PTSD in Survivors of Cardiac Arrest Raises CV Event Risk for at Least a Year

November 07, 2018

CHICAGO — Of more than 100 patients who left a major tertiary care center after experiencing cardiac arrest, about 30% showed early signs of post-traumatic stress disorder (PTSD). The group with PTSD also showed a threefold increased adjusted risk for death or cardiac events over the next year compared with the rest.

Those who tested positive for PTSD were younger and more likely to be female than those without PTSD, but the analysis had adjusted for those factors, as well as for comorbidities and whether they had shown a nonshockable initial rhythm at cardiac arrest.

Further adjustment for whether the patient had a history of psychiatric disorders didn't greatly alter the results.

A future goal for patients who survive cardiac arrest would be to screen for those likely to develop PTSD "and start working on some kind of intervention before hospital discharge," Sachin Agarwal, MD, MPH, Columbia University, New York City, told | Medscape Cardiology.

Agarwal is scheduled to report the findings here November 11 at the Resuscitation Science Symposium held during the American Heart Association Scientific Sessions 2018. They are consistent with a body of literature showing high rates of PTSD and associated mortality risk in patients who have experienced myocardial infarction (MI), implantable defibrillator shocks, or cardiac arrest.

The current study, which included only survivors of in-hospital or out-of-hospital cardiac arrest who were mentally capable of self-reporting PTSD symptoms soon after discharge, is unusual for its prospective nature and long follow-up, Agarwal and colleagues observed.

The PTSD-CV Outcomes Link

Development of PTSD after cardiac arrest could potentially trigger CV events by both direct and indirect mechanisms, Agarwal noted.

For example, chronic anxiety after the event can prolong what would otherwise be short fight-or-flight physiologic responses, leading to inflammation and autonomic dysfunction that elevates blood pressure and promotes endothelial dysfunction.

"The second mechanism that has been tested in PTSD models is behavioral dysregulation," he said. For example, "the same medications that are supposed to help you and reduce your CV risk become reminders of your condition, and you stop taking the medications."

And, "with small increases in heart rate and small increases in blood pressure, they think they're going to have an event again. Then they reduce their physical activity and sedentary behavior kicks in. And to offset this stress response, people also start taking more tobacco and alcohol."

The PTSD, he said, "is less about the about the event and more about the enduring somatic reminders of their mortality."

Possible Confounders

Psychiatric evaluations for survivors of cardiac arrest are rare, and "we think it should probably be more common," said Samuel F. Sears, PhD, who directs the Cardiac Psychology Research Lab at East Carolina University, Greenville, North Carolina, in an interview.

Agarwal and his colleagues "did a nice job merging the worlds of cardiovascular clinical trial outcomes and a psychologic diagnosis."

Sears, who isn't connected with the study, said the current findings are "new enough, but not unexpected." And he cautioned, as do the authors, that the analysis adjusted for only a few of many potential confounders.

For example, he said, how many went to cardiac rehabilitation sessions, were on optimal CV medications, received psychiatric counseling, or were prescribed psychiatric meds?

"We don't know if the risk is simply from PTSD patients being unable to take as good care of themselves, or whether there is a more pathophysiologic process that PTSD triggers," he said.

"It may be simply that patients disengage from memories, and disengage from the recovery process, and they simply are trying to escape what is a very aversive set of thoughts and feelings."

Of the 114 survivors of cardiac arrest, 35 tested positive for PTSD symptoms on the PTSD Checklist-Specific (PCL-S) self-assessment instrument, using cut-off values appropriate for the disorder in medical settings.

Ten patients died and 29 experienced a major adverse cardiac event (MACE) over a mean of 12.4 months, for rates of 8.8% and 25.4%, respectively. MACE was defined here as hospitalization for nonfatal MI, unstable angina, heart failure, urgent or emergent coronary revascularization procedures, or urgent implantation of a cardiac rhythm device.

For those with vs without PTSD, the hazard ratio (HR) for death from any cause or MACE, the primary end point, was 3.2 (95% CI, 1.7 - 6.1) adjusted for age, sex, Charlson comorbidity index, and nonshockable initial rhythms (none of which were independently predictive on their own).

Further adjustment for psychiatric history didn't make much difference: HR 3.1 (95% CI, 1.6 - 5.9).

In a sensitivity analysis, all-cause mortality by itself was significantly increased in the PTSD group, HR 4.4 (95% CI, 1.2 - 15.8), as was rehospitalization for MI, unstable angina, or heart failure, at HR 3.1 (95% CI, 1.2 - 8.3).

It's unclear what early interventions would be best in survivors of arrest who show signs of PTSD, Sears noted.

"So, where should we start? My guess would be that some PTSD patients need psychologic support. Specifically, they might need treatment for their PTSD. But since that's not always commonly available, they also they need careful attention to re-engagement in the recovery process, whether that be medication adherence, dietary changes, exercise adherence, or other things."

Neither Agarwal nor his colleagues on the study had disclosures. Sears has recently disclosed receiving honoraria or consulting fees from Medtronic, Boston Scientific, Spectranetics, St Jude Medical, and Zoll Medical; and research grants from Medtronic and Zoll Medical.

Resuscitation Science Symposium at the American Heart Association (AHA) Scientific Sessions 2018: Abstract 13. To be presented November 11, 2018.

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