Valsartan and atenolol in patients with severe essential hypertension

Cífková, Renata; Peleskã, Jan; Hradec, J; Rosolová, Hana; E, Pintérová; Zeman, Karel; Oddou-Stock, Pascale; Thirlwell, J.; Botteri, Florence

doi:10.1038/sj.jhh.1000615

Cited by 29 publications

(13 citation statements)

References 13 publications

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“…The development of AT 1 receptor antagonists has provided a new class of therapeutic agents that may interfere with the effects of A-II at the level of target organs. These agents have been shown to be effective in mild-to-moderate hypertension and are associated with a lower incidence of cough and angioedema than ACE inhibitors [7,8], but there are only limited reports on their use in severe hypertension [9][10][11].…”

Section: Introductionmentioning

confidence: 98%

Efficacy and Safety of Eprosartan in Severe Hypertension

Sega

1999

Blood Pressure

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The efficacy of eprosartan, a highly selective, orally-active non-biphenyl, non-tetrazole, type 1 angiotensin II (AT1) receptor antagonist, was compared with that of the angiotensin-converting enzyme (ACE) inhibitor, enalapril, with the addition of hydrochlorothiazide (HCTZ) when necessary in patients with severe hypertension (sitting diastolic blood pressure [sitDBP] > or = 115 mmHg and < or = 125 mmHg). Patients (n = 118) were randomized into an 8-week, double-blind titration phase and were started on oral eprosartan 400 mg total daily dose, given b.i.d., or oral enalapril 10 mg total daily dose, given o.d. The dose of eprosartan was increased to 600 and 800 mg daily, given b.i.d., and that of enalapril to 20 and 40 mg daily, given o.d., at weeks 2 and 4 if sitDBP was > or = 90 mmHg. If blood pressure remained uncontrolled on maximum doses of eprosartan or enalapril at week 6, HCTZ 25 mg o.d. was added to the treatment regimen. Patients whose blood pressure was deemed medically acceptable by the investigator at week 8 entered a 2-week maintenance phase on the final dose used in the titration phase. The primary efficacy measure was the difference between treatments of the mean reduction from baseline in sitDBP at the end of the study. Eprosartan and enalapril caused a similar reduction in sitDBP at study endpoint. The mean change in sitDBP at the end of the study for the eprosartan group was -20.1 mmHg vs -16.2 mmHg for the enalapril group. However, eprosartan produced significantly greater decreases in both sitting and standing systolic blood pressure (sitSBP and staSBP, respectively) than enalapril. The mean decrease in sitSBP was 29.1 mmHg for eprosartan compared with 21.1 mmHg for enalapril (p = 0.025). The mean reduction in staSBP was 27.8 mmHg for eprosartan compared with 20.0 mmHg for enalapril (p = 0.032). At the end of the study, the response rate (sitDBP < 90 mmHg or decreased from baseline by at least 15 mmHg) was 69.5% in the eprosartan group and 54.2% in the enalapril group. The proportion of patients in each treatment group who required addition of HCTZ was similar. Eprosartan was well tolerated; the overall incidence of adverse events was comparable to that in the enalapril group. These results demonstrate that in patients with severe hypertension, eprosartan is well tolerated and may be more effective than enalapril in reducing systolic blood pressure.

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Section: Introductionmentioning

confidence: 98%

Efficacy and Safety of Eprosartan in Severe Hypertension

Sega

1999

Blood Pressure

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“…This was maintained over 6 months during which the decline in glomerular filtration rate was less, although not significantly, than that following treatment with placebo. In patients with severe hypertension (diastolic blood pressure 110–119 mm Hg), a drug regimen based on valsartan was as effective as one based on atenolol in reducing blood pressure [31]demonstrating that valsartan is compatible with other antihypertensive agents and can be used easily as part of combination therapy. In that study and in other comparative studies, valsartan had a clear advantage over comparator drugs in tolerability [23, 25, 26, 27, 32].…”

Section: Introductionmentioning

confidence: 99%

Clinical Advantage of Valsartan

McInnes¹

1999

Cardiology

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Valsartan is a specific angiotensin II receptor antagonist with high selectivity for the AT₁ receptor subtype. After oral administration of single or repeated once-daily doses, valsartan 40–80 mg inhibits the pressor response to angiotensin II for 24 hours. In patients with mild-to-moderate hypertension, efficacy of valsartan appears to be independent of age, sex, and race, and is at least equivalent to that of calcium antagonists, ACE inhibitors, or thiazide diuretics. Response rate to valsartan 160 mg o.d. is significantly greater than after receiving losartan 100 mg o.d. Valsartan has additive effects with other antihypertensive drugs and combination therapy is effective in severe hypertension and in hypertension with renal insufficiency, where renal function is well maintained. Valsartan has good tolerability with a side-effect profile indistinguishable from placebo and superior to that of comparable drugs. Valsartan does not cause cough or adverse metabolic effects; first dose hypotension and rebound hypertension on abrupt withdrawal have not been encountered. Valsartan has clear clinical advantage in the management of hypertension. Its impact on prognosis in patients with a high risk of cardiovascular morbidity and mortality is under evaluation.

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“…Since the major fraction of administered drug is excreted in the bile, a reduced dose may be appropriate for patients with biliary duct obstruction or severe liver disease [58]. As valsartan is not metabolised to any significant degree and clearance from plasma occurs mainly by biliary excretion of the unchanged substance, it is suitable for administration together with a wide range of other drugs [19,28,37,[59][60][61][62][63]. Valsartan has been found in the mammary glands and is excreted in the milk of rats.…”

Section: Safety and Tolerabilitymentioning

confidence: 99%

“…Clinical trials in the elderly show good efficacy and high responder rates with the same doses as in younger patients [35,36]. Valsartan is effective as an antihypertensive treatment in both mild-tomoderate and severe cases of hypertension [34,37].…”

Section: Major Phase III Studiesmentioning

confidence: 99%

Valsartan in The Treatment of Hypertension

et al. 2005

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Valsartan is a widely used, efficacious and very well-tolerated antihypertensive agent. By specifically blocking the action of angiotensin II on the angiotensin Type 1 receptor, valsartan reduces unwanted effects of angiotensin II, such as aldosterone, vasopressin and endothelin secretion, vasoconstriction, diuresis, endothelial cell hyperplasia, mitogenesis, induction of growth factors and production of collagen. Valsartan has a simple pharmacokinetic profile and requires no metabolism to become active. The dose-related efficacy of valsartan has been clearly demonstrated and the tolerability profile is similar to placebo. Clinical trials in elderly patients show good efficacy and high responder rates with the same doses as in younger patients. Valsartan is available as 80-, 160-and 320-mg tablets, and also in the same doses in combination with hydrochlorothiazide, 12.5 or 25 mg. Availability varies between countries. Beyond the reduction of blood pressure, valsartan is indicated for use in several countries in patients with heart failure and in patients post myocardial infarction, based on the results of the large-scale Valsartan Heart Failure Trial and VALsartan In Acute myocardial iNfarcTion trials. Valsartan has also been shown, in the Valsartan Antihypertensive Long-term Evaluation trial, to reduce the risk of developing new-onset diabetes in hypertensive patients at high risk of cardiac events.

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Valsartan and atenolol in patients with severe essential hypertension

Cited by 29 publications

References 13 publications

Efficacy and Safety of Eprosartan in Severe Hypertension

Efficacy and Safety of Eprosartan in Severe Hypertension

Clinical Advantage of Valsartan

Valsartan in The Treatment of Hypertension

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