Vous êtes sur la page 1sur 5
Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond) Senior Lecturer for Medipass Intensive
Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond)
Senior Lecturer for Medipass Intensive MRCP II Courses
Table Of Contents
MANAGEMENT OF ACUTE NON-ST ELEVATION MYOCARDIAL INFARCTION (NSTEMI)
3
DIAGNOSIS OF
NSTEMI
3
1.
TREATMENT OPTIONS
3
TREATMENT PROTOCOL
4
1. IMMEDIATE TREATMENTS
4
2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION
5
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by
4 2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION 5 Reproduced from A Rapid Review of Clinical Medicine by

Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond) Senior Lecturer for Medipass Intensive MRCP II Courses

Management Of Acute Non-ST Elevation Myocardial Infarction (NSTEMI)

Of Acute Non-ST Elevation Myocardial Infarction (NSTEMI) NSTEMI included subendocardial, nontransmural, ST

NSTEMI included subendocardial, nontransmural, ST depression, or intramural infarction.

nontransmural, ST depression, or intramural infarction. The entity of non-Q wave myocardial infarction (NQWMI) which
nontransmural, ST depression, or intramural infarction. The entity of non-Q wave myocardial infarction (NQWMI) which
nontransmural, ST depression, or intramural infarction. The entity of non-Q wave myocardial infarction (NQWMI) which

The entity of non-Q wave myocardial infarction (NQWMI) which is conventionally termed non ST segment elevation MI (NSTEMI), is part of the continuum of acute coronary syndromes, in which coronary thrombosis

of acute coronary syndromes, in which coronary thrombosis compromises blood flow to a region of viable
of acute coronary syndromes, in which coronary thrombosis compromises blood flow to a region of viable
of acute coronary syndromes, in which coronary thrombosis compromises blood flow to a region of viable
of acute coronary syndromes, in which coronary thrombosis compromises blood flow to a region of viable
of acute coronary syndromes, in which coronary thrombosis compromises blood flow to a region of viable

compromises blood flow to a region of viable myocardium. It is characterized by an elevation in cardiac enzymes but a lack of ST segment elevation or pathologic Q waves on the electrocardiogram (ECG). Previous names for

an

The reason why Q waves do or do not develop following coronary occlusion is related to the duration of occlusion and the extent to which the collateral vessels maintain myocardial viability during occlusion. Coronary arteriography, performed in the acute period following NSTEMI, demonstrates that the infarct-related artery is patent in more than 50 percent of cases.

artery is patent in more than 50 percent of cases. Patients with NSTEMI SHOULD NOT RECEIVE
artery is patent in more than 50 percent of cases. Patients with NSTEMI SHOULD NOT RECEIVE

Patients with NSTEMI SHOULD NOT RECEIVE A THROMBOLYTIC AGENT, in contrast to those with an acute

MI

(PTCA) in NSTEMI remains uncertain. http://www.utdol.com/application/topic.asp?file=CHD/39496

associated with ST segment elevation. The benefit of primary percutaneous transluminal coronary angioplasty

This initial approach should be followed by the administration of different drugs that may improve the long-term prognosis . The goals of therapy following acute NSTEMI include:

. The goals of therapy following acute NSTEMI include: 1. Prevention of progression to full thickness

1. Prevention of progression to full thickness myocardial infarction.

2. Prevention of left ventricular remodeling with an angiotensin converting enzyme (ACE) inhibitor.

with an angiotensin converting enzyme (ACE) inhibitor. 3. Identification of patients at continued ischemic risk
with an angiotensin converting enzyme (ACE) inhibitor. 3. Identification of patients at continued ischemic risk
with an angiotensin converting enzyme (ACE) inhibitor. 3. Identification of patients at continued ischemic risk

3. Identification of patients at continued ischemic risk with assessment of clinical factors and a predischarge exercise tolerance test

clinical factors and a predischarge exercise tolerance test The long-term goal is atherothrombotic risk reduction
clinical factors and a predischarge exercise tolerance test The long-term goal is atherothrombotic risk reduction
clinical factors and a predischarge exercise tolerance test The long-term goal is atherothrombotic risk reduction
clinical factors and a predischarge exercise tolerance test The long-term goal is atherothrombotic risk reduction

The long-term goal is atherothrombotic risk reduction including cessation of smoking, control of hypertension if present, and cholesterol lowering in patients with hypercholesterolemia.

cholesterol lowering in patients with hypercholesterolemia. Diagnosis Of NSTEMI The diagnosis of NSTEMI is based on
cholesterol lowering in patients with hypercholesterolemia. Diagnosis Of NSTEMI The diagnosis of NSTEMI is based on
cholesterol lowering in patients with hypercholesterolemia. Diagnosis Of NSTEMI The diagnosis of NSTEMI is based on

Diagnosis Of NSTEMI

The diagnosis of NSTEMI is based on a raised serum cardiac troponin in the context of ischaemic symptoms and non ST elevation ECG changes indicative of myocardial ischaemia.

1. TREATMENT OPTIONS

Patients with an NSTEMI should be treated with an early medical regimen similar to that used in a Q wave MI with one exception: there is no evidence of benefit from thrombolysis in this setting and these agents are therefore not indicated. Patients presenting with an NSTEMI have a lower in-hospital mortality than those with STEMI but a similar long-term outcome. These relationships can be illustrated by results from the GUSTO-IIb trial in which patients with an NSTEMI had a lower 30 day mortality (3.8 versus 6.1 percent for a Q wave MI, p<0.001) but the same mortality at six months and one year (8.8 versus 9.6 percent).

at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in
at six months and one year (8.8 versus 9.6 percent). The substantial persistent coronary risk in

The substantial persistent coronary risk in patients with NSTEMI suggests that medical interventions targeted at preventing death, reinfarction, arrhythmias, and remodeling should have a beneficial impact on subsequent outcomes.

should have a beneficial impact on subsequent outcomes. The information presented below is derived from studies
should have a beneficial impact on subsequent outcomes. The information presented below is derived from studies
should have a beneficial impact on subsequent outcomes. The information presented below is derived from studies

The information presented below is derived from studies that were limited to patients with NSTEMI and from subgroup analyses of studies in unselected patients with unstable angina or acute myocardial infarction. A series of guidelines for the treatment of patients with a non ST-segment (NSTEMI) have been published by the ACC/AHA (algorithm).

Treatment Protocol

Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond) Senior Lecturer for Medipass Intensive MRCP II Courses

1. IMMEDIATE TREATMENTS

Medipass Intensive MRCP II Courses 1. I MMEDIATE TREATMENTS 1. ASPIRIN Treatment with ASPIRIN in the

1. ASPIRIN

MRCP II Courses 1. I MMEDIATE TREATMENTS 1. ASPIRIN Treatment with ASPIRIN in the acute setting
MRCP II Courses 1. I MMEDIATE TREATMENTS 1. ASPIRIN Treatment with ASPIRIN in the acute setting

Treatment with ASPIRIN in the acute setting of NSTEMI significantly reduces the incidence of death and recurrent MI.

reduces the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE
reduces the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE
reduces the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE
reduces the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE
reduces the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE
reduces the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE

2. CLOPIDOGREL.

the incidence of death and recurrent MI. 2. CLOPIDOGREL . 3. HEPARIN . The CURE study

3. HEPARIN.

The CURE study showed better outcomes in patients treated with both aspirin and clopidogrel versus aspirin alone. The combination should be continued for a year.

alone. The combination should be continued for a year. The ACC/AHA task force recommended that LMW

The ACC/AHA task force recommended that LMW heparin can be used as an alternative to unfractionated heparin in patients with a NSTEMI There are two advantages to low molecular weight heparin that have led some physicians to recommend its use: a lower incidence of heparin-associated thrombocytopenia; and ease of administration without the need for monitoring.

4. BETA BLOCKERS.

without the need for monitoring. 4. BETA BLOCKERS . Controlled trials have repeatedly documented the beneficial

Controlled trials have repeatedly documented the beneficial effects of beta blockers in patients with acute myocardial infarction; however, there have been no randomized trials specifically addressing the efficacy of these drugs in NSTEMI. The only available data come from subgroup analyses of the acute MI trials. These analyses have provided conflicting results with some showing benefit, a finding not confirmed in other studies. A retrospective analysis of 201,752 patients from the Cooperative Cardiovascular Project found that the reduction in mortality from beta blockers was equivalent in those with a Q wave and NSTEMI subgroup. Given the proven efficacy in unselected acute MI and the absence of harm in NSTEMI, we recommend therapy with a beta blocker similar to that used in Q wave myocardial infarction. These recommendations are in accord with guidelines for management of patients with an acute coronary syndrome published in 2000 by an ACC/AHA Task Force.

syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in
syndrome published in 2000 by an ACC/AHA Task Force. 5. INTRAVENOUS NITROGLYCERIN is very useful in

5. INTRAVENOUS NITROGLYCERIN is very useful in the management of ischaemic pain.The current ACC/AHA guidelines recommend the use of nitrates for the first 24 to 48 hours in patients with acute MI who have an indication for nitrate therapy such as recurrent ischemia, heart failure, or hypertension.

6. GLYCOPROTEIN IIB/IIIA RECEPTOR ANTAGONISTS

Glycoprotein IIb/IIIa receptor antagonists appear to be of some benefit in patients with unstable angina and NSTEMI. In the PRISM trial in which patients with an acute coronary syndrome were randomly assigned to tirofiban or h e p a r in , the patients with NSTEMI who received tirofiban had significant reductions in the 30 day risk of death (1.6 versus 6.2 percent for heparin, p = 0.004) and MI (2.7 versus 6.8 percent, p = 0.01). These drugs should be reserved for patients with dynamic ST segment changes, on-going ischaemic symptoms, arrhythmias and cardiac decompensaion in the setting of myocardial ischaemia.

decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin
decompensaion in the setting of myocardial ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin

7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS

ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin converting enzyme (ACE) inhibitors appear to
ischaemia. 7. ANGIOTENSIN CONVERTING ENZYME INHIBITORS Angiotensin converting enzyme (ACE) inhibitors appear to

Angiotensin converting enzyme (ACE) inhibitors appear to beneficial after unselected acute MI in patients with an anterior infarct or reduced left ventricular function.

There is less information concerning efficacy in NSTEMI. Thus, administration of ACE inhibitors may be beneficial in NSTEMI, particularly those with an anterior MI. However, the HOPE trial, the results of which were published after the guidelines, showed that high-risk patients without an acute MI benefit from ACE inhibition with a reduced incidence of cardiovascular death, MI, and stroke. This observation provides a rationale for treating all post-MI patients with an ACE inhibitor, particularly since the follow-up period in

Reproduced from A Rapid Review of Clinical Medicine by Sanjay Sharma, with kind permission from Manson publishing.

Find more revision resources at www.medibyte.com

Page 4

Author: Dr Sanjay Sharma BSc (Hons), FRCP (UK), MD (Lond) Senior Lecturer for Medipass Intensive MRCP II Courses

the HOPE trial (4.5 years) was much longer than the one to six month follow-up periods in the trials in which all post-MI patients were treated. ACEI should be administered within 24 hours and should be continued for 6 weeks in those with an EF > 40% and indefinitely in those patients with an EF < 40%.

8.

STATINS

in those patients with an EF < 40%. 8. STATINS Lipid lowering is indicated even if
in those patients with an EF < 40%. 8. STATINS Lipid lowering is indicated even if

Lipid lowering is indicated even if there are only borderline high serum total or LDL-cholesterol concentrations. The value of this approach was illustrated in the CARE trial which evaluated the effects of pravastatin (40 mg/day) versus placebo in 4,159 survivors of acute myocardial infarction with baseline total cholesterol levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]).

levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated
levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated
levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated
levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated
levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated
levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated
levels <240 mg/dL (mean of 209 mg/dL [5.4 mmol/L]). After five years, pravastatin treatment was associated

After five years, pravastatin treatment was associated with reductions in the combined incidence of coronary death and nonfatal MI (10.2 versus 13.2 percent, p = 0.003) and in the need for revascularization with CABG or PTCA (14.1 versus 18.8 percent, p<0.001). Subgroup analysis found that a significant number of cardiovascular events could be prevented among patients with average LDL- cholesterol levels above 125 mg/dL (3.2 mmol/L) by the administration of lipid-lowering therapy. In the placebo group, the event rate was increased by 28 percent for every 25 mg/dL (0.65 mmol/L) increment in LDL-cholesterol and by 10 percent for every 10 mg/dL (0.26 mmol/L) decrease in HDL-cholesterol.

every 10 mg/dL (0.26 mmol/L) decrease in HDL-cholesterol. 2. C ORONARY ANGIOGRAPHY +/- REVASCULARISATION . Patients
every 10 mg/dL (0.26 mmol/L) decrease in HDL-cholesterol. 2. C ORONARY ANGIOGRAPHY +/- REVASCULARISATION . Patients

2. CORONARY ANGIOGRAPHY +/- REVASCULARISATION.

Patients who do not become pain free after administration of medical therapy should be considered candidates for immediate angiography and revascularization based upon measures of left ventricular function, clinical status, and the extent of coronary disease. In general all patients fit for coronary revascularisation should undergo pre- discharge coronary angiography given the relatively high long term mortality based on medical therapy

RISK FACTOR REDUCTION

mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension
mortality based on medical therapy RISK FACTOR REDUCTION Risk factor modification includes treatment of hypertension

Risk factor modification includes treatment of hypertension and hyperlipidemia and the following changes in lifestyle:

and hyperlipidemia and the following changes in lifestyle:  Smoking cessation  Cardiac rehabilitation and an
and hyperlipidemia and the following changes in lifestyle:  Smoking cessation  Cardiac rehabilitation and an

Smoking cessation

Cardiac rehabilitation and an exercise program

Stress reduction

rehabilitation and an exercise program  Stress reduction Reproduced from A Rapid Review of Clinical Medicine
rehabilitation and an exercise program  Stress reduction Reproduced from A Rapid Review of Clinical Medicine
rehabilitation and an exercise program  Stress reduction Reproduced from A Rapid Review of Clinical Medicine
rehabilitation and an exercise program  Stress reduction Reproduced from A Rapid Review of Clinical Medicine
rehabilitation and an exercise program  Stress reduction Reproduced from A Rapid Review of Clinical Medicine