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SAN DIEGO -- Patients with post-traumatic stress disorder (PTSD) have cardiac inflammatory profiles that may put them at risk for major cardiovascular events, researchers reported here.

Patients with PTSD who underwent computed tomography angiography (CTA) had worse vascular dysfunction as measured by the coronary distensibility index (CDI) than those who didn't have PTSD (3.3 versus 4.5, P=0.001), according to Naser Ahmadi, MD PhD, of the University of California Los Angeles, and colleagues.

These patients also had less brown epicardial adipose tissue (bEAT), which is known to be anti-inflammatory, and more white epicardial adipose tissue (wEAT), which has inflammatory functions, Ahmadi reported during a poster session at the here.

Also, cardiovascular event rates were higher among those PTSD patients with vascular dysfunction compared with controls who didn't have PTSD, the researchers found.

"This study demonstrated the prognostic value of CDI, bEAT, and wEAT on risk stratification of PTSD at risk for major adverse cardiovascular events," Ahmadi told 番茄社区app.

Vascular dysfunction is associated with reduced cerebral blood flow, blood-brain barrier disturbances, neuronal dysfunction, neuroinflammation and neurodegeneration, Ahmadi explained, which may play a role in psychological disorders. But the relationship between measures of cardiac inflammation and PTSD hasn't been well-studied, he noted.

They chose to focus on CDI, a measure of vascular dysfunction, and on both white epicardial adipose tissue and brown epicardial adipose tissue; wEAT has a distinct pro-inflammatory component while bEAT has anti-inflammatory functions. Increased wEAT and decreased bEAT is associated with multiple markers of inflammation, vascular dysfunction, and oxidative stress, and is a marker for major cardiovascular events. CDI has also been associated with decreased bEAT and increased wEAT, as well as the presence and severity of atherosclerosis.

Overall, the researchers enrolled 246 patients, among whom 53 had PTSD; the remaining 193 did not. The mean age was 64 and the majority (67%) were male.

In addition to worse scores on the CDI, patients with PTSD had significantly lower amounts of bEAT (46.3 versus 52.6, P=0.001) and significantly higher amounts of wEAT (102.6 versus 66.5, P=0.001).

After adjustment for risk factors, there was a negative relationship between PTSD and levels of CDI and bEAT, and a strong positive relationship between PTSD and wEAT (P<0.05), they reported.

And those inflammatory profiles were tied to cardiovascular outcomes: the researchers observed a significant link between decreased bEAT, impaired CDI, and PTSD with increased major adverse cardiovascular events (MACE).

Indeed, the hazard ratio of MACE was eight-fold higher in PTSD with decreased bEAT, impaired CDI, and increased wEAT, compared to those without PTSD (P<0.05), Ahmadi and colleagues reported.

He concluded that the findings "highlight the important role of neurovascular and neuroendocrine responses of inflammation on PTSD, and its role in identifying individuals with PTSD at risk for MACE."

"The take home-message here for psychiatrists," Ahmadi told 番茄社区app, "is to consider evaluating the cardiac health of their PTSD patients as well as their psychological health."