According to the world health organization, cardiovascular disease is the leading cause of death worldwide, as well as in Pakistan. Of those, a large proportion is caused by heart attacks, also known as acute myocardial infarctions, or just myocardial infarctions, sometimes just called MI. The word infarction means that some area of tissue has died due to a lack of blood flow, and therefore a lack of oxygen. “Myo” refers to the muscle, and “cardial” refers to the heart tissue. So with a heart attack or MI, you have the death of heart muscle cells because of a lack in blood flow, a process called necrosis. Now the heart’s main job is to pump blood to your body’s tissues. Well, the heart also needs blood, and so it also pumps blood to itself, using coronary circulation.
This mound of stuff has two parts to it, the soft cheesy-textured interior and the hard outer shell which is called the fibrous cap. Collectively this whole thing’s ominously called plaque. Usually, though, it takes years for plaque to build up, and this slow blockage only partially blocks the coronary arteries, so even though less blood makes it to heart tissue, there’s still blood. Heart attacks happen when there’s a sudden complete blockage or occlusion of a coronary artery—so let’s see how that can happen. Since these plaques sit right in the lumen of the blood vessel, they’re constantly being stressed by mechanical forces from blood flow, and interestingly it’s often the smaller plaques with softer caps rather than the larger ones with harder caps that are especially prone to break or get ripped off.
Notice that the majority of these
areas supply the left ventricle—most heart attacks, therefore, involve the left
ventricle, where the right ventricle and both atria—the upper chamber—aren’t as
often affected. Each of these areas is called the artery’s zone of perfusion. And,
if we take a closer look at one of these zones, we’ll see that basically you’ve
got the endocardium, which is the smooth membrane on the inside of the heart,
and then the myocardium, all the heart muscle, and then, the epicardium, the
outer surface of the heart, which is where the coronary arteries live. Let’s
say the LAD gets blocked, the area of perfusion is now at serious risk, and
within about a minute, the muscle cells in this zone don’t see enough oxygen
and become ischemic, and the muscle layer’s ability to contract is severely
reduced.
This initial stage is extremely
sensitive since the ischemic damage to cells in the perfusion zone is
potentially reversible. After about 20-40 minutes, though, damage starts to
become irreversible and the cells start to die, and this zone changes to a zone
of necrosis, or dead tissue. Once lost, these cells will never return or
regrow—that’s why quickly identifying and treating an MI quickly is super
important. The first area affected is the inner third of the myocardium, since
it’s farthest from the coronary artery and the last area to receive blood and
it’s subject to higher pressures from inside the heart. If the blockage
suddenly lyses or breaks down and blood flow returns, sometimes patients’ damage
will be limited to the inner third, and this would be called a sub-endocardial infarct.
An ECG, or electrocardiogram, done at this point typically shows an ST-segment
depression, or in other words, it doesn’t show ST-segment elevation, so sometimes
we call this an NSTEMI which stands for non-ST elevation myocardial infarction.
Other causes of this sort of
subendocardial infarcts would be severe atherosclerosis and hypotension—anything
that ultimately leads to poor perfusion of the heart tissue. After about 3 to 6
hours, though, the zone of necrosis extends through the entire wall thickness,
called a transmural infarct, which this time shows up as ST-segment elevation on
ECG, which is why they’re sometimes called STEMIs, or ST-elevation myocardial
infarctions. So the difference between NSTEMIs and STEMIs is that NSTEMIs don’t
have ST-segment elevation, and these are caused by partial infarct of the wall,
whereas STEMIs have ST-segment elevation and involve the whole wall thickness. Patients
that have an MI will most commonly have severe and crushing chest pain or
pressure, that might radiate up to the left arm or jaw, they might have diaphoresis
or sweating, nausea, fatigue, and dyspnea.
All of these are either a direct
result of an end-organ like the heart or the brain not getting enough
perfusion—so think chest pain and dizziness. Or from the sympathetic response
from the body to help the heart work harder and preserve blood pressure—so
think sweating and clammy skin. Many people also have referred pain where the
nerves in the heart are irritated, but that pain can be felt in the jaw,
shoulder, arm, or back instead. In addition to an ECG, labs can be very useful
in diagnosing an MI. When there’s been irreversible damage to heart cells, their
membranes become damaged, and the proteins and enzymes inside escape, and can
enter the bloodstream. Three key ones are troponin I, Troponin T, and CK-MB,
which is a combination of creatine kinase enzymes M and B. d Both troponin I
and T levels can be elevated in the blood within 2-4 hours after infarction,
and usually peak around 48 hours, but stay elevated for 7-10 days.
CK-MB starts to rise 2-4 hours after
infarction, peaks around 24hours and returns to normal after 48 hours. Since
CK-MB returns to normal more quickly, it can be useful to diagnose re-infarction,
a second infarction that happens after 48 hours but before troponin levels go
back to normal. A second heart attack happens following 10% of MIs. A major
complication with MIs is arrhythmias, or abnormal heart rhythms, with the
highest risk being immediately following an MI since the damage or injury can disrupt
how the cells conduct electrical signals. Kind of along the same lines,
depending on how much contractile or muscle tissue is affected, patients’
hearts might not be able to pump enough blood to the body, resulting in
cardiogenic shock.
In the days following infarction,
the tissue around the infarcted area becomes inflamed and is invaded by
neutrophils, which can lead to pericarditis, and inflammation of the pericardium. In
the next couple of weeks, macrophages invade the tissue, and the healing process
begins with the formation of granulation tissue, which is the new connective tissue
that’s yellow and soft. At this phase, the tissues are most at risk of myocardial rupture.
After 2 weeks to several months, the cardiac tissue scarring process finishes, and
the resulting tissue becomes grayish-white in color. Since the scar tissue
doesn’t help pump blood, over time the remaining heart muscle can grow or
change shape to try and compensate for these lost cells and pump harder, but they
ultimately continue to fail, which can lead to heart failure. Now a potentially
life-saving treatment that can be performed immediately following an MI, is
fibrinolytic therapy, which uses medications to break down fibrin in blood
clots.
An angioplasty might also be done,
which is a minimally invasive endovascular procedure where a deflated balloon is inserted into the blockage and then inflated to open the artery up. And finally, a
percutaneous coronary intervention (PCI) might also be performed, where a tiny
catheter is used to place a stent in the coronary artery to physically open up
a blood vessel. Each of these focuses on re-establishing blood flow to the
dying heart cells—since time is tissue. If early enough following blockage,
some of these cells that haven’t entered into the irreversible stage can be
salvaged and saved, while the others will be destroyed and removed. This can
improve both short and long-term function as well as prevent further damage and
reduce the overall zone of necrosis.
Now an important complication of
re-establishing perfusion, or reperfusion therapy, is reperfusion injury, where
tissue is damaged by returning blood flow. And, this is thought to happen
because of a couple mechanisms. First, blood flowing back to cells brings this
influx of calcium, and since calcium leads to muscle contraction, the
irreversibly damaged cells contract, and since they’ve been irreversibly damaged,
they get stuck like that and can’t relax. This shows up on histology as this
characteristic contraction band necrosis. Also though, blood brings along
oxygen. But, that oxygen, paradoxically, can actually lead to more cellular
damage. The conditions in an ischemic heart seem to cause an increased
conversion of the returning oxygen to reactive oxygen species, which go on to
damage more heart cells.
In addition to re-establishing blood
flow though, there are a number of medications that might be given in the acute
setting including anti-platelet meds like aspirin, anticoagulants like heparin,
nitrates which relax the coronary arteries and help lower preload, beta-blockers that slow down the heart rate and thereby cardiac demand, pain
medication to help relieve the discomfort, and statins which help improve a patient’s
lipid profile. Now there are many individual factors to consider when it comes to the acute management of myocardial infarction, and of course many long-term
issues to consider as well—the most important of which is to address the
underlying risk factors like an improved diet and quitting smoking.
All right, time for a quick recap… heart attack, also known as myocardial infarction, or MI, is the death of heart muscle cells due to the lack of blood flow, most commonly caused by atherosclerosis of the coronary arteries. The most common symptoms of MI include crushing chest pain or pressure that might radiate up to the left arm or jaw, sweating, nausea, and dyspnea. Treatment of MI includes re-establishing blood flow using medications, angioplasty, or percutaneous coronary intervention (PCI). Underlying risk factors should be addressed for long-term management.
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