Association between non-alcoholic hepatic steatosis and hyper reactive blood pressure response on the exercise treadmill test.

AIMS: Non-alcoholic hepatic steatosis (HS) is associated with hypertension and increased cardiovascular risk. While Blood pressure hyper-reactive response (HRR) during peak exercise indicates an increased risk of incident hypertension and increased cardiovascular risk, no data on the association of non-alcoholic HS and HRR exists. In this study, we have evaluated the association of HS with HRR. METHODS: We included 13 410 consecutive individuals with a mean age: 42.4 ± 8.9 years, 3561 (26.6%) female with normal resting blood pressure and without a previous diagnosis of hypertension, who underwent symptom limited exercise treadmill test, abdominal ultrasonography and clinical and laboratory evaluation. HS was detected by abdominal ultrasonography. HRR was defined by a peak exercise systolic blood pressure >220 mmHg and/or elevation of 15 mmHg or more in diastolic blood pressure from rest to peak exercise. RESULTS: The prevalence of HS was 29.5% (n = 3956). Overall, 4.6% (n = 619) of the study population presented a HRR. Subjects with HS had a higher prevalence of HRR (8.1 vs. 3.1%, odds ratio 2.8, 95% CI 2.4-3.3, P < 0.001). After adjustment for body mass index, waist circumference, fasting plasma glucose and low density lipoprotein cholesterol, HS (odds ratio 1.4, 95% CI 1.1-1.6, P = 0.002) remained independently associated with HRR. HS was additive to obesity markers in predicting exercise HRR. CONCLUSIONS: Non-alcoholic HS is independently associated with hyper-reactive exercise blood pressure response.

Cardiovascular disease prevention: matching evidence-based algorithms with individualized care.

The appropriate use of statins in primary prevention remains a matter of debate. Although statins reduce cardiovascular events at all levels of baseline risk, they are associated with rare but important side effects including incident diabetes. Herein, we review strategies for statin allocation ranging from strict "evidence-based" adherence to randomized controlled clinical trial (RCT) entry criteria to more "personalized" risk assessment using high-sensitivity C-reactive protein (hsCRP), coronary artery calcification (CAC), or genetic testing. Current guidelines advocate an unusual middle ground between an evidence-based approach and a personalized approach.

In vivo demonstration that parathyroid hormone and parathyroid hormone-related protein stimulate expression by osteoblasts of interleukin-6 and leukemia inhibitory factor.

We have previously reported that parathyroid hormone (PTH) and PTH related protein (PTHrP) stimulate expression of interleukin-6 (IL-6) and leukemia inhibitory factor (LIF) in osteoblasts in vitro. In the current study, we have developed a model of hormone injection into the subcutaneous space overlying mouse parietal bones to demonstrate that similar processes occur in osteoblasts in vivo. Specifically, PTH and PTHrP rapidly and transiently induce expression of the mRNAs encoding IL-6 and LIF. The effects are dose-dependent, with a maximal stimulation of approximately 50-fold for each cytokine. Although PTH and PTHrP activate both adenyl cyclase and phospholipase C-dependent signal transduction pathways, stimulation of IL-6 and LIF depends on adenyl cyclase since it is not reproduced by PTH(3-34), a partial agonist that only activates phospholipase C. These results confirm our previous in vitro studies and support the hypothesis that IL-6 and/or LIF are physiologically important mediators of at least some of the actions of PTH and PTHrP.