Coronary angiography may be hazardous for patients with obesity, with complication rates in excess of those experienced by normal weight patients. The Blue Cross Blue Shield of Michigan Cardiovascular Consortium registry is one of the largest registries from which CV outcomes in patients with morbid obesity have been assessed. In 2013, analysis of data from 227,044 patients in the registry undergoing percutaneous coronary intervention revealed that compared with overweight patients, patients with morbid obesity experienced more vascular complications, almost twice the rate of contrast-induced nephropathy, a fourfold increased risk of contrast nephropathy requiring dialysis, and an increased risk of mortality (odds ratio, 1.63).27 This increased risk of mortality has been confirmed in other publications.28,29 Other problematic elements of coronary angiography include three to four times the typical quantity of radiation exposure, increased contrast use and lengthened procedural time.30
For patients with morbid obesity requiring cardiothoracic surgery, risks remain elevated above baseline. Australian data suggest that morbid obesity is associated with prolonged ventilation, deep sternal wound infection, renal failure, return to intensive care and longer length of hospital stay.31 International studies have confirmed these elevated risks32 and associated increased costs,33 and have stated that the increased number of patients with obesity undergoing cardiothoracic surgery ‘demands attention’.
Can cardiovascular morbidity be reversed by weight loss?
It can be dispiriting to connect the links between increased CV risk in obesity and consequent worsened outcomes. However, data increasingly suggest that patients can remodel their hearts and health outcomes by losing weight. Some of the most powerful data in this area are Australian and may ultimately dramatically shape future guidelines on CV care of patients with obesity. GPs will have a key role in this new paradigm of obese CV care (Table 3).
It is increasingly being recognised that successful weight loss may alleviate the ‘metabolic syndrome’, with reductions in hypertension, dyslipidaemia and insulin resistance. One of the most powerful trials to date bearing out this association was the STAMPEDE (Surgical Treatment And Medications Potentially Eradicate Diabetes Effectively) trial.34 In this trial, published in The New England Journal of Medicine in 2012, 150 obese patients with type 2 diabetes mellitus received either medical treatment for their obesity or a combination of surgical (gastric bypass or sleeve gastrectomy) and medical treatment. Although external validity is limited by its nature as a single-centre, nonblinded study, results were highly significant. Patients in the combined surgical and medical arm of the trial lost an average of 27 kg of weight over 12 months. This weight loss was associated with mean improvement in HbA1c from 9.4% to 6.5%, a 28.4% improvement in HDL-cholesterol readings, and a 43% improvement in triglyceride levels. Particularly impressive was the significant reduction in patients’ requirement for diabetes medications and lipid-lowering, antihypertensive and antithrombotic agents following surgery. These outcomes, including the degree of weight loss, were largely sustained at the three-year follow up in 2014.10
The findings of this trial suggest that significant weight loss achieved by surgery may outperform many of our currently available medications in terms of reducing hypertension, dyslipidaemia and insulin requirements. In some cases, weight loss appeared to have induced complete remission of these conditions, with remission sustained for at least three years’ follow up.
A South Australian cardiac team has provided further support for the key role of weight loss in improving CV health, this time in the context of AF. As described earlier, AF may be mechanistically linked to obesity via systemic hypertension, cardiac hypertrophy, fatty infiltration of cardiac muscle and electroanatomic remodelling. Obesity is now the second-highest population attributable risk for AF behind hypertension.35 Pathak and colleagues have shown that weight loss has a dose-dependent effect in reducing patients’ burden of AF.36 Patients who were able to lose more than 10% of their body weight had a sixfold greater probability of remaining free from AF. This reduction in AF has also been shown to be associated with structural improvements in cardiac measurements, with partial reversal of pathological cardiac remodelling.37