Russia has developed a substance that reduces the severity of heart damage during a heart attack.

During a myocardial infarction, doctors typically have only minutes to provide emergency care. Recent research has shown that, in addition to standard medical and surgical procedures to restore blood flow to the heart muscle or place arterial stenting, the heart can be helped by essentially tricking it. Researchers from the Bashkir State Medical University, together with their Chinese colleagues, have developed for the first time a substance that can significantly reduce the extent of heart muscle damage during a heart attack. An MK correspondent visited the laboratory where this substance was tested on an isolated, living heart suspended above a table.

The Laboratory for Small Targeted Molecules at the Belarusian State Medical University of the Russian Ministry of Health specializes in synthesizing new molecules and then transferring them into clinical or preclinical trials. During the current decade of science and technology, its staff developed a molecule that reduces the area of ​​cardiac tissue necrosis during myocardial infarction.

Irina Krylova, a young scientist and assistant professor at the Department of Pharmacology at Bashkir State Medical University, explains the causes of coronary heart disease, its progression to an acute form called a heart attack, and the mechanism of action of a recently discovered molecule: "Usually, someone who has suffered from coronary heart disease for a long time is diagnosed with atherosclerosis, the so-called plaques in the vessels. The heart's function becomes significantly more difficult, it begins to suffer from a lack of nutrition and oxygen, and at some point, blood flow to this area of ​​the heart is blocked, leading to ischemia. The heart begins to die, but this doesn't happen immediately. There is a zone where cardiomyocytes (heart muscle cells) have already died, and there is a region where they are no longer active, but are not yet completely dead. While the patient waits for an ambulance, enzymes responsible for clearing the body of dead cells mistake these half-alive, half-dead cardiomyocytes for dead ones and remove them from the body along with the dead ones, preventing them from being reactivated. A special protein marks them as dead. It can also be called a signaling molecule, which attracts the "recycling" enzymes. Our substance targets this protein. By reducing its activity, the necrotic zone does not increase—the half-alive cardiomyocytes await help to be revived, and the person's chances of survival increase."

...We go into a laboratory where scientists model heart attacks ex vivo (outside the body) and in vivo (in a living rat), and then test the effects of a new molecule on them.

"During preclinical trials, our substance must be administered after an infarction has occurred. "Therefore, we begin our work by modeling it," explains Irina Krylova.

We are approaching the installation of an isolated heart using the Langendorff method. This is the gold standard for research prior to selecting substances for cardiac protection. Only those that pass the selection will be transferred to another part of the lab for testing in a living organism.

"Why should we test prototypes of future drugs on an isolated heart? Its owner, the rat, dies when it's removed anyway."

"The body produces many hormones under stress. These hormones themselves can aggravate myocardial damage and increase the area of ​​necrosis. Therefore, to ensure the integrity of the experiment, we isolate the heart after first placing the animal into a drug-induced coma."

They show us a suspended heart that is still beating!

"Why shouldn't it fight?" says Irina Krylova. "After all, it's connected to tubes that mimic the composition of blood, and they're also supplied with oxygen and carbon dioxide, and the temperature is maintained at 37 degrees Celsius—everything just like a living organism."

Once the heart adapts to the new conditions, we begin simulating a heart attack: a special switch blocks the flow of simulated blood. Since a heart attack only lasts 40 minutes—that's how long it takes for doctors to provide emergency care to a patient—we in the lab also strive to achieve the same timeframe. A new substance, which is supposed to save heart muscle cells, is administered to the suspended heart slightly before the onset of the heart attack.

"The heart beats, then stops...," the scientist comments on what's happening in the Langendorff device. "But after 40 minutes, we restore blood flow, and it starts beating again. The extent to which the necrotic zone has shrunk as a result isn't visible to the naked eye—that's what morphologists will later determine when they examine the heart muscles under a microscope."

According to Krylova, initial findings show that after drug-induced blockade of the "scavenger" protein, significantly more viable tissue remained in the heart after 40 minutes of infarction than in the control heart. While it will still be years before a drug is developed, there is already hope that scientists may be able to extend that 40-minute window of hope for lifesaving.