A higher prevalence of coronary heart disease, cardiac and overall mortality is associated with obesity. The development of obesity appears in different adaptations in the morphology of cardiac structure and function. Obesity causes eccentric hypertrophy and changes in diastolic function of left ventricle. A systolic on diastolic heart dysfunction results from the breakdown of compensatory pace to raised wall stress and dilatation of chambers. Obesity does not possess primary cause and effect relationship with cardiovascular disease, such as LDL cholesterol. It is regarded as a means of facilitating factors such as hypertension, diabetes or cigarette smoking. Adipose tissue in this manner works as the hormone generating tissue, secreting various peptides and secondary messengers and inflammatory cytokines. Pharmacotherapy can be a useful component in the global fight against obesity. Besides repeating re-evaluations of weight loosing drug treatment with respect to efficiency or safety for continuous use, one must not underappreciate the pretreatment risk-assessments and expected benefits of treatment, along with impact on the patient’s quality of life and motivation. Pharmacotherapy of obesity is reserved for obese people with body mass index (BMI) ≥ 30 kg/m2 but also in individuals with BMI 27 .0 and 29 .9 kg/m2 and obesity related comorbidities as obstructive sleep apnea, hypertension, dyslipidemias, diabetes and metabolic syndrome. Although connections between obesity and cardiovascular diseases (CVD) are acknowledged for over dozen of years, there is still a lack of scientific research into the field and it is a challenge for future studies.