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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) effectively interfere with the renin-angiotensin system and exert various beneficial actions on cardiac and vascular structure and function, beyond their blood pressure-lowering effects. Randomized, controlled clinical trials have shown that ACE inhibitors improve endothelial function, cardiac and vascular remodeling, retard the anatomic progression of atherosclerosis, and reduce the risk of myocardial infarction, stroke, and cardiovascular death. Therefore, these agents are recommended in the treatment of a wide range of patients at risk for adverse cardiovascular outcomes, including those with coronary disease, prior stroke, peripheral arterial disease, high-risk diabetes, hypertension, and heart failure. ARBs are effective blood pressure- lowering and renoprotective agents and can be used in heart failure in patients who do not tolerate ACE inhibitors. The role of ARBs in the prevention of atherosclerosis and its sequelae is currently under investigation. The use of combined ACE inhibitor plus ARB therapy offers theoretical advantages over the use of each of these agents alone and is also under investigation in large, randomized clinical trials.
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PMID:Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in atherosclerosis. 1216 36

The renin-angiotensin-aldosterone system (RAAS) plays a fundamental role in the development of atherosclerosis and adverse cardiovascular events. Traditionally, the pathologic effects of the RAAS were assumed to result from vasoconstriction induced by angiotensin II, and salt and water retention due to aldosterone. However, these hormones also have powerful trophic effects, stimulating increased mass in both the arterial wall and left ventricle. In addition, angiotensin II and aldosterone predispose to vascular inflammation, thrombosis, oxidative stress, and sudden cardiac death. Therapy directed at RAAS overactivity is essential for normalizing the prognosis of most patients with atherosclerosis. An angiotensin-converting enzyme (ACE) inhibitor improves the prognosis of patients with atherosclerosis and/or diabetes even in the setting of normal baseline blood pressure. Angiotensin receptor blocking agents also improve cardiovascular structure and prognosis. Although these agents are better tolerated than ACE inhibitors, they do not appear to be as effective in reducing event rates. Aldosterone receptor blocking agents also improve cardiovascular structure, function, and prognosis. Aldosterone receptor blockers appear to provide additive benefit when used in conjunction with either an ACE inhibitor or an angiotensin receptor blocker.
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PMID:The renin-angiotensin-aldosterone system as a target in coronary disease. 1257 98

The renin-angiotensin-aldosterone system (RAAS) exerts a principal influence in maintaining vascular tone, optimal salt and water homeostasis, and forward cardiac output in human beings. Overactivity of the RAAS can lead to pathologic consequences in states of diabetic nephropathy, hypertension, renal artery stenosis, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure. In addition to fluid and hemodynamic effects, the RAAS may have a critical role in the activation of the sympathetic nervous system, the progression of atherosclerosis, the dysregulation of endothelial function, and the inhibition of the fibrinolytic system. Accumulated basic and clinical evidence supports the use of inhibitors of the RAAS, including aldosterone antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers, in treating hypertension, improving diabetic nephropathy, preventing or ameliorating congestive heart failure, and optimizing the prognosis after myocardial infarction.
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PMID:Renin-angiotensin-aldosterone system: fundamental aspects and clinical implications in renal and cardiovascular disorders. 1267 84

The cardiovascular continuum describes the way from risk factors to atherosclerosis, acute cardiovascular events (unstable angina and myocardial infarction), and development of terminal heart failure and its complications. Following this way, advances are reported in the prevention of cardiovascular disease, in noninvasive diagnostics and revascularization of coronary artery disease, and in new therapeutic options of acute myocardial infarction. The following issues are reported in detail: (1) significance of statins, inhibition of platelet aggregation and vitamins in primary and secondary prevention of cardiovascular disease, (2) comparison of the angiotensin receptor blocker losartan and the beta-blocker atenolol in hypertension (LIFE study), (3) magnetic resonance angiography for the detection of coronary stenoses, (4) advantages and disadvantages of operative and interventional coronary revascularization considering elderly patients and sirolimus-eluting stents, and (5) efficacy of glycoprotein IIb/IIIa inhibition and low molecular weight heparin in acute myocardial infarction.
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PMID:[From risk factors to symptomatic coronary artery disease. Update cardiology 2001/2002--part I]. 1271 45

The cardiovascular continuum describes the way from risk factors to atherosclerosis, acute cardiovascular events (unstable angina and myocardial infarction), and development of terminal heart failure and its complications. Following this way, advances are reported in the therapy of acute coronary syndrome, heart failure, ventricular and supraventricular tachyarrhythmias, and stroke in patients with patent foramen ovale. The following issues are reported in detail: (1) significance of statins and statin withdrawal, glycoprotein IIb/IIIa receptor blocker, acute coronary interventions, aspirin and clopidogrel in unstable coronary syndromes, (2) pathogenesis of acute pulmonary edema associated with hypertension, (3) cardiac regeneration capability after transplantation and myocardial infarction, (4) beta-blocker therapy, efficacy of additional angiotensin receptor blocker therapy and multisite biventricular pacing in symptomatic (advanced) heart failure, (5) prognosis after ablation of the atrioventricular node in patients with atrial fibrillation, (6) primary prevention with an implantable defibrillator and resumption of driving after implantation, and (7) therapeutic options after cryptogenic stroke and patent foramen ovale.
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PMID:[Update cardiology 2001/2002-part II. From unstable coronary syndrome to terminal heart failure]. 1281 17

Arterial hypertension is a major risk factor for the clinical syndrome of angina pectoris, in which the ECG is abnormal but the coronary arteries are normal. Structural and functional abnormalities in coronary circulation as well as extravascular factors (eg, left-ventricular hypertrophy, fibrosis with diastolic dysfunction) compromise the adequate ratio of coronary blood flow to oxygen demand causing angina, dyspnea, and major cardiac events. Recent studies stress the importance to functional disturbances of coronary microvasculature leading to profound morphologic changes associated with impaired coronary conductance. In patients without epicardial coronary stenosis hypertensive microvascular disease can be qualitatively assessed by noninvasive diagnostic approaches based on new Doppler echocardiography techniques and may also be monitored by widely available stress tests. For ultimate quantitative assessment, invasive procedures are still required. Beyond guidelines to control blood pressure in hypertensive individuals, restoration of functional and structural integrity of the coronary microvasculature represents the ultimate therapeutic goal in hypertensive patients with coronary insufficiency and without angiographic evidence of atherosclerosis. Concomitant factors reducing coronary conductance such as left-ventricular hypertrophy and diastolic dysfunction should be reversed in parallel. Currently, therapeutic intervention in the renin-aldosterone-angiotensin-II-system using ACE inhibitors, angiotensin receptor blockers, and low doses of aldosterone antagonists represent the most promising strategy to achieve these goals. Using the knowledge of these recent results we should refine the overall management of our hypertensive patients with coronary insufficiency but without atherosclerosis.
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PMID:Management of the hypertensive patient with coronary insufficiency but without atherosclerosis. 1285 22

The renin-angiotensin-aldosterone system (RAAS) plays an integral role in maintaining vascular tone, optimal salt and water homeostasis, and cardiac function in humans. However, it has been recognized in recent years that pathologic consequences may also result from overactivity of the RAAS. Clinical disease states such as renal artery stenosis, hypertension, diabetic and nondiabetic nephropathies, left ventricular hypertrophy, coronary atherosclerosis, myocardial infarction, and congestive heart failure (CHF) are examples. Part of the adverse cardiorenal effects of the RAAS may be related to the prominent role that this system plays in the activation of the sympathetic nervous system, the dysregulation of endothelial function and progression of atherosclerosis, as well as inhibition of the fibrinolytic system. Also, direct profibrotic actions of angiotensin II and aldosterone in the kidney and heart promote end organ injury. Current basic science and clinical research supports the use of inhibitors of the RAAS, including angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists in treating hypertension, improving diabetic nephropathy and other forms of chronic kidney disease, preventing or ameliorating CHF, and optimizing prognosis after myocardial infarction.
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PMID:The renin-angiotensin-aldosterone system: cardiorenal effects and implications for renal and cardiovascular disease states. 1286 Nov 21

In view of the pro-oxidant and proinflammatory effects of angiotensin II, we have tested the hypothesis that valsartan, an angiotensin receptor blocker, may exert a suppressive action on reactive oxygen species (ROS) generation, nuclear factor kappa B (NF-kappa B) in mononuclear cells. Four groups of eight normal subjects were given 1) 160 mg daily of valsartan, 2) 80 mg daily of simvastatin, 3) 40 mg quinapril, or 4) no treatment. Fasting blood samples were obtained before treatment and at d 1, 8, and 14 (7 d after the cessation of the drug). After valsartan, ROS generation by polymorphonuclear cells and mononuclear cells fell significantly by more than 40% (P < 0.01). NF-kappa B binding activity and the expression of total cellular p65, a protein component of NF-kappa B, fell significantly (P < 0.01). The expression of inhibitor kappa B (I kappa B) increased significantly (P < 0.05). Plasma C-reactive protein (CRP) concentration fell significantly (P < 0.01). All indices, except I kappa B, reverted toward baseline, 7 d after the cessation of the drug. I kappa B persisted in an elevated state. Neither quinapril nor simvastatin given for 7 d produced a suppression of ROS generation, intranuclear NF-kappa B, p65, or CRP, and these two agents did not alter cellular I kappa B either. The untreated controls also did not demonstrate a change in their ROS generation or NF-kappa B binding activity or plasma CRP concentration. We conclude that valsartan at a modest dose exerts a profound and rapid ROS and inflammation-suppressive effect that may be relevant to its potential beneficial effects in atherosclerosis, diabetes, and congestive cardiac failure. In contrast, quinapril and simvastatin produced no similar effect over the period of 1 wk. Our observations may also have implications to clinical situations in which a rapid antiinflammatory effect is required.
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PMID:Angiotensin II receptor blocker valsartan suppresses reactive oxygen species generation in leukocytes, nuclear factor-kappa B, in mononuclear cells of normal subjects: evidence of an antiinflammatory action. 1297 Mar 29

The Maillard reaction involves the non enzymatic combination of carbohydrates such as glucose with protein aminogroups to yield schiff bases and Amadori protein adducts evolving into irreversible advanced glycation end products (AGEs). This phenomenon, part of normal ageing, is accelerated in diabetes, as a result of hyperglycaemia, and in renal failure, as a consequence of the accumulation of reactive carbonyl compounds (RCOs). AGEs and RCOs are implicated in uraemic toxicity both at the biochemical and the clinical level (dialysis amyloidosis, atherosclerosis, alterations of peritoneal membrane permeability). Reduction of plasma AGEs and RCOs is an interesting avenue to reduce uraemic toxicity. Therapeutic strategies involve dialysis technique (haemodialysis membranes, daily haemodialysis, ultrapure dialysate, RCO free peritoneal dialysate) as well as drugs inhibiting AGE formation (aminoguanidine and the less toxic angiotensin converting enzyme inhibitors or angiotensin receptor blockers).
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PMID:Advanced glycation in uraemic toxicity. 1455 90

The renin-angiotensin system (RAS) is well recognized for its importance in regulation of BP, electrolyte balance and vascular growth. Pharmacological suppression of the RAS, through ACE inhibition and/or angiotensin receptor blockade, is a proven effective therapeutic approach to the treatment of a range of cardiovascular diseases. Renin is the enzyme that catalyzes the first and rate-limiting step of RAS, the cleavage of angiotensinogen to angiotensin I (A-I). A-I is then further converted by ACE to the biologically active vasoconstrictor, A-II. Interruption of the generation of A-II by renin inhibitors at this highly specific initial step of the cascade would be expected to have similar but not identical effects to those of the already well established RAS antagonists. Due to the lack of effective alternative enzyme pathways, blockade of A-II production may be more effective with renin inhibition than with ACE inhibition, and because of the high specificity of renin for only one substrate, namely angiotensinogen, adverse effects would be expected to be less frequent. It is currently unclear whether blockade of angiotensin II type 1 receptors (AT(1)), leaving other A-II receptors unblocked, is preferable to the reduction in plasma and tissue A-II levels achieved with either ACE or renin inhibition. The development of early peptidic and peptidomimetic renin inhibitors was hampered by problems with oral bioavailability and high costs of synthesis. However recent work has led to the synthesis of a potent non-peptidic inhibitor of renin, aliskiren, which has acceptable oral bioavailability. This renin inhibitor has been shown to effectively reduce A-II levels in normal volunteers and to lower BP in patients with mild to moderate hypertension. It appears likely that aliskiren is the first of a new class of agents that may prove useful in the management of patients with nephropathy, heart failure and atherosclerosis in addition to hypertension.
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PMID:Therapeutic potential of renin inhibitors in the management of cardiovascular disorders. 1472 59


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