Surgical Removal of Blood Clots Reverses PH But Not Sleep Issues in CTEPH Patients, Study Finds

Vijaya Iyer, PhD avatar

by Vijaya Iyer, PhD |

Share this article:

Share article via email
CTEPH sleep disorders

Surgery to remove blood clots from the arteries improves pulmonary hypertension (PH) symptoms but not underlying sleep disorders in patients with chronic thromboembolic pulmonary hypertension (CTEPH), according to a study.

The study, “Chronic thromboembolic pulmonary hypertension: Reversal of pulmonary hypertension but not sleep-disordered breathing following pulmonary endarterectomy,” was published in the International Journal of Cardiology.

CTEPH patients have blood clots in their blood vessels, resulting in increased pressure in the arteries causing pulmonary hypertension.

The arterial blockage caused by the blood clots may induce the remodeling of pulmonary vasculature, causing patients to stop breathing, partially or completely, several times during sleep. Many CTEPH patients experience these abnormal breathing patterns, known as sleep-disordered breathing (SDB).

To remove these clots, patients can undergo an elective surgery known as a pulmonary endarterectomy.

Because a pulmonary endarterectomy removes the blockage, the researchers assessed whether this procedure has an influence on the occurrence of sleep-disordered breathing in CTEPH patients.

The team analyzed 50 adult CTEPH patients who had a pulmonary endarterectomy. Cardiorespiratory tests were performed the night before and one month after the surgery.

The Apnea-Hypopnea Index, or AHI — the number of apnea events, where breathing completely stops, or hypopnea events, where breathing partially stops — was used to determine sleep-disordered breathing.

Patients were divided into three groups: dominant central sleep apnea (CSA), where AHI is equal to five or higher, and more than 50% of AHI events cause very slow breathing during sleep; dominant obstructive sleep apnea (OSA) where AHI is equal to five or higher, and more than 50% of AHI events cause a complete stop in breathing during sleep; and no sleep disorder, with an AHI of less than five.

In addition, a pulse oximeter was placed on the patient’s finger to detect oxygen levels in the blood. Nasal airflow pressure was also monitored throughout the study.

As previously reported, results showed that there was a significant improvement of PH symptoms in CTEPH patients after the surgery. It resulted in a more than 50% reduction in both pulmonary arterial pressure and resistance required to pump blood, or pulmonary vascular resistance.

The cardiac index — a measure of the amount of blood the heart pumps — also increased by more than 20% post-surgery.

However, the improvements observed in PH did not alleviate sleep-disordered breathing.

There was no significant difference in the number of patients with overall sleep-disordered breathing reported before (64%) and after surgery (68%). However, there was a marked change in obstructive and central sleep apnea patterns — before the intervention, 18 patients had no sleep disorder, 22 had obstructive sleep apnea, and 10 had central sleep apnea; after the surgery, 16 patients had no sleep disorder, 30 had obstructive sleep apnea, and four had central sleep apnea.

Five patients with central sleep apnea moved to the obstructive sleep apnea group post-surgery. The researchers noted that PH parameters had significantly improved in CTEPH patients who moved from the central to the obstructive sleep apnea group. Before surgery, PH likely induced central sleep apnea in these patients, which masked the underlying sleep disorder pattern, the team hypothesized.

Based on the results, the researchers concluded that “SDB is high in patients with CTEPH even after resolution of PH,” namely obstructive sleep apnea, suggesting that this sleep disorder “may play a role in the development of chronic thromboembolic pulmonary hypertension.”

The team suggests that tests focused on sleep might be needed when assessing CTEPH patients, and that further studies “are required to define the role of OSA in the pathogenesis or progression of CTEPH and the value of its active treatment.”