Failure to address PE may result in CTEPH

William Kuo

HOLLYWOOD, Fla. — Unresolved pulmonary embolism often leads to chronic thromboembolic pulmonary hypertension, a condition associated with very poor outcomes, a speaker said at the International Symposium on Endovascular Therapy (ISET).

“Chronic thromboembolic pulmonary hypertension (CTEPH) occurs when a pulmonary embolism fails to undergo complete dissolution, and may happen despite anticoagulation,” William Kuo, MD, FSIR, FCCP, FSVM, FCIRSE, professor of vascular and interventional radiology at Stanford University School of Medicine, said. “The hallmark of CTEPH is fibrotic transformation of pulmonary arterial thrombus leading to mechanical obstruction of pulmonary arteries.”

Therefore, he said, it is crucial to determine whether early thrombolytic therapy in patients with PE, especially those ineligible for pulmonary endarterectomy, can prevent CTEPH, but evidence is currently unclear.

Among patients with PE for the first time, approximately 4% to 9% go on to develop CTEPH, but chronic cardiopulmonary disability and breathlessness occur at a higher rate, Kuo said.

In a meta-analysis of 3,671 patients with PE followed for a median of 18 months, 18% had right ventricular dysfunction, 33% had NYHA class II or greater HF and mean 6-minute walk distance was 415 m, in the 4th percentile of age- and sex-matched norms, he said.

Unfortunately, he said, median time between symptom onset and diagnosis of CTEPH is more than 1 year, because the condition presents similarly to other cardiac and pulmonary diseases.

He said CTEPH can be defined as mean pulmonary artery pressure 25 mm Hg and mean pulmonary artery wedge pressure 15 mm Hg as determined by invasive right heart catheterization, as well as the presence of consistent flow-limiting thrombi and/or emboli in the elastic pulmonary arteries despite 3 months of anticoagulation.

“CTEPH is a dual vascular disorder including major-vessel vascular obliteration and peripheral pulmonary arteriopathy resembling classic pulmonary arterial hypertension in many patients,” he said.

Inflammation represents a significant risk factor for CTEPH, and inflammatory disorders concomitant with CTEPH confer a negative impact on survival, according to Kuo, who noted that hypothyroidism is another CTEPH risk factor.

Although CTEPH often stems from acute venous thromboembolism, as many as 40% of patients with the condition have no known history of acute PE, he said.

Numerous studies have demonstrated that CTEPH confers worse quality-of-life and mental health outcomes, he noted.

There is little definitive evidence on how best to prevent CTEPH, Kuo said. In one study of patients with submassive PE, those assigned IV tissue plasminogen plus heparin had no increase in estimated systolic pulmonary artery pressure at 6 months, but among those assigned heparin alone, 27% had an increase.

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Likewise, in the MOPETT trial of patients with moderate PE, those who had thrombolytic therapy were less likely to have pulmonary hypertension than those who had anticoagulation, Kuo said.

In a meta-analysis, patients with PE treated with thrombolysis had a lower risk for moderate or worse functional impairment vs. those treated with anticoagulation, but the difference was not statistically significant, he said.

Pulmonary endarterectomy is a solution in some, but not all, patients. “CTEPH is potentially curable with pulmonary endarterectomy, but only in patients who meet specific surgical criteria,” he said.

References:

Kuo W. Session III: Advances in PE Management. Presented at: the International Symposium on Endovascular Therapy (ISET); Feb. 3-7, 2018; Hollywood, Fla.

Kline JA, et al. Chest. 2009;doi:10.1378/chest.08-2988.

Sharifi M, et al. Am J Cardiol. 2013; 10.1016/j.amjcard.2012.09.027.

Sista AK, et al. Vasc Med. 2017;doi:10.1177/1358863X16670250.

Disclosure : Kuo reports he is a consultant for WalkVascular.