Heart disease deaths dropping, but we can do better

Apr 11 2011 Published by under Medicine

Here's a re-post on an important topic.  New posts to follow.  --PalMD


Sixty years ago,  the world was full of miracles.  Western Europe was recovering from the devastation of World War II, an agricultural revolution promised to banish the fear of starvation in large parts of the world, and the mythical Mad Men era gave Americans a taste of technology-dependent peace and prosperity unlike any in the past.  Despite the technological progress that would soon send animals into space and return them relatively unharmed, Americans, and westerners in general, were still dying of heart disease at a frightening rate.  If you, as a middle aged American,  experienced chest pain and were lucky enough to make it to a hospital (about 20% of all sufferers would die immediately), you would probably be given nitroglycerin and morphine to control you pain, put on bed rest, and could expect to live a few more years, with limited physical activity.

Heart disease continues to be a top killer of Americans, but there has been a dramatic decline in heart disease mortality in the last 60 years, with age-specific mortality rates dropping 60%.  Fewer people are developing heart disease, and those that have it are living longer.   It is estimated that in 2000 alone,  there were 341,745 fewer heart disease deaths than would have been expected if rates had remained unchanged.

The trend has been going on for many decades, and has been accelerating, although current trends in diabetes and obesity put us at risk for more overall cases of heart disease in the future.  So what are we doing right?  How have we managed to cut the death rate from heart disease so dramatically?

Several studies have helped illuminate the answers.  There have been different relative contributions from primary prevention (preventing  new cases of heart disease) and secondary prevention (preventing recurrent cases).  A recent study in the American Journal of Public Health analysed data from 1980-2000.  The authors found that most of the reduction in deaths from heart disease (nearly 80%) were due to primary prevention, specifically decreasing smoking rates, and improvements in blood pressure and cholesterol levels.  Society-wide reductions in smoking, blood pressure, and cholesterol are saving hundreds of thousands of lives in the U.S. every year.

The smoking rate in the US is still hovering around 24%.   More than half of people with known high blood pressure do not have their blood pressure under control.  This study shows us that we can easily prevent more heart attack deaths through education and through better adherence to extant treatment guidelines.   Reducing heart disease deaths isn't hard, and it won't take miracles. We just have to want to do it.

*Similar trends have been seen in other English-speaking countries


Hurlburt CW (1927). THE CARDIAC CRIPPLE. Canadian Medical Association journal, 17 (11), 1305-9 PMID: 20316574

Sytkowski PA, Kannel WB, & D'Agostino RB (1990). Changes in risk factors and the decline in mortality from cardiovascular disease. The Framingham Heart Study. The New England journal of medicine, 322 (23), 1635-41 PMID: 2288563

FRY J (1964). CORONARY HEART DISEASE IN GENERAL PRACTICE: NATURAL HISTORY OVER TWELVE YEARS (1950-1961). Proceedings of the Royal Society of Medicine, 57, 39-42 PMID: 14114173

Centers for Disease Control and Prevention (CDC) (1999). Decline in deaths from heart disease and stroke--United States, 1900-1999. MMWR. Morbidity and mortality weekly report, 48 (30), 649-56 PMID: 10488780

Young, F., Capewell, S., Ford, E., & Critchley, J. (2010). Coronary Mortality Declines in the U.S. Between 1980 and 2000 Quantifying the Contributions from Primary and Secondary Prevention American Journal of Preventive Medicine, 39 (3), 228-234 DOI: 10.1016/j.amepre.2010.05.009

Wijeysundera HC, Machado M, Farahati F, Wang X, Witteman W, van der Velde G, Tu JV, Lee DS, Goodman SG, Petrella R, O'Flaherty M, Krahn M, & Capewell S (2010). Association of temporal trends in risk factors and treatment uptake with coronary heart disease mortality, 1994-2005. JAMA : the journal of the American Medical Association, 303 (18), 1841-7 PMID: 20460623

15 responses so far

  • D. C. Sessions says:

    I'm a lot less interested in trends of mortality rates than I am in trends of age at death.

    I mean, I have to die of something and a honking MI has a lot to recommend it compared to, say, metastatic prostate cancer (what got my father and $HERSELF's respectively.) However, it also matters a bunch whether I check out at 62 like my father or well into my 80s like hers.

    BTW, one factor not mentioned, but near to home: sleep apnea. Probably the primary cause of my father's arterial disease and ultimately his death, certainly a big factor in his quality of life for most of the time I had him. We do vastly better at that than we did forty years ago.

  • PalMD says:

    I suspect sleep apnea is underdiagnosed and under treated, but i don't know the data to back that up.

    • D. C. Sessions says:

      Always room for improvement -- we're not going to run out of thing like that to learn in any of our lifetimes.

      In the meantime, we just do the best we can (which is sometimes pretty damn good, says /me while breaking in a new knee.)

    • antipodean says:

      Prevalence will be rising in tune with the rising mean age and BMI. Massively undertreated. Associatied with marked morbidity and mortality.

    • daedalus2u says:

      Sleep apnea is probably due to low NO. The nasal passages are a significant source of NO, they produce ~200 ppb NO in the air inhaled through the nose. Humming greatly increases NO production due to oscillatory flow past the NO producing cells. Snoring is probably adaptive.

      Breathing is triggered by low O2, high CO2 and high S-nitrosothiols. The RSNO pathway is the least understood and the most complicated. It couples to O2 through reduction of nitrite to NO and to CO2 through reduction of nitrite by carbonic anhydrase and probably through disproportionation of nitrite at lower pH and maybe some other things too. Exactly where all those things happen is not clear.

      It is the RSNO pathway that is out of whack in COPD, Cheyenne-Stokes, and sleep apnea (my hypothesis). What happens when the RSNO pathway gets out of whack, the O2 and CO2 pathways have to get farther out of range to trigger taking a breath and so you get slight chronic hypoxia and chronic hypercapnea. Breathing frequency gets less chaotic and becomes more regular. Regular is bad. You really want all of your control systems to be operating chaotically.

      • D. C. Sessions says:

        Sleep apnea is probably due to low NO.

        No. Monomania aside, it's primarily mechanical. Sleeping on your back, the tongue rolls back to block the airway. This is especially so when age softens the tone of the soft palate and the uvula becomes pendulous.

        The patient falls asleep, the airway becomes blocked, and breathing cessation causes the usual blood gas problems -- followed by the patient waking partially, airway opening, breathing, fall back asleep, etc. Maintaining continuous positive airway pressure (CPAP) breaks the cycle.

        A co-worker had one of the most severe cases of sleep apnea I've ever heard of. He literally fell asleep upright in his chair at work while talking to me. After his jaw was rearchitected, tongue tied forward, uvula ablated, and soft palate scarred to harden it -- after all that, he told me that before he was allowed solid food he had the seven best nights' sleep of his adult life. He went on to lose an amazing amount of weight, his BP dropped like a stone to healthy levels, he was more alert than any of us could remember, etc.

        Mechanical. The breathing reflex is doing fine, but the airway is blocked.

        ABC. Always ABC.

        • daedalus2u says:

          It can also be due to low NO, which is why PDE5 inhibitors make it worse and need to be used with extreme care in OSA. The PDE5 inhibitor increases cGMP levels which then feedback inhibits NO production which then lowers basal NO levels (my hypothesis).


          Because the triggering of breathing by RSNOs is not mediated through cGMP, I think the adverse effects of PDE5 inhibitor has to be via a feedback inhibition effect.

          • Tsu Dho Nimh says:

            Hey, I know you luvs ur NO but when a purely mechanical fix (surgery) gets rid of the sleep apnea, it's hard to accept a chemical as the culprit.

          • antipodean says:

            and you have no data and you think that every disease is caused by NO

  • Karen says:

    I watched my mother die for nearly two decades as smoking and post-hysterectomy obesity took her life; she suffered terribly from atherosclerosis and later from arryhythmia. We talked often about diet and healthy eating, but she never had a meaningful conversation with her doctor on that score, and she ignored my suggestions.

    As her health decayed, and she was kept together more and more by the duct tape and baling wire of pharmaceuticals, her life diminished frighteningly. Walking caused extreme pain (because of the lack of blood to her legs) and so she gave up all exercise; the worse she felt, the more she lost interest in life; and there was nothing anyone could do to revive it. She was undeniably depressed and refused treatment for it. It was a gift that she spent the last month of her life, with organs failing and treatment largely ineffective, in a coma.

    Her last fully-conscious act was probably smoking a cigarette.

    I have my own obesity-related health issues (though not related to smoking -- I've never done that!) and my own doctor is a staunch advocate of diet -- and he's explicit about it, and will gladly refer me to a nutritionist if I don't get it -- and managing arthritic pain for exercise, and whatnot. Did my mother have an advocate for a doctor? Did she ignore him? I don't know. I'll never know.

    But I do wish she would have been able to quit smoking. It wasn't as though she didn't try, but it never worked for long.

    And I also wish it wasn't so damned hard to lose weight and keep it off.

  • Karen says:

    RE: sleep apnea: it seemed to me out of the blue, my allergist decided I should be tested for both waking and sleeping oxygen in my blood. Turns out I'm fine while awake, but there's a problem while I sleep, so now I breathe the output of an oxygen concentrator at night.

    This has greatly increased my energy during the day, so maybe I was suffering from sleep apnea. But neither my PCP or any other specialist thought about it...

  • Natalie Sera says:

    My father had early heart disease -- first heart attack before the age of 53, and died at 69 from his 5th. My mother died of COPD from asthma and smoking. I've had diabetes for 20 years, although neither of my parents had it. I also had a coronary artery spasm when I was 44, but my arteries were clear at the time.

    Best news is, now age 63, I just had an angiogram, and my arteries were clear, cardiac wall motion normal, and ejection fraction 67%, which is excellent! I attribute it to careful diabetes control over the years. I never had an A1c out of the 6's -- I think the goal of 7% is too high. The goal should be 6.5% tops, and 6.0% is even better. I'm doing a low-carb diet, and my blood glucose is rarely over 140. And I've lost 27 lb., and am now down to a BMI of 24.0. I have a pump and a continuous glucose monitor, which help immensely. Better diabetes care would help reduce the heart disease and stroke rate even further.

  • Jason says:

    If their were more free public health screenings for blood sugar, cholesterol, & high blood pressure at places like Walmart and other grocery stores I think it would definitely help with awareness of the problem.

  • khan says:

    Given family history, heart will be the last thing to go.
    I want to know how to make the first stroke be the last stroke.