Szymon Pacho

Mean Platelet Volume Predicts Early Death in Acute Pulmonary Embolism

Background Recently, mean platelet volume (MPV) was reported to predict venous thromboembolism. Moreover, MPV correlates with platelet reactivity and indicates poor outcome in acute coronary syndromes. Objective To examine the hypothesis that in acute pulmonary embolism (APE) MPV is elevated and may predict mortality. Methods and results The study included consecutive 192 patients with APE, (79M/113F, 64±18 years) and 100 controls matched for age, sex and concomitant diseases. On admission blood samples were collected for MPV and troponin measurements. Although MPV did not differ between patients with APE and controls (10.0±1.2 vs 10.1±0.8 fl), it differed between low- and intermediate- or high-risk APE (9.4±1.2 fl, 10.3±1.1 fl, 10.3±1.8 fl; respectively, p<0.0001). Eighteen (9%) patients with APE died during the 30-day observation. MPV was higher in non-survivors than survivors (10.7±1.4 fl vs 9.9±1.2fl, p<0.01). The areas under receiver operating characteristic curves of MPV were 0.658 (95% CI 0.587 to 0.725) for predicting 30-day mortality, and 0.712 (95% CI 0.642 to 0.775) for 7-day mortality. MPV >10.9 fl, showed sensitivity, specificity, positive predictive value and negative predictive value for death within 30 days (39%, 81%, 18%, 93%, respectively) and for 7-day mortality (54%, 82%, 18%, 96%). Multivariable analysis showed that MPV was an independent mortality predictor for 7- and 30-day all-cause mortality (HR=2.0 (95% CI 1.3 to 3.0), p<0.001)) and 1.7 (95% CI 1.2 to 2.5), p<0.01)), respectively). MPVs were higher in patients with myocardial injury than in those without troponin elevation (10.2±1.1 fl vs 9.8±1.2 fl; p=0.02). There were correlations between MPV and right ventricular diameter and right ventricular dysfunction (r=0.28, p<0.01 and r=0.19, p<0.02, respectively). Conclusion MPV is an independent predictor of early death in APE. Moreover, MPV in APE is associated with right ventricular dysfunction and myocardial injury.

Assessment of renal dysfunction improves troponin‐based short‐term prognosis in patients with acute symptomatic pulmonary embolism

Summary.  Objective: Current risk stratification in acute pulmonary embolism (APE) includes assessment of clinical status, right ventricular overload and plasma troponin concentrations. As impaired renal function is one of the important predictors of mortality in cardiovascular diseases, we hypothesized that it is an independent early mortality marker in APE. Material and methods: In prospective cohort study, we observed 220 consecutive patients (86M/134F, 64 ± 18 years) with APE proven by spiral computed tomography (CT). On admission, echocardiography was performed and blood samples were collected for troponin and creatinine assays. Results: The calculated glomerular filtration rate (GFR) differed significantly between 81 pts with low‐, 131 pts with moderate‐ and 8 pts with high‐risk APE [71 (19–181) vs. 55 (9–153) vs. 41 (14–68) mL min−1; respectively P < 0.0001]. Twenty‐three patients died during the 30‐day observation. Importantly, GFR was lower in non‐survivors than in survivors [35 (9–92) vs. 63 (14–181) mL min−1, P < 0.0001]. The area under the curve (AUC) of the GFR receiver‐operating characteristic (ROC) curve for predicting mortality was 0.760 (95% CI: 0.698–0.815). In multivariable analysis, independent mortality predictors were GFR, troponin, heart rate and history of chronic heart failure. In normotensive patients, the GFR and cardiac troponins (cTn) ROC curves for prediction of mortality showed no difference (AUC 0.789 and 0.781, respectively). However, Kaplan–Meier analysis showed an additive prognostic value of renal dysfunction. Thus, troponin‐positive patients with a GFR ≤ 35 mL mn−1 showed 48% 30‐day mortality, whereas troponin‐positive patients with a GFR > 35 mL mn−1 had 11% mortality, and troponin‐negative patients with a GFR > 35 mL mn−1 had good prognosis, P < 0.0001. Conclusion: Impaired kidney function, present in 47% of APE patients, is related to all‐cause mortality. In initially normotensive patients, a GFR < 35 mL min−1 predicts 30‐day mortality. Moreover, GFR assessment can improve troponin‐based risk stratification of APE.

Electrocardiographic differentiation between acute pulmonary embolism and non-ST elevation acute coronary syndromes at the bedside.

Background: Clinical picture of acute pulmonary embolism (APE), with wide range of electrocardiographic (ECG) abnormalities can mimic acute coronary syndromes.

Endothelin is not elevated in acute pulmonary embolism

INTRODUCTION In acute pulmonary embolism (APE) the increase of pulmonary vascular resistance depends on the thromboli load and potentially on the pulmonary bed contraction caused by neurohormonal reaction. Plasma levels of endothelin were reported to be elevated in pulmonary arterial hypertension. However, there are only a few studies assessing endothelin in patients with APE. MATERIALS & METHODS Therefore in our study we evaluated endothelin concentration in 55 patients (29M, 26F, age 57+/-19 yrs) with confirmed APE for potential value in risk stratification. Patients were compared with 24 healthy volunteers at similar age. On admission blood samples were collected for plasma endothelin concentration. The quantitative assessment of right ventricular (RV) function was performed by echocardiography. RESULTS Endothelin concentrations were similar in APE patients and in control group (1.41(0.22-9.68)pg/mL vs. 1.62(0.27-8.92)pg/mL; p = NS). There was no differences in endothelin levels between APE patients with and without RV dysfunction (1.46(0.38-4.54)pg/mL vs. 1.41(0.22-9.68)pg/mL; p = NS). Endothelin concentration did not differ between patients with serious adverse events and APE group with event-free clinical course (3.19(0.38-4.27)pg/mL vs. 1.38(0.22-9.68)pg/mL; p = NS). There was no significant correlation between endothelin levels and blood saturation, time from the first symptoms, heart rate, blood pressure, tricuspid valve regurgitation pressure gradient and other echocardiographic parameters. CONCLUSIONS We concluded that plasma endothelin concentrations assessed on admission are not elevated in patients with APE and it does not play as important role in acute phase of increase of pressure in pulmonary arteries as in chronic pulmonary hypertension.

d-Dimer Assessment Improves the Simplified Pulmonary Embolism Severity Index for In-Hospital Risk Stratification in Acute Pulmonary Embolism:

d-dimer (DD) levels are used in the diagnostic workup of suspected acute pulmonary embolism (APE), but data on DD for early risk stratification in APE are limited. In this post hoc analysis of a prospective observational study of 270 consecutive patients, we aimed to optimize the discriminant capacity of the simplified pulmonary embolism severity index (sPESI), an APE risk assessment score currently used, by combining it with DD for in-hospital adverse event prediction. We found that DD levels were higher in patients with complicated versus benign clinical course 7.2 mg/L (25th-75th percentile: 4.5-27.7 mg/L) versus 5.1 mg/L (25th-75th percentile: 2.1-11.2 mg/L), P = .004. The area under the curve of DD for serious adverse event (SAE) was 0.672, P = .003. d-dimer =1.35 mg/L showed 100% negative predictive value for SAE and identified 11 sPESI ≥1 patients with a benign clinical course, detecting the 1 patient with SAE from sPESI = 0. d-dimer >15 mg/L showed heart rate for SAE 3.04 (95% confidence interval [CI]: 1-9). A stratification model which with sPESI + DD >1.35 mg/L demonstrated improved prognostic value when compared to sPESI alone (net reclassification improvement: 0.085, P = .04). d-dimer have prognostic value, values <1.35 mg/L identify patients with a favorable outcome, improving the prognostic potential of sPESI, while DD >15 mg/L is an independent predictor of SAE.

Age-adjusted plasma D-Dimer levels in suspected acute pulmonary embolism - a retrospective, single center study.

INTRODUCTION The conventional D‑dimer threshold (CDD) is characterized by high sensitivity and low specificity in diagnosing acute pulmonary embolism (PE) in older patients. A higher cut‑off level for D‑dimer has been proposed, aiming at increasing the specificity while maintaining high sensitivity. It is calculated by multiplying the patients age in years by a coefficient of 10 (YADD10). OBJECTIVES The aim of this study was to validate the clinical value of YADD10 in patients with suspected acute PE and to optimize this threshold to achieve increased specificity paired with high sensitivity. PATIENTS AND METHODS The medical records of 1022 patients with suspected acute PE, hospitalized between the years 2014 and 2016, were retrospectively analyzed. Patients older than 50 years, with complete medical records and good quality of multislice computed tomography (CT) scans were enrolled. The sensitivity, specificity, negative predictive value, positive predictive value, and accuracy of the proposed thresholds were calculated and compared with those of the CCD. The number of computed tomography scans that could have been avoided with higher thresholds was determined. RESULTS The final analysis included 321 patients (176 women; mean age, 74.2 years; range, 51-101 years). Acute PE was confirmed in 135 patients. The sensitivity of CDD was 100%, and specificity-5.4%. The use of the YADD10 and YADD11 thresholds (obtained by multiplying by the coefficients of 10 and 11, respectively) resulted in maintaining high sensitivity, with increased specificity of 8.6% (YADD10) and 12.4% (YADD11). The number of unnecessary CT scans was reduced by 7%. CONCLUSIONS The YADD thresholds are characterized by high sensitivity and increased specificity when compared with CDD, thus allowing for a safe reduction of the number of CT scans. A prospective study should be conducted to validate these results.

Ocena przebiegu klinicznego u chorych z ostrą zatorowością płucną i skrzeplinami w jamach prawego serca. Doświadczenia jednego ośrodka

Introduction. Assessment of the clinical course of patients with acute pulmonary embolism (PE) and a right heart thrombus (RiHT). Material and methods . The analysis included 13 consecutive patients with echocardiographically detected RiHT and acute PE who were treated in our department. The endpoints were 30-day all-cause mortality and 30-day acute PE-related mortality. When a clear alternative cause of death was reported, a non-acute PE-related death was diagnosed and this contributed to 30-day all-cause mortality. All other fatalities were classified as related to acute PE. Results. High risk acute PE was diagnosed in 4 of 13 patients, and intermediate risk acute PE was diagnosed in the remaining 9 patients. Thrombolysis was the first-choice treatment in 4 (31%) patients, 6 (46%) patients were only anticoagulated, and the remaining 3 (23%) patients underwent surgical treatment. The main indication for embolectomy was RiHT entrapped in a patent foramen ovale (PFO). Two patients died during the first 30 days; they were hemodynamically unstable and deaths occurred within 48 hours since the diagnosis. No hemodynamically stable patients died within 30 days since the diagnosis. Conclusions . Thirty-day mortality in patients with RiHT depended mostly on the patient’s clinical condition and was not related to the presence or morphology of the thrombus. Patients with shock or hypotension may possibly benefit more from primary invasive treatment compared to drug therapy.