Chest Pain / Angina Pectoris: Difference between revisions

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===Additional Research===
===Additional Research===
If the ECG made during exercise testing does not show any abnormalities angina pectoris becomes very unlikely. If the ECG does show abnormalities during exercise testing additional research needs to be done.<cite>Fox2</cite> Depending on the hospital one of the below standing research will be done.  
If the ECG made during exercise testing does not show any abnormalities angina pectoris becomes very unlikely. If the ECG does show abnormalities during exercise testing additional research needs to be done.<cite>Fox</cite> Depending on the hospital one of the below standing research will be done.  
# Exercise echocardiography means that an echocardiography is made directly after exercise. The poorly perfused parts of the heart will show less activity.<cite>Amanullah</cite>
# Exercise echocardiography means that an echocardiography is made directly after exercise. The poorly perfused parts of the heart will show less activity.<cite>Amanullah</cite>
# Myocardium Perfusion Scintigraphy (MPS) is able to show the perfusion of the heart during exercise and at rest.<cite>Brown</cite>
# Myocardium Perfusion Scintigraphy (MPS) is able to show the perfusion of the heart during exercise and at rest.<cite>Brown</cite>
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==Coronary Angiography==
==Coronary Angiography==
In patients with unstable angina pectoris early coronary angiography possibly followed by revascularization is usually performed within 4 to 24 hours of admission in the hospital. In most clinical trials this strategy has shown a reduction in the incidence of death or nonfatal myocardial infraction.<cite>Anderson2</cite>
In patients with unstable angina pectoris early coronary angiography possibly followed by revascularization is usually performed within 4 to 24 hours of admission in the hospital. In most clinical trials this strategy has shown a reduction in the incidence of death or nonfatal myocardial infraction.<cite>Anderson</cite>


A CAG is an X ray examination of the coronary arteries, a catheter is inserted into the femoral artery or into the radial artery. The tip of the catheter is positioned at the beginning of the coronary arteries and contrast fluid is injected. Contrast is visible by X ray and the images that are obtained are called angiograms.
A CAG is an X ray examination of the coronary arteries, a catheter is inserted into the femoral artery or into the radial artery. The tip of the catheter is positioned at the beginning of the coronary arteries and contrast fluid is injected. Contrast is visible by X ray and the images that are obtained are called angiograms.
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In patients with stable angina pectoris percutaneous coronary intervention does not offer any benefit in terms of death, myocardial infarction, or the need for subsequent revascularization compared with conservative medical treatment.<cite>Katritsis</cite>
In patients with stable angina pectoris percutaneous coronary intervention does not offer any benefit in terms of death, myocardial infarction, or the need for subsequent revascularization compared with conservative medical treatment.<cite>Katritsis</cite>


Initial treatment of stable angina pectoris therefore focuses on medication to keep the workload of the heart as low as possible. β blockers lower heart rate and blood pressure, this decreases the oxygen demand of the heart.<cite>Garcia</cite> Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood.<cite>Abrams2</cite> Anticoagulants (aspirin) to reduce the risk of development of a thrombus in the coronary arteries.<cite>Hennekens</cite>
Initial treatment of stable angina pectoris therefore focuses on medication to keep the workload of the heart as low as possible. β blockers lower heart rate and blood pressure, this decreases the oxygen demand of the heart.<cite>Garcia</cite> Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood.<cite>Abrams</cite> Anticoagulants (aspirin) to reduce the risk of development of a thrombus in the coronary arteries.<cite>Hennekens</cite>


Apart from starting medication the patient needs to minimize any present risk factors like smoking, overweight and drinking alcohol. ''See chronic coronary diseases''.
Apart from starting medication the patient needs to minimize any present risk factors like smoking, overweight and drinking alcohol. ''See chronic coronary diseases''.
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==History==
==History==
Classic presentation of a myocardial infarction is acute chest pain which lasts longer than a few minutes. PMID 16304077 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. PMID 10099685 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. PMID 10866870, PMID 10751787
Classic presentation of a myocardial infarction is acute chest pain which lasts longer than a few minutes.<cite>Swap</cite> 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.<cite>Foreman</cite> 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.<cite>Canto</cite>,<cite>Pope</cite>


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).  
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. PMID 15289388
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.<cite>Antman</cite>


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


==Physical Examination==
==Physical Examination==
On physical examination evidence of systemic hypoperfusion can be found such as hypotension, tachycardia, impaired cognition, pale and ashen skin. PMID 15289388
On physical examination evidence of systemic hypoperfusion can be found such as hypotension, tachycardia, impaired cognition, pale and ashen skin.<cite>Antman</cite>


If during auscultation pulmonary crackles are heard and pitting oedema of the ankles is seen heart failure is complicating the myocardial infarction.  
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. PMID 15289388
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.<cite>Antman</cite>
 
==Electrocardiogram==
An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected myocardial infarction.<cite>Antman</cite>
An ECG is important to differentiate between myocardial ischemia and infarction:
* 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.<cite>Antman</cite>
 
An 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
 
==Cardiac Markers==
Cardiac markers are essential for confirming the diagnosis of infarction. Elevated CK MB and Troponin I indicate damage of the myocardium. Cardiac Troponin I concentration begins to rise two to three hours after myocardial ischemia.<cite>Macrae</cite>
It can take 4-6 hours before the CK MB concentration is elevated. The advise is to repeat the measurements after 4-6 hours.<cite>Puleo</cite>
A pitfall concerning elevated Troponin I can be patients with renal failure or pulmonary embolism.<cite>Thygesen</cite> Although cardiac markers are helpful for confirming the diagnosis reperfusion should not always wait till the cardiac markers are known.
 
=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.<cite>Antman</cite>
 
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. <cite>Anderson2</cite>, <cite>Bassand</cite>
Revascularisation can be achieved by fibrinolysis or PCI.
 
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. PMID 14532318
• Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction. PMID 16186438, PMID 12472924
 
Or when PCI has a better outcome:
 
• Patients who present three hours to four hours after the onset of the symptoms. PMID 12559937
• Patients with a non diagnostic ECG or a atypical history a coronary angiography with the ability to perform a PCI is preferred. PMID 12559937
 
FIBRINOLYSIS
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.<cite>Bassand</cite>
Because re occlusion after fibrinolysis is possible patients should be transferred to a PCI qualified hospital once fibrinolysis is done. PMID 15769784
 
 
PERCUTANEOUS CORONARY INTERVENTION (PCI)
 
Table 3 Considerations for selecting primary percutaneous coronary intervention (PCI) for reperfusion therapy in patients with ST elevation myocardial infarction (STEMI)
 
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.
 
 
 
 




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#Constant pmid=6831781
#Constant pmid=6831781
#Anderson pmid=17692738
#Anderson pmid=17692738
#Anderson2 pmid=17692738
#Anderson2 pmid=8712096
#Abrams pmid=3925741
#Abrams pmid=3925741
#Abrams2 pmid=3925741
#Henrikson pmid=14678917
#Henrikson pmid=14678917
#Antman pmid=15289388
#Antman pmid=15289388
#Fox pmid=17162834
#Fox pmid=17162834
#Fox2 pmid=17162834
#Amanullah pmid=1352191
#Amanullah pmid=1352191
#Brown pmid=2007701
#Brown pmid=2007701
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#Hennekens pmid=9355934
#Hennekens pmid=9355934
#Davies3 pmid=11084798
#Davies3 pmid=11084798
 
#Swap pmid=16304077
#Macrae pmid=16556688
#Thygesen pmid=17951284
#Puleo pmid=7702648
#Bassand pmid=16311237
#Ref1 pmid=8375424
#Ref1 pmid=8375424
</biblio>
</biblio>
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