Heart attacks, referred to as ‘myocardial infarction’ in the medical field, involve the blockage or reduced flow of blood through the coronary arteries, which are the blood vessels that supply the myocardium, the heart’s muscle tissue. Blockages are most commonly due to clotting of the blood. The narrowing of the coronary arteries mainly causes the reduction of blood flow due to fat accumulation within the arterial wall. These effects lead to much higher levels of work needed by the heart to continue blood circulation normally, causing a person to experience tiredness and shortness of breath while doing low-energy tasks.
When a heart attack is experienced, its severity is determined by the heart’s workload and which coronary vessel is being blocked. For example, suppose a blockage occurs at the beginning of the left main coronary artery (which wraps around the outside of the heart), the damage done to the heart can be catastrophic since this artery supplies blood to the circumflex artery that branches to the left of the heart and the anterior descending coronary arteries. Together they cover nearly the entire blood supply to the heart’s tissues. On the other hand, if a blockage happens at the bottom of the left anterior descending artery (LAD, the largest coronary artery, which goes from the bottom of the heart to the top), this may only cause a mild myocardial infarction only noticeable during high workloads. This is because the LAD is relatively isolated from other vessels supplying the heart, and it does not supply any main vessels as the left main coronary artery does.
The Pathophysiological Mechanism Leading to Heart Attacks
The damage of the myocardium begins with low blood flow to the heart. Blood supplies the heart’s muscle tissues with oxygen, and so if blood flow is low, oxygen levels will also drop. In hypoxic conditions, the heart cannot receive enough oxygen to meet the energy production demands of its cells. Thus, it must rely more on anaerobic metabolism, which is not ideal. Energy is produced and stored in the form of a molecule called ATP, which acts as a cellular currency. In other words, if you want something done, you need to have the cash (or the ATP) to pay for it. ATP is produced by an organelle called the mitochondria. If the mitochondria do not have enough oxygen to continue ATP synthesis, mitochondrial dysfunction occurs, eventually leading to apoptosis or cell death.
The electron transport chain (ETC) is how a mitochondrion produces ATP. Electrons are carried into the mitochondria by NADH in the form of hydrogen. NADH passes its H molecule off to complex I and becomes NAD, making it ready to accept a new electron from the environment. The transport complexes are embedded in the innermost of the mitochondria’s two membranes, and as they pass H molecules down the chain, the complexes pump out protons, creating an imbalance. The electrical imbalance is corrected when protons push themselves through ATP synthase, and as they do so, the ATP synthase enzyme harnesses their energy to produce ATP.
When oxygen becomes scarce, the electron transport chain in the mitochondria will back up because complex IV requires oxygen to transfer its electrons to, opening it up to receive the next electron in the chain. But since there is not enough oxygen for complex IV to offload electrons to, it cannot accept new electrons, and a sort of molecular pileup ensues. As a result, the electrons build up in the electron transport chain. NADH, the molecule that carries electrons in the form of hydrogen, does not become NAD+, preventing the regeneration of electron carriers. The body has to turn to lactic acid fermentation, which requires the cell to turn glucose into lactic acid to continue producing hydrogen ions. With nowhere for these ions to go, large amounts of H+ may build up and induce cellular apoptosis since a high concentration of these ions increases protein degradation. Since the cell has reduced amounts of functional proteins important for the maintenance of the cell, it will undergo apoptosis and become scar tissue, making the condition of the heart even worse.
Ways to Prevent Heart Attacks
Fortunately, preventing heart attacks is simple, but many neglect these important practices highlighted below.
- Exercise: One key method of preventing heart attacks is through regular exercise; even as little as a 20-minute daily walk is beneficial for the heart and overall body.
- Good Nutrition: Reducing the number of fats will lower cholesterol and reduce the narrowing of arterie. In turn, the heart is protected from any pressure that results in heart attacks.
- Healthy Weight: Maintaining healthy weight makes it easier for blood to travel in the body and helps control blood pressure and keep heart attacks at bay. Keep in mind to consult with your doctor about what a healthy weight looks like for you, since it isn’t necessarily the average weight for people your age.
- Healthy Habits: Generally, practice good habits significant to your overall health and avoid harmful habits like smoking.
At the moment, there are not many therapies for heart attack prevention since it involves cell death and the creation of scar tissue. The closest researchers have come to reversing the effects of cell death (apoptosis) is to regenerate heart tissue, which is not currently a mastered technique and is still being researched. Adult heart cells (cardiomyocytes) do not express genes that cause proliferation (like stem cells do), so the idea is to introduce those genes externally to start cell division.
There are 15 genes during cell proliferation that can be transplanted into mature cardiomyocytes using viral vectors. This may look promising, but when combinations of these genes are expressed in a cell derived from cardiomyocytes, they cause issues with cell cycle re-entry (which is required for division) and ultimately damage DNA causing cell death. Different combinations of these genes could accomplish proliferation and minimize death resulting from DNA damage. Research into various gene combinations shows some promise in regenerating heart tissue and reverse the effects of apoptosis.
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