Association between different lipid-lowering treatment strategies and blood pressure control in the Brisighella Heart Study

Borghi, Claudio; Dormi, Ada; Veronesi, Maddalena; Sangiorgi, Z.; Gaddi, Antonio Vittorino

doi:10.1016/j.ahj.2004.02.003

Cited by 94 publications

(67 citation statements)

References 27 publications

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“…The investigators demonstrated a significant decrease in BP in the upper 2 quartiles of SBP (Ն140 mm Hg) over a 5-year period and showed that this decrease was greater in subjects treated with cholesterol-lowering medication and greatest for those treated with a statin. 12 In another study, there was no decrease in BP among normotensive subjects. 22 Glorioso et al 23 conducted a trial of pravastatin in 30 hypertensive, hypercholesterolemic subjects and demonstrated that, compared with placebo, treatment with pravastatin significantly decreased systolic, diastolic, and pulse pressures and blunted the BP increase induced by the cold pressor test.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 Small trials have looked at the effect of lipid lowering on BP. 11,12 Additional prospective data on the association of lipids with hypertension will help us clarify the relationship.We, therefore, prospectively examined whether total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and non-high density lipoprotein cholesterol (non-HDL-C) are associated with the risk of developing hypertension in men initially free of hypertension. …”

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Dyslipidemia and the Risk of Incident Hypertension in Men

Halperin

Sesso²,

Ma³

et al. 2006

Hypertension

286

190

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Abstract-Evidence suggests that hypertension may share a similar pathophysiology with cardiovascular disease (CVD).Thus, dyslipidemia, a strong predictor of CVD, may also predict incident hypertension. We analyzed 3110 men free of hypertension, CVD, and cancer from the Physicians' Health Study, who provided baseline blood samples from which we measured total cholesterol (TC) and HDL cholesterol (HDL-C), and calculated non-HDL-C and the TC/HDL-C ratio. We categorized each lipid parameter into quintiles and considered National Cholesterol Education Project clinical cut points. Other risk factor information was provided from self-reports on the baseline questionnaire. Incident hypertension was defined as either the initiation of antihypertensive treatment, self-reported systolic blood pressure Ն140 mm Hg, or diastolic blood pressure Ն90 mm Hg. Over a mean follow-up of 14.1 years, 1019 men developed hypertension. In Cox proportional hazards models adjusted for lifestyle and clinical risk factors, men in the highest quintile of TC, non-HDL-C, and TC/HDL-C ratio had increased risks of developing hypertension of 23%, 39%, and 54%, respectively, compared with participants in the lowest quintile. Furthermore, men in the highest quintile of HDL-C had a 32% decreased risk of developing hypertension compared with those in the lowest quintile. Models using National Cholesterol Education Project cut points demonstrated similar associations with hypertension. Models excluding men with diabetes and obesity maintained an independent association between baseline lipids and hypertension. These prospective cohort data suggest that dyslipidemias may lead to the subsequent development of hypertension. Thus, plasma lipids may be useful in the identification of men at risk for hypertension. Key Words: cholesterol Ⅲ lipids Ⅲ hypertension Ⅲ blood pressure Ⅲ men Ⅲ prospective studies H ypertension is a common condition that affects Ͼ50 million Americans 1 and is an important risk factor for cardiovascular disease. Although several risk factors for the development of hypertension have been identified, 2 its etiology is still not fully understood. 1 Hypertension is commonly associated with other cardiovascular risk factors, such as obesity, diabetes, and dyslipidemia. 3 The presence of these cardiovascular risk factors and the resulting endothelial dysfunction may play a role in the pathophysiology of hypertension. 4 Dyslipidemia, a strong predictor of cardiovascular disease, 5 causes endothelial damage, 6 -8 and the loss of physiological vasomotor activity that results from endothelial damage may become manifested as increased blood pressure (BP). Therefore, factors like dyslipidemia that cause endothelial dysfunction may lead to hypertension. Cross-sectional studies have suggested a link between abnormal lipids and hypertension. 4,9,10 A few studies have prospectively examined the relationship between plasma lipids and the future development of hypertension, finding that there is an association between plasma lipids and development of hyp...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Dyslipidemia and the Risk of Incident Hypertension in Men

Halperin

Sesso²,

Ma³

et al. 2006

Hypertension

286

190

View full text Add to dashboard Cite

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“…In fact, much evidence has shown the pleiotropic effects of statins in improving or restoring endothelial function, enhancing the stability of atherosclerotic plaques, and decreasing oxidative stress and vascular inflammation (38). Recent data from the Brisighella Heart Study demonstrated that the use of lipid-lowering measures could significantly improve BP control in patients with both hypercholesterolemia and hypertension, enhancing the reduction in BP in patients who are treated with statins (39). Patients who present with CKD experience higher mortality and adverse CV event rates, which remains significant after adjustment for conventional CVRF (40).…”

Section: Treatment Of Patients With Ckdmentioning

confidence: 99%

Chronic Kidney Disease as a Situation of High Added Risk in Hypertensive Patients

Segura¹,

García-Donaire²,

Praga³

et al. 2006

Journal of the American Society of Nephrology

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Recent guidelines for the management of hypertension have recognized the relevance of renal function on cardiovascular prognosis of hypertensive patients. In fact, growing evidences have confirmed that as soon as renal function exhibits minor derangements, cardiovascular risk starts a continuous rise until the development of end-stage renal disease. Both estimated glomerular filtration rate and urinary albumin excretion are associated with an increased incidence of cardiovascular events and death among hypertensive patients and in general population. Consequently, hypertensive patients presenting with chronic kidney disease are considered by guidelines as high-risk patients, and strict blood pressure control should be considered as a part of an integrative therapeutic approach, including correction of anemia, treatment of dyslipidemia, cessation of tobacco use, and antiplatelet therapy. This paper briefly reviews the most recent evidences about pharmacologic therapies in high-risk patients, focusing on benefits related to improvement of cardiovascular risk factors in hypertensive patients with chronic kidney disease.

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“…11,12 Several previous experimental and retrospective studies suggest that statins reduce blood pressure in animals and humans with and without hypertension. [13][14][15][16] However, randomized trials have reached conflicting results. 17,18 We analysed blood pressure data from a previously conducted randomized trial, which examined the cardiovascular benefits of pravastatin 40 mg daily compared with placebo.…”

Section: Introductionmentioning

confidence: 99%

Effect of pravastatin on blood pressure in people with cardiovascular disease

et al. 2006

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Experimental evidence and several small studies in humans suggest that HMG-CoA (3-hydroxy 3-methylglutaryl coenzyme A) reductase inhibitors (statins) reduce blood pressure, perhaps through effects on endothelial function or by reducing inflammation. We tested the hypothesis that pravastatin would reduce blood pressure at 3 months and the risk of developing new hypertension over a follow-up period of 5 years. This was a post hoc subgroup analysis of a randomized double-blind placebo-controlled trial of pravastatin 40 mg daily vs placebo in 4159 participants with previous myocardial infarction and total plasma cholesterol o240 mg/dl (6.2 mmol/l). The primary outcome was the unadjusted change in mean arterial pressure (MAP) from baseline to 3 months. We also considered systolic and diastolic blood pressure (SBP and DBP) and pulse pressure. Analysis of covariance was used to calculate the adjusted effect of treatment on change in these outcomes at 3, 6, 12 and 24 months postrandomization, after controlling for potential confounders. Logistic regression was used to calculate the adjusted effect of treatment on incident hypertension (blood pressure X140/90 in those without known hypertension at baseline). This analysis included 4126/4159 (99.2%) participants for whom blood pressure was measured at baseline and during at least one follow-up visit. Median duration of follow-up was 57.8 months. The unadjusted and adjusted change in MAP, SBP, DBP or pulse pressure from baseline was not significantly different for pravastatin or placebo recipients at 3, 6, 12 or 24 months after randomization, or at last follow-up. Pravastatin did not reduce the adjusted risk of incident systolic hypertension (odds ratio 0.99, 95% CI 0.80-1.23), or incident diastolic hypertension (odds ratio 0.97, 95% CI 0.73-1.27). In summary, pravastatin 40 mg daily did not reduce blood pressure in survivors of myocardial infarction without overt hypercholesterolaemia.

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Association between different lipid-lowering treatment strategies and blood pressure control in the Brisighella Heart Study

Cited by 94 publications

References 27 publications

Dyslipidemia and the Risk of Incident Hypertension in Men

Dyslipidemia and the Risk of Incident Hypertension in Men

Chronic Kidney Disease as a Situation of High Added Risk in Hypertensive Patients

Effect of pravastatin on blood pressure in people with cardiovascular disease

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