**1. Introduction**

During the past half-century, the advances in the prevention, diagnosis, and management of cardiovascular disease (CVD) have been spectacular. The cardiovascularrelated deaths have declined by about two-thirds in industrialized nations [1].

Heart failure is characterized by an increased rate of cell death, which has been attributed to a variety of conditions: oxidative stress; abnormal elevations in circulating neurohormones; toxins, such as alcohol or cancer chemotherapeutic drugs; excessive adrenergic activity; inflammation; and infiltrative processes. Apoptosis is a highly regulated type of cell death that normally increases with aging. It has been suggested that, over time, the resulting deletion of myocytes leads to heart failure [2, 3].

The metabolic demand is increased in obesity; this is due to different factors as increasing blood volume, greater adipose tissue and lean mass, and as such, increased preload to the heart. In addition, in obese patients there are vascular alterations impacting arterial stiffness, and resistance increases afterload to the heart. In adults with obesity, both eccentric and concentric hypertrophies have been noted and are impacted by the duration and the degree of the obesity [4, 5].
