What's the mildest "heart attack"?

[Sampiro]

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

[spingears]

Originally Posted by Sampiro

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

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

[Sampiro]

Originally Posted by spingears

MILD??
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.

[KarlGauss]

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.

[St. Urho]

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.

[KarlGauss]

Originally Posted by St. Urho

it would depend on how much blockage there is and where the blockage occurs.

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).

[picunurse]

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.

[Maera]

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?

[pudytat72]

Originally Posted by Maera

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!

[KGS]

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.

[picunurse]

Originally Posted by Maera

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?

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.

[picunurse]

Originally Posted by KGS

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.

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.

[MLS]

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

[picunurse]

Originally Posted by MLS

Question:
Will a silent MI show up on an EKG (A) always or (B) usually or (C) 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.

[Qadgop the Mercotan]

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.

[picunurse]

Originally Posted by Qadgop the Mercotan

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.


_{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.}

[St. Urho]

Originally Posted by KarlGauss

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).

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

[Metacom]

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" ?

[KarlGauss]

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)

[KarlGauss]

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.

[Metacom]

So the risk factors for a heart attack are the same as for a stroke? Why are heart attacks more common (or are they?)?

[KarlGauss]

Yes, indeed, there is considerable overlap between stroke risk factors and heart attack risk factors:

- high blood pressure
- high cholesterol
- diabetes
- smoking

I should point out that about 1 in 8 or so strokes are NOT due to blockages in the arteries giving blood to the brain. Rather, they are due to a burst blood vessel within the brain, i.e. intracerebral hemorrhage. There is no corresponding phenomenon in the heart.

Lastly, a major risk factor for strokes is the condition called atrial fibrillation. People with atrial fibrillation can have a risk of stoke as high as 20 percent per year.

[Waterman]

While I had been on blood pressure medication for several years, I never knew I had a heart attack until an EKG was performed (as part of a job physical for a job I really needed) and the doctor who oversaw the clinic called me two days later and asked me when I had my heart attack.

Needless to say I was like what heart attack. I went in shortly thereafter to have a nuclear stress test done and then went in a week later for an angiogram and ended up having double bypass surgery the very next day. That was 7 years ago.

[picunurse]

Originally Posted by KarlGauss

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.

I'll add that the liver has amazing regererative capability, where the heart and brain do not.

Originally Posted by KarlGauss

Lastly, a major risk factor for strokes is the condition called atrial fibrillation. People with atrial fibrillation can have a risk of stoke as high as 20 percent per year.

Also, A Fib is often caused by a heart attack.

One reason people think heart attacks are more common than strokes, in my opinion, is that heart attacks have had more agressive treatments available for a longer period of time than strokes. Also drug companies have focused on heart attack pervention with various drugs, so more press.

[MLS]

Originally Posted by KarlGauss

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)

Yeah, I saw that in my late father. He'd had two successful bypass operations, but toward the end we saw his mental function deteriorate significantly and we guessed that he had some blood flow decrease there. But he also apparently had awful circulation in his legs. Combining the two, the gangrene on his feet had progressed quite far before it was brought to anyone's attention. I don't know how a person could have parts of his feet turning black without deciding he needed to consult a doctor about that. (He was a widower, so ordinarily nobody saw his bare feet.) And let me tell you, it was disgusting to see. He had to have portions of his feet amputated right away, but the legs were not getting enough circulation either, and things just went from bad to worse. In those last few months it became apparent that blood just wasn't flowing well anywhere.

[serious lark]

Originally Posted by Metacom

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" ?

As someone else has already responded, other parts of the body are also susceptible to blockages of their blood supply resulting in no oxygen reaching a given portion of that tissue or organ, resulting in turn in death of those cells if this blockage is not relieved in a short time.

Most areas of the body have overlapping arterial supply or collateral vessels that (if one artery is blocked) there is another route for oxygenated blood to get to that area. Organs like the heart, brain, kidney etc are organs where either

(1) only one artery supplies that organ so if that artery gets blocked , short of undoing the block quickly there's no other way to get oxygenated blood to that organ OR

(2) there are a few arteries supplying that organ, but each artery covers separate portions of that organ, so that when one artery is blocked, a significant portion of that organ will be starved of oxygen. This is why they are more vulnerable to infarcts.

In the case of the heart, there are typically 2 arteries supplying oxygen to the heart muscle: the left and right coronary arteries, that both feed directly off of the aorta. While there is some overlap, large parts of the heart are typically only supplied by one or the other artery.

To quote from my old anatomy textbook: "Although there is a rich anastomosis between arterioles, this supply is inadequate to supply the requirements of cardiac muscle when there is a sudden blockage of a major branch. As a result, the region supplied by the blocked branch becomes infarcted (i.e. rendered virtually bloodless) and soon undergoes necrosis (i.e., dies)."

Some people only have one coronary artery, so you can imagine what that means for their risks if that vessel spasms or blocks off.

[St. Urho]

Originally Posted by serious lark

Some people only have one coronary artery, so you can imagine what that means for their risks if that vessel spasms or blocks off.

Wow! Do you have a cite for that?

[irishgirl]

Vascular patients always scare me.

All the diabetic feet (people with diabetes are prone to getting ulcers and gangrene in their feel abecause of poor blood supply) tended to put me off my breakfast.

Calf claudication is a symptom that is easily overlooked, one lady had no other symptoms suggestive of cardiac or atherosclerotic disease, and a normal ECG. Her problem was that the claudication in her legs gave her such severe pain that she had to sleep in a chair, and then only for 2 or 3 hours at a time. She ended up with a bilateral femoral-popliteal bypass, which is a major surgical procedure.

What always bothers me is the heavy smokers and drinkers who don't even give up after an MI. Most people are terrified into sorting their lifestyle out a bit...some people aren't, and they worry me.

[serious lark]

Originally Posted by St. Urho

Wow! Do you have a cite for that?

Not for the actual risk estimate, but here's a pretty dense E-Medicine article on the topic of coronary artery anomalies.

[Dr_Paprika]

I suppose the smallest possible heart attack would be one where the heart muscle is deprived of oxygen for enough time to kill one cell of heart muscle. Not all heart attcks cause enormous damage to the heart, but of course, many do. Many people still die from heart attacks.

MIs or Acute cornonary syndrome can be a difficult diagnosis to make. Stories and pains can be very atypical (and I have seen MIs present as an itchy throat or without symptoms). Many people have atypical ECGs which, while not normal, do not suggest MI. Blood tests can take many hours to show evidence of MI, or show evidence without ECG changes.

Strokes can be harder to diagnose than MIs since i) symptoms are often far more subtle, ii) there is the perception less can be done for strokes than a heart attack (fewer strokes require an operation, stroke management is very time dependent, for example), iii) diagnosis depends on tests which are more expensive and harder to obtain (most ambulances could do an ECG, not many ambulances can do a CT scan).

I manage a lot of heart attacks. I get scared by the guys who (no kidding!) have been thrombolyzed four of five times but don't take their aspirin or blood pressure medicine and keep smoking their two packs a day. I've seen quite a few very sick, non-compliant patients who, despite all expectations, recover from deadly illness after deadly illness and live to a ripe old age. Of course, most of these folks do not.

[St. Urho]

Originally Posted by serious lark

Not for the actual risk estimate, but here's a pretty dense E-Medicine article on the topic of coronary artery anomalies.

Cool, thanks.

[easy e]

Originally Posted by KarlGauss

Lastly, a major risk factor for strokes is the condition called atrial fibrillation. People with atrial fibrillation can have a risk of stoke as high as 20 percent per year.

I work for a medical device company that makes a lot of products to diagnose and treat atrial fibrillation. AF has a whole host of risk factors, including the typical ones for cardiovascular disease (high cholesterol, high blood pressure, etc.), but there are also congenital conditions. Additonally, people who have had some sort of heart surgery in the past are at higher risk. Just getting old is a risk factor.

What happens in AF is that the atria (the upper chambers) start beating in an uncoordinated fashion. This allows blood to pool, especially in the atrial appendages (they look a bit like ears sticking off the atria). When blood pools, it can clot, and if it clots it can break off and go someplace else (like the heart or the brain).

We have a lot of devices that are designed to measure ECGs from inside the heart. Incidentally, this is one way to estimate the size of a heart attack--you'll get no ECG if the catheter is touching dead tissue. To try to stop AF, an electrophysiogist will go and try to burn away the part of myocardium (muscle cell) that's causing problems.

We do both left-side and right-side work. On the left side, you have to be very careful that your device is nonthrombogenic and that it doesn't have anything that could fall off, because if that happened, the patient could get an MI or a stroke. On the right side, the blood goes into the lungs before goig to the left side, so it's not considered as crucial. Granted, we don't want to give the patient a massive pulmonary embolism, but there's considered to be more room for error. I know whether a device is left-side or right-side affects the regulatory path it takes.

I've also seen another way to estimate the size of an MI. I attended an animal study where they were using purposely infarcted pigs (they created the infarc by inflating a balloon catheter in a coronary artery for several minutes). The animals I saw were 3 months post-infarc. They were put in an MRI scanner and gadolinium contrast was injected into their blood. The vasculature in the MI was really tiny and the contrast tended to collect there, giving a big white spot on the MRI. Additionally, you could see the thinner layers of myocardium without even using contrast.