DOCSLIB.ORG

Angiotensin-Converting Enzyme (ACE) Inhibitors Single Entity Agents

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Angiotensin-Converting Enzyme (ACE) Inhibitors Single Entity Agents Therapeutic Class Overview Angiotensin-Converting Enzyme (ACE) Inhibitors Single Entity Agents Therapeutic Class Overview/Summary: The renin-angiotensin-aldosterone system (RAAS) is the most important component in the homeostatic regulation of blood pressure.1,2 Excessive activity of the RAAS may lead to hypertension and disorders of fluid and electrolyte imbalance.3 Renin catalyzes the conversion of angiotensinogen to angiotensin I. Angiotensin I is then cleaved to angiotensin II by angiotensin- converting enzyme (ACE). Angiotensin II may also be generated through other pathways (angiotensin I convertase).1 Angiotensin II can increase blood pressure by direct vasoconstriction and through actions on the brain and autonomic nervous system.1,3 In addition, angiotensin II stimulates aldosterone synthesis from the adrenal cortex, leading to sodium and water reabsorption. Angiotensin II exerts other detrimental cardiovascular effects including ventricular hypertrophy, remodeling and myocyte apoptosis.1,2 The ACE inhibitors block the conversion of angiotensin I to angiotensin II, and also inhibit the breakdown of bradykinin, a potent vasodilator.4 Evidence-based guidelines recognize the important role that ACE inhibitors play in the treatment of hypertension and other cardiovascular and renal diseases. With the exception of Epaned® (enalapril solution) and Qbrelis® (lisinopril solution), all of the ACE inhibitors are available generically. Table 1. Current Medications Available in Therapeutic Class5-19 Generic Food and Drug Administration Approved Dosage Generic (Trade Name) Indications Form/Strength Availability Benazepril Hypertension Tablet: (Lotensin®*) 5 mg 10 mg 20 mg 40 mg Captopril* Diabetic nephropathy, heart failure, hypertension, Tablet: left ventricular dysfunction post-myocardial 12.5 mg infarction 25 mg 50 mg 100 mg Enalapril Asymptomatic left ventricular dysfunction, heart Solution: (Vasotec®*, failure, hypertension 1 mg/mL Epaned®) Tablet: 2.5 mg 5 mg 10 mg 20 mg Enalaprilat* Hypertension Injection: 1.25 mg/mL Fosinopril* Heart failure, hypertension Tablet: 10 mg 20 mg 40 mg Lisinopril Acute myocardial infarction to improve survival, Solution: (Prinivil®*, heart failure, hypertension 1 mg/mL Qbrelis®, Zestril®*) Tablet: 2.5 mg 5 mg 10 mg 20 mg Page 1 of 6 Copyright 2016 • Review Completed on 09/13/2016 Therapeutic Class Overview: angiotensin-converting enzyme (ACE) inhibitors-single entity Generic Food and Drug Administration Approved Dosage Generic (Trade Name) Indications Form/Strength Availability 30 mg 40 mg Moexipril* Hypertension Tablet: 7.5 mg 15 mg Perindopril Hypertension, stable coronary artery disease to Tablet: (Aceon®*) reduce the risk of cardiovascular mortality or 2 mg nonfatal myocardial infarction 4 mg 8 mg Quinapril Heart failure, hypertension Tablet: (Accupril®*) 5 mg 10 mg 20 mg 40 mg Ramipril Heart failure post myocardial infarction, Capsule: (Altace®*) hypertension, reduce the risk of myocardial 1.25 mg infarction, stroke and death from cardiovascular 2.5 mg causes 5 mg 10 mg Trandolapril Heart failure post-myocardial infarction, Tablet: (Mavik®*) hypertension, left ventricular dysfunction post- 1 mg myocardial infarction 2 mg 4 mg *Generic available in at least one dosage form or strength. Evidence-based Medicine Angiotensin-converting enzyme (ACE) inhibitors have been shown to be effective for coronary artery disease and to reduce the risk of cardiovascular mortality, myocardial infarction and stroke.19-30 Clinical Trials have demonstrated the efficacy of ACE inhibitors in reducing mortally associated with congestive heart failure.31-47 ACE inhibitors have demonstrated efficacy for the treatment for hypertension and for the use in diabetic nephropathy.48-79 Key Points within the Medication Class According to Current Clinical Guidelines:80-97 o Treatment guidelines for the management of stable angina recommend angiotensin- converting enzyme (ACE) inhibitors in patients with a left ventricular ejection fraction <40% and in those with hypertension, diabetes or chronic kidney disease. ACE inhibitors are also recommended in patients at lower risk (mildly reduced or normal left ventricular ejection fraction) in whom cardiovascular risk factors remain well controlled and revascularization has been performed. o Treatment guidelines for the management of unstable angina/non-ST elevation myocardial infarction recommend the use of ACE inhibitors in the first 24 hours in patients with or without pulmonary congestion or left ventricular ejection fraction of <40%. ACE inhibitors are recommended in patients with heart failure, left ventricular dysfunction, diabetes or hypertension. In addition, ACE inhibitors are a reasonable for patients with heart failure and left ventricular ejection fraction >40% and patients without hypertension or diabetes. The guidelines are similar for the management of ST-elevation myocardial infarction. o Treatment guidelines recommend ACE inhibitors in patients who are at risk for the development of heart failure. ACE inhibitors are recommended for the management of heart failure in patients who have cardiac structural abnormalities or remodeling who have not Page 2 of 6 Copyright 2016 • Review Completed on 09/13/2016 Therapeutic Class Overview: angiotensin-converting enzyme (ACE) inhibitors-single entity developed heart failure symptoms, especially in patients with reduced left ventricular ejection fraction and a history of myocardial infarction. o Treatment guidelines for hypertension recommend the use of ACE inhibitors as a first line option in all patients as well as in hypertensive patients with certain compelling indications including heart failure, post-myocardial infarction, left ventricular dysfunction, high coronary disease risk, diabetes, chronic kidney disease, and recurrent stroke prevention. o Treatment guidelines for the management of hypertension in patients with diabetes recommend a regimen including an ACE inhibitor. In patients with known cardiovascular disease, a regimen including an ACE inhibitor should be used to reduce the risk of cardiovascular events. In patients with type 1 diabetes, with hypertension and any degree of albuminuria, ACE inhibitors have been shown to delay the progression of nephropathy. In patients with type 2 diabetes, hypertension and microalbuminuria, ACE inhibitors have been shown to delay the progression to macroalbuminuria. Other Key Facts: o Clinical trials have not demonstrated significant differences when ACE inhibitors were compared to angiotensin II receptor blockers. o With the exception of Epaned® (enalapril solution) and Qbrelis® (lisinopril solution), all of the ACE inhibitors are available generically. References 1. Saseen JJ, Carter BL. Hypertension. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 6th edition. New York (NY): McGraw-Hill; 2005. p. 185-217. 2. Parker RB, Patterson JH, Johnson JA. Heart failure. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 6th edition. New York (NY): McGraw-Hill; 2005. p. 219-60. 3. Reid IA. Vasoactive peptides. In: Katzung BG, editor. Basic and clinical pharmacology [monograph on the Internet]. 11th ed. New York (NY): McGraw-Hill: 2009 [cited 2011 Mar 25]. Available from: http://online.statref.com. 4. Benowitz NL. Antihypertensive agents. In: Katzung BG, editor. Basic and clinical pharmacology [monograph on the Internet]. 11th ed. New York (NY): McGraw-Hill: 2009 [cited 2011 Mar 25]. Available from: http://online.statref.com. 5. Drug Facts and Comparisons 4.0 [database on the Internet]. St. Louis: Wolters Kluwer Health, Inc.; 2014 [cited 2014 Apr 18]. Available from: http://online.factsandcomparisons.com. 6. Micromedex® Healthcare Series [database on the Internet]. Greenwood Village (CO): Thomson Reuters (Healthcare) Inc.; Updated periodically [cited 2014 Apr 18]. Available from: http://www.thomsonhc.com/ 7. Lotensin® [package insert]. Suffern (NY): Novartis Pharmaceuticals Corporation; 2015 Jul. 8. Captopril [package insert]. Morgantown (WV): Mylan Pharmaceuticals Inc.; 2015 Jun. 9. Epaned® [package insert]. Greenwood Villaige (Co): Silvergate Pharmaceuticals, Inc.; 2016 Jan. 10. Vasotec® [package insert]. Bridgewater (NJ): Valeant Pharmaceuticals North America, LLC; 2015 Aug. 11. Fosinopril [package insert]. Fort Lauderdale (FL): Andrx Pharmaceuticals, Inc.; 2004 Jan. 12. Prinivil® [package insert]. Whitehouse Station (NJ): Merck&Co., Inc.; 2015 Aug. 13. Qbrelis® [package insert]. Greenwood Village (CO): Silvergate Pharmaceuticals, Inc.; 2016 Jul. 14. Zestril® [package insert]. Wilmington (DE): AstraZeneca Pharmaceuticals, LP; 2014 Jun. 15. Moexipril [package insert]. Mahwah (NJ): Glenmark Pharmaceuticals, Inc.; 2014 Dec. 16. Perindopril [package insert]. Baltimore (MD): Lupin Pharmaceuticals, Inc.; 2010 Jan. 17. Accupril® [package insert]. New York (NY): Pfizer Inc; 2015 Sep. 18. Altace® [package insert]. Bristol (TN): King Pharmaceuticals; 2015 Sep. 19. Mavik® [package insert]. North Chicago (IL): AbbVie, Inc.; 2016 Jan. 20. Swedberg K, Held P, Kjekshus J, et al. Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction results of the cooperative New Scandinavian enalapril survival study II (CONSENSUS II). N Engl J Med. 1992 Sep 3;327(10):678-84. 21. Pitt B, Reichek N, Willenbrock R, Zannad F, Philips RA, Roniker B, et al. Effects of eplerenone, enalapril, and eplerenone/enalapril
Load more

Recommended publications
  • Selective Mtorc2 Inhibitor Therapeutically Blocks Breast Cancer Cell Growth and Survival
    Author Manuscript Published OnlineFirst on January 22, 2018; DOI: 10.1158/0008-5472.CAN-17-2388 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Selective mTORC2 inhibitor therapeutically blocks breast cancer cell growth and survival Thomas A. Werfel1, 3, Shan Wang2, Meredith A. Jackson1, Taylor E. Kavanaugh1, Meghan Morrison Joly3, Linus H. Lee1, Donna J. Hicks3, Violeta Sanchez4, Paula Gonzalez Ericsson4, Kameron V. Kilchrist1, Somtochukwu C. Dimobi1, Samantha M. Sarett1, Dana Brantley-Sieders2, Rebecca S. Cook1,3,4* and Craig L. Duvall1* 1Department of Biomedical Engineering, Vanderbilt University, Nashville, TN 37232 USA 2Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232.USA 3Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232 USA 4Breast Cancer Research Program, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37232 USA Running Title: A selective mTORC2 inhibitor blocks breast cancer growth Key Words: Breast Cancer, mTOR, Rictor, RNA interference, Nanomedicine *To whom correspondence should be addressed: Craig L. Duvall, PhD Vanderbilt University School of Engineering Department of Biomedical Engineering Nashville, TN 37232 Phone: (615) 322-3598 Fax: (615) 343-7919 Email: [email protected] Rebecca S. Cook, PhD Vanderbilt University Medical Center Department of Cancer Biology Nashville, TN 37232 Phone: (615) 936-3813 Fax: (615) 936-3811 Email: [email protected] Funding. This work was supported by Specialized Program of Research Excellence (SPORE) grant NIH P50 CA098131 (VICC), Cancer Center Support grant NIH P30 CA68485 (VICC), NIH F31 CA195989-01 (MMW), NIH R01 EB019409, DOD CDMRP OR130302, NSF GFRP 1445197, and CTSA UL1TR000445 from the National Center for Advancing Translational Sciences.
    [Show full text]
  • Introduction to Hospital and Health-System Pharmacy Practice 59 Tients with a Specific Disease State Or for Activities Related to Self Governance Diagnosis
    Part II: Managing Medication Use CHAPTER 4 Medication Management Kathy A. Chase ■■ ■■■ Key Terms and Definitions Learning Objectives ■■ Closed formulary: A list of medica- After completing this chapter, readers tions (formulary) which limits access should be able to: of a practitioner to some medications. 1. Describe the purpose of a formulary A closed formulary may limit drugs to system in managing medication use in specific physicians, patient care areas, or institutions. disease states via formulary restrictions. 2. Discuss the organization and role of the ■■ Drug formulary: A formulary is a pharmacy and therapeutics committee. continually updated list of medications 3. Explain how formulary management and related information, representing works. the clinical judgment of pharmacists, 4. List the principles of a sound formulary physicians, and other experts in the system. diagnosis and/or treatment of disease 5. Define key terms in formulary manage- and promotion of health. ment. ■■ Drug monograph: A written, unbi- ased evaluation of a specific medica- tion. This document includes the drug name, therapeutic class, pharmacology, indications for use, summary of clinical trials, pharmacokinetics/dynamics, ad- verse effects, drug interactions, dosage regimens, and cost. ■■ Drug therapy guidelines: A document describing the indications, dosage regi- mens, duration of therapy, mode(s) of administration, monitoring parameters and special considerations for use of a specific medication or medication class. ■■ Drug use evaluation (DUE): A process used to assess the appropriate- ness of drug therapy by engaging in the evaluation of data on drug use in a given health care environment against predetermined criteria and standards. ◆■ Diagnosis-related DUE: A drug use evaluation completed on pa- INTRODUCTION TO HOSPITAL AND HEALTH-SYSTEM PHARMACY PRACTICE 59 tients with a specific disease state or for activities related to self governance diagnosis.
    [Show full text]
  • Utilization and Program Costs of Statins for Wisconsin Medicaid
    To: Prescribing Physicians, Pharmacies From: Wisconsin Medicaid, Division of Health Care Financing January 2004 Utilization and Program Costs of Statins for Wisconsin Medicaid PRIOR AUTHORIZATION GUIDELINES (atorvastatin), Zocor (simvastatin), Pravachol (pravastatin), Crestor (rosuvastatin), Lescol (fluvastatin), and Lescol XL In order to encourage the use of generic lovastatin, the Wis- (fluvastatin XL). Products that contain an HMG-CoA reductase consin Medicaid program began requiring prior authorization inhibitor combined with another ingredient (e.g. Advicor) were for brand name HMG-CoA reductase inhibitors on April 15, not included in this analysis. 2003. Prior authorization was made available through the STAT-PA system. Only recipients new to statin drugs are re- The generic form of lovastatin is significantly less expen- quired to try lovastatin first. The criteria for determining prior sive to the Medicaid program than brand name products. authorization includes: Average cost to the Wisconsin Medicaid Program for generic 1 · Any recipient currently on an effective brand name statin lovastatin 40 mg is $1.20 per tablet and for a brand name will be granted PA to continue on that statin drug. HMG-CoA reductase inhibitors (including the brand name · Any recipient who requires >35% reduction in low-density forms of lovastatin) range from $1.65 to $4.18 per equipotent dosage2 (table 1). lipoprotein (LDL) cholesterol will be granted PA to start on the brand name statin drugs. Table I · Any recipient who has impaired renal function will be Cost Per Tablet for Wisconsin Medicaid granted PA to start on the brand name statin drugs. · Any recipient who is at high risk for drug interactions will be granted PA to start on the brand name statin drugs.
    [Show full text]
  • S1 Table. List of Medications Analyzed in Present Study Drug
    S1 Table. List of medications analyzed in present study Drug class Drugs Propofol, ketamine, etomidate, Barbiturate (1) (thiopental) Benzodiazepines (28) (midazolam, lorazepam, clonazepam, diazepam, chlordiazepoxide, oxazepam, potassium Sedatives clorazepate, bromazepam, clobazam, alprazolam, pinazepam, (32 drugs) nordazepam, fludiazepam, ethyl loflazepate, etizolam, clotiazepam, tofisopam, flurazepam, flunitrazepam, estazolam, triazolam, lormetazepam, temazepam, brotizolam, quazepam, loprazolam, zopiclone, zolpidem) Fentanyl, alfentanil, sufentanil, remifentanil, morphine, Opioid analgesics hydromorphone, nicomorphine, oxycodone, tramadol, (10 drugs) pethidine Acetaminophen, Non-steroidal anti-inflammatory drugs (36) (celecoxib, polmacoxib, etoricoxib, nimesulide, aceclofenac, acemetacin, amfenac, cinnoxicam, dexibuprofen, diclofenac, emorfazone, Non-opioid analgesics etodolac, fenoprofen, flufenamic acid, flurbiprofen, ibuprofen, (44 drugs) ketoprofen, ketorolac, lornoxicam, loxoprofen, mefenamiate, meloxicam, nabumetone, naproxen, oxaprozin, piroxicam, pranoprofen, proglumetacin, sulindac, talniflumate, tenoxicam, tiaprofenic acid, zaltoprofen, morniflumate, pelubiprofen, indomethacin), Anticonvulsants (7) (gabapentin, pregabalin, lamotrigine, levetiracetam, carbamazepine, valproic acid, lacosamide) Vecuronium, rocuronium bromide, cisatracurium, atracurium, Neuromuscular hexafluronium, pipecuronium bromide, doxacurium chloride, blocking agents fazadinium bromide, mivacurium chloride, (12 drugs) pancuronium, gallamine, succinylcholine
    [Show full text]
  • Interaction of the Sympathetic Nervous System with Other Pressor Systems in Antihypertensive Therapy
    Journal of Clinical and Basic Cardiology An Independent International Scientific Journal Journal of Clinical and Basic Cardiology 2001; 4 (3), 185-192 Interaction of the Sympathetic Nervous System with other Pressor Systems in Antihypertensive Therapy Wenzel RR, Baumgart D, Bruck H, Erbel R, Heemann U Mitchell A, Philipp Th, Schaefers RF Homepage: www.kup.at/jcbc Online Data Base Search for Authors and Keywords Indexed in Chemical Abstracts EMBASE/Excerpta Medica Krause & Pachernegg GmbH · VERLAG für MEDIZIN und WIRTSCHAFT · A-3003 Gablitz/Austria FOCUS ON SYMPATHETIC TONE Interaction of SNS J Clin Basic Cardiol 2001; 4: 185 Interaction of the Sympathetic Nervous System with Other Pressor Systems in Antihypertensive Therapy R. R. Wenzel1, H. Bruck1, A. Mitchell1, R. F. Schaefers1, D. Baumgart2, R. Erbel2, U. Heemann1, Th. Philipp1 Regulation of blood pressure homeostasis and cardiac function is importantly regulated by the sympathetic nervous system (SNS) and other pressor systems including the renin-angiotensin system (RAS) and the vascular endothelium. Increases in SNS activity increase mortality in patients with hypertension, coronary artery disease and congestive heart failure. This review summarizes some of the interactions between the main pressor systems, ie, the SNS, the RAS and the vascular endothelium including the endothelin-system. Different classes of cardiovascular drugs interfere differently with the SNS and the other pressor systems. Beta-blockers, ACE-inhibitors and diuretics have no major effect on central SNS activity. Pure vasodilators including nitrates, alpha-blockers and DHP-calcium channel blockers increase SNS activity. In contrast, central sympatholytic drugs including moxonidine re- duce SNS activity. The effects of angiotensin-II receptor antagonist on SNS activity in humans are not clear, experimental data are discussed in this review.
    [Show full text]
  • Angiotensin-Converting Enzyme (ACE) Inhibitors
    Angiotensin-Converting Enzyme (ACE) Inhibitors Summary Blood pressure reduction is similar for the ACE inhibitors class, with no clinically meaningful differences between agents. Side effects are infrequent with ACE inhibitors, and are usually mild in severity; the most commonly occurring include cough and hypotension. Captopril and lisinopril do not require hepatic conversion to active metabolites and may be preferred in patients with severe hepatic impairment. Captopril differs from other oral ACE inhibitors in its rapid onset and shorter duration of action, which requires it to be given 2-3 times per day; enalaprilat, an injectable ACE inhibitor also has a rapid onset and shorter duration of action. Pharmacology Angiotensin Converting Enzyme Inhibitors (ACE inhibitors) block the conversion of angiotensin I to angiotensin II through competitive inhibition of the angiotensin converting enzyme. Angiotensin is formed via the renin-angiotensin-aldosterone system (RAAS), an enzymatic cascade that leads to the proteolytic cleavage of angiotensin I by ACEs to angiotensin II. RAAS impacts cardiovascular, renal and adrenal functions via the regulation of systemic blood pressure and electrolyte and fluid balance. Reduction in plasma levels of angiotensin II, a potent vasoconstrictor and negative feedback mediator for renin activity, by ACE inhibitors leads to increased plasma renin activity and decreased blood pressure, vasopressin secretion, sympathetic activation and cell growth. Decreases in plasma angiotensin II levels also results in a reduction in aldosterone secretion, with a subsequent decrease in sodium and water retention.[51035][51036][50907][51037][24005] ACE is found in both the plasma and tissue, but the concentration appears to be greater in tissue (primarily vascular endothelial cells, but also present in other organs including the heart).
    [Show full text]
  • Beta-Blockers for Hypertension: Time to Call a Halt
    Journal of Human Hypertension (1998) 12, 807–810 1998 Stockton Press. All rights reserved 0950-9240/98 $12.00 http://www.stockton-press.co.uk/jhh FOR DEBATE Beta-blockers for hypertension: time to call a halt DG Beevers University Department of Medicine, City Hospital, Birmingham B18 7QH, UK Beta-blockers are not very effective at lowering blood the endorsement of beta-blockers by the British Hyper- pressure in elderly hypertensive patients or in Afro- tension Society and other guidelines committees, Caribbeans and these two groups represent a large pro- except possibly for severe resistant hypertension, high portion of people with raised blood pressure. Further- risk post-infarct patients and those with angina pectoris. more they do not prevent more heart attacks than the The time has come to move across to newer, safer, more thiazide diuretics. Beta-blockers can also be dangerous tolerable and more effective antihypertensive agents in many hypertensive patients and even when these whilst continuing to use thiazide diuretics in low doses drugs are not contraindicated, they cause subtle and in the elderly as first choice, providing there are no depressing side effects which should preclude their contraindications. usefulness. The time has come therefore to reconsider Keywords: beta-blockers; hypertension Introduction Safety and tolerability Beta-adrenergic blockers were first introduced in the There is little doubt that the beta-blockers are the early 1960s for the treatment of angina pectoris. most unsafe of all antihypertensive drugs. They can Their antihypertensive properties were not fully precipitate or worsen heart failure in patients with recognised until the celebrated paper by Pritchard myocardial damage and they are contraindicated in and Gillam in 1964.1 They rapidly became popular patients with asthma.
    [Show full text]
  • 3. Diuretics for Hypertension-A Review and Update
    REVIEW Diuretics for Hypertension: A Review and Update George C. Roush1 and Domenic A. Sica2 Downloaded from https://academic.oup.com/ajh/article-abstract/29/10/1130/2622231 by Xenia Agorogianni user on 17 July 2019 This review and update focuses on the clinical features of hydrochlo- ectopy and reduce the risk for sudden cardiac death relative to thi- rothiazide (HCTZ), the thiazide-like agents chlorthalidone (CTDN) and azide-type diuretics used alone. A recent synthesis of 44 trials has indapamide (INDAP), potassium-sparing ENaC inhibitors and aldos- shown that the relative potencies in milligrams among spironolac- terone receptor antagonists, and loop diuretics. Diuretics are the sec- tone (SPIR), amiloride, and eplerenone (EPLER) are approximately ond most commonly prescribed class of antihypertensive medication, from 25 to 10 to 100, respectively, which may be important when SPIR and thiazide-related diuretics have increased at a rate greater than is poorly tolerated. SPIR reduces proteinuria beyond that provided by that of antihypertensive medications as a whole. The latest hyper- other renin angiotensin aldosterone inhibitors. EPLER also reduces tension guidelines have underscored the importance of diuretics for proteinuria and has beneficial effects on endothelial function. While all patients, but particularly for those with salt-sensitive and resist- guidelines often do not differentiate among specific diuretics, this ant hypertension. HCTZ is 4.2–6.2 systolic mm Hg less potent than review demonstrates that these distinctions are important for man- CTDN, angiotensin-converting enzyme inhibitors, beta blockers, and aging hypertension. calcium channel blockers by 24-hour measurements and 5.1 mm Hg systolic less potent than INDAP by office measurements.
    [Show full text]
  • Calcium Channel Blockers
    Calcium Channel Blockers Summary In general, calcium channel blockers (CCBs) are used most often for the management of hypertension and angina. There are 2 classes of CCBs: the dihydropyridines (DHPs), which have greater selectivity for vascular smooth muscle cells than for cardiac myocytes, and the non-DHPs, which have greater selectivity for cardiac myocytes and are used for cardiac arrhythmias. The DHPs cause peripheral edema, headaches, and postural hypotension most commonly, all of which are due to the peripheral vasodilatory effects of the drugs in this class of CCBs. The non-DHPs are negative inotropes and chronotropes; they can cause bradycardia and depress AV node conduction, increasing the risk of heart failure exacerbation, bradycardia, and AV block. Clevidipine is a DHP calcium channel blocker administered via continuous IV infusion and used for rapid blood pressure reductions. All CCBs are substrates of CYP3A4, but both diltiazem and verapamil are also inhibitors of 3A4 and have an increased risk of drug interactions. Verapamil also inhibits CYP2C9, CYP2C19, and CYP1A2. Pharmacology CCBs selectively inhibit the voltage-gated L-type calcium channels on cardiac myocytes, vascular smooth muscle cells, and cells within the sinoatrial (SA) and atrioventricular (AV) nodes, preventing influx of extracellular calcium. CCBs act by either deforming the channels, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the major cellular calcium store, the endoplasmic reticulum. Calcium influx via these channels serves for excitation-contraction coupling and electrical discharge in the heart and vasculature. A decrease in intracellular calcium will result in inhibition of the contractile process of the myocardial smooth muscle cells, resulting in dilation of the coronary and peripheral arterial vasculature.
    [Show full text]
  • Drug Class Review on Targeted Immune Modulators
    Drug Class Review on Targeted Immune Modulators Final Report December 2005 The purpose of this report is to make available information regarding the comparative effectiveness and safety profiles of different drugs within pharmaceutical classes. Reports are not usage guidelines, nor should they be read as an endorsement of, or recommendation for, any particular drug, use or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Gerald Gartlehner, MD, MPH Richard A. Hansen, PhD Patricia Thieda, MA Beth Jonas, MD Kathleen N. Lohr, PhD Tim Carey, MD, MPH Produced by RTI-UNC Evidence-based Practice Center Cecil G. Sheps Center for Health Services Research University of North Carolina at Chapel Hill 725 Airport Road, CB# 7590 Chapel Hill, NC 27599-7590 Tim Carey, MD, MPH, Director Oregon Evidence-based Practice Center Mark Helfand, MD, MPH, Director Copyright © 2005 by Oregon Health & Science University Portland, Oregon 97201. All rights reserved Final Report Drug Effectiveness Review Project TABLE OF CONTENTS List of Abbreviations ............................................................................................................................... 4 Introduction............................................................................................................................................... 6 Scope and Key Questions ............................................................................................................. 12 Methods
    [Show full text]
  • Annrheumdis-2019-216655.Full.Pdf
    Recommendation Ann Rheum Dis: first published as 10.1136/annrheumdis-2019-216655 on 22 January 2020. Downloaded from EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease- modifying antirheumatic drugs: 2019 update Josef S Smolen ,1 Robert B M Landewé,2,3 Johannes W J Bijlsma,4 Gerd R Burmester,5 Maxime Dougados,6 Andreas Kerschbaumer ,1 Iain B McInnes,7 Alexandre Sepriano ,8 Ronald F van Vollenhoven,9 Maarten de Wit ,10 Daniel Aletaha,1 Martin Aringer ,11 John Askling,12 Alejandro Balsa,13 Maarten Boers,14 Alfons A den Broeder,15 Maya H Buch ,16 Frank Buttgereit,5 Roberto Caporali,17 Mario Humberto Cardiel,18 Diederik De Cock,19 Catalin Codreanu,20 Maurizio Cutolo ,21 Christopher John Edwards,22 Yvonne van Eijk- Hustings ,23 Paul Emery ,24 Axel Finckh,25 Laure Gossec ,26 Jacques-Eric Gottenberg,27 Merete Lund Hetland,28 Tom W J Huizinga ,29 Marios Koloumas,30,31 Zhanguo Li,32 Xavier Mariette,33 Ulf Müller- Ladner,34 Eduardo F Mysler,35 Jose A P da Silva ,36 Gyula Poór,37 Janet E Pope ,38 Andrea Rubbert- Roth ,39 Adeline Ruyssen- Witrand,40 Kenneth G Saag,41 Anja Strangfeld,42 Tsutomu Takeuchi,43 Marieke Voshaar,44 René Westhovens,19 Désirée van der Heijde 29 Handling editor Dimitrios T ABStract fails, any other bDMARD (from another or the same Boumpas Objectives To provide an update of the European class) or tsDMARD is recommended. On sustained For numbered affiliations see League Against Rheumatism (EULAR) rheumatoid remission, DMARDs may be tapered, but not be stopped.
    [Show full text]
  • Information Presse an Antihypertensive Drug Improves Corticosteroid-Based Skin Treatments
    Paris, le 18 mars 2015 Information presse An antihypertensive drug improves corticosteroid-based skin treatments Basic research on blood pressure has led researchers from Inserm (Inserm Unit 1138, “Cordeliers Research Centre”) to obtain unexpected results: drugs used to treat hypertension (high blood pressure) reduce side effects from corticosteroid-based creams used to treat certain skin diseases. This work is published in the Journal of Investigative Dermatology. Corticosteroid-based dermatological creams are indicated for the symptomatic treatment of inflammatory skin conditions, such as atopic dermatitis and psoriasis, for example. However, they have frequent side effects, such as a slight burning sensation, and very often end by inducing skin atrophy (thinning of the skin, which becomes fragile), which is inconvenient for the patient, and for which there is presently no treatment. The researchers from Inserm formulated a hypothesis whereby this harmful effect might be related to the inappropriate activation by these creams of mineralocorticoid receptors located in the epidermis. These receptors, which are present in the kidney, heart, eye, and certain neurons in particular, reacted with aldosterone, a hormone that regulates the blood pressure. Moreover, previous studies also showed them to be highly sensitive to corticosteroids. Application of corticosteroids to cultured skin causes it to become thinner: in 6 days, the thickness of the epidermis was reduced by one-third. The researchers then induced a pharmacological blockade of the receptors by adding specific antagonists to the corticosteroid treatment. The inability of the corticosteroid to bind to the mineralocorticoid receptors restores proliferation of the epidermal cells, and partially corrects epidermal atrophy. From the clinical point of view, it turns out that spironolactone, a drug used for a very long time as an antihypertensive drug (and which has marketing authorisation), is an antagonist of the mineralocorticoid receptor.
    [Show full text]