Right Ventricular Infarction in a Patient With Acute Pulmonary Embolism and Normal Coronary Arteries

Pruszczyk, Piotr; Szulc, Marcin; Horszczaruk, Grzegorz J.; Gurba, Hubert; Kobylecka, Małgorzata

doi:10.1001/archinte.163.9.1110

Cited by 21 publications

(14 citation statements)

References 5 publications

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“…[12][13][14] Moreover, autopsy and scintigraphic case series reported RV MIs in patients with major APE. 15,16 Therefore, larger RV dimension and higher Tei index found at follow-up in the APE group may result from damage-induced RV remodelling.…”

Section: Discussionmentioning

confidence: 99%

Long‐term effects of acute pulmonary embolism on echocardiographic doppler indices and functional capacity

Ciurzyński

Kurzyna²,

Bochowicz

et al. 2004

Clinical Cardiology

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SummaryBackground and hypothesis: Hemodynamic and functional consequences of acute pulmonary embolism (APE) are believed to be reversible with antithrombotic treatment. To verify this hypothesis, we reassessed our patients at least 1 year after an episode of APE.Methods: We compared echo Doppler indices and 6-min walking test parameters (6-MWT) of 36 patients (13 men, 23 women, age 66 ± 11 years), studied on average 3.1 ± 2.2 years after an acute episode of pharmacologically treated massive or submassive APE, with data of 30 age-matched subjects (12 men, 18 women, age 67 ± 12 years).Results: At least 1 year after APE, right ventricular (RV) diameter remained increased in patients compared with controls (27 ± 2 vs. 23 ± 2 mm, p < 0.001). Also, acceleration time of pulmonary ejection (AcT) was markedly shorter (97 ± 19 vs. 123 ± 19 ms, p < 0.001) and the diameter of the pulmonary trunk was significantly larger in patients than in controls (21 ± 2.6 vs. 18 ± 2.2, p < 0.001). Although the mean value of the tricuspid valve peak systolic gradient (TVPG) in the APE group at follow-up was similar to that in controls, TVPG > 30 mmHg was recorded in three patients with APE (8.3%). There was no difference in the distance of 6-MWT between both groups; however, the mean desaturation after 6-MWT was higher in the APE group than in controls (3.04 ± 2.08 vs. 1.45 ± 0.69%, p = 0.0005).

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Section: Discussionmentioning

confidence: 99%

Long‐term effects of acute pulmonary embolism on echocardiographic doppler indices and functional capacity

Ciurzyński

Kurzyna²,

Bochowicz

et al. 2004

Clinical Cardiology

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“…Pulmonary embolism can cause right ventricular infarction. 183,184 Hypotension, hypertension and tachycardia could contribute with or without concomitant coronary artery disease. Troponin elevations are more likely to occur in patients with shock 185,186 and clinical variables 187,188 associated with poor outcome.…”

Section: Other Clinical Situations In Which Troponin Levels May Be Elmentioning

confidence: 99%

Troponin: the biomarker of choice for the detection of cardiac injury

Babuin¹

2005

Canadian Medical Association Journal

550

390

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T roponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated. The biology of troponinThe 3-unit troponin complex (troponin I, T and C) along with tropomyosin is located on the actin filament and is essential for the calcium-mediated regulation of skeletal and cardiac muscle contraction. 1 There are tissue-specific isoforms of troponin I, T and C. 2,3 Because the cardiac isoform of troponin C is shared by slow-twitch skeletal muscles, troponin C does not have cardiac specificity and thus is not used in assays for the diagnosis of cardiac injury. 4 There is one cardiac troponin I (cTnI) isoform in myocardial tissue. 5 This isoform has a post-translational tail of 32 amino acids on the N-terminus. 6,7 This sequence and the 42% and 45% dissimilarity with sequences of the other isoforms 8 have made possible the generation of highly specific monoclonal antibodies without cross-reactivity with other noncardiac forms. 9 Three genes control cardiac troponin T (cTnT). 10 These genes and alternative mRNA splicing produce a series of isoforms 10,11 with variable sequences close to the regions of the N-terminus and C-terminus. 10,12 Human cardiac muscle contains 4 troponin T isoforms, but only one is characteristic of the normal adult heart. 13,14 Highly specific antibodies have been made to the N-terminus-specific sequence of this cTnT isoform. 15 The skeletal isoforms present in the fetal heart are replaced by cTnI and cTnT late during fetal development. 16,17 cTnI is not expressed in skeletal muscle or other tissues during development 17 or in response to degenerative or regenerative muscle disease processes. 18 Thus, it is unlikely to be reexpressed in damaged tissues. The situation is more complex for cTnT. Re-expression of fetal forms occurs in cardiac tissue 12 and in diseased skeletal muscle. 19 With the firstgeneration cTnT assay, this problem was compounded by a nonspecific tag antibody that cross-reacted with troponin T in skeletal muscle. 20 Once this antibody was replaced by one with high specificity, false-positive elevations from skeletal muscle were eliminated. 15 Studies using immunohistochemistry and polymerase chain reaction have confirmed that these fetal isoforms are not detected by the assay used today. 21,22 Thus, the assay used to measure cTnT levels has cardiac specificity equivalent to that of assays for cTnI. Characteristics of troponin assaysMost troponin is found in the 3-unit complex (troponin I, T and C) of the c...

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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). 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 Infarction in a Patient With Acute Pulmonary Embolism and Normal Coronary Arteries

Abstract: Figure 2. Heart scintigraphy with technetium Tc 99m pyrophosphate detected abnormal isotope uptake within the right ventricle and left ventricular inferior wall (omega sign), suggestive of acute myocardial damage. LAO indicates left anterior oblique plane.

Cited by 21 publications

References 5 publications

Long‐term effects of acute pulmonary embolism on echocardiographic doppler indices and functional capacity

Long‐term effects of acute pulmonary embolism on echocardiographic doppler indices and functional capacity

Troponin: the biomarker of choice for the detection of cardiac injury

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

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