ 0.79) mm/mmHg (P = 0.002). Conclusions: In line with previous reports, after major lung resection the increase in afterload reduces the RV function, but the impairment remains clinically not relevant. The different clinical picture of an acute cor pulmonale due to PE implies that the pathogenesis of cardiac failure involves more pathways than the mere mechanic occlusion of the blood flow. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Supplemental Index
الوصف
تدمد:22114122
DOI:10.4103/jcecho.jcecho_17_23