Relation Among Clot Burden, Right-Sided Heart Strain, and Adverse Events After Acute Pulmonary Embolism




Computed tomography pulmonary angiogram (CTPA) provides a volumetric assessment of clot burden in acute pulmonary embolism (PE). However, it is unclear if clot burden is associated with right-sided heart strain (RHS) or adverse clinical events (ACE). We prospectively enrolled Emergency Department patients with PE (in CTPA) from 2008 to 2011. We assigned 1 to 9 points as clot burden score, based on whether emboli were saddle, central, lobar, segmental, and subsegmental. We evaluated a novel score (the “CT-PASS”) based on the sum (in millimeters) of the largest filling defects in the right and left pulmonary vasculature. Our primary outcome was RHS, defined by imaging (echocardiography or CTPA) or cardiac biomarkers. Our secondary outcomes included 5-day ACE. We included 271 patients (50% women), with a mean age of 59 ± 17 years. Based on CTPA, 131 patients (48%) had central PE (clot burden score ≥5 points). The median CT-PASS was 9.1 mm (interquartile range 4.9 to 16.4). In univariate analysis, higher clot burden (highest quartile CT-PASS) was associated with RHS (p = 0.003). In multivariate analysis, after adjusting for RHS, age, and gender, central PE (odds ratio [OR] 2.92, 95% confidence interval [CI] 1.10 to 7.81) and CT-PASS >20 mm (OR 3.54, 95% CI 1.39 to 8.97) were significantly associated with ACE. However, this association of central PE with ACE was not statistically significant after excluding patients with shock index >1 (OR 2.56, 95% CI 0.62 to 10.64). In conclusion, highest quartile CT-PASS was associated with RHS and central PE and ACE, but this association was not statistically significant in hemodynamically stable PE.


Acute pulmonary embolism (PE) is a major health problem, accounting for >250,000 hospitalizations in the United States every year. The severity of short-term outcomes after acute PE varies, and clinicians must be able to risk-stratify patients to identify adverse clinical events (ACE). Risk stratification of PE requires clinicians to weigh various factors including age, co-morbid illnesses, physical examination findings, biomarkers, and imaging results. Computed tomography pulmonary angiography (CTPA) is generally available and is the preferred diagnostic technique for PE. CTPA demonstrates the location and quantity of clot, right and left ventricular sizes, and other measures of PE severity. Assessment of clot burden can be performed using semi-quantitative scoring systems, such as those proposed by Qanadli et al and Mastora et al. However, these scoring systems have not consistently correlated with ACE or right-sided heart strain (RHS)—a predictor of ACE and short-term mortality after PE. Moreover, these complex clot quantification systems are relatively time consuming and are not commonly used in routine radiology practice. Our goal was to create and evaluate 2 simple and reproducible classifications of clot burden in patients with PE. We first quantified the location of clot burden according to categories commonly reported in clinical radiology reports: based on whether emboli were saddle, central, lobar, segmental, or subsegmental and whether clot was single or multiple. We also developed a scoring system, the CTPA severity score (CT-PASS) that objectively quantified clot burden size using a method that is easily understandable and reproducible. We investigated the association of these 2 scoring systems with objective markers of RHS and ACE.


Methods


We performed a prospective observational cohort study from October 2008 to December 2011 in the Emergency Department (ED) of Massachusetts General Hospital, an urban, tertiary referral center with an annual emergency department census of 95,000 visits. The study was approved by the Human Research Committee of Partners HealthCare Inc. Consecutive adult (≥18 years) patients diagnosed with PE within 24 hours of ED registration who could provide informed consent were deemed eligible for enrollment. Subjects were enrolled in accordance with Strengthening the Reporting of Observational Studies in Epidemiology guidelines. We limited our analysis to patients with a filling defect in a pulmonary artery in CTPA. Patients were excluded if they were <18 years, could not provide informed consent, did not have CTPA available for review at our institution, or had inadequate follow-up data (e.g., homeless, prisoners). We also excluded patients if their PE appeared chronic according to published criteria. Trained study staff used a standard form to collect demographics, co-morbid illness, ED/inpatient vitals, and treatment data.


We obtained CTPA images using a 16- or 64-section scanner (GE Lightspeed; GE Medical Systems, Milwaukee, Wisconsin). Patients received 90 to 110 ml of contrast medium (Isoview-300 or Isoview-370; Bracco Diagnostics, Princeton, New Jersey) and a 40-ml isotonic sodium chloride solution flush through an 18-gauge needle with a flow rate of 4 ml/s using a power injector (Medrad Power Injector; Medrad, Indianola, Pennsylvania, or E-Z-EM EmpowerCT; E-Z-EM, Lake Success, New York). We used a bolus tracking system (Smart Prep; GE Medical Systems) with the region of interest in the main pulmonary arteries. Alternatively, we used a fixed delay of 22 seconds for the 16-section CT scanner and 26 seconds for the 64-section CT scanner. We imaged the thorax from a caudal to cranial direction starting at the adrenal glands and ending at the apices of the lungs, in the helical mode, in standard algorithm with a large field of view.


We coded the location of PE (saddle, main pulmonary artery, lobar, segmental, or subsegmental artery) in the final CTPA interpretations documented by board-certified attending radiologists and also noted whether PE was single or multiple. Subsequently, we retrieved index CTPAs from our picture archiving and communication system after patient enrollment. Two independent board-eligible radiologist readers (PM and FH), blinded to the outcomes, reviewed images for quality by determining the smallest vessel that could be confidently assessed considering vessel enhancement, motion artifacts, or noise. We defined acute PE as the presence of an endoluminal central filling defect partially or completely occluding a pulmonary artery. We interpreted scans using axial images, supplemented with reconstructed coronal and sagittal images. Disagreements were resolved by consensus among PM, FH, and CK.


We defined our clot burden score (CBS) a priori. We quantified the clot burden as 1 to 9 points based on the final CTPA report as detailed in Table 1 . We assigned saddle PE a CBS = 9 points. For the purposes of analysis, we defined central PE as a CBS ≥5 points (i.e., at least 1 PE in a lobar or more proximal vessel) and noncentral PE as a CBS <5 points (all PE in segmental or more distal vessels). We measured the size of the largest filling defect in a pulmonary artery by measuring the widest dimension (in millimeters) orthogonal to the long axis of the occluded vessel in each lung and added these to determine the CT-PASS. For all clots, especially those in central vessels, we found that the maximum short-axis dimension was best assessed using sagittal and coronal reformats and axial images. CT-PASS for saddle PE was calculated as the sum of thrombus size extending into the right and left pulmonary artery. To assess correlation with RHS and clinical outcomes, the scores of the 2 independent radiologist readers were averaged.


<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='CT-PASS=Largestfillingdefectintherightlung(mm)+largestfillingdefectintheleftlung(mm)’>CTPASS=Largestfillingdefectintherightlung(mm)+largestfillingdefectintheleftlung(mm)CT-PASS=Largestfillingdefectintherightlung(mm)+largestfillingdefectintheleftlung(mm)
CT – PASS = Largest filling defect in the right lung ( mm ) + largest filling defect in the left lung ( mm )

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Nov 20, 2016 | Posted by in CARDIOLOGY | Comments Off on Relation Among Clot Burden, Right-Sided Heart Strain, and Adverse Events After Acute Pulmonary Embolism

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