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 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Knowledge of predictors of diabetes mellitus (DM) development in patients with coronary artery disease (CAD) who use antihypertensive therapy could contribute to decreasing this adverse metabolic consequence. This is particularly relevant because the standard of care, beta blockers combined with diuretics, may contribute to adverse metabolic risk. The INternational VErapamil SR-trandolapril STudy compared a calcium antagonist-based (verapamil SR) and a beta-blocker-based (atenolol) strategy with trandolapril and/or hydrochlorothiazide added to control blood pressure (BP) in patients with CAD. The 16,176 patients without DM at entry were investigated with regard to newly diagnosed DM during follow-up. Newly diagnosed DM was less frequent in the verapamil SR versus atenolol strategy (7.0% vs 8.2%, hazard ratio 0.85, 95% confidence interval 0.76 to 0.95, p <0.01). Characteristics associated with risk for newly diagnosed DM included United States residence, left ventricular hypertrophy, previous stroke/transient ischemic attack, Hispanic ethnicity, coronary revascularization, hypercholesterolemia, greater body mass index, and higher follow-up systolic BP. Addition of trandolapril to verapamil SR decreased DM risk and addition of hydrochlorothiazide to atenolol increased risk. In conclusion, clinical findings associated with more severe vascular disease and Hispanic ethnicity identify a group at high risk for developing DM, whereas lower on-treatment BP and treatment with verapamil SR-trandolapril attenuated this risk.
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PMID:Predictors of development of diabetes mellitus in patients with coronary artery disease taking antihypertensive medications (findings from the INternational VErapamil SR-Trandolapril STudy [INVEST]). 1699 68

The objective of the present study was to assess the risk factors for stroke in patients undergoing coronary artery bypass grafting (CABG) surgery. We conducted a nested case-control study from a 9-year, prospective hospitalization cohort (n = 6245). Inclusion in the cohort included CABG between October 1993 and June 2002. Exclusion criteria included any other simultaneously performed surgery. Cases were defined as patients who underwent CABG and experienced a stroke (171 cases, 2.7% of the total), and controls were patients who underwent CABG without a stroke. Cases were matched to controls at a ratio of 1:3 (513 controls). The 39 predictor variables were pump time, body surface area, creatinine, previous percutaneous transcoronary angioplasty (PTCA), clamp time, coronary perfusion time, previous cardiac surgeries, hypertension, race, sex, previous myocardial infarction, family history of coronary disease, history of cerebrovascular disease, preoperative neurologic disease, pulmonary hypertension, aortic disease, previous intervention within 30 days, angina history, bleeding history, previous vascular surgery, diabetes, age, myocardial findings, chronic obstructive pulmonary disease, New York Heart Association class, previous gastrointestinal disease, current vascular disease, systemic diseases, vessels at last PTCA, PTCA result, current smoking, tobacco history, dialysis, current anticoagulant therapy, character of operation, left ventricular hypertrophy, hypercholesterolemia, and chronic corticosteroid therapy. There were 13 significant predictors of stroke. Regression analysis revealed 3 independent predictors of stroke: age >70 years (odds ratio [OR], 4.61; 95% confidence interval [CI], 2.84-6.07), poor preoperative neurologic status (OR, 4.24; 95% CI, 2.02-5.79), and previous cardiac surgery (OR, 1.75; 95% CI, 1.05-2.91). We conclude that in patients undergoing CABG surgery, the independent predictors for stroke, in order of risk, are age >70 years, poor preoperative neurologic status, and previous cardiac surgery.
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PMID:Predictors of stroke in patients undergoing coronary artery bypass grafting surgery: a prospective, nested, case-control study. 1790 72

Late nephrology referral of patients with chronic kidney disease (CKD) has been suggested as increasing mortality after the initiation of dialysis. The aim of this study was to assess the impact of nephrology referral on the initiation of haemodyalisis (HD) and mortality during HD treatment in end-stage renal disease (ESRD) patients who have died in our institution over a five-year period. We studied data from all 117 patients on HD treatment in our institution who died (after 90 days of HD treatment) in the period between 01.01. 2002 and 31.12. 2006. Early (ER) and late referral (LR) were defined by the time of follow-up by a nephrologist greater than or less than 6 months, respectively, before the initiation of haemodialysis. Out of a total of 117 patients, 37.6% (44 patients) started HD in the ER group and 62.4% (73 patients) in the LR group. At the start of HD, LR patients were older, had a higher proportion of temporary catheters and had a significantly lower levels of haemoglobin and diuresis. Creatinine clearance was less in the LR (7.67 +/- 3.86 ml/min/1.73 m2) vs. the ER group (8.70 +/- 3.62 ml/min/1.73 m2), but not significantly different. Cardiovascular disease (CVD), defined by a history of myocardial infarction, cerebral vascular disease, peripheral arteriopathy, and/or heart failure, was also significantly more common among LR patients compared to ER (56%; 27%, p = 0.002). During the haemodyalisis treatment, the LR group had significantly lower levels of haemoglobin and haematocrit. CVD accounted for about 64% of deaths observed in the LR group. According to echocardiography data, there were no significant differences in the left ventricular mass index (LVMI) between the LR and ER groups at the time of dialysis initiation, but during haemodialysis treatment the LR group had significantly greater LVMI than the ER group (232,96 +/- 92,48 g/m2 vs.184,09 +/- 51,74 g/m2; p = 0,031). The time until death in months during dialysis treatment was significantly different between the LR and ER group, (69.51 +/- 64.03 vs.113.27 +/- 89.03, p = 0.0025). LR patients experienced a greater degree of anaemia and a high prevalence of CVD at the time of dialysis initiation. Our data suggest that the anaemia, CV damage and progression of left ventricular hypertrophy (LVH) in the LR patients during haemodialysis treatment are associated with poor survival on haemodialysis.
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PMID:Effect of nephrology referral on the initiation of haemodyalisis and mortality in ESRD patients. 1835 83

Diastolic dysfunction is frequent in elderly subjects and in patients with left ventricular hypertrophy, vascular disease and diabetes mellitus. Patients with diastolic dysfunction demonstrate a reduced exercise capacity and might suffer from congestive heart failure (CHF). Presence of symptoms of CHF in the setting of a normal systolic function is referred to as heart failure with normal ejection fraction (HFNEF) or, if evidence of an impaired diastolic function is observed, as diastolic heart failure (DHF). Reduced exercise capacity in diastolic dysfunction results from a number of pathophysiological alterations such as slowed myocardial relaxation, reduced myocardial distensibility, elevated filling pressures, and reduced ventricular suction forces. These alterations limit the increase of ventricular diastolic filling and cardiac output during exercise and lead to pulmonary congestion. In healthy subjects, exercise training can enhance diastolic function and exercise capacity and prevent deterioration of diastolic function in the course of aging. In patients with diastolic dysfunction, exercise capacity can be enhanced by exercise training and pharmacological treatment, whereas improvement of diastolic function can only be observed in few patients.
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PMID:Diastolic dysfunction in exercise and its role for exercise capacity. 1875 43

Inflammatory cytokine interleukin (IL)-6 is elevated in the serum and lungs of patients with pulmonary artery hypertension (PAH). Several animal models of PAH cite the potential role of inflammatory mediators. We investigated role of IL-6 in the pathogenesis of pulmonary vascular disease. Indices of pulmonary vascular remodeling were measured in lung-specific IL-6-overexpressing transgenic mice (Tg(+)) and compared to wild-type (Tg(-)) controls in both normoxic and chronic hypoxic conditions. The Tg(+) mice exhibited elevated right ventricular systolic pressures and right ventricular hypertrophy with corresponding pulmonary vasculopathic changes, all of which were exacerbated by chronic hypoxia. IL-6 overexpression increased muscularization of the proximal arterial tree, and hypoxia enhanced this effect. It also reproduced the muscularization and proliferative arteriopathy seen in the distal arteriolar vessels of PAH patients. The latter was characterized by the formation of occlusive neointimal angioproliferative lesions that worsened with hypoxia and were composed of endothelial cells and T-lymphocytes. IL-6-induced arteriopathic changes were accompanied by activation of proangiogenic factor, vascular endothelial growth factor, the proproliferative kinase extracellular signal-regulated kinase, proproliferative transcription factors c-MYC and MAX, and the antiapoptotic proteins survivin and Bcl-2 and downregulation of the growth inhibitor transforming growth factor-beta and proapoptotic kinases JNK and p38. These findings suggest that IL-6 promotes the development and progression of pulmonary vascular remodeling and PAH through proproliferative antiapoptotic mechanisms.
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PMID:Interleukin-6 overexpression induces pulmonary hypertension. 1907 75

Untreated hypertension increases cardiovascular risk 2-fold to 3-fold, leading to serious cardiovascular problems that include left ventricular hypertrophy, stroke, ischemic heart disease, myocardial infarction, vascular disease, renal disease, and death. Exercise conditioning is recommended as one of the initial treatments for hypertension. The purpose of this pretest-posttest study was to quantify the effects of a 12-week home-based low-intensity exercise conditioning (walking) program in hypertensive men and women on systolic and diastolic blood pressure, heart rate, and autonomic modulation of heart rate. A total of 20 mildly hypertensive men and women who were assigned to a structured exercise (walking) program were compared with a control group of 20 nonexercising mildly hypertensive participants. Electrocardiographic heart rate and R-R interval data and beat-by-beat arterial blood pressure data were collected continuously for 10 min with participants in the supine and standing postures and during low-intensity steady-state exercise. The results show that systolic and diastolic blood pressure and R-R interval decreased and spontaneous baroreflex sensitivity increased in the exercise group. The decline in blood pressure was significant statistically and clinically. The increase in spontaneous baroreflex sensitivity indicates that the ability of the cardiovascular system to respond rapidly to changing stimuli improved after the 12-week walking protocol. The low-intensity exercise conditioning program achieved a training effect in this population.
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PMID:Effects of low-intensity exercise conditioning on blood pressure, heart rate, and autonomic modulation of heart rate in men and women with hypertension. 1915 Sep 92

Cardiovascular disease remains the leading cause of death world wide. Although atheroma is clearly important, the role of arteriosclerotic vascular disease is often overlooked. Arteriosclerosis causes increased arterial stiffness, with consequent systolic hypertension and left ventricular hypertrophy. Serum phosphate is increasingly being recognised as a cardiovascular risk factor and has been implicated in the development of arteriosclerosis and arterial calcification. Its determinants are unclear, but both diet and minor reductions in renal function may be important. Diets in affluent populations are high in phosphate because of increased consumption of animal protein and the use of phosphate-containing preservatives. This viewpoint suggests that the consumption of a phosphate-rich diet, exacerbated by the high prevalence of chronic kidney disease found in ageing populations, accelerates the development of arteriosclerosis. It is hypothesised that reducing phosphate intake will attenuate the progression of arterial stiffness with major beneficial effects upon cardiovascular mortality and morbidity.
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PMID:Is lowering phosphate exposure the key to preventing arterial stiffening with age? 1932 94

Recent advances in our understanding of the excess mortality of chronic kidney disease (CKD) due to cardiovascular complications, obtained through observational studies, demonstrate that vascular calcification and hyperphosphatemia are major cardiovascular risk factors. Mechanistic studies demonstrate that these two risk factors are related and that hyperphosphatemia directly stimulates vascular calcification. The role of hyperphosphatemia in stimulating vascular calcification in CKD is associated with a block to the skeletal reservoir function in phosphate balance due to excess bone resorption. This has led to the realization that renal osteodystrophy is linked to vascular calcification by disordered mineral homeostasis (phosphate) and that a multiorgan system fails in CKD, leading to cardiovascular mortality. In children with renal disease, the multiorgan system fails, just as in adults, but the outcomes have been less well studied, and perceptions of differences from adults are possibly incorrect. Vascular calcification and cardiovascular mortality are less prevalent among pediatric patients, but they are present. However, CKD-induced vascular disease causes stiffness of the arterial tree causing, in turn, systolic hypertension and left ventricular hypertrophy as early manifestations of the same pathology in the adult. Because of the role of the skeleton in these outcomes, renal osteodystrophy has been renamed as the CKD mineral bone disorder (CKD-MBD). This review, which focuses on the pediatric patient population, describes our current state of knowledge with regards to the pathophysiology of the CKD-MBD, including the new discoveries related to early stages of CKD. As a new necessity, cardiovascular function issues are incorporated into the CKD-MBD, and new advances in our knowledge of this critical component of the disorder will lead to improved outcomes in CKD.
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PMID:Cardiovascular risk in chronic kidney disease (CKD): the CKD-mineral bone disorder (CKD-MBD). 1989 75

Right ventricular hypertrophy (RVH) and RV failure contribute to morbidity and mortality in pulmonary arterial hypertension (PAH). The cause of RV dysfunction and the feasibility of therapeutically targeting the RV are uncertain. We hypothesized that RV dysfunction and electrical remodeling in RVH result, in part, from a glycolytic shift in the myocyte, caused by activation of pyruvate dehydrogenase kinase (PDK). We studied two complementary rat models: RVH + PAH (induced by monocrotaline) and RVH + without PAH (induced by pulmonary artery banding (PAB)). Monocrotaline RVH reduced RV O(2)-consumption and enhanced glycolysis. RV 2-fluoro-2-deoxy-glucose uptake, Glut-1 expression, and pyruvate dehydrogenase phosphorylation increased in monocrotaline RVH. The RV monophasic action potential duration and QT(c) interval were prolonged due to decreased expression of repolarizing voltage-gated K(+) channels (Kv1.5, Kv4.2). In the RV working heart model, the PDK inhibitor, dichloroacetate, acutely increased glucose oxidation and cardiac work in monocrotaline RVH. Chronic dichloroacetate therapy improved RV repolarization and RV function in vivo and in the RV Langendorff model. In PAB-induced RVH, a similar reduction in cardiac output and glycolytic shift occurred and it too improved with dichloroacetate. In PAB-RVH, the benefit of dichloroacetate on cardiac output was approximately 1/3 that in monocrotaline RVH. The larger effects in monocrotaline RVH likely reflect dichloroacetate's dual metabolic benefits in that model: regression of vascular disease and direct effects on the RV. Reduction in RV function and electrical remodeling in two models of RVH relevant to human disease (PAH and pulmonic stenosis) result, in part, from a PDK-mediated glycolytic shift in the RV. PDK inhibition partially restores RV function and regresses RVH by restoring RV repolarization and enhancing glucose oxidation. Recognition that a PDK-mediated metabolic shift contributes to contractile and ionic dysfunction in RVH offers insight into the pathophysiology and treatment of RVH.
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PMID:The inhibition of pyruvate dehydrogenase kinase improves impaired cardiac function and electrical remodeling in two models of right ventricular hypertrophy: resuscitating the hibernating right ventricle. 1994 38

The effectiveness of hypertension treatments is attributed either to the change in blood pressure, independent of the means used, or to an important contribution of appropriate drug selection: this debate probably stems from an inappropriate comparison. Treating essential hypertension in relatively healthy patients without advanced vascular disease and co-morbidities affords cardio-vascular protection by the lowering of the mechanical shear stress determined by blood pressure per se: thus, lowering blood pressure is the critical step, while the methods used can only differ through side effects. This treatment is, in fact, a lifetime prophylaxis, as hypertension, rather than a disease, is a symptom affecting one tail of the Gaussian distribution of blood pressure across the normal population. Treating hypertension in the context of diseases, like diabetes mellitus, congestive heart failure, left ventricular hypertrophy, and advanced atherosclerosis, would be improper if focused on just one symptom, while the appropriate treatment must include options which exhibit a more extended profile to include effectiveness on cardiac hypertrophy, insulin resistance, cardiac output, and systemic hemodynamics: thus, drugs may be different in their effectiveness and in the cardio-vascular protection afforded, even though the trials quoted in favour of this thesis were designed to compare drugs in their ability to lower blood pressure rather than in improving the overall complex clinical derangements. In conclusion, while the answer to the question is a sharp YES when dealing with primary prevention, it might be a NO, still clouded by contradictory and inconclusive evidence when dealing with secondary prevention and/or treatment of complex disease conditions and co-morbidities.
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PMID:Treating high blood pressure: is reaching the target more important than the means? Yes, the target is more important. 2111 29


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