Reward System Activation Improves Recovery from Acute Myocardial Infarction

Research at the Technion demonstrated that activation of the brain’s reward system can boost recovery from a heart attack. The study was led by Ph.D. student Hedva Haykin under the supervision of Prof. Asya Rolls (Ruth and Bruce Rappaport Faculty of Medicine) and Prof. Lior Gepstein (Ruth and Bruce Rappaport Faculty of Medicine and Director of the Cardiology Department at Rambam Health Care Campus).

It has long been known that emotional states are able to influence cardiac function. For example, in an extreme case known as “Broken Heart Syndrome,” acute stress is liable to trigger a condition that mimics a heart attack. Broken heart syndrome is a condition where some of the heart muscle weakens rapidly, but there is no evidence of blocked coronary arteries. Similarly, psychological processes have a known impact on recovery from a heart attack, and on cardiovascular disease in general. For instance, anxiety and depression can worsen the heart’s condition, whereas positive emotional states can improve it. The physiological mechanisms at the foundation of the heart-brain connection, however are still unclear.

In this study, published in Nature Cardiovascular Research, the research group focused on the reward system, a brain network activated in positive emotional states and motivation and evaluated its potential in improving recovery from acute myocardial infarction (AMI, commonly known as a heart attack). They demonstrated how the activation of this system significantly reduces the extent of the resulting infarct scarring and improves the clinical outcomes of AMI in mice.

More specifically, the authors found that activating a specific part of the brain called the ventral tegmental area (VTA), which is involved in feelings of reward and motivation, can improve recovery after AMI in mice. VTA activation was found alter the immune response in the heart, reducing inflammation and promoting healing. It also affected the liver, causing it to produce more of a protein called complement component 3 (C3). C3 and other liver-produced proteins helped form new blood vessels in the damaged heart tissue. When C3 was inhibited, the benefits of VTA stimulation disappeared, indicating that C3 is crucial for the positive effects.

The research findings establish a causal connection between the reward system and recovery from AMI, introducing potential therapeutic avenues for intervention.

The study was assisted by the Technion Smoler Proteomics Center and was supported by the European Research Council (ERC), the Howard Hughes Medical Institutes (HHMI), the Wellcome Trust, Israel Science Foundation (ISF), and the Mirian and Sheldon G. Adelson Medical Research Foundation.

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