A heart attack is a critical and often life-altering event that strikes suddenly, but its underlying causes develop over time. The heart, our body's vital pump, relies on a steady supply of oxygen-rich blood to function effectively. However, when that supply is disrupted, the consequences can be devastating. Understanding what happens during a heart attack—how the heart muscle suffers from the lack of oxygen and the chain reaction that follows—is key to grasping why prompt medical attention and preventive care are so crucial. In this article, we'll explore the intricate processes that unfold during a heart attack, illuminating the biological cascade that damages the heart, and explore potential ways to prevent and treat heart attacks.
Heart attack—also known as a myocardial infarction—occurs when blood flow to a part of the heart is restricted, depriving the heart muscle of oxygen. A lack of blood flow leads to the production of reactive oxygen species. The heart’s cells are forced to switch from aerobic metabolism to anaerobic metabolism, leading to inefficient energy production and the accumulation of metabolic byproducts that cause cellular and molecular damage. Without oxygen, the heart’s cells undergo apoptosis and necrosis, or cell death. As cells die, they release proinflammatory signals that worsen cellular and tissue damage. This cardiac cascade can lead to long-term reductions in the heart’s pumping efficiency and, eventually, heart failure.
The most significant risk factors for premature heart attack, defined as a heart attack occuring in men aged 18 to 55 years or women aged 18 to 65 years, are mostly modifiable and include:[1]
Heart attack recovery hinges on more than just reestablishing blood flow—it’s about helping the heart regenerate. This involves rebuilding blood vessels, strengthening heart cells, and adapting to new energy demands. Interventions that target these pathways might be effective in reducing the damage from a heart attack or enhancing the recovery process. This includes pharmacological interventions, early screening and risk assessment, public health policies, and most importantly, lifestyle modifications including physical activity, weight management, smoking cessation, and diet.
By harnessing the power of metabolic switching, intermittent fasting might offer a promising, non-invasive strategy to support heart health and accelerate recovery following cardiac events.
A recent study showed just that—practicing time-restricted eating in the 6 months after a heart attack led to robust improvements in cardiac function and rejuvenation—improvements that weren’t observed in patients who stuck to their regular meal timing. This was accompanied by a significant reduction in blood pressure and body weight.[2]
Just one month after their heart attack, participants assigned to 16:8 time-restricted eating experienced a 6.6% increase in a measure of their heart’s pumping efficiency known as left ventricular ejection fraction (LVEF) compared to a mere 1.5% increase in the regular diet group.
That wasn’t the most surprising part. The improvement in the heart’s pumping efficiency persisted and was even larger at 3 months and 6 months of intermittent fasting—increasing by 8.4% and 10.3%, respectively. The longer the participants practiced intermittent fasting, the more their heart function continued to improve!
In contrast, the heart’s pumping efficiency only improved by 2.2% and 2.5% in the regular diet group at 3 and 6 months, respectively.
Both groups lost some weight and improved their BMI—the intermittent fasting group’s BMI fell by 1.34 kg/m2 and the regular diet group’s BMI dropped by 0.58 kg/m2—with the intermittent fasting group experiencing a larger change. The only other major difference was in diastolic blood pressure, which fell from 81 mmHg to 71 mmHg in the intermittent fasting group after 3 weeks and remained at this level for the remaining 6 months. On the other hand, diastolic blood pressure increased from 73 mmHg to as high as 79 mmHg in the regular diet group between 4 weeks and 6 months.
One patient in the regular diet group died during the follow-up period, while zero deaths occurred in the intermittent fasting group.
What’s so incredible about the findings of this (albeit smaller) study is that the improvements in heart function with fasting were similar to those observed for other clinical treatments. In one study where heart attack patients received stem cell therapy, the heart’s pumping efficiency improved by 8.5% after 4 months.[3] Another study in which stem cells were injected into the patients’ hearts observed a 4.3% improvement in the heart’s pumping efficiency 6 months after their heart attack.[4] Empagliflozin, a sodium-glucose cotransporter 2 (SGLT-2) inhibitor, improved the heart’s pumping efficiency by 4.7% after 6 months.[5]
This means that 6 months of 16:8 TRE (in addition to guideline-based secondary prevention medication including a statin and blood-pressure-lowering therapy) improved cardiac function to the same degree as pharmacological and experimental invasive treatments. That's the power of fasting.