TY - JOUR
T1 - Correlation between CT-derived cardiac chamber volume, myocardial injury and mortality in acute pulmonary embolism
AU - Granot, Yoav
AU - Rozenbaum, Zach
AU - Ziv-Baran, Tomer
AU - Fares, Rabeeh
AU - Milwidsky, Assi
AU - Berliner, Shlomo
AU - Aviram, Galit
N1 - Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/9
Y1 - 2021/9
N2 - Introduction: The release of troponin in patients with acute pulmonary embolism (PE) is assumed to be secondary to elevated intracardiac chamber pressure. Since right ventricular (RV) hypertrophy does not develop in the acute setting, pressure overload correlates with chamber dilatation, causing myocardial injury. The aim of the present study was to investigate correlations between cardiac chamber volume, troponin and subsequent early mortality in patients with acute PE and refine risk stratification. Materials and methods: Patients who underwent a computerized tomographic pulmonary angiogram (CTPA) and a troponin test within 24 h of the CTPA were included. Automated software calculated the volumes of the four cardiac chambers indexed to body surface area (BSA) and correlated them to troponin and early all-cause mortality. Results: The final cohort consisted of 370 patients (56% females) with acute PE. RV volume and right to left ventricular volume ratio (VVR) were the most significant indicators for elevated troponin (receiving operating characteristic [ROC] 0.796, confidence interval [CI]: 0.749–0.843, p < 0.001, and ROC 0.802, CI: 0.753–0.851, p < 0.001, respectively). VVR cutoff values, which are predictive of elevated troponins, correlated with higher 30-day mortality (odds ratio = 3.1, CI 1.5–6.7, p = 0.003) for a VVR >3 compared to a VVR <2. Conclusion: Cardiac chamber volume correlates to elevated troponin in patients with acute PE. A higher VVR reflects an increased likelihood for myocardial ischemia, as well as an increased short-term mortality risk. These data are available seconds after CTPA performance and may contribute to refining patients' risk stratification.
AB - Introduction: The release of troponin in patients with acute pulmonary embolism (PE) is assumed to be secondary to elevated intracardiac chamber pressure. Since right ventricular (RV) hypertrophy does not develop in the acute setting, pressure overload correlates with chamber dilatation, causing myocardial injury. The aim of the present study was to investigate correlations between cardiac chamber volume, troponin and subsequent early mortality in patients with acute PE and refine risk stratification. Materials and methods: Patients who underwent a computerized tomographic pulmonary angiogram (CTPA) and a troponin test within 24 h of the CTPA were included. Automated software calculated the volumes of the four cardiac chambers indexed to body surface area (BSA) and correlated them to troponin and early all-cause mortality. Results: The final cohort consisted of 370 patients (56% females) with acute PE. RV volume and right to left ventricular volume ratio (VVR) were the most significant indicators for elevated troponin (receiving operating characteristic [ROC] 0.796, confidence interval [CI]: 0.749–0.843, p < 0.001, and ROC 0.802, CI: 0.753–0.851, p < 0.001, respectively). VVR cutoff values, which are predictive of elevated troponins, correlated with higher 30-day mortality (odds ratio = 3.1, CI 1.5–6.7, p = 0.003) for a VVR >3 compared to a VVR <2. Conclusion: Cardiac chamber volume correlates to elevated troponin in patients with acute PE. A higher VVR reflects an increased likelihood for myocardial ischemia, as well as an increased short-term mortality risk. These data are available seconds after CTPA performance and may contribute to refining patients' risk stratification.
KW - CT pulmonary angiography
KW - Cardiac troponin
KW - Mortality
KW - Pulmonary embolism
KW - Volumetric analysis
UR - https://www.scopus.com/pages/publications/85109654529
U2 - 10.1016/j.thromres.2021.07.005
DO - 10.1016/j.thromres.2021.07.005
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C2 - 34265604
AN - SCOPUS:85109654529
SN - 0049-3848
VL - 205
SP - 63
EP - 69
JO - Thrombosis Research
JF - Thrombosis Research
ER -