Obesity produces hemodynamic alterations that contribute to the development of cardiac structural abnormalities and impairment of left and right ventricular function.1–5 Recent studies, predominantly in animal models, suggest that various neurohormonal and metabolic disturbances associated with obesity may contribute to these abnormalities.1–5 Changes in cardiac structure and function may predispose to heart failure (HF), even in the absence of comorbidities such as hypertension, coronary heart disease, or other underlying causes.1–6 Heart failure due predominantly or entirely to severe obesity is referred to as obesity cardiomyopathy.1–6 This review discusses the epidemiology of HF in obesity and describes the changes in cardiac performance and morphology associated with obesity that may predispose to HF. It characterizes the clinical features of obesity cardiomyopathy and discusses the prognosis of HF associated with obesity, including the role of cardiorespiratory fitness (CRF). Finally, it describes the effects of purposeful weight loss on these factors.
CLASSIFICATION OF OBESITY
The World Health Organization classification of body weight (including obesity), based on body mass index (BMI), is as follows: underweight (BMI <18.5 kg/m2); normal weight (BMI of 18.5-24.9 kg/m2); overweight (BMI of 25.0-29.9 kg/m2); class I obesity (BMI of 30.0-34.9 kg/m2); class II obesity (BMI of 35.0-39.9 kg/m2); and class III obesity, also known as severe or morbid obesity (BMI ≥402,3 kg/m2).7 In recent years, the term super-obesity has been applied to a BMI, that is, 50 kg/m2 or more.2
In a study of 6 076 hospitalized patients who were discharged with a diagnosis of HF, Owan et al reported a prevalence of obesity of 41.4% in subjects with a preserved left ventricular (LV) ejection fraction (LVEF) and 35.5% in those with a reduced LVEF.8 It has been estimated that obesity is present in up to 86% of all patients with HF. Many of these individuals are elderly.2,3,9
Heart failure is common with class III obesity. In such patients, the prevalence of HF is related to duration of obesity.2,3,10 In 1 study of class III obese patients, the prevalence of HF was 70% at 20 years and 90% in 30 years.10 Obesity is a risk factor for HF in overweight persons, and in class I and class II obesity as well. Kenchaiah and colleagues11 studied 5 881 participants in the Framingham Heart Study. The mean age of this study population was 55 years, and 54% were women. Followup was conducted over a mean duration of 14 years. During this interval, 496 (8.4%) developed HF. After adjustment for traditional risk factors, there was an increased risk of HF of 7% in women and 5% in men for each unit increase in BMI. This risk of HF was significantly greater in overweight than in normal weight subjects, and greater still in classes I and II obese participants in both women and men. In a study of a low-risk Mediterranean population, obesity was an independent risk factor for HF.12 Recent studies suggest that abdominal obesity may independently predict an increased risk of HF, especially in the elderly.13
It is difficult to fully assess the comparative contribution of obesity to the development of HF. Obesity is a major risk factor for hypertension, which facilitates the development of coronary heart disease, and directly promotes abnormal LV geometry and subsequent HF.14 Obesity is also linked to other cardiovascular risk factors such as diabetes mellitus, dyslipidemia, and inflammation, and contributes to a low level of CRF, which itself is a potent risk factor for HF.1–3,14 Considering these combined effects, overweight and obesity should probably be considered on even par with coronary heart disease and hypertension for the development of HF.14
Hemodynamic Alterations With Obesity
Excessive fat produces an increase in total and central blood volume.2,3,14,15,19 In normotensive persons, there is a decrease in systemic vascular resistance that facilitates an increase in cardiac output.2,3,15,16 Since heart rate changes little in the setting of obesity, the increase in cardiac output is due predominantly to an augmentation in LV stroke volume.2,3,15,16,19 Left ventricular stroke work, LV work, and cardiac work have all been reported to be elevated in obese subjects.2,3,15–17 The increase in cardiac output together with systemic hypertension and possibly certain metabolic factors predispose to LV hypertrophy, LV diastolic dysfunction, and LV systolic dysfunction in some individuals.2,3 Left ventricular filling pressure and pulmonary capillary wedge pressure are commonly increased in severely obese persons.2,3–6,15–19 The increase in LV filling pressure augments pulmonary venous pressure and pulmonary capillary wedge pressure.2,3,15–18 This leads to elevation of pulmonary artery pressure and to an increase in right ventricular end-diastolic and right atrial pressures. This process is facilitated by the presence of sleep apnea and obesity hypoventilation, which are particularly common in severely obese persons.2,3 Hypoxemia and pulmonary artery vasoconstriction in such patients contribute to pulmonary arterial hypertension, although LV failure remains the predominant cause.2,3 In such patients, it is not unusual to observe a diastolic pressure gradient across the pulmonary vascular bed.2,3,16
In classes II and III obese persons, exercise produces a substantial increase in total and central blood volumes, stroke volume, cardiac output, stroke work, LV filling pressure, pulmonary capillary wedge pressure, and in some cases pulmonary artery pressure.2,3,20,21 The effect of exercise on blood pressure and systemic vascular resistance is more variable.2,3,20,21
In obese persons with systemic hypertension, cardiac output remains relatively high, but somewhat lower than in normotensive obese individuals.2,3,22,23 Left ventricular filling pressure is often higher than in normotensive obese patients.21,22 Systemic vascular resistance in hypertensive obese patients is higher than in normotensive obese patients but is lower than in lean hypertensive persons with similar degrees of blood pressure elevation.2,3,22,23
Originally, the elevation of cardiac output associated with obesity was attributed to increased adipose mass. However, blood flow per unit of adipose tissue is relatively low at 2 to 3 mL/min and is insufficient to fully account for the high cardiac output state.2,3 Recent reports indicate that in classes I and II obese patients, increased nonosseous fat-free mass predicts cardiac output to a greater extent than adipose mass.2,3 It is uncertain whether this is also true in class III obesity.
High cardiac output may not be present in all forms of obesity. Recent evidence suggests that in centrally obese subjects, cardiac output is lower and systemic vascular resistance is higher than in peripherally obese persons.24 Hemodynamic alterations with obesity are summarized in Table 1.
Cardiac Morphology in Obesity
Post-mortem studies by Smith and Willius,25 which included all classes of obesity, described increased heart weight, but the authors attributed this to increased epicardial fat. Three additional post-mortem studies, consisting of a total of 33 class III obese patients, reported (1) increased heart weight and microscopic evidence of LV hypertrophy in all cases; (2) increased LV mass in 32 subjects with right ventricular hypertrophy in 6 patients; and (3) excess epicardial fat occurred in 21%.26–28 In a post-mortem study comparing 43 classes II to III obese patients with 409 lean patients with HF, a specific etiology for HF other than obesity was present in 23.3% of obese and 64.5% of normal weight patients, an observation that supported the existence of a cardiomyopathy of obesity.18 The predominant pathological finding in obese patients was LV hypertrophy.
Studies that noninvasively assessed LV mass using echocardiography or cardiac magnetic resonance imaging consistently reported significantly higher values of LV mass in all classes of obesity compared with lean controls.2–6,29 Those with HF (predominantly class III obese patients) had significantly greater LV mass than similarly obese patients without HF. In most, but not all noninvasive studies of LV morphology, LV diastolic chamber size or volume was significantly greater in obese compared with normal weight subjects.2–6,29–41
Traditionally, the increase in LV chamber size and LV mass has been attributed to adverse LV loading conditions relating to altered hemodynamics.2–6,29 In the normotensive obese state, the increase in central blood volume and cardiac output was thought to predispose to LV enlargement (increased preload) resulting in increased LV wall stress. Eccentric LV hypertrophy was thought to ensue in an attempt to reduce LV wall stress. This model appears to be valid in studies of uncomplicated (normotensive) obesity.2–6,29,33,35,41,42 In hypertensive obese patients, elevated blood pressure may disproportionately augment afterload and increase LV wall stress, resulting in concentric LV remodeling or hypertrophy.2,3,30 Indeed, multiple recent studies have reported that among obese subjects with abnormal LV geometry, concentric LV remodeling or hypertrophy occurs as or more commonly than eccentric LV hypertrophy.2,3,30,34,37,40,43 Most of these studies did not adjust for the presence of hypertension, and those that did failed to account for the relative duration and severity of obesity and hypertension. Thus, while it is clear that obesity contributes to increased LV mass, the effect of obesity on LV geometry remains uncertain.
Several studies have demonstrated a relationship between duration of obesity and LV morphology.2,3,35 There is a significant positive correlation between duration of normotensive class III obesity and both LV diastolic chamber size and LV mass, both in patients with and without HF.2,3,10,30,34
In addition to hemodynamic alterations and duration of obesity, certain metabolic and neurohormonal abnormalities that occur commonly in human obesity have been shown to produce increased LV mass in animal models and, to a lesser extent, in humans.2,3 These include insulin resistance with hyperinsulinemia, leptin resistance with hyperleptinemia, and activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. Abnormalities of cardiac morphology associated with obesity are summarized in Table 1.
Obesity and LV Function
As previously noted, LV filling pressure is frequently elevated in classes II and III obese individuals, and increases substantially with exercise in such individuals, often exceeding the threshold likely to produce pulmonary edema.2,3,15–17 Noninvasive studies of LV diastolic function in all classes of obesity have consistently shown impairment of LV diastolic filling or relaxation relative to lean controls.2,3,44–50 Moreover, the incidence of LV diastolic dysfunction, on the basis of transmitral flow, increases progressively with higher classes of obesity, from 12% in class I to 35% in class II and to 45% in class III obesity.46 Class III obese patients with HF exhibit greater impairment of LV diastolic filling than those without HF.10
Causes of impaired LV diastolic filling and relaxation in such individuals may be related to increased LV mass and the adverse loading conditions that contribute to it.2,3 In 1 study of class III obese patients, only those with LV hypertrophy exhibited impairment of LV diastolic filling.47 As with LV mass, duration of obesity also appears to contribute to impairment of LV diastolic filling.32
Adverse LV loading conditions and their sequelae may not be the only explanation for LV diastolic dysfunction in obesity. Studies employing tissue Doppler imaging, ostensibly a load-independent technique, have reported decreased mitral annular velocities in diastole in obese subjects.49,50 In addition, studies of transgenic murine models of lipotoxicity have reported LV diastolic dysfunction with selected abnormalities of enzyme or protein metabolism.2–4,57
Most studies assessing LV systolic function in obesity have reported normal LV ejection phase indices.2–5,51–54 Some have reported supranormal values.2,3 Even in studies where LV systolic function of obese subjects was significantly lower than in lean controls, it was only marginally so in most cases, and still within the normal range.2–5,52–55 In class III obese patients, moderate LV systolic dysfunction occurs with higher frequency, particularly in those with HF.10,53 However, severe LV systolic dysfunction is rare in uncomplicated obesity. The presence of severe LV dysfunction should elicit a search for comorbidities.
Duration of class III obesity is also an important contributor.32 As with LV diastolic dysfunction, LV systolic dysfunction has been reported in some transgenic murine models of lipotoxicity.2–5,51
Recent studies employing tissue Doppler imaging have shown reduced mitral annular velocities in systole, even when LV ejection phase indices are normal.54,55 This suggests the possible presence of subclinical impairment of LV systolic function in obesity, independent of loading conditions. Changes in LV diastolic and systolic function associated with obesity are summarized in Table 1.
Pathophysiology of Obesity Cardiomyopathy
Although the aforementioned alterations in cardiac performance occur in class I and class II obesity, they are most pronounced in class III and super-obesity. Figure 1 summarizes the pathophysiology of obesity cardiomyopathy.
CLINICAL FEATURES OF OBESITY CARDIOMYOPATHY
Obesity may serve as a risk factor for or as the predominant cause of HF.2,3,56,57 Obesity cardiomyopathy may be defined as HF due predominantly or entirely to obesity.2,3 Obesity cardiomyopathy occurs mainly in class III or super-obese patients.2,3,56 Such individuals have usually been severely obese for 10 years or more.10 Heart failure exacerbations tend to follow recent weight gain and may be accompanied by episodes of atrial fibrillation or flutter.2,3,56 Obstructive sleep apnea is present in 50% or more of such persons, and severe hypoventilation is encountered in approximately 10%.56 These abnormalities contribute to right heart failure in obesity cardiomyopathy, but LV failure remains the predominant cause of right ventricular decompensation.2,3,56
Obesity cardiomyopathy shares some clinical manifestations with HF from other causes but is associated with some that are unique to severe obesity.2,56 Symptoms include fatigue, shortness of breath with exertion, paroxysmal nocturnal dyspnea, increasing abdominal girth, and edema of the lower extremities.2,56 Physical signs include gallop rhythm, jugular venous distension, ascites, hepatomegaly, and lower extremity edema (often brawny).2,56 Other clinical features include plethora or cyanosis in the presence of polycythemia, a periodic breathing pattern, somnolence, conjunctival suffusion, retinal venous congestion, and in some papilledema.2,56 These latter features are sometimes referred to as the “Pickwickian syndrome,” a term derived from the Dickens description of the fat boy Joe in his novel, Pickwick Papers.2
Obesity and Exercise
Obesity has substantial impact on the response to exercise.58–60 The acute response to exercise differs in obese and lean individuals.58–60 Prior to exercise, obese persons typically have similar or slightly higher resting heart rates and higher levels of both systolic and diastolic blood pressures compared with lean individuals.58–60 With exercise, the heart rate response in obese individuals is blunted relative to persons with normal weight.58–60 Blood pressure increases to a similar or greater extent in obese as in lean individuals. Overall exercise capacity or CRF is lower in obese persons, with an approximate 0.4 mean metabolic equivalent (MET) reduction in exercise capacity for every 1 kg/m2 increase in BMI.59,60 However, exercise testing data, such as the assessment of CRF, have similar prognostic value in lean and obese subjects.58,59
There are limitations to stress testing for myocardial ischemia in obese patients. Most treadmills used in treadmill exercise testing can accommodate patients whose body weight is ≤350 pounds (158 kg). An alternative for exercise stress testing in patients whose weight exceeds that limit is arm crank ergometry. Dobutamine stress echocardiography, using intravenous contrast, is favored over pharmacologic perfusion imaging in severely obese patients for detection of myocardial ischemia because there are weight limits for tables for patients undergoing myocardial perfusion imaging. Moreover, artifact occurs more commonly in severely obese patients than in patients at normal weight or with lesser degrees of obesity. Transesophageal dobutamine stress echocardiography has been proposed as a diagnostic technique for detection of myocardial ischemia in severely obese patients but is seldom used.
Cardiopulmonary exercise testing remains the diagnostic standard for assessing CRF in obese patients who are able to perform treadmill exercise.60,61 Key variables to be assessed in obese patients during aerobic exercise testing are peak oxygen consumption, oxygen consumption at the ventilatory threshold, peak respiratory exchange ratio, ratio of minute ventilation to carbon dioxide production, oxygen uptake efficiency slope, blood pressure, heart rate recovery, and perception of dyspnea.60,61
The Obesity Paradox in Patients With HF: General Considerations
Although overweight and all classes of obesity are clearly risk factors for the development of HF, evidence is accumulating that mortality risk in overweight and classes I and II obese patients with HF is lower than in underweight or normal weight persons with comparable degrees of severity of HF.62–69 This phenomenon is known as the “obesity paradox.”2,3
Although most obesity paradox studies have used BMI to define obesity status, the obesity paradox has been demonstrated using percentage body fat, waist circumference/central obesity, in addition to BMI in patients with HF3,69 and with percentage body fat, waist circumference/central obesity, and BMI in patients with coronary heart disease.66,70–72
In general, when discussing the obesity paradox, most references are to patients with chronic diseases, such as HF, coronary heart disease, or other chronic diseases.3,73–81 However, Flegal and colleagues82 recently reported a meta-analysis of 97 studies in 2.9 million “healthy” subjects. They showed that optimal survival occurred in the overweight BMI group, who had a significant 6% lower mortality than did the normal BMI group. Although the obese group had higher mortality, this was due to the very high mortality in class II and class III obesity, whereas those with class I obesity actually had a 5% lower mortality than did the normal BMI patients. This study, however, did not evaluate physical activity or CRF.
In a meta-analysis of 29 209 subjects with HF reported by Oreopoulos et al,62 the all-cause mortality rate was 16% and 33% lower, respectively, in overweight and obese patients than that observed in normal weight subjects. Similarly, cardiovascular mortality was 19% and 40% lower, respectively, in overweight and obese patients than that noted in normal weight subjects.62
The obesity paradox, as it relates to HF, occurs in diverse populations including women, men, the elderly, patients with a reduced or preserved LVEF, and in those with acute or chronic HF.2,3,63–66 The worst prognosis occurs in underweight subjects.2,3 Although not studied extensively, the mortality rates of class III and super-obese subjects are also high, substantially greater than those of overweight and classes I and II obese patients.2,3,73–76 Possible causes of the obesity paradox in HF patients include nonpurposeful weight loss in lean or underweight patients due to catabolic diseases, earlier presentation due to the presence of dyspnea or edema, a lower prevalence of cigarette smoking, less frailty, greater metabolic reserves, higher blood pressure facilitating the use of HF medications known to improve survival, and better CRF.3
CRF and Prognosis in Obesity
Substantial evidence during the past 2 decades indicates the importance of CRF to predict prognosis and survival from all causes and, particularly, from cardiovascular diseases.3,67–72 In fact, CRF may be the strongest of the major cardiovascular risk factors.68 Certainly, levels of CRF are typically lower in overweight and obese subjects compared with lean patients. A recent study of 5328 male nonsmokers (mean age 51.8 years) demonstrated an inverse relationship between body weight and estimated level of CRF.60 Compared with 1370 normal weight subjects who had a MET value of 12.7 ± 3.0, the 2 333 overweight subjects and 1 625 obese subjects had mean MET values of 11.2 ± 2.5 and 9.7 ± 2.3, respectively, indicating progressively lower estimated CRF with increasing weight. Nevertheless, age- and sex-related functional aerobic capacity predicted survival equally well across BMI groups.
Substantial evidence also indicates that CRF substantially affects the relationship between obesity status and subsequent major health outcomes, particularly from cardiovascular diseases.3,69 Both higher body weight or obesity status and lower CRF are associated with more adverse cardiovascular risk factors and higher risk of cardiovascular diseases. Nevertheless, the relative and combined importance of fitness versus fatness remains somewhat controversial.69
Recently, Barry and colleagues70 analyzed 10 studies and quantified the joint association of obesity status and CRF, demonstrating that compared with subjects who have normal BMI and preserved fitness, those who are unfit had a 2-fold higher risk of all-cause mortality regardless of their level of BMI. In contrast, overweight and obesity with preserved levels of CRF had a similar mortality risks similar to that of as normal weight subjects. Clearly, in this meta-analysis, CRF was more important than weight for predicting major health outcomes.
Others have studied changes over time in both CRF and adiposity and predictors of subsequent health outcomes.68,69 In a study of 14 345 men, a 1 MET increase in CRF on 2 maximal exercise stress tests separated by an average of 6.3 years was associated with a 15% lower risk of all-cause mortality and a 19% lower risk of cardiovascular disease mortality after adjusting for changes in CRF and other risk factors.71 In another study of 3148 healthy adults, although changes in both BMI and CRF predicted the development of hypercholesterolemia, hypertension, and metabolic syndrome, the impact of CRF seemed greater than adiposity for predicting future risks of these disorders.72 Therefore, the preponderance of evidence indicates that CRF may be more important than obesity status regarding long-term health outcomes.
CRF and the Obesity Paradox
The contribution of CRF to the obesity paradox has recently been reviewed in detail.69 Recent evidence in patients with HF and coronary heart disease suggests that the level of CRF is an important predictor of prognosis and alters the relationship of adiposity to subsequent prognosis.77,83 In a study of 9 563 patients with coronary heart disease, only those in the bottom tertile for age and sex-related CRF demonstrated an obesity paradox, with leaner patients by BMI, body fat, and waist circumference-central obesity having a higher all-cause and cardiovascular mortality than do heavier patients who are also unfit.77 Conversely, coronary heart disease patients who were not in the lowest of age and sex CRF tertiles had a favorable prognosis regardless of their BMI, body fat, or central obesity. On a similar note, in 2 066 patients with systolic HF, CRF was assessed by cardiopulmonary stress testing, where peak oxygen uptake (
o2) was utilized to divide HF patients into relatively fit (peak
o2 ≥ 14 mL/kg/min).83 Those HF patients with low CRF had a poor prognosis, and survival was related to BMI, showing the best survival with BMI ≥30 kg/m2, worst survival with BMI 18.5 to 24.9 kg/m2, and intermediate survival in the overweight BMI group. On the contrary, HF patients with relatively preserved CRF had a good survival, regardless of BMI, and no obesity paradox was noted. These data indicate that CRF markedly affects the obesity paradox.
Treatment of HF Exacerbations
Heart failure exacerbations in patients with obesity cardiomyopathy are treated in a similar manner as HF from other causes.56,57 In such patients, sodium restriction, supplemental inspired oxygen, and loop diuretics serve as the cornerstone of therapy. Renin-angiotensin-aldosterone system antagonists should be considered in those with severe LV systolic dysfunction. In patients with atrial fibrillation, digitals may be used for ventricular rate control in patients with severe LV systolic dysfunction who do not respond to the aforementioned measures (doses should not be weight based). The role of direct acting vasodilators, β-blockers, calcium channel blockers, and centrally or peripherally active sympatholytics for treatment of HF in this population has not been established.
Reduction of blood pressure in hypertensive obese patients has the potential to reduce the risk of HF in such individuals. Because central blood volume is increased in most hypertensive obese patients and because there is activation of the renin-angiotensin-aldosterone system in such persons, it would seem reasonable to treat hypertensive obese individuals with diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers. Indeed, such drugs are commonly used to reduce blood pressure in hypertensive obese patients. However, there are no studies that demonstrated superior efficacy of any 1 form of antihypertensive drug therapy in such patients.
Effects of Purposeful Weight Loss
The most effective long-term treatment of obesity cardiomyopathy is substantial purposeful weight loss.1–3,10,84–93 Purposeful weight loss reverses most of the abnormalities of cardiac structure and function associated with severe obesity and produces improvement in many of the clinical features of obesity cardiomyopathy and metabolic abnormalities associated with obesity.1,2,10,84–93
Substantial purposeful weight loss reduces total and central blood volume, oxygen consumption, arteriovenous oxygen difference, stroke volume, cardiac output, stroke work, and blood pressure.1,2,18,84–86 Left ventricular end-diastolic pressure and pulmonary capillary wedge pressure, when elevated, decreased in some studies but remained unchanged in others.1,2,18,80,84–86
Systemic vascular resistance increases with weight loss in uncomplicated obesity but is more variable in hypertensive obese patients depending on the relative reductions in blood pressure and cardiac output.1,2,80,84–86 Right-sided pressures are variably affected by weight loss, depending on the response of LV filling pressure and also on improvements in sleep apnea and obesity hypoventilation.1,2,18,84–86
Substantial weight loss consistently produces regression of LV hypertrophy in severely obese patients.1,2,10,23,82–88 Left ventricular diastolic chamber size decreases in most but not all patients. Similarly, the response of LV wall thickness to purposeful weight loss is variable.1,2,10,29,30,87–91 One recent study demonstrated a reduction in abnormal LV geometry from 70.7% to 42.5% after substantial weight loss from bariatric surgery in class III obese patients.89
Multiple studies have demonstrated improvement in LV diastolic filling and relaxation in classes II and III obese subjects.1,2,10,44,47,89–91 This may relate to reduction of LV mass and improvement of LV loading conditions in such patients. Weight loss generally produces no significant change in LV systolic function since preweight loss LV ejection phase indices in such individuals are usually normal.1,2,52,53,57,89–91 In 1 study of class III obese subjects, LV systolic function improved significantly with substantial weight loss in those with depressed preweight loss LV systolic function.53
Limited information exists concerning the effect of weight loss on clinical manifestation of HF and CRF in obesity. Small studies suggest that substantial purposeful weight loss is capable of reversing some of the manifestations of the sleep apnea/obesity hypoventilation syndrome and is associated with improved functional capacity and quality of life in most severely obese patients with HF.92,93
Purposeful weight loss in the context of a cardiac rehabilitation program produces an increase in functional capacity and an improvement in CRF in all classes of obesity.94–99 Other benefits include an improvement in serum lipids (increase in high-density lipoprotein levels, reduction in total and low-density lipoprotein levels and triglyceride levels), a decline in blood homocysteine levels, a decrease in inflammatory markers, improvement of endothelial function, lowering of blood viscosity, improvement in depression and anxiety scores, a decrease in hostility scores, reduction in hospital costs, and a decrease in the risk of nonfatal myocardial infarction and total mortality.58,59,96,98 Blood pressure is frequently decreased in such patients.
Prior to entry into an exercise training program, patients with established heart disease and those deemed at risk for cardiac disease on the basis of symptoms, signs, or the presence of cardiovascular risk factors should undergo appropriate diagnostic evaluation. The American College of Sports Medicine has provided recommendations for physical activity in obese patients, which are applicable to individuals for whom moderate aerobic exercise has been deemed medically safe: (1) 150 minutes per week to maintain and improve health; (2) 150 to 250 minutes per week to prevent weight gain; (3) 225 to 420 minutes per week to promote clinically significant weight loss; and (4) 200 to 300 minutes per week to prevent weight gain after weight loss.94 Exercise sessions should be performed at least 5 days, and preferably 7 days per week.
This is particularly important for obese patients in cardiac rehabilitation exercise training (CRET) programs, as exercise sessions in phase II CRET programs are generally 30 to 45 minutes in duration, 3 times per week. Therefore, emphasis on longer exercise durations, even at lower intensities, and the promotion of physical activity on many of the non-CRET days is even more important for obese compared with lean patients. Comorbidities may require modification of exercise modalities in some obese patients, particularly those who are severely obese and more deconditioned at baseline, where initial prescription of exercise intensity will be initiated at much lower exercise workloads, generally based on CRET entry stress testing results.
Aerobic exercise is thought to be superior to pedometer-based physical activity in effecting weight loss.94 Exercise training in combination with caloric restriction has traditionally been advocated for weight reduction; however, Ades et al97 recently reported that a high-caloric, high-intensity exercise training program doubled weight loss compared with a standard exercise training program coupled with caloric restriction. Nevertheless, emphasizing dietary caloric restriction is another important aspect of CRET programs for obese patients, with special emphasis on dietary education and adherence.
Obesity, especially severe obesity, is capable of producing alterations in cardiac performance and morphology that may predispose to HF. Obesity serves as a risk factor for HF, even when it is not the primary cause. Despite this risk, an obesity paradox exists for all-cause and cardiovascular mortality in HF patients who are overweight or who have class I, and possibly class II obesity. Cardiorespiratory fitness is impaired in severe obesity and has important prognostic implications, not only in patients with HF, but also in those with coronary heart disease. Substantial purposeful weight loss reverses most of the hemodynamic alterations and LV morphologic abnormalities associated with obesity. Weight loss causes improvement in LV diastolic filling and LV systolic function (when impaired) in obese patients and may produce improvement in the clinical manifestations and quality of life of patients with obesity cardiomyopathy. Since obese patients have lower levels of CRF and more cardiovascular risk factors than nonobese CRET patients, and because changes in CRF strongly predicts prognosis in CRET patients, this group may particularly benefits from formal CRET programs.98,99
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