To date, the majority of trials seeking to evaluate the cardiovascular impact of bariatric surgery have only presented the cardiovascular risk endpoints of hypertension, diabetes, hyperlipidemia, inflammatory markers, and risk prediction scores, with far fewer reporting actual cardiovascular events or mortality. Among cardiologists, reliance on cardiovascular risk markers as indicators of reduced clinical risk after bariatric surgery is regarded with suspicion, because of prior instances where CVD risk surrogates have not translated into an actual survival benefit. Hence, there is now interest in designing bariatric surgery trials focused on the collection of longer-term data on actual cardiovascular events, cardiovascular mortality, and all-cause mortality. Ideally, such studies should randomize subjects to surgical vs. nonsurgical management of obesity. As all the existing cardiovascular outcomes data is from nonrandomized, matched cohorts, it remains possible that features specific to obese patients who pursue a surgical intervention, as compared to those who do not opt for surgery, are currently confounding the relationship between bariatric surgery and CV outcomes.

There is limited data examining the outcomes of bariatric surgery in cohorts of obese patients with preexisting cardiac disease. The safety of RYGB with preexisting CAD was assessed in a cohort of 52 patients (with prior coronary revascularization, >30 % angiographic coronary stenosis, prior myocardial infarction, or a positive stress test). There were no in-hospital deaths among the 52 CAD patients or 507 surgical patients without CAD. Three CAD patients (5.8 %, 95 % CI, 0–12.2 %) and 7 without CAD (1.4 %, 95 % CI, 0.4–2.4 %) had perioperative cardiac complications (p = 0.06). Postoperative cardiovascular event data is more abundant for the full population of patients undergoing bariatric surgery. One study of 575 high-risk VA bariatric surgery patients, 42 % with BMI ≥50 kg/m², revealed 1.6 % and 0.5 % rates for perioperative cardiac arrest and myocardial infarction, respectively. The overall mortality in this group was 1.4 %, slightly exceeding the national published rates which are under 1 % [74]. Torquati et al. reported a rate of 1 % for CV events in the 5 years after bariatric surgery within a cohort of 500 RYGB patients [75]. SOS investigators have reported cardiovascular outcomes for their 2010 surgical patients and matched nonoperative controls, up to a median follow-up of 14.7 years [3]. Despite an excess of smoking and higher baseline weights and blood pressures in the surgical cohort, bariatric surgery was associated with a lower number of total first-time cardiovascular events (9.9 % vs. 11.5 % adjusted HR, 0.67; 95 % CI, 0.54–0.83; p < 0.001), fatal myocardial infarctions, and total myocardial infarctions than controls. Cardiovascular deaths were also reduced, with 1.4 % cardiovascular mortality in subjects vs. 2.4 % in controls, adjusted hazard ratio 0.47 (95 % CI, 0.29–0.76, p = 0.002). The baseline degree of insulin resistance was far more predictive of cardiovascular benefit than baseline BMI in this study, supporting the hypothesis of the importance of metabolic dysfunction in the relationship between adipose tissue and cardiac outcomes. Cardiovascular outcomes have also been investigated specific to patients with diabetes. An adjusted hazard ratio of 0.56 (95 % CI, 0.34–0.93, p = 0.025) for myocardial infarction was seen at 2 years for 345 SOS surgical subjects compared to 262 nonsurgical controls, all with diabetes [76].

Mortality outcomes after bariatric surgery are considered in greater detail in Chap. 45, but as cardiovascular mortality findings are relevant to the consideration of cardiac benefit from surgical weight loss, they are also outlined here. The favorable mortality rate over 9 years in 154 RYGB patients vs. 78 controls (who were referred for surgery but did not undergo the procedure) was primarily due to a lower rate of CV death [77]. An observational study of 1,035 predominantly open RYGB patients and 5,746 matched controls demonstrated that the surgical subjects had 50 % fewer hospitalizations during the 5-year follow-up and developed significantly fewer cardiovascular diagnoses (4.73 % vs. 26.79 %, RR 0.18, 95 % CI, 0.12–0.22) [78]. At 5 years, the same cohort also showed significantly decreased incidences of new pulmonary edema (RR 0.42, 95 % CI, 0.18–0.96), angina (RR 0.53, 95 % CI, 0.40–0.70), coronary artery bypass grafting (RR 0.28, 95 % CI, 0.14–0.61), and coronary angioplasty (RR 0.36, 95 % CI, 0.19–0.66) in the postsurgical subjects compared to controls, although the decrease in myocardial infarctions (RR 0.71, 95 % CI, 0.50–1.00) did not reach significance (p = 0.05) [79]. There was favorable all-cause mortality, and also a specific reduction in death from CAD (59 % risk reduction, p = 0.006), observed among 7,925 RYGB patients vs. 7,925 severely obese matched control subjects [10]. Further details of the patient characteristics and major results from the 14 largest studies reporting cardiovascular outcomes after bariatric surgery are presented in Table 2.

The cardiac effects of excess weight and surgical weight loss have been predominantly considered in terms of the impact on atherosclerotic CAD progression and rates of myocardial infarction or other cardiovascular events. However, the direct impact of obesity on the structure and function of the myocardium is also becoming increasingly evident. Obesity is strongly associated with left ventricular hypertrophy (thickening of the walls of the main pumping chamber) and diastolic dysfunction (abnormal relaxation of the left ventricle during chamber filling) [80–82]. It has been established, in cohort sizes of 16–60 patients, that obese individuals without overt cardiac disease can show improvements in left ventricular mass and the echocardiographic markers of diastolic function in the 3 months to 3.6 years after bariatric surgery [83–87]. Furthermore, there is evidence that the regression of left ventricular mass is independent of changes in blood pressure post-bariatric surgery [83]. Prolongation of the isovolumic relaxation time is probably the most consistent diastolic abnormality seen in obesity, with left atrial volume, tissue Doppler velocities, and mitral inflow patterns also showing derangement in obese subjects [88, 89].

Most of the current data is from echocardiography studies, but cardiac magnetic resonance imaging (MRI) also has a developing role in defining structural and functional changes after bariatric surgery and can provide superior volumetric assessments. Thirty obese subjects without cardiac risk factors underwent MRIs at baseline and 1-year post-weight loss (bariatric surgery or diet) [90]. There was a 10 % mean reduction in left ventricular mass and a 40 % reduction in right ventricular mass. Left ventricular end-systolic volume, stroke volume, and cardiac output also fell with weight loss. An early echocardiographic study of left ventricular systolic, as well as diastolic, function was published with 38 SOS surgical subjects who underwent echocardiography pre- and post-gastroplasty. An improvement in left ventricular ejection fraction (LVEF) was reported at 1 year postoperatively, but the mean baseline and follow-up LVEFs in both groups were >50 %, so any statistical differences after surgery were not clinically meaningful. Similarly, there was a statistically significant improvement in LVEF at 3 years post-bariatric surgery in another 23-patient cohort, but the baseline LVEF mean was already supranormal at 71 % [88].

More sensitive echocardiographic techniques than LVEF are now available for detecting subtle changes in systolic function, particularly in the setting of left ventricular hypertrophy [91]. Two-dimensional speckle tracking-derived strain and strain rate imaging have highlighted the subclinical systolic dysfunction that can be associated with obesity [92, 93]. Barbosa and colleagues demonstrated slight differences in left ventricular global strain (22.5 % ± 3.5 vs. 24.4 % ± 2.5, p < 0.005) between 92 patients with class III obesity and 31 healthy controls, despite no differences in LVEF between subjects and controls, suggesting incipient systolic dysfunction with obesity. Of note, these authors reported that only 9 patients (9 % of the cohort) had a technically inadequate echocardiogram that was not amendable to strain analysis. Thirteen obese patients with LVEFs above 40 % demonstrated regression of these subclinical abnormalities of myocardial deformability in the 6–24 months after bariatric surgery [94].

Several cross-sectional and prospective studies have demonstrated that increasing BMI or waist circumference is independently associated with development of incident heart failure (HF) [95–97]. A prospective Framingham study of 5,881 participants, stratified by BMI at enrollment, found that the risk of clinically symptomatic HF increased by 5 % for men and 7 % for women per unit BMI increase, despite adjustments for demographics and known CAD risk factors [98]. In a prospective study of 4,080 men age 60–79 years without baseline HF followed for a mean period of 9 years, the adjusted hazard ratios associated with a 1-standard deviation (SD) increase in BMI were 1.37 (95 % CI, 1.09–1.72) and 1.18 (95 % CI, 1.00–1.39) in men with and without CHD, respectively. Increased leptin was significantly associated with an increased risk of HF in men without preexisting CHD, independent of BMI and potential mediators (adjusted HR for a 1-SD increase in log leptin 1.30, 95 % CI, 1.06–1.61, p = 0.01) [43].

The evidence suggesting improvements in obesity-associated diastolic and systolic dysfunction after bariatric surgery raises the possibility of echocardiographic and clinical improvements in obese patients who have a preoperative clinical diagnosis of heart failure. Indeed, there are a handful of early case reports describing HF recovery after surgical weight loss [99–101]. Such reports do, however, feature very obese individuals who were young and predominantly affected by systolic HF, and so the results may not be generalizable.

Beyond case reports, the published evidence in favor of improvements in HF after bariatric surgery is limited to three small studies. The first is a prospective analysis of fractional shortening performed pre- and post-vertical band gastroplasty that incorporated 13 subjects with low preoperative systolic function [102]. There were modest improvements in fractional shortening (22 ± 2 % to 31 ± 2 % p < 0.01) at a mean of 4.3 months after weight loss plateaued, accompanied by reductions in left ventricular end-diastolic diameter and mean arterial blood pressure. The same group published a study of fractional shortening pre- and post-vertical band gastroplasty in 14 subjects with clinical diagnoses of HF and an average fractional shorting that lies just below the lower limit of normal [103]. This cohort showed improvements in New York Heart Association functional class from III to II in four patients, III to I in three patients, and II to I in five patients but no statistically significant improvements in systolic function. However, these postoperative echocardiograms occurred at only 4.5 ± 1.2 months postoperatively, and the older procedure of vertical band gastroplasty is not associated with the same degree of metabolic recovery as malabsorptive bariatric surgery.

An overlapping cohort of HF patients that underwent bariatric surgery generated two publications [104, 105]. The Ramani study utilized an independent echocardiogram reader. Twelve patients with a mean age of 41 years, BMI of 53 kg/m², and LVEF of 22 ± 7 % were retrospectively reviewed. Nine underwent RYGB, two received sleeve gastrectomies, and one underwent gastric banding. Subjects were matched to ten controls who received diet and exercise counseling only. At 1 year, hospital readmission in bariatric patients was significantly lower than controls (0.4 ± 0.8 vs. 2.5 ± 2.6, p = 0.04). There was a significant improvement in mean LVEF for the bariatric group (35 ± 15 %, p = 0.005) but not for controls, and the NYHA class improved in bariatric patients (2.3 ± 0.5, p = 0.02) but deteriorated in controls. The third cohort was a subset of 9 patients with LVEF ≤ 50 %, within a 57-patient cohort of obese subjects with mean BMI of 49 kg/m², who underwent RYGB. Although there did appear to be a trend towards increased LVEF in these 9 patients (preoperative LVEF 44.8 ± 7 to postoperative LVEF 59.5 ± 10.1, no p value presented), there was a similar rise in mean LVEF in the nonsurgical controls with initial LVEF ≤ 50 % (44.9 ± 7.9 to 58.6 ± 14.1) [83].

Despite the suggestions of improvements in symptoms and systolic function after bariatric surgery for patients with HF, HF patients with higher BMIs actually show more favorable survival rates than their leaner counterparts [106–108]. Each incremental 5 kg/m² BMI increase was associated with 10 % lower in-hospital mortality among 108,927 decompensated HF patients [109]. A cohort of 2,271 chronic systolic heart failure patients (mean age 71.9 ± 11.3 years, 74.6 % male) was followed for a median of 1,785 days, during which time 912 patients died. Measures of body mass were strong univariable predictors of outcome, and body surface area (χ ² = 71.3) was the strongest predictor followed by height (χ ² = 68.6), weight (χ ² = 57.4), then BMI (χ ² = 15.2). The greater the patient’s overall size, the greater the likelihood of survival. Body surface area was the single strongest predictor of outcome in a multivariable model including 14 variables [110]. However, the survival advantage of obesity may be lost in individuals with diabetes. Of 2,153 chronic mild to moderate systolic HF patients with diabetes, of whom 798 (37 %) were obese, all-cause mortality occurred in 38 % of obese patients and 39 % of nonobese patients (hazard ratio, 0.99; 95 % CI, 0.80–1.22; p = 0.915) [111].

The paradoxical survival relationship noted in HF populations has also been observed in patients with CAD but may disappear when survival is correlated to waist circumference, rather than the cruder parameter of BMI [112]. Conversely, the paradox persists with anthropometric measurements of obesity in HF and was recently demonstrated in advanced systolic HF patients stratified by BMI and waist circumference (WC) [113]. Both high WC and the combination of high WC/high BMI were associated with improved mortality, or freedom from urgent heart transplant, in this cohort.

Analysis of chronic systolic HF subjects in the SOLVD and V-HeFT II trials revealed that the loss of more than 6 % of body weight during the study duration was an independent predictor of mortality [114]. Lower BMIs may simply be a marker of cardiac cachexia and more advanced HF, but the possibility remains that weight loss may be detrimental to survival in obese patients with HF. Heart failure with preserved ejection fraction is also more frequently seen in obese patients than their lean counterparts and is also associated with a survival paradox with increasing BMI (hazard ratio for mortality 0.67, 95 % CI, 0.56–0.81) [115]. These survival observations have sparked interest in a hypothesis that although some of the adipokine and gut hormone changes associated with obesity may promote cardiac dysfunction, others may potentially become protective once HF is established.

Atherosclerosis and myocardial dysfunction are not the only cardiac effect of obesity; obese individuals also have an increased risk of arrhythmias and sudden death. It is postulated that the myocardial of obese patients is vulnerable to ventricular repolarization abnormalities. Russo et al. reported a significant postoperative decrease in the heterogeneity of ventricular repolarization among 100 bariatric surgery patients with pre- and postoperative electrocardiograms [116]. Decreased QT interval and QT dispersion have also been observed in 85 patients post-biliopancreatic diversion [117]. Such electrophysiological modulation may reduce the substrate for ventricular arrhythmias in this high-risk patient population. Obesity also increases the risk for atrial arrhythmias such as atrial fibrillation. Significant regression of P-wave dispersion, a marker of atrial refractoriness heterogeneity and a risk factor for atrial fibrillation, has been reported after bariatric surgery [118]. This suggests that surgical weight loss may hold potential for reducing incident atrial fibrillation, or the incidence of new atrial fibrillation, after bariatric surgery.