Myocardial Infarction: Difference between revisions

From Textbook of Cardiology
Jump to navigation Jump to search
No edit summary
Line 1: Line 1:
In 2006 425.425 people died from a heart attack, 1.255.000 new and recurrent coronary attacks took place, about 34% died, 17.600.000 victims of angina, heart attack and other forms of coronary heart disease are still living.  
Each year, more than 2 million Americans have a heart attack or stroke, and more than 800,000 of them die; cardiovascular disease is the leading cause of death in the United States and the largest cause of lower life expectancy among blacks.  


These numbers only account for the United States.


===Pathofysiology===
== PATHOPHYSIOLOGY ==
[[File:Atherosclerosis.svg|thumb|right|200px|Atherosclerosis can stabilize or result in occlusion and myocardial infarction]]
An acute coronary syndrome (ACS) is most commonly caused by rupture or erosion of an atherosclerotic plaque with superimposed thrombus formation. The underlying process is atherosclerosis, a chronic disease in which artery walls thicken by deposition of fatty materials such as cholesterol and inflammatory cells. The accumulation of this material results in the formation of an atherosclerotic plaque, encapsulated by connective tissue, which can narrow the lumen of the arteries significantly and progressively causing symptoms as angina pectoris or lead to an ACS. Depending on the presence of myocardial damage and typical ECG characteristics, ACS can be divided into ST-segment elevation myocardial infarction (STEMI), and non-ST-segment ACS including non-ST-segment elevation MI (NSTEMI) and unstable angina. In the case of STEMI and NSTEMI, there is biochemical evidence of myocardial damage (infarction). <Cite>REFNAME1</Cite>: 11084798
A heart attack or myocardial infarction (MI) is an acute presentation of a process that has been going on much longer. The process responsible is atherosclerosis. Atherosclerosis is a chronic disease of the arteries in which artery walls thicken by deposition of fatty materials such as cholesterol. The result over decades are plaques, which can narrow the lumen of the arteries significantly and progressively causing symptoms as angina pectoris. Plaques can also suddenly rupture, trigger a cascade which results in a thrombus and thereby cause myocardial infarction.


===History===
== HISTORY ==
[[File:Heart_attack_pain_areas.svg|thumb|left|100px|Typical anginal chest pain distribution]]
The most typical characteristic of an ACS is acute prolonged chest pain. PMID 16304077 The pain does not decrease at rest and is only temporarily relieved with nitroglycerin. Frequent accompanying symptoms include a radiating pain to shoulder, arm, back and/or jaw. PMID 10099685 Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patient groups like elderly and diabetics might present with aspecific symptoms. PMID 10866870, PMID 10751787
Classic presentation of a myocardial infarction is acute chest pain which lasts longer than a few minutes. The pain does not decrease at rest and is only temporarily relieved with nitroglycerin. Common accompanying symptoms are radiating pain to shoulder, arm, back and/or jaw. Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patients not really complain about chest pain but more about abdominal pain so as with angina pectoris the presentation can be very a specific.  


It is important to complete the history with information about past history (prior history of ischemic events or vascular disease), risk factors for cardiovascular disease (o.a. smoking, hypertension, hyperlipidemia, obesity) and family history (direct family with myocardial infarction and/or sudden cardiac death).


Signs of heart failure such as orthopnea (not able to sleep without a pillow), progressive dyspnoea and oedematous ankles are indicative for the extent of the problem.  
It is important to complete the history with information about the medical history (prior history of ischemic events or vascular disease), risk factors for cardiovascular disease (a.o. diabetes mellitus, current smoking, hypertension, hyperlipidemia) and family history (first degree relatives with myocardial infarction before the age 55 of (males) or 65 (females) and/or sudden cardiac death). PMID15138242


A suspected myocardial infarction should be rapidly evaluated to initiate appropriate therapy.


===Physical Examination===
Symptoms of heart failure such as orthopnea (dyspnoea when lying flat), progressive dyspnoea and peripheral oedema are indicative for the extent of the problem. PMID 15289388
On physical examination evidence of systemic hypoperfusion can be found such as hypotension, tachycardia, impaired cognition, pale and ashen skin.
If during auscultation pulmonary crackles are heard and pitting oedema of the ankles is seen heart failure is complicating the myocardial infarction.  


History and physical examination are helpful to determine myocardial infarction as diagnosis and to exclude other causes of chest pain, such as angina pectoris, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems.


===Electrocardiogram===
== PHYSICAL EXAMINATION ==
[[File:TBC00002.jpg|200px|thumb|right|ST elevation in a patient with acute myocardial infarction]]
The focus of the physical examination should be to recognize signs of systemic hypoperfusion such as hypotension, tachycardia, impaired cognition, pale and ashen skin. PMID 15289388


An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected myocardial infarction.


An ECG is important to differentiate between myocardial ischemia and infarction:
Furthermore, signs of heart failure are important, such as pulmonary crackles during auscultation and pitting oedema of the ankles.
* ST elevation in myocardial infarction
* ST depression in myocardial ischemia


And to differentiate between STEMI and NSTEMI:
* STEMI stands for ST elevated (>20 min) Myocardial Infarction
* NSTEMI stand for Non ST elevated Myocardial Infarction


It can however take 90 minutes after the onset of the symptoms to see abnormalities on the ECG. Therefore it is important to make a serial ECG, certainly if a patient has ongoing symptoms.  
In more stable ACS patients, history and physical examination are helpful to exclude other causes of chest pain, such as angina pectoris, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems. PMID 15289388


An ECG is also helpful in localising the ischemia:
== ELECTROCARDIOGRAM ==
Anterior wall ischemia - One or more of leads V1-V6
An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected ACS. PMID 15289388
Anteroseptal ischemia - Leads V1 to V3
Apical or lateral ischemia - Leads aVL and I, and leads V4 to V6
Inferior wall ischemia - Leads II, III, and aVF


===Cardiac Markers===
[[File:Trop_ckmb.svg|thumb|right|300px|CK-MB and Troponine levels rise and fall differently after coronary obstruction with or without recovery of flow]]
Cardiac markers are essential for confirming the diagnosis of infarction. Elevated CK MB and Troponin I indicate damage of the myocardium. It can however take 4-8 hours, after the symptoms started, before the cardiac markers are elevated.  The advise is to repeat the measurements after 4-6 hours. A pitfall concerning elevated Troponin I can be patients with renal failure or pulmonary embolism. Although cardiac markers are helpful for confirming the diagnosis reperfusion should not always wait till the cardiac markers are known.


===Treatment===
The ECG is an important and easy modality which can assist in the diagnosis and prognostication of ACS.
It can however take 90 minutes after the onset of the symptoms to see abnormalities on the ECG. Furthermore, the ECG does not reflect the dynamic pathophysiology of the ACS. Therefore it is important to make serial ECGs, certainly if a patient has ongoing symptoms. PMID 15289388


===ST elevated Myocardial Infarct===


Initial treatment of STEMI is relief of ischemic pain, stabilize the hemodynamic status and reduce the ischemia as quickly as possible by fibrinolysis or primary percutaneous coronary intervention (PCI). Meanwhile other measures as continuous cardiac monitoring, oxygen and intravenous access are necessary to guarantee the safety of the patient.
Furthermore, the ECG is also helpful in localising the ischemia:
:Anterior wall ischemia - One or more of leads V1-V6
:Anteroseptal ischemia - Leads V1 to V3
:Apical or lateral ischemia - Leads aVL and I, and leads V4 to V6
:Inferior wall ischemia - Leads II, III, and aVF
:Posterior wall – Leads V7-V9
:Right ventricle – Leads V3R, V4R
:Left main coronary artery ischemia – Lead aVR


Rapid revascularisation is essential to minimize the impact of the myocardial infarction and thereby reduce mortality. In the first hours after symptom onset the amount of salvageable myocardium by reperfusion is greatest. Revascularisation can be achieved by fibrinolysis or PCI.
== CARDIAC MARKERS ==
Cardiac markers are essential in order to confirm the diagnosis of MI, indicated by elevated Creatine Kinase isoenzyme MB (CK MB) and/or (high-sensitive) troponins. Troponins are more specific and sensitive than CK MB. The cardiac troponin concentration begins to rise around 4 hours after the onset of myocardial cell damage. PMID 16556688


PCI is, if available, the preferred revascularisation method for patients with STEMI.
But not all hospitals are qualified to perform PCI and therefore fibrinolysis is still used. There are however some circumstances in which transfer to a PCI qualified hospital is essential:


* Patients with contraindications for fibrinolysis as active bleedings, recent dental surgery, past history of intracranial bleeding.  
With high-sensitive troponins, myocardial cell damage can be detected even earlier.  
* Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction.  
It can take 4-6 hours before the CK MB concentration is elevated. Serial measurements are advised in order to estimate infarct size and increase the sensitivity of the (older) assays. PMID 7702648


Or when PCI has a better outcome:
* Patients who present three hours to four hours after the onset of the symptoms.
* Patients with a non diagnostic ECG or a atypical history a coronary angiography with the ability to perform a PCI is preferred.


===Fibrinolysis===
A pitfall concerning mildly elevated cardiac markers can be patients with renal failure or pulmonary embolism. PMID: 17951284 Although cardiac markers are helpful for confirming the diagnosis, reperfusion should not always wait till the cardiac markers are known if the ECG or symptoms are evident.  
Fibrinolytics like streptokinase stimulate the conversion of plasminogen to plasmin. Plasmin demolishes fibrin which is an important constituent of the thrombus. Fibrinolytics are most effective the first hours after the onset of symptoms, after twelve hours the outcome will not improve. Because re occlusion after fibrinolysis is possible patients should be transferred to a PCI qualified hospital once fibrinolysis is done.  


===Percutaneous Coronary Intervention (PCI)===
== TREATMENT ==
{| class="wikitable" border="0"
As the formation of an intracoronary thrombus is the most common cause of the ACS and (recurrent) subsequent outcomes, the cornerstone in the treatment of ACS is antithrombotic treatment. All patients diagnosed with ACS should start with aspirin and a P2Y12 receptor blocker (clopidogrel, prasugrel or ticagrelor). PMID: 21873419 Aspirin and the P2Y12 receptor blocker are both platelet aggregation inhibitors. The treatment of ACS also focuses on medication to keep the workload of the heart as low as possible. β blockers lower heart rate and blood pressure, to decrease the oxygen demand of the heart. PMID 16735367 Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood. PMID 3925741
|-
| <flashow>http://pcipedia.org/images/b/bb/MM0079.swf|align=right|height=300px|width=300px</flashow>
| <flashow>http://pcipedia.org/images/5/51/MM0078.swf|align=right|height=300px|width=300px</flashow>
|-
| Right coronary artery (RCA) occlusion before PCI
| Reflow in the RCA after PCI
|}


The procedure of PCI starts off as a coronary angiography (see CAG). When the stenosis is visualized a catheter with an inflatable balloon will be brought at the site of the stenosis. Inflation of the balloon within the coronary artery will crush the atherosclerosis and eliminate the stenosis. To prevent that the effect of the balloon is only temporarily a stent is positioned at the site of the stenosis. To reduce the risk of coronary artery stent thrombosis antiplatelet therapy should be given.


===Coronary Artery Bypass Graft===
Depending on the (working) diagnosis STEMI or NSTE-ACS, the reperfusion strategy differs.
When the coronary arteries contain too many or too severe stenoses for PCI a coronary artery bypass graft (CABG) is indicated. Especially when the stenoses are located proximally of the three major coronary arteries, causing occlusion of many ramifications and high risk of severe myocardial damage.
[[File:Lima_vsm.svg|thumb|right|300px|In coronary artery bypass grafting the LIMA (left internal mammalian artery) is often used to revascularise the left anterior decending (LAD) coronary artery. Also, saphenous veins grafts can be used.]]
CABG does not eliminate the stenosis like PCI does. Using the internal thoracic arteries or the saphenous veins from the legs a bypass is made around the stenosis. The bypass originates from the aorta and terminates directly after the stenosis. Thereby restoring the blood supply to the ramifications. A bypass can be single or multiple, multiple meaning that there are several coronary arteries bypassed using the same bypass.  


Major surgery is not preferable in patients with STEMI, but CABG is inevitable when fibrinolysis and/or PCI failed or when the patient develops cardiogenic shock, life threatening ventricular arrhymthmias or three vessel disease.
=== ST-segment elevation Myocardial Infarction ===
Initial treatment of STEMI is relief of ischemic pain, stabilize the hemodynamic status and restoration of coronary flow and myocardial tissue perfusion. Reperfusion therapy should be initiated as quickly as possible within 12 hours after symptom onset by preferably primary percutaneous coronary intervention (PCI) or otherwise fibrinolysis. Meanwhile other measures as continuous cardiac monitoring, oxygen and intravenous access are necessary to guarantee the safety of the patient. PMID 15289388


===Medication to start after MI===
β blockers lower heart rate and blood pressure, this decreases the oxygen demand of the heart.
Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood. Anticoagulants reduce the risk of development of a thrombus in the coronary arteries.
Statins:
Apart from starting medication the patient needs to minimize any present risk factors like smoking, overweight and drinking alcohol.


===Non ST elevated Myocardial Infarct===
Rapid revascularisation is essential to minimize the size of the myocardial infarction and thereby reduce mortality. In the first hours after symptom onset the amount of salvageable myocardium by reperfusion is greatest. PMID 8712096, PMID16311237 There is no consensus whether reperfusion after 12 hours from the onset of symptoms is still beneficial.  
Initial treatment in NSTEMI is to reduce ischemia, stabilize the hemodynamic status, make serial ECG and to repeat measurements of the cardiac markers. Depending on the early risk stratification a choice has to be made between early invasive therapy or conservative therapy with medicines.  


Early risk stratification is helpful to identify patients at high risk who need a more aggressive therapeutic approach to prevent further ischemic events.
* Age ≥65 years
* Presence of at least three risk factors for coronary heart disease (hypertension, diabetes, dyslipidemia, smoking, or positive family history of early MI)
* Prior coronary stenosis of ≥50 percent
* Presence of ST segment deviation on admission ECG
* At least two anginal episodes in prior 24 hours
* Elevated serum cardiac biomarkers
Patients with a score of 0 to 1 are at low risk, score 2 to 3 are at intermediate risk, score 4 to 6 are at high risk.


===Conservative Therapy===
Primary PCI is the preferred revascularisation method for patients with STEMI. It is an effective method of securing and maintaining coronary patency and avoids the higher bleeding risk associated with fibrinolysis. If a patient is referred to a non-PCI-capable hospital, and transfer to a PCI-capable hospital in order to perform PCI within 2 hours after the onset of symptoms is not possible, fibrinolytic therapy is recommended.  
The main objective of in hospital conservative therapy is to relieve ischemic pain by intensifying medical therapy with aspirin and clopidogrel orally and nitro-glycerine, heparin and a beta blocker intravenously. If the patients becomes asymptomatic on these medication and is still asymptomatic when the medication is stopped, rest and stress imaging testing will be performed. The advantage of conservative therapy is reduction of the number of unnecessary revascularizations. The disadvantage is a prolonged stay in the hospital.
There are some circumstances in which transfer to a PCI qualified hospital is essential:
*  Patients with contraindications for fibrinolysis, such as:  active bleedings, recent dental surgery, past history of intracranial bleeding. PMID 14532318
* Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction. PMID 16186438, PMID 12472924


===Rest and Stress Imaging Tests===
Rest and stress testing is indicated in patients with:
# Angina pectoris with ECG abnormalities during exercise ECG testing
# Asymptomatic NSTEMI after in hospital conservative therapy


Exercise echocardiography means that an echocardiography is made directly after exercise. The poorly perfused parts of the heart will show less activity.  
Available data support the pre-hospital initiation of fibrinolytics if this reperfusion strategy is indicated. Fibrinolytics like streptokinase stimulate the conversion of plasminogen to plasmin. Plasmin demolishes fibrin which is an important constituent of the thrombus. Fibrinolytics are most effective the first hours after the onset of symptoms, and a benefit is observed in terms of reducing mortality within the first twelve hours. PMID 16311237  The hazards of thrombolysis are the increased bleeding risk, including strokes. Because re occlusion after fibrinolysis is possible patients should be transferred to a PCI qualified hospital once fibrinolysis is done. PMID 15769784 


Myocardium Perfusion Scintigraphy (MPS) is able to show the perfusion of the heart during exercise and at rest.


MRI can be done with vasodilatory dobutamine or stimulating adenosine to assess how the heart behaves during exercise.
There are circumstances in which CABG could be indicated, such as failed fibrinolysis and/or PCI, when the patient develops cardiogenic shock, life threatening ventricular arrhythmias, has three vessel disease, or mechanical complications of the MI. PMID:18191746


===Invasive Therapy===
=== Non-ST-segment elevation Acute Coronary Syndrome ===
High risk patients, patients with persistent symptoms despite medication or a positive stress test need invasive therapy. Depending on what is seen during coronary angiography PCI or a CABG is indicated. (see PCI/CABG)
Comparable to STEMI, revascularization in NSTE-ACS relieves symptoms, shortens hospital
stay, and improves prognosis. However, NSTE-ACS patients represent a heterogenous population, and indication and timing of revascularization depend on many factors, including the baseline risk of the patient. According to current guidelines, depending on early risk stratification a choice has to be made between a routine invasive or a selective invasive (or “conservative strategy”) PMID 15289388


Fibrinolytic therapy is not used in NSTEMI .
 
Early risk stratification is helpful to identify patients at high risk who might benefit the most from a more aggressive therapeutic approach in order to prevent further ischemic events. PMID 10938172
Early risk stratification can be performed using one of the validated risk scores, such as the TIMI risk score:
:- Age ≥65 years
:- Presence of at least three risk factors for coronary heart disease (hypertension, diabetes, dyslipidemia, smoking, or positive family history of early MI)
:- Prior coronary stenosis of ≥50 percent
:- Presence of ST segment deviation on admission ECG
:- At least two anginal episodes in prior 24 hours
:- Elevated serum cardiac biomarkers
:- Use of aspirin in the prior seven days
 
 
Patients with a score of 0 to 1 are at low risk, score 2 to 3 are at intermediate risk, score 4 to 6 are at high risk. 
 
Regarding treatment strategies in NSTE-ACS, many randomized controlled trials (RCTs) and meta-analyses have assessed the effects of a routine invasive vs. conservative or selective
invasive approach in the short and long term. One of the most recent meta-analysis has shown a benefit of the routine invasive management that was mainly visisble in intermediate- to high-risk patients. (referentie)
 
=== Selective invasive (“or conservative”) management ===
Patients undergoing a selective invasive (“or conservative”) management are initially stabilized by optimal medication, including aspirin and clopidogrel orally and nitro-glycerine, heparin and a beta blocker intravenously. If the patients becomes unstable or has refractory angina, he/she is referred for coronary angiography. Patients stabilized on medical therapy should undergo ischemia detection test before discharge. Potential advantages of this treatment strategy are a reduction of the number of catherization procedures. A potential disadvantage is a prolonged stay in the hospital. Although meta-analyses suggest the superiority of a routine invasive management, trials in which the selective invasive strategy was characterized by high rates of revascularization show equivalence of the two strategies.
 
=== Routine invasive management ===
The routine invasive strategy consists of routine, early coronary angiography (tijd noemen, ik dacht < 24 uur) and subsequent revascularization by PCI or CABG based on the angiographic findings.
 
 
The optimal timing of coronary angiography with an intended routine invasive management is still a topic for debate.

Revision as of 14:04, 13 January 2012

Each year, more than 2 million Americans have a heart attack or stroke, and more than 800,000 of them die; cardiovascular disease is the leading cause of death in the United States and the largest cause of lower life expectancy among blacks.


PATHOPHYSIOLOGY

An acute coronary syndrome (ACS) is most commonly caused by rupture or erosion of an atherosclerotic plaque with superimposed thrombus formation. The underlying process is atherosclerosis, a chronic disease in which artery walls thicken by deposition of fatty materials such as cholesterol and inflammatory cells. The accumulation of this material results in the formation of an atherosclerotic plaque, encapsulated by connective tissue, which can narrow the lumen of the arteries significantly and progressively causing symptoms as angina pectoris or lead to an ACS. Depending on the presence of myocardial damage and typical ECG characteristics, ACS can be divided into ST-segment elevation myocardial infarction (STEMI), and non-ST-segment ACS including non-ST-segment elevation MI (NSTEMI) and unstable angina. In the case of STEMI and NSTEMI, there is biochemical evidence of myocardial damage (infarction). [1]: 11084798

HISTORY

The most typical characteristic of an ACS is acute prolonged chest pain. PMID 16304077 The pain does not decrease at rest and is only temporarily relieved with nitroglycerin. Frequent accompanying symptoms include a radiating pain to shoulder, arm, back and/or jaw. PMID 10099685 Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patient groups like elderly and diabetics might present with aspecific symptoms. PMID 10866870, PMID 10751787


It is important to complete the history with information about the medical history (prior history of ischemic events or vascular disease), risk factors for cardiovascular disease (a.o. diabetes mellitus, current smoking, hypertension, hyperlipidemia) and family history (first degree relatives with myocardial infarction before the age 55 of (males) or 65 (females) and/or sudden cardiac death). PMID15138242


Symptoms of heart failure such as orthopnea (dyspnoea when lying flat), progressive dyspnoea and peripheral oedema are indicative for the extent of the problem. PMID 15289388


PHYSICAL EXAMINATION

The focus of the physical examination should be to recognize signs of systemic hypoperfusion such as hypotension, tachycardia, impaired cognition, pale and ashen skin. PMID 15289388


Furthermore, signs of heart failure are important, such as pulmonary crackles during auscultation and pitting oedema of the ankles.


In more stable ACS patients, history and physical examination are helpful to exclude other causes of chest pain, such as angina pectoris, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems. PMID 15289388

ELECTROCARDIOGRAM

An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected ACS. PMID 15289388


The ECG is an important and easy modality which can assist in the diagnosis and prognostication of ACS. It can however take 90 minutes after the onset of the symptoms to see abnormalities on the ECG. Furthermore, the ECG does not reflect the dynamic pathophysiology of the ACS. Therefore it is important to make serial ECGs, certainly if a patient has ongoing symptoms. PMID 15289388


Furthermore, the ECG is also helpful in localising the ischemia:

Anterior wall ischemia - One or more of leads V1-V6
Anteroseptal ischemia - Leads V1 to V3
Apical or lateral ischemia - Leads aVL and I, and leads V4 to V6
Inferior wall ischemia - Leads II, III, and aVF
Posterior wall – Leads V7-V9
Right ventricle – Leads V3R, V4R
Left main coronary artery ischemia – Lead aVR

CARDIAC MARKERS

Cardiac markers are essential in order to confirm the diagnosis of MI, indicated by elevated Creatine Kinase isoenzyme MB (CK MB) and/or (high-sensitive) troponins. Troponins are more specific and sensitive than CK MB. The cardiac troponin concentration begins to rise around 4 hours after the onset of myocardial cell damage. PMID 16556688


With high-sensitive troponins, myocardial cell damage can be detected even earlier. It can take 4-6 hours before the CK MB concentration is elevated. Serial measurements are advised in order to estimate infarct size and increase the sensitivity of the (older) assays. PMID 7702648


A pitfall concerning mildly elevated cardiac markers can be patients with renal failure or pulmonary embolism. PMID: 17951284 Although cardiac markers are helpful for confirming the diagnosis, reperfusion should not always wait till the cardiac markers are known if the ECG or symptoms are evident.

TREATMENT

As the formation of an intracoronary thrombus is the most common cause of the ACS and (recurrent) subsequent outcomes, the cornerstone in the treatment of ACS is antithrombotic treatment. All patients diagnosed with ACS should start with aspirin and a P2Y12 receptor blocker (clopidogrel, prasugrel or ticagrelor). PMID: 21873419 Aspirin and the P2Y12 receptor blocker are both platelet aggregation inhibitors. The treatment of ACS also focuses on medication to keep the workload of the heart as low as possible. β blockers lower heart rate and blood pressure, to decrease the oxygen demand of the heart. PMID 16735367 Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood. PMID 3925741


Depending on the (working) diagnosis STEMI or NSTE-ACS, the reperfusion strategy differs.

ST-segment elevation Myocardial Infarction

Initial treatment of STEMI is relief of ischemic pain, stabilize the hemodynamic status and restoration of coronary flow and myocardial tissue perfusion. Reperfusion therapy should be initiated as quickly as possible within 12 hours after symptom onset by preferably primary percutaneous coronary intervention (PCI) or otherwise fibrinolysis. Meanwhile other measures as continuous cardiac monitoring, oxygen and intravenous access are necessary to guarantee the safety of the patient. PMID 15289388


Rapid revascularisation is essential to minimize the size of the myocardial infarction and thereby reduce mortality. In the first hours after symptom onset the amount of salvageable myocardium by reperfusion is greatest. PMID 8712096, PMID16311237 There is no consensus whether reperfusion after 12 hours from the onset of symptoms is still beneficial.


Primary PCI is the preferred revascularisation method for patients with STEMI. It is an effective method of securing and maintaining coronary patency and avoids the higher bleeding risk associated with fibrinolysis. If a patient is referred to a non-PCI-capable hospital, and transfer to a PCI-capable hospital in order to perform PCI within 2 hours after the onset of symptoms is not possible, fibrinolytic therapy is recommended. There are some circumstances in which transfer to a PCI qualified hospital is essential:

  • Patients with contraindications for fibrinolysis, such as: active bleedings, recent dental surgery, past history of intracranial bleeding. PMID 14532318
  • Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction. PMID 16186438, PMID 12472924


Available data support the pre-hospital initiation of fibrinolytics if this reperfusion strategy is indicated. Fibrinolytics like streptokinase stimulate the conversion of plasminogen to plasmin. Plasmin demolishes fibrin which is an important constituent of the thrombus. Fibrinolytics are most effective the first hours after the onset of symptoms, and a benefit is observed in terms of reducing mortality within the first twelve hours. PMID 16311237 The hazards of thrombolysis are the increased bleeding risk, including strokes. Because re occlusion after fibrinolysis is possible patients should be transferred to a PCI qualified hospital once fibrinolysis is done. PMID 15769784


There are circumstances in which CABG could be indicated, such as failed fibrinolysis and/or PCI, when the patient develops cardiogenic shock, life threatening ventricular arrhythmias, has three vessel disease, or mechanical complications of the MI. PMID:18191746

Non-ST-segment elevation Acute Coronary Syndrome

Comparable to STEMI, revascularization in NSTE-ACS relieves symptoms, shortens hospital stay, and improves prognosis. However, NSTE-ACS patients represent a heterogenous population, and indication and timing of revascularization depend on many factors, including the baseline risk of the patient. According to current guidelines, depending on early risk stratification a choice has to be made between a routine invasive or a selective invasive (or “conservative strategy”) PMID 15289388


Early risk stratification is helpful to identify patients at high risk who might benefit the most from a more aggressive therapeutic approach in order to prevent further ischemic events. PMID 10938172 Early risk stratification can be performed using one of the validated risk scores, such as the TIMI risk score:

- Age ≥65 years
- Presence of at least three risk factors for coronary heart disease (hypertension, diabetes, dyslipidemia, smoking, or positive family history of early MI)
- Prior coronary stenosis of ≥50 percent
- Presence of ST segment deviation on admission ECG
- At least two anginal episodes in prior 24 hours
- Elevated serum cardiac biomarkers
- Use of aspirin in the prior seven days


Patients with a score of 0 to 1 are at low risk, score 2 to 3 are at intermediate risk, score 4 to 6 are at high risk.

Regarding treatment strategies in NSTE-ACS, many randomized controlled trials (RCTs) and meta-analyses have assessed the effects of a routine invasive vs. conservative or selective invasive approach in the short and long term. One of the most recent meta-analysis has shown a benefit of the routine invasive management that was mainly visisble in intermediate- to high-risk patients. (referentie)

Selective invasive (“or conservative”) management

Patients undergoing a selective invasive (“or conservative”) management are initially stabilized by optimal medication, including aspirin and clopidogrel orally and nitro-glycerine, heparin and a beta blocker intravenously. If the patients becomes unstable or has refractory angina, he/she is referred for coronary angiography. Patients stabilized on medical therapy should undergo ischemia detection test before discharge. Potential advantages of this treatment strategy are a reduction of the number of catherization procedures. A potential disadvantage is a prolonged stay in the hospital. Although meta-analyses suggest the superiority of a routine invasive management, trials in which the selective invasive strategy was characterized by high rates of revascularization show equivalence of the two strategies.

Routine invasive management

The routine invasive strategy consists of routine, early coronary angiography (tijd noemen, ik dacht < 24 uur) and subsequent revascularization by PCI or CABG based on the angiographic findings.


The optimal timing of coronary angiography with an intended routine invasive management is still a topic for debate.

Retrieved from "https://www.textbookofcardiology.org/index.php?title=Myocardial_Infarction&oldid=597"