Although obesity remains an important risk marker and mechanism for nearly all cardiovascular diseases, some data show that having stable obesity increases chances of survivability in patients with established chronic heart failure.

These were among the findings highlighted by Ramachandran S. Vasan, MD, professor of medicine at Boston University School of Medicine, at the Heart Failure Society of America 11th Annual Scientific Meeting.

Vasan discussed data from a variety of large clinical trials, including the Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) study that examined the impact of obesity on prognosis of patients with established HF. He also selected data from the Framingham Heart Study to illustrate that obesity is a risk factor for developing new-onset HF.

“What was less clear when we began our investigation seven years ago was whether obesity was associated with the risk of developing clinical HF,” Vasan said. “Data from Framingham shows that if you take 2,500 women, divide them into three groups based on their BMI and follow them up for 20 years, the HF experience of the three groups is radically different, with higher heart failure rates as BMI increases. Just using BMI, you see three separate trend lines fairly early. When the men are looked at, you get a similar pattern, although the lines take a bit longer to diverge.”

The obesity paradox

According to Vasan, the relationships between BMI measurements and all-cause mortality are more complicated when looking at it in patients with established HF.

“In the CHARM trial, nearly 7,600 people were followed for three years. If you classify people according to their BMI categories and look at the mortality experience, you see a pattern that is very different,” said Vasan. “The bottom of the curve shows the lowest mortality of people with stage I obesity or BMI between 30 and 35. Just above that are people with stage II obesity … There is a strong consistency in the data in patients with chronic HF, indicating that a higher BMI, especially in ambulatory patients with stable chronic HF, is associated with better survival.”

Vasan provided some possible explanations for the obesity paradox. First, it may be questioned that patients with HF who are obese may not have HF and an incorrect diagnosis has been made.

“I do not accept that condition, because we see the obesity paradox with a lot of other conditions, and we do not doubt the diagnosis of those conditions,” Vasan said. “Perhaps it is because obese patients with HF are earlier in the time course of natural progression of the disease. If you look at the CHARM data, you find that obese patients with HF are on average about five years younger, and maybe the lean patients are further along in the natural history of the disease. Another alternate explanation, and an even more plausible one in my opinion, is that perhaps the HF patients with lower BMI are sicker and have more advanced disease.”

Vasan concluded that more research was needed to examine the paradox and to establish practical clinical protocols regarding weight management strategies in obese patients with HF.

“You see your patient John Doe with metabolic syndrome initially, and you tell him he needs to lose weight. You tell him to come back in a year and see how he’s doing with BP, lipids and glucose intolerance,” Vasan said. “Mr. Doe comes back one year later with HF. You tell him, ‘Mr. Doe, I encouraged you to lose weight a year ago. Now I’m going to tell you not to lose weight but maintain it at the current level.’ Where does that place you? What level of comfort do practitioners have in these contradictory recommendations?”

  Editor’s note: This is an interesting consideration. Obesity has never been an independent predictor for mortality for any kind of heart disease. That’s because it contributes to hypertension, hyperlipidemia and diabetes, which we know make you more likely to develop heart disease. So, what you have to do is say that obesity by itself is not an independent risk factor but that obesity is clearly an associated risk factor for those other three components. If you have good enough genetics that you happen to avoid those complications from obesity, then in fact you may be a privileged group. What we need to find out is if that genetically-privileged group fared better lean or obese after they lost weight. They may fare well or they may not. More research is needed to examine this.

  — Frank W. Smart, MD, Member, Myocardial Disorders, HF and Transplantation, Cardiology Today Editorial Board.

  Each patient is different; in some, obesity might be good and signal the fact that the HF is not triggering an inflammatory state that might be the cause of the weight loss. The observations may be an epidemiologic phenomenon. I do not think that there are other implications and certainly would not want my chronic patients with HF becoming more obese.

  — James B. Young, MD, Section Editor, Myocardial Disorders, HF and Transplantation, Cardiology Today editorial board.

  For more information:

      * Kenchaiah S, Popcock S, Wang D, et al. Body mass index and prognosis in patients with chronic heart failure: Insights from the Candesartan in heart failure: Assessment of reduction in mortality and morbidity (CHARM) program. Circulation. 2007;116:627-636.
      * Vasan R. Clinical perspective: Obesity and heart failure. Presented at: Heart Failure Society of America Annual Scientific Meeting; Sept. 16-19, 2007; Washington.

by Eric Raible
Cardiology Today