The Mediterranean diet and incidence of hypertension: the Seguimiento Universidad de Navarra (SUN) Study

The Mediterranean diet is receiving increasing attention in cardiovascular epidemiology. The association of adherence to the Mediterranean diet with the incidence of hypertension was evaluated among 9,408 men and women enrolled in a dynamic Spanish prospective cohort study during 1999–2005. Dietary intake was assessed at baseline with a validated semiquantitative food frequency questionnaire, and a 9-point Mediterranean diet score was constructed. During a median follow-up period of 4.2 years (range, 1.9–7.9), 501 incident cases of hypertension were identified. After adjustment for major hypertension risk factors and nutritional covariates, adherence to the Mediterranean diet was not associated with hypertension (the hazard ratio was 1.10 (95% confidence interval (CI): 0.81, 1.41) for moderate adherence and 1.12 (95% CI: 0.79, 1.60) for high adherence). However, it was associated with reduced changes in mean levels of systolic blood pressure (moderate adherence, 2.4 mm Hg (95% CI: 4.0, 0.8); high adherence, 3.1 mm Hg (95% CI: 5.4, 0.8)) and diastolic blood pressure (moderate adherence, 1.3 mm Hg (95% CI: 2.5, 0.1); high adherence, 1.9 mm Hg (95% CI: 3.6, 0.1)) after 6 years of follow-up. These results suggest that adhering to a Mediterranean-type diet could contribute to the prevention of age-related changes in blood pressure

The Mediterranean diet and incidence of hypertension: the Seguimiento Universidad de Navarra (SUN) Study

The Mediterranean diet is receiving increasing attention in cardiovascular epidemiology. The association of adherence to the Mediterranean diet with the incidence of hypertension was evaluated among 9,408 men and women enrolled in a dynamic Spanish prospective cohort study during 1999–2005. Dietary intake was assessed at baseline with a validated semiquantitative food frequency questionnaire, and a 9-point Mediterranean diet score was constructed. During a median follow-up period of 4.2 years (range, 1.9–7.9), 501 incident cases of hypertension were identified. After adjustment for major hypertension risk factors and nutritional covariates, adherence to the Mediterranean diet was not associated with hypertension (the hazard ratio was 1.10 (95% confidence interval (CI): 0.81, 1.41) for moderate adherence and 1.12 (95% CI: 0.79, 1.60) for high adherence). However, it was associated with reduced changes in mean levels of systolic blood pressure (moderate adherence, 2.4 mm Hg (95% CI: 4.0, 0.8); high adherence, 3.1 mm Hg (95% CI: 5.4, 0.8)) and diastolic blood pressure (moderate adherence, 1.3 mm Hg (95% CI: 2.5, 0.1); high adherence, 1.9 mm Hg (95% CI: 3.6, 0.1)) after 6 years of follow-up. These results suggest that adhering to a Mediterranean-type diet could contribute to the prevention of age-related changes in blood pressure

Role of lysyl oxidase in myocardial fibrosis: from basic science to clinical aspects

Because of its dynamic nature, the composition and structure of the myocardial collagen network can be reversibly modified to adapt to transient cardiac injuries. In response to persistent injury, however, irreversible, maladaptive changes of the network occur leading to fibrosis, mostly characterized by the excessive interstitial and perivascular deposition of collagen types I and III fibers. It is now becoming apparent that myocardial fibrosis directly contributes to adverse myocardial remodeling and the resulting alterations of left ventricular (LV) anatomy and function present in the major types of cardiac diseases. The enzyme lysyl oxidase (LOX) is a copper-dependent extracellular enzyme that catalyzes lysine-derived cross-links in collagen and elastin. LOX-mediated cross-linking of collagen types I and III fibrils leads to the formation of stiff collagen types I and III fibers and their subsequent tissue deposition. Evidence from experimental and clinical studies shows that the excess of LOX is associated with an increased collagen cross-linking and stiffness. It is thus conceivable that LOX upregulation and/or overactivity could underlie myocardial fibrosis and altered LV mechanics and contribute to the compromise of LV function in cardiac diseases. This review will consider the molecular aspects related to the regulation and actions of LOX, namely, in the context of collagen synthesis. In addition, it will address the information related to the role of myocardial LOX in heart failure and the potential benefits of controlling its expression and function

Role of lysyl oxidase in myocardial fibrosis: from basic science to clinical aspects

Because of its dynamic nature, the composition and structure of the myocardial collagen network can be reversibly modified to adapt to transient cardiac injuries. In response to persistent injury, however, irreversible, maladaptive changes of the network occur leading to fibrosis, mostly characterized by the excessive interstitial and perivascular deposition of collagen types I and III fibers. It is now becoming apparent that myocardial fibrosis directly contributes to adverse myocardial remodeling and the resulting alterations of left ventricular (LV) anatomy and function present in the major types of cardiac diseases. The enzyme lysyl oxidase (LOX) is a copper-dependent extracellular enzyme that catalyzes lysine-derived cross-links in collagen and elastin. LOX-mediated cross-linking of collagen types I and III fibrils leads to the formation of stiff collagen types I and III fibers and their subsequent tissue deposition. Evidence from experimental and clinical studies shows that the excess of LOX is associated with an increased collagen cross-linking and stiffness. It is thus conceivable that LOX upregulation and/or overactivity could underlie myocardial fibrosis and altered LV mechanics and contribute to the compromise of LV function in cardiac diseases. This review will consider the molecular aspects related to the regulation and actions of LOX, namely, in the context of collagen synthesis. In addition, it will address the information related to the role of myocardial LOX in heart failure and the potential benefits of controlling its expression and function

Association of the peroxisome proliferator-activated receptor α gene L162V polymorphism with stage C heart failure

OBJECTIVE: To analyze whether genetic variants of PPARA are associated with the development of stage C heart failure. METHODS: We analyzed the distribution of the rs1800206, rs4253778 and rs135551 polymorphisms in genomic DNA extracted from peripheral blood cells of 534 patients in different heart failure stages and 63 healthy individuals. The mRNA expression of the peroxisome proliferator-activated receptor (PPAR)α target genes long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and medium-chain acyl-CoA dehydrogenase (MCAD) was measured in myocardial biopsies of a subgroup of stage B and C patients. Functional studies were performed in HL-1 cardiomyocytes. RESULTS: The V162 allele of the rs1800206 polymorphism was more frequent in stage C patients than in stage A and B patients and healthy individuals. Patients with the V162 allele exhibited decreased myocardial LCHAD and MCAD mRNA expression as compared to L162 homozygote patients. In addition, stage C patients exhibited lower myocardial LCHAD and MCAD mRNA expression than stage B patients. Cardiomyocytes transfected with the V162 allele presented decreased PPARα transcriptional activity, LCHAD mRNA expression and ATP production compared to cardiomyocytes transfected with the L162 variant. CONCLUSIONS: These findings suggest that the V162 allele of the human PPARA gene can be a new risk factor in the development of stage C heart failure, likely via depressed cardiac PPARα activit

Association of the peroxisome proliferator-activated receptor α gene L162V polymorphism with stage C heart failure

OBJECTIVE: To analyze whether genetic variants of PPARA are associated with the development of stage C heart failure. METHODS: We analyzed the distribution of the rs1800206, rs4253778 and rs135551 polymorphisms in genomic DNA extracted from peripheral blood cells of 534 patients in different heart failure stages and 63 healthy individuals. The mRNA expression of the peroxisome proliferator-activated receptor (PPAR)α target genes long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and medium-chain acyl-CoA dehydrogenase (MCAD) was measured in myocardial biopsies of a subgroup of stage B and C patients. Functional studies were performed in HL-1 cardiomyocytes. RESULTS: The V162 allele of the rs1800206 polymorphism was more frequent in stage C patients than in stage A and B patients and healthy individuals. Patients with the V162 allele exhibited decreased myocardial LCHAD and MCAD mRNA expression as compared to L162 homozygote patients. In addition, stage C patients exhibited lower myocardial LCHAD and MCAD mRNA expression than stage B patients. Cardiomyocytes transfected with the V162 allele presented decreased PPARα transcriptional activity, LCHAD mRNA expression and ATP production compared to cardiomyocytes transfected with the L162 variant. CONCLUSIONS: These findings suggest that the V162 allele of the human PPARA gene can be a new risk factor in the development of stage C heart failure, likely via depressed cardiac PPARα activit