Association of suboptimal blood pressure control with body size and metabolic abnormalities.

BACKGROUND: Blood pressure control is disappointingly suboptimal in populations. Whether metabolic abnormalities influence blood pressure control is unclear. We evaluated the relationship between metabolic risk factors and blood pressure control in a large population of patients with hypertension. METHODS: From our Hypertension Centre, 4551 subjects (43.4% women; age 51 +/- 12 years) were selected with available data for metabolic and cardiovascular evaluation (no prevalent cardiovascular disease), at the last control visit. A modified Adult Treatment Panel III definition of metabolic syndrome was adopted changing waist girth for body mass index (>or= 30 kg/m2). Blood pressure was considered controlled when supine office blood pressure was below 140/90 mmHg, or uncontrolled if this target was not achieved. Blood pressure control has been evaluated in relation to metabolic risk factors, adjusting for age, sex, and the number of antihypertensive medications. RESULTS: The metabolic syndrome phenotype was found in 1444 individuals (31.72%). The probability of uncontrolled blood pressure was 43% higher in patients with the metabolic syndrome than in those without, independently of covariates. This probability was also confirmed in 728 untreated patients. The probability of uncontrolled blood pressure significantly and independently increased with the increasing number of metabolic risk factors. Uncontrolled blood pressure was also independently associated with the prescription of more medications. CONCLUSION: Insufficient control of blood pressure is independently associated with the presence of the metabolic syndrome. Blood pressure control worsens with the increasing number of metabolic risk factors associated with hypertension, despite the use of a greater number of medications.

[Usefulness of a telematic system and image analysis in the follow-up of high-risk patients: a new health service model]. / L'approccio telematico nella riduzione del rischio cardiovascolare: un nuovo modello organizzativo assistenziale.

BACKGROUND: Inadequate blood pressure control in hypertensive patients is in contrast with the evidence from clinical studies of effectiveness of the same antihypertensive compounds used in clinical practice. These results may be due to follow-up management of hypertensive patients and in particular to the interaction between general practitioners (GPs) and hypertension specialists. The aim of this study was to assess the effectiveness of an internet-based digital network, connecting specialists and GPs in the Campania Region, on blood pressure control and major cardiovascular events. METHODS: A network between the Hypertension Center of "Federico II" University, 14 specialist centers and 60 GPs was done in the Campania Region (Campania Salute Project, CS). Randomized GPs enrolled in CS could update online clinic records of patients (n = 1979). As a control group, we included 2045 patients referred to the specialist centers by GPs from outside the network. All patients completed a 2-year follow-up. RESULTS: CS determined a significant reduction in systolic and diastolic blood pressure (CS group 144 +/- 18/91 +/- 11 vs 136 +/- 17/86 +/- 10 mmHg; control group 144 +/- 17/90 +/- 10 vs 139 +/- 15/87 +/- 9 mmHg, p < 0.001). Indeed, the CS group showed less frequent fatal and non-fatal major cardiovascular events (2.9 vs 4.3%, chi2 = 5.047, p < 0.02). CONCLUSIONS: Our results support the hypothesis that telematic connections may contribute to improve blood pressure control and reduce major cardiovascular events.

The use of a telematic connection for the follow-up of hypertensive patients improves the cardiovascular prognosis.

BACKGROUND: Inadequate blood pressure (BP) control could be due to incorrect management of hypertensives caused by the lack of interaction between general practitioners (GP) and hypertension specialists. OBJECTIVES: To test the effectiveness on BP and total cardiovascular risk (TCVR) control of an internet-based digital network connecting specialists and GPs. METHODS: We created a network among the Hypertension Clinic, Federico II University (Naples, Italy), 23 hospital-based hypertension clinics and 60 GPs from the area (CampaniaSalute Network, CS). Randomized GPs enrolled in CS could update online records of patients (n = 1979). As a control, we included 2045 patients referred to the specialist clinics by GPs from outside the network. All patients completed a 2-year follow-up. RESULTS: CS provided a larger reduction in BP [systolic/diastolic BP (SBP/DBP): 7.3 +/- 0.4/5.4 +/- 0.3 versus 4.1 +/- 0.4/3.1 +/- 0.26 mmHg, CS versus control; P < 0.001 for both] and percentage of patients with BP < 140/90 mmHg (CS versus control: baseline, 33 versus 34%, NS; end of follow-up, 51 versus 47%, chi = 13.371; P < 0.001). A European Society of Hypertension-European Society of Cardiology (ESH/ESC) TCVR score was calculated [from 1 (average) to 5 (very high TCVR)]. The CS group showed a reduction in the mean TCVR score (CS: from 3.5 +/- 0.02 to 3.2 +/- 0, P < 0.01, ANOVA; control group: 3.5 +/- 0.03 to 3.4 +/- 0.03, NS) and, accordingly, fatal and non-fatal major cardiovascular events (MACE) were less frequent (2.9 versus 4.3%; chi = 5.047, P < 0.02). CS predicts fewer MACE in multiple binary regression analysis (beta:-7.27, P < 0.008) reducing the risk for MACE compared to control [odds ratio (OR): 0.838; 95% confidence interval (CI): 0.73-0.96]. CONCLUSION: Our results support the idea that telemedicine can achieve better control of BP and TCVR.

AKT participates in endothelial dysfunction in hypertension.

BACKGROUND: In hypertension, reduced nitric oxide production and blunted endothelial vasorelaxation are observed. It was recently reported that AKT phosphorylates and activates endothelial nitric oxide synthase and that impaired kinase activity may be involved in endothelial dysfunction. METHODS AND RESULTS: To identify the physiological role of the kinase in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), we used adenoviral vectors to transfer the human AKT1 gene selectively to the common carotid endothelium. In vitro, endothelial vasorelaxations to acetylcholine, isoproterenol, and insulin were blunted in control carotids from SHR compared with WKY rats, and human AKT1 overexpression corrected these responses. Similarly, blood flow assessed in vivo by Doppler ultrasound was reduced in SHR compared with WKY carotids and normalized after AKT1 gene transfer. In primary cultured endothelial cells, we evaluated AKT phosphorylation, activity, and compartmentalization and observed a mislocalization of the kinase in SHR. CONCLUSIONS: We conclude that AKT participates in the settings of endothelial dysfunction in SHR rats by impaired membrane localization. Our data suggest that AKT is involved in endothelium dysfunction in hypertension.

Physical training increases eNOS vascular expression and activity and reduces restenosis after balloon angioplasty or arterial stenting in rats.

The effects of dynamic exercise on restenosis after vascular injury are still unknown. The consequences of balloon dilation-induced injury on neointimal hyperplasia, vascular negative remodeling, and reendothelialization were assessed in sedentary and trained rats. Ex vivo eNOS vascular expression and activity were investigated in carotid arteries isolated from sedentary and exercised rats. The in vivo effects of eNOS inhibition by L-NMMA on vessel wall after balloon dilation were evaluated in sedentary and exercised rats. We also investigated the effects of exercise on neointimal formation in a rat stent model of vascular injury. Compared with sedentary group, the arteries isolated from trained rats showed higher levels of eNOS protein expression and activity 7 days after balloon dilation. A significant reduction of both neointimal hyperplasia and negative remodeling was observed 14 days after balloon injury in trained compared with sedentary rats. Moreover, we demonstrated that exercise training produced accelerated reendothelialization of the balloon injured arterial segments compared with sedentary. L-NMMA administration eliminated the benefits of physical training on vessel wall after balloon dilation. Finally, a decrease of neointimal hyperplasia as well as of platelet aggregation was observed after stent deployment in trained rats compared with sedentary. In conclusion, physical exercise could favorably affect restenosis after balloon angioplasty and stenting. Increase in eNOS expression and activity might contribute to the potential beneficial effects of exercise on the vessel wall after vascular injury.

Hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin prevents cardiac hypertrophy induced by pressure overload and inhibits p21ras activation.

BACKGROUND: Patients with cardiac hypertrophy are at increased cardiovascular risk. It has been hypothesized that hydroxymethylglutaryl coenzyme A reductase inhibitors may exert beneficial effects other than their cholesterol-lowering actions. The aims of the study were to assess the in vivo effects of simvastatin (SIM) on cardiac hypertrophy and on Ras signaling in rats with ascending aorta banding. METHODS AND RESULTS: Wistar rats were randomized to receive either treatment with SIM or placebo, and then short-term (group I) and long-term (group II) left ventricular pressure overload was performed by placing a tantalum clip on ascending aorta. At the end of treatment period, left and right ventricular weight, body weight, and tibial length were measured and echocardiographic evaluations were performed. Ras signaling was investigated by analyzing Ras membrane localization and activation, ERK2 phosphorylation, and p27(kip1) and cdk4 levels. In SIM-treated rats, a significant reduction of left ventricular weight/body weight, echocardiographic left ventricular mass, and left ventricular end-diastolic diameter and end-diastolic pressure was found. In rats with pressure overload, SIM treatment significantly reduced Ras membrane targeting, Ras in vivo activation, ERK2 phosphorylation, and the ratio cdk4/p27(kip1). CONCLUSIONS: HMG CoA inhibitor SIM inhibits in vivo Ras signaling and prevents left ventricular hypertrophy development in aortic-banded animals.

Rat carotid artery dilation by PTCA balloon catheter induces neointima formation in presence of IEL rupture.

The best animal angioplasty model is the porcine model, which is expensive and not available in all laboratories. The aim of this study was to describe a new rat model of angioplasty. An injury was induced with the use of a standard percutaneous transluminal coronary angioplasty (PTCA) 1.5-mm balloon catheter. The neointimal tissue, arterial dimensions, and the injury index were assessed following angioplasty. Ki-67 expression was detected to evaluate cell turnover after balloon angioplasty. In contrast with the standard Clowes model, a significant neointimal formation was detected only in the presence of ruptured internal elastic lamina (IEL). A positive correlation between the percentage of ruptured IEL and the amount of neointimal tissue was also demonstrated. The percentage of IEL fracture correlates with the proliferation index by anti-Ki-67 immunolabeling 7 and 14 days after the angioplasty. Significant arterial negative remodeling was observed following PTCA balloon dilation. In conclusion, our inexpensive animal model of restenosis after angioplasty may have great relevance toward a better understanding of the mechanisms and toward assessment of new therapeutical strategies for this phenomenon.