Saturday, August 17, 2013

Perspectives on the Bush stenting case: lifestyle modifications and the risk of cardiovascular disease

Significant controversy (examples here, here, and here) has surrounded whether former President George W. Bush should have undergone percutaneous coronary intervention (PCI) and stent placement. Many have called PCI an overly aggressive strategy based on his clinical presentation, citing studies that have shown no advantages with PCI among patients with stable coronary artery disease (CAD) [1]. However, the purpose of this entry is not to discuss the clinical appropriateness of the stent (as few individuals outside of the team taking care of Bush have the data to determine this), but instead how his case has refocused attention on the pathophysiology of CAD (for an elegant explanation of this, see John M's blog) and more importantly, how living a healthy lifestyle is not always the be-all end-all strategy for reducing one's cardiovascular risk.

First, let me be clear that the association between cardiovascular disease and many of the characteristic features of an unhealthy lifestyle (e.g., poor nutrition, excess sodium intake, physical inactivity) is undeniable. In fact, the growing prevalence of these traits is largely responsible for the rate at which cardiovascular disease has overtaken malnutrition and infectious diseases as the most common cause of worldwide morbidity and mortality.

Unfortunately, these associations have also been used to stigmatize many patients with cardiovascular disease as simply paying the dues for a lifetime of poor decisions, and how easily their problems could be "fixed" with healthier choices (or by that same token, why health care benefits should not be provided to them for their past indiscretions). Often these statements come from individuals who can ably afford a gym membership (or live in a neighborhood where it is safe enough to exercise outside), can purchase fresh foods (not to mention having the time to properly prepare them), or who were raised in homes or school systems where they were taught the importance of nutrition and exercise.  In Bush's case, we have an individual who purportedly eats healthy, exercises regularly (he recently completed a 100-km bike ride), and has access to the best preventative care in the world, yet has CAD significant enough to at least warrant discussion of coronary stent placement.

While making healthy lifestyle decisions can undoubtedly reduce one's risk of cardiovascular disease, the risk never evaporates entirely. More importantly, the impact of these decisions on cardiovascular risk is a complex interplay of genetic, physiologic, and biochemical interactions, many of which we do not understand or have any influence upon. Even if we did reach consensus on what exaxctly constitutes a healthy lifestyle (for example, what should the daily limit of sodium be?), it is not clear that everyone would respond favorably, if at all. A recent example of this was observed in the Look AHEAD trial, where aggressive changes in diet and increased physical activity failed to improve outcomes among overweight patients with diabetes [2].

A predisposition to developing cardiovascular disease has already been well-characterized among several congenital disease states and conditions, such as type 1 diabetes, familial hypercholesterolemia, and a number of kidney disorders. Even cardiovascular risk factors traditionally characterized as being under the influence of lifestyle decisions (e.g., hypertension, type 2 diabetes) can be impacted significantly by underlying genetic differences.  For example, African Americans are known to demonstrate enhanced sodium retention as well as low plasma renin activity, making them more susceptible to hypertension and conferring differences in how they respond to certain classes of antihypertensive medications [3]. Similar effects have also been observed with diabetes, where both African Americans and American Indians have been shown to be at higher risk for developing insulin resistance compared to other ethnic groups [4].  While some are quick to point out the socioeconomic and cultural features that may lead to these differences, an independent association between ethnicity and disease often remains, even after controlling for dietary and other lifestyle factors.

In summary, while it is clear that therapeutic lifestyle modifications can have a signficant impact on the development and progression of cardiovascular disease, it is not yet clear how many of these risk factors -- and to what extent -- are under our control.  While we should emphasize to patients that healthy lifestyle decisions can be an effective strategy for reducing their risk (which I believe should also include attempts at removing barriers that would prevent them from otherwise making healthy choices), we should recognize that cardiovascular disease may still occur anyway, as it did in the case of former President Bush.  Because it is capable of prevailing in the face of even the most intensive lifestyle interventions, cardiovascular disease should be a villain against whom we are all opposed, not as fair and just punishment for a few unhealthy decisions.

  1. Boden WE, O'Rourke RA, Weintraub WS, et al; for the COURAGE Trial Research Group. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007 Apr 12;356(15):1503-16.
  2. Wing RR, Bolin P, Yanovski SZ, et al; for the Look AHEAD Research Group. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med. 2013 Jul 11;369(2):145-54.
  3. Gibbs CR, Beevers DG, Lip GY. The management of hypertensive disease in black patients. QJM. 1999 Apr;92(4):187-92.
  4. Steinberger J, Daniels SR; for the American Heart Association Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young); American Heart Association Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Obesity, insulin resistance, diabetes, and cardiovascular risk in children. Circulation. 2003 Mar 18;107(10):1448-53.

No comments: