Patients with sarcoidosis have lower coronary flow velocity reserve (CFVR), a measure of disturbances in blood flow in heart muscles, compared to healthy volunteers, researchers found.
CFVR is the maximum increase in blood flow through the coronary arteries above the normal resting flow. Low CFVR indicates that there is coronary microvascular dysfunction, a malfunction in tiny vessels in the heart muscle.
A total of 40 patients with sarcoidosis, age 18 and older, without known atherosclerotic coronary artery disease (a condition in the arteries supplying blood to the heart in which plaque builds up inside the artery walls) or risk factors for atherosclerosis, were enrolled in the study, along with 42 healthy volunteers.
The peak velocity of blood flow was 60.5 in sarcoidosis patients and 68.9 in healthy controls. CFVR was 2.08 in patients and 3.03 in controls. Both measures were thereore lower in patients with sarcoidosis.
Older age and high blood pressure were also found to be associated with a lower CFVR in sarcoidosis patients.
The drop in CFVR seen in patients did not relate to the severity of sarcoidosis, the duration of disease, or the degree of inflammation. Instead, it was associated with the presence of sarcoidosis itself.
“Our findings indicate that the majority of patients with sarcoidosis have an abnormal CFVR and mean CFVR is significantly lower than healthy volunteers, suggesting that an impairment in flow reserve is a common condition in patients with sarcoidosis even when clinically manifest cardiac involvement is not present,” the team wrote.
An abnormal CFVR may indicate a clinically undetectable myocardial involvement (involvement of the heart muscle) in sarcoidosis, the researchers pointed out, stating that poorer health outcomes in patients with sarcoidosis may result from it. However, additional studies are needed.
“Coronary flow velocity reserve is reduced in patients with sarcoidosis even in the absence of risk factors for CAD [coronary artery disease], thus strongly suggesting that coronary microvascular function is disturbed in these patients,” the team concluded, adding that “further studies are needed to elaborate on the mechanisms of microvascular dysfunction in patients with sarcoidosis.”