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Query: UMLS:C0018801 (heart failure)
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Ramipril is safe and effective in the treatment of hypertension and heart failure, but this is not reviewed here. Ramipril is a lipophilic angiotensin-converting enzyme inhibitor suitable for once-daily administration. In addition to decreasing angiotensin II and increasing bradykinin levels, ramipril increases the levels of vasodilatory renal medullary neutral lipids and inhibits platelet-derived growth factor-induced proliferation of glomerulus cells. Ramipril also decreases transforming growth factor-beta in the kidney. Changes in kidney structure and proteinuria are characteristics of the streptozotocin (STZ) rat model of diabetes, and these are prevented by ramipril. In STZ diabetes, doses of ramipril that have no effect on blood pressure reverse vascular hypertrophy. In animal models of kidney failure (subtotal nephrectomy, stroke-prone spontaneously hypertensive rats), ramipril is renoprotective and some of this renoprotective effect is independent of blood pressure lowering. In humans, clinical doses of ramipril probably do not modify glucose metabolism but do reduce the levels of LDL- and HDL-cholesterol. In clinical trials of renal effects, ramipril has been shown to increase cortical nephron flow in hypertension and to reduce proteinuria in patients with and without diabetes and/or hypertension. Some of the smaller clinical trials showed beneficial effects on kidney function with low doses of ramipril that do not lower blood pressure. A large clinical trial in nondiabetic proteinuria, the Ramipril Efficacy in Nephropathy (REIN) trial, has shown that ramipril 1.25 mg/day, which does not lower blood pressure, arrested the decline in glomerular filtration rate and prolonged the time to end-stage renal failure. In diabetic patients who have had a previous cardiovascular event or having one other cardiovascular risk factor, the MICRO-HOPE clinical trial showed that ramipril lowers the combined risk of myocardial infarction, stroke and cardiovascular death by 25%. In conclusion, ramipril has proven beneficial effects in kidney disease alone or in association with diabetes and in diabetes without kidney disease, and is the pril for diabetes and kidney disease. (c) 2001 Prous Science. All rights reserved.
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PMID:Is Ramipril the pril for diabetes and kidney disease? 1276 20

Blood pressure reduction and intensive antihypertensive treatment are effective in reducing both microvascular and macrovascular complications in type 2 diabetes. Blood pressure target levels < 130/85 or 130/80 mmHg are now recommended. Antagonism of the renin-angiotensin-aldosterone system seems to be an important goal in the treatment of hypertension and diabetes-related complications. The renoprotective role of angiotensin-converting enzyme (ACE)-inhibitors has been well documented in type 1 diabetes; in type 2 diabetes ACE-inhibitors have been deemed more effective than other traditional drugs in reducing the onset of overt nephropathy in microalbuminuric patients (secondary prevention) but not in reducing renal dysfunction in patients with clinical proteinuria (tertiary prevention). Recently, four large trials performed on type 2 diabetes showed that angiotensin II receptor blockers (ARBs) prevent the development of clinical proteinuria in microalbuminuric patients (IRMA and MARVAL studies) and delay the progression of nephropathy towards end-stage renal failure in patients with overt nephropathy (IDNT and RENAAL studies). Moreover, ARBs have been deemed more effective in reducing hospitalizations for heart failure compared to placebo (IDNT and RENAAL studies) and in reducing cardiovascular morbidity and mortality compared to conventional therapy (LIFE study) in type 2 diabetes. In conclusion, ARBs are effective in preventing and delaying renal damage in type 2 diabetes. Thus, the recent guidelines for the prevention and treatment of diabetic nephropathy state that ACE-inhibitors are the first-choice drugs in type 1 diabetes while ARBs are considered as the first-choice drugs in secondary prevention, the same as ACE-inhibitors, and are the unique first-choice drug in tertiary prevention of end-stage renal failure in type 2 diabetes. Finally, ACE-inhibitors and ARBs are both first-choice drugs in cardiovascular prevention in type 2 diabetes.
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PMID:[The role of angiotensin II AT1-receptor antagonists in renal and cardiac protection in type-2 diabetes mellitus]. 1278 55

Hypertension is a nutritional-hygienic disease. Long-term caloric intake in excess of energy expenditures, chronic supraphysiological intake of dietary sodium, excessive alcohol consumption, and psychosocial stressors all contribute to the development of hypertension throughout the world. Elevated BP, particularly systolic BP, has been linked to multiple adverse clinical outcomes including stroke, heart failure, myocardial infarction, renal insufficiency/failure, peripheral vascular disease, retinopathy, dementia, and premature mortality. These undesirable clinical outcomes are typically, although not invariably, preceded by pressure-related target-organ injury such as left ventricular hypertrophy, renal insufficiency and proteinuria. The relation of BP and CKD and, in turn, the prevention of CKD or forestalling its progression by hypertension treatment, will be the focus of this manuscript. In hypertensive persons with reduced kidney function and/or proteinuria, lowering BP with multidrug therapy that is inclusive of pharmacologic modulators of the renin-angiotensin-aldosterone-kinin system is an effective strategy to forestall the progressive loss of kidney function. The totality of data support low therapeutic BP targets for persons with proteinuria >1 g/d. Nevertheless, in persons with CKD, even those with proteinuria below the dipstick positive level (approximately 300 mg/d or urine protein to creatinine ratio of 0.22), aggressive BP control also may be warranted because of the high risk of nonrenal cardiovascular disease. Multiple antihypertensive drugs will be required in the vast majority of patients with diabetes and/or reduced kidney function to attain BP goal. Renin-angiotensin system (RAS) modulator therapy is indicated among persons with diabetes mellitus and CKD. Available data support the use of angiotensin receptor blockers in persons with type 2 diabetes and overt nephropathy for preservation of kidney function. Among persons with type I diabetes with or without overt nephropathy, type 2 diabetes without overt nephropathy and in nondiabetic CKD, the available clinical data support the use of angiotensin-converting enzyme inhibitors as the RAS modulator of choice. Low therapeutic target BP levels <130/80 mmHg in persons with type 2 diabetes mellitus also appear warranted based on available data mostly for reducing the risk of nonrenal cardiovascular disease and overall mortality.
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PMID:Prevention of hypertension and its complications: theoretical basis and guidelines for treatment. 1281 10

The majority of patients seen at the renal clinic of the University Hospital of the West Indies (UHWI) are of African descent. The case notes of patients with systemic lupus erythematosus (SLE) with class 4 nephritis and who were given standard pulse intravenous cyclophosphamide therapy during the period 1990-2000 were retrospectively reviewed. Primary outcomes were doubling of serum creatinine and development of end stage renal disease (ESRD). Secondary outcomes were return of proteinuria to normal and renal remission. A total of 117 patients had a renal biopsy for SLE nephritis at the UHWI between 1990 and 2000. Of the patients, 34 (29%) had diffuse proliferative glomerulonephritis (WHO class 4), of which 29 were reviewed. Twenty-two patients of 24 in whom it was measured (92%) had significant proteinuria at presentation. The 24-hour proteinuria was measured at final review in 16 patients and in 10 patients it went into complete remission. At the beginning of therapy, 24 patients (83%) had renal impairment. Of the 18 who had final creatinine values, the renal function returned to normal in eight patients (44%) and an additional six patients showed a significant improvement in renal function at final review. Six patients developed end stage renal disease (ESRD). The risk (95% confidence interval) of developing ESRD at one year was 16.2% (CI, 6.4-37.6) and at two years was 23.2% (CI, 10.0-48.5). There were three deaths, two from sepsis and one from heart failure. The one-year mortality (95% CI) was 8% (CI, 2.0-28.5), the two-year mortality was 15.6% (CI, 4.9-43.5) and the five-year mortality was also 15.6% (CI, 4.9-43.5). Intravenous pulse cyclophosphamide for Jamaican patients with SLE and diffuse proliferative glomerulonephritis is an ineffective form of treatment.
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PMID:Severity of systemic lupus erythematosus with diffuse proliferative glomerulonephritis and the ineffectiveness of standard pulse intravenous cyclophosphamide therapy in Jamaican patients. 1294 26

In the individual patient, the goal of antihypertensive treatment is to lower the blood pressure (BP) to a level that minimizes the patient's risk of cardiovascular complications. However, most of our knowledge regarding what this level of BP should be is derived from population studies and large clinical trials. Population studies have shown that elevated BP is associated with an increased risk of morbidity and mortality from coronary heart disease, stroke, heart failure, and renal failure. Cardiovascular risk begins to increase when BP exceeds 115/75 mm Hg and doubles with each increment of 20 mm Hg in systolic BP and 10 mm Hg in diastolic BP.The clinical benefit of BP reduction in patients with hypertension is well established. Thus, patients with less severe elevations in BP (high-normal) are at increased risk. Patients with diabetes or proteinuria benefit from even more aggressive reductions in BP. Despite the well-established benefits of BP reduction, hypertension is still not well treated, underscoring the need for more aggressive detection and better management. Although data from large clinical trials have provided valuable information to help guide treatment, application of clinical trial results to individual patients is limited by the heterogeneity of patient populations with respect to patient risk, comorbidities, and differences in genetic and environmental background. Ultimately, the treatment decisions should be tailored to each patient, integrating as much information as possible concerning the patient's history, risk, pathophysiology, and lifestyle.
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PMID:Examining therapeutic goals: population versus individual-based approaches. 1462 57

Decreasing levels of renal function act as a major adverse prognostic factor after contrast exposure with or without percutaneous coronary intervention. In chronic kidney disease, the most important risk factor for the development of contrast-induced nephropathy (CIN) is an estimated glomerular filtration rate </= 60 mL/min/1.73 m2. Additional risk factors include diabetes, proteinuria, volume depletion, heart failure, and intraprocedural events. Overall, CIN occurs in approximately 15% of radiocontrast procedures, with < 1% requiring dialysis. CIN is directly related to increases in hospitalization length, cost, and long-term morbidity. For those patients who require dialysis, a 30% in-hospital mortality rate and 80% 2-year mortality rate can be expected. CIN is predictable and presents an opportunity to utilize preventive strategies, given the increasing numbers of patients undergoing contrast procedures worldwide.
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PMID:Epidemiology of contrast-induced nephropathy. 1466 4

The development of drugs which block the renin-angiotensin system (RAS) has been proven a major advance in cardiovascular medicine. Angiotensin converting enzyme (ACE) inhibitors, which block the formation of angiotensin II from the inactive angiotensin I, are widely used as first line treatment in hypertension, heart failure and diabetic nephropathy. More recently, selective antagonists of the angiotensin type-1 receptor (AT1R) have become available for clinical use. Accumulating evidence suggests that AT1R antagonists have similar effects to ACE inhibitors in hypertension, heart failure and diabetic nephropathy. Although ACE inhibitors and AT1R antagonists block the same system, experimental evidence suggest that their mechanisms of action differ in several respects, such as increased bradykinin and angiotensin 1-7 levels with ACE inhibitors and AT2R activation with AT1R antagonists. Nevertheless, the clinical significance of these differences remains largely unknown and, in practice, the only clear advantage of AT1R antagonists over ACE inhibitors is the absence of cough as a side effect. Recent clinical data suggest that combined ACE inhibition and AT1R antagonism offer additive effects in reducing blood pressure in hypertension, in reducing proteinuria in nephropathy and in improving prognosis in heart failure. Further evidence suggests that some hypertensive patients may have a good antihypertensive response with ACE inhibition but not with AT1R antagonism, or the reverse. These data suggest that these two drug classes have important similarities, because they act on the same system, but they also appear to have important differences, which are not only of theoretical but also of clinical importance.
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PMID:Renin-angiotensin system blockade at the level of the angiotensin converting enzyme or the angiotensin type-1 receptor: similarities and differences. 1496 13

Anemia can be the cause of heart failure, but also its consequence. The pathogenesis of anemia in chronic heart failure (CHF) has yet to be fully elucidated, but is likely to be complex. Epidemiologic studies suggest that kidney dysfunction (by reducing the erythropoietic response to anemia), inflammation (by inducing erythropoietin resistance), decreased body mass index, old age, female gender, and poor clinical status may be important factors in the development of anemia in CHF. Intestinal malabsorption, chronic aspirin use, and proteinuria predisposes to iron deficiency. Proinflammatory cytokines are likely to play a significant role in anemia in CHF by generating the "anemia of chronic illness" that is a hallmark of inflammatory conditions. Few studies have investigated the mechanisms of anemia in CHF. There is a need for such studies.
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PMID:Anemia in chronic heart failure: pathogenetic mechanisms. 1500 93

The goal of antihypertensive therapy is to prevent cardiovascular complications of hypertension, such as heart failure, stroke, end stage renal disease, and death, not just to normalize blood pressure. Recently, several clinical trials investigated the beneficial effects of angiotensin II antagonists (AIIAs) in patients with hypertension, heart failure or diabetic nephropathy utilizing proven clinical outcomes (e.g., all-cause mortality) rather than surrogate outcomes (e.g., blood pressure or proteinuria). The AIIAs may offer therapeutic advantages with respect to particular outcomes in certain types of patients. Evidence is also emerging that losartan may possess beneficial pharmacological properties such as effects on uric acid, platelets, sexual dysfunction, and cognitive function, that may set it apart from other members of the AIIA class. However, further studies are needed to delineate fully these potential pharmacological differences among the AIIAs and their possible clinical relevance. This paper reviews recent AIIA outcomes studies in patients with hypertension, heart failure, or diabetic nephropathy and also examines data suggesting that molecular differences exist within the AIIA class, differences that may assist in explaining the outcomes achieved in these recent trials.
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PMID:AII antagonists in hypertension, heart failure, and diabetic nephropathy: focus on losartan. 1502 37

Diabetic nephropathy has become the single most important cause of end-stage renal disease in the USA, Europe and Japan. The earliest marker of incipient diabetic nephropathy is the transition of normoalbuminuria to microalbuminuria at an albumin excretion rate of 20 microg/min. Human studies in patients both with and without diabetic kidney diseases have shown that the severity of baseline proteinuria is an important predictor of the rate of loss of renal function. Moreover, the reduction in protein excretion rate when patients with nephropathies are being treated with antihypertensive agents predicts the efficacy of subsequent renoprotection. Experimental and clinical observations provide the rationale for targeting the renin-angiotensin system as a renoprotective approach in diabetic and nondiabetic proteinuric nephropathies. Losartan (Cozaar, Merck Sharpe and Dohme) is a potent, orally active and highly specific angiotensin-type 1 receptor blocker. In addition to its antihypertensive efficacy, losartan decreases the left ventricular mass index in patients with hypertension, left ventricular end-diastolic and end-systolic volume in subjects with heart failure and prevents cardiovascular morbidity and death, predominantly stroke, independent of blood pressure reduction. Short-term studies in Type 1 diabetic patients with overt nephropathy have demonstrated that losartan and angiotensin-converting enzyme inhibitors have similar beneficial effects on albumin excretion rate, blood pressure and renal hemodynamics. Losartan also lowered albumin excretion rate in microalbuminuric patients with Type 2 diabetes mellitus. Moreover, the large multicenter Reduction of End points in Noninsulin dependent diabetes mellitus with the Angiotensin II Antagonist Losartan (RENAAL) trial has shown that blockade of angiotensin-type 1 receptor with losartan is superior to conventional antihypertensive therapy in slowing the progression of overt Type 2 diabetic nephropathy. Together, data from clinical trials demonstrate the beneficial effect of angiotensin-type 1 receptor blockers, including losartan, in the primary and secondary prevention of renal disease progression in diabetic patients. Nevertheless, it can be expected that the positive results achieved so far with this class of drugs may be further implemented by including angiotensin-type 1 receptor antagonists as a part of the multidrug approach that may hold more promise for the future of renoprotection in diabetic patients with chronic nephropathy.
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PMID:Losartan in diabetic nephropathy. 1522 8

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