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The term metabolic syndrome or cardiometabolic syndrome describes the clustering of several cardiovascular and renal risk factors, including type 2 diabetes mellitus, central obesity, hypertension, and dyslipidemia. Over the past 15 years, several studies have examined the association between the metabolic/cardiometabolic syndrome or its central component, insulin resistance, with the presence of elevated urine albumin excretion. Intrarenal changes associated with the cardiometabolic syndrome result in elevated glomerular filtration rate, impaired pressure natriuresis, endothelial dysfunction related to changes in nitric oxide and, hence, impaired renal autoregulation and enhanced chronic inflammation. The aforementioned changes that occur in the cardiometabolic syndrome all contribute to the development of renal injury. While this review focuses on the epidemiology and mechanisms associated with vascular/renal injury, it must be remembered that prevention and treatment of kidney disease require a multifactorial approach. Weight loss through diet and exercise can reverse many of these pathophysiologic adaptations. Pharmacologic intervention should be aimed at achieving guideline goals and include insulin sensitizers to aid in tight glycemic control, lipid control, blockade of the renin-angiotensin-aldosterone system for blood pressure reduction, and anti-inflammatory therapies.
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PMID:Cardiometabolic syndrome and chronic kidney disease: what is the link? 1767 96

The regulation of blood glucose levels involves a finely tuned relationship between insulin sensitivity, hepatic glucose output, and production of insulin. The cardiometabolic syndrome includes in its definition criteria a disturbance of normal glucose tolerance and implies development of both insulin resistance and beta-cell dysfunction. There is now abundant evidence pointing toward a central role of dysregulation of the beta-cell function and mass in the development of impaired glucose tolerance. Mechanisms implicated in beta-cell dysfunction include genetic abnormalities, prenatal and early postnatal insults, and environmental events along with obesity, dyslipidemia-lipotoxicity, glucotoxicity, oxidative stress, chronic low-grade inflammation, amyloid deposition, and activation of the local renin-angiotensin system. Novel therapeutic characteristics of known medications such as metformin, thiazolidinediones, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and novel medications such as exendin-4 promise encouraging possibilities to battle against the cardiometabolic syndrome and the future development of cardiovascular disease.
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PMID:The role of beta-cell dysfunction in the cardiometabolic syndrome. 1767

Chronic kidney disease (CKD) is increasingly recognized not only as a cause of end-stage renal disease but also as a cause of cardiovascular disease. Importantly, it is intimately associated with non-healthy lifestyles such as obesity, metabolic syndrome, hypertension, diabetes mellitus, smoking, and heavy drinking. To define CKD direct measurement of GFR or estimation of GFR (eGFR) is required. Japan Society of Nephrology is asking nationwide project to create "original" equation without using ethnic factor to obtain eGFR. Early detection and early treatment are vital to prevent not only CKD progression but also cardiovascular events. A comprehensive health education campaign and screening of the general populace are needed in order to detect CKD early. The control of hypertension, dyslipidemia, proteinuria, obesity, are intervention strategies that retard or prevent progression of CKD. Blockade of the renin-angiotensin system can be beneficial, especially if proteinuria is present.
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PMID:[New concept of chronic kidney disease and blockade of renin-angiotensin system]. 1787 2

In the last years there has been increasing evidence suggesting that the treatment of cardiovascular risk factors must be done on a global rather than on a separate approach, because they have additive effects and share common pathways leading to atherothrombosis. Of special interest is the relationship between hypertension and dyslipidemia. An excessive activity of the renin-angiotensin system (RAS), that plays an important role in hypertension, contributes to endothelial dysfunction, vascular inflammation and thrombosis. Dyslipidemia induces the same effects through similar mechanisms. In fact, combined therapy with statins and RAS modulators shows synergic beneficial effects in the treatment of atherosclerosis. Then, in the future, the traditional hypertension and dyslipidemia units should probably evolve into global cardiovascular risk management Units. Also, polypills combining antihypertensive and lipid-lowering drugs will make easier the treatment of these conditions. These changes would provide us the necessary tools to treat our patients in accordance with the current strategies of cardiovascular therapy and prevention.
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PMID:Common pathways of hypercholesterolemia and hypertension leading to atherothrombosis: the need for a global approach in the management of cardiovascular risk factors. 1796 82

The identification and treatment of high-risk patients for cardiovascular disease reduces the risk of morbidity and mortality. Significant risk factors for cardiovascular events in hypertensive patients over and above dyslipidemia, smoking, and obesity include coronary heart disease, peripheral arterial disease, cerebrovascular/carotid artery disease, and diabetes. Treatment options for the reduction of cardiovascular events in hypertensive patients include diuretics, beta-blockers, alpha-blockers, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists. All of these agents, in various combinations, have been found to reduce the risk of cardiovascular events, even in high-risk patients. The use of ACE inhibitors or ARBs (usually in combination with a diuretic) has proven especially effective in reducing cardiovascular events in diabetes and, although both classes of drugs target the renin-angiotensin-aldosterone system, each has a different mechanism of action. Some investigators believe that combination therapy with an ACE inhibitor and ARB, usually given with other medications, may be more effective than either agent alone with other drugs. The Ongoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial (ONTARGET) is evaluating the cardioprotective effect of an ACE inhibitor (ramipril) plus an ARB (telmisartan) in high-risk patients.
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PMID:Evolving treatment options for prevention of cardiovascular events in high-risk hypertensive patients. 1797 96

Type 2 diabetes has reached epidemic proportions and is now recognized as a coronary heart disease equivalent. While the most common metabolic abnormality associated with diabetes is hyperglycemia, there are also abnormalities in carbohydrate, fat and protein metabolism. These abnormalities increase oxidative stress and activate the renin-angiotensin system leading to endothelial dysfunction and, thereafter, to systemic atherosclerosis. This systemic atherosclerosis is responsible for the increased cardiovascular morbidity and mortality related to diabetes. In this article, we review the evidence and discuss the rationale for comprehensive risk reduction to prevent and treat vascular disease in individuals with diabetes mellitus. The components of comprehensive risk reduction strategy consist of lifestyle changes, glycemic control, control of dyslipidemia and hypertension.
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PMID:Diabetes and vascular disease. 1809 12

The main components of the metabolic syndrome (MS) are abdominal obesity, atherogenic dyslipidemia, raised blood pressure, insulin resistance with or without glucose intolerance, and proinflammatory and prothrombotic states. The clustering of these metabolic risk factors significantly increases the risk of type 2 diabetes and promotes vascular endothelial dysfunction, inflammation, and increased oxidative stress. The net result is an increase in the risk of atherosclerotic cardiovascular disease. Therefore, management of MS is of utmost importance, especially considering its rapidly increasing prevalence in a population with rising obesity rates and its significant cardiovascular implications. The primary management of this syndrome involves the correction of the underlying risk factors--obesity, physical inactivity, and an atherogenic diet--with lifestyle modifications including increased physical activity and dietary modification. Smoking cessation also should be encouraged. However, pharmacologic therapies are often required to address cardiovascular risk factors. These agents can be categorized broadly into 1) anorectic agents, 2) insulin-sensitizing agents, 3) statins, and 4) renin-angiotensin system antagonists. Emerging therapies include adipokines, endocannabinoid inhibitors, and metabolic modulators, such as perhexiline and trimetazidine. To date, these therapies have not been shown to normalize the metabolic and cardiovascular burden of MS, and there still is no single therapeutic agent for its management.
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PMID:Management of the metabolic syndrome in cardiovascular disease. 1832 5

This study investigated the association of blood pressure with blood oxidative stress-related parameters in normotensive and hypertensive subjects. A cross-sectional design was applied to 31 hypertensive patients and 35 healthy normotensive subjects. All subjects were men between the ages of 35 and 60 years. Exclusion criteria were obesity, dyslipidemia, diabetes mellitus, smoking and current use of any medication. All patients underwent 24-h ambulatory blood pressure monitoring and sampling of blood and urine. Antioxidant enzymes activity, reduced/oxidized glutathione ratio (GSH/GSSG), and lipid peroxidation (malondialdehyde) were determined in erythrocytes. Parameters measured in the plasma of test subjects were plasma antioxidant status, lipid peroxidation (8-isoprostane), plasma vitamin C and E, and the blood pressure modulators renin, aldosterone, endothelin-1 and homocysteine. Daytime systolic and diastolic blood pressures of hypertensives were negatively correlated with plasma antioxidant capacity (r=-0.46, p<0.009 and r=-0.48, p<0.007), plasma vitamin C levels (r=-0.53, p<0.003 and r=-0.44, p<0.02), erythrocyte activity of antioxidant enzymes, and erythrocyte GSH/GSSG ratio, with hypertensives showing higher levels of oxidative stress. Blood pressures showed a positive correlation with both plasma and urine 8-isoprostane. Neither plasma vitamin E nor the assessed blood pressure modulator levels showed significant differences between the groups or correlation with blood pressures. These findings demonstrate a strong association between blood pressure and some oxidative stress-related parameters and suggest a possible role of oxidative stress in the pathophysiology of essential hypertension.
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PMID:Relationship between oxidative stress and essential hypertension. 1834 20

To evaluate survival after acute myocardial infarction (AMI) in nonagenarians, we conducted a retrospective chart review of 177 consecutive patients > or =90 years of age admitted from 2000 to 2006 with a primary diagnosis of AMI confirmed by peak troponin I > or =1.5 microg/L. Mean follow-up was 3.7 years (range 4 months to 6.7 years). Mean age was 93 years, 34% were men, and 60% were Caucasian. Common co-morbidities included hypertension (67%), dyslipidemia (28%), atrial fibrillation (28%), renal insufficiency (27%), dementia (23%), and previous cerebrovascular events (22%). Mean peak troponin was 20 mug/L (range 1.5 to 183 microg/L). Cardiac catheterization was performed within 48 hours in 42 patients (24%) and after 48 hours in 14 patients (8%); 40 patients (23%) received an intervention. Hospital mortality was 15% (n = 27). Survival at 30 days, 90 days, and 1 year were 78%, 69%, and 47%. Independent predictors of shorter survival time by Cox analysis included body mass index <25 kg/m2 (p <0.001), creatinine > or =2.0 mg/dl (p = 0.001), hemoglobin <11.0 g/dl (p = 0.016), and dementia (p = 0.027). Patients receiving aspirin, clopidogrel, beta blockers, and renin-angiotensin system inhibitors appeared to have a lower mortality. In conclusion, AMI in nonagenarians is associated with high mortality, with over 50% of patients dying within one year of presentation; elevated creatinine and lower hemoglobin are strong predictors of adverse prognosis, and lower body mass index and the presence of dementia add independent prognostic significance.
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PMID:Outcomes of acute myocardial infarction in nonagenarians. 1847 45

The coexistence of hypertension and type 2 diabetes considerably increases the risk for cardiovascular and renal complications, not only after manifestation of the diseases, but also in the range of high-normal blood pressures and prediabetic states. According to recent guidelines, patients with type 2 diabetes should be treated if the blood pressure is in the high-normal (previously normal) range (130-139/85-90 mmHg), sometimes even with blood pressures in the normal oder low prehypertensive range (120-129/80-85 mmHg). In any case, blood pressure should be reduced < 130/80 mmHg, if tolerated < 125/75 mmHg. The target for diabetic patients with microalbuminuria or nephropathy is below 125/75 mmHg. All blood pressure goals cited refer to office or clinic blood pressure measurements. The corresponding values for home (self) or ambulatory blood pressure measurement during the day are lower by 5-10 mmHg for systolic and 5 mmHg for diastolic blood pressures. The proper management of patients with type 2 diabetes has to be multifactorial, aiming at controlling blood pressure, hyperglycemia and dyslipidemia by using both lifestyle changes (reduction of sodium and fat intake, regular physical activity, weight loss in overweight patients, smoking cessation) and drug therapy. Antihypertensive treatment should be started with a (fixed) combination, preferably containing an inhibitor of the renin-angiotensin system such as ACE inhibitors or AT(1)-receptor blockers and either a diuretic (preferably indapamide) or a calciumantagonist rather than combining thiazide diuretics and beta-blockers.
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PMID:[Treatment of hypertensive type 2 diabetics: too late, too little]. 1856 13


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