What's the mildest "heart attack"?

I know there are infarctions, events, etc., but what is the “mildest” form of heart attack? Odd question I know, but…

No such thing.
Any heart attack is as serious a a catash…tin.

Yes, but there are degrees. I’m curious as to how they’re classified (other than “mild”, “massive”, etc.). Some people have had heart attacks and been sent home within hours, others (like the men in my family) simply wake up dead with their first one. I’m curious what the former ones are called.

I’d be surprised if anyone with an honest-to-goodness heart attack was sent home within hours.

Now, to answer your question …

Nowadays, the term acute coronary syndrome (ACS) is being used to denote a number of conditions which had, previously, been considered separately. They are:

  1. unstable angina
  2. non-Q wave myocardial infarction
  3. Q-wave myocardial infarction

Angina is (chest) pain due to inadequate blood flow to the heart muscle itself. Unstable angina means that such pain is happening more frequently and/or with less provocation and/or is harder to relieve.

A myocardial infaction (MI) is what people mean when they say “heart attack”. An MI means there has been death of heart muscle cells due to lack of blood flow to those cells.

Q-waves are patterns that appear on ECG’s following an MI. They indicate that there has been full-thickness death of part of the heart muscle.

A non-Q wave MI means there has been death of heart muscle cells but not as extensively as in a Q wave MI.

It is important to distinguish among the three possible causes of ACS since management and prognosis differs.

I’ll note in passing, that since the advent of very sensitive biochemical markers of heart muscle cell death, the frequency of non-Q wave MI’s has, of course, seemed to have increased.

AFAIK, there’s no established system for rating the severity of MIs. However, generally speaking, it would depend on how much blockage there is and where the blockage occurs. Also, the more distal the blockage, the less heart tissue is affected. For example, someone with 100% occlusion of the distal end of an artery will fare much better than someone with 100% occlusion of the Left Main Coronary Artery.

This may determine the severity of the underlying coronary artery disease, but doesn’t tell us at all about the size of the infarct.

Infarct size (i.e. size of area of dead heart muscle) is difficult to determine, short of autopsy. Surrogate measures of infarct size are levels of CK (an enzyme released from dead/dying heart muscle), levels of other heart cell enzymes, and development of Q waves. An echocardiogram (or nuclear scan) will also tell how much, and which part of, heart muscle is not working (and thus presumably dead).

Ok first, a little anatomy lesson. The heart is a musclular pump. It carries blood to all parts of the body, including itself. It supplies its own blood and oxygen via the coronary arteries. They can be compromised by a clot or occlusion from plaque build-up.
When a coronary artery becomes obstructed, it no longer carries oxygen to the part of the heart it normally feeds. The area first becomes oxygen starved, causing angina, a fancy word for chest pain. If the blockage isn’t corrected, that part of the muscle dies. This is called an infarction or infarct. Any type of tissue can infarct, if its deprived of oxygen. When the heart is the tissue in question, its called an MI or Myocardial Infarction.

The severity of the attack is predicated on the size of the infarct, and which artery is involved.
These same arteries supply blood to the parts of the heart that cause it to beat, called the conduction system.
If the infarct severely damages the conduction system, the heart beat may become uncoordinated and random, making it impossible to pump blood to vital areas.
It the infarct is large, the muscle may actually rupture.
These are worst case.
When Joe gets sweaty and short of breath, with a crushing pain in his chest and left arm, he needs a ride in the big loud truck. These are the classic signs. Classic doesn’t mean universal.
The symptoms can range from none at all, called a silent heart attack, your doctor finds on a routine EKG, to being DRT (dead right there, medical slang). Some have nausea, some dizziness, with or without pain, or any combination. I had one pateint who only had pain in her left thumb.

If someone goes to the ER and is sent home, they didn’t have an actual heart attack. They may have had a temporary loss of blood flow to a portion of the heart. Sometimes when an artery is partly obstructed, the vessel can spasm for a short time, cutting blood flow, then relaxing, to allow flow to resume.
Chest pain is called angina. Angina is caused by ischemia, a fancy word for lacking oxygen, or by infarction.
If it goes away with rest, and/or minimal medicine, its stable. If it doesn’t go away, its called unstable, and requires immediate treatment.
The area of the heart compromised is a factor in survivability, but I won’t go into that now.

Just curious, what made you suspect a heart attack in the patient with pain only in her thumb? I mean, why would you even test for that?

When someone has symptoms that don’t match up with the history and physcal findings, you have to start thinking of other possibilities.

Several years ago, I was working in a minor emergency clinic. A gentleman came in with “throat pain”. We were busy at the time so he sat in the waiting room for **several hours ** before being seen by the nurse and placed in the examining room.
When I saw him, he said, “My throat hurts, but it doesn’t hurt to swallow”. No pain or restriction of neck motion, no redness, no swelling, and his exam was normal except for high blood pressure. Since heart pain can refer to the neck, I ordered an electrocardiogram and it showed BIG changes indicating a heart attack, and we called 911 and had him sent to the hospital.
Shortly after that, the clinic changed it’s policy and required all patients to be seen by the nurse within 10 minutes of coming into the clinic, no matter what their complaint was!

Anecdote time:

My grandpa had two heart attacks. The first one, in his mid-50’s, was so minor he didn’t even know what it was, probably passed it off as acid reflux or something. It wasn’t until years later while getting a routine medical checkup that his doctor said, “So…when did you have your heart attack?” Somehow, the doc was able to know.

His second attack, in his mid-80’s, was considerably more fatal. :frowning:

Well, I hate to put this out there, but sometimes its just intuition. It was a night shift, she was awakened out of a sound sleep by it, there was no obvious injury, so I did an EKG. It showed that she was in the process of having a big MI. I got the doctor out of bed to deal with it. From then on, he never questioned me if I told him I thought something was wrong.
We moved her to the ICU, where she did fine, if I remember correctly.

The earlier one was an example of the silent MI I metioned in my first post. The doctor probably did a routine EKG, that showed the changes to the electrical conduction. The heart will re-route the conduction around the wounded area, changing the way the EKG pattern looks.

Will a silent MI show up on an EKG (A) always or (B) usually or © sometimes?

Always, otherwise, it wouldn’t be an MI.
As I said, the infarction is an area of dead tissue. The electrical footprint on the EKG is predictable in a normal, undamaged heart. So, when there is damage, the electrical footprint is different, thus, the EKG is different.

Someone experienced in reading 12 lead EKGs can even tell which part of the heart is damaged.
The 12 electrodes are placed at specific points on the chest. As the channels switch, the graph “looks” at the heart from different angles, giving a graphical analysis of the three dimentional heart.

Gotta disagree, picunurse. Lots of MIs don’t show significant changes at all on EKGs. Just google “non Q-wave MI” sometime. My EKG didn’t change a damn during or after my MI, only the troponin level tipped off that it wasn’t unstable angina. And I’ve seen many patients for whom I had EKGs before and after enzyme-documented MIs whose EKGs didn’t change a whit.

And let’s face it. That makes sense. A small MI may knock off only a few hundred myocardial cells, or less. That change may not even be enough to elevate troponin levels, much less change the electrical conduction pattern.

So frankly the answer to MLS’ question is C) Sometimes.

I bow to your broader experience. That does make sense.
Even though I’ve taken several EKG courses, I never remember much. I have always prefered patients that warn me, by bleeding or spiking fevers, and such, before they start circling the drain.
So often cardiac patients say, “I don’t feel good.” then die. Its just not polite.
[sub] For those of you not in the medical profession, the preceeding was a bit of the black humor that keeps us sane. If it offended, I sincerely apologize.[/sub]

You’re right, of course. I meant to add more to my post.

Thanks for the heart attack overview, picunurse.

A question: Why is the heart particularly susceptible to getting stopped up? Why do we hear so much about heart attacks, but never about “brain attacks” or “liver attacks” or “holy-shit-my-left-calve-just-died attacks” ?

Actually, we hear lots about “brain attacks”, but they’re called strokes. Often, strokes are secondary to blockages in the arteries delivering blood to the brain.

The (muscles in the) calves can also be affected by inadequate blood flow. However, that tissue is not nearly as dependent on uninterrupted blood flow as, say, the heart muscle. Interestingly, when the calf muscles don’t get enough blood, one experiences claudication, a pain in the calves, which is similar to angina from the heart.

Although the legs aren’t usually affected by sudden blockages in their arteries unlike the heart or brain, they can be chronically deprived. Eventually, the tissues of the leg and foot ulcerate and/or get infected and/or become gangenous (i.e. dead)

I neglected to mention that the liver has a dual blood supply, with the major portion coming from the veins going to the liver. Veins don’t development atherosclerosis (cholesterol blockages) so the liver is pretty well guaranteed of getting an uniterrupted flow of blood even if the artery to the liver gets blocked for whatever reason.

Of course, this is a generalization. Indeed, the portal vein can thrombose, get compressed, etc.