7.2 Relation between Adrenergic Tone, Insulin Resistance and Left Ventricular Hypertrophy in Human Obesity

Introduction: Recent studies have shown that factors other than the haemodynamic ones (metabolic, neurohumoral, etc) are involved in the development of hypertensive left ventricular hypertrophy. No data are available on the role of sympathetic and metabolic factors in the pathogenesis of obesity-related left ventricular hypertrophy.

Methods: In 32 male patients with abdominal obesity (age 42.7±2.8 yrs, mean ± SEM) and in 10 age-matched healthy male controls, we measured beat-to-beat mean arterial pressure (MAP, Finapres), heart rate (EKG), and efferent postganglionic muscle sympathetic nerve traffic (microneurography, MSNA) at rest and during arterial baroreceptor stimulation and deactivation via the vasoactive drug infusion technique. Measurements also included left ventricular mass index (echocardiography) and HOMA index.

Results: Based on blood pressure and left ventricular mass index data, obese patients were classified as normotensives without LVH [O, n=8, BMI: 33.7±0.7 kg/m2, MAP: 96.3±2.5 mmHg, LVMI: 107.5±6], normotensives with LVH [OLV n=7, BMI: 34.2±0.5 kg/m2, MAP: 98.4±2.2 mmHg, LVMI: 131.4±7 g/m2], hypertensives without LVH [OH n=9, BMI: 34.2±0.5Kg/m2, MAP: 122.6±2.4 mmHg, LVMI: 118.2±7 g/m2] and hypertensives with LVH [OHLV n=8, BMI: 35.6±0.8 Kg/m2, MAP: 125.6±2.4 mmHg, LVMI: 138.9 ±8 g/m2]. The MSNA and HOMA index values displayed by the 4 obese groups were significantly greater than C. More importantly, MSNA and HOMA index values were significantly greater in OLV than in O (57.5±3.4 vs 47.2±3.6 bs/100hb and 4.9±0.4 vs 3.3±0.3 a.u., respectively, p in OHLV as compared to OH (71.5±4.1 vs 60.9±3.9 bs/100 hb and 5.1±0.4 vs 3.9±0.3 a.u.. respectively.

Conclusions: Thus in human obesity the presence of cardiac hypertrophy is associated with greater sympathetic and metabolic alterations. This is true not only when obesity is accompanied by a normotensive state but also when it is complicated by hypertension, suggesting the relevance of the insulin resistance state as well as of the adrenergic activation in the pathogenesis of end-organ damage.