Contributions of cardiorespiratory fitness and visceral adiposity to six-year changes in cardiometabolic risk markers in apparently healthy men and women.

CONTEXT: Both excess visceral adipose tissue (VAT) and low cardiorespiratory fitness (CRF) levels are associated with a deteriorated cardiometabolic risk profile. OBJECTIVE: The aim of the study was to examine the respective contributions of changes in VAT accumulation vs. changes in CRF to 6-yr longitudinal changes in cardiometabolic risk markers. DESIGN, SETTINGS, AND PARTICIPANTS: We conducted a prospective, population-based study with an average follow-up of 5.9 ± 0.8 yr. We followed 132 middle-aged participants from the Quebec Family Study (mean age, 35.3 ± 13.9 yr). VAT was measured by computed tomography, whereas the level of CRF was assessed by a submaximal physical working capacity test at baseline and at follow-up. A complete cardiometabolic risk profile, including systolic and diastolic blood pressure, fasting glucose and insulin levels, C-reactive protein (n = 72), as well as a standard lipoprotein-lipid profile, was obtained at baseline and at follow-up. MAIN OUTCOME MEASURES: We measured changes in CRF, VAT, and cardiometabolic risk profile over 6 yr. RESULTS: After adjusting for age and sex, 6-yr changes in VAT were negatively correlated with changes in CRF (r = -0.38; P < 0.001). In a multivariate model that included age, sex, changes in VAT, changes in CRF, as well as baseline levels of the above cardiometabolic risk factors, 6-yr changes in VAT were the most important predictor of the change in the metabolic syndrome score (R(2) = 13.2%; P < 0.001). Adding 6-yr changes in CRF levels significantly improved the predictability of the model (R(2) = 19.7%; P = 0.002). CONCLUSIONS: Changes in both VAT and CRF levels observed over 6 yr are associated with changes in parameters of the lipoprotein-lipid profile, glucose-insulin homeostasis, and inflammatory markers. Thus, maintaining a low level of VAT and a high level of CRF are important targets for maintenance of cardiometabolic health.

Left ventricular response to sustained volume overload from chronic aortic valve regurgitation in rats.

OBJECTIVES: Aortic regurgitation (AR) induces left ventricular (LV) eccentric hypertrophy in response to chronic volume overload. Patients suffering from this disease often remain asymptomatic for decades before progressive LV dysfunction develops silently. Because of this slow evolution, large clinical trials with long-term follow-up on subjects with chronic AR are hard to perform. To overcome this problem, animal models have been developed in the past but results were very heterogeneous. METHODS: Helped by echocardiography, we refined a known technique to induce homogeneous degrees of severe AR in Wistar-Kyoto rats. The effects on LV function without treatment and with nifedipine (25 mg/kg daily) (a drug currently recommended in humans with chronic AR) were evaluated by echocardiography. RESULTS: Over 6 months, nontreated animals developed progressive LV dilatation and eccentric hypertrophy, characteristic of chronic LV volume overload. The animals also developed progressive LV systolic dysfunction, mimicking closely the evolution of the disease in humans. Abnormal filling parameters were also detected in the majority of animals. Systolic and diastolic abnormalities were prevented but only partially in the group treated with nifedipine. CONCLUSION: This model can be used to study chronic AR and LV dysfunction associated with the disease. Nifedipine seems to protect the LV against chronic volume overload but only partially. Treatment strategies currently used in humans deserve further investigation.