News article about patients suffering from depression and their recovery after heart attack using sertaline
People with depression do not recover as well from heart attacks, reported The Daily Telegraph. These people “may be at increased risk of having a second, and possibly, fatal attack” said the newspaper. It went on the explain that “it was unclear why, but that depression is known to have an effect on hormone levels, heart rate and inflammation responses”.
The newspaper story is based on a study looking at heart rate variability – changes in the heartbeat that are used to indicate heart health – in 290 depressed people who had “suffered attacks” and were treated with the antidepressant sertaline, or a placebo.
The study highlighted differences in heart rate variability, but it did not look at the effect of antidepressants on the risk of heart attack. Larger, long-term studies would be needed to assess these effects.
Alexander Glassman and colleagues from Columbia University College of Physicians and Surgeons, USA, and Queens University, Canada, and Pfizer Inc, carried out this research. The study was funded by a NARSAD Distinguished Investigator Award, the Suzanne C. Murphy Foundation, the Thomas and Caroline Royster Research Fund, and Pfizer. It was published in the peer-reviewed medical journal, Archives of General Psychiatry.
This was a secondary analysis of an earlier double blind randomised controlled trial, the Sertraline Antidepressant Heart Attack Randomized Trial (SADHART).
The researchers looked at recordings of heart rate variability (HRV) in 258 of the 369 participants in the SADHART trial. Other studies have suggested that people who have a low HRV after a heart attack are at a greater risk of death than those with a high HRV. In this trial, adults with a major depressive disorder who had been admitted to hospital because of acute coronary syndrome (a slightly broader range of heart conditions which includes a ‘heart attack’, in addition to other events where electrical heart changes and blood markers are suggestive of heart muscle damage) were randomised to receive either an antidepressant (sertraline) or inactive placebo.
Most of the participants had their HRV measured at the start of the study (before they took any medication) and after 16 weeks of taking sertraline or a placebo. Researchers looked at the differences in HRV between people treated with sertraline and those treated with placebo. They also looked at whether HRV differed between those people whose depression had improved significantly and those whose depression had not.
Overall, researchers found that there were no significant improvements in HRV over 16 weeks in either group. However, HRV was significantly better in those people who had taken sertraline than in those who had taken a placebo at 16 weeks. People whose depression had improved significantly had greater HRV than people whose depression didn’t improve significantly, whether or not they took sertraline. These differences were mostly due to worsening of HRV in the placebo group, and in people whose depression did not improve.
The researchers concluded that HRV does not improve as expected after acute coronary syndrome in people with depression. Sertraline increases HRV compared to placebo, and improvements in depression are also associated with increased HRV.
This was a well designed and conducted study. When interpreting this study there are a few limitations to note, some of which the authors acknowledge:
It must also be considered how reliable a measure of prognosis variation in heart rate is. There are many other factors that affect the risk of death following heart attack and other acute coronary syndromes, such as extent of heart muscle damage, presence of irregular heart rhythms, whether the patient is in heart failure, and the presence of other coexisting medical disease and risk factors. Even if depression is considered to be a risk factor for poor prognosis, it cannot be said that it is the illness itself that is the direct cause of this. For example, depressed patients may be less likely to take their prescribed heart medications correctly, and this may be the cause of worse prognosis. Until further research has been carried out, any conclusions into the links between depression and prognosis after a heart attack should not be drawn.
It will come as no surprise to many people that the mind affects the body; what is a surprise to some people is the fact that doctors often seem to forget this fact.