I have more flesh than another man; and therefore more frailty. William Shakespeare (Henry IV Part I, Act III Scene III)

The link between obesity and physical frailty has long been recognized. Obesity and overweight have reached epidemic proportions in the United States. Two-thirds of American adults are overweight or obese, and more than 30 % are obese. In addition, the greatest rate of increase in this population is seen in those who are morbidly obese (body mass index greater than 40 kg/m²).

The overweight and obesity problem is associated with multiple comorbid conditions and an increased mortality. Obesity in general, and visceral adiposity specifically, is associated with an increased mortality. The overall relative risk of mortality is approximately 2.00 for men and 1.65 for women with a BMI > 35 kg/m², compared to the normal weight population [12]. In fact, trends suggest that obesity will overtake smoking as the primary preventable cause of death in the United States [13]. Obesity in an otherwise healthy population in the fifth decade of life is associated with frailty decades later [14].

Obesity is associated with significant comorbid conditions. These maladies affect almost every system in the body and include the musculoskeletal, pulmonary, endocrine, immune, and cardiovascular systems. The cardiovascular system is especially affected with multiple physiologic changes that often lead to adverse outcomes. Thus, concurrent with the dramatic increase in the prevalence of obesity in the United States and worldwide over the past several decades, reaching epidemic proportions [15, 16], the American Heart Association issued a “call to action” in response [17]. In it, the AHA reclassified obesity as a “major, modifiable risk factor for coronary heart disease” and in doing so focused more resources to understanding the role of obesity in cardiovascular disease.

One of the early changes with obesity is an increase in total blood volume, leading to an increase in filling pressures, cardiac output, and cardiac workload [18]. Concurrently, obese patients are more likely to be hypertensive, eventually leading to cardiac chamber dilation, left ventricular hypertrophy, and abnormal diastolic filling pressures. In fact, diastolic dysfunction is thought to be frequently present in asymptomatic patients who are morbidly obese [19]. Indeed, obesity is considered an independent predictor of developing CAD [20]. However, the relationship between obesity and cardiovascular disease appears to be much more complex. In fact, obesity lowers systemic vascular resistance and thus may provide a protective component, leading to the “obesity paradox.”

Patients who are overweight and obese have an increased prevalence of cardiac risk factors and have an increased risk of cardiovascular disease in general, including CAD and heart failure. The increase in risk is directly proportional to incremental increase in body mass index. However, multiple studies suggest that overweight and obese patients with known cardiovascular disease are actually predicted to have a better event-free survival compared to normal or underweight cohorts [21–23]. Thus, it seems that obesity increases the initial risk for cardiovascular disease, but it may confer some protective benefit from mortality in those already afflicted with heart failure or CAD. The mechanism for this observation is not clear, although there is some evidence to suggest that the BMI is not the proper parameter to be measured. Rather, waist circumference (WC) and waist-hip ratio (WHR), as proxies for central adiposity, may be more predictive of mortality in patients with CAD. In addition, it is uncertain whether the findings still hold true in the severe or morbidly obese. A large systematic review and collaborative analysis found that increasing central obesity was associated with higher mortality in patients with CAD and the use of WC in addition to WHR is a more effective indicator than either measurement alone [24]. Nonetheless, the PDAY (Pathobiological Determinants of Atherosclerosis in Youth) study provided convincing data to suggest that obesity in adolescents and young adults (ages 15–34 years) accelerates the progression of atherosclerosis 10–20 years before any clinical symptoms [25]. From available evidence, it is clear that earlier onset of obesity, corresponding to a longer period of time spent with obesity, leads to a lifetime increased risk of cardiovascular disease and mortality. A younger obese population has a higher mortality than a BMI-matched older population [26, 27].

It has long been recognized that fat tissue is not a simple storage cell of fat but is metabolically highly active and is responsible for systemic secretion of molecules that impact cardiovascular homeostasis [28]. Of these factors, the concentrations of plasminogen activator inhibitor-1, angiotensin II, CRP, fibrinogen, and TNF-α(alpha) are directly affected by BMI, and concentrations of IL-6 directly affect CRP levels [29].

Along with obesity, insulin resistance has been implicated in the development of CAD, leading to the insulin resistance syndrome or metabolic syndrome concepts that correlate the concurrent pathophysiology of obesity, insulin resistance, dyslipidemia, and cardiovascular disease. Obesity is a leading cause of insulin resistance, which implies a peripheral tissue resistance to the effects of circulating insulin, mainly glucose metabolism [30]. It affects all ethnic groups and is apparent in the entire BMI spectrum of overweight and obesity. The target tissues affected are hepatocytes, skeletal muscle, and adipocytes. In the adipocytes, lipogenesis and lipid storage and metabolism are directly affected, resulting in an increased systemic load of free fatty acids. But again, it appears that central adiposity has the greatest impact on insulin resistance and its effects. The hyperinsulinemic state is also implicated as a growth factor with direct deleterious cardiac effects. While the exact mechanism is not yet fully elucidated, it is clear that insulin resistance is part of a syndrome whose hallmark is obesity and that significantly increases the risk of cardiovascular disease [31].

Obstructive sleep apnea (OSA) is directly associated with obesity and directly impacts cardiac function. Obesity, in and of itself, is a common cause of alveolar hypoventilation and is considered the most important modifiable risk factor for sleep-disordered breathing [31, 32]. Obesity and OSA so often coexist in the same population that it can be difficult to identify diagnoses that are correlated with one and not the other. Those patients with sleep apnea have an increased mortality as well as a risk of diurnal hypertension, nocturnal dysrhythmias, pulmonary hypertension, right and left ventricular failure, myocardial infarction, and stroke [33, 34].

Whether related to OSA or not, the risk of acute arrhythmia leading to sudden death is markedly increased in the obese population. In the Framingham study, obesity was found to be a major modifiable risk factor for sudden cardiac death in both men and women [35]. Prolongation of the QTc interval seen on ECG (electrocardiogram) is considered a risk of increased risk of arrhythmia and cardiovascular mortality. In fact, both prolongation and shortening of the QT interval was found to be associated with all-cause mortality, cardiovascular disease, and ventricular arrhythmia and sudden death. For prolonged QT, the increased risk is seen for both males and females at an interval of 420–450 ms [36, 37].

Meanwhile, weight loss in the morbidly obese population, and specifically loss of central adiposity, is associated with a reduction in cardiovascular risk factors and overall mortality. Despite this, there is some uncertainty whether intentional weight loss is beneficial to patients with known cardiovascular disease. This point of controversy is based on several studies that have shown increased risk of arrhythmia and negative outcomes in patients with aggressive dietary restrictions, meal replacements and very low-calorie diets, or pharmacotherapy with cardiac toxicity [18]. This is typically manifested through the prolongation of the QTc interval often observed in these situations. Fatal or life-threatening arrhythmias have been observed after radical dieting or liquid protein meal replacements.

Nonetheless, it is clear that weight loss in the obese population improves obesity-related risk factors for cardiovascular disease. Even modest medical weight loss in overweight and obese patients directly correlates with a reduction of CRP, lipids, and glucose, with a lower total mortality as well [38]. In general, weight loss by any means leads to improvement of cardiovascular risk factors and is strongly recommended for the asymptomatic obese population [39]. Total blood volume, stroke volume, and systemic arterial pressure all decline. Consequently, filling pressures decrease and left ventricular stroke work diminishes, and oxygen consumption decreases [39].

But weight loss also benefits the symptomatic obese population already diagnosed with cardiovascular disease. A healthy eating protocol along with structured exercise training is central in this population with known heart disease. A study of 377 patients with cardiovascular disease who lost weight had a 38 % relative risk reduction relative to patients who did not lose weight, in all-cause mortality and cardiovascular events that included myocardial infarction, stroke, and heart failure [40, 41]. Although long-term cardiac-specific survival data after intentional weight loss is lacking, there is strong data to support that weight loss in the overweight and obese population decreases nearly all identified risk factors for cardiovascular disease. To date, bariatric surgery has proven to be the only durable treatment method for significant weight loss in the obese population. Thus, weight loss surgery is a rational approach to the treatment of obesity in patients at risk for cardiovascular disease. Due to their higher risk for cardiac events, the preoperative evaluation is especially significant.

Obesity independently increases cardiovascular risk factors, and many obese patients may have underlying cardiovascular disease but are asymptomatic when they present for evaluation for bariatric surgery. Thus, the cardiac evaluation of obese patients preparing to undergo surgery is especially important. In fact the National Institutes of Health Consensus Development Program Statement specifically advocates a multidisciplinary approach to these patients, suggesting a thorough medical evaluation as part of the preoperative work-up, and it is common practice to include an evaluation by a cardiologist to assess for cardiac risks [42].

There is no consensus approach to the preoperative work-up of the bariatric patient, but general guidelines are followed by most. A thorough history and physical examination are used to identify comorbid conditions with specific surgical implications and those that can affect cardiovascular risk, such as the presence of dyspnea on exertion, daytime sleepiness, and nighttime snoring; the presence of hypertension, diabetes, or insulin resistance; or the use of medications that may prolong the QT interval. The degree of central obesity should be assessed by physical examination, as it relates to cardiovascular risk more strongly than BMI.

A routine preoperative laboratory evaluation should also include the known biochemical markers previously discussed, including a full lipid profile, CRP, and fasting insulin levels. Other biochemical markers that may be informative preoperatively and followed in the postoperative period include lipoprotein(a) and homocysteine.

It is common for the obese patient to undergo at least one adjunct study as part of the preoperative work-up. Although the utility of routine chest X-rays is debated, it may be useful to obtain in the bariatric population, which has a high prevalence of asymptomatic cardiopulmonary disease. Findings of cardiomegaly or cephalization of pulmonary vessels may suggest cardiovascular disease and prompt further work-up.

The electrocardiogram (ECG), however, should be considered a mandatory part of the preoperative evaluation of the bariatric patient. Structural cardiac changes that are induced by obesity may influence the appearance of the ECG. These include cardiac displacement, ventricular hypertrophy, a distant heart due to chest wall adiposity, and elevated pulmonary pressures [28]. As a result, multiple findings are expected in the obese patient who has cardiac morphological changes. Of patients preparing for bariatric surgery, 62 % were found to have specific ECG abnormalities [43]. Included were LVH, RVH, short PR, bundle branch block, ST-T wave abnormalities, AV block, tachycardia, ectopy, and prolonged QT. In and of itself, the finding of an abnormal echocardiogram may predict a more complicated postoperative course and need for intensive care utilization [44].

Those patients with a significant cardiac history, cardiac symptoms, an especially low functional capacity, or abnormalities uncovered in the initial evaluation should undergo a noninvasive functional cardiac evaluation or cardiac stress testing. While myocardial nuclear perfusion imaging may provide valuable information, table weight and torso diameter limitations may make it impractical in some of these patients [45]. Stress echocardiography is widely used to evaluate known or suspected coronary artery disease. However, the image quality in the obese population may be significantly compromised, decreasing the efficacy of the test. Subepicardial fatty tissue, for example, may commonly result in a false positive for a pericardial effusion or conversely underestimate the amount of pericardial fluid [46]. On the other hand, many have advocated for the use of dobutamine stress echocardiography. It can provide the practicality of an echocardiogram, with enhanced image quality. Echocardiograph contrast agents improve the fidelity of the test and may be used in stress and nonstress testing. In a study of 590 morbidly obese patients, the transthoracic dobutamine stress echocardiograph was inconclusive in only 6.4 % of patients and was found to be safe and effective [45, 47].

Other noninvasive cardiac imaging studies include the single-photon emission computed tomography (SPECT), positron emission tomography (PET), and computed tomographic (CT) coronary angiography. The utility and cost-effectiveness of these studies are unclear.