Cardiovascular effects of weight loss. Studies of human obesity

Abstract

Obesity is an important determinant of cardiovascular disease. Although several cardiovascular risk factors may improve following weight loss the effects of weight reduction on the heart and vascular system are unclear. The present study examines the effects of obesity and large, sustained weight losses on various features of cardiovascular structure and function. Forty one patients treated with gastric surgery, 31 obese patients receiving conventional dietary recommendations and 43 normal weight subjects were included. Body weight and blood pressure measurements were obtained and metabolic risk factors, as well as urinary norepinephrine excretion, were analysed. Two-dimensional and Doppler echocardiography were performed to evaluate cardiac structure and function and 24-hour Holter recordings used to assess heart rate variability. Carotid ultrasonography was performed to determine intima-media thickness, an estimate of atherosclerosis. All the study groups were investigated at baseline and the two obese groups were re-examined after one to four years of follow-up. In addition, 1,290 obese surgical cases and 1,099 matched obese control subjects, followed for two years, were compared with respect to symptoms of breathlessness and chest pain and levels of leisure-time physical activity. Patients with obesity had higher blood pressure, larger left ventricular mass and increased relative wall thickness compared with lean subjects. They also had impaired left ventricular filling and reduced left ventricular ejection fraction. Heart rate variability was lower and norepinephrine excretion was higher in obese subjects than in lean subjects. An adverse metabolic risk factor profile was noted in patients with obesity, who also had increased intima-media thickness in the carotid artery bulb, compared with lean controls. Obese patients treated with surgery displayed substantial weight losses, whereas the average weight in the obese control group remained essentially unchanged. Following weight loss, blood pressure, left ventricular mass and relative wall thickness diminished and left ventricular filling patterns, as well as ejection fraction, were favourably affected. Heart rate variability increased and norepinephrine excretion decreased. The weight loss group also showed improvements in metabolic risk factors and appeared to have a lower progression rate of carotid bulb intima-media thickness than the group with persistent obesity. Finally, weight loss was associated with the marked relief in symptoms of dyspnea and chest pain and increased levels of leisure-time physical activity. In conclusion, sustained weight losses in people with severe obesity are associated with improvements in cardiac structure and function, the correction of cardiac autonomic balance and an apparent reduction in carotid atherosclerotic progression rate. Weight reduction also contributes to a recovery from breathlessness and chest discomfort and promotes increased physical activity. Taken as a whole, these cardiovascular improvements are likely to have favourable effects on the long-term prognosis and support the view that obesity should be treated.