American Journal of Cardiology
Volume 105, Issue 1, Supplement , Pages 30A-35A, 4 January 2010

Renin–Angiotensin System Blockade and Cardiovascular and Renal Protection

  • Byron J. Hoogwerf, MD

      Affiliations

    • Corresponding Author InformationAddress for reprints: Byron J. Hoogwerf, MD, 2237 Demington Drive, Cleveland Heights, Ohio 44106-3320

Department of Endocrinology, Diabetes, and Metabolism, Cleveland Clinic, Cleveland, Ohio, USA; and Lilly USA, LLC, (Endocrinology), Indianapolis, Indiana, USA

The renin–angiotensin–aldosterone system (RAAS) plays an important role in the pathogenesis of a variety of clinical conditions, including atherosclerosis, hypertension, left ventricular hypertrophy, myocardial infarction, and heart failure. Inhibition of the RAAS with either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (ARBs) has been shown to be effective in lowering blood pressure and reducing cardiovascular mortality and morbidity in various at-risk patient populations. A number of studies have shown that these 2 classes are effective in reducing the rate of renal disease progression in patients with diabetic nephropathy, although more long-term vascular outcome studies are needed in patients with chronic kidney disease. The Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) was the first study to show comparable reno- and cardioprotective effects between an ARB (telmisartan) and ramipril in a broad section of at-risk patients, on top of usual standard care. However, telmisartan showed better tolerability than ramipril in ONTARGET, with less cough and angioedema. This difference was obtained despite patients having been selected for tolerability to both drugs at study entry.

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

 Statement of author disclosure: Please see the Author Disclosures section at the end of this article.

 This work was supported by Boehringer Ingelheim GmbH.

PII: S0002-9149(09)02484-9

doi:10.1016/j.amjcard.2009.10.009

American Journal of Cardiology
Volume 105, Issue 1, Supplement , Pages 30A-35A, 4 January 2010