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Angiotensin receptor blockers for chronic heart failure and acute myocardial infarction.
| Content Provider | Semantic Scholar |
|---|---|
| Author | McMurray, John J. V. |
| Copyright Year | 2001 |
| Abstract | wo landmark clinical trials, CONSENSUS I and SOLVD-T, have shown, unequivocally, that angiotensin converting enzyme (ACE) inhibitors reduce all cause mortality in patients with chronic heart failure (CHF) and underlying left ventricular systolic dysfunction. 1 2 These and other trials have also confirmed that ACE inhibitors reduce morbidity, as manifest by hospital admission, in patients with CHF. 3 A number of other key randomised, controlled , trials have also shown that ACE inhibitors reduce the risk of all cause mortality and major clinical events (sudden death, reinfarction, heart failure) after myocardial infarction. w1–3 These benefits are most clearly seen in patients with left ventricular systolic dysfunction or clinical evidence of heart failure. w4 The ATLAS study has shown that higher doses of ACE inhibitor give greater morbidity/ mortality benefits. w5 Recently, another drug known to block a component of the renin-angiotensin-aldosterone system (RAAS), spironolactone (an aldosterone antagonist), has also been shown to reduce mortality and morbidity in CHF, even when added to an ACE inhibitor (this was demonstrated in RALES). w6 The question arises, therefore, as to what the role of the newest agents available for RAAS inhibition, the angiotensin II receptor antagonists or blockers (ARBs), might be in CHF and acute myocardial infarction? ARB–ACE inhibitor comparison studies Though, logically, the first question to ask of ARBs might be whether these new drugs are better than placebo, the first comparison actually made in a large scale trial was with an ACE inhibitor. The first of these—the ELITE-1 trial—addressed tolerability, whereas the hypothesis of the larger ELITE-2 trial was that losartan would be more eYcacious than capto-pril. The approach of the ELITE trials was based on the belief that: (1) ARBs are more eVective inhibitors of the RAAS than ACE inhibitors; and (2) bradykinin, the breakdown of which is blocked by ACE inhibitors, is directly or indirectly responsible for cough and possibly other adverse eVects of these agents. 4 There is some scientific basis for the view that ARBs might be more eYcacious than ACE inhibitors at blocking the RAAS. If it is accepted that ACE inhibitors bring about benefit through reducing the actions of angiotensin II, then the recent demonstration that angio-tensin II generating pathways that bypass ACE exist in human myocardium and arteries is of some significance (fig 1). w7–9 Clearly, these observations suggest that ARBs oVer a potentially more eVective means of inhibiting the actions of angiotensin II. … |
| Starting Page | 97 |
| Ending Page | 103 |
| Page Count | 7 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://heart.bmj.com/content/heartjnl/86/1/97.full.pdf |
| PubMed reference number | 11410575v1 |
| Volume Number | 86 |
| Issue Number | 1 |
| Journal | Heart |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Aldosterone Angiotensin II Angiotensin Receptor Antagonists Angiotensin-Converting Enzyme Inhibitors Angiotensins Bradykinin Catabolism Coughing Heart failure Hospital admission Inhibition Large Left ventricular systolic dysfunction Losartan Morbidity - disease rate Myocardial Infarction Myocardium Patients Peptidyl-Dipeptidase A Renin-angiotensin system Spironolactone Sudden death TNFSF12-TNFSF13 gene Ventricular Dysfunction, Left benefit bypass |
| Content Type | Text |
| Resource Type | Article |
