Acute coronary insufficiency due to pulmonary embolism

Dack, Simon; Mastér, Arthur M.; Horn, Henry; Grishman, Arthur; Field, Leonard E.

doi:10.1016/0002-9343(49)90396-4

Cited by 74 publications

(15 citation statements)

References 32 publications

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“…It has also been predicted that severe PE increases RV wall tension, causing both shear force injury to myocytes and compression of the right coronary artery (23,24). 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).…”

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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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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“…As a consequence, the right ventricle reacts with acute dilatation [15,16] and increased coronary perfusion [12] with resulting positive inotropic effect. However, if the pulmonary hypertension persists, these protective mechanisms fail and contribute to ischemic damage: the right ventricular dilatation, in fact, affects the left ventricular diastolic compliance determining a decrease in the left ventricular output with subsequently reduced coronary perfusion of the right ventricle and ischemic damage due to the combination of lower coronary supply and increased demand for oxygen [3,[17][18][19]. Even if this theory is generally accepted, morphological evidence of ischemic damage is still missing: Iwadate et al [7,11] could not demonstrate ischemic changes at the right ventricle in cases of PT, but could observe a tendency to increased macrophage infiltrates in cases of PT.…”

Section: Introductionmentioning

confidence: 99%

Morphological identification of right ventricular failure in cases of fatal pulmonary thromboembolism

et al. 2010

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Pulmonary thromboembolism is a life-threatening event potentially determining right ventricular failure. Even if the pathophysiology of this phenomenon has been widely investigated, no morphological demonstration of right ventricular ischemic damage determining right ventricular failure in cases of fatal pulmonary embolism has been reported till now. We performed an immunohistochemical investigation with the markers fibronectin and C5b-9 in 26 cases of fatal pulmonary thromboembolism (16 ♀, 10 ♂, mean age 56.4 years), as well as in 25 cases of myocardial infarction (16♀, 9♂, mean age 60.8 years) and 20 cases of hanging (3♀, 17♂, mean age 40.8 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 prepared. The reactions were semiquantitatively classified and the groups compared. In the study group, the occurrence of ischemic changes at the right ventricle was significantly higher than in cases of myocardial infarction and global hypoxia due to hanging. The determining aspect of the immunohistochemical examination is the identification of 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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“…It has been suggested that coronary insuffi ciency occurs in patients with PE since right ventricular infarction has been described during the acute phase of high-risk PE, with angiographically normal coronary arteries [22,23]. However, Stein et al, reported that coronary blood fl ow was not reduced except for terminal stages [24].…”

Section: Discussionmentioning

confidence: 99%