Abdullah H Alsaghir1, Soror A Alaithan1. 1. Consultant Pulmonary and Critical Care Medicine, Dammam Medical Complex, Dammam, Saudi Arabia. E-mail: asaghir4000@yahoo.com.
Sir,We read with interest the study by Al Otair et al.,[1] in the recent issue of Annals of Thoracic Medicine entitled “Outcome of pulmonary embolism (PE) and clinico-radiological predictors of mortality: Experience from a university hospital in Saudi Arabia.” They prospectively studied 105 patients with PE diagnosed by computed tomography pulmonary angiography (CTPA) and followed until death or hospital discharge. Their conclusion included there was no significant difference in localization of the embolus or obstruction score between survivors and non-survivors.I agree with their conclusion, as the anatomical distribution and burden of embolic occlusion of pulmonary artery has conflicting results and hence is not currently recommended for prognostic purpose when compared with the assessment based on hemodynamic consequences of PE. A recent meta-analysis by Vedovati et al. showed no correlation was observed between obstruction index (according to the Qanadli scoring system) and 30 days mortality rate, but can be used for risk stratification in patients with acute PE.[2] In the contrary, some studies have reported that increase in right-to-left ventricular dimension ratio correlate with mortality. The 30 day mortality of patients with a right-to-left ventricular dimension ratio >0.9 was 16% versus 8% mortality of patients without right ventricular (RV) dilation.[3] Other CTPA signs of right-heart overload potentially contributing to risk stratification include the shape of the interventricular septum, main pulmonary artery width, pulmonary artery-to-aorta width ratio, decreased width of the left atrium and pulmonary veins.[4]The other point which is worth commenting is the importance of measurement of the myocardial injury markers that includes cardiac troponins (troponins T and I) and the overload markers natriuretic peptides (brain natriuretic peptide [BNP]). In PE, elevation of cardiac troponin levels has been suggested to reflect its severity and is primarily used for risk stratification in hemodynamically stable normotensive patients. Some studies have shown that elevation of troponin level reflects RV dysfunction and is associated with increased mortality in PE patients. A meta-analysis investigating troponin levels in acute PE determined that any increase was associated with up to a five-fold increase in the risk of death.[5] Another meta-analysis has shown that increases in BNP levels are associated with a ninefold increase in the risk of death in normotensive PE patients.[6]
Authors: Doo Kyoung Kang; Christian Thilo; U Joseph Schoepf; J Michael Barraza; John W Nance; Gorka Bastarrika; Joseph A Abro; James G Ravenel; Philip Costello; Samuel Z Goldhaber Journal: JACC Cardiovasc Imaging Date: 2011-08
Authors: U Joseph Schoepf; Nils Kucher; Florian Kipfmueller; Rene Quiroz; Philip Costello; Samuel Z Goldhaber Journal: Circulation Date: 2004-11-08 Impact factor: 29.690
Authors: Hadil A K Al Otair; Ahmad A Al-Boukai; Gehan F Ibrahim; Mashael K Al Shaikh; Ahmed Y Mayet; Mohamed S Al-Hajjaj Journal: Ann Thorac Med Date: 2014-01 Impact factor: 2.219