Unstable angina pectoris: Difference between revisions
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[[File:AP Ateroskleróza.png|thumb|Atherosclerosis of the coronary artery causing obstruction of 70% or more, resulting in angina pectoris.]] | |||
[[File:AP | |||
'''Unstable angina pectoris''' (NAP) is an '''acute coronary syndrome without ST elevation'''' on [[ECG]]. | '''Unstable angina pectoris''' (NAP) is an '''acute coronary syndrome without ST elevation'''' on [[ECG]]. | ||
Among '''[[acute coronary syndrome]] | <big>'''ACS, Unstable Angina pectoris:'''</big> {{Video | url=https://youtu.be/UYOKE-aUw6w?t=1275}} | ||
Among '''[[acute coronary syndrome]]s''' (ACS) we include:<ref name="Běl">{{Cite | |||
| type = article | | type = article | ||
| surname1 = | | surname1 = Bělohlávek | ||
| name1 = J | | name1 = J | ||
| surname2 = Aschermann | | surname2 = Aschermann | ||
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}} | }} | ||
</ref> | </ref> | ||
#unstable angina pectoris; | #unstable angina pectoris; | ||
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==Etiopathogenesis== | ==Etiopathogenesis== | ||
The pathophysiological essence of all ACS is intracoronary [[thrombosis]] superimposed on a superficially damaged (rupture, erosion, fissure), unstable [[atherosclerosis|atherosclerotic plaque]]. In the case of NAP, the resulting obstruction of the coronary artery is incomplete, so myocardial [[Necrosis|necrosis]] | The pathophysiological essence of all ACS is intracoronary [[thrombosis]] superimposed on a superficially damaged (rupture, erosion, fissure), unstable [[atherosclerosis|atherosclerotic plaque]]. In the case of NAP, the resulting obstruction of the coronary artery is incomplete, so myocardial [[Necrosis|necrosis]] '''does not occur''', so the levels of [[Cardiospecific markers|cardiospecific markers]] do not '''increase'''.<ref name="ceska">{{Cite | ||
| type = book | | type = book | ||
| isbn = 978-80-7387-423-0 | | isbn = 978-80-7387-423-0 | ||
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</ref> | </ref> | ||
The causes of NAP include:<ref name="Běl"> | The causes of NAP include:<ref name="Běl"> | ||
</ref><ref>{{Cite | |||
</ref><ref>{{ | |||
| type = article | | type = article | ||
| surname1 = Aschermann | | surname1 = Aschermann | ||
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| issn = 1803-7712 | | issn = 1803-7712 | ||
}} | }} | ||
</ref><ref name="gregor">{{ | </ref><ref name="gregor">{{Cite | ||
| type = article | | type = article | ||
| surname1 = Gregor | | surname1 = Gregor | ||
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*progressing atherosclerotic process; | *progressing atherosclerotic process; | ||
*progressive neointimal hyperplasia with the emergence of restenosis; | *progressive neointimal hyperplasia with the emergence of restenosis; | ||
*focal epicardial coronary artery spasm (''Prinzmetal's AP''); | *focal epicardial coronary artery spasm ('''Prinzmetal's AP'''); | ||
*inflammation of the coronary artery wall; | *inflammation of the coronary artery wall; | ||
*a number of extracardiac mechanisms (tachycardia, [[thyrotoxicosis]], fever, anemia, hypoxemia, hypotension). | *a number of extracardiac mechanisms (tachycardia, [[thyrotoxicosis]], fever, anemia, hypoxemia, hypotension). | ||
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:{| class="wikitable" | :{| class="wikitable" | ||
|- | |- | ||
! colspan="2" |Clinical forms of NAP<ref name="Běl"> | ! colspan="2" |Clinical forms of NAP<ref name="Běl"> | ||
</ref> | </ref> | ||
|- | |- | ||
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| range = 855 | | range = 855 | ||
}} | }} | ||
</ref><ref name="Běl"> | </ref><ref name="Běl"> | ||
</ref> | </ref> | ||
|- | |- | ||
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==Clinical symptoms== | ==Clinical symptoms== | ||
Patients report | Patients report '''pressure/tightening/burning pain in the chest (angina)''', the pain can radiate to the neck, lower jaw, upper limbs, back and abdomen. The pain usually subsides within 20 minutes. In addition, anxiety, nausea, vomiting, sweating, dizziness, a feeling of fainting, a feeling of [[shortness of breath]]i may be present. | ||
==Diagnosis== | ==Diagnosis== | ||
*'''History:''' risk factors (smoking, [[hyperlipoproteinemia]], [[DM]], [[hypertension]])?, positive family history?, CHD?, previous MI?, exertional AP?, coronary angioplasty?, intracoronary stent?, aortocoronary [[bypass]]? other diseases? permanent medication? allergies?.<ref name="gregor">{{ | *'''History:''' risk factors (smoking, [[hyperlipoproteinemia]], [[DM]], [[hypertension]])?, positive family history?, CHD?, previous MI?, exertional AP?, coronary angioplasty?, intracoronary stent?, aortocoronary [[bypass]]? other diseases? permanent medication? allergies?.<ref name="gregor">{{Cite | ||
| type = article | | type = article | ||
| surname1 = Gregor | | surname1 = Gregor | ||
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| issn = 1801-7606 | | issn = 1801-7606 | ||
}} | }} | ||
</ref><ref name="Běl"> | </ref><ref name="Běl"> | ||
</ref> | </ref> | ||
*'''Physical examination:''' mostly normal. Tachycardia and increased blood pressure (sympathetic activation) may be present.<ref name="gregor">{{Cite | *'''Physical examination:''' mostly normal. Tachycardia and increased blood pressure (sympathetic activation) may be present.<ref name="gregor">{{Cite | ||
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| range = 855 | | range = 855 | ||
}} | }} | ||
</ref><ref name="Běl"> | </ref><ref name="Běl"> | ||
</ref> | </ref> | ||
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| year = 2001 | | year = 2001 | ||
}} | }} | ||
</ref><ref name="gregor">{{ | </ref><ref name="gregor">{{Cite | ||
| type = article | | type = article | ||
| surname1 = Gregor | | surname1 = Gregor | ||
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:{| class="wikitable" | :{| class="wikitable" | ||
|- | |- | ||
! colspan="2" |Initial treatment of a patient with ACS. Taken from <ref name="Běl"> | ! colspan="2" |Initial treatment of a patient with ACS. Taken from <ref name="Běl"> | ||
</ref>. | </ref>. | ||
|- | |- | ||
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[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Pathophysiology]] | [[Category:Pathophysiology]] | ||
[[Category:Missing link to the original WikiScripta article]] |
Latest revision as of 21:08, 2 October 2023
Unstable angina pectoris (NAP) is an acute coronary syndrome without ST elevation' on ECG.
ACS, Unstable Angina pectoris:
Among acute coronary syndromes (ACS) we include:[1]
- unstable angina pectoris;
- acute myocardial infarction without ST segment elevations (NSTEMI);
- acute myocardial infarction with ST segment elevations (STEIMI).
These conditions are an acute manifestation of ischemic heart disease and need to be addressed urgently. A patient with NAP must be hospitalized in a coronary unit.
Etiopathogenesis[edit | edit source]
The pathophysiological essence of all ACS is intracoronary thrombosis superimposed on a superficially damaged (rupture, erosion, fissure), unstable atherosclerotic plaque. In the case of NAP, the resulting obstruction of the coronary artery is incomplete, so myocardial necrosis does not occur, so the levels of cardiospecific markers do not increase.[2]
The causes of NAP include:[1][3][4]
- non-occluding thrombosis encroaching on an unstable atherosclerotic plaque;
- progressing atherosclerotic process;
- progressive neointimal hyperplasia with the emergence of restenosis;
- focal epicardial coronary artery spasm (Prinzmetal's AP);
- inflammation of the coronary artery wall;
- a number of extracardiac mechanisms (tachycardia, thyrotoxicosis, fever, anemia, hypoxemia, hypotension).
Clinical forms and classification[edit | edit source]
|
|
Clinical symptoms[edit | edit source]
Patients report pressure/tightening/burning pain in the chest (angina), the pain can radiate to the neck, lower jaw, upper limbs, back and abdomen. The pain usually subsides within 20 minutes. In addition, anxiety, nausea, vomiting, sweating, dizziness, a feeling of fainting, a feeling of shortness of breathi may be present.
Diagnosis[edit | edit source]
- History: risk factors (smoking, hyperlipoproteinemia, DM, hypertension)?, positive family history?, CHD?, previous MI?, exertional AP?, coronary angioplasty?, intracoronary stent?, aortocoronary bypass? other diseases? permanent medication? allergies?.[4][1]
- Physical examination: mostly normal. Tachycardia and increased blood pressure (sympathetic activation) may be present.[4]
- Nitroglycerin test: Nitroglycerin is given for chest pain. If the pain subsides within 2 minutes, it is probably angina pectoris. Pain relief after more than 10 minutes is non-specific.[5]
- ECG: ST segment depression, T wave inversion, new A-V block?, new bundle branch block?. Outside of an anginal attack, the ECG is usually completely normal. If the ECG picture is normal even during an angina attack, this usually indicates against NAP (possibly against acute ischemia).[4]
- Biochemical markers of myocardial necrosis: are negative in NAP (myocardial necrosis does not occur in NAP).[4][2]
- Selective coronary angiography: should be performed in all patients with NAP. For hemodynamically stable patients, we perform it early, i.e. within 48–72 hours. We perform it immediately in hemodynamically unstable patients. Diagnostic coronary angiography can be followed by PCI (percutaneous coronary intervention) or CABG (coronary artery bypass grafting).[2][1]
Differential diagnosis[edit | edit source]
Differential diagnostics should exclude:
- other causes of chest pain (STEMI, NSTEMI, ischemia of non-coronary origin, aortic dissection, aortic aneurysm, pericarditis, myocarditis, pulmonary embolism, pneumothorax, vertebrogenic algic syndrome etc.).[6][4]
Treatment[edit | edit source]
A patient with NAP must be hospitalized in an intensive care unit with permanent monitoring of vital signs and ECG (preferably in a coronary unit).
-
introduction of i.v. cannulas
recording of a 12-lead ECG
Initial treatment of a patient with ACS. Taken from [1]. continuous monitoring of vital functions and ECG oxygen delivery 4–8 l/min blood sampling for the determination of markers of myocardial necrosis analgosedation (opiates) ASA 150–300 mg i.v. or p.o.[7] heparin 5000 j i.v./enoxaparin 1 mg/kg s.c./i.v. clopidogrel 300–600 mg i.v. (consider IIb/IIIa inhibitors) metoprolol i.v. according to the clinical condition
- Antithrombotic treatment: ASA, clopidogrel, IIb/IIIa inhibitors.
- Anticoagulation treatment: heparin, low molecular weight heparin.
- Antiischemic treatment: β-blocker (metoprolol), nitrate, calcium channel blocker (amlodipine, felodipine).
- Hypolipidemic treatment: statin.
Links[edit | edit source]
Related Articles[edit | edit source]
External links[edit | edit source]
References[edit | edit source]
- ↑ Jump up to: a b c d e f g BĚLOHLÁVEK, J – ASCHERMANN, M. Recommended procedure for diagnosis and treatment of acute coronary syndromes without ST segment elevations on ECG. Cor et Vasa [online]. 2008, y. 50, vol. Suppl, p. 1S7–1S23, Available from <http://www.kardio-cz.cz/resources/upload/data/141_aschermann_supl.pdf/>. ISSN 1803-7712.
- ↑ Jump up to: a b c d CZECH, Richard, et al. Intern. 1. edition. Prague : Triton, 2010. 855 pp. ISBN 978-80-7387-423-0.
- ↑ ASCHERMANN, Michael. Recommendations for the diagnosis and treatment of unstable angina pectoris - revision 2002. Cor et Vasa [online]. 2002, y. 44, vol. 7-8, p. K123–K143, Available from <http://www.kardio-cz.cz/index.php?&desktop=clanky&action=view&id=86>. ISSN 1803-7712.
- ↑ Jump up to: a b c d e f GREGOR, P – JIRMAŘ, R. Unstable angina pectoris. Cardioforum [online]. 2003, y. 2, vol. -, p. 13-15, Available from <http://www.kardiologickeforum.cz/pdf/kf_03_02_02.pdf\>. ISSN 1801-7606.
- ↑ ČEŠKA, Richard, ŠTULC, Tomáš, Vladimír TESAŘ and Milan LUKÁŠ, et al. Intern. 3. edition. Prague: Stanislav Juhaňák - Triton, 2020. 964 pp. 189-200. ISBN 978-80-7553-780-5.
- ↑ HRADEC, Jaromir – HE SLEPT, George. Internal medicine. Volume II, Cardiology, angiology. 1. edition. Prague : Galen :&nbsCaroline, 2001. ISBN 80-7262-106-8.
- ↑ P. Widimsky, et al. Summary of the 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Prepared by the Czech Society of Cardiology. Cor et Vasa 58 (2016) e4–e28, as published in the online version of Cor et Vasa at <http://www.sciencedirect.com/science/article/pii/S0010865016000059>