The preliminary autopsy of actor Corey Haim shows he died of an enlarged heart.
However the Wikipedia article doesn’t say much about it. What exactly is it? What causes it? And how dangerous is it? Is it very dangerous if known about and treated properly? How would one know if one had it?
Just any useful info would be appreciated. Thanks
The Cleveland clinic has a nice summary here: Hypertrophic Cardiomyopathy.
Edit function is acting weird.
Of course, he might have had a Dilated Cardiomyopathy instead.
Not applicable in this case, but many people who exercise heavily have an “athlete’s heart.” This heart is also enlarged due to stronger muscles, especially of the left ventricle. One whose heart labors due to diseased arteries will also have an enlarged left ventricle. AFAIK, there are several differences, both in the anatomy and physiology. Anatomically, an athlete’s heart muscles will be stronger and the left ventricle chamber will not be enlarged. A diseased heart will have a larger chamber. I’m not sure of that, but I am sure of the physiological differences:
An athlete’s heart will be adequately supported by coronary arteries. The arteries will be healthy; whereas, in a diseased heart, the arteries struggle to provide blood to the heart. In addition, an athlete’s heart will pump more blood with each beat, close to 75%, which is the max. A weakened enlarged heart may pump only 30%, or even less. Since the athlete pumps more blood with each beat, his heart doesn’t have to beat as much. Some have been known to have a resting pulse of 30. 40 is not uncommon. A diseased, enlarged heart will have to beat more often than the normal range.
It’s not strictly correct to say death was “from” an enlarged heart. It would be better to say that at autopsy an enlarged heart was present. In the cite you give about Mr Haim, pulmonary congestion is also mentioned.
While neither of these are actual diagnoses, the combination suggests heart failure as a possible cause of death. Most (though not all) causes of an abnormally large heart reflect underlying pathologic conditions, and a partial list is found in the Wikipedia cite you give.
If the underlying cause is not congenital (particularly valvular abnormalities, septal defects and primary disorders of the heart muscle such as Hypertrophic Cardiomyopathy), other commonly found underlying causes are things like post-viral cardiomyopathies which can leave the heart muscle flabby and dilated, and heart failure from hypertension–this can be a generally enlarged heart from an overworked heart muscle, or it can be a dilated cardiomyopathy when the ventricle begins to fail and becomes flabby. It’s also possible to have ischemic damage from heart attacks that leaves part of the heart muscle thin and dilated (called a cardiac aneurysm). There are, of course, many many other possibilities…in general “an enlarged heart” is too non-specific a term to give any sort of detail around cause, treatment or prognosis.
In a young man with a history of substance abuse (and I have no idea if this would apply to Mr Haim) it would not be unusual for an overindulgence in nose candy over a long enough period of time to produce heart failure in conjuction with an enlarged heart. Cocaine and smilar stimulants can produce spikes of high blood pressure that take a toll on the heart, leading to pump failure.
The heart enlarges when it has to work harder (like most muscles).
The ‘good’ cause for this is as barbitu8 mentioned, an athletes heart. They practice & train their bodies to an exceptional degree of effort, and their heart will enlarge correspondingly. Even in animals: after his death, Secretariat’s heart was about twice the normal size for a horse. But this type of enlarged heart is good; it developed in response to a planned training regimen, to meet the demands on it.
The ‘bad’ cause is where the heart is forced to enlarge because the heart/lungs/circulatory system is not functioning properly, and the body responds by directing the heart to pump faster/harder, and so the heart enlarges to try to do this. This kind of enlarged heart indicates a last ditch attempt by the body to keep things going, despite some underlying problem. There are lots of different problems that can cause this reaction: problems with heart valves that don’t work properly; problems with the lungs where oxygen exchange is not happening properly; problems with clogged arteries where the blood & oxygen is not being distributed efficiently – all of these can result in an enlarged heart. And like Chief Pedant said, people generally don’t die from an enlarged heart. They usually die from the underlying health problem, the one that caused the heart to enlarge.
Yes. And no.
It is CRITICAL to distinguish between hypertrophy of the heart muscle and dilation of the heart chambers. The former can be physiologic (as in an athlete) but the latter is never normal - it means the heart (ventricle) is failing. It is also important to note that in clinical medicine, “enlarged” means dilated.
When you examine someone and note that their heart is “enlarged”, you are stating that the point of their heartbeat’s maximum thrust is situated beyond its usual confines. That can only be due to dilation of the heart chamber (ventricle). A heart (ventricle) that’s hypertrophied does not change the point of where you feel that maximum thrust. It may make the thrust last longer (be sustained), but it does not place the point of maximum thrust beyond the normal site.
The same applies for the findings and terminology with respect to echocardiograms. “Enlarged” on echo means the chamber is dilated. Hypertrophy means the wall muscle is thickened. As with the clinical usage, the terms hypertrophy and enlargement (dilation) in this setting carry very different implications (and prognosis).
ETA: Dilation means the chamber (ventricle) is overloaded with volume. That is always pathological. Hypertrophy means the ventricle is dealing with high pressure (or with lots of ‘normal’ pressures as in an athlete). That may, or may not, be abnormal.
Hmmm…
In so-called “physiologic” left ventricular hypertrophy (aka “athlete’s heart”) there is some debate around whether or not the condition has any pathologic consequences–i.e. whether it’s truly “physiologic” (meaning not harmful). It’s not entirely settled, in summary, about whether or not this is good for you or not over the long haul.
The layman’s term “enlarged heart” is quite vague and encompasses several notions: 1) the heart’s overall outside dimension is larger than a normal range, or 2) the heart’s total mass is larger than normal, or 3) both the total mass and total outside dimensions are larger than normal.
So, for example, a big floppy heart could be described as “enlarged” even though it doesn’t weigh more than normal. Dilated cardiomyopathies give rise to this. Or a pure left ventricle hypertrophy which diminishes the left ventricle volume but doesn’t really increase the outside dimension might be described as an “enlarged” heart because the muscle mass is greater than normal…
In physiologic LVH both the overall size of the heart and the overall mass of muscle in the left ventricle are greater than normal. The volume (specifically, the end-diastolic volume) of the left ventricle is higher than normal–i.e. the LV is mildly dilated–but filling pressures are normal and hypertrophy is relatively concentric (as opposed to the pathologic condition of Hypertrophic Cardiomyopathy, say). The point of maximal impulse (PMI) on the chest would be shifted from that patient’s baseline (pre-training) state because the actual outside dimension of such a heart is bigger; the hypertrophy does not simply take up space formerly occupied by the LV cavity.
Yeah, this is where it gets confusing. But mostly because of using “enlarged” or “displaced” in a literal sense. In other words, yes, hypertrophy does displace the apex - the thickened ventricle expands not just into the cavity, but also in the other direction. Given that outward expansion, the PMI must be displaced, I agree. But . . .
. . . it’s all a matter of degree. So, even though hypertrophy displaces the apex, it only does so to a very small extent. Maybe a centimeter or so. On the other hand, the displacement of the PMI that results from ventricular dilation dwarfs that amount - I’m sure you’ve seen PMIs that are out to the anterior axillary line (or beyond).
So, when we (?I) talk about a displaced apex or PMI, it’s referring to the gross displacement that occurs as a result of ventricular dilation, not the much more modest, often imperceptible displacement that can arise due to ventricular hypertrophy per se.
One of the reasons so many pro wrestlers die young is an enlarged heart from taking steroids or HGH. This combined with cocaine or speed usage can be deadly.
I happen to have a hypertrophic heart due to an intense exercise regimen, which was much more intense 30 years ago, when I was running at least 70 miles a week, completed a 50-miler, etc. My EKG has always been abnormal, so doctors had me undergo a thallium stress test (around 1981) which was negative. My initial TP here in Charleston detected a partial left bundle block on one EKG. He said that a quick repolarization was diagnostic of that and had nothing to do with an “athlete’s heart.” The following year he had me undergo an echocardiogram. When I went for a follow-up visit, the doctor left the office for a while, so I peaked at the cardiologist’s summary. (I had the right to see it, anyway.) The cardiologist noted that the apex of the left ventricle moved slowly, but there was no shunting (whatever that meant.) Anyway, the cardiologist wanted another echocardiogram from a different viewpoint, below the apex. I never did find out the results of that one, but when I asked my TP about the LBBB, he seemed perplexed, as the EKG no longer showed it.