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      The Value of Electrocardiographic Abnormalities in the Prognosis of Pulmonary Embolism: A Consensus Paper : Pulmonary Embolism & ECG

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          Abstract

          Electrocardiographic (ECG) abnormalities in the setting of acute pulmonary embolism (PE) are being increasingly characterized and mounting evidence suggests that ECG plays a valuable role in prognostication for PE. We review the historical 21-point ECG prognostic score for the severity of PE and examine the updated evidence surrounding the utility of ECG abnormalities in prognostication for severity of acute PE. We performed a literature search of MEDLINE, EMBASE, and PubMed up to February 2015. Article titles and abstracts were screened, and articles were included if they were observational studies that used a surface 12-lead ECG as the instrument for measurement, a diagnosis of PE was confirmed by imaging, arteriography or autopsy, and analysis of prognostic outcomes was performed. Thirty-six articles met our inclusion criteria. We review the prognostic value of ECG abnormalities included in the 21-point ECG score, including new evidence that has arisen since the time of its publication. We also discuss the potential prognostic value of several ECG abnormalities with newly identified prognostic value in the setting of acute PE.

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          Most cited references61

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          2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism.

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            Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II.

            Selection of patients for diagnostic tests for acute pulmonary embolism requires recognition of the possibility of pulmonary embolism on the basis of the clinical characteristics. Patients in the Prospective Investigation of Pulmonary Embolism Diagnosis II had a broad spectrum of severity, which permits an evaluation of the subtle characteristics of mild pulmonary embolism and the characteristics of severe pulmonary embolism. Data are from the national collaborative study, Prospective Investigation of Pulmonary Embolism Diagnosis II. There may be dyspnea only on exertion. The onset of dyspnea is usually, but not always, rapid. Orthopnea may occur. In patients with pulmonary embolism in the main or lobar pulmonary arteries, dyspnea or tachypnea occurred in 92%, but the largest pulmonary embolism was in the segmental pulmonary arteries in only 65%. In general, signs and symptoms were similar in elderly and younger patients, but dyspnea or tachypnea was less frequent in elderly patients with no previous cardiopulmonary disease. Dyspnea may be absent even in patients with circulatory collapse. Patients with a low-probability objective clinical assessment sometimes had pulmonary embolism, even in proximal vessels. Symptoms may be mild, and generally recognized symptoms may be absent, particularly in patients with pulmonary embolism only in the segmental pulmonary branches, but they may be absent even with severe pulmonary embolism. A high or intermediate-probability objective clinical assessment suggests the need for diagnostic studies, but a low-probability objective clinical assessment does not exclude the diagnosis. Maintenance of a high level of suspicion is critical.
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              Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling.

              The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening. In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening. In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law. The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05). In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.
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                Author and article information

                Journal
                Annals of Noninvasive Electrocardiology
                Ann Noninvasive Electrocardiol
                Wiley
                1082720X
                May 2015
                May 2015
                May 20 2015
                : 20
                : 3
                : 207-223
                Affiliations
                [1 ]Department of Medicine, Kingston General Hospital; Queen's University; Kingston Ontario Canada
                [2 ]Department of Cardiology and Internal  Medicine; Specialistic Hospital; Gorlice Poland
                [3 ]Department of Cardiology, Taihe Hospital; Hubei University of Medicine; Shiyan City China
                [4 ]Clinical Unit of Electrocardiography, Heart Institute (InCor), Clinic Hospital, Faculty of Medicine, Sao Paulo University; Sao Paulo; Brazil
                [5 ]Telecardiology Center; Institute of Cardiology; Warsaw Poland
                [6 ]Iberoamerican Forum of Arrhythmias in the Internet, (FIAI), Buenos Aires; Argentina
                [7 ]The Heart Research Follow-up Program, Cardiology Unit; University of Rochester Medical Center; Rochester NY
                [8 ]ICCC-Hospital Sant Pau; Barcelona Catalunya Spain
                [9 ]Department of Internal Medicine and Cardiology; Medical University of Warsaw; Warszawa Poland
                Article
                10.1111/anec.12278
                6931801
                25994548
                0dbe25c7-4995-48e2-ab20-bdaef98cf467
                © 2015

                http://doi.wiley.com/10.1002/tdm_license_1.1

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