Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new ramipril research articles will be listed here shortly after becoming available to us.
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Medical research on ramipril
Cardioprotective effects of telmisartan in uncomplicated and complicated hypertension.
J Renin Angiotensin Aldosterone Syst. 2008 Jun; 9(2): 66-74
Grassi G, Quarti-Trevano F, Mancia G
The development of angiotensin II receptor blockers (ARB) as a new class of drugs for the management of hypertension has elicited the attention of many clinicians worldwide with the aim of improving blood pressure (BP) control as well as cardiovascular protection. Among ARB telmisartan has been shown to be characterised by an antihypertensive efficacy fully covering the 24-hour period, thereby allowing to antagonise the adverse effects of early morning BP rise on cardiovascular risk. Other specific effects of the drug are represented by its favourable metabolic profile (particularly on insulin sensitivity) and neutral effects on sympathetic cardiovascular function. These properties are coupled with cardioprotective effects, documented by the evidence that the drug: 1) is effective in favouring the regression of cardiac and vascular organ damage, 2) reduces arterial stiffness and improves vascular distensibility and 3) reverses the endothelial dysfunction typical of the hypertensive state particularly when complicated by renal failure, diabetes, obesity or metabolic syndrome. Several of these properties can account for the results of the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET), documenting the beneficial effects on the drug on cardiovascular morbidity and mortality.
Eur J Heart Fail. 2008 Jun 24;
Chen CY, Lee BC, Hsu HC, Lin HJ, Chao CL, Lin YH, Ho YL, Chen MF
OBJECTIVES: In this study, we used a proteomic approach to investigate the potential proteins regulated by ramipril in post-infarction left ventricular remodelling in the rabbit. METHODS AND RESULTS: Myocardial infarction (MI) was induced in male New Zealand White rabbits (2.5-3 kg) by ligation of the left anterior descending coronary artery. Two months later, the rabbits were either left untreated (MI group) or were treated daily for one month with 0.1 mg/kg wt of ramipril (ramipril group), then sacrificed. One month of ramipril treatment resulted in a significant improvement in the LV ejection fraction (LVEF) and a decrease in hydroxyproline content. The protein profiles of LV tissue showed that ramipril caused upregulation of glutathione peroxidase, superoxide dismutase (SOD), and heart-type fatty acid binding-protein (h-FABP) and downregulation of HSP27 and cyclophilin A. Ramipril treatment caused an increase in catalase, glutathione peroxidase, and SOD activity in the LV tissue. Oxidized glutathione levels and the GSSG/GSH ratio in the heart tissue were lower in the ramipril group than in the MI group. CONCLUSIONS: Ramipril increased antioxidative protein expression and enzyme activity, which could partly explain the role of ramipril in attenuating LV remodelling. In addition, the present study identifies several potential protein targets which may help to explain the mechanism by which ramipril exerts its effect in post-infarction LV remodelling in the rabbit.
Liver Transpl. 2008 Jun 25; 14(7): 1020-1028
Galioto A, Semplicini A, Zanus G, Fasolato S, Sticca A, Boccagni P, Frigo AC, Cillo U, Gatta A, Angeli P
The aim of this study was to compare nifedipine and carvedilol in the treatment of de novo arterial hypertension after orthotopic liver transplantation (OLT). The study included 50 patients who developed arterial hypertension after OLT. Twenty-five patients received nifedipine (group A), and 25 received carvedilol (group B). Patients were defined as intolerant to nifedipine or carvedilol if severe adverse effects developed. These patients stopped the first drug and were switched to the other one. Patients were defined as full responders to monotherapy if there was normalization of blood pressure, and they were defined as partial responders by the need to add a second antihypertensive drug, ramipril. The 2 groups of patients were similar for baseline conditions. At the end of the study, patients intolerant to monotherapy were 48% of group A and 12.5% of group B (P < 0.01). Full responders were 20% of group A and 33.33% of group B (P < 0.01). Partial responders were 22% of group A and 54.1% of group B (P < 0.01). The addition of ramipril normalized blood pressure in 19% of partial responders to monotherapy (75% in partial responders to nifedipine and 30% in partial responders to carvedilol, P < 0.01). In responders to either monotherapy or combined therapy, there was a significant improvement of renal function. In responders to carvedilol, but not in responders to nifedipine, the daily dose of tacrolimus at 1 year should be reduced to 50% compared to the baseline dose to maintain the blood trough level in the therapeutic range. Liver Transpl 14:1020-1028, 2008. (c) 2008 AASLD.
Rev Med Liege. 2008 Apr; 63(4): 213-9
Scheen AJ, Krzesinski JM
ONTARGET ("ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial") compared the angiotensin converting enzyme inhibitor ramipril (10 mg/day), the angiotensin-receptor blocker telmisartan 80 mg/day, and the combination of the two drugs in 25,620 patients with vascular disease or high-risk diabetes. After a median follow up of 56 months, no significant differences were observed between the three groups neither in the primary composite outcome (death from cardiovascular causes, myocardial infarction, stroke, or hospitalization for heart failure), nor in each of its components, total mortality and other secondary outcomes. Telmisartan was equivalent to ramipril (non inferiority criterion), but was better tolerated (less cough and angioedema). The combination of the two drugs in this population (without congestive heart failure and proteinuric nephropathy) did not bring increased benefit (no superiority), but was associated with more adverse events (hypotension, syncope and renal dysfunction). In this population, the choice of the molecule in monotherapy remains optional and the use of a dual blockade is not justified in order to have a better cardiovascular protection.
Am J Hypertens. 2008 Jun 19;
Fogari R, Derosa G, Ferrari I, Corradi L, Zoppi A, Lazzari P, Santoro T, Preti P, Mugellini A
BackgroundThis study compared the effect of antihypertensive treatment with valsartan or ramipril on atrial fibrillation (AF) recurrence, on P-wave dispersion, (PWD) and on serum procollagen type I carboxy terminal peptide (PIP).MethodsA total of 369 mild hypertensive (systolic blood pressure (SBP) >140 and/or 90 < diastolic blood pressure (DBP) < 110 mm Hg) outpatients in sinus rhythm but with at least two episodes of AF in the previous 6 months were randomized to valsartan (n = 122), ramipril (n = 124), or amlodipine (n = 123) for 1 year. Clinic blood pressure (BP) and a 24-h electrocardiogram (ECG) were evaluated monthly. Patients were asked to report any episode of symptomatic AF and to perform an ECG as early as possible. PWD and serum PIP levels were evaluated before and after each treatment period.ResultsSBP and DBP were significantly reduced by the three treatments (P < 0.001). A total of 46 (47.4%) patients treated with amlodipine had a recurrence of AF as did 26 (27.9%) patients treated with ramipril (P < 0.01 vs. amlodipine) and 16 (16.1%) patients treated with valsartan (P < 0.01 vs. amlodipine and P < 0.05 vs. ramipril). The Kaplan-Meyer analysis showed a significant reduction of AF episodes in the valsartan group (P = 0.005 log-rank test) as well as in the ramipril group (P = 0.021), even if at a lesser degree. PWD values were significantly reduced by ramipril (-4.2 ms, P < 0.05) and even more by valsartan (-11.2 ms, P < 0.01), the difference being significant (P < 0.01). Serum PIP levels were reduced by ramipril (-49.7 mug, P < 0.001) and valsartan (-49.3 mug, P < 0.001).ConclusionsDespite similar BP lowering, valsartan and ramipril were more effective than amlodipine in preventing new episodes of AF, but the effect of valsartan was greater than that of ramipril. This could be related to the greater PWD reduction observed with valsartan.American Journal of Hypertension (2008). doi:10.1038/ajh.2008.217American Journal of Hypertension (2008). doi:10.1038/ajh.2008.217.
Effect of ramipril on renal function in patients with intermittent claudication.
Vasc Health Risk Manag. 2008; 4(2): 471-5
Hobbs SD, Claridge MW, Wilmink AB, Adam DJ, Thomas ME, Bradbury AW
BACKGROUND: The Heart Outcomes Prevention Study (HOPE) demonstrated that ramipril resulted in a blood-pressure-independent 25% reduction in cardiovascular events in patients with peripheral arterial disease (PAD). Despite this, general practitioners and vascular surgeons remain reluctant to prescribe ACE inhibitors in this group of patients because of concerns about renal artery stenosis (RAS). We aimed to define the effect of ramipril on renal function in patients with intermittent claudication (IC). METHODS AND RESULTS: Of 132 unselected patients with IC entering the study 78 (59%) were excluded due to: current ACE inhibitor use (38%), renal impairment (serum creatinine above normal range) (15%), known severe RAS (1%) or unwillingness to participate (5%). The remaining 54 patients were titrated to 10 mg ramipril and renal function was monitored at 1, 5, and 12 weeks. Treatment was discontinued during titration in 5 patients due to symptoms (3) or lack of compliance (2). In the remainder, median [IQR] serum creatinine increased (94 [85.8-103.3] to 98 [88.0-106.5] micromol/L, p < or = 0.001) and median [IQR] GFR decreased (71.5 [64.6-82.3] to 68.7 [59.8-74.7] mL/min per 1.73 m2, p < or = 0.001) between baseline and 5 weeks. These changes were not considered clinically significant. By 12 weeks these values had returned almost to baseline (Cr 95.5 [88.0-103.25] micromol/L, GFR 71.8 [65.3-77.4] mL/min). No patient had a serum creatinine rise > 30%. CONCLUSION: Most of patients with IC and a normal serum creatinine can be safely commenced on ramipril provided they are screened, titrated and monitored as described above. Studies in patients with borderline renal impairment (serum creatinine up to 30% above baseline) are on-going.
Eur J Pharmacol. 2008 May 16;
Ismael MA, Talbot S, Carbonneau CL, Beauséjour CM, Couture R
Glucose-fed rat is a model of insulin resistance that displays sensory polyneuropathy and hypertension. This study aimed at comparing the beneficial effects of N-Acetyl-l-Cysteine (NAC, antioxidant) and ramipril (angiotensin-1 converting enzyme inhibitor) on tactile and cold allodynia induced by chronic glucose feeding. Impact of these treatments was also assessed on hypertension, plasma glucose and insulin concentrations, insulin resistance and kinin B(1) receptor expression. Male Wistar rats (50-75 g) were given 10% d-glucose in their drinking water for 11 weeks or tap water (controls). Glucose-fed rats were treated either with NAC (1 g/kg/day, gavage), ramipril (1 mg/kg/day in drinking water) or no drug during the last 5 weeks. Glucose feeding for 6 weeks induced a significant increase in systolic blood pressure and hyperglycaemia which was accompanied by tactile and cold allodynia. At 11 weeks, plasma insulin, insulin resistance (HOMA index), kinin B(1) receptor mRNA in spinal cord and renal cortex and B(1) receptor binding sites in spinal cord were enhanced in glucose-fed rats. NAC and ramipril caused a progressive to complete inhibition of tactile and cold allodynia from 6 to 11 weeks. High systolic blood pressure, hyperinsulinemia, insulin resistance and kinin B(1) receptor expression were also normalized or attenuated in glucose-fed rats by either treatment. Results suggest that chronic treatment with an antioxidant or an ACE inhibitor provides similar beneficial effects on sensory polyneuropathy, hypertension and insulin resistance in glucose-fed rats. Both therapies were associated with a reduction of the expression of the pro-nociceptive kinin B(1) receptor.
J Hypertens. 2008 Jul; 26(7): 1487-1496
Lüders S, Schrader J, Berger J, Unger T, Zidek W, Böhm M, Middeke M, Motz W, Lübcke C, Gansz A, Brokamp L, Schmieder RE, Trenkwalder P, Haller H, Dominiak P,
BACKGROUND: The prevention of hypertension with the angiotensin-converting enzyme inhibitor ramipril in patients with high-normal blood pressure study addresses the issue of whether progression to manifest hypertension in patients with high-normal blood pressure can be prevented with treatment. METHODS: A total of 1008 participants with high-normal office blood pressure were randomized to ramipril treatment group (n = 505) and a control group (n = 503). The patients were followed up for 3 years. Primary endpoint was to prevent or delay the progression to manifest hypertension. Secondary endpoints were reduction in the incidence of cerebrovascular and cardiovascular events, as well as the development of hypertension as defined by ambulatory blood pressure monitoring. FINDINGS: One hundred and fifty-five patients (30.7%) in the ramipril group, and 216 (42.9%) in the control group reached the primary endpoint (relative risk reduction 34.4%, P = 0.0001). Ramipril also proved to be more effective in reducing the incidence of manifest office hypertension in patients with baseline ambulatory blood pressure monitoring high-normal blood pressure. The incidence of cerebrovascular and cardiovascular events showed no statistically significant differences between the two groups. Cough was more frequent in the ramipril group (4.8 vs. 0.4%). INTERPRETATION: There is now good clinical evidence that patients with high-normal blood pressure (prehypertension) are more likely to progress to manifest hypertension than patients with optimal or normal blood pressure. Additional ambulatory blood pressure monitoring seems to be essential to achieve correct diagnosis. Treatment of patients with high-normal office blood pressure with the angiotensin-converting enzyme inhibitor was well tolerated, and significantly reduced the risk of progression to manifest hypertension.
Kardiologiia. 2008; 48(5): 72
Liakishev AA
[Choroidal effusion after uncomplicated cataract surgery.]
Klin Monatsbl Augenheilkd. 2008 Jun; 225(6): 591-3
Fromberg I, Krause M, Brückner K, Lang M, Seitz B
BACKGROUND: Intake of ACE inhibitors may promote angioedema which can appear months and years after the medication has been stopped. Surgery and local anaesthesia can further aggravate angioedema. A 61-year-old patient with age-related cataract was admitted to our hospital for elective out-patient cataract surgery. A few days after surgery, the patient complained of pain and reduced vision in the operated eye. RESULTS: Postoperative findings were elevated intraocular pressure (28 mmHg) and a significant reduction of vision. The anterior chamber was shallow. Ophthalmoscopy showed a circumferential choroidal and focal exsudative retinal detachment. Local and systemic therapy with antiglaucomatous medications as well as steroids (methylprednisolone) and antibiotics (ciprofloxacine) resulted in control of the eye pressure and an increase of vision. After two weeks, the choroidal detachment disappeared. Important preexisting diseases included a minimal change glomerulonephritis under treatment with low doses of cortisone (4 mg), as well as arterial hypertension. An ACE inhibitor (ramipril) was taken. CONCLUSIONS: ACE inhibitor intake might be associated with choroidal effusion. A preoperative change to another antihypertensive medication should be considered in patients with a tendency to develop angioedema. A glomerulonephritis might also support edema. Patients with such edema should undergo diagnostic evaluation and receive treatment before cataract surgery.