BE WARY OF “ACS”
Acute Coronary Syndrome is only Acute Coronary Syndrome
When It’s Caused by a Change in the Coronaries

I had written in the past about acute cardiac ischemia and referred to an article published by the American Heart Association and the American College of Cardiology in which they discussed “Guidelines for Diagnosis and Management of Unstable Angina/NSTEMI (non-ST-elevation myocardial infarction).  The major issue I presented was that unstable angina or non-ST-elevation MI can occur from two basic causes:

1. rupture of a coronary plaque or
2. inadequate delivery of oxygenated blood to the heart at times of need

The former is TRUE ACS.  The latter is caused by supply/demand mismatch.  This is to say that, with whatever limitations there may be to existing blood supply to the heart itself through the coronaries, either increased cardiac work in the face of stable blood supply or decreased oxygenated blood supply to the heart through the coronaries can cause ischemia to the heart muscle.

If the ischemia is mild, there may be signs and symptoms of classic angina, with chest pain in the classical distribution or atypical angina, with fatigue or dizziness being the substitute for chest pain.  But generally, this won’t respond normally to nitroglycerine because you haven’t treated the cause.

If the ischemia is great enough, some cells of the heart can die, causing elevation of blood markers such as troponin levels but usually no EKG changes – and this is a non-ST-elevation MI.

In neither of these cases is there rupture of a coronary plaque, so despite being “:unstable angina” or a “NSTEMI,” there is NO ACS.

Let’s look at how this happens.  The heart muscle is supplied with blood through the coronary arteries.  Each of these originates in the depths of a cusp of the aortic valve.  As the leaflets of the aortic valve are open during systole, they are in a position that closes off the openings to the coronary arteries.  So the coronary arteries fill during the part of the heart cycle when the left ventricle relaxes – diastole.  When the heart rate is normal, we systole (eject blood into the aorta) – diastole (fill the coronaries), systole (eject blood into the aorta) – diastole (fill the coronaries).  You need time to pass during diastole to fill the coronaries.  However, when a patient has a very rapid heart rate, we get systole-systole-systole-systole … 160 – 180 – 220 times a minute.  There is no time during diastole for the coronaries to fill.  So, at a time that the heart is being called upon to beat very rapidly, to expend tons of energy, when it needs blood supply the most, there AIN’T NONE.

Now, depending on the rate, depending on the amount of oxygenated blood the heart muscle fibers need to carry on without dying, there may be chest pain – and that chest pain is unstable angina.  It will not respond to nitrates – you need to slow the heart rate – then the chest pain stops.  And what do the docs call it?  Chest pain.  If the rate is so fast that the heart cells farthest from the start of the coronaries cannot survive, some die and troponin is released as well as other cardiac enzymes.  These cells are right under the inner lining of the ventricle – the subendocardium.  And a sub-endocardial MI or non-ST-elevation MI occurs.  The docs in the ED are working feverishly to slow the heart rate or it can get worse.  Remember, it’s the tachycardia, not the atrial fibrillation that kills this way!

The most grave presentation of this is experienced with ventricular tachycardia leading to ventricular fibrillation and sudden cardiac death (SCD).  This is why there are defibrillators in airports.

But rate isn’t the only thing that can cause this supply/demand mismatch to take place.  The heart needs oxygenated blood to be delivered through the coronaries, right? 

Well, there may be either inadequate oxygen in the blood as in instances of suffocation or carbon monoxide poisoning or progressive chronic lung disease and acute respiratory failure – and there just won’t be enough oxygen in the blood that is delivered to avoid myocardial ischemia.  Nothing happened to the coronaries – they’re just fine.  Myocardial ischemia which can lead to unstable angina or to NSTEMI – and it’s NOT ACS.

Conversely, there may be plenty of oxygen getting to the body through the lungs, but there isn’t enough blood – or red blood cells – as can happen with progressive anemias, such as anemia of chronic kidney disease or of malignancy or chemo treatment where the red cell count can drop lower and lower and all of the organs suffer some.  If the delivery of oxygen to the myocardium isn’t enough for the cells to survive, the patient may develop angina or NSTEMI – and it’s NOT ACS.

If the patient is in shock, with all of the cells in the body pleading for oxygenated blood, regardless of the origin of the shock (anaphylactic, cardiogenic, septic, hemorrhagic, etc.), there is inadequate perfusion of all organs.  Patients develop “altered mental status” which represents metabolic encephalopathy, acute renal failure which is due to acute tubular necrosis, heart failure, liver failure – and they may inadequately perfuse the coronaries and the patient may develop angina or NSTEMI – and it’s NOT ACS.

An article was published in Circulation and other world-wide heart journals which gave a “Universal Definition of Myocardial Infarction.”  This is a great article for us to read – for the internists, family practitioners, emergency physicians and cardiologists to read.  It presents exactly what we’ve described above and gives criteria for evaluation by the physician so as to be able to make a determination if an abnormal cardiac enzyme elevation is likely to represent an acute MI.  It also presents a table, dividing heart attacks into categories which I believe will result in code sets being defined in the future, because it represents a valuable epidemiologic tool for data gathering.  See what you think:

Type 1 – Spontaneous MI from ischemia from a primary coronary artery event (erosion of a plaque, rupture, fissuring, dissection of a plaque) – TRUE ACS

Type 2 – Ischemic MI due to supply/demand mismatch with no change in the coronary artery status – due to increased demand or decreased supply

Type 3 – Sudden Cardiac Death (SCD) where you can’t tell if it was the chicken or the egg that came first because the patient died too quickly for chemical change to be available for analysis – whether an MI caused ventricular fibrillation or ventricular fibrillation caused an MI – you just can’t tell

Type 4 – MI related to angioplasty.  This is divided into:
            4a.       MI during angioplasty (with or without stent insertion) with either showering of small particles of a coronary plaque that happened during the balloon dilation or excessive time of occlusion of the artery by the balloon and death of some myocardial fibers beyond the balloon
            4b.       MI occurring later because of occlusion of a stent documented by angiography or autopsy

Type 5 – MI associated with coronary artery bypass grafting (CABG).

(http://circ:ahajournals.org/cgi/content/full/116/22/2634.  You may need your cardiologists to get to this for you.)

That’s pretty good, don’tcha think?

Anyhow, discuss this with the heart docs at your hospital.  Download the article and read it yourself.  Keep it on the side for them.  This may help avoid the phrases “shock with elevated troponins” or “troponin leak” when the clinical circumstances truly represent non-ST-elevation myocardial infarction.  But also realize that not all troponin elevations represent an MI.  As sensitive as this test is, elevations can occur in certain conditions and not represent myocardial fiber death – and those aren’t MIs.