Association of Persistent Right Ventricular Dysfunction at Hospital Discharge After Acute Pulmonary Embolism With Recurrent Thromboembolic Events

Grifoni, Stefano; Vanni, Simone; Magazzini, Simone; Olivotto, Iacopo; Conti, Alberto; Zanobetti, Maurizio; Polidori, Gianluca; Pieralli, Filippo; Nazerian, Peiman; Becattini, Cecilia; Agnelli, Giancarlo

doi:10.1001/archinte.166.19.2151

Cited by 110 publications

(64 citation statements)

References 17 publications

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“…Notably, three out of four patients with persistent PH underwent PEA. The detection of right ventricular dysfunction during the acute phase of PE in a cohort of 301 patients with a first acute episode of PE was associated with an almost four-fold risk of VTE recurrences after a 3-yr follow-up (hazard ratio 3.79, 95% CI 1.8-7.8) [33]. However, the question remains whether early detection of significantly elevated pulmonary arterial pressures is related to true acute PE with right ventricular strain, or to an early manifestation of CTEPH.…”

Section: Coagulation and Fibrinolysismentioning

confidence: 99%

Risk factors and basic mechanisms of chronic thromboembolic pulmonary hypertension: a current understanding

et al. 2012

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All available evidence today indicates that chronic thromboembolic pulmonary hypertension (CTEPH) is primarily caused by venous thromboembolism, as opposed to primary pulmonary vascular in situ thrombosis. Both the initial magnitude of clot and pulmonary embolism (PE) recurrence may contribute to the development of CTEPH. Only few specific thrombophilic factors, such as phospholipid antibodies, lupus anticoagulant and elevated factor VIII, are statistically associated with CTEPH.A mechanistic view of CTEPH as a disease caused by obliteration of central pulmonary arteries by pulmonary emboli is too simplistic. Based on available data one may speculate that PE may be followed by a pulmonary vascular remodelling process modified by infection, immune phenomena, inflammation, circulating and vascular-resident progenitor cells, thyroid hormone replacement or malignancy. Both plasmatic factors (hypercoagulation, ''sticky'' red blood cells, high platelet counts and uncleavable fibrinogens) and a misguided vascular remodelling process contribute to major vessel and small vessel obliteration. Endothelial dysfunction and endothelialmesenchymal transition may be important, but their precise roles remain obscure. There exists no animal model for CTEPH; therefore, experimentation in the future must include human tissues and clinical data in parallel.

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Section: Coagulation and Fibrinolysismentioning

confidence: 99%

Risk factors and basic mechanisms of chronic thromboembolic pulmonary hypertension: a current understanding

et al. 2012

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“…25 The presence of persistent RV dysfunction after acute PE is associated with higher rates of recurrent PE, deep vein thrombosis, and PE-related death. 26 Moreover, presence of myocardial necrosis in PE, as determined by elevation in troponin, is associated with significantly worse prognosis. 27 Taken together these findings highlight the vulnerability of patients with submassive PE.…”

Section: Discussionmentioning

confidence: 99%

Submassive Pulmonary Embolism

et al. 2013

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ForewordInformation about a real patient is presented in stages (boldface type) to expert clinicians (Drs Louis J. Dell'Italia and David C. McGiffin) who respond to the information, sharing his or her reasoning with the reader (regular type). A discussion by the authors follows.A 67-year-old black woman presents to the emergency department with a 1-day history of dyspnea, which began the previous morning initially with moderate exertion now progressing to dyspnea at rest. She denies chest pain, cough, palpitations, nausea, diaphoresis, lower extremity swelling, paroxysmal nocturnal dyspnea, orthopnea, presyncope, or syncope. Her medical history is notable for hypertension, diabetes mellitus, and hypothyroidism. Her medications include metoprolol tartrate 12.5 mg twice daily, metformin 1000 mg twice daily, levothyroxine 25 μg daily, and estradiol 1 mg daily for symptomatic management of hot flashes. She lives alone and is a retired schoolteacher. She does not smoke, drink alcohol, or use illicit drugs. Family history is not significant. Travel history is notable for round-trip plane flight from Alabama to Utah, arriving home 2 days previously.On physical examination her temperature is 98.4°F, pulse is 94 beats/min, blood pressure is 112/55 mm Hg in the right arm, 110/58 mm Hg in the left arm, respiratory rate 26 breaths/min, and oxygen saturation 90% on room air. She is an obese black woman (body mass index 32 kg/m 2 ) in mild distress secondary to shortness of breath. Jugular venous pressure is estimated at 14 cm H 2 0. Lungs are clear to auscultation. The heart rhythm is regular with a normal S1 and S2. No murmurs, rubs, or gallops are appreciated. Peripheral pulses are brisk and symmetrical with trace pretibial pitting edema. Abdominal examination is benign. Dr Louis J. Dell'Italia:This patient presents with a 24-hour history of dyspnea progressing from symptoms with exertion to now occurring at rest. Probable causes for this presenting complaint often involve serious cardiopulmonary pathology. The history and physical examination is helpful in narrowing the differential and raises particular concern for acute pulmonary thromboembolism (PE). Certain risk factors increase suspicion for venous thrombosis in this patient, including obesity, hormone replacement therapy, and recent plane flight. However, air travel less than 6 hours is associated with a very low incidence of venous thromboembolism and therefore does not represent an identifiable risk factor for thrombosis.1 Rapid onset dyspnea at rest or exertion, as with this case, is the most common presenting symptom for acute PE. Currently the patient appears hemodynamically stable, although β-blockade may blunt a tachycardic response. Coupled with the history is an examination that is remarkable for an obvious elevation of the jugular venous pressure with clear lung fields, suggestive of right heart failure. Combined with sudden dyspnea and hypoxia, these findings strongly suggest the diagnosis of acute PE. It would be prudent to evaluate for deep vein thro...

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“…Persistent RV dysfunction is a predictor of adverse long-term prognosis. 23,24 Grifoni et al reported that persistence of RV dysfunction at hospital discharge is a frequent finding, occurring in approximately 20% of patients with a first episode of PE not complicated with concomitant cardiopulmonary disease. 24 In the present study, RV overload persisted in only 1 patient (3.1%) among those without concomitant cardiopulmonary disease and this favorable result may be related to the early effect of monteplase with catheter-based treatment.…”

Section: Discussionmentioning

confidence: 99%

Thrombolysis With a Novel Modified Tissue-Type Plasminogen Activator, Monteplase, Combined With Catheter-Based Treatment for Major Pulmonary Embolism

Yamamoto

Murai

Tokita

et al. 2009

Circ J

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Circ J 2009; 73: 106 -110 ajor pulmonary embolism (PE) is a life-threatening disorder with high mortality and morbidity. [1][2][3] Most of the deaths of patients presenting in shock occur within the first hour after presentation, 1 so rapid therapeutic action is essential to save lives. Thrombolysis with a tissue-type plasminogen activator (t-PA) produces a much faster improvement in vascular obstruction and hemodynamics than heparin treatment 4 and is the established treatment for acute major PE. 5 In Japan, a novel modified t-PA, monteplase, was approved in 2005 for high-risk patients with acute PE. Compared with the properties of native t-PA, the third-generation, bioengineered thrombolytic agent, monteplase, has a longer half-life, greater clot sensitivity, and more rapid lytic capacity. 6 In a double-blinded, randomized study of patients with acute myocardial infarction, monteplase administration led to greater rates of coronary recanalization and at an earlier stage than was achieved with native t-PA. 6 Initial experience of thrombolysis with the third-generation agents for acute PE has been reported, 7,8 the efficacy and safety of the third-generation thrombolytic agents, including monteplase, with or without catheter-based treatment in patients with major PE has not been clarified and were examined in the present study. Methods Patient PopulationAll patients referred with symptoms suggestive of acute major PE were considered for inclusion in the study. Major PE included massive and submassive types in severity; 9 definitions followed the guideline of the European Society of Cardiology. 10 Massive PE involves shock or hypotension and the subgroup of patients with submassive PE can be identified by the echocardiographic findings of right ventricular (RV) overload without hypotension. All patients had confirmation of PE by pulmonary angiography. A total of 50 patients were included in the study between June 2003 and March 2008. During the same period, 13 patients with major PE were not included because of a contraindication to thrombolytic therapy (n=4), use of urokinase as the initial thrombolytic agent (n=5), anticoagulation only with unfractionated heparin (n=3), and 1 death soon after admission. Treatment Regimen and Assessment of EfficacyOf the 50 patients, 46 received monteplase (Cleactor, Eisai, Japan) through a catheter tip placed in the most diseased segment of the pulmonary artery and 4 were adminis- Background A novel modified tissue-type plasminogen activator, monteplase, has been approved for acute major pulmonary embolism (PE) in Japan. Monteplase has rapid and sustained lytic effects because of a steep rise in concentration after bolus infusion and a longer half-life. Methods and ResultsTo assess the efficacy and safety of thrombolysis with monteplase in combination with catheter-based treatment, acute hemodynamic changes and clinical outcomes were assessed in 50 patients with angiographically confirmed major PE. Thrombolysis with monteplase in combination with embolus fragmentation and t...

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Association of Persistent Right Ventricular Dysfunction at Hospital Discharge After Acute Pulmonary Embolism With Recurrent Thromboembolic Events

Abstract: Persistent RVD at hospital discharge after an acute pulmonary embolism is associated with recurrent VTE.

Cited by 110 publications

References 17 publications

Risk factors and basic mechanisms of chronic thromboembolic pulmonary hypertension: a current understanding

Risk factors and basic mechanisms of chronic thromboembolic pulmonary hypertension: a current understanding

Submassive Pulmonary Embolism

Thrombolysis With a Novel Modified Tissue-Type Plasminogen Activator, Monteplase, Combined With Catheter-Based Treatment for Major Pulmonary Embolism

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