This morning, I want to talk about the number one killer of Americans: heart attacks- or, more specifically, what we like to call “Ischemic Heart Disease”.
Ischemic heart disease is a sort-of catch all term for things like all coronary artery disease, including (but not limited to) myocardial infarction (heart attack). Basically, what it means the supply of coronary blood can't meet the demand of the heart for oxygen and nutrients.
The problem here is that, contrary to the population depiction of coronary events, there isn't really a definitive line for having a "heart attack"- it's a continuum. You don't go from sitting there, minding your own business, being 100% healthy to BOOM! Heart attack (unless it's caused by an outside precipitating event, like a lightning strike or trauma of some sort, but that's a bit different).
So when we say "ischemic heart disease", we're including transient ischemic syndromes with this- stable angina (chest pain), silent angina, prinzmetal angina- as well as acute coronary syndromes, like Non-ST Elevation Acute Coronary Syndromes (which includes both unstable angina and non-ST segment elevation myocardial infarction), and the most well known, ST-segment elevation myocardial infarction or STEMI, which is the sort-of "classic heart attack".
Those "STEMIs", or "classic heart attacks", are currently the #1 killer in the United States. They are highly prevalent, affecting over a third of men, and about a quarter of women in their later years. Men are more likely to have ischemic heart disease, but women are much more likely to die from it.
Unfortunately, this is not well known; most women, if you survey them, think that breast cancer is the #1 killer of women. Breast cancer is a big and legitimate health concern for women, but it's way down the list. The problem with women and heart disease is that women are much more likely than men to have chest pain and be told, "Oh, don't worry about it- you're just having some anxiety. It's nothing to worry about. You're just being a 'woman'."
Yes, that’s right- if anyone tries to write off someone saying “Sexism kills” as hyperbole, you point ‘em straight to this fact right here.
Mortality trends for coronary artery disease are down quite a bit, thanks to advanced in medical technology and interventions. We do a really good job of saving folks who're having cardiac events, especially if we can get them in a hospital quickly. Alzheimer's has gone up significantly in exchange of that; however, there's a significant school of thought that infectious disease will be the #1 cause of death again soon, with the coming antibiotic apocalypse. Very ominous, huh? Sleep tight.
Anyway, as I said before, when you have transient myocardial ischemia (injury), it's because there's an imbalance between demand and supply. The stereotypical episode of cardiac ischemia, which occurs with "stable angina", is when you have chest pain on exertion; you're working hard and you get chest pain because you can't keep up with your cardiac tissues' demand for oxygen. This also causes changes in how the heart conducts electricity, which is why we do EKGs to take a picture of the heart's conduction of electricity, and why we do stress tests on people. We hook them up to those wires and set 'em on the treadmill, and watch- if the electrical conductivity of their heart changes, we figure pretty much for certain that they've got something bad going on.
If you increase your cardiac workload slowly, like, say, by walking and gradually ramping up your speed, you might not notice anything is different, either. If you ramp things up slowly, collateral perfusion (blood going down other pathways) mean that the chance of infarction- actual tissue death- is very low. Your body is good at autoregulation of itself to keep it running at peak efficiency. The danger is when you have a rapid increase in cardiac output and your body can't keep up with it (the stereotypical event of this is shoveling snow in the winter). Even so, even with a rapid increase, we often don't see symptoms until an artery is 60-75% occluded.
So, when your heart can't get enough oxygen, it shifts itself over to an anaerobic metabolism. Anyone who's done physical training is probably familiar with aerobic exercise, and anyone who's done training for performance exercise- competitive weightlifting, etc- is familiar with anaerobic exercise. Anaerobic exercise are VERY hardcore ones, that exhaust our cell's onhand oxygen and so require glucose and other chemicals for them to continue to operate effectively. People that do "tough mudder" or "Iron Man" competitions engage in anaerobic exercise. Aerobic activities, on the other hand, include activities such as walking, long slow runs, rowing, and cycling require a great deal of oxygen to generate the energy needed for prolonged exercise.
Your heart is an aerobic machine. It needs oxygen to do it's job right; it's a long-distance jogger, not a PX-90 exercise nut. But, just like your other muscles, your heart CAN shift over to anaerobic metabolism- but it's not a fun process. Granted, it's not a fun process in any muscles, but your heart is (for obvious reasons) the most important out of any of them, and one you really don't want to have undergo that. Anaerobic metabolism is VERY inefficient, it's only a fraction as efficient as aerobic metabolism. You can't get as much energy out of anaerobic metabolization, and you get things like your lactate levels increasing (lactic acidosis). So then your heart doesn't beat as effectively, meaning your ejection fraction diminishes (can't pump as much blood), which can back fluid up into your lungs and give you poor circulation into your peripheral tissues.
Remember that pain you get after working out, particularly the next day? When your muscles are all sore and you can barely move. That's what chest pain due to a cardiac event is. Same sort-of process, but it's in your heart, not in your quads from doing all those squats. And it can affect nearby nerves, which is why often we'll see chest pain radiate to the neck, jaw, left shoulder, and left arm.
Similarly, while working out your quads can lead to muscle remodeling, that's *not* a good thing when it involves your heart. We don't want that muscle remodeled; your heart is already the size and shape we want it to be to work optimally. Any resizing it does is BAD.
Now, there's a few ways we can discern which arteries are being blocked, important to know for treating any sort of myocardial ischemia. The right-circumflex artery, for instance, in most people help run the AV nodes- so if we look on a person's EKG, we can often suggest there might be certain changes in conduction patterns ("heart block") that might suggest we have a block of the right circumflex artery. The Left anterior descending artery and the left circumflex artery supply the heart's left ventricle with blood, so if that ventricle doesn't work, we might instead see heart failure-like symptoms.
The problem is that most times, it's not just one blood vessel that's affected; it's usually a bunch. One in particular might be causing this episode of whatever's going on, but often there are multiple vessels in multiple states of block; the more vessels involved, obviously, the worse the prognosis of a person. In fact, people that have multiple partially-obstructed arteries are at a huge risk for developing heart failure even if they never have a heart attack.
Now, that's all for what we call "stable angina", which is the "normal", stereotypical presentation. But it's far from the only presentation; things often times don't work out quite so easily as that. There's also "silent" angina, which is very common in elderly patients, in women, and in diabetics, as well as in men aged 45-65 suffering from mental stress. Diabetics, for instance, have something called "neuropathy", meaning the excess sugar in their blood has jacked with the way they feel pain. So if you don't feel pain the same way, you can't feel chest pain the same way. Obviously a small population, but we find this to be true with transplant patients, too, which makes perfect sense if you think about it.
As mentioned before, we also worry about women with this. If a diabetic woman comes to you and says they just don't feel right, they feel like they're going to die, you need to BELIEVE THEM. That ominous sense of doom can be what we call "status dramaticus", sure, but normally people don't profess a feeling of "I feel like I'm going to die" wantonly, and it's a legitimate feeling for these certain types of things. Take it seriously; if it turns out to be nothing, great!
ACUTE CORONARY SYNDROMES
But things don't always work quite as nicely as we've laid out about. Lots of people have fatty buildups or plaques in their arteries that are almost completely non-obstructive. Whether it's because those buildups are relatively "flat", instead of growing out into the vessel lumen, or because they've burrowed their way into the vessel wall or endothelium, they rupture suddenly and with no warning. Those are the really scary ones, that's usually what you know happened if someone keels over dead from a heart attack with no warning whatsoever. That's what we call "unstable angina".
The fatty plaques that line cell walls of the heart are generally made of LDL lipids, the "bad" cholesterol you often hear about. They lay themselves over the wall of a blood vessel, and your immune system HATES that. Oh, man, does it ever. It sends white blood cells called macrophages after these fat cells, and then engulfs them and walls them off- but then there's nowhere for them to go, and they just build up on the wall of the artery.
Most plaques like this, as they start out, have a very thin cap on the top of them, but will eventually end up with a "thick" cap. Some of these will also more or less go away, but a small percentage remain, and remain with a thin cap. The thinner the cap on this plaque, the more "unstable" it is, because that makes it more liable to break off and block something suddenly, rather than slowly over time with a "thick" cap. Genes and environment contribute a lot to determining which type of plaques develop- it's one reason why you see the drive against trans-fatty acids, for instance. We're also looking at new treatments that'll keep people from developing these unstable plaques, though these are a number of years off.
What are some triggers for this to happen? An important thing to know is, once again, none of this happens in a day. It develops over time. This was first noticed in the Vietnam War, when they would conduct autopsies on 18, 19-year old soldiers. What they discovered was that even the very fit ones had already developed fatty streaks in their arteries, which is the precursor to everything we're discussing here. Indeed, new research suggests that 95-99% of all people in the Western world have these in their arteries as early as age 10. Some of these "fatty streaks" progress, some don't, again a lot depending on genes and environmental factors. The bottom line is, and it can't be overstressed enough, is that these things don't happen overnight.
But if you've developed an unstable plaque, what can lead it to break off? Well, we know you're more likely to have an MI in the morning, in the winter, if you're suffering from emotional stress, or if you are physically exerting yourself. All of these things increase tension on that thin plaque cap, compresses them, flexes them; and all of those states also can confer dysfunctional coagulability states on your body (making your blood easier to clot) and vasoconstricting (narrowing of arteries) because they trigger your body's inflammatory processes.
When this plaque breaks off, it's just like having a blood clot suddenly obstruct a vein- you get a thrombosis. If you have intermittent occlusion, you get what we call an NSTEMI- a non-ST segment elevation myocardial infarction, meaning that if I look at the readout of your heart on an EKG, I won't see any elevation in the ST waves. If you have persistent occlusion, though, you'll get a STEMI- where the ST-segment is elevated. Somewhat ominous, if you see an ST-elevation on an EKG, it looks an awful lot like a tombstone- but that's appropriate, I suppose, since that's pretty much what it signifies.
Aspirin is a front-line medication to give if we suspect this, because it's mostly safe and easily available, and because most of these clots have some component of platelet aggregation with them. Ie, they're not JUST fat, there have been platelets clumping together at the plaque site- and we want to disrupt that process as fast as we can. Aspirin needs to be on the front line of any first-aid response to a suspected heart attack.
Now, these unstable clots; once they form, they may go away quickly; clots can dissolve or be broken up before they cause any lasting damage to the heart. That's what we call "unstable angina"; it means you can get chest pain even at rest. If you're at risk of unstable angina, it also means doing a stress test to see if you're at risk is probably ineffective. The pain is unpredictable. The only thing that prevents you from having a severe myocardial infarction with unstable angina is whether or not a clot breaks up before it's had a chance to block your coronary arteries for long enough. We take unstable angina so seriously we basically group it with an "actual" heart attack for how aggressively we treat it.
If a coronary artery stays blocked for longer than 10-20 minutes, that's where you get to the level of an "myocardial infarction". "Infarction" signifies that part of your heart muscle has died, as opposed to "ischemia", which is theoretically reversible injury. Obviously this is on a continuum, too; if your artery is unblocked in exactly 9:59, it doesn't mean you magically escape with no heart damage at all. There isn't a threshold, and everyone's a little different.
With "unstable" angina, too, some of the normal diagnostic markers will show up positively, but at levels WAY below that of a "normal" MI, so they're hard to rely on.
An interesting corollary to this is that if you look at someone (sadly, generally under autopsy), and see their cardiac artery lesions, you'll most often note that they're all about the same size, shape, and age. So, what does this mean? We're actually not entirely sure. Something clearly happened, and they all started growing at about the same time. Doesn't really make sense, does it? It's puzzling. But what it does tell us is that if someone has one unstable plaque, then they're pretty likely to have another unstable plaque in a different place.
There are actually five different kinds of myocardial infarction, but a Type I Myocardial Infarction is the biggest deal. To be an "official" type-I MI, you need to be able to detect a rise in their troponin level, and you need at least one symptom of ischemia, like
- Chest pain
- a change on their EKG
- a change on their echocardiogram;
- or to confirm it on an autopsy, but obviously this is our least preferred route.
When you have a thrombus in your vessel, it probably goes without saying- the longer it stays, the more damage it causes. If the clot stays long enough, past the point of having "unstable angina", you're almost certain to have an "infarction" of your cardiac tissue. And the parts of the heart farthest from blood flow are generally the ones that "infarct" first.
The first place that gets damaged is the inside of your heart. This is why, when we do a cardiac test in the ER, we pull multiple sets of cardiac enzymes and do multiple EKGs, usually over the course of a few hours- or will sometimes have folks spend the night for the same thing. Because that damage won't show up fully until the damaged tissue spreads from the inside of your heart, all the way to the outer wall. That's when we see EKG changes (colloquially known as "fireman's hats" or "tombstones" based on how the cardiac rhythm appears on an EKG); so a "normal" EKG doesn't rule out problems.
These "internal infarctions" used to be called "Subendocardial myocardial infarctions", but now we just call them NSTEMIs- meaning your EKG is okay, but you still got problems.
So, we figure out you're having a cardiac event, and we go in and fix it- suck that clot right out. Problem solved, right?
Wrong. We've discovered something called "myocardial stunning", and it's a real problem. If you make a tissue ischemic, meaning we take it's oxygen away, even if we go in and do a cardiac intervention right away, it takes awhile for that tissue to recover. This is kind-of like if you take someone and hit them on the head, they'll wonder where they are for a few minutes even if you don't keep hitting them on the head. Thus, "stunning".
How much of the heart is "stunned", and how long your cardiac event lasts, is a big part of surviving the first twenty-four hours of your post "heart attack" period. It also plays a huge role in your overall outcomes- how you recover, your life expectancy, etc. New research has made us wonder if insulin might play a role in helping recover from this stunning; if we can restore cellular balance quickly with how much sugar is available to cells, to help them recover from stunning, the thought is recovery will improve sooner- but the jury is still out on this one.
HOW THIS RELATES TO POLITICS
Our medical system has been focused on fixing emergent and dangerous things, like heart attacks, severe trauma from car accidents, etc- which is great. Those are important things. But we need to be focusing more on primary care to keep us from having to get there, and for managing people after they've had these events.
For instance, everyone who's had a heart attack is going to get ACE inhibitors and beta blockers once they stablize. If they get a stent, they need to be on lifelong Plavix to help keep them from re-occluding those stents. Which means they need a primary care provider to be able to help prescribe, and keep them up to date on those things. To check in with them, and catch those conditions before they get to the extent of needing to take dramatic (and expensive as heck) measure to save their life.
The way Trumpcare and other "Go to the ER"-care proposals are structured, it only makes our ability to do this worse. Republicans in the House and Senate can deny and pretent this isn't the case all they want to, but we're all paying for this stuff now, as it is. From $900 tylenols to $4500 CT Scans, we're all paying for everyone in this country to have access to healthcare- but we're paying for it in the least efficient and comprehensive way possible.
Single payer, "Medicare for All", is the answer- hands down. It's the most "fiscally conservative" and overall most comprehensive way to get it done. And that's exactly what we need to do to get it done- period. It’s one of the things I’m fighting for in my run for the Virginia State Legislature this year, and I think that needs to be the goal for anyone running for public office- and we shouldn't rest until we get there.
Kellen Squire is an emergency department nurse from Barboursville, VA, running for the Virginia House of Delegates this fall in the 58th District.
Saturday, Jul 29, 2017 · 1:54:11 PM +00:00 · SquireForYou
Per a request in the comments, someone asked what they should do at the first sign you might be having a heart attack. This can be:
- Chest pain, generally left sided or substernal (right in the middle)
- Pain that may radiate to your jaw, chin, or left arm
- “An elephant is sitting on my chest”
- A feeling of impending doom- if you want to make a healthcare provider go pale, tell them you have that sense of impending doom, like you’re going to die, because people are too often right about that.
As I mention in the article, women often present with nebulous, less “classical” heart attack symptoms, which is unfortunate because there is also a tendency to dismiss women having these nebulous symptoms as “you’re just having anxiety” or other “womanly” things. I have seen it personally, where a woman in her mid-50s died because she was convinced to ignore her chest tightness and sense of impending doom as having an anxiety attack until it was too late.
Thus, the first thing to do is, if you are able to medically (if you’re not, you probably know) and haven’t had any aspirin yet today, is try to chew and swallow at least a baby aspirin, but preferably a full 324mg tablet. Well, I take that back- the first thing you need to do is seek immediate medical attention, preferably at a hospital emergency department. Our cardiac unit’s motto is “TIME IS HEART”. But, if you are delayed for some reason in doing that, the aspirin should be the next step.