Obesity, the heart under pressure: why today's cardiologist must intervene earlier

For many years, obesity was considered primarily an aesthetic or, at best, a metabolic problem. Today we know that it is a real chronic, progressive and relapsing disease, with the capacity to profoundly alter the cardiovascular system. This is why the cardiologist can no longer limit himself to treating the consequences - heart attack, heart failure, atrial fibrillation, stroke - but must intervene early on the causes.

Obesity now affects more than 10% of the Italian population, with numbers growing even among the young. Moreover, it has been shown that life expectancy decreases with increasing BMI (Body Mass Index) and thus with obesity. Excess adipose tissue is not just an energy store: it is a metabolically active organ that produces chronic low-grade inflammation, alters vessel function, and promotes diabetes, hypertension and dyslipidaemia. In other words, it creates the ideal breeding ground for the development of cardiovascular disease.

The heart of a person with obesity works harder and worse. The volume of blood to be put into circulation, oxygen consumption and haemodynamic stress increase. Over time, the heart muscle becomes hypertrophic and stiffer with altered diastolic function, leading to heart failure, a condition that is increasingly common in obese patients. Furthermore, the accumulation of visceral and pericardial fat is associated with an increased risk of arrhythmias, particularly atrial fibrillation.

There is also a cultural aspect to be overcome: the idea that it is enough to 'eat less and move more'. A correct lifestyle with proper nutrition and physical activity remain fundamental, but unfortunately, not always sufficient. Obesity is a complex disease, influenced by genetic, neuro-hormonal, environmental and social factors. Blaming the patient does not help; instead, effective and multidisciplinary treatment paths must be built.

In recent years, research has opened up a new phase. New molecules with both 'incretin' and 'non-incretin' action, such as GLP-1 receptor agonists (GLP1-ra) and so-called dual-agonists (GLPI-ra + GIP), are changing the therapeutic approach. Their advent has made it possible to significantly reduce the therapeutic gap between correct lifestyle and bariatric surgery. However, these are not simply drugs that promote weight loss: clinical trials show a significant reduction in major cardiovascular events in high-risk patients. It is a paradigm shift. For the first time, we have therapies that act simultaneously on body weight, metabolic control and cardiovascular protection. It must be emphasised that drug therapy should not be regarded as a cosmetic approach, but rather as a true pathway that must begin with the awareness of lifestyle modification.