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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extensive animal studies and a growing number of human clinical trials have now definitively demonstrated the central role of the renin-angiotensin-aldosterone system in the expression and modulation of cardiovascular disease. In contrast to the original hypothesis, the benefits of angiotensin antagonism do not emanate from the antihypertensive effect alone. Subsequent extensive investigations of angiotensin blockade suggest that the benefits of this approach may also result from the pharmacologic alteration of endothelial cell function and the ensuing changes in the biology of the vasculature. The more recent availability of direct antagonists of the AT(1) angiotensin receptor has introduced an element of doubt into this realm of clinical decision making. The receptor antagonists and the more widely studied converting-enzyme inhibitors share many endpoint attributes. Nevertheless, the partially overlapping mechanisms of action for the two classes of angiotensin antagonists confer distinct pharmacologic properties, including side effect profiles, mechanisms of action, and theoretic salutary effects upon the expression of cardiovascular disease. The current review will attempt to contrast the biology of angiotensin converting-enzyme inhibition with angiotensin II receptor antagonism. A discussion of the differential effects of these drug classes on endothelial cell function and on the modulation of vascular disease will be utilized to provide a theoretic framework for clinical decision making and therapeutics.
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PMID:Formulating clinical strategies for angiotensin antagonism: a review of preclinical and clinical studies. 1133 Oct 59

The most common etiologies for mitral regurgitation (MR) include mitral valve prolapse syndrome, coronary artery disease, infective endocarditis, rheumatic heart disease, collagen vascular disease, and, recently, anoretic drugs have also been reported to cause MR. In chronic severe MR, forward cardiac output is maintained for the development of afterload reduction with increase in compensatory left ventricular (LV) end-diastolic volume and LV ejection fraction. It is well established that some patients with asymptomatic mitral regurgitation develop irreversible contractile dysfunction of the LV, which is often masked by the afterload-reducing effect of the regurgitant flow; cardiologist have to use some variables, like LV chamber elastance, LV End-Systolic dimensions and volumes, left atrial area combined with ejection fraction, in their clinical evaluations tube able to predict surgery mortality. Careful and periodic evaluation of left ventricular function and size is essential to optimize the timing of surgical intervention in these patients. After symptoms occur, outcome is improved with surgical interventions compared to medical therapy, with a reported survival of only 45% at 5 years without surgical intervention. Vasodilators, diuretics, and recently, angiotensin receptor antagonists have been used in MR medical therapy. Long-term carvedilol therapy in patients with chronic heart failure may prevent or partially reverse progressive left ventricular dilatation. Concomitant by, it has been associated with recovery of diastolic reserve and a decrease in mitral regurgitation.
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PMID:[Heart failure and pure mitral failure. Prognostic impact and its best treatment]. 1200 70

Arterial hypertension and diabetes are potent independent risk factors for cardiovascular, cerebral, renal and peripheral (atherosclerotic) vascular disease. The prevalence of hypertension in diabetic individuals is approximately twice that in the non-diabetic population. Diabetic individuals with hypertension have a greater risk of macrovascular and microvascular disease than normotensive diabetic individuals. Hypertension is a major contributor to morbidity and mortality in diabetes, and should be recognized and treated early. Type 2 diabetes and hypertension share certain risk factors such as overweight, visceral obesity, and possibly insulin resistance. Life-style modifications (weight reduction, exercise, limitation of daily alcohol intake, stop smoking) are the foundation of hypertension and diabetes management as the definitive treatment or adjunctive to pharmacological therapy. Additional pharmacological therapy should be initiated when life-style modifications are unsuccessful or hypertension is too severe at the time of diagnosis. All classes of antihypertensive drugs are effective in controlling blood pressure in diabetic patients. For single-agent therapy, ACE-inhibitors, angiotensin receptor blocker, beta-blockers, and diuretics can be recommended. Because of concerns about the lower effectiveness of calcium channel blockers in decreasing coronary events and heart failure and in reducing progression of renal disease in diabetes, it is recommended to use these agents as second-line drugs for patients who cannot tolerate the other preferred classes or who require additional agents to achieve the target blood pressure. The choice depends on the patients specific treatment indications since each of these drugs have potential advantages and disadvantages. In patients with microalbuminuria or clinical nephropathy, both ACE-inhibitors and angiotensin receptor blockers are considered first line therapy for the prevention of and progression of nephropathy. Since treatment is usually life-long, cost effectiveness should be included in treatment evaluation.
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PMID:[Treatment of hypertension in type 2 diabetes mellitus--2002 update]. 1223 35

Diabetes mellitus increases the risk for hypertension and associated cardiovascular diseases, including coronary, cerebrovascular, renal and peripheral vascular disease. The risk for developing cardiovascular disease is increased when both diabetes and hypertension co-exist; in fact, over 11 million Americans have both diabetes and hypertension. These numbers will continue to climb, internationally, since the leading associated risk for diabetes development, obesity, has reached epidemic proportions, globally. Moreover, the frequent association of diabetes with dyslipidemia, as well as coagulation, endothelial, and metabolic abnormalities also aggravates the underlying vascular disease process in patients who possess these comorbid conditions. The renin-angiotensin-aldosterone system (RAS) and arginine vasopressin (AVP) are overactivated in both hypertension and diabetes. Drugs that inhibit this system, such as ACE inhibitors and more recently angiotensin receptor antagonists (ARBs), have proven beneficial effects on the micro- and macrovascular complications of diabetes, especially the kidney. The BRILLIANT study showed that lisinopril reduces microalbuminuria better than CCB therapy. Numerous other long-term studies confirm this association with ACE inhibitors including the HOPE trial. Furthermore, the European Controlled trial of Lisinopril in Insulin-dependent Diabetes (EUCLID) study, showed that lisinopril slowed the progression of renal disease, even in individuals with mild albuminuria. In fact, there are now five appropriately powered randomized placebo-controlled trials to show that both ACE inhibitors and ARBs slow progression of diabetic nephropathy in people with type 2 diabetes. These effects were shown to be better than conventional blood pressure lowering therapy, including dihydropyridine CCBs. In patients with microalbuminuria, ACE inhibitors and ARBs reduce the progression of microalbuminuria to proteinuria and provide a risk reduction of between 38 and 60% for progression to proteinuria. This is important since microalbuminuria is known to be associated with increased vascular permeability and decreased responsiveness to vasodilatory stimuli. Recently, increased AVP levels have been lined to microalbuminuria and hyperfiltration in diabetes. The microvascular and macrovascular benefits of ACE inhibition, ARBs and possible role of AVP antagonists in diabetic patients will be discussed, as will be recommendations for its clinical use.
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PMID:Treatment of the diabetic patient: focus on cardiovascular and renal risk reduction. 1243 44

Control of hypertension in the vascular patient is clearly a priority. However, these patients often will have significant co-morbidities that may influence the choice of medication, a decision that also may be affected by cost or Health Plan directives. Wherever possible, monotherapy should be attempted first, although in select circumstances combination therapy may be more appropriate. The 5 main categories of drugs used in the initial treatment of hypertensive vascular diseases are (1). diuretics, (2). beta-adrenergic blockers, (3). calcium channel blockers, (4). angiotensin-converting enzyme (ACE) inhibitors, and (5). angiotensin receptor blockers (ARBs). There are also other less commonly used drugs. Each of the antihypertensive agents is roughly equally effective, producing a good antihypertensive response in 40% to 60% of cases. Some antihypertensives, especially ACE and ARBs, also may have beneficial effects on the vascular and metabolic systems separate from their blood pressure lowering effects, which suggests they may be beneficial even if blood pressure is well maintained with other agents. This report covers the basic information required for the vascular surgeon to become familiar with the various medications and their indications, dosage, and side effects. It also provides some guidelines in selecting relevant antihypertensive treatment regimens for the elderly patient with arterial vascular disease.
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PMID:Treatment of hypertension from volume to vasoconstriction: The ACE up your sleeve. 1247 97

Diabetes mellitus is the leading cause of end-stage renal disease and also increases the risk of atherosclerotic vascular disease. Hypertension amplifies both problems. Detection of microalbuminuria, a common and early manifestation of diabetic nephropathy and a marker for cardiovascular risk, permits early treatment to reduce progression of nephropathy and vascular disease in diabetes. Although optimal glycemic control is essential to reduce the risk of nephropathy, aggressive blood pressure lowering to a level of 130/80 mg Hg or below in hypertensive diabetic patients is as important as glycemic control. Initial drug therapy for nephropathy should include an angiotensin-converting enzyme inhibitor (or if contra-indicated, an angiotensin receptor blocker), as several large randomized double-blinded multicenter clinical trials have demonstrated an independent renoprotective effect with renin angiotensin system inhibition. The role of advanced glycation end products in the pathogenesis of renal and vascular disease in diabetes is becoming more clearly established. However, the use of therapeutic strategies directed at blocking their effect still awaits further investigation. A multifaceted intervention program that combines optimal glycemic control, lifestyle modification/cardiovascular prevention guidelines such as lipid control and smoking cessation, with appropriate antihypertensive therapy when indicated, will prevent or delay both the occurrence and progression of diabetic nephropathy.
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PMID:Combating diabetic nephropathy with drug therapy. 1264 11

The use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) has significantly reduced morbidity and mortality across the continuum of vascular disease. The utilization of these agents, however, remains suboptimal. The drugs are not prescribed in many patients because of concerns regarding their effects on renal function. Despite overwhelming evidence in favor of renoprotection, it is not uncommon for the glomerular filtration rate (GFR) to decrease shortly after starting treatment with an ACE inhibitor or ARB. This response is functional in nature and should be expected based on renal physiology and its dependence on the renin-angiotensin system to maintain GFR. Unfortunately, this phenomenon sometimes is viewed as an adverse effect or an indicator of underlying pathology. Although somewhat counterintuitive, early elevations in serum creatinine concentration are associated with improved long-term renal outcomes in patients with renal insufficiency and thus support, rather than condemn, continued treatment. Clinicians should be aware of the physiologic course associated with blockade of the renin-angiotensin system so that these agents will not be withheld unnecessarily.
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PMID:Elevations in serum creatinine concentration: concerning or reassuring? 1452 53

Numerous studies document an almost linear association between the level of albuminuria and risk for a cardiovascular event. Recent data also demonstrate a strong association between the presence of microalbuminuria and elevations in C-reactive protein. Therefore, the increased membrane permeability that generates microalbuminuria might be secondary to an inflammatory process. Progression from microalbuminuria to macroalbuminuria indicates worsening of vascular disease and presence of kidney disease. Recent pharmacologic interventions have resulted in significant delay and even arrest of progression of microalbuminuria to macroalbuminuria as well as kidney disease progression. Therefore, focus should be placed on use of antihypertensive agents that not only lower blood pressure but also lower or normalize albuminuria levels. All recent guideline statements support the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). Further lowering of albuminuria may be achieved by adding verapamil, diltiazem, or an ARB to an ACE inhibitor.
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PMID:Clinical importance of microalbuminuria in diabetes and hypertension. 1534 86

Albuminuria is recognized in all hypertension guideline statements as a cardiovascular risk factor and indicator of kidney disease. Recent data also demonstrate a strong association between the presence of microalbuminuria and elevations in C-reactive protein. Thus, the increased membrane permeability that generates microalbuminuria may be secondary to an inflammatory process. Progression from microalbuminuria (>30 and < or =300 mg albumin/g creatinine) to macroalbuminuria (>300 mg albumin/g creatinine) indicates a worsening of vascular disease and the presence of kidney disease. Recent outcome trials of kidney disease progression have demonstrated the best results among those with reductions in albuminuria in concert with blood pressure (BP) reduction. Thus, use antihypertensive agents that not only lower BP but also lower or normalize albuminuria levels. All recent guideline statements support the use of agents that block the renin-angiotensin-aldosterone system as part of a regimen to achieve the BP goal. Further lowering of albuminuria may be achieved by adding either a nondihydropyridine calcium antagonist such as verapamil or diltiazem, or aldosterone receptor blockers. Use of an angiotensin receptor blocker added to an angiotensin-converting enzyme inhibitor or vice versa can further lower albuminuria by an additional 30%-40%, which is not true of the additional lowering of BP.
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PMID:Implications of albuminuria on kidney disease progression. 1553 7

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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