An Osmosis Video: Heart Attack Explained

According to the world health organization,
cardiovascular disease is the leading cause of death worldwide, as well as in the US. Of those, a large proportion are 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 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 right? Well, the heart also needs blood, and so it
also pumps blood to itself, using the coronary circulation. The coronary circulation is this system of
small arteries and veins that help keep the heart cells supplied with fresh oxygen. Heart attacks happen when these small arteries
become blocked and stop supplying blood to the heart tissue, and if this happens for
long enough, heart tissue dies. Almost all heart attacks are ultimately a
result of endothelial cell dysfunction, which relates to anything that irritates or inflames
the slippery inner lining of the artery—the tunica intima. One classic irritant are the toxins found
in tobacco which float around in the blood and damage these cells. That damage then becomes a site for atherosclerosis,
a type of coronary artery disease where deposits of fat, cholesterol, proteins, calcium, and
white blood cells build up and start to block blood flow to the heart tissue. 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, and 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. Once that happens the inner cheesy filling
which remember is this mix of fat, cholesterol, proteins, calcium, and white blood cells,
is thrombogenic, and this means that it tends to form clots very quickly. So platelets, or blood-clotting components
in the blood, flow by and get excited; and they adhere to the exposed cheesy material. In addition to piling up, the platelets also
release chemicals that enhance the clotting process. Now this happens super fast, think about how
quickly a small cut stops bleeding, that’s a very similar process—it happens in a matter
of minutes, right? And now that coronary artery is fully occluded. So now let’s change views a bit, If we take
a slice of the heart like this, this side being posterior, or back, and this being anterior,
or the front, with the left and right ventricles here, and then we have the three most commonly
blocked arteries—the left anterior descending, or LAD which supplies blood to the anterior
wall and septum of the left ventricle which accounts for 40-50% of cases, the right coronary
artery, or the RCA which covers the posterior wall, septum and papillary muscles of the
left ventricle—accounts for about 30-40% of cases, and finally, the left circumflex
artery, or LCX which supplies to the lateral wall of the left ventricle —about 15-20%
of cases. 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 subendocardial 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 24 hours, and returns to normal after 48 hours. Since CK-MB returns to normal more quickly,
it can be useful to diagnose reinfarction, 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 are 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 an infarction, the tissue
around the infarcted area becomes inflamed and is invaded by neutrophils, which can lead
to pericarditis, inflammation of the pericardium. In the next couple weeks, macrophages invade
the tissue, and the healing process begins with the formation of granulation tissue,
which is new connective tissue that’s yellow and soft. At this phase, the tissue’s 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 inserted into the
blockage then inflated to open the artery up. And finally a percutaneous coronary intervention
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 the dying heart 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, right? Yeah it does. 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 reestablishing blood flow though,
there are a number of medications that might be given in the acute setting including antiplatelet
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 acute management of a 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. Underlying risk factors should be addressed
for long term management.



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