Apr

27

This blog post gives some very stunning data on "coronary heart disease", which I assume means "heart attacks". Supposedly the rate of death per year per 100,000 people has gone from over 500 in the 1970s to 20 now. People just stopped dying from heart attacks.

What's up with that? Is the data misleading in some way? Has coronary heart disease started getting re-classified as something else? (And for that matter, isn't "coronary heart disease" redundant?)

Seems like a good topic for Dr. Lillienfeld.

Dr Lillienfeld responds: 

A few thoughts:

First, the commentator in the link should not be confused with the UNC ob-gyn epidemiologist David Grimes.

Second, coronary heart disease, in which atherosclerosis is present in the coronary arteries supplying blood to the heart musculature, differs from valvular heart disease (in which one or more valves malfunctions and needs to be replaced) and other manifestations of heart disease. Syphilitic heart disease referred to in the blog is, I think, a reference to dissecting thoracic aortic aneurysms, which used to be a major problem in the US, but with control of syphilis, it's declined in occurrence.

Third, as for the main issue, there has been a substantial decline in CHD mortality in the US and in the UK. The peak in the US was in 1968 and in the UK, 1970. Stroke mortality has similarly declined. There are lots of questions as to what is actually taking place in the population—is it better treatment? is it reduction in exposure to risk factors? We know that there's been a significant reduction in risk factor prevalence—smoking rates have declined from 60% or so in the US to 20%. (The impact of the e-cig boom isn't clear as yet). There have been significant reductions in air pollution, especially in the small particulate portion, and the consumption of a fat/cholesterol-based/laced diet has also declined.

Hypertension has come under control (though in the early 1980s, with budget cuts in public health clinics, hypertension control lessened, and for a period of about 8 years, stroke incidence went up). Oral contraceptive use—a significant factor in heart attacks in younger women and also strokes—have reduced their estrogen content (we're now on the 3rd generation), and with that reduction, the associated risk of a heart attack or a pulmonary embolism has declined, too. (There's parts of this story in Foundations of Epidemiology 2nd edition and 3rd edition), but we didn't include it in the first edition—that was much of a lung cancer-cigarette smoking focus.

So far, so good. Except that the decline began in the US in 1968, just after the role of oral contraceptives in heart disease in young women was discovered (and before any reductions in estrogen content had been undertaken). (By the early 1970s, something like 60% of American women under the age of 50 had used oral contraceptives for at least 18 months; it was a widely used medication-especially among women who smoked—and smoking acted synergistically with oral conceptive use in increasing the risk of a heart attack. Hypertension control was introduced into the US during the 1960s. It would be difficult to say that it was widely prevalent by the end of the 1960s. During my residency in Minnesota in the mid1980s, we undertook many different ways to get everyone in the population screened for hypertension, and we know we didn't succeed nearly enough to suggest that there was effective control of high blood pressure in the population. In any case, control of high blood pressure really took hold only after the decline began. (It has had an impact—on chronic kidney disease; it has reduced hypertensive renal failure significantly. And since Medicare covers the expense of dialysis, the use of those anti-hypertensives has saved a lot of money. Whether Medicare should have ever covered the cost of chronic renal failure, much as whether it should have covered coronary bypass surgery, is a matter of contestation.)

Similarly with blood lipids. Cholesterol levels have declined, but the impact of the statins (the effects of which have been shown in a number of randomized trials) would have been felt only since the mid 1990s; lovastatin wasn't even introduced in the US until the late 1970s, and atorvastatin (Lipitor) wasn't until 1997. In other words, the big three risk factors for heart disease—blood lipids, smoking, and high blood pressure—have declined, though lagging the decline in mortality. Then there's Europe. Smoking in Europe did not decline nearly as much, nor as fast, as in the US. I don't know about the extent to which high blood pressure control occurred in Europe, but I doubt if it was any faster than in the US. Yet the decline took place to the same degree as in the US.

Ah, I hear you say, that's because it's the result of better treatment. All that money wasted on disease prevention programs. Except that the data supporting that contestation are as out of sync with the decline as were the risk factors. Many cardiologists have declared that the decline is a demonstration of the impact of all the coronary care units built during the 1960s and 1970s. CCUs were the crowning jewel in many academic medical centers. There were high tech and they were effectively black holes for money. Despite many efforts by epidemiologists to subject CCUs to randomized trials, cardiologists insisted (much as psychiatrists were doing at the same time) that to deny access to the CCU to any patient meeting criteria for admission to the CCU was unethical. But CCUs were an American creation. The UK and much of the rest of Europe didn't build them until the decline was well underway. That build-out wasn't completed until much of the decline had happened. The same is true for coronary bypass surgery and the use of stents.

 Bill Rothstein looked at this issue (to a degree) in his book (http://www.amazon.com/Public-Health-Risk-Factor-Revolution/dp/1580461271). Bill got into quite a heated discussion when he presented his first paper on the subject at the 2012 American Association for the History of Medicine meeting in Baltimore (esp with Bruce Fye, who I think is still at Mayo), and more recently at the 2013 meeting in Atlanta with Henry Blackburn (from U Minnesota). Henry's compiled his own online history of cardiovascular epidemiology (http://www.epi.umn.edu/cvdepi/people_list.asp), but at least when I last spoke with him late last year, he had no response to Rothstein.

Frankly put, no one understands the decline, and to suggest that statins and the like had little contribution to it doesn't make sense given the extensive clinical trial data showing significant effects. Lipitor can reduce the blood lipid level by a third, for instance. The only thing everyone agrees on is that there was indeed a decline. Maybe it's lots of little contributions, except that the lag times don't concord with that explanation, either.

I hope that helps.

Charles Pennington writes: 

Yes, that was masterful, seriously. I am still digesting it. Thanks!

If you still have energy left, I would also like to know about the left hand side of the curve–the enormous accelerating increase that took place from 1910 (when the rate was very close to zero) through the 70s. Was that at least partly a reporting/diagnostic issue — that they just didn't recognize this mechanism of death in 1910?

David Lillienfeld replies: 

Let's start with what we know and work from there. We know that by the 1960s, there were many heart attacks occurring in the US male population—women would catch up in a couple of decades (yes, Benson and Hedges had it right, just in the additional context of disease as well as social conventions, occupational opportunities, and so on). The phrase "He had a coronary" was part of everyday discussions. For a middle-aged American male, having a heart attack was almost a part of life's passages, much like one's first love, marriage, children, and so on. Heart attacks were diagnosed by EKG until the 1960s, when wide-scale availability of serum chemistry analyzers in medical laboratories facilitated the development and use of elevations in different enzymes as indicative of a heart attack. At the same time, the idea of a "silent MI," as it was called, was developed, in which some myocardial tissue died from a mini-heart attack that did not cause sufficient pain or shortness of breath to cause the individual to present to a physician. That's how we came to know that there were a lot of heart attacks in men during the 1960s (which is not to suggest there wasn't lots of heart disease in women, too).

How did we get to the point of having so much heart disease in the first place? Heart attacks have been known as a distinct clinical entity for a long time. In Major's Classic Descriptions of Disease (I think I have the second edition, but I can't find it immediately), the credit for the first observation of a heart attack is given to Adam Hammer, a physician in St. Louis, who published the description during the late 1870s. Angina pectoris, as a distinct entity, would await William Osler, but I don't remember the date. It was later than Hammer.

During the first part of the 20th century, there's general agreement that the majority of cases of heart disease were rheumatic, ie, sequelae to a case of rheumatic fever; specifically, there was damage to the heart valves. (While there was some controversy about the diagnosis of rheumatic fever and what might be its cause up until the 1940s, when T. Duckett Jones put forth a standardized set of criteria that have served since as the basis for making the diagnosis, the cardiovascular effects were accepted as such back by the turn of the century.) While there are some controversies outstanding about how exactly rheumatic heart disease develops, its clinical diagnosis can be made with assurance using the medical technology and skills available in the early part of the 20th century. It seems unlikely, then, that there were many heart attacks misdiagnosed, unless one posited that there were lots of silent heart attacks. I don't know of anyone putting forth that idea, though.

Two big factors weighed on the population's health during the turn of the century—better nutrition and, for reasons not well understood, a declining frequency of active tuberculosis. The two may be coupled, but again, that's controversial. Suffice it to say that American diets included many dairy products, providing a source of animal-based fats. This was the "anti-tuberculosis diet" of the early 20th century. It provided sufficient calories that even in the presence of an active case of tuberculosis, the patient was not literally consumed by the infection (this is why TB was known as consumption). The problem was that that same diet was also fantastic at creating fatty plaques the lumens of the coronary arteries (other arteries too). As the population became wealthier, consumption of meat and processed dairy goods increased. Concurrent with that was an increase in the prevalence of smoking. Prior to 1900, there wasn't nearly as much smoking as there was in the mid-20th century. And the vast majority of that smoking was among men. The incubation period for smoking on heart attacks is much shorter than dietary fat or hypertension. WW2 didn't help matters—the cig cos gave the cigs out free to soldiers—a whole generation hooked on smoking.

Hypertension is a little more challenging. No one's really sure when it really did first appear. Until the 1950s/60s, increasing BP with age was considered OK.

The bottom line is that there was a confluence of factors, all of which were increasing at the same time—a trifecta if you will. Or a perfect storm.


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