Acute myocardial ischemia occurs when blood flow is restricted in the heart. This usually leads to cardiovascular issues, but treatments have advanced quite far. However, one thing that still plagues patients experiencing acute myocardial ischemia is the development of ventricular tachycardia.
Ventricular tachycardia is when your heart consistently beats above 100 beats per minute. This causes strain on your heart and your blood vessels, which can lead to damage. Acute myocardial ischemia patients who develop ventricular tachycardia have a four times higher risk of death than those who don’t. Therefore, it is crucial to identify tachycardia indicators to catch it early, and possibly even treat it.
A team out of the University of Cologne in Germany decided to tackle the problem using nitro-oleic acid. Nitro-oleic acid is a molecule your body produces naturally and is known to act as an anti-inflammatory that can treat several cardiovascular disorders. Their new study tested whether nitro-oleic acid could be used against ventricular tachycardia.
The team used a mouse model to see if nitro-oleic acid treatment before inducing ventricular tachycardia could prevent tachycardia. Pretreated mice did not develop ventricular tachycardia as frequently as those who were not.
Calcium signaling is an essential component of proper muscle contraction, so the team investigated if nitro-oleic acid affected the system. They induced dysfunction to calcium signaling in cardiac cells and found the nitro-oleic acid could recover normal signaling. Further investigation pointed to nitro-oleic acid seemed to inhibit a critical calcium regulator CaMKII, which stabilized calcium signaling.
This study showed that nitro-oleic acid, a molecule already known to treat several cardiovascular diseases, can prevent the development of ventricular tachycardia in mice. The team isolated the mechanism of action to CaMKII inhibition, which prevented abnormal calcium signaling and stabilized heart contractions. The findings still need to be confirmed in a more extensive study before moving on to human testing.
The study concluded, “we show for the first time that, by inhibiting CaMKII, NO2-OA modulates a critical pathway of electrical remodeling following AMI and thus has potential as a pre-emptive anti-arrhythmic strategy for patients at risk for developing AMI.”