Sixty-six nondiabetic patients with CKD and proteinuria and 36 healthy subjects were enrolled. Patients were treated with either ramipril 5 mg daily or valsartan 160 mg daily for 3 months. Proteinuria, ADMA, symmetric dimethyl arginine (SDMA), flow-mediated dilatation (FMD) and HOMA index measurements were performed both before and after the treatment.
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Multiple switches per prescription are uncommon and multiple different products are rarely supplied on repeats of the same prescription. The rules of the brand substitution policy appear to be adequate in allowing brand choice for patients, without leading to multiple switches per prescription.
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Subchronic bolus administration of the angiotensin-converting-enzyme inhibitor ramipril caused a dose-dependent (0.1 to 10 mg.kg-1.d-1), yet each in his own way 24-hour sustained, reduction in arterial blood pressure in conscious unrestrained spontaneously hypertensive rats with telemetric recording, and 0.01 mg.kg-1.d-1 was a no-effect dose. This was accompanied by dose-dependent attenuation of heart rate lowering during periods of low locomotor activity. Neither effect persisted for more than a few days after cessation of the medication with full restoration of pretreatment levels. No dosage altered the circadian rhythm of blood pressure, heart rate and locomotor activity of the rats.
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Inhibition of the renin-angiotensin system contributes to reductions in proteinuria and in progression of chronic kidney disease. Indeed, monotherapy with either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) has been shown to decrease proteinuria and slow the decline of chronic kidney disease, but incompletely. Therefore, there is increasing interest in whether combination strategies will provide more complete blockade of the renin-angiotensin system, which may translate into superior renoprotective and cardioprotective effects compared with either agent alone. There have been several reports on combination strategies. However, the recent report of the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) has received much of the attention. The renal outcomes in ONTARGET suggest that combined ACE inhibitor and ARB therapy contributes to a higher rate of adverse renal outcomes than monotherapy. Therefore, this review explores data from ONTARGET in relation to other available evidence on the use of combination therapies.
Among all patients, increases in apical regional wall stress were associated with LV volume changes (P -trend =.015). The relationship between apical regional wall stress and change in LV volume was strongest in the low-dose ramipril group (r = 0.53, P =.002) and remained significant after adjustment for end-diastolic volume, infarct size, ejection fraction, and systolic blood pressure yet was attenuated in the full-dose ramipril group.
In our studies, we investigated the vasodepressor effects of bradykinin in vivo in normotensive and hypertensive subjects. Bradykinin was injected intravenously and intra-arterially (40-6,050 pM/kg) and was infused intra-arterially (40-6,050 pM/kg/min). The investigations were performed in 21 normotensive and 15 hypertensive patients. Bradykinin injections were performed after the following pharmacological interventions: salt restriction (10 mmol of Na/day), salt loading (300 mmol of Na/day), captopril (50 mg), ramipril (5 mg), lisinopril (20 mg), ketotifen (2 X 1 mg), indomethacin (2 X 50 mg), and propranolol (80 mg). The results show that bradykinin lowers blood pressure in a dose-related manner by marked reduction in peripheral vascular resistance. The blood pressure reduction was strongly correlated with the increase in kinin concentration. This effect of bradykinin appears to be independent of changes in sodium metabolism, beta-adrenoceptors, histamine-1 receptors, and prostaglandins. ACE inhibitors protentiate the blood pressure-lowering effect of bradykinin approximately 20- to 50-fold. In the case of intra-arterial injection of bradykinin, only 2-5% of the intravenously used dose of bradykinin are needed to produce an identical fall in blood pressure. From these experiments, a pulmonary clearance rate of bradykinin of over 95% can be calculated. In the pulmonary arteries, bradykinin has no effect on vascular resistance. In patients suffering from primary or renovascular hypertension, the blood pressure response to bradykinin was enhanced. The bradykinin potentiating effect of the ACE inhibitors was not altered in the hypertensives. In patients suffering from borderline hypertension or primary hyperaldosteronism, bradykinin caused the same blood pressure lowering effect as in the normotensives.
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Nitrates are often administrated with a variety of other pharmacologic agents in the management of chronic heart failure (CHF). However, limited information is available concerning the long-term effects in patients with evidence of left ventricular (LV) dysfunction after acute myocardial infarction (AMI) already treated with standard heart failure therapy.
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A total of 87 patients were assessed at baseline and following 9 weeks treatment with the angiotensin-receptor blocker telmisartan (final dose, 80 mg; n = 45) or the angiotensin-converting enzyme inhibitor ramipril (final dose, 10 mg; n = 42). Adiponectin levels were measured in plasma by radioimmunoassay.
In Wistar rats, four experiments were carried out, studying specific inhibitors for ACE (angiotensin-converting enzyme), such as captopril, enalapril, lisinopril, ramipril and cilazapril, in presence of 20% and 95% ethanol induced gastric lesions. The effect of lisinopril and angiotensin I on the same injury was also studied. Subsequently, drugs with known role in gastric mucosa cytoprotection, such as enprostil, paracetamol, ketotiphen, levamisole, diazepam, bromocriptine, dopamine and clonidine, before and after absolute ethanol gastric injury were also studied. Finally, to examine the potential role of ACE in gastric cytoprotection, pretreatment with enalapril, followed by cytoprotective drugs, was carried out. We conclude that all ACE blockers aggravate the gastric lesion induced by 20% and 95% ethanol and are similar to the findings with angiotensin I. The gastric ACE probably plays an important role in the gastric mucosa defense. On the other hand, gastric ACE, as a physiologic regulator of microcirculation, acts by a double mechanism. a) converting the vasopressor amine, angiotensin I in angiotensin II. b) activating vasoactive peripheric receptors such as DA 2 dopaminergic and alfa 2 adrenoreceptors.
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In the HOPE trial, 9297 high-risk men and women, >/=55 years of age with previous cardiovascular disease or diabetes plus 1 risk factor, were randomly assigned to ramipril (up to 10 mg/d), vitamin E (400 IU/d), their combination, or matching placebos. During the mean follow-up of 4.5 years, there were 482 (10.4%) patients with clinical MI and unexpected cardiovascular death in the ramipril group compared with 604 (12.9%) in the placebo group [relative risk reduction (RRR), 21% (95% CI) (11,30); P<0.0003]. Ramipril was associated with a trend toward less fatal MI and unexpected death [4.0% versus 4.7%; RRR, 16% (-3, 31)] and with a significant reduction in nonfatal MI [5.6% versus 7.2%; RRR, 23% (9,34)]. Risk reductions in MI were documented in participants taking or not taking beta-blockers, lipid lowering, and/or antiplatelet agents. Although ramipril had no impact on hospitalizations for unstable angina [11.9% versus 12.2%; RRR, 3% (-9,14)], it reduced the risk of worsening and new angina [27.2% versus 30.0%; RRR, 12% (5,18); P<0.0014] and coronary revascularizations [12.5% versus 14.8%; RRR, 18%; (8,26) P<0.0005].
Compared with placebo, MDL decreased blood pressure (P < 0.001) and prevented left ventricular hypertrophy (P < 0.001), being as effective as ramipril. Hypertrophy and dilatation of the aorta and hypertrophy of the resistance arterioles were all prevented by MDL. Plasma aldosterone was decreased by MDL (P < 0.001), but not by ramipril. Icatibant blunted the decrease in blood pressure (P < 0.001), decreased cGMP concentrations and blunted the decrease in cross-sectional area of the resistance arteries in MDL-treated, but not in ramipril-treated, transgenic rats. In 3-month-old transgenic rats, MDL normalized blood pressure, regressed left ventricular hypertrophy and decreased adrenomedullin concentrations.
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Inhibition of the angiotensin-converting enzyme (ACE) exerts a renoprotective effect in adult patients with chronic kidney disease. We evaluated prospectively changes in blood pressure (BP), protein excretion and renal function after administration of the long-acting ACE inhibitor ramipril as monotherapy during 6 months in 14 moderately hypertensive children aged 5-18 years with various nephropathies. Four patients initially had a decreased glomerular filtration rate (GFR below 60 ml/min/1.73 m2). BP was evaluated by ambulatory 24-h monitoring. After 2 weeks of treatment by oral ramipril (1.5 mg/m2 once daily), mean values of systolic and diastolic 24-h ambulatory BP fell by more than 5 mmHg in nine patients. In eight patients the dose was doubled. At the end of the study systolic BP was below the 95th percentile in 9 and diastolic BP in 13 patients. The initially reduced nocturnal dip increased significantly. Of 11 patients with an increased albumin excretion (median 1.3 g/g creatinine), 6 responded to ramipril by a median reduction of 78% (range 24-83%), whilst in 5 albuminuria increased (median +19%). GFR was well preserved and no other adverse effects from the drug were noted. The study demonstrates that ramipril is an efficacious antihypertensive agent in children with renal hypertension. It is well tolerated, even in mild renal insufficiency. In addition, the drug has a persistent antiproteinuric action in about half of the patients contributing to conserve renal function.
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Placebo for 14 days, followed by full-dose (10 mg) ramipril until day 90; low-dose (0.625 mg) ramipril for 90 days; or full-dose ramipril for 90 days. All patients underwent reperfusion therapy.
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Microalbuminuria is reduced significantly by ramipril treatment in type 1 diabetic patients without hypertension. Although the magnitude of the response was greater, there is no significant difference between responses to 1.25 or 5 mg ramipril. Small but highly significant reductions in systolic and mean arterial pressures occur in ramipril-treated patients. GFR is stable at this stage of the evolution of diabetic nephropathy and is unaffected by ramipril treatment for 2 years.
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This study compares the effect of two different strategies to inhibit the renin-angiotensin system in the setting of acute myocardial infarction (MI). Male Wistar rats were treated with placebo, the angiotensin-converting enzyme (ACE) inhibitor ramipril (1 mg/kg/day), or the AT1 receptor antagonist, olmesartan (1 mg/kg/day), both initiated 1 week before induction of MI and continued for 6 weeks after MI. The inflammatory reaction in the heart was investigated 7 days post-MI by determination of macrophage infiltration and the expression of tumor necrosis factor (TNF-alpha), interleukin (IL)-1beta and IL-6 at mRNA and protein levels. Six weeks post-MI, cardiac function was measured following chronic implantation of catheters in the LV and femoral artery, and cardiac morphology and coronary structure were investigated in picrosirius-red stained hearts. In placebo-treated rats, macrophage infiltration was accompanied by upregulation of IL-1beta and IL-6 mRNA in the peri-infarct zone. TNF-alpha and IL-1beta mRNA and protein were also upregulated in the non-infarcted myocardium. Whereas both treatment regimes significantly reduced IL-6 upregulation, olmesartan additionally reduced macrophage infiltration and IL-1beta expression. Six weeks post-MI, placebo-treated MI animals developed an impaired cardiac function with structural remodeling of the myocardium and coronaries. While olmesartan and ramipril both improved cardiac function and reduced infarct size and myocardial/coronary remodeling, olmesartan was more effective not only in increasing vascular perimeter, inner vascular diameter and septal thickness but also in lowering media thickness of coronary arteries, inner left ventricular diameter, left ventricular circumference and left ventricular end-diastolic pressure than ramipril. Thus, following MI the AT1 receptor blocker, olmesartan, attenuated cardiac inflammatory reactions and protected myocardial/coronary structure and function of the failing heart proving to be of similar, in some cases superior effectiveness in this respect than the ACE inhibitor, ramipril.
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p38 mitogen-activated protein kinase (p38 MAPK) inhibition exerts beneficial effects on left ventricular (LV) remodeling and dysfunction. p38 MAPK activity is transiently increased soon after myocardial infarction (MI), suggesting brief inhibition may afford the same benefit as long-term inhibition. We examined chronic 12-week p38 MAPK inhibition compared with short-term (7-day) inhibition, and then we discontinued inhibition after MI. Post-MI rats at day 7 received either vehicle, 4-[4-(4-fluorophenyl)-1-(3-phenylpropyl)-5-(4-pyridinyl)-1H-imidazol-2-yl]-3-butyn-1-ol (RWJ67657; RWJ) for 12 weeks (long term; LT-RWJ), RWJ for 1 week and discontinued for 11 weeks (1-week RWJ), or continuous ramipril for 12 weeks. In separate groups of animals, 24 h after MI, vehicle or RWJ was administered for 7 days. Cardiac function was assessed by echocardiography and hemodynamic measurements. Percentage of fractional shortening improved after LT-RWJ and ramipril, but not after 1-week RWJ treatment. Likewise, LV contractility and maximal first derivative of left ventricular pressure (dP/dt(max)) was improved (12.5 and 14.4%) and LV end diastolic pressure (LVEDP) was reduced (49.4 and 54.6%) with both treatments. Functional outcomes were accompanied by regression of interstitial collagen I and alpha-smooth muscle actin expression in LV noninfarct, border, and infarct regions with LT-RWJ and ramipril treatment. Hypertrophy was reduced in noninfarct (18.3 and 12.2%) and border regions (16.3 and 12.0%) with both treatments, respectively. Animals receiving RWJ 24 h after MI for 7 days showed similar improvements in fractional shortening, dP/dt(max), LVEDP, including reduced fibrosis and hypertrophy. In vitro experiments confirmed a dose-dependent reduction in hypertrophy, with RWJ following tumor necrosis factor-alpha stimulation. Continuous but not short-term p38 MAPK blockade attenuates post-MI remodeling, which is associated with functional benefits on the myocardium.
The administrative databases did not contain detailed clinical information, and unmeasured factors associated with a patient's risk for death may have influenced physicians' prescription choices.
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Our experience suggests that treatment of anthracycline-induced CHF with an ACE inhibitor should start soon after clinical improvement on digoxin/diuretic regardless of the severity of symptoms rather than waiting for clinical deterioration.
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An open and multicentric study was conducted with 66 patients with mild to severe diastolic arterial hypertension and echocardiographic left ventricular hypertrophy, the evolution of diastolic function, by means of doppler transmitral flow echocardiography, under treatment with ramipril, an angiotensin converting enzyme inhibitor, at a dose of 2.5 and 5 mg/day, or combined with a diuretic, after three and six months of treatment. Despite not obtaining the tensional control in all patients, a decrease in the mass, both in absolute values and mass index, was obtained. This decrease was observed both in male and female patients from the first three months, which went on until the sixth month, thus suggesting an independent action of the hemodynamic load decrease for the obtention of this effect. There was also a change in the ventricular geometry with a displacement of patients from concentric enlargement to normal, remodelling and eccentric enlargement. The diastolic function improved both for the early and for the late maximal filling velocity, relationship between both, and deceleration time, although the time during which this improvement occurred was different for each parameter, thus indicating the different influence of the dynamic and structural factors on these parameters. No correlation was found between the improvement in diastolic function and hypertrophy regression. We can conclude that ramipril is useful for the control of the left ventricular hypertrophy and diastolic function, irrespective of arterial tension values.
Although prescribing and the resulting outpatient use of cardiovascular drugs (ATC group C) that were reimbursed by the Republic Fund for Health was increased approximately by 13% in 2004 in comparison with 2000 (67.98 vs. 60.17 DDD/1000 inh./day), we did not find a statistically significant difference (p > 0.05). Prescribing of ACE inhibitors (C09A) increased approximately by 45% during the investigated period (15.30 vs. 22.17 DDD/1000 inh./day). The selection of drugs was also altered: cilazapril, ramipril and quinapril were left out, captopril and enalapril were more prescribed, and a newly-induded fosinopril was prescribed mostly (31.5%). Calcium-channel blockers (C08) were prescribed 33.7% more (7.12 vs. 9.52 DDD/1000 inh./day), mostly because of seven times higher prescribing of amlodipine in 2004. Pentaerythritol tetranitrate was left out, but isosorbide dinitrate and isosorbide mononitrate were prescribed more frequently. High-priced atorvastatin was replaced with the older simvastatin, that was prescribed three times more.