Myocardial Infarction: Difference between revisions

Latest revision as of 07:53, 2 March 2021

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). [1]

A myocardial infarction results from a coronary occlusion (1) with necrosis of myocardial tissue (2) distal to the occlusion

History

Different terminology is used during different phases of the chest pain workup. The ECG classifies into ST elevtion or not. Troponine definitely classifies into myocardial infarction (damage) or not.

The most typical characteristic of an ACS is acute prolonged chest pain. [2] 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. [3] Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patients including elderly and diabetics may present with aspecific symptoms. [4], [5]

It is important to complete 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). [6]

Symptoms of heart failure such as orthopnea (dyspnoea when lying flat), progressive dyspnoea and peripheral oedema are indicative of the extent of the problem. [7]

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. [7]

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 aortic valve stenosis, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems. [7]

Electrocardiogram (ECG)

An electrocardiogram (ECG) should be made on arrival in every patient with suspected ACS. [7]

The ECG is an important and easy modality which can assist in the diagnosis and prognostication of ACS. However, a single ECG may not reflect the dynamic pathophysiology of the ACS. Therefore it is important to make serial ECGs, certainly if a patient has ongoing symptoms. [7]

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

Anterior wall ischemia - One or more of leads V2-V5
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, V1
Left main coronary artery ischemia – Lead aVR

More information abou the ECG during myocardial infarction can be found on ECGpedia.

Cardiac Markers

Rise and fall of several cardiac markers based on whether the myocardium was reperfused or not

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.[8]

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 useful in order to estimate infarct size and increase the sensitivity of the (older) assays. [9]

A pitfall concerning mildly elevated cardiac markers can be patients with renal failure or pulmonary embolism. [10]

Treatment

Reperfusion strategies. The thick arrow indicates the preferred strategy.

As the formation of an intracoronary thrombus is a central mechanism in 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). [11] Aspirin and the P2Y12 receptor blocker are both platelet aggregation inhibitors. The treatment of ACS also focuses on medication to reduce the workload of the heart. ß blockers lower heart rate and blood pressure, to decrease the oxygen demand of the heart. [12] Nitrates dilatate the coronary arteries. [13]

Depending on the (working) diagnosis STEMI or NSTE-ACS, the revascularisation strategy varies.

ST-segment elevation Myocardial Infarction

Initial treatment of STEMI is relief of ischemic pain, stabilisation of hemodynamic status and restoration of coronary flow and myocardial tissue perfusion. Reperfusion therapy should be initiated as quickly as possible by preferably primary percutaneous coronary intervention (PCI) or fibrinolysis. Reperfusion is beneficial up to 12 hours after the onset of symptoms. In case of severe hemodynamic compromise, reperfusion therapy may be attempted up to 24 hours after symptom onset. Meanwhile other measures as continuous ECG monitoring, oxygen supply and intravenous access are indicated. [7]

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 circumstances in which transfer to a PCI qualified hospital is recommended:

Patients with contraindications for fibrinolysis, such as: active bleedings, recent surgery, past history of intracranial bleeding. [14]
Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction. [15], [16]

Available data support the pre-hospital initiation of fibrinolytics if this reperfusion strategy is indicated. Fibrinolytics like streptokinase and rtPA stimulate the conversion of plasminogen to plasmin. Plasmin degrades 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. [17] The hazards of thrombolysis are increased bleeding risk, including hemorrhagic strokes. Because re occlusion after fibrinolysis is possible patients should be transferred if possible to a PCI qualified hospital once fibrinolysis is done. [18]

In rare cases, CABG is indicated, such as failed fibrinolysis with coronary anatomy unsuited for PCI and/or failed PCI, when the patient develops cardiogenic shock, life threatening ventricular arrhythmias, has three vessel disease, or mechanical complications of the MI. [19]

Non-ST-segment elevation Acute Coronary Syndrome

The GRACE risk score model

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”) [20]

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. [21]

Risk Category	low	Intermediate	High
GRACE risk score
NSTEMI Probability of Death In-hospital (%)	<1	1-3	>3
NSTEMI 6 Month Post-discharge Mortality	<3	3-8	>8
STEMI In-hospital Mortality (%)	<2	2-5	>5
STEMI 6 Month Post-discharge Mortality	<4.4	4.5-11	>11

Early risk stratification can be performed using one of the validated risk scores, such as the GRACE risk score. GRACE calculates the probability of death while in hospital. The following characteristics are taken into account:

Age
Heart rate and systolic BP
Creatinine
Killip class
Cardiac arrest at admission
Elevated cardiac markers
ST segment deviation

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. Recent meta-analyse suggest a benefit of the routine invasive management that is mainly visible in intermediate- to high-risk patients. (referentie)

Selective invasive (“or conservative”) management

Patients undergoing a selective invasive (“or conservative”) management are initially stabilized by medication only, including aspirin and clopidogrel orally and nitro-glycerin, heparin and a beta blocker intravenously. If the patients is unstable or has refractory angina, he/she is referred for coronary angiography. Patients stabilized on medical therapy should undergo a stress 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 within 24 hours after admission and subsequent revascularization if appropriate by PCI or CABG based on the angiographic findings. The optimal timing of coronary angiography with an intended routine invasive management is debated. In patients with high risk features, including hypotension, ventricular arrhythmias or a large myocardial area at risk, should undergo urgent angiography (<2 hours).

Cardiac rehabilitation

Cardiac rehabilitation reduces mortality, helps the patient to regain confidence and to resocialise, and helps to reduce risk factors for atherosclerosis. Post-ACS patient should be referred for cardiac rehabilitation.

References

All Medline abstracts: PubMed | HubMed

@@ 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.
+[[File:MyocardialInfarction.svg|thumb|right|400px|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>
+[[File:AMI_scheme.png|thumb|right|200px|A myocardial infarction results from a coronary occlusion (1) with necrosis of myocardial tissue (2) distal to the occlusion]]
-These numbers only account for the United States.
+==History==
+[[File:chest_pain_to_NSTEMI_STEMI_v2.svg|thumb|400px|right|Different terminology is used during different phases of the chest pain workup. The ECG classifies into ST elevtion or not. Troponine definitely classifies into myocardial infarction (damage) or not.]]
+The most typical characteristic of an ACS is acute prolonged chest pain. <Cite>REFNAME2</Cite> 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. <Cite>REFNAME3</Cite> Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patients including elderly and diabetics may present with aspecific symptoms. <Cite>REFNAME4</Cite>, <Cite>REFNAME5</Cite>
-===Pathofysiology===
+It is important to complete 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). <Cite>REFNAME6</Cite>
-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===
+Symptoms of heart failure such as orthopnea (dyspnoea when lying flat), progressive dyspnoea and peripheral oedema are indicative of the extent of the problem. <Cite>REFNAME7</Cite>
-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).
+==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. <Cite>REFNAME7</Cite>
-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.
+Furthermore, signs of heart failure are important, such as pulmonary crackles during auscultation and pitting oedema of the ankles.
-A suspected myocardial infarction should be rapidly evaluated to initiate appropriate therapy.
+In more stable ACS patients, history and physical examination are helpful to exclude other causes of chest pain, such as aortic valve stenosis, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems. <Cite>REFNAME7</Cite>
-===Physical Examination===
+==Electrocardiogram (ECG)==
-On physical examination evidence of systemic hypoperfusion can be found such as hypotension, tachycardia, impaired cognition, pale and ashen skin.
+An electrocardiogram (ECG) should be made on arrival in every patient with suspected ACS. <Cite>REFNAME7</Cite>
-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.
+The ECG is an important and easy modality which can assist in the diagnosis and prognostication of ACS. However, a single ECG may not reflect the dynamic pathophysiology of the ACS. Therefore it is important to make serial ECGs, certainly if a patient has ongoing symptoms. <Cite>REFNAME7</Cite>
-===Electrocardiogram===
+Furthermore, the ECG is also helpful in localising the ischemia:
-An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected myocardial infarction.
+*Anterior wall ischemia - One or more of leads V2-V5
+*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, V1
+*Left main coronary artery ischemia – Lead aVR
-An ECG is important to differentiate between myocardial ischemia and infarction:
+More information abou the [http://en.ecgpedia.org/wiki/Myocardial_Infarction ECG during myocardial infarction] can be found on ECGpedia.
-* ST elevation in myocardial infarction
-* ST depression in myocardial ischemia
-And to differentiate between STEMI and NSTEMI:
+==Cardiac Markers==
-* STEMI stands for ST elevated (>20 min) Myocardial Infarction
+[[File:Cardiac_markers.png|thumb|right|Rise and fall of several cardiac markers based on whether the myocardium was reperfused or not]]
-* NSTEMI stand for Non ST elevated Myocardial Infarction
+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.<Cite>REFNAME12</Cite>
-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.
+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 useful in order to estimate infarct size and increase the sensitivity of the (older) assays. <Cite>REFNAME13</Cite>
-An ECG is also helpful in localising the ischemia:
+A pitfall concerning mildly elevated cardiac markers can be patients with renal failure or pulmonary embolism. <Cite>REFNAME14</Cite>
-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
-===Cardiac Markers===
+==Treatment==
-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.
+[[File:Figure_2_-_Reperfusion_strategies.svg|thumb|right|500px|Reperfusion strategies. The thick arrow indicates the preferred strategy.]]
-===Treatment===
+As the formation of an intracoronary thrombus is a central mechanism in 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). <Cite>REFNAME15</Cite> Aspirin and the P2Y12 receptor blocker are both platelet aggregation inhibitors. The treatment of ACS also focuses on medication to reduce the workload of the heart. ß blockers lower heart rate and blood pressure, to decrease the oxygen demand of the heart. <Cite>REFNAME16</Cite> Nitrates dilatate the coronary arteries. <Cite>REFNAME17</Cite>
-===ST elevated Myocardial Infarct===
+Depending on the (working) diagnosis STEMI or NSTE-ACS, the revascularisation strategy varies.
-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.
+===ST-segment elevation Myocardial Infarction===
-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.
+Initial treatment of STEMI is relief of ischemic pain, stabilisation of hemodynamic status and restoration of coronary flow and myocardial tissue perfusion. Reperfusion therapy should be initiated as quickly as possible by preferably primary percutaneous coronary intervention (PCI) or fibrinolysis. Reperfusion is beneficial up to 12 hours after the onset of symptoms. In case of severe hemodynamic compromise, reperfusion therapy may be attempted up to 24 hours after symptom onset. Meanwhile other measures as continuous ECG monitoring, oxygen supply and intravenous access are indicated. <Cite>REFNAME7</Cite>
+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 circumstances in which transfer to a PCI qualified hospital is recommended:
+*Patients with contraindications for fibrinolysis, such as:  active bleedings, recent surgery, past history of intracranial bleeding. <Cite>REFNAME21</Cite>
+*Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction. <Cite>REFNAME22</Cite>, <Cite>REFNAME23</Cite>
+Available data support the pre-hospital initiation of fibrinolytics if this reperfusion strategy is indicated. Fibrinolytics like streptokinase and rtPA stimulate the conversion of plasminogen to plasmin. Plasmin degrades 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. <Cite>REFNAME20</Cite> The hazards of thrombolysis are increased bleeding risk, including hemorrhagic strokes. Because re occlusion after fibrinolysis is possible patients should be transferred if possible to a PCI qualified hospital once fibrinolysis is done. <Cite>REFNAME25</Cite>
+In rare cases, CABG is indicated, such as failed fibrinolysis with coronary anatomy unsuited for PCI and/or failed PCI, when the patient develops cardiogenic shock, life threatening ventricular arrhythmias, has three vessel disease, or mechanical complications of the MI. <Cite>REFNAME26</Cite>
+===Non-ST-segment elevation Acute Coronary Syndrome===
+[[Image:Non-ST-segment elevation Acute Coronary Syndrome.svg|thumb|right|400px]]
+[[Image:Non-ST-segment elevation Acute Coronary Syndrome2.svg|thumb|right|400px]]
+[[Image:Swe.jpg|thumb|right|400px|link=http://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html|The [http://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html GRACE risk score model]]]
+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”) <Cite>REFNAME27</Cite>
+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. <Cite>REFNAME28</Cite>
+{| class="wikitable" cellpadding="0" cellspacing="0" border="0" width="500px"
+|-
+|colspan="5" align="center"|'''GRACE risk score'''
+|-
+!Risk Category
+!low
+!Intermediate
+!High
+|-
+|NSTEMI Probability of Death In-hospital (%)
+|<1
+|1-3
+|>3
+|-
+|NSTEMI 6 Month Post-discharge Mortality
+|<3
+|3-8
+|>8
+|-
+|STEMI In-hospital Mortality (%)
+|<2
+|2-5
+|>5
+|-
+|STEMI 6 Month Post-discharge Mortality
+|<4.4
+|4.5-11
+|>11
+|}
+Early risk stratification can be performed using one of the validated risk scores, such as the GRACE risk score. GRACE calculates the probability of death while in hospital. The following characteristics are taken into account:
+*Age
+*Heart rate and systolic BP
+*Creatinine
+*Killip class
+*Cardiac arrest at admission
+*Elevated cardiac markers
+*ST segment deviation
+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. Recent meta-analyse suggest a benefit of the routine invasive management that is mainly visible in intermediate- to high-risk patients. (referentie)
+====Selective invasive (“or conservative”) management====
+Patients undergoing a selective invasive (“or conservative”) management are initially stabilized by medication only, including aspirin and clopidogrel orally and nitro-glycerin, heparin and a beta blocker intravenously. If the patients is unstable or has refractory angina, he/she is referred for coronary angiography. Patients stabilized on medical therapy should undergo a stress 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 within 24 hours after admission and subsequent revascularization if appropriate by PCI or CABG based on the angiographic findings.
+The optimal timing of coronary angiography with an intended routine invasive management is debated. In patients with high risk features, including hypotension, ventricular arrhythmias or a large myocardial area at risk, should undergo urgent angiography (<2 hours).
+====Cardiac rehabilitation====
+Cardiac rehabilitation reduces mortality, helps the patient to regain confidence and to resocialise, and helps to reduce risk factors for atherosclerosis. Post-ACS patient should be referred for cardiac rehabilitation.
+== References ==
+<biblio>
+#REFNAME1 pmid=11084798
+#REFNAME2 pmid=16304077
+#REFNAME3 pmid=10099685
+#REFNAME4 pmid=10866870
+#REFNAME5 pmid=10751787
+#REFNAME6 pmid=15138242
+#REFNAME7 pmid=15289388
+#REFNAME12 pmid=16556688
+#REFNAME13 pmid=7702648
+#REFNAME14 pmid=17951284
+#REFNAME15 pmid=21873419
+#REFNAME16 pmid=16735367
+#REFNAME17 pmid=3925741
+#REFNAME18 pmid=15289388
+#REFNAME19 pmid=8712096
+#REFNAME20 pmid=16311237
+#REFNAME21 pmid=14532318
+#REFNAME22 pmid=16186438
+#REFNAME23 pmid=12472924
+#REFNAME24 pmid=16311237
+#REFNAME25 pmid=15769784
+#REFNAME26 pmid=18191746
+#REFNAME27 pmid=15289388
+#REFNAME28 pmid=10938172
+</biblio>

Myocardial Infarction: Difference between revisions

Latest revision as of 07:53, 2 March 2021

Contents

History

Physical Examination

Electrocardiogram (ECG)

Cardiac Markers

Treatment

ST-segment elevation Myocardial Infarction

Non-ST-segment elevation Acute Coronary Syndrome

Selective invasive (“or conservative”) management

Routine invasive management

Cardiac rehabilitation

References

Navigation menu

Myocardial Infarction: Difference between revisions

Latest revision as of 07:53, 2 March 2021

History

Physical Examination

Electrocardiogram (ECG)

Cardiac Markers

Treatment

ST-segment elevation Myocardial Infarction

Non-ST-segment elevation Acute Coronary Syndrome

Selective invasive (“or conservative”) management

Routine invasive management

Cardiac rehabilitation

References

Navigation menu

Search