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Tenormin I.V. (Atenolol) - Summary

 
 



BOX WARNING

BOXED WARNING

Cessation of Therapy with TENORMIN

Patients with coronary artery disease, who are being treated with TENORMIN, should be advised against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction and ventricular arrhythmias have been reported in angina patients following the abrupt discontinuation of therapy with beta blockers. The last two complications may occur with or without preceding exacerbation of the angina pectoris. As with other beta blockers, when discontinuation of TENORMIN is planned, the patients should be carefully observed and advised to limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that TENORMIN be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue TENORMIN therapy abruptly even in patients treated only for hypertension. (See DOSAGE AND ADMINISTRATION.)

 

TENORMIN I.V. SUMMARY

TENORMIN
(atenolol)
I.V. INJECTION

TENORMIN® (atenolol), a synthetic, beta1-selective (cardioselective) adrenoreceptor blocking agent.

TENORMIN is indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Treatment can be initiated as soon as the patient's clinical condition allows. (See DOSAGE AND ADMINISTRATION, CONTRAINDICATIONS, and WARNINGS.) In general, there is no basis for treating patients like those who were excluded from the ISIS-1 trial (blood pressure less than 100 mm Hg systolic, heart rate less than 50 bpm) or have other reasons to avoid beta blockade. As noted above, some subgroups (eg, elderly patients with systolic blood pressure below 120 mm Hg) seemed less likely to benefit.
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NEWS HIGHLIGHTS

Published Studies Related to Tenormin I.V. (Atenolol)

Identifying iatrogenic depression using confirmatory factor analysis of the Center for Epidemiologic Studies Depression Scale in patients prescribed a verapamil-sustained-release-led or atenolol-led hypertension treatment strategy. [2011.11.29]
BACKGROUND: beta-blockers and calcium channel blockers are highly effective medications indicated for treatment and prevention of hypertension. However, the literature regarding the potential depressive effects of beta-blockers and calcium channel blockers is equivocal regarding whether one or both are associated with depression. OBJECTIVES: To determine whether self-reported depressive symptoms of older persons with hypertension and coronary artery disease and who were randomly assigned to a verapamil-sustained-release-led (Ve-led) or atenolol-led (At-led) hypertension treatment strategy were similar using confirmatory factor analytical models of the Center for Epidemiologic Studies Depression Scale (CES-D)... CONCLUSIONS: The domains indicating less happiness and more depressive symptoms were most likely to be unfavorably impacted by the At-led treatment strategy. Given a choice between these equally effective high blood pressure treatment strategies, it may be prudent to use the Ve-led strategy. This is especially true if the risk of the occurrence of a mood-related side effect of the beta-blocker outweighs its other benefits in comparison. Copyright (c) 2011 Elsevier Inc. All rights reserved.

[Study of the efficacy and safety of losartan versus atenolol for aortic dilation in patients with Marfan syndrome]. [2011.06]
INTRODUCTION AND OBJECTIVES: Marfan syndrome is an inherited disease of the connective tissue. Recent trials have indicated the use of losartan (a transforming growth factor beta inhibitor) in these patients prevents aortic root enlargement. The aim of our clinical trial is to assess the efficacy and safety of losartan versus atenolol in the prevention of progressive dilation of the aorta in patients with Marfan syndrome... CONCLUSIONS: Efficacy of losartan versus atenolol in the prevention of progressive dilation of the aorta, improved aortic distensibility, and prevention of adverse events (aortic dissection or rupture, cardiovascular surgery, or death) will be assessed in this study. It will also show the possible treatment benefits at different age ranges and with relation to the initial level of aortic root dilation. Copyright (c) 2011 Sociedad Espanola de Cardiologia. Published by Elsevier Espana. All rights reserved.

Comparison of the effects of ivabradine and atenolol on heart rate and echocardiographic variables of left heart function in healthy cats. [2011.05]
BACKGROUND: Ivabradine is a novel negative chronotropic drug used for treatment of ischemic heart disease in people. Little is known about its effects and safety in cats.Clinical studies in cats with hypertrophic cardiomyopathy are needed to validate these findings.

Effect of atenolol vs metoprolol succinate on vascular function in patients with hypertension. [2011.01]
BACKGROUND: We evaluated the effect of atenolol vs metoprolol succinate on vascular function in patients with essential hypertension. HYPOTHESIS: Given intrinsic differences between these agents, we hypothesized that atenolol and metoprolol succinate would have disparate effects on vascular function... CONCLUSIONS: Although atenolol and metoprolol succinate have similar effects on blood-pressure reduction, they have different effects on vascular function. Compared with metoprolol succinate, atenolol increases peripheral AIx. Neither drug has an effect on vascular endothelial function. These findings may have clinical implications, depending on the indication for treatment in an individual patient. (c) 2011 Wiley Periodicals, Inc.

beta(1)-Adrenergic receptor gene polymorphisms and the acute response to atenolol in healthy young Japanese subjects. [2011]
Polymorphisms at codons 49 and 389 of the beta(1)-adrenergic receptor gene have been shown to alter the receptor function in vitro, whereas it remains controversial whether they influence the response to beta-blocker in vivo. In the present study, we investigated whether these polymorphisms influence the acute changes of heart rate and blood pressure induced by the beta(1)-adrenergic receptor-selective blocker atenolol in healthy young Japanese...

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Clinical Trials Related to Tenormin I.V. (Atenolol)

Effects of Losartan Versus Atenolol on Aortic and Cardiac Muscle Stiffness in Adults With Marfan Syndrome [Completed]
Marfan syndrome is an inherited connective tissue disorder with morbidity and mortality from aortic dilation and dissection. The degree of aortic dilation and response to beta-blockade (standard of care) vary in adults with Marfan syndrome. However, aortic stiffness is often present, and can be a predictor of aortic dilation and cardiovascular complications. In addition, adults with Marfan syndrome develop left ventricular diastolic dysfunction, which can progress to heart failure. Aortic stiffness and diastolic dysfunction are important and logical therapeutic targets in adults with Marfan syndrome. TGF-beta mediates disease pathogenesis in Marfan syndrome and contributes to aortic stiffness. The angiotensin receptor blocker, losartan, inhibits TGF-beta activity and reverses aortic wall pathology in a Marfan mouse model. Losartan also decreases aortic stiffness and improves diastolic function in hypertension, renal disease and hypertrophic cardiomyopathy. This trial is a randomized, double-blind trial of 50 adults with Marfan syndrome, treated with 6 months of atenolol vs. losartan. Arterial tonometry for aortic stiffness and echocardiography for diastolic function will be performed at the beginning and end of treatment. A blood draw for serum markers of extracellular matrix turnover and inflammation will also be performed at 0 and 6 months. We plan to determine whether losartan decreases aortic stiffness and left ventricular diastolic dysfunction significantly more than atenolol.

Comparison Study of the Effect of Aliskiren Versus Negative Controls on Aortic Stiffness in Patients With Marfan Syndrome Under Treatment With Atenolol [Recruiting]
Marfan syndrome (MFS) is an inherited disorder of connective tissue with morbidity and mortality from aortic dilatation and dissection. The current standard of care is beta-blocker (BB) treatment and therapeutic target is heart rate. The degree of aortic dilatation and response to BB vary in adults with MFS. However, aortic stiffness is often present, and can be a predictor of aortic dilatation and cardiovascular complications. Aortic stiffness is a logical therapeutic target in adults with MFS. Transforming growth factor beta(TGF-beta) mediates disease pathogenesis in MFS and contributes to aortic stiffness. Cross-talk between TGF-beta system and renin-angiotensin system (RAS) has been demonstrated. The angiotensin receptor blocker (ARB), losartan, inhibits TGF-beta activity and reverses aortic wall pathology in a Marfan mouse model. In a small cohort study, the use of ARB therapy (losartan or irbesartan) significantly slowed the rate of progressive aortic dilatation in patients with MFS, after BB therapy had failed to prevent aortic root dilatation. In another study, angiotensin converting enzyme inhibitor, perindopril, reduced both aortic stiffness and aortic root diameter in patients with MFS taking standard BB therapy. Renin inhibitor, aliskiren, has not been studied to reduce aortic stiffness and attenuate aortic dilatation in patients with MFS. This trial is a randomized, open-label trial of 32 patients with Marfan syndrome, treated with 6 months of aliskiren vs. negative controls in patients with MFS under atenolol treatment. MRI for aortic pulsed wave velocity (PWV) and distensibility, measurements of central BP (CBP) and augmentation index (AIx) will be performed at the beginning and end of treatment. A blood drawn for serum markers of TGF-beta, extracellular matrix turnover and inflammation will also be performed at 0 and 6 months. We plan to determine whether aliskiren decreases aortic stiffness significantly more than negative controls in patients with MFS under atenolol treatment.

Effect of SLCO2B1 Genotype and Apple Juice on Pharmacokinetics of Atenolol After Oral Administration in Healthy Male Korean [Completed]

Comparison of Peripheral and Cerebral Arterial Flow in Acute Ischemic Stroke: Fimasartan vs. Valsartan vs. Atenolol [Active, not recruiting]
Confirm central blood pressure reduction effect of Fimasartan, Valsartan and Atenolol and compare correlation with the measured peripheral (central blood pressure, pulse wave velocity, and flow-mediated dilation) and cerebral blood flow factors (transcranial doppler findings, cerebral blood flow volume) in acute ischemic stroke patients with hypertension.

Evaluation of The Effects of Nebivolol in Comparison to Atenolol on Wall Shear Stress and Rupture Prone Coronary Plaques [Completed]
Nebivolol is a novel blood pressure lowering drug with an additional effect on the inner lining of blood vessels to release a compound called nitric oxide that can relax blood vessels. Atenolol is a blood pressure reducing agent without the ability to release nitric oxide and effect additional blood vessel relaxation. The goal of this proposal is to compare Nebivolol and Atenolol with respect to the following parameters:

- Plaque within arteries supplying the heart in terms of its volume and composition as

assessed by ultrasound within these arteries.

- Ability of small arteries in the heart to open up and deliver an enhanced blood supply

in response to drug called Adenosine (routinely used in the cardiac catheterization laboratory) as assessed by pressure and flow detecting catheters within these arteries.

- Ability of the inner lining of arteries that supply the heart to release a relaxing

compound called nitric oxide in response to injection of Acetylcholine (also used in the cardiac catheterization laboratory) as assessed by squirting dye into these arteries

- Local forces that affect blood flow in the arteries supplying the heart as assessed by

superimposing the above data into complex maps created offline at Georgia Institute of Technology. It is likely that Nebivolol causes the plaque within arteries supplying the heart to change from the 'vulnerable' type to the 'stable' type plaque. There are several features of "vulnerable plaques" that can be detected in arteries of the heart using intravascular ultrasound (a small ultrasound camera that goes in the arteries of the heart). The investigators hypothesis is that Nebivolol will prove superior to Atenolol in reducing 'vulnerable plaques', improve blood flow within the small arteries and the health of inner lining of these arteries at the 1 year time point. The investigators plan to enroll 20 patients into the study (26 patient including dropouts) who will be randomized in a 1: 1 manner to Nebivolol Vs Atenolol for 1 year and repeat evaluation at that time point.

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Page last updated: 2011-12-09

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