What causes heart attacks?

I recently had a “near death” experience, which led to my becoming very confused about heart disease.

I was a runner all my life, and ate only the “right” foods, until I ended up in the ICU. While recovering from my heart attack, I was told the following story by my cardiologist:

The diet-leads-to-heart-disease, and exercise-is-healthy theory apparently is not the whole story. And may, in fact, be wrong.

Apparently, some research was done about 20 - 30 years ago in which it was found that it didn’t make any difference what you ate, or how much cholesterol there was in your blood, or clogging your arteries; you could still get a heart attack. Just as many people with squeaky clean arteries as those with plugged arteries have heart attacks.

The people who did this research took tissue samples from the arteries of people who had died of heart attacks, and found that 100% of them had a particular bacterial infection in the tissue.

According to them, the bacterial infection inflames the arteries. The body reacts to this inflammation by depositing cholesterol over the inflammation. If the inflammation is big enough, it precipitates a blood clot. If the blood clot breaks loose, this can cause a heart attack or stroke.

This theory seems to be substantiated by the fact that stents that are impregnated with antibiotics are more effective and last longer than those without.

Similarly, the pattern of heart disease apparently follows a pattern characteristic of those caused by infective agents. Ie: the incidence of heart disease peaked in the early 1970’s, and bottomed out about five years ago. It is now on the rise again.

I am not qualified to say whether this story is right or wrong, but since it was told to me by a very prominent cardiologist as I was lying in bed hooked up to a whole bunch of machines and drips, it does have credibility.

Anyone know anything about this?

Heart attacks can certainly occur in people who have all the following attributes (at once):

Low cholesterol
Low blood pressure
Long term low fat diet
Prolific exercisers
Non smokers

However, for each of the above attributes that does not apply to you your chances of a heart attack increase. In some cases (high fat diet, long term heavy smokers who don’t exercise) very considerably.

Of course, most of us know at least one person who breaks every rule and lives to 90+.

Welcome to the Straight Dope Message Boards, Grateful-UnDead, we’re definitely glad to have you with us.

You’ve started this thread in a forum devoted to comments on Cecil’s Columns, and I think your question is really NOT related to a past column (at least, not directly.) I’m therefore moving it to a forum where I think it will get more attention and better responses.

If I’m wrong and this is indeed in response to one of Cecil’s columns, please email me and I’ll move it back. No biggie, and, as I say, welcome!

Well, I am (very much NOT) a doctor, but I do lots of reading on this subject as a hobby, and have enough confidence in it to put it into personal practice. There is considerable doubt that there is any basis to the “lipid hypothesis”, that is, that consumption of saturated fat and/or cholesterol causes cardiovascular disease, and more evidence that such disease is due to our intakes of sugar, starches, grains, wheat (yes, “healthy whole grains/wheat”) and the like. I won’t attempt to explain it all, but can point you to some reading so you can make up your own mind.

Book: Good Calories, Bad Calories, by Gary Taubes
One suggested website, by a cardiologist, Dr. William Davis. He keeps it just technical enough to be useful, but not overwhelming. He explains the wheat/grains statement I gave above.

Basically, what you are asking is what is atherosclerosis (“hardening of the arteries”). The Wiki article on the subjectlooks fairly comprehensive and should be a good place to start, especially with respect to the underlying cause(s) of atherosclerosis. Among other features, it has an interesting list of risk factors for atherosclerosis (factors which are associated with it, but do not necessarily cause it).

Despite many people’s claims and “common sense”, the root causes of atherosclerosis remain obscure. We know many of the processes involved, but not a lot about what sets them in motion, and what protects against their development and progression. IMO, for many putative causes, it is still debatable whether they are really, at the bottom, just associations.

It is beyond debate (IMO) that lowering cholesterol prevents heart attacks and atherosclerosis in general. Still, that is far, far from the whole story and, more importantly, does not imply that dietary intake of cholesterol (or other fats) has anything to with their blood levels or their role in atherosclerosis (indeed, most cholesterol is made by the body, itself, and has little or nothing to do with diet).

Empirically, for most of us, the most potent risk factors for atherosclerosis seem to be genetics (i.e. your family history), diabetes, and kidney disease. Most people (>80 to 90 percent) in the latter two groups will die of atherosclerosis. Likewise, if you have a certain genetic makeup, you will have a heart attack by your teens, at the latest (e.g. familial hypercholesterolemia). Other, common risk factors pale in comparison in terms of their predictive power for the development of atherosclerosis.

For me (and I cannot emphasize too strongly that these things are individual), it was smoking. I was obese–I still am–but the day I had my heart attack 45 years ago, I stopped smoking. I was 28. Oh I lost a fair bit of weight, but I put it back on, lost some again. When I underwent an echocardiogram about 6 or 7 years, they could detect no scar tissue. Now I am 73 and, while I do have some heart problems (atrial fib, required a pacemaker), I feel fine and I have concluded that the heart attack, by getting me to stop smoking, may have been the best thing that ever happened.

By contrast, my father had a heart attack when he was 41, never stopped smoking, and died of a heart attack at 63. Both of us had an ashy complexion, but mine turned pink when I stopped smoking. My layman’s conjecture is that we were both unusually sensitive to CO.

But I emphasize, YMMV.

There isn’t a short answer to your question. Thousands of studies and ongoing research haven’t really answered it fully.

The Framingham Study is one of the most popularized ones to look at what is associated with heart disease, and all of the things you normally hear about–smoking; genes; high cholesterol; diabetes; sedentary lifestyle…–are seen as being associated with heart disease. The odd thing, though, is that it’s much tougher to prove they cause it, per se, and it’s really been tough to show that altering lifestyles–diet and exercise, e.g.–affect heart disease much. Most of your lipids are endogenously made, and a guy with crappy genes will make plenty of lipids from an ordinary diet; a guy with good genes can eat butter and have perfectly fine levels. Physicians, the public, and industry all have accepted on intuition that healthy lifestyles must be good for your heart if heart disease is associated with all those other things, but frankly the Framingham Study peeps have had to sort of admit that medical intervention into lifestyles hasn’t been particularly helpful. So, for instance, diet and exercise control of lipids is pretty much useless. On the other hand, lipid-lowering agents do help control lipids and probably to reduce mortality.

The role of “inflammatory” processes is currently still poorly defined.

In short, if you want to be heart-healthy, get some good genes and don’t ever smoke, not even while young. With good genes you can eat what you want and your arteries will still be fine. If you have crappy genes, you may get diabetes and hypertension no matter what you do; diet and moderate excercise might moderate those diseases and may even help diminish the complications of them, including heart disease. Lipid-lowering agents might be a good addition, but the actual sub-populations we should use them in are still being defined.

Nothing new here, huh? Sorry.

Some very interesting responses; they, in general do seem to substantiate the substance of what my cardiologist told me; Ie: it doesn’t matter what you do, or eat; whether or not you get heart disease is a matter of chance.

Interestingly, he also told me that the Framingham(?) and numerous other related studies have in recent years had their raw data re-examined by expert statisticians. This re-examination apparently shows no co-relation between diet and heart disease. That is to say, the reported results of those studies are not supported by their own data.

This would also seem to be supported by the fact that he also told me that he treats a couple of hundred people a year. They range in body type from the morbidly obese to the skeletal; from the meat and potato type to the vegan; and the iron man exercise fanatic, to the guy who only gets off the couch to get another burger and beer. Yet they all present with the same heart disease.

In that respect, he also told me that his clinical observation is that taking cholesterol lowering drugs, in fact, increase your chance of having a heart attack. His theory is that blood cholesterol levels are, in part, an immune system response to an infective agent. So by artificially lowering their level, conditions favorable to the infective process are maintained. The result is an increased chance of heart attack.

Also, are “atherosclerosis” and “heart disease” the same thing? I think he told me that heart disease is specifically a condition relating to the coronary arteries, whereas the other is a general systemic thing; and both have different and distinct causes.

I admit that I was high on happy pills at the time we were having this discussion, so I may have got some of this stuff wrong, but I think I have the gist right.

So, assuming I have got it right, and the responses from the other contributors above are also right, all of this all raises the big question: if there is no connection between what we eat and heart disease, why are we subject to a constant barrage in which we are told: “don’t eat this, that or the other thing; do this, do that, and don’t do the other!”

If, in reality, diet and exercise have no bearing on heart disease, why are we being told otherwise?

The book referenced above by Angel of Doubt, Good Calories, Bad Calories, by Gary Taubes, explains very well the history of why we’re being told otherwise. Basically it boils down to the fact that it sounded very plausible, and it seemed to make sense to recommend what intuitively should work, if it had the chance of saving lives. When studies were done that didn’t bear out the recommendations, they usually didn’t get published, because the authors thought there must have been flaws. When Taubes would ask them why they didn’t publish, they’d say things like “We didn’t get the results we were expecting.” I recommend this book highly. Taubes is one of the most respected science journalists in the country, and he has no hidden agenda. He spent many years re-evaluating the studies your doctor referred to, and is one of the key people in determining that the studies weren’t supported by their own data.

Because it does appear to matter for some people. And even if it’s not a cure-all to diet and exercise, you may be helping yourself in other ways not directly related to heart disease but possibly related to other diseases/syndromes that can screw you up royally. Type II diabetes, for instance, is strongly influenced by diet, smoking, exercise, and level of alcohol consumption.

Question to Karl Gauss and the others:

I keep reading that (as the OP said) arterioscleriosis is started by bacterial infection (and then apparently worsened by the fats etc.), and the source of these bacterias might be … bad teeth, as well established. So much that the first advice in the general area is to get your teeth in order, not only in regards to caries, but also parodontitis, before getting to diet and exercise.

Also, as to why we are told about diet and exercise: if you do exercise and eat enough vitamins instead of fast-food, your body will recover quicker from stress, in addition to what Ferret Herder said about other diseases.


Bad teeth are conclusively linked to both heart disease and diabetes, and I have seen studies indicating an increased risk of some types of cancer. The primary cause of periodontal disease is the acidic waste of certain types of oral bacteria that happen to live and thrive on carbohydrate in the mouth. Dietary intake of carbohydrate has always been linked to periodontal disease, and is now being linked to the development of heart disease, diabetes, and some types of cancer. Additionally, nutrients not found in high levels in a diet primarily composed of carbohydrate contribute to the healing (remineralization) of teeth, and are being linked to reduced risk factors for the other conditions… omega-3 fatty acids and vitamin D have been getting big press lately.

Somehow we haven’t all connected the dots on this one, yet.

This is simply not the case. Many, high quality research studies have shown the exact opposite - lowering cholesterol reduces your chance of having a heart attack.

That being said, I will be the first to admit that the net benefit of cholesterol lowering is usually overstated. For example, as shown on this Wiki linkeven among “high risk” men (age 40 to 79, with high blood pressure and at least three other cardiovascular risk factors), you have to treat one hundred patients for over three years with cholesterol lowering drugs to prevent one heart attack. This is similar to, but not quite the same as saying, you must treat more than 300 such men for one year to prevent one heart attack. Phrased differently yet again, in any given year, more than 299 men will take cholesterol lowering medicines unnecessarily for every man who gets his heart attack prevented.

On the other hand, for people who already have had a heart attack, the effect of cholesterol lowering is more impressive. In one of the earliest studies in this regard, it was shown that you need treat about 15 heart attack survivors for five years to prevent another heart attack, or 33 heart attack survivors for five years to prevent one death. These numbers may not seem too impressive, but it seldom gets much better than that in Medicine.

Yes, infection, or more generally inflammation, is thought by many to play an important role in the development of atherosclerosis (here is a relatively recent view on the subject which I think is free). Suffice it to say, the various mechanisms involved are not completely understood.

In terms of infection specifically, the evidence would suggest, ‘no’, it’s not that simple. For example, a number of studies have shown that treating people with antibiotics (i.e. antibiotics that should cure the type of infection postulated to cause atherosclerosis) has no effect on atherosclerosis. Cites available on request.

No, but they are closely related. In particular, atherosclerosis is the term used to describe the condition where the blood vessels (arteries) in your body get clogged up. Eventually, blood can’t flow through them. At that point, whatever part of the body that was getting its blood supply from the clogged artery will die (from lack of blood, i.e. lack of oxygen). In fact, it’s very often the heart itself which doesn’t get adequate blood flow as a result of clogging of the arteries (atherosclerosis). In other words, the blood vessels (arteries) supplying the heart itself with oxygen can get clogged. Eventually, not enough blood/oxygen can get to the heart and it dies, or part of it dies. That is a heart attack.

So, atherosclerosis is one cause of heart disease. Specifically, the blood vessels which supply the heart itself with oxygen are called the coronary arteries. When the coronary arteries are affected by atherosclerosis, it’s called coronary artery disease or even coronary heart disease. Whatever it’s called, this disease process can eventually lead to inadequate supply of blood/oxygen to the heart itself. When that happens, the heart, or part of it, can die. And that is called a heart attack.

Really? I just haven’t been able to find many. For men over 40 who have many risk factors and/or a history of heart disease and heart attacks - yes, there are some good studies inditcating that cholesterol-lowering drugs have been found to reduce risk of heart attack in a very small proportion of patients (not nearly helpful enough IMO to justify the use of statins for a majority of patients, with all the side-effects they have). For everyone else it seems there is no evidence indicating they are helpful, and some evidence they might be harmful. So why are we putting women of all ages on statins?


I just assumed the OP and others were talking about cholesterol lowering (primarily with statins) in people for whom such treatment is indicated. Who said anything about treating, say, asymptomatic young women?

IMO, and I think the evidence backs me up, cholesterol lowering with statins is a reasonable and beneficial approach (i.e. prevents heart attacks and possibly death and/or stroke) in the following groups:

  • all people who’ve had heart attacks already
  • all people with atherosclerosis (e.g. previous stroke, “peripheral vascular disease”)
  • all people with diabetes (whether or not they’ve had heart attacks or have any evidence of atherosclerosis)
  • all people with significant impairment of kidney function (whether or not they’ve had heart attacks or have any evidence of atherosclerosis)
  • most people at “high risk” for heart attacks (e.g. a 10-year “Framingham risk” for heart attack of > 20 percent, i.e. people with high cholesterol and risks such as older age, male sex, smoking, hypertension, and low HDL)

(FYI, here are the free, full-text Canadian Cardiovascular Society recommendations which include the “Framingham risk engine”).

Again, I must stress that no one I work with, and certainly not me, is advocating the use of statins in “the majority of patients”. Who says such a thing?

Finally, statements such as “statins . . . with all the side-effects they have”, are misleading and not based on the evidence accrued from their use in literally millions of people. Yes, like all drugs, they can have unintended or side-effects, but serious ones are uncommon, if not rare. More to the point, the potential benefits of statins in the groups of people I’ve listed above far outweigh the chance and risk of such effects.

My former primary care physician, for one. I was resisting going on a statin, which annoyed him no end. “Most cardiologists think statins should be put in the water,” was what he told me.

I like this rubric, and wish more doctors would follow it. My mother, of healthy BMI, no cardiac history, no diabetes, no kidney problems, etc. was put on statins because and only because her cholesterol level is elevated.

She’s not alone, just the one whose medical history I know the most about. I’m fighting off the doctors myself now, as I share her genetic predisposition to elevated cholesterol levels. I’ve been “granted” 6 months to get my cholesterol down by other means before they “make” me take statins. (Luckily, I *do *know my medical rights. I’ll let them test me again in 6 months just so I know what sort of impact all this weight loss has had, but I’ll find another doctor or no doctor at all before I take statins with no other major risk factors.)

Maybe it’s a US thing. Docs here are statin happy. I haven’t had a *single *patient in Clinicals yet who wasn’t on them.

As a non medical layman, this discussion is starting to get really interesting now; as a matter of fact, it has got me sitting up very straight and paying rapt attention.

Let me go out on an uninformed limb with regard to blood cholesterol: I understand (from high school biology) that the primary source of cholesterol in the body is synthesis in the liver; and the input from dietary sources is negligible.

If the dietary intake is excessive, then synthesis in the liver is proportionately reduced. This is part of the internal biological control system that acts to maintain the levels of all kinds of bodily metabolites within predetermined limits (homeostasis???).

Also, I understand cholesterol is a crucial metabolite both in brain function and in the formation of cell walls.

So, if somebody’s cholesterol level is “high”, then homeostasis is not working. So, is this not indicative of a pathological condition?

If so, shouldn’t that pathological condition be treated; as opposed to the symptom being treated with cholesterol lowering drugs?

If the cholesterol level is artificially lowered, would that not then impair the brain and cell functions which are dependent on cholesterol?

PS: “Angel of Doubt” I have placed an order for “Good Calories, Bad Calories”; I don’t know if I will be able to sleep nights after reading all this.

Remember that “high” is defined only in relation to the range of cholesterol levels of in the general population. In other words, just because a person’s cholesterol level is higher than most other people’s, doesn’t mean it’s “high” for him/her (and vice versa), or that it’s necessarily abnormal. So rather than reflecting a “pathological condition”, it may be totally normal. (Is someone who’s seven feet tall suffering from pathology? Or mightn’t they be perfectly ‘normal’ except they happen to be taller than most everyone else? I’d say that it’s not that their “homeostasis isn’t working” so much as that they may have a ‘set point’ that’s higher than most. On the other hand, if their unusually tall status is associated with things like abnormalities of the lens in the eyes, or heart valve problems, one might suspect that their height does reflect pathology (in this example, Marfan Syndrome).

As an aside, it’s interesting to consider that for pretty well all blood test results, “high” levels are simply defined as those greater than 95 percent of the population. This practice has the effect of causing all blood abnormalities (and any diseases such abnormalities may reflect) to have the same prevalence - 5 percent! Obviously, that’s nonsense; not all conditions have the same frequency.

At the end of the day, what counts may not be the underlying theory which may (or may not) explain a disease or disease process, but rather, reality and observation, e.g. independent of any speculation or theorizing, do people treated with statins experience fewer heart attacks?

This is a great example of why what counts should probably be data and experimental results and not the more abstract theoretical underpinnings. Specifically, a number of studies have shown that there is no increase in things like trauma, suicide, or dementia as a result of statin use, all of which might have been expected if statins caused an adverse change in brain function (in fact, if anything, there is some evidence to suggest that statins may protect against the development of dementia.)