The basic components of lifestyle modification to prevent and manage heart disease, including HF, and its comorbidities begin with 3 basic interventions: avoid tobacco in all forms, follow a nutritionally balanced diet, and stay physically active.
33 For example, the Jackson Heart Study,
34 a prospective observational study of 4129 black participants without a history of HF or CAD at enrollment showed that persons who smoked cigarettes had a significantly increased risk for left ventricular hypertrophy, systolic dysfunction, and incident HF hospitalization at a median follow-up of 8 years. Diets recommended for patients with heart disease have traditionally involved restriction of dietary sodium. However, data to support this approach for HFrEF are inconsistent. This controversy is manifested in the ACC/AHA guidelines. In 2013, the ACC/AHA guidelines downgraded the recommendation for sodium restriction to class IIa (reasonable) with C level of evidence.
1 More specific information concerning sodium intake comes from the multihospital Heart Failure Adherence and Retention Trial,
35 which enrolled 902 patients with New York Heart Association class II and III HF and followed up with them for a median of 36 months. Sodium restriction was associated with a significantly higher risk of the composite end point of HF hospitalization or death. This increase was predominantly driven by hospitalization for HF; the increase in death was not statistically significant.
35 A subgroup analysis suggested that patients were most likely to have increased risk if they were not receiving an ACEI or ARB. This hypothesis-generating study
35 represents a challenge to the conventional wisdom that dietary sodium restriction is a cornerstone in the management of HF.
Obesity has a moderately strong inverse relationship with HF outcomes. However, there is weak clinical trial evidence for modulating this comorbidity.
4 This finding is complex because it has been reported that after PCI, patients with obesity had a better prognosis, with a lower incidence of HF.
36 This obesity paradox has some nuance because body mass index does not discriminate between body fat and lean muscle. A study
37 of 570 consecutive patients with HF demonstrated that arm circumference, a marker of muscle mass, predicted more accurately the favorable prognosis of patients with obesity and HF than abdominal girth, which is a marker of central obesity.
The Physician's Health Study
38 demonstrated a beneficial effect of vigorous physical activity in all categories of baseline covariants, including weight, age, smoking, hypertension, and hyperlipidemia. Both skeletal muscle mass and muscle strength are protective against HF through a variety of physiologic mechanisms.
37
The
Physical Activity Guidelines for Americans39 issued by the US Department of Health and Human Services recommends that adults do at least 150 minutes of moderate-intensity exercise per week for substantial health benefits. The new guidelines recognize that adults with chronic conditions may not be able to meet this goal. In that case, they recommend that every adult “just move.”
39
Obesity contributes to the development of HF through multiple mechanisms. However, the population of people with HF is no more successful at sustained weight loss through diet than the general population. Bariatric surgery provides long-term protection against the development of HF.
40,41 A nonrandomized, prospective, controlled study
42 of 2010 patients who were treated with bariatric surgery were compared with matched controls in Sweden. At a follow-up of 14.7 years, a significant reduction in cardiovascular deaths and cardiac events was found. A self-controlled study
43 of 524 patients with HF had a reduced incidence of hospitalization or emergency department visits after bariatric surgery compared with obese patients who had other types of surgery. These preliminary data suggest that bariatric surgery can play a significant role in the management of obesity in patients with established HFrEF.