Author + information
- Steve R. Ommen, MD∗ ( and )
- Francisco Lopez-Jimenez, MD, MSc
- ↵∗Reprint requests and correspondence:
Dr. Steve R. Ommen, Mayo Clinic, College of Medicine, Division of Cardiovascular Diseases and Internal Medicine, 200 First Street SW, Rochester, Minnesota 55905.
The impact of obesity on the cardiovascular system continues to reveal itself. In this issue, Olivotto et al. (1) share the results of a 3-center collaboration on body mass index and its relation to left ventricular morphology in patients with hypertrophic cardiomyopathy (HCM). The investigators found that obese HCM patients had significantly larger left ventricular mass, left ventricular mass index, and higher subsequent rates of symptom development. These results suggest that environmental/situational factors can influence ventricular morphology in a condition that is genetically inherited. Notably, only 25% of the patients in this study fell into the normal weight classification. So, like the age-old question, can we tell which came first? Is it a more severe expression of HCM that leads to obesity, or is it the general trend of increasing body weight in Western society that complicates HCM?
Because this was an observational study, we cannot tell the direction of the association. There are numerous potential pathophysiologic mechanisms by which obesity could result in more hypertrophy. These include increased sympathetic tone, increased leptin levels, myocardial fatty infiltration, insulin resistance, and enhanced renin-angiotensin activity (2). Likewise, a more severe phenotypic expression of HCM could readily lead to a less active life with all the attendant negative impacts, including increasing body mass. While at baseline, the study subjects had statistically similar symptom status; there is no indication of daily activity levels, nor objective measures of exercise capacity. In the end, treating patients with HCM and obesity will necessarily involve treating both aspects.
The impact of obesity on symptom status is a troubling clinical conundrum. Obesity is a well-known cause of heart failure, and has been shown to result in worsening diastolic function independent of other comorbid conditions (3,4). Patients with obesity have higher overall oxygen requirements as well as abnormal myocardial function as evidenced by strain and strain rate imaging (5). In the Olivotto et al. study, the patients with obesity were more likely to have left ventricular outflow tract obstruction, and to be receiving diuretics, and/or pure vasodilators as part of their therapy. Those medications are well known to exacerbate left ventricular outflow tract obstruction.
Why is this a problem in patients with HCM? Other than defibrillators for prevention of sudden cardiac death, all therapies in HCM have the sole indication of symptom relief (6). The therapies employed, including medications and invasive procedures, can be quite effective when combating symptoms due to hemodynamic derangements, but not likely to be effective at when directed at problems such as deconditioning and excess oxygen requirements. Similarly, the need to consider surgical or invasive therapy is based on persistent symptoms that are unresponsive to pharmacologic therapy. However, if the symptoms are persistent because they are primarily related to the obesity, then the medications (and the subsequent procedures) have little chance of making an impact on symptoms.
So, when facing an obese patient with HCM and deciding whether to start, increase, or decrease therapy one has to make important considerations of the balance between hemodynamics and excess body weight. By the time such patients have become highly symptomatic, the combination of sedentary status, deconditioning, and increased tendency to outflow tract obstruction may make therapeutic lifestyle change untenable. Yet, treating the hemodynamic abnormalities will lead to less than satisfying results unless weight loss and healthy habits are taught to and adopted by the patients.
How does one then approach this situation? With cardiopulmonary exercise testing we can determine whether patients exercise capacity is limited by cardiac output limitations based on a plateau in the peak oxygen consumption (VO2). Conversely, if a patient is purely limited due to deconditioning and obesity, then the peak oxygen consumption (VO2) will continue to rise through the point at which the patient has to stop exercising. Armed with this information, appropriate therapeutic decisions and focused counseling can help our patients understand the expected impact, and their role in achieving a better quality of life. Even with completely successful treatment of hemodynamic considerations, the obese patient needs to understand this is the first step in their path to improved functional capacity. Long-term exercise and dietary modifications will need to continue. Importantly, therapeutic lifestyle change, particularly if the cardiac hemodynamic abnormalities are mild, may represent the most important step to recovery. Whether purposeful weight loss in symptomatic patients with HCM improves left ventricular morphology and hemodynamics is yet to be determined.
The study by Olivotto et al. (1) suggested that some of these findings were independent of comorbid conditions. However, as clinicians we must not discount the increased rates of hypertension, diabetes, coronary artery disease, and sleep apnea have important roles not only in the cardiovascular system but in general well-being. Furthermore, each of these conditions has been shown to be associated with adverse outcomes in patients with HCM. Treating and caring for patients with HCM means not just understanding the pathophysiology of diastole and outflow tract obstruction, but must incorporate treating comorbid conditions aggressively.
Another of the management considerations for patients with HCM deserves mention. Many patients perceive, or are in fact inappropriately counseled by their physicians, that they should not engage in regular exercise. This stems from the fact that sudden cardiac death among competitive athletes is most often related to HCM such that competitive athletics are discouraged for these patients. To extend that discouragement to regular, noncompetitive exercise is a travesty. Counseling and encouraging healthy habits, including mild to moderate intensity exercise, is an important aspect of caring for patients.
Hypertrophic cardiomyopathy is generally well tolerated, with a good prognosis, and completely compatible with a normal lifestyle (often with no therapeutic interventions). That obesity modifies the ventricular morphology, and the overall well-being of our patients, provides further evidence that we need to actively teach our patients about healthy choices. Which comes first? Maybe we will find out one day, but for now it is our responsibility to treat both. Clinically, we treat people, not just pathophysiology.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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