Journals / MN Kardiyoloji / 2006 / Cilt: 13 - Sayı: 4

Inhibition of RAA system in patients with left ventricular dysfunction

Sol ventrikül fonksiyon bozukluğu olan olgularda RAA sistemi inhibisyonunun yeri

Pages
286–291
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Due to these studies ACE inhibitors are recommended to MI patients with the evaluation of safety, tolerability and cost effectiveness specific to patient and disease considering these studies.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Congestive heart failure, as a result of acute myocardial infarction, is a clinical syndrome in which dysfunctioning myocardium fails to supply metabolic requirements of peripheral tissues.
📊
Key Findings & Data:Existent angiotensin II causes detrimental effects to all over the cardiovascular system through the angiotensin II T1 receptors and also AT II activates neurohumoral mechanisms including increase in sympathetic adrenergic system, activation vazopressin/antidiuretic hormon release, endothelin and free oxygen radicals levels.
💡
Conclusion & Impact:Due to these studies ACE inhibitors are recommended to MI patients with the evaluation of safety, tolerability and cost effectiveness specific to patient and disease considering these studies.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Renin-anjiyotensin sistemi · Anjiyotensin II · Anjiyotensin dönüştürücü enzim inhibitörleri

Abstract

Congestive heart failure, as a result of acute myocardial infarction, is a clinical syndrome in which dysfunctioning myocardium fails to supply metabolic requirements of peripheral tissues. It is the leading determinant of mortality. Renin-angiotensin-aldosteron (RAA) system has the most important role in the progression of this disease. Existent angiotensin II causes detrimental effects to all over the cardiovascular system through the angiotensin II T1 receptors and also AT II activates neurohumoral mechanisms including increase in sympathetic adrenergic system, activation vazopressin/antidiuretic hormon release, endothelin and free oxygen radicals levels. Angiotensin-converting enzyme inhibitors acutely remove vasoconstriction due to AT II. Previous studies support the data that ACE inhibitors prevent infarct expansion, improve ventricular remodelling process and improve survivel in patients with ventricular dysfunction. Also, in long term, they restrict aldosteron release, decrease sodium retantion and potassium loss, decrease proliferation and remodelling of myocardial cells and vessel smooth muscle cells , they have many beneficial effects. In recent studies, these drugs have shown to provide additional benefit at end points in MI patient groups when added to other agents. Due to these studies ACE inhibitors are recommended to MI patients with the evaluation of safety, tolerability and cost effectiveness specific to patient and disease considering these studies.

Özet

Akut miyokard infarktüsü (AMI) sonucu oluşan kalp yetersizliği (KY) kalp kasının fonksiyonlarının bozulmasına bağlı olarak dokuların metabolik ihtiyaçlarını karşılamakta yetersiz kaldığı bir klinik sendromdur ve mortalitenin en önemli belirleyicisidir. Kalp yetersizliğinin ilerlemesinde renin-anjiyotensin-aldosteron (RAA) sistemi en önemli role sahiptir. Oluşan anjiyotensin II, anjiyotensin II T1 reseptörleri ile tüm kardiyovasküler sistemde zararlı etkilere neden olmakta ve AT II aynı zamanda sempatik adrenerjik sistemin aktivasyonu, vazopressin/antidiüretik hormon salınımı, endotelin, serbest oksijen radikallerinin düzeyinde artış gibi diğer zararlı nörohümoral mekanizmaları da aktive etmektedir. Anjiotensin konverting enzim inhibitörleri (ACEİ), anjiyotensin II’nin yol açtığı vazokonstriksiyonu akut olarak ortadan kaldırır. Akut dönemde infarktüs yayılmasına engel olduğu, ventriküler yeniden şekillenme olayına olumlu etki yaptığı ve ventrikül disfonksiyonu olan hastalarda surveyi iyileştirdiği çalışmalar ile desteklenmiştir. Uzun dönemde de aldosteron salınımını kısıtlayıp sodyum retansiyonu, potasyum kaybını, kalp ve damar düz kas hücrelerinde proliferasyonu ve yeniden yapılanmayı azaltarak olumlu etkilerde bulunurlar.Yapılan çalışmalarda MI grubu hastalarda sonlanım noktalarında diğer ajanlara eklendiğinde ek bir fayda sağlamaktadır.Bu ajanların MI grubu hastalarda, çalışmaların ışığında, hastaya ve hastalığa spesifik, güvenlik, tolerabilite ve maliyet değerlendirilerek ACE inhibitörü ajanlarından birisinin başlanması önerilmektedir.

🔖

Cite This Article

ÖZCAN, T., AKÇAY, B. (2006). Inhibition of RAA system in patients with left ventricular dysfunction. MN Kardiyoloji, Cilt: 13 - Sayı: 4, 286–291. https://ajindex.com/articles/297541

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (10)

  1. Garg R, Yusuf S. Overview of randomized trials of angiotensin-converting- enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials. JAMA. 1995; 273:1450-56.
  2. Flather MD, Yusuf S, Kober L, et al. Long-term ACE-mhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual piatients. ACE-Inhibitor Myocardial Infarction Collaborative Group. Lancet. 2000; 355:1575-81.
  3. Latini R, Tognoni G, Maggioni AP, et aL. Clinical effects of early angiotensin-converting enzyme inhibitor treatment for acute myocardial infarction are similar in the presence and absence of aspirin: systematic overview of individual data from 96,712 randomized patients. Angiotensin-converting Enzyme Inhibitor Myocardial Infarction Collaborative Group. J Am Coll Cardiol. 2000; 35:1801-07.
  4. Jaramillo LP, Casas JP: Endothelial dysfunction, angiotensinconverting enzyme inhibitors and calcium antagonists. J Hum Hypertens 2002; 16:34-37.
  5. Sheth T, Parker T, Block A, et al: The IMPRESS Investigators. Comparison of the effects of omapatrilat and lisinopril on circulating neurohormones and cytokines in patients with chronic heart failure. Am J Cardiol 2002; 90:496-500.
  6. Guidi E, Minetti EE, Cozzi MG: Acute and long-term effects of ACE inhibition on renal haemodynamics in glomerular and interstitial nephropathies. J Renin Angiotensin Aldosterone Syst 2002; 3:40-45.
  7. Pitt B, Chang P, Timmermans PB. Angiotensin II receptor antagonists in heart failure: rationale and design of the evaluation of losartan in the elderly (ELITE) trial. Cardiovasc Drugs Ther. 1995; 9:693-700.
  8. Witherow FN, Helmy A, Webb DJ, et aL. Bradykinin contributes to the vasodilator effects of chronic angiotensin converting enzyme inhibition in patients with heart failure. Circulation. 200I; 104:2177-81.
  9. Witherow FN, Dawson P, Ludlam CA, et aL. Marked bradykinin-induced tissue plasminogen activator release in patients with heart failure maintained on long-term angiotensin- converting enzyme inhibitor therapy. J Am Coll Cardiol. 2002; 40:961-6.
  10. Abadir PM, Carey RM, Siragy HM. Angiotensin AT 2 receptors directly stimulate renal nitric oxide in bradykinin B2-receptor-null mice.Hypertension. 2003; 42:600-4 Pfeffer MA.Left ventrieular remodeling after acute myacardial infarctian. Ann Rev Med. 1995; 46:455 Ambrosioni E, Borghi C, Magnani B. et al: Effects of the early administratian of zofenopril on mortality and morbidity i