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Query: UMLS:C0007222 (cardiovascular disease)
 65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that the most effective method of reducing cardiovascular disease (CVD) is to define overall CVD risk and apply fixed doses of anti-hypertensive, hypolipidaemic and anti-platelet therapies, using the evidence base from clinical outcome studies. Such studies have examined large numbers of patients with a wide representation of subgroups and demon-Welwyn strated equivalent benefits in all subsets. In so doing, there may be over-interpretation of the data leading to large-scale applicability of the findings to individuals who were not genuinely represented in the study populations. Most lipid-lowering studies have been unable to consider the possibility that optimal correction of dyslipidaemia would have been more effective than the use of a fixed dose of statins. Studies of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockade have produced contradictory findings regarding unique non-hypotensive beneficial CVD effects, and suboptimal control of mild hypertension was a frequent finding in the study populations. Scrutiny of concomitant therapy in studies that focus on a particular issue such as LDL (low-density lipoprotein) cholesterol or blood pressure supports the notion that benefits from the agent may be attenuated by other drugs. Widespread application of fixed doses of all these agents to at-risk cases will increase the incidence of inappropriate use and side effects. Clinical experience with modulators of the renin-angiotensin system in hypertensive diabetic renal disease confirms reduced efficacy, and more frequent deterioration of renal function than observed in clinical trials. Measurement of individual biomedical CVD risk factors along with overall risk estimation should continue to be the mainstay of clinical practice. This will allow appropriate case selection for different agents, optimisation of dosage or better assessment of compliance where treatment is less efficacious, and monitoring for adverse effects of therapy. Pragmatic individualisation of care should remain the basis for treating asymptomatic CVD risk factors.
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PMID:Drug therapy for prevention of cardiovascular disease--should surrogate measures be abandoned? 1601 Dec 22

Prolonged hyperglycemia, dyslipidemia and oxidative stress in diabetes result in the production and accumulation of AGEs. It is now clear that AGEs contribute to the development and progression of cardiovascular disease in diabetes, as well as other complications. AGEs are thought to act through receptor-independent and dependent mechanisms to promote vascular damage, fibrosis and inflammation associated with accelerated atherogenesis. As a result, novel therapeutic agents to reduce the accumulation of AGEs in diabetes have gained interest as potential cardioprotective approaches. A variety of agents have been developed which are examined in detail in this review. These include aminoguanidine, ALT-946, pyridoxamine, benfotiamine, OPB-9195, alagebrium chloride, N-phenacylthiazolium bromide and LR-90. In addition, it has been demonstrated that a number of established therapies have the ability to reduce the accumulation of AGEs in diabetes including ACE inhibitors, angiotensin receptor antagonists, metformin, peroxisome proliferators receptor agonists, metal chelators and some antioxidants. The fact that many of these inhibitors of AGEs are effective in experimental models, despite their disparate mechanisms of action, supports the keystone role of AGEs in diabetic vascular damage. Nonetheless, the clinical utility of AGE inhibition remains to be firmly established. Optimal metabolic and blood pressure control, that is achieved early and sustained indefinitely, remains the best recourse for inhibition of AGEs until more specific interventions become a clinical reality.
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PMID:The role of AGEs and AGE inhibitors in diabetic cardiovascular disease. 1602 65

Type 2 diabetes is a cardiovascular disease equivalent that is associated with accelerated atherosclerosis and significant mortality. However, the metabolic syndrome and prediabetes are associated with increased cardiovascular mortality, indicating that atherogenic vascular changes begin prior to the onset of overt diabetes. At the core of diabetes and the metabolic syndrome is insulin resistance (IR), which sets the stage for dyslipidemia, hypertension, and inflammation. Endothelial dysfunction is the first stage of the atherosclerosis process and results from exposure to cardiovascular risk factors, such as IR and diabetes. IR and atherosclerosis follow parallel paths as they progress in severity. Thiazolidinediones, angiotensin-converting enzyme inhibitors, angiotensin receptor-AT1 blockers, and statins are widely used in the treatment of diabetes. Emerging evidence indicates that these pharmacologic agents have added mechanisms of action, especially on the endothelium and in the prevention of diabetes.
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PMID:Insulin resistance and the endothelium. 1603 73

Hypertension is both a disease and risk factor for cardiovascular disease (CVD) and each 20/10 mm Hg rise in blood pressure (BP) doubles the risk for CVD. Although BP reduction through lifestyle modification and/or antihypertensive therapy has been shown to dramatically reduce the risk for CVD, recent evidence has shown that many patients with hypertension do not have adequate BP control. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) provides comprehensive guidelines on the diagnosis, classification, and management of hypertension and related CV conditions. The JNC 7 guidelines recommend that most patients receive first-line therapy with thiazide diuretics, but the majority of patients will require 2 or more antihypertensive agents to achieve adequate BP control. The selection of additional antihypertensive therapies should be based on the presence of concomitant CV and metabolic conditions as well as patient-specific factors such as race. An important role exists for angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and beta-blockers, particularly in patients with comorbid CV or metabolic conditions. Clinical evidence suggests that these agents may offer benefits beyond simple BP lowering. Furthermore, synergies among antihypertensive classes may improve BP control and combination therapy may also permit the use of smaller doses of each medication and reduce the risk of dose-related adverse effects.
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PMID:Treating hypertension with cardioprotective therapies: the role of ACE inhibitors, ARBs, and beta-blockers. 1614 81

We examined the efficacy of candesartan in reducing cardiovascular events in hypertensive patients with coexisting chronic kidney disease and cardiovascular diseases. This open-label, prospective study was conducted from 1999 to 2002, and 141 hypertensive subjects 60 to 75 years old with non-diabetic chronic renal insufficiency were enrolled. Before randomization of the patients, we examined their past medical history and found that 69 patients had been hospitalized due to myocardial infarction (MI) or stroke. Therefore, the patients were divided into 2 groups, one with previous histories of MI or stroke and the other with no previous history of Ml or stroke. The patients were randomized to receive either the angiotensin receptor blocker candesartan or conventional treatment. The mean duration of follow-up was 3.1 +/- 0.4 years. The primary outcome was a primary cardiovascular event (MI, stroke, or heart failure) verified by hospitalization. At the end of the study, in the patients with past history of cardiovascular diseases, blood pressure was reduced from 146.4 +/- 7.2/79.2 +/- 5.1 to 34.4 +/- 6.1/72.3 +/- 4.0 mmHg in the candesartan group and from 145.3 +/- 5.1/80.1 +/- 3.8 to 133.4 +/- 5.8/73.8 +/- 4.2 mmHg in the conventional treatment group. In the patients without past history of cardiovascular diseases, blood pressure was reduced from 143.2 +/- 4.3/78.3 +/- 4.8 to 133.8 +/- 5.3/ 73.1 +/- 3.8 mmHg in the candesartan group and from 143.9 +/- 6.8/78.1 +/- 4.2 to 132.6 +/- 5.4/74.5 +/- 4.4 mmHg in the conventional treatment group at the end of the study. There were no significant differences between the candesartan group and the conventional treatment group in the reduction of blood pressures. Among patients with a past history of cardiovascular disease, the serum creatinine concentration increased from 1.49 +/- 0.38 to 1.58 +/- 0.42 by candesartan treatment and from 1.50 +/- 0.32 to 1.89 +/- 0.37 by conventional treatment. On the other hand, in patients with no past history of cardiovascular disease, the serum creatinine concentration increased from 1.44 +/- 0.42 to 1.46 +/- 0.40 by candesartan treatment and from 1.46 +/- 0.44 to 1.51 +/- 0.38 by conventional treatment. Although, there was no significant difference in the incidence of cardiovascular events between the 2 groups with the candesartan-based and conventional-based antihypertensive treatment, in patients without cardiovascular events (12/36 vs. 7/34: these figures indicate events per total participated persons per 3 years; following figures are the same as this), treatment with candesartan reduced the incidence of cardiovascular events in the patients with past history of cardiovascular diseases (20/33 vs. 32/ 38). In particular, candesartan-based treatment reduced the incidence of congestive heart failure by 66.4% in these patients. In conclusion, this prospective, open-labeled randomized study suggests that 1) previous history of cardiovascular diseases is a major risk factor for cardiovascular events; and 2) candesartan is effective for reduction of cardiovascular events in hypertensive patients with coexisting chronic kidney disease and cardiovascular diseases, especially for prevention of congestive heart failure.
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PMID:An angiotensin receptor blocker reduces the risk of congestive heart failure in elderly hypertensive patients with renal insufficiency. 1615 5

The diagnostic categories of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) were stablished in an effort to identify populations at risk for developing type 2 diabetes mellitus (T2DM). Both IGT and IFG are associated with increased risk of developing T2DM, but recent analyses found that the thresholds of risk vary among different populations and an even lower diagnostic threshold of IFG may be appropriate. IGT has been linked with an increased risk of cardiovascular events and some analyses have demonstrated an increased mortality risk compared with patients with normal glucose tolerance. In contrast, a continuum of increased risk of microvascular manifestations of T2DM has been demonstrated with IFG but an association of IFG with cardiovascular events has not been well established. Although both IGT and IFG are associated with resistance to insulin and increased insulin secretion, they do not identify the identical patient populations and are not equivalent in predicting development of T2DM or cardiovascular events. IFG and IGT have been associated with other features of insulin resistance, including dyslipidaemia, hypertension, abdominal obesity, microalbuminuria, endothelial dysfunction, and markers of inflammation and hypercoagulability, traits collectively referred to as the metabolic syndrome. Analyses of combinations of these components have also been associated with progression to T2DM, cardiovascular disease and increased mortality. The foundation of treatment for IGT, IFG, and the metabolic syndrome is lifestyle modification, including both dietary change and routine exercise. To date, several clinical trials have found that lifestyle modification is the most efficacious strategy to prevent progression to T2DM. Alternative treatments include pharmacotherapy with metformin or acarbose, both of which have been demonstrated to decrease the development of T2DM. Ongoing clinical trials are evaluating newer pharmacotherapies, including angiotensin converting enzyme inhibitors, angiotensin receptor antagonists, metglitinides and thiazolidinediones, to prevent both T2DM and cardiovascular events. In combination with lifestyle modification, these therapies offer hope for effective prevention of T2DM and its consequences in high-risk patients.
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PMID:Impaired glucose tolerance and impaired fasting glucose--a review of diagnosis, clinical implications and management. 1630 67

The role of potassium in cardiovascular disease and the importance of preserving potassium balance have emerged as clinical hot points, particularly as they relate to cardioprotective and renoprotective therapies that secondarily promote potassium retention. Antihypertensive medications that most commonly influence serum potassium levels and/or total body potassium include beta blockers and potassium-wasting and potassium-sparing diuretics as well as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Uncertainty exists as to the best way to monitor potassium levels when any of these drug therapies are used, particularly in the setting of chronic kidney disease and/or heart failure. Guidelines for the monitoring of serum potassium levels in the setting of antihypertensive therapy are at best makeshift and often drawn from the know-how of the treating physician.
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PMID:Antihypertensive therapy and its effects on potassium homeostasis. 1640 94

Although strict blood pressure control is essential for the prevention of cardiovascular disease, there are many hypertensive patients whose current hypertension treatments are inadequate. Therefore, we designed a clinical study to evaluate the efficacy achieving a blood pressure reduction by combination therapy with losartan and a low-dose diuretic. In the 10 hypertensive patients treated with candesartan at 8 mg/day for more than 2 months, combination therapy with losartan at 50 mg/day and hydrochlorothiazide (HCTZ) at 12.5 mg/day was conducted for 3 months after the cessation of treatment with candesartan. Either immediately before the onset of combination therapy or 3 months after the treatment, the 24 hour ambulatory blood pressure(ABP) and pulse rate were measured every 30 minutes. Pulse wave velocity(PWV) and homeostasis model assessment insulin resistance index(HOMA-R) with fasting blood were also measured after 3 months. In the treatment with candesartan, the ABP was 134.4 +/- 8.7/88.1 +/- 6.1 mmHg at 24 hours, 139.7 +/- 8.4/91.3 +/- 7.1 mmHg in the daytime, 123.8 +/- 11.6/81.6 +/- 5.9 mmHg in the nighttime, and 139.3 +/- 10.3/92.3 +/- 7.3 mmHg in the early morning(6 : 00-8 : 00). After the switch to the combination therapy with losartan and HCTZ, the blood pressure changed to 126.8 +/- 9.3/81.6 +/- 7.0 mmHg (p < 0.05/p < 0.05) at 24 hours, 130.6 +/- 12.0/84.2 +/- 8.5 mmHg (p < 0.05/p < 0.05) in the daytime, 119.3 +/- 8.7/76.6 +/- 6.5 mmHg (NS/NS) in the nighttime, and 129.7 +/- 11.7/84.0 +/- 9.2 mmHg(p < 0.05/p < 0.05) in the early morning. However, both the changes in heart rate and PWV, and the differences in blood glucose, lipid and HOMA-R were not significant. Nonetheless, the blood pressure control for 24 hours was better using the combination therapy with losartan at 50 mg/day and HCTZ of 12.5 mg/day than in the treatment with candesartan at 8 mg/day alone. Since losartan decreases uric acid unlike other angiotensin receptor blockers, the combination therapy of losartan and a diuretic can be expected to provide one of the best therapies for essential hypertensive patients.
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PMID:[Beneficial effects of combination therapy with losartan and low-dose hydrochlorothiazide in the treatment of essential hypertension]. 1640 30

Blood pressure (BP) measured at home early in the morning (HBP) has been recognized as a useful predictor for organ damage and has been viewed as an important therapeutic target in patients with hypertension. The present study was aimed to determine whether this notion holds true in patients with progressive renal disease. The study enrolled patients with mild to moderate renal impairment. They were all directed to record self-measured HBP to evaluate the adequacy of BP control. In addition to the conventional antihypertensive therapy, intensive treatment to more efficiently reduce elevated morning HBP was applied, especially in patients with diabetic nephropathy. The results were as follows: 1) The status of BP control assessed using HBP and office/clinic BP (OBP) shows predominance of morning hypertension. The prevalence of patients with well-controlled systolic HBP was 38%, those with poorly-controlled HBP 30%, masked hypertension 20% and white coat hypertension 12%. 2) Early morning systolic HBP in diabetics was significantly higher than that in non-diabetics. However, when evaluated on systolic OBP, both groups were comparable.3)Logistic regression analysis showed that the predictive variables to explain morning hypertension (more than 130 mmHg and increased systolic HBP) were age, amount of daily urinary protein excretion and left ventricular mass index (LVMI).4)Following conventional therapy, intensive antihypertensive therapy consisting of calcium channel blockers (CCB) and/or diuretics given in the morning, and angiotensin receptor blockers (ARB) given in the evening, together with alpha1-blockers given at bedtime, efficaciously reduced elevated HBP in the morning. This result was associated with significant reduction in daily urinary protein excretion and in serum plasminogen-activator inhibitor (PAI-1) concentration. The present study indicates that, regardless of ongoing conventional antihypertensive therapy, the majority of patients with renal disease had morning hypertension, suggesting that these patients are at a higher risk for cardiovascular disease. For the purpose of improving morning hypertension, intensive treatments with combined CCB, ARB and alpha1-blockers could have substantial benefit on the morbidity and prognosis in patients with diabetic nephropathy.
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PMID:Morning blood pressure predicts hypertensive organ damage in patients with renal diseases: effect of intensive antihypertensive therapy in patients with diabetic nephropathy. 1641 38

Endothelium-derived nitric oxide (NO) is the most potent endogenous vasodilator and, by virtue of its anti-inflammatory and anti-thrombotic effects, it is an endogenous anti-atherogenic agent. Accordingly, impairment of NO synthesis or bioactivity may increase the risk of vascular disease. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of the NO synthase pathway. Plasma levels of ADMA are increased in patients with vascular disease, or with risk factors for vascular disease. Preclinical and clinical studies indicate that ADMA may mediate the adverse effects of traditional risk factors on endothelial vasodilator function. By impairing endothelial function, ADMA may contribute to pulmonary or systemic hypertension, as well as to vascular disease. Several drugs known to treat cardiovascular disease also reduce plasma ADMA levels, such as angiotensin receptor antagonists, converting enzyme inhibitors, and insulin sensitizing agents. Plasma ADMA may be a common mediator of endothelial dysfunction induced by vascular risk factors. Insights into the mechanisms by which plasma ADMA is regulated may lead to new therapeutic knowledge.
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PMID:ADMA: its role in vascular disease. 1644 64


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