Right ventricular damage due to pulmonary embolism: examination of the number of infiltrating macrophages

Iwadate, Kimiharu; Doi, Mikio; Tanno, Kozo; Katsumura, Seiko; Itô, Haruo; Sato, Keita; Yonemura, Isamu; Ito, Yohko

doi:10.1016/s0379-0738(03)00138-5

Cited by 46 publications

(46 citation statements)

References 20 publications

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“…The relationship between elevated WBC count and left ventricular dysfunction in patients with acute coronary syndrome and the various potential mechanisms of myocardial injury mediated by leukocytes have been described in detail [3]. There is growing evidence from animal and autopsy studies that acute PE with at least moderately severe pulmonary hypertension results in right ventricular myocyte lysis and infiltration by neutrophils, macrophages, and lymphocytes in humans and rats [12][13][14][15]17] and that this inflammation independently amplifies injury [25]. Therefore, an elevated WBC count may indicate PE-related right heart dysfunction, a known factor for adverse prognosis in patients with PE [11].…”

Section: Discussionmentioning

confidence: 99%

“…Early death after PE is strongly associated with right ventricular dysfunction [11]. Animal and autopsy studies demonstrated that neutrophils are not only involved in the development of venous thrombosis but that an influx of neutrophils and other WBCs may contribute to right ventricular dysfunction following PE [12][13][14][15][16][17]. Moreover, the WBC count also correlates with levels of fibrinogen, factor VII, and factor VIII and thus, may be a marker for hypercoagulability [18].…”

Section: Introductionmentioning

confidence: 99%

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White blood cell count and mortality in patients with acute pulmonary embolism

et al. 2013

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Although associated with adverse outcomes in other cardiovascular diseases, the prognostic value of an elevated white blood cell (WBC) count, a marker of inflammation and hypercoagulability, is uncertain in patients with pulmonary embolism (PE). We therefore sought to assess the prognostic impact of the WBC in a large, state‐wide retrospective cohort of patients with PE. We evaluated 14,228 patient discharges with a primary diagnosis of PE from 186 hospitals in Pennsylvania. We used random‐intercept logistic regression to assess the independent association between WBC count levels at the time of presentation and mortality and hospital readmission within 30 days, adjusting for patient and hospital characteristics. Patients with an admission WBC count <5.0, 5.0–7.8, 7.9–9.8, 9.9–12.6, and >12.6 × 109/L had a cumulative 30‐day mortality of 10.9%, 6.2%, 5.4%, 8.3%, and 16.3% (P < 0.001), and a readmission rate of 17.6%, 11.9%, 10.9%, 11.5%, and 15.0%, respectively (P < 0.001). Compared with patients with a WBC count 7.9–9.8 × 109/L, adjusted odds of 30‐day mortality were significantly greater for patients with a WBC count <5.0 × 109/L (odds ratio [OR] 1.52, 95% confidence interval [CI] 1.14–2.03), 9.9–12.6 × 109/L (OR 1.55, 95% CI 1.26–1.91), or >12.6 × 109/L (OR 2.22, 95% CI 1.83–2.69), respectively. The adjusted odds of readmission were also significantly increased for patients with a WBC count <5.0 × 109/L (OR 1.34, 95% CI 1.07–1.68) or >12.6 × 109/L (OR 1.29, 95% CI 1.10–1.51). In patients presenting with PE, WBC count is an independent predictor of short‐term mortality and hospital readmission. Am. J. Hematol. 88:677–681, 2013. © 2013 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

White blood cell count and mortality in patients with acute pulmonary embolism

et al. 2013

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“…The possibility of detecting necrosis only with a very early marker probably indicates a very rapid evolution from the occurrence of the ischemic damage to death. Inflammatory changes at the sub-endocardial region were reported in cases of pulmonary embolism [43,44] and may represent a late reaction to ischemia in cases of non-fatal embolism.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical identification of prevalent right ventricular ischemia causing right heart failure in cases of pulmonary fat embolism

et al. 2009

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Pulmonary fat embolism is a life-threatening event that may result to potentially determining right ventricular failure. Even if the pathophysiology of this phenomenon has been widely investigated, no immunohistochemical demonstration of right ventricular failure following pulmonary fat embolism has been reported till now. We performed an immunohistochemical investigation with the markers fibronectin and C5b-9 in 21 cases of polytrauma with bone fractures (study group-nine females and 12 males; mean age 64.6 years) compared to a control group of 21 forensic cases with various causes of death (nine females and 12 males; mean age 68.6 years). In each case at least one tissue slide from both cardiac ventricles (free wall of the right ventricle, anterior and/or posterior wall of the left ventricle) was available. The reactions were semi-quantitatively classified, and the two groups were compared. In the study group, the occurrence of ischemic changes at the right ventricle was significantly higher than in controls. The determining aspect, however, seems to be the prevalent ischemic lesion at the right ventricle compared to the left one. This may indicate the primary involvement of the right ventricle, thus, demonstrating a right ventricular failure.

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“…Histological studies of human RV tissue taken postmortem demonstrated the presence of neutrophil and monocyte/macrophage cells in a small series of human PE cases (27,28), but the contribution of those inflammatory cells to cardiac injury has not been defined in the clinical setting. To study mechanisms of cardiac injury, we have successfully developed a rat model of PE that employs polystyrene microspheres as emboli (29,32,34).…”

Section: Discussionmentioning

confidence: 99%

“…Although case reports have associated massive PE with frank RV infarction, and patients with RV dysfunction do liberate contractile proteins such as troponins into the blood, no study has shown evidence to support RV tissue necrosis as the primary cause of RV contractile dysfunction observed after PE (25,26). Indeed, postmortem histological analyses of RV muscle from humans with fatal PE demonstrated the accumulation of neutrophils and monocyte/macrophages in the RV but without histological evidence of infarction (27,28).…”

Section: Inhibition Of Cinc-1 Decreases Right Ventricular Damage Causmentioning

confidence: 99%

Inhibition of CINC-1 Decreases Right Ventricular Damage Caused by Experimental Pulmonary Embolism in Rats

Zagorski

Gellar

Obraztsova

et al. 2007

The Journal of Immunology

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Right ventricular (RV) dysfunction is a strong risk factor for poor clinical outcome following pulmonary embolism (PE), the third most prevalent cardiovascular disease. Previous studies in our laboratory demonstrated that RV failure during PE is mediated, in part, by neutrophil-dependant cardiac inflammation. In this study we use DNA microarray analysis of gene expression to demonstrate that PE results in increased expression of the CXC chemokines CINC-1 and CINC-2 between 6 and 18 h after the start of PE in a rat model of PE. Neutrophils accumulate in RV tissue by 18 h, and this inflammation is associated with decreased right heart function. Treatment of rats with Abs to CINC-1 significantly suppressed neutrophil accumulation in RVs during PE (52% reduction in tissue myeloperoxidase) and ameliorated RV failure. In addition, plasma concentration of cardiac troponin I, an established diagnostic marker for cardiac damage, was reduced by 90%. These results suggest that selective anti-inflammatory therapies targeted at neutrophil chemoattractants will reduce cardiac inflammation and reduce RV damage in the setting of PE.

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Right ventricular damage due to pulmonary embolism: examination of the number of infiltrating macrophages

Cited by 46 publications

References 20 publications

White blood cell count and mortality in patients with acute pulmonary embolism

White blood cell count and mortality in patients with acute pulmonary embolism

Immunohistochemical identification of prevalent right ventricular ischemia causing right heart failure in cases of pulmonary fat embolism

Inhibition of CINC-1 Decreases Right Ventricular Damage Caused by Experimental Pulmonary Embolism in Rats

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