Effect of a high-fiber diet vs a fiber-supplemented diet on C-reactive protein level.

BACKGROUND: Diets high in fiber are associated with lower levels of inflammatory markers. This study examined the reduction in inflammation from a diet supplemented with fiber compared with a diet naturally high in fiber. METHODS: Randomized crossover intervention trial of 2 diets, a high-fiber (30-g/d) Dietary Approaches to Stop Hypertension (DASH) diet or fiber-supplemented diet (30 g/d), after a baseline (regular) diet period of 3 weeks. There were 35 participants (18 lean normotensive and 17 obese hypertensive individuals) aged 18 to 49 years. RESULTS: The study included 28 women and 7 men; 16 (46%) were black, the remainder white. The mean (SD) fiber intake on baseline diets was 11.9 (0.3) g/d; on the high-fiber DASH diet, 27.7 (0.6) g/d; and on the supplemented diet, 26.3 (0.4) g/d. Overall, the mean C-reactive protein (CRP) level changed from 4.4 to 3.8 mg/L (-13.7%; P = .046) in the high-fiber DASH diet group and to 3.6 mg/L (-18.1%) in the fiber-supplemented diet group (P = .03). However, CRP levels decreased in the 18 lean normotensive participants in either intervention diet group (2.0 mg/L [baseline] vs 1.4 mg/L [high-fiber DASH] vs 1.2 mg/L [supplemented]); P<.05) but did not change significantly (7.1 mg/L [baseline] vs 6.2 mg/L [high-fiber DASH] vs 6.5 mg/L [supplemented]; P>.05) in obese hypertensive participants. Neither age nor race influenced the response of CRP levels to the diets. No evidence of a crossover effect was detected. CONCLUSIONS: The results demonstrate that fiber intake of about 30 g/d) from a diet naturally rich in fiber or from a supplement can reduce levels of CRP. Further research is needed to more clearly elucidate the differential effect seen in lean vs obese individuals and whether modification of dietary fiber may be helpful in modulating inflammation and its consequent cardiovascular consequences.

Platelet and white blood cell counts are elevated in patients with the metabolic syndrome.

Platelet and white blood cell counts are higher among some insulin-resistant patients and may contribute to atherothromboembolic complications. Metabolic syndrome patients are insulin resistant, often hypertensive, and at high cardiovascular disease risk, yet the relationship of platelets to the metabolic syndrome is unknown. Platelet and white blood cell counts were obtained from 135 volunteers who had measurements of blood pressure, fasting triglycerides, high-density lipoprotein cholesterol, and glucose. A body mass index >30 kg/m2 served as a surrogate for increased waist circumference. Subjects were subdivided into three groups by the number of metabolic syndrome criteria, i.e., no metabolic syndrome risk factor (MS-0; n = 40), one or two metabolic syndrome risk factors (MS1-2; n = 61), and three to five metabolic syndrome risk factors (MS3-5; n = 34). Platelet counts were increased significantly from 226+/-8 to 257+/-8 and 276+/-10 (x10(3)/mm3) in the MS-0, MS1-2, and MS3-5 groups, respectively (p < 0.01), after adjustment for age, gender, ethnicity, total cholesterol, and low-density lipoprotein cholesterol. White blood cell counts were also increased across the three groups (5.4+/-0.2, 6.2+/-0.2, and 6.6+/-0.3 [x10(3)/mm3]; p < 0.01) after multivariate adjustment. Compared with patients with zero to two metabolic syndrome risk factors, metabolic syndrome patients have higher platelet and white blood counts, which may serve as markers of a prothrombotic and proinflammatory state and contributors to atherothromboembolic risk.

Angiotensin receptor blockade improves arterial distensibility and reduces exercise-induced pressor responses in obese hypertensive patients with the metabolic syndrome.

Patients with the metabolic syndrome have three or more of five cardiovascular risk factors and increased oxidative stress, arterial stiffness and pressor responses to exercise, which may contribute to their threefold greater risk for coronary heart disease. In addition to lowering basal blood pressure (BP), angiotensin receptor blockers (ARBs) may benefit metabolic syndrome patients by reducing oxidative stress, arterial stiffness, and pressor responses to exercise. Twelve patients, 7 women and 5 men, with the metabolic syndrome (aged 45 +/- 2 years, BP 145 +/- 5/85 +/- 2 mm Hg, waist girth 110 +/- 3 cm, triglycerides 186 +/- 23 mg/dL, HDL cholesterol 44 +/- 2 mg/dL, glucose 99 +/- 3 mg/dL) were studied off medications, while on modest sodium restriction ( approximately 100 mmol/d). Patients were randomized to the ARB losartan or placebo for 3 weeks then crossed over to the complement for 3 weeks. Studies were performed at the end of each phase following an overnight fast. Serum lipids and biomarkers of oxidative stress (F2-isoprostanes, thiobarbituric acid reacting substances) were unchanged by losartan, whereas large artery elasticity at rest, measured with the HDI PulseWave, increased from 13.6 +/- 0.7 on placebo to 16.2 +/- 1.1 mL/mm Hg on losartan, P <.05. Losartan lowered systolic BP pre-exercise from 142 +/- 3 to 131 +/- 3 mm Hg (P <.001) and systolic BP after 6 min of treadmill exercise from 192 +/- 6 to 169 +/- 5 mm Hg (P <.001). Losartan lowered systolic BP (-23 +/- 3 v -11 +/- 2 mm Hg, P <.05) and pulse pressure (-4 +/- 1 v -15 +/- 2 mm Hg, P <.05) more during exercise than rest. Losartan reduces the pressor response to exercise, perhaps by enhancing arterial compliance. In addition to lowering basal BP, angiotensin receptor blockade in patients with metabolic syndrome improves arterial compliance and reduces pressor reactivity to exercise.

Severe mitral annular calcification predicts chronic kidney disease.

BACKGROUND: Mitral annular calcification (MAC) is common in the elderly and is associated with atherosclerosis, sharing many of the same risk factors. It is also frequent among dialysis patients. We hypothesized that in general cardiology patients without kidney failure, MAC, especially when severe, may be a marker for renal dysfunction. METHODS: Forty-one subjects were identified by searching outpatient echocardiogram reports for phrases indicating severe MAC. These were divided into subgroups based on greater or lesser overall intracardiac calcification. The "MAC mobile" subgroup had calcification largely limited to the posterior annulus with normal anterior mitral leaflet mobility. In the "MAC restricted" subgroup, calcification extended to the anterior annulus and limited anterior mitral leaflet mobility. These latter patients also had more severe aortic valve calcification. Seventy-seven controls with minimal or no intracardiac calcification were used for comparison. RESULTS: The total MAC group had worse renal function, measured by creatinine and glomerular filtration rate (GFR), than controls (p<0.001 for both comparisons). Nearly 60% had chronic kidney disease as defined by a GFR<60 ml/min/1.73 m(2) with a relative risk of 1.8 versus controls. GFR was observed to decline in a graded fashion as calcification increased (control versus "MAC mobile" versus "MAC restricted"). Though this trend did not remain statistically significant after controlling for age and gender, GFR was substantially lower in "MAC restricted" versus "MAC mobile" patients (p=0.03). CONCLUSIONS: Severe MAC on echocardiogram points to a strong likelihood of chronic kidney disease. Further study is needed to explore a possible graded relationship between severity of MAC and severity of renal dysfunction.

Therapeutic inertia is an impediment to achieving the Healthy People 2010 blood pressure control goals.

Therapeutic inertia (TI), defined as the providers' failure to increase therapy when treatment goals are unmet, contributes to the high prevalence of uncontrolled hypertension (> or =140/90 mm Hg), but the quantitative impact is unknown. To address this gap, a retrospective cohort study was conducted on 7253 hypertensives that had > or =4 visits and > or =1 elevated blood pressure (BP) in 2003. A 1-year TI score was calculated for each patient as the difference between expected and observed medication change rates with higher scores reflecting greater TI. Antihypertensive therapy was increased on 13.1% of visits with uncontrolled BP. Systolic BP decreased in patients in the lowest quintile of the TI score but increased in those in the highest quintile (-6.8+/-0.5 versus +1.8+/-0.6 mm Hg; P<0.001). Individuals in the lowest TI quintile were &33 times more likely to have their BP controlled at the last visit than those in highest quintile (odds ratio, 32.7; 95% CI, 25.1 to 42.6; P<0.0001). By multivariable analysis, TI accounted for &19% of the variance in BP control. If TI scores were decreased &50%, that is, increasing medication dosages on &30% of visits, BP control would increase from the observed 45.1% to a projected 65.9% in 1 year. This study confirms the high rate of TI in uncontrolled hypertensive subjects. TI has a major impact on BP control in hypertensive subjects receiving regular care. Reducing TI is critical in attaining the Healthy People 2010 goal of controlling hypertension in 50% of all patients.