Persistent Post-Embolic Pulmonary Hypertension

Soyza, Neil de; Murphy, Marvin L.

doi:10.1378/chest.62.6.665

Cited by 66 publications

(17 citation statements)

References 11 publications

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“…37 Long-term follow-up studies have consistently demonstrated that incomplete perfusion recovery, even years after acute PE, occurs in one-third to more than two-thirds of patients. [38][39][40][41] Up to 15% of acute PE patients remain symptomatically compromised 2 years after treatment 42 and may have abnormal pulmonary gas exchange (O 2 gradients, dead space, etc) as well. 43 These findings suggest that incomplete clot resolution has clinical manifestations in a significant proportion of acute PE patients, the most severe of which is CTEPH.…”

Section: Discussionmentioning

confidence: 99%

High prevalence of dysfibrinogenemia among patients with chronic thromboembolic pulmonary hypertension

Morris

Marsh

Chiles

et al. 2009

Blood

157

114

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The mechanism by which chronic thromboembolic pulmonary hypertension (CTEPH) develops after acute pulmonary thromboembolism is unknown. We previously reported that fibrin from CTEPH patients is relatively resistant to fibrinolysis in vitro. In the present study, we performed proteomic, genomic, and functional studies on fibrin(ogen) to investigate whether abnormal fibrin(ogen) might contribute to the pathogenesis of CTEPH. Reduced and denatured fibrinogen from 33 CTEPH patients was subjected to liquid chromatography-mass spectrometry analysis. Fibrinogen from 21 healthy controls was used to distinguish atypical from commonly occurring mass peaks. Atypical peaks were further investigated by targeted genomic DNA sequencing. Five fibrinogen variants with corresponding heterozygous gene mutations (dysfibrinogenemias) were observed in 5 of 33 CTEPH patients: B␤ P235L/␥ R375W, B␤ P235L/␥ Y114H, B␤ P235L, A␣ L69H, and A␣ R554H (fibrinogens San Diego I-V ). B␤ P235L was found in 3 unrelated CTEPH patients. Functional analysis disclosed abnormalities in fibrin polymer structure and/or lysis with all CTEPH-associated mutations. These results suggest that, in some patients, differences in the molecular structure of fibrin may be implicated in the development of CTEPH after acute thromboembolism. (Blood. 2009;114: 1929-1936

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Section: Discussionmentioning

confidence: 99%

High prevalence of dysfibrinogenemia among patients with chronic thromboembolic pulmonary hypertension

Morris

Marsh

Chiles

et al. 2009

Blood

157

114

View full text Add to dashboard Cite

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“…To date, we do not know for sure which cases will become chronic; those with pulmonary artery pressure higher than 40 mmHg at the moment of the acute event are known to have a higher probability of developing chronic pulmonary involvement 5,18,19 . Remy-Jardin et al 20 demonstrated involvement of a larger pulmonary area in patients who did not present complete resolution of the acute episode.…”

Section: Resultsmentioning

confidence: 99%

Avaliação da hipertrofia da camada média nos pacientes com embolia pulmonar: estudo anatomopatológico

Arnoni¹,

Jatene²,

Bernardo³

et al. 2007

Arq. Bras. Cardiol.

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SummaryObjective: To compare the arterial response of cases of acute and chronic embolism, seeking to associate ischemic pulmonary remodeling with progression to chronicity.Methods: Retrospective analysis of 61 necropsies of patients who died in the Instituto do Coração (31 cases of pulmonary embolism and 30 cases of acute myocardial infarction). Slides of pulmonary tissue were obtained from all cases and analyzed qualitative and quantitatively (medial thickness measurement).Results: Qualitative analysis enabled the differentiation between cases of embolism and the control group, thus characterizing the two groups and defining the adequate choice of the control group. The alterations predominated in patients with embolism (alveolar inflammation and edema, infarction, vasoconstriction, concentric intimal proliferation, presence of thrombus). Quantitative analysis demonstrated higher percent medial thickness in the cases of embolism than in the control group; among the cases of embolism, no differences in intra (acute -19.74 and chronic -20.04) and pre-acinar (acute -18.85 and chronic -18.68) arteries were observed.Conclusion: The lack of difference among the groups with embolism and the higher values of percent medial thickness in the peripheral arteries allow the conclusion that the vascular response is more intense and starts in these arteries. (Arq Bras Cardiol 2007;88(6):584-589)

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“…If residual throm boemboli continue to accumulate, chronic pulmonary hypertension may result, with chronic cor pulmonale becoming clinically evident in patients with the most severe pul monary hypertension. The development of chronic cor pulmonale is shown below: That chronic pulmonary hypertension may result from PE treated with conven tional anticoagulants was made evident by de Soyza and Murphy [10] who recatheterized 13 patients with previous PE, after an aver age time interval of 49 months. Nine of the 13 patients had pulmonary hypertension at rest and during exercise.…”

Section: Thrombolytic Therapy and The Pulmonary Microcirculationmentioning

confidence: 99%