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Cortisol concentration linked to acute coronary syndrome
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The 12th European Congress of Endocrinology
Growing evidence suggests that serum cortisol levels are associated with increased cardiovascular mortality in patients with chronic heart failure, according to research presented this week at the 12th European Congress of Endocrinology.
“These findings show for the first time that serum cortisol levels are strongly linked to higher death rates in patients with coronary syndrome,” Andreas Tomaschitz, MD, of the division of endocrinology and nuclear medicine at Medical University of Graz, Austria, said in a press release. The data “suggest that cortisol might play an important role in worsening CV damage.”
Data were generated using the ongoing, prospective Ludwigshafen Risk and CV Health (LURIC) study. The researchers assessed data from 1,036 patients referred for coronary angiography who were found to have acute coronary syndrome.
The researchers found little variation in mean serum cortisol concentration range between patients with and without acute coronary syndrome (22.5 vs. 22.2). Norepinephrine levels were also similar (P=.378), as was the frequency of severe heart failure (NYHA Class III/IV; P=.156) and left ventricular dysfunction (P=.062).
During a mean follow-up of eight years, 14.1% of patients with acute coronary syndrome and elevated cortisol levels at baseline had died as a result of CV causes, according to the researchers.
Patients with the highest levels of cortisol were significantly more likely to die from CV events compared with those with the lowest levels (HR=1.89; 95% CI, 1.12-3.19), according to multivariate analysis. When the researchers added plasma aldosterone and norepinephrine levels to the adjusted model, they did not significantly affect the association (HR=1.85; 95% CI, 1.04-3.27).
“Until now, cortisol has been thought of as a non-specific stress indicator, but given that there was no real difference between the acute coronary syndrome and non-acute coronary syndrome groups, we may have to reconsider this,” Tomaschitz said. “In the future, we will need to understand the complex way in which cells react to cortisol and how this causes CV damage to people with acute coronary syndrome.”
For more information:
- Tomaschitz A. OC #4.6. Presented at: 12th European Congress of Endocrinology; April 24-28, 2010; Prague, Czech Republic.
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