ST elevation myocardial infarction inhibition of the renin-angiotensin-aldosterone system at discharge
| Myocardial infarction | |
| ICD-10 | I21-I22 |
|---|---|
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
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Inhibition of the renin-angiotensin-aldosterone system is a key therapeutic maneuver in patients with STEMI. The best known regulator of blood pressure and determinant of target organ damage from hypertension is the renin-angiotensin-aldosterone system. Overexpression of renin and its metabolic products predisposes to increased blood pressure and even frank hypertension, as well as target organ damage. Renin reacts with angiotensinogen to produce the decapeptide angiotensin I, which is biologically inactive. Angiotensin I is cleaved by a variety of enzymes, including angiotensin converting enzyme (ACE) and other proteolytic enzymes, e.g. the serine protease chymase, to generate angiotensin II, an octapeptide that is responsible for most of the known biological activity of the system. In addition, non-renin-enzymes, including tonin and cathepsin, are capable of generating angiotensin II directly from angiotensinogen. The angiotensin peptides, angiotensin I and II, are susceptible to digestion at a number of sites by angiotensinases. The resultant peptide fragments are found in the circulation and have functions that may be distinct from those of angiotensin II. For example, angiotensin III (the 2-8 peptide) has functions identical to those of angiotensin II, while angiotensin IV (the 3-8 peptide) may bind selectively to a novel receptor (AT4) and stimulate release of plasminogen activator inhibitor-1 (PA1-1), a potent anti-thrombolytic, and the (1-7) peptide may bind to the AT3 receptor to stimulate vasodilation and potentiate bradykinin. The biological significance of these novel peptides has yet to be fully elucidated.
Angiotensin II elevates blood pressure by a variety of mechanisms, including direct vasoconstriction, potentiation of sympathetic nervous system activity at both central and peripheral levels, stimulation of aldosterone synthesis and release with consequent sodium and fluid retention by the kidney and stimulation of arginine vasopressin release. In addition, angiotensin II has a variety of actions that damage blood vessels directly. For example, it stimulates NADH and NADPH activity, raising the oxidative potential of vascular tissue. Angiotensin II also plays a role in the vascular injury response, stimulating leukocyte adhesion to the site of injury and favoring superoxide and peroxynitrite formation and proliferation and migration of various cell types toward the luminal site of injury. The events that follow cause cellular components of the arterial wall to transform their phenotypes, resulting in atherosclerotic plaque or fibrous neointima formation. Angiotensin II and some of its constituent peptides also stimulate synthesis of the antithrombolytic agent, PAI-1, suggesting that activation of the renin-angiotensin-aldosterone system predisposes to atherosclerosis and thromboembolic events, including heart attack and stroke.
Mechanism of Benefit
Pharmacological agents that antagonize the renin-angiotensin-aldosterone system at the level of ACE, the angiotensin II receptor, and more recently, the aldosterone (mineralocorticoid) receptor, have come into prominence in the treatment of hypertension, heart failure and postmyocardial infarction cardiac remodeling. These agents are highly effective in lowering blood pressure and, particularly in the case of the angiotensin II receptor antagonists, are extremely well tolerated. The major questions asked regarding the clinical utilization of the angiotensin receptor antagonists and the ACE inhibitors are: Do they have clinical benefits beyond blood pressure lowering? Are their advantages sufficient to justify their high cost? Is one class superior to the other with respect to preventing target organ damage and cardiovascular events? Are the therapeutic effects of the two classes additive or synergistic? Clinical trial evidence to date is inconclusive on these points. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]
Clinical Trial Data
Additional long-term controlled clinical trials are needed to clarify the benefits and risks of cardiovascular outcomes associated with blood pressure reduction induced by antihypertensive agents that antagonize components of the renin-angiotensin-aldosterone system in patients with multiple cardiovascular risk factors. The ongoing NHLBI-sponsored Antihypertensive and Lipid Lowering to Prevent Heart Attack (ALLHAT) trial is the largest of these ongoing trials, including over 42,000 high-risk hypertensive subjects with diverse ethnic backgrounds. ALLHAT is comparing ACE inhibitor or calcium channel blocker therapy to a diuretic based regimen with respect to prevention of major cardiovascular disease outcomes. This massive trial should provide important answers to many of these pressing questions. For the rest, we need more fundamental information about the biology of the renin-angiotensin-aldosterone system in human subjects.[21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33]
Dosing
Side Effects
Guidelines
Guidelines for ACE Inhibitors Therapy [34]
Guidelines for Angiotensin Receptor Blockers Therapy [34]
Guidelines for Aldosterone Blockers Therapy [34]
Guidelines for Inhibition of the Renin-Angiotensin-Aldosterone System [34]
References
- ↑ "Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators". Lancet. 342 (8875): 821–8. 1993. PMID 8104270. Unknown parameter
|month=ignored (help) - ↑ Køber L, Torp-Pedersen C, Carlsen JE; et al. (1995). "A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group". N. Engl. J. Med. 333 (25): 1670–6. PMID 7477219. Unknown parameter
|month=ignored (help) - ↑ "ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group". Lancet. 345 (8951): 669–85. 1995. PMID 7661937. Unknown parameter
|month=ignored (help) - ↑ "GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction. Gruppo Italiano per lo Studio della Sopravvivenza nell'infarto Miocardico". Lancet. 343 (8906): 1115–22. 1994. PMID 7910229. Unknown parameter
|month=ignored (help) - ↑ Swedberg K, Held P, Kjekshus J, Rasmussen K, Rydén L, Wedel H (1992). "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. 327 (10): 678–84. PMID 1495520. Unknown parameter
|month=ignored (help) - ↑ Pfeffer MA (1998). "ACE inhibitors in acute myocardial infarction: patient selection and timing". Circulation. 97 (22): 2192–4. PMID 9631866. Unknown parameter
|month=ignored (help) - ↑ Rutherford JD, Pfeffer MA, Moyé LA; et al. (1994). "Effects of captopril on ischemic events after myocardial infarction. Results of the Survival and Ventricular Enlargement trial. SAVE Investigators". Circulation. 90 (4): 1731–8. PMID 7923656. Unknown parameter
|month=ignored (help) - ↑ Pfeffer MA, McMurray JJ, Velazquez EJ; et al. (2003). "Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both". N. Engl. J. Med. 349 (20): 1893–906. doi:10.1056/NEJMoa032292. PMID 14610160. Unknown parameter
|month=ignored (help) - ↑ Pitt B, Remme W, Zannad F; et al. (2003). "Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction". N. Engl. J. Med. 348 (14): 1309–21. doi:10.1056/NEJMoa030207. PMID 12668699. Unknown parameter
|month=ignored (help) - ↑ Pfeffer MA, Greaves SC, Arnold JM; et al. (1997). "Early versus delayed angiotensin-converting enzyme inhibition therapy in acute myocardial infarction. The healing and early afterload reducing therapy trial". Circulation. 95 (12): 2643–51. PMID 9193433. Unknown parameter
|month=ignored (help) - ↑ Tokmakova M, Solomon SD (2006). "Inhibiting the renin-angiotensin system in myocardial infarction and heart failure: lessons from SAVE, VALIANT and CHARM, and other clinical trials". Curr. Opin. Cardiol. 21 (4): 268–72. doi:10.1097/01.hco.0000231394.79609.24. PMID 16755193. Unknown parameter
|month=ignored (help) - ↑ Pitt B (2003). "Aldosterone blockade in patients with systolic left ventricular dysfunction". Circulation. 108 (15): 1790–4. doi:10.1161/01.CIR.0000086776.15268.22. PMID 14557343. Unknown parameter
|month=ignored (help) - ↑ Latini R, Maggioni AP, Flather M, Sleight P, Tognoni G (1995). "ACE inhibitor use in patients with myocardial infarction. Summary of evidence from clinical trials". Circulation. 92 (10): 3132–7. PMID 7586285. Unknown parameter
|month=ignored (help) - ↑ Ambrosioni E, Borghi C, Magnani B (1995). "The effect of the angiotensin-converting-enzyme inhibitor zofenopril on mortality and morbidity after anterior myocardial infarction. The Survival of Myocardial Infarction Long-Term Evaluation (SMILE) Study Investigators". N. Engl. J. Med. 332 (2): 80–5. PMID 7990904. Unknown parameter
|month=ignored (help) - ↑ Oral captopril versus placebo among 13,634 patients with suspected acute myocardial infarction: interim report from the Chinese Cardiac Study (CCS-1). Lancet 1995;345
- ↑ "Oral captopril versus placebo among 13,634 patients with suspected acute myocardial infarction: interim report from the Chinese Cardiac Study (CCS-1)". Lancet. 345 (8951): 686–7. 1995. PMID 7885123. Unknown parameter
|month=ignored (help) - ↑ "Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomized trials. ACE Inhibitor Myocardial Infarction Collaborative Group". Circulation. 97 (22): 2202–12. 1998. PMID 9631869. Unknown parameter
|month=ignored (help) - ↑ Teo KK, Yusuf S, Pfeffer M; et al. (2002). "Effects of long-term treatment with angiotensin-converting-enzyme inhibitors in the presence or absence of aspirin: a systematic review". Lancet. 360 (9339): 1037–43. PMID 12383982. Unknown parameter
|month=ignored (help) - ↑ Meune C, Mahe I, Mourad JJ; et al. (2000). "Interaction between angiotensin-converting enzyme inhibitors and aspirin: a review". Eur. J. Clin. Pharmacol. 56 (9–10): 609–20. PMID 11214765. Unknown parameter
|month=ignored (help) - ↑ Sigurdsson A, Swedberg K (1994). "Left ventricular remodelling, neurohormonal activation and early treatment with enalapril (CONSENSUS II) following myocardial infarction". Eur. Heart J. 15 Suppl B: 14–9, discussion 26–30. PMID 8076657. Unknown parameter
|month=ignored (help) - ↑ The Acute Infarction Ramipril Efficacy—AIRE—Study Investigators : Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet 1993; 342:821-828.
- ↑ Kober L, Torp-Pedersen C, Carlsen JE, Bagger H, Eliasen P, Lyngborg K, Videbaek J, Cole DS, Auclert L, Pauly NC: A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group. N Engl J Med 1995; 333:1670-1676.
- ↑ ISIS-4 Collaborative Group: ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet 1995; 345:669-685.
- ↑ Gruppo Italiano per lo Studio della Sopravvivenza nell'infarto Miocardico : GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute myocardial infarction. Lancet 1994; 343:1115-1122.
- ↑ Swedberg K, Held P, Kjekshus J, Rasmussen K, Ryden L, Wedel H: 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; 327:678-684.
- ↑ Rutherford JD, Pfeffer MA, Moye LA, Davis BR, Flaker GC, Kowey PR, Lamas GA, Miller HS, Packer M, Rouleau JL, et al: Effects of captopril on ischemic events after myocardial infarction. Results of the Survival and Ventricular Enlargement trial. SAVE Investigators. Circulation 1994; 90:1731-1738.
- ↑ Pfeffer MA, Greaves SC, Arnold JM, Glynn RJ, LaMotte FS, Lee RT, Menapace Jr. FJ, Rapaport E, Ridker PM, Rouleau JL, Solomon SD, Hennekens CH: Early versus delayed angiotensin-converting enzyme inhibition therapy in acute myocardial infarction. The healing and early afterload reducing therapy trial. Circulation 1997; 95:2643-2651.
- ↑ Tokmakova M, Solomon SD: Inhibiting the renin-angiotensin system in myocardial infarction and heart failure: lessons from SAVE, VALIANT and CHARM, and other clinical trials. Curr Opin Cardiol 2006; 21:268-272.
- ↑ Latini R, Maggioni AP, Flather M, Sleight P, Tognoni G. ACE inhibitor use in patients with myocardial infarction: summary evidence from clinical trials. Circulation 1995;92:3132-7.
- ↑ Ambrosioni E, Borghi C, Magnani B, for the Survival Myocardial Infarction Long-Term Evaluation (SMILE) Study Investigators. The effect of the angiotensin-converting-enzyme inhibitor zofenopril on mortality and morbidity after anterior myocardial infarction. N Engl J Med 1995;332:80-5.
- ↑ Oral captopril versus placebo among 13,634 patients with suspected acute myocardial infarction: interim report from the Chinese Cardiac Study (CCS-1). Lancet 1995;345:686-7.
- ↑ ACE Inhibitor Myocardial Infarction Collaborative Group. Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomized trials. Circulation 1998; 97:2202-12.
- ↑ Sigurdsson A, Swedberg K. Left ventricular remodelling, neurohormonal activation and early treatment with enalapril (CONSENSUS II) following myocardial infarction. Eur Heart 1994;15(Suppl B):14-9; discussion 26.
- ↑ 34.0 34.1 34.2 34.3 Antman EM, Hand M, Armstrong PW, Bates ER, Green LA, Halasyamani LK, Hochman JS, Krumholz HM, Lamas GA, Mullany CJ, Pearle DL, Sloan MA, Smith SC Jr; 2004 Writing Committee Members, Anbe DT, Kushner FG, Ornato JP, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Halperin JL, Hunt SA, Lytle BW, Nishimura R, Page RL, Riegel B, Tarkington LG, Yancy CW. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee. Circulation 2008 Jan 15;117(2):296-329 PMID 18071078