Login | Users Online: 1684  
Home Print this page Email this page Small font sizeDefault font sizeIncrease font size   
Home | About us | Editorial board | Search | Ahead of print | Current Issue | Archives | Submit article | Instructions | Subscribe | Advertise | Contact us

Year : 2003  |  Volume : 4  |  Issue : 4  |  Page : 3 Table of Contents     

Optimizing Management of Acute Coronary Syndromes Without St Segment Elevation: Update 2004

Professor of Cardiology & Chief of Cardiology Department, University Hospital Pole Couer Poumons, Besancon Cedex, France

Date of Web Publication22-Jun-2010

Correspondence Address:
Jean-Pierre L Bassand
Professor of Cardiology & Chief of Cardiology Department, University Hospital Pole Couer Poumons, Besancon Cedex
Login to access the Email id

Source of Support: None, Conflict of Interest: None

Rights and PermissionsRights and Permissions

How to cite this article:
Bassand JPL. Optimizing Management of Acute Coronary Syndromes Without St Segment Elevation: Update 2004. Heart Views 2003;4:3

How to cite this URL:
Bassand JPL. Optimizing Management of Acute Coronary Syndromes Without St Segment Elevation: Update 2004. Heart Views [serial online] 2003 [cited 2023 Dec 7];4:3. Available from: https://www.heartviews.org/text.asp?2003/4/4/3/64425

Acute coronary syndromes (ACS) are different clinical expressions of acute myocardial ischemia, which is the result of a common underlying pathophysiological mechanism: atherosclerotic plaque rupture or erosion with different degrees of superimposed thrombosis and distal embolization. Nowadays, we distinguish between ACS with and without persistent ST segment elevation. ACS with ST segment elevation is usually due to plaque rupture and total occlusion of a major epicardial vessel with a fibrin-rich thrombus. The ECG typically shows ST segment elevation in these patients.

ACS without persistent ST segment elevation usually results from plaque rupture or erosion with a platelet-rich thrombus that may be partial or intermittently occlusive. In these cases, the ECG shows ST segment depression, T-wave inversion, and can sometimes be normal or near normal.

Non-ST segment elevation ACS is further divided into unstable angina (if no markers of cell death are released) and non-Q wave myocardial infarction (when markers of cell death, namely CK-MB or troponin, are released). Non-ST segment elevation ACS is quite frequent. In the Euro Heart Survey and GRACE registries, involving more than 10,000 patients each, the proportion of patients without ST segment elevation was higher than the proportion of patients with ST segment elevation. The prognosis is quite serious with a rate of death and non-fatal myocardial infarction in the range of 13% to 15% at 6 months.

The ESC guidelines on the management of non-ST segment elevation ACS were recently updated [1] . The guideline distinguishes 5 categories of treatment. Thrombolytic therapy is NOT included because they have not been shown to be effective and could possibly even be deleterious in these patients. Anti-ischemic agents, such as beta-blockers, calcium inhibitors and nitrates must be prescribed in these patients to control ischemia, but they have never been demonstrated capable of improving prognosis in terms of death and myocardial infarction.

Anti-thrombin agents are mandatory since they result in a 35% risk reduction compared to placebo. It has consistently been shown in several trials that low molecular weight heparins are at least as effective and as safe as unfractionated heparin, but with a better bio-availability, fixed doses, and no need for coagulation monitoring. They are the preferred anti-thrombotic agents at the moment. Pooled data from TIMI 11B and ESSENCE trials led to the idea that enoxaparin might be superior to unfractionated heparin in this particular setting.

Anti-platelet agents are the second line of mandatory treatment. Aspirin has been shown to reduce the risk of death and MI by virtually 50%. More recently, clopidogrel in the CURE trial was shown to improve further the prognosis of these patients by reducing the risk of death, MI and stroke by 20% when added to standard therapy, including aspirin. Risk reduction is uniform with clopidogrel, whatever the initial risk level of the patient. This is the main difference with glycoprotein IIb/IIIa inhibitors, which are particularly efficient in high-risk patients, especially those submitted to revascularisation by PCI, diabetics, and patients with troponin release. Of course, the use of potent anti-platelet therapy may lead to increased risk of bleeding. Interestingly, it has consistently been shown that while the risk of major bleeding is increased, the risk of intra-cranial hemorrhage is not significantly modified by an intense anti-platelet regimen.

The fourth therapeutic option is systematic revascularization, which has constantly been shown, in the most recent and modern trials, such as TACTICS-TIMI18, FRISC 2 and RITA 3, to lead to improved prognosis in terms of death and MI at 6 months, and death at one year (at least in FRISC 2). Revascularization must now be considered as a mandatory therapeutic option whenever possible.

In daily routine practice, risk assessment is a first step after the diagnosis has been ascertained. The acute risk is marked by recurrent ischemia, ST segment depression, dynamic ST changes, elevated troponins, diabetes, and renal failure. The long-term risk is linked to the underlying coronary artery disease, and to biological markers, particularly CRP.

In practical terms, the first line of treatment is heparin (low molecular weight or unfractionated), aspirin, clopidogrel, beta-blockers and nitrates. Patients at high risk must receive IIb/IIIa inhibitors in addition to this treatment, and should be considered for coronary angiography and early revascularisation, if possible within 4 to 48 hours. Patients at low risk, that is to say without recurrence of chest pain, with normal ECG or T-wave inversion, and without troponin release, can be managed conservatively and should be risk-stratified by non-invasive exercise stress testing. If necessary, coronary angiography should be considered but not urgently.

Long term management is based on aggressive risk factor modification, aspirin (75 to 100mg/day for life), clopidogrel for 9 to 12 months, in addition to aspirin, beta blockers, statins, preferably simvastatin 40mg/day (demonstrated to reduce risk of death by 25% at 5 years), and ACE inhibitors. This last therapy has been proven 0 to reduce the risk of death and MI by 20% in the HOPE trial (ramipril in high risk patients), and in the Europa trial (perindopril, 8mg/day in moderate to low risk patients).

Last but not least, it has consistently been shown through different registries that the implementation of guidelines is poor, and moreover, that the lack of implementation of guidelines leads to deterioration of patient prognosis. Efforts have to be made in the implementation of the best possible medical practice, as summarised in the clinical guidelines.

   References Top

1.Bertrand ME, Simoons ML, Fox KA, Wallentin LC, Hamm CW, McFadden E, De Feyter PJ, Specchia G, Ruzyllo W. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2002;23:1809-1840.  Back to cited text no. 1      


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article

 Article Access Statistics
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal