Open Access
Feature Article

The cardiac complications of obesity

Open Access
Feature Article

The cardiac complications of obesity

Elizabeth Paratz, Sonny Palmer, Justin Mariani

Figures

© LIGHTSPRING/SHUTTERSTOCK
© LIGHTSPRING/SHUTTERSTOCK
Dr Paratz is a Cardiologist at St Vincent’s Hospital and the Baker Heart & Diabetes Institute, Melbourne. Associate Professor Palmer is an Interventional and Structural Cardiologist at St Vincent’s Hospital, Melbourne. Associate Professor Mariani is an Interventional Heart Failure Specialist at The Alfred Hospital, Melbourne, Vic.

Obesity and cardiovascular risk

Physiology

The impact of obesity on CV risk is multifactorial and self-amplifying. Obesity augments CV risk by multiple mechanisms, as illustrated in the Figure. The direct mechanical effect of excess adipose tissue increases total body blood volume, cardiac filling pressures and sympathetic activation, leading to an increased cardiac workload and cardiac hypertrophy. Adipose tissue also increases cardiac afterload and chest-wall resistance, enabling the development of both systemic hypertension and obstructive sleep apnoea.6

Adipose tissue is more than just a mechanical load, however, creating a web of metabolic consequences. It is very active metabolically, both in synthesising and in metabolising numerous substances. These substances are predominantly pro-inflammatory and prothrombotic (tumour necrosis factor-alpha, interleukin-6, plasminogen-activator inhibitor 1, oestrogen) or worsen insulin resistance and lipid metabolism (leptin, adiponectin, insulin-like growth factor, insulin-binding-protein 3).7

Clinical events

The physiological effects of obesity directly elevate the risks of multiple cardiac conditions (Table 2).8-17 Hypertension and dyslipidaemia are widely prevalent in patients with obesity, and the association of hypertension, dyslipidaemia and central obesity has been formally recognised in ‘the metabolic syndrome’. Type 2 diabetes is also strongly associated with obesity, which has led to the coining of the term ‘diabesity’.18

The presence of obesity as a contributing risk factor for several cardiac conditions now features prominently on several risk scores (e.g. STOP-BANG score for obstructive sleep apnoea and Q-RISK3 score for cardiovascular risk). Further, the presence of obesity is a feature of the H2FPEF score for heart failure with preserved ejection fraction (HFpEF).19 This reflects that obesity is very strongly associated with HFpEF,20 with up to 80% of patients with HFpEF either having overweight or obesity.21

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The combination of cardiac hypertrophy and direct fatty infiltration creates a substrate for arrhythmias. The most common arrhythmia observed is AF, and the dose-dependent link between obesity and AF is now well established. Pathak and colleagues have quoted an increased risk of 3 to 7% for developing AF for each incremental unit of BMI.14

Patients who have obesity also have an elevated incidence of ventricular dysrhythmias, raising the risk of sudden cardiac death.22,23 Obesity is now the leading cause of nonischaemic sudden cardiac death in young people,17,24 responsible for approximately 25% of cases. Cardiopulmonary resuscitation is more difficult in those with obesity, potentially further compromising outcomes.

A 2008 study of more than 100,000 patients with acute coronary syndromes demonstrated that morbid obesity is now the most powerful risk factor for premature CV events, lowering the age of first coronary syndrome by a mean of 12 years.5 By contrast, smoking lowered the age of first coronary syndrome by a mean of only 9.7 years.5

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With an increasing morbidly obese population, cardiologists are seeing an increase in young patients with ST-segment elevation infarctions (STEMIs). A 2011 study into the high prevalence of obesity in young patients with STEMIs found that almost 80% of young patients (men aged less than 45 years, women less than 55 years) who experienced a STEMI had obesity.16

Appreciation of the adverse effects of obesity has driven recommendations in societal guidelines. For instance, in the NHMRC guidelines on the management of obesity, doctors are strongly advised to inform their patients who have obesity of their elevated CV risk profile and mortality (Table 3).9

Morbid obesity and procedural complications and outcomes

Despite typically being younger, patients with morbid obesity and coronary syndromes may be prone to increased procedural complications and poorer outcomes than normal weight patients. Cardiac work-up of patients with obesity is problematic, both in the difficulty of these patients exercising and in the poor image quality achieved across a range of investigational modalities. The ECG from such patients often has baseline abnormalities that obscure correct interpretation (for example, axis deviation or diffusely low QRS voltages).25 In addition, false-positive results suggesting ischaemia have been recorded at higher frequency for patients with morbid obesity undergoing echocardiography, stress echocardiography and stress thallium testing.26

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