Renal Insufficiency as a Predictor of Cardiovascular Outcomes and the Impact of Ramipril: The HOPE Randomized Trial
Department of Nephrology and Hypertension, Schwabing General Hospital, LMU, Kolner Platz 1, D-80804 Munchen, Germany. Annals of internal medicine
(Impact Factor: 17.81).
04/2001; 134(8):629-36. DOI: 10.1016/S1062-1458(01)00373-7
The cardiovascular risk associated with early renal insufficiency is unknown. Clinicians are often reluctant to use angiotensin-converting enzyme inhibitors in patients with renal insufficiency.
To determine whether mild renal insufficiency increases cardiovascular risk and whether ramipril decreases that risk.
Post hoc analysis.
The Heart Outcomes and Prevention Evaluation (HOPE) study, a randomized, double-blind, multinational trial involving 267 study centers.
980 patients with mild renal insufficiency (serum creatinine concentration >/= 124 micromol/L [>/=1.4 mg/dL]) and 8307 patients with normal renal function (serum creatinine concentration < 124 micromol/L [<1.4 mg/dL]) Patients with a baseline serum creatinine concentration greater than 200 micromol/L (2.3 mg/dL) were excluded.
The primary outcome measure was incidence of cardiovascular death, myocardial infarction, or stroke.
Cumulative incidence of the primary outcome was higher in patients with renal insufficiency than in those without (22.2% vs. 15.1%; P < 0.001) and increased with serum creatinine concentration. Patients with renal insufficiency had a substantially increased risk for cardiovascular death (11.4% vs. 6.6%) and total mortality (17.8% vs. 10.6%) (P < 0.001 for both comparisons). The effect of renal insufficiency on the primary outcome (adjusted hazard ratio, 1.40 [95% CI, 1.16 to 1.69]) was independent of known cardiovascular risks and treatment. Ramipril reduced the incidence of the primary outcome in patients with and those without renal insufficiency (hazard ratio, 0.80 vs. 0.79; P > 0.2 for the difference).
In patients who had preexisting vascular disease or diabetes combined with an additional cardiovascular risk factor, mild renal insufficiency significantly increased the risk for subsequent cardiovascular events. Ramipril reduced cardiovascular risk without increasing adverse effects.
Available from: Ioannis Goutos
- "It is a relatively late complication of T1DM, but often established at the time of diagnosis of T2DM. Nephropathy is a marker for other diabetes related complications , including cardiovascular disease and cerebrovascular accidents    and can lead to end stage renal insufficiency necessitating renal replacement therapy or transplantation  . The implications of diabetic renal impairment are multiple and apart from the need for careful fluid management include: "
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ABSTRACT: The number of diabetic patients presenting to burn services is predicted to increase significantly over the next decades. Diabetes mellitus represents an independent risk factor for sustaining burn injuries and mediates alterations to key physiological systems including the vascular, renal, nervous, gastrointestinal and immune system. The effects of the pathophysiological permutations need to be carefully considered during both the acute as well as the long-term rehabilitation phase of injury. The purpose of the first part of this review is to outline the metabolic permutations observed in diabetes mellitus pertinent to the clinical presentation and management of burn patients.
Available from: Verónica Guarner
- "voia et al . , 2011 ; Touyz , 2005 ) . In the HOPE ( Heart Outcome and Prevention Evaluation ) trials , renal insufficiency was associated with increased risk for cardiovascular events , and the ACEi ( Angiotensin Converted Enzyme inhibitor ) ramipril reduced the incidence of cardiovascular events in patients with and without renal insufficiency ( Mann et al . , 2001 ) . Even if these secondary analyses appear promising , trials specifically designed in CKD populations are still needed to properly assess the effect of RAS blockade on arterial remodeling and cardiovascular prognosis ( Briet and Burns , 2012 ) ."
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ABSTRACT: Aging impairs blood vessel function and leads to cardiovascular disease. The mechanisms underlying the age-related endothelial, smooth muscle and extracellular matrix vascular dysfunction are discussed. Vascular dysfunction is caused by: 1) Oxidative stress enhancement. 2) Reduction of nitric oxide (NO) bioavailability, by diminished NO synthesis and/or augmented NO scavenging. 3) Production of vasoconstrictor/vasodilator factor imbalances. 4) Low-grade pro-inflammatory environment. 5) Impaired angiogenesis. 5) Endothelial cell senescence. The aging process in vascular smooth muscle is characterized by: 1) Altered replicating potential. 2) Change in cellular phenotype. 3) Changes in responsiveness to contracting and relaxing mediators. 4) Changes in intracellular signaling functions.
Systemic arterial hypertension is an age-dependent disorder, and almost half of the elderly human population is hypertensive. The influence of hypertension on the aging cardiovascular system has been studied in models of hypertensive rats. Treatment for hypertension is recommended in the elderly. Lifestyle modifications, natural compounds and hormone therapies are useful for initial stages and as supporting treatment with medication but evidence from clinical trials in this population is needed. Since all antihypertensive agents can lower blood pressure in the elderly, therapy should be based on its potential side effects and drug interactions.
Available from: Wookyung Chung
- "Therefore, preventive measures for CVD are of great importance in patients with CKD. Previous studies have demonstrated that efforts to lower blood pressure ,  and lipid levels  are effective for reducing the risk of CVD in patients with CKD. However, the importance of other potential preventive therapies, such as antiplatelet agents, remains controversial. "
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Chronic kidney disease (CKD) is a major risk factor for the development of cardiovascular disease (CVD). Previous trials have investigated the effects of low-dose aspirin on CVD prevention in patients with diabetes; however, patients with CKD were not examined. The role of aspirin in diabetics is controversial, and the available literature is contradictory. Therefore, we studied whether low-dose aspirin would be beneficial for patients with CKD, a group that is at high risk for CVD.
From a total of 25340 patients with CKD, 1884 recipients of low-dose aspirin (100 mg/day) were paired 1∶1 with non-recipients for analysis using propensity score matching. The primary endpoint was the development of atherosclerotic CVD, including coronary arterial disease, stroke, and peripheral arterial disease. Secondary endpoints included death from any cause, bleeding events, doubling of serum creatinine, and renal death.
The incidence of a primary endpoint of any atherosclerotic CVD was significantly higher in the aspirin users than in the non-users (P<0.001). Secondary endpoints, including all-cause mortality and composite bleeding events, were not significantly different between the aspirin users and the non-users. However, the doubling of serum creatinine levels (P = 0.001) and renal death (P = 0.042) were significantly associated with the use of aspirin.
These results suggest that the use of low-dose aspirin in patients with CKD may have harmful consequences related to the development of CVD and renal progression.
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