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

The roundtable discussion, "Managing Cardiovascular Disease in African Americans: Emerging Strategies for Optimizing Care, " was convened to review the evidence that supports best practices for the management of cardiovascular disease and its complications in African Americans. Treatment guidelines are reviewed, as is the clinical evidence supporting the use of diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and beta-blockers. The ultimate goals of this work are to improve the understanding of the links among hypertension, diabetes, the metabolic syndrome, and cardiovascular disease, all of which disproportionately affect African Americans, and to increase physician awareness of the unique impact of these conditions in the often underserved African-American population.
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PMID:Executive summary of the African-American Initiative. 1743 35

The cardiovascular complications of Marfan syndrome (MFS) remain the primary source of morbidity and mortality in affected patients. Over the last decade, the underlying pathogenesis of these cardiovascular abnormalities has been the focus of much research. Such research has shed light on the potential role of several novel medical therapies and their ability to prevent cardiovascular disease progression. This paper summarizes the research underlying new medical therapies and provides a review of the scientific foundation underlying all current medical therapies used for prevention of cardiovascular disease in patients with MFS, including beta-adrenoceptor antagonists, calcium channel antagonists, ACE inhibitors, and angiotensin receptor antagonists.
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PMID:Cardiovascular pharmacotherapy in patients with Marfan syndrome. 1750 82

Effective blood pressure control with a large arsenal of conventional antihypertensive drugs, such as diuretics, beta-adrenergic blockers, and calcium channel blockers, significantly reduce the morbidity and mortality associated with cardiovascular disease. However, blood pressure control with these drugs does not reduce cardiovascular disease risks to the levels in normotensive persons. Only two drug classes that inhibit or antagonize portions of the renin-angiotensin system (RAS), angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor type-1 (AT(1) receptor) blockers, have protective and beneficial effects unrelated to the degree of blood pressure reduction. These drugs may prevent the blood pressure related functional and structural abnormalities of the cardiovascular system and reduce the end organ-damage. The first part of this review presents the components of the RAS, biological actions of angiotensin peptides, and the functions of the enzymes that generate and metabolize angiotensins, including the likely effect of manipulating them. Special attention is devoted to renin, ACE, ACE2, chymase, and neprilysin. The second part of this review presents the rationale for targeting the RAS, based on clinical studies of the ACE inhibitors and AT(1) receptor blockers. Finally, we present the investigational agents acting on the RAS that have a potential for clinical usage, and give the perspective of pharmacological, immunological and gene targeting of the RAS for treatment of cardiovascular disease.
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PMID:Pharmacological, immunological, and gene targeting of the renin-angiotensin system for treatment of cardiovascular disease. 1750 30

With the rising epidemic of type 2 diabetes worldwide, including the United States, the death and disability due to the suboptimal control of cardiovascular disease associated with this epidemic has made prevention of type 2 diabetes emerge as a primary strategic intervention. Several modalities have been assessed in large randomized controlled trials for diabetes prevention such as lifestyle interventions and various pharmacologic agents. Included in these agents are metformin, thiazolidinediones, acarbose, angiotensin converting enzyme inhibitors, as well as angiotensin receptor blockers. Abrogation of oxidative stress appears to be a common soil hypothesis that explains the favorable effects of these agents on glucose metabolism, including the prevention of diabetes and its complications. This comprehensive review highlights the role of oxidative stress in the pathogenesis of diabetes, with emphasis on the major clinical trials conducted on prevention of type 2 diabetes.
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PMID:Oxidative stress, glucose metabolism, and the prevention of type 2 diabetes: pathophysiological insights. 1750 14

Dihydropyridine calcium channel antagonists have been maligned in recent years because of concerns regarding their cardiovascular and overall safety profile. Specifically, it was widely publicised in the mid-1990s that these agents might increase the risk of myocardial infarction, gastrointestinal bleeding and cancer. Data linking these agents with increased cardiovascular risk were based on nonrandomised studies and implicated short-acting, immediate-release agents. These results were inappropriately extrapolated to longer-acting compounds, extended-release products, and to the non-dihydropyridine class. Fortunately, recent studies have vindicated the class from safety allegations. These studies are reviewed herein. Compared with both diuretics and contemporary agents, amlodipine decreases cardiovascular events to a similar or greater extent without evidence for increased coronary heart disease, gastrointestinal bleeding or cancer. Despite these data, initial concerns have had lasting repercussions, as the use of dihydropyridine calcium channel antagonists appears to lag behind what emerging data would support. Dihydropyridine calcium channel antagonists have several noteworthy attributes that merit consideration in the management of hypertension. The blood pressure response to this class of drugs is less contingent on patient factors such as age and race compared with other antihypertensive agents (e.g. ACE inhibitors). Dihydropyridine calcium channel antagonists may exert effects that protect against stroke that are independent of their blood pressure-lowering mechanism. Unlike diuretics and beta-adrenoceptor anatagonists (beta-blockers), dihydropyridine calcium channel antagonists are lipid neutral and do not disturb glucose homeostasis. Dihydropyridine calcium channel antagonists demonstrate a highly desirable profile when administered as part of combination therapy. Combinations of dihydropyridine calcium channel antagonists and ACE inhibitors or angiotensin receptor antagonists display additive efficacy and an enviable adverse-effect profile. Collectively, the cardiovascular benefit, metabolic neutrality and homogeneous blood pressure response illuminated in recent studies, and reviewed here, represent a reaffirmation of the benefit of long-acting dihydropyridine calcium channel antagonists and should serve to help reinforce the critical importance of these agents in the therapeutic armamentarium against cardiovascular disease.
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PMID:Dihydropyridine calcium channel antagonists in the management of hypertension. 1754 73

Metabolic syndrome (MetS) has been defined in different ways. However, key components common to most definitions are a constellation of risk factors including abdominal adiposity, impaired fasting glucose, hypertension, and dyslipidemia. A major mediator of MetS appears to be insulin resistance, which relates to the development of the vascular and metabolic dysfunctions that precede overt cardiovascular disease and type 2 diabetes. Evidence suggests that the mechanisms underlying the elevated cardiovascular risk associated with MetS begin with subclinical organ damage. Therapy for MetS targets individual components of the syndrome and includes lifestyle interventions, lipid-modifying therapy, and antihypertensive agents, particularly those that inhibit the renin-angiotensin system. Results of trials of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have demonstrated reductions in new-onset diabetes and cardiovascular events in a wide range of patients. Clinical trials to investigate further the role of these drugs in the primary prevention of type 2 diabetes in patients with MetS are currently under way. The purpose of this paper is to review the MetS from the perspective of the cardiology workforce with the hope that a better understanding of the links between MetS and cardiovascular disease could lead to improved management of persons at risk.
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PMID:Metabolic syndrome and cardiovascular disease: challenges and opportunities. 1760 58

Cardiovascular disease represents a continuum that starts with risk factors, such as hypertension, and progresses to atherosclerosis, target organ damage, and ultimately leads to heart failure or stroke. Renin-angiotensin-aldosterone system (RAAS) blockade with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) has been shown to be beneficial at all stages of this continuum. Both classes of agent can prevent or reverse endothelial dysfunction and atherosclerosis, thereby potentially reducing the risk of cardiovascular events. Such a reduction has been shown with ACE inhibitors in patients with coronary artery disease, but no such data are currently available for ARBs. Both ACE inhibitors and ARBs have been shown to reduce damage in target organs, such as the heart and kidney, and to decrease cardiovascular mortality and morbidity in patients with congestive heart failure. Trials, such as the Ongoing Telmisartan Alone in Combination with Ramipril Global Endpoint Trial (ONTARGET) and the Telmisartan Randomised Assessment Study in ACE-Intolerant Subjects with Cardiovascular Disease (TRANSCEND), that compare telmisartan, ramipril, and their combination in high-risk patients with vascular end-organ damage, should provide important new insights into the benefits of intervention with RAS blockade along the cardiorenovascular continuum.
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PMID:Angiotensin receptor blockers versus angiotensin-converting enzyme inhibitors: where do we stand now? 1830 33

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) differ in their actions on the renin-angiotensin-aldosterone system (RAAS). ACE inhibitors prevent the formation of angiotensin II, although angiotensin II may still be generated by alternative pathways. However, ACE inhibitors interrupt bradykinin breakdown, which in turn potentially enhances nitric oxide and prostacyclin mechanisms. In contrast, ARBs selectively prevent the binding of angiotensin II to the angiotensin type 1 (AT(1)) receptor while leaving the potentially beneficial effects of the AT(2) receptor unaffected. The supposition is that dual blockade of the RAAS effectively overcomes the harmful effects of angiotensin II mediated by the AT(1) receptor while offering the additional effects of the ACE inhibitor. This concept was first evaluated clinically more than a decade ago in small-scale studies that were not sufficiently powered to conclusively demonstrate benefits from dual blockade. Subsequently, larger-scale trials have been conducted to determine the effects of a combination of an ACE inhibitor and an ARB in combating the effects of angiotensin II at different stages of cardiovascular and renal disease. This review explores these data in areas, such as hypertension, renal disease, and cardiovascular disease, and draws on this preliminary evidence to support the rationale for the Ongoing Telmisartan Alone in Combination with Ramipril Global Endpoint Trial (ONTARGET) program, which aims to fully explore the clinical end points and effects of dual RAAS blockade in patients at high risk for cardiovascular outcomes.
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PMID:New opportunities in cardiovascular patient management: a survey of clinical data on the combination of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. 1766 98

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

Cardiovascular disease is a continuum, starting with risk factors resulting from physiological changes and extending to vascular pathology associated with adverse clinical outcomes. The overactivation of the renin-angiotensin-aldosterone system has been related to the development and worsening of risk factors associated with cardiovascular diseases such as hypertension and heart failure. Treatment at each stage along the continuum may prevent, or at least delay, the next one, and so it is crucial to initiate therapy as early as possible in such patients so as to provide optimal care. Candesartan, a long-acting angiotensin receptor antagonist, has been shown to be an effective, and well-tolerated therapy, in both the early and late phases of cardiovascular disease (prehypertension, hypertension, left ventricular hypertrophy and heart failure). This article reviews the data supporting the use of candesartan in cardiovascular medicine, with a focus on left ventricular hypertrophy and ultimately heart failure. Particular emphasis is given to the Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) program, which has shown a positive impact of candesartan in patients with chronic heart failure in terms of reducing the incidence of cardiovascular deaths and chronic heart failure hospitalizations.
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PMID:Candesartan: from left ventricular hypertrophy to heart failure, a global approach. 1786 13


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