Chronic thromboembolic pulmonary hypertension

Hoeper, Marius M.; Madani, Michael M.; Nakanishi, Norifumi; Meyer, Bernhard; Cebotari, Serghei; Rubin, Lewis J.

doi:10.1016/s2213-2600(14)70089-x

Cited by 186 publications

(169 citation statements)

References 91 publications

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“…Both the extent of proximal occlusion of the pulmonary arteries and secondary small-vessel arteriopathy are considered to contribute to the elevated pulmonary artery resistance. 31) Thus, many aspects of endothelial function in patients with CTEPH remain unclear. In the present study, 123 I-MIBG uptake in patients with San Diego class III CTEPH was not significantly different from that in controls.…”

Section: Discussionmentioning

confidence: 99%

Impairment of Iodine-123-Metaiodobenzylguanidine (<sup>123</sup>I-MIBG) Uptake in Patients with Pulmonary Artery Hypertension

et al. 2018

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SummaryAccording to recent studies, lung uptake of iodine-123-metaiodobenzylguanidine ( 123 I-MIBG) is impaired in many lung diseases and low lung uptake of 123 I-MIBG suggests endothelial dysfunction of the pulmonary artery. The 21 patients with PH were categorized into those with pulmonary artery hypertension (PAH, n = 12) and those with chronic thromboembolic pulmonary hypertension (CTEPH, n = 9). The mean pulmonary artery pressure was not significantly different between patients with CTEPH and PAH (37.7 ± 6.8 versus 32.3 ± 5.3 mmHg respectively; P = 0.054). There were no significant differences in any other hemodynamic parameters between the two groups. The lung uptake of 123 I-MIBG in PAH patients (early image: 1.54 ± 0.18, delayed image: 1.41 ± 0.16) was significantly lower than that of CTEPH patients (early image: 2.17 ± 0.25, P < 0.0001; delayed image: 1.99 ± 0.20, P = 0.0001, adjusted for age and World Health Organization classification) and controls (early image: 2.32 ± 0.27, P = 0.0007; delayed image: 1.92 ± 0.19, P = 0.0007). In conclusion, we found for the first time that the lung uptake of 123 I-MIBG in patients with PAH is lower than that in patients with CTEPH and controls.(Int Heart J 2018; 59: 112-119)

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Section: Discussionmentioning

confidence: 99%

Impairment of Iodine-123-Metaiodobenzylguanidine (<sup>123</sup>I-MIBG) Uptake in Patients with Pulmonary Artery Hypertension

et al. 2018

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“…Patients with suspected CTEPH should be referred to a specialist centre for right-heart catheterization and pulmonary angiography. Surgical pulmonary endarterectomy is still the treatment of choice for CTEPH and is associated with excellent longterm results and a high probability of cure [4]. Although several studies have shown that homocysteine levels can be reduced by vitamin supplementation, it has yet to be proven that this reduction leads to a reduced risk of cardiovascular morbidity and mortality [12].…”

Section: Discussionmentioning

confidence: 99%

“…Hyperhomocysteinemia is another accepted risk factor for pulmonary thromboembolism [3]. Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare condition presenting in 2-4% of patients after acute pulmonary embolism but characterized by significant morbidity and mortality [4,5]. The association of NS and hyperhomocysteinemia with CTEPH is extremely rare.…”

Section: Introductionmentioning

confidence: 99%

Hereditary hyperhomocysteinemia associated with nephrotic syndrome complicated by artery thrombosis and chronic thromboembolic pulmonary hypertension: A case report

Ruggeri¹,

Bello²,

Nucera³

et al. 2017

Monaldi Arch Chest Dis

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We present here the case of a 30-year-old man with a long term history of nephrotic syndrome (NS) who developed an episode of acute left main pulmonary artery thrombosis complicated by a lung abscess. During the hospital admission was also identified a concomitant hyperhomocysteinemia. After an atypical resection of the left upper pulmonary lobe and the starting of long term anticoagulation the patient was discharged but did not attend the planned follow up visits until one year later when he was seen again for severe dyspnea and exercise intolerance. At this time chronic thromboembolic pulmonary hypertension (CTEPH) was diagnosed by lung perfusion scintigraphy and right heart catheterization. He initially refused the surgical treatment but, after six months, for the presence of worsening dyspnea was referred for bilateral pulmonary endarterectomy followed by a cardio-thoracic rehabilitation program. After a follow-up of seven years the patient is alive and in stable conditions. NS and hyperhomocysteinemia are both known risk factors for pulmonary embolism (PE), but their association with CTEPH is extremely rare. We discuss here the possible mechanisms linking these conditions. CTEPH must be suspected in any patient with NS, with or without hyperhomocysteinemia, and unexplained dyspnea.

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“…Single lung transplantation (SLT x ), double lung transplantation (DLT x ), and combined heart and lung transplantation (HLT x ) have been performed worldwide in adults for the primary indication of PAH [68]. In PAH patients undergoing lung transplantation, the International Society for Heart and Lung Transplantation registry reports 1-, 3-, 5-, and 10-year survivals of 66%, 57%, 47%, and 27%, respectively [68].…”

Section: Atrial Septostomymentioning

confidence: 99%

Treatment of Pulmonary Hypertension

Madden¹

2015

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SummaryPulmonary arterial hypertension (PAH) is a chronic progressive disease of the pulmonary vasculature characterized by elevated pulmonary arterial pressure and secondary right ventricular failure. PAH is considered a life-threatening condition unless treated. This article provides a comprehensive review of controlled and uncontrolled trials to define the risk-benefit for different therapeutic options of this clinical disorder. Relevant published articles were identified through searches of the National Center for Biotechnology PubMed database. All therapeutic measures for PAH were discussed. Six drugs have been approved in the United States for the treatment of PAH. Extensive medical advancement has been achieved in treatment of PAH. However, none of the approved therapies have shown ability to cure the disease. New research should be performed to develop promising new therapies. Full-text PDF:

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Chronic thromboembolic pulmonary hypertension

Cited by 186 publications

References 91 publications

Impairment of Iodine-123-Metaiodobenzylguanidine (<sup>123</sup>I-MIBG) Uptake in Patients with Pulmonary Artery Hypertension

Impairment of Iodine-123-Metaiodobenzylguanidine (<sup>123</sup>I-MIBG) Uptake in Patients with Pulmonary Artery Hypertension

Hereditary hyperhomocysteinemia associated with nephrotic syndrome complicated by artery thrombosis and chronic thromboembolic pulmonary hypertension: A case report

Treatment of Pulmonary Hypertension

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