Arterial Stiffness Early Marker of CTEPH After Embolism

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by Marta Figueiredo PhD |

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In people experiencing a pulmonary embolism, higher-than-normal arterial stiffness at the time of hospital discharge increased the risk of pulmonary arterial hypertension (PAH) when evaluated one month later, according to a study in Italy.

Given that this patient population is at risk of chronic thromboembolic pulmonary hypertension (CTEPH) — a rare type of pulmonary hypertension caused by blood clots in the lungs — these findings suggest that increased arterial stiffness in these patients may be an early marker of CTEPH.

Notably, the data also highlighted the usefulness of cardio-ankle vascular index (CAVI), a non-invasive method of measuring arterial stiffness, and its scores to determine a high-risk threshold that may help identify patients at risk of developing CTEPH, the researchers noted.

The study, “Peripheral Arterial Stiffness in Acute Pulmonary Embolism and Pulmonary Hypertension at Short-Term Follow-Up,” was published in the Journal of Clinical Medicine and conducted by a team from Italy.

Pulmonary embolism is a sudden blockage of an artery in the lung, mostly caused by blood clots from deep veins in the legs that travel to and become stuck in the lungs. These clots restrict blood flow through the lungs, which causes a localized increase in blood pressure and limits oxygen transport to the rest of the body.

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CTEPH is “a severe and under-recognized complication of acute pulmonary embolism,” the researchers wrote. It is characterized by blood clot-associated chronic PAH that forces the heart to work harder to pump blood, which can lead to heart failure if unrecognized and left untreated.

Multiple risk factors are associated with CTEPH, such as younger age, non-O type blood group, spleen removal, cancer, inflammatory disease, and underlying autoimmune or blood-related disorders.

Notably, previous studies have shown that higher pulmonary arterial pressure, as measured through an echocardiogram, in pulmonary embolism patients, was associated with a “higher risk of developing pulmonary hypertension and should trigger a high suspicion of CTEPH development at the time of hospital discharge,” the team wrote.

Now, a team of researchers at the Sapienza University of Rome and the Sandro Pertini Hospital, also in Rome, evaluated whether, in people with pulmonary embolism, arterial stiffness, as measured with CAVI, could be an early marker of the blood vessel remodeling mechanisms that drive CTEPH.

Increased arterial stiffness, or arteries with less elastic properties (important for blood flow), is associated with high blood pressure and is a risk factor of cardiovascular disease.

CAVI is a non-invasive method of measuring arterial stiffness that involves the placement of electrocardiogram electrodes on both wrists, a microphone on the sternum (breastbone), and four blood pressure cuffs wrapped around the legs and arms.

Notably, CAVI is easier to acquire and less affected by blood pressure than pulse wave velocity, the most widely used measure for arterial stiffness.

The researchers analyzed arterial stiffness at the time of hospital discharge and signs of pulmonary hypertension — assessed through an echocardiogram within one month from hospital discharge — in 40 people referred to their hospital due to a pulmonary embolism from June to December 2019.

For comparison analyses, these patients, with a mean age of 69 years and 55% being women, were matched for age and sex to 45 idiopathic — no known cause — pulmonary arterial hypertension (IPAH) patients, 40 people with high blood pressure (hypertension), and 40 healthy people.

Results showed that patients with either pulmonary embolism or IPAH had comparable arterial stiffness (CAVI values), which were significantly higher than those of healthy individuals and people with hypertension.

Higher arterial stiffness in pulmonary embolism patients may be explained by the known association between arterial stiffness and systemic inflammation, which is a known consequence of pulmonary embolism, the team noted.

Also, high CAVI values were associated significantly with echocardiography-derived high risk of PAH.

Particularly, the pulmonary embolism patients with CAVI values of 9 or higher at the time of hospital discharge had a 60% or greater chance of having echocardiographic signs of PAH at the one-month assessment.

Notably, CTEPH was confirmed after three months of anti-clotting treatment in the four pulmonary embolism patients with CAVI values greater than 9 at hospital discharge

These findings highlight “a possible positive predictive role of CAVI as an early marker for the development of CTEPH,” suggesting that assessing CAVI in patients with pulmonary embolism “could improve risk stratification for the development of CTEPH,” the researchers wrote.

The data also points to increased arterial stiffness as “a reflection of pulmonary vascular remodeling induced by PE [pulmonary embolism],” the team added, noting this may boost research on the molecular changes in the systemic circulation induced by pulmonary embolism that lead to increased arterial stiffness, PAH, and ultimately CTEPH.

Still, larger studies are needed to confirm the association between CAVI and CTEPH development in this patient population.