Acute coronary syndromes: Difference between revisions
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The pathophysiology of acute coronary syndromes depends on [[atherosclerosis|coronary atherosclerotic plaque]] which includes:<ref name="pmid3286036">{{cite journal| author=Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ, Chesebro J| title=Insights into the pathogenesis of acute ischemic syndromes. | journal=Circulation | year= 1988 | volume= 77 | issue= 6 | pages= 1213-20 | pmid=3286036 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3286036 }} </ref><ref name="pmid11457759">{{cite journal| author=Libby P| title=Current concepts of the pathogenesis of the acute coronary syndromes. | journal=Circulation | year= 2001 | volume= 104 | issue= 3 | pages= 365-72 | pmid=11457759 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11457759 }} </ref> | The pathophysiology of acute coronary syndromes depends on [[atherosclerosis|coronary atherosclerotic plaque]] which includes:<ref name="pmid3286036">{{cite journal| author=Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ, Chesebro J| title=Insights into the pathogenesis of acute ischemic syndromes. | journal=Circulation | year= 1988 | volume= 77 | issue= 6 | pages= 1213-20 | pmid=3286036 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3286036 }} </ref><ref name="pmid11457759">{{cite journal| author=Libby P| title=Current concepts of the pathogenesis of the acute coronary syndromes. | journal=Circulation | year= 2001 | volume= 104 | issue= 3 | pages= 365-72 | pmid=11457759 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11457759 }} </ref> | ||
'''Initiation and | '''Initiation and Progression of Coronary Atherosclerotic Plaque''' | ||
*The [[endothelium]] of [[coronary arteries]] are damaged by the risk factors resulting in [[endothelium|endothelial dysfunction]], leading to the formation of [[Atherosclerosis|atherosclerotic plaque]]. | *The [[endothelium]] of [[coronary arteries]] are damaged by the risk factors resulting in [[endothelium|endothelial dysfunction]], leading to the formation of [[Atherosclerosis|atherosclerotic plaque]]. | ||
*The [[macrophages]] in the atherosclerotic plaque release matrix [[metalloproteinases]], leading to plaque disruption. <ref name="pmid1728735">{{cite journal| author=Fuster V, Badimon L, Badimon JJ, Chesebro JH| title=The pathogenesis of coronary artery disease and the acute coronary syndromes (2). | journal=N Engl J Med | year= 1992 | volume= 326 | issue= 5 | pages= 310-8 | pmid=1728735 | doi=10.1056/NEJM199201303260506 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1728735 }} </ref> | *The [[macrophages]] in the atherosclerotic plaque release matrix [[metalloproteinases]], leading to plaque disruption. <ref name="pmid1728735">{{cite journal| author=Fuster V, Badimon L, Badimon JJ, Chesebro JH| title=The pathogenesis of coronary artery disease and the acute coronary syndromes (2). | journal=N Engl J Med | year= 1992 | volume= 326 | issue= 5 | pages= 310-8 | pmid=1728735 | doi=10.1056/NEJM199201303260506 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1728735 }} </ref> | ||
*The balance between [[smooth muscle cells]] and [[macrophages]] in the plaque plays a major role in plaque vulnerability and the propensity to rupture. | *The balance between [[smooth muscle cells]] and [[macrophages]] in the plaque plays a major role in plaque vulnerability and the propensity to rupture. | ||
'''Plaque | '''Plaque Vulnerability''' | ||
The plaque vulnerability depends on the following factors:<ref name="pmid8044947">{{cite journal| author=Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT| title=Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. | journal=Circulation | year= 1994 | volume= 90 | issue= 2 | pages= 775-8 | pmid=8044947 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8044947 }} </ref><ref name="pmid8518056">{{cite journal| author=Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J| title=Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. | journal=Br Heart J | year= 1993 | volume= 69 | issue= 5 | pages= 377-81 | pmid=8518056 | doi= | pmc=1025095 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8518056 }} </ref><ref name="pmid10330380">{{cite journal| author=Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC et al.| title=Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. | journal=Circulation | year= 1999 | volume= 99 | issue= 19 | pages= 2503-9 | pmid=10330380 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10330380 }} </ref><ref name="pmid10330380">{{cite journal| author=Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC et al.| title=Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. | journal=Circulation | year= 1999 | volume= 99 | issue= 19 | pages= 2503-9 | pmid=10330380 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10330380 }} </ref><ref name="pmid11602491">{{cite journal| author=Herman MP, Sukhova GK, Libby P, Gerdes N, Tang N, Horton DB et al.| title=Expression of neutrophil collagenase (matrix metalloproteinase-8) in human atheroma: a novel collagenolytic pathway suggested by transcriptional profiling. | journal=Circulation | year= 2001 | volume= 104 | issue= 16 | pages= 1899-904 | pmid=11602491 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11602491 }} </ref> | The plaque vulnerability depends on the following factors:<ref name="pmid8044947">{{cite journal| author=Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT| title=Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. | journal=Circulation | year= 1994 | volume= 90 | issue= 2 | pages= 775-8 | pmid=8044947 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8044947 }} </ref><ref name="pmid8518056">{{cite journal| author=Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J| title=Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. | journal=Br Heart J | year= 1993 | volume= 69 | issue= 5 | pages= 377-81 | pmid=8518056 | doi= | pmc=1025095 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8518056 }} </ref><ref name="pmid10330380">{{cite journal| author=Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC et al.| title=Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. | journal=Circulation | year= 1999 | volume= 99 | issue= 19 | pages= 2503-9 | pmid=10330380 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10330380 }} </ref><ref name="pmid10330380">{{cite journal| author=Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC et al.| title=Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. | journal=Circulation | year= 1999 | volume= 99 | issue= 19 | pages= 2503-9 | pmid=10330380 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10330380 }} </ref><ref name="pmid11602491">{{cite journal| author=Herman MP, Sukhova GK, Libby P, Gerdes N, Tang N, Horton DB et al.| title=Expression of neutrophil collagenase (matrix metalloproteinase-8) in human atheroma: a novel collagenolytic pathway suggested by transcriptional profiling. | journal=Circulation | year= 2001 | volume= 104 | issue= 16 | pages= 1899-904 | pmid=11602491 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11602491 }} </ref> | ||
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==Diagnosis== | ==Diagnosis== | ||
===High-sensitivity | ===High-sensitivity Cardiac Troponin (hs-cTn)=== | ||
{| class="wikitable" | {| class="wikitable" | ||
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High sensitivity troponin levels have reduced predictive value when prevalence is low<ref name="pmid30580773">{{cite journal| author=Lee KK, Noaman A, Vaswani A, Gibbins M, Griffiths M, Chapman AR et al.| title=Prevalence, Determinants, and Clinical Associations of High-Sensitivity Cardiac Troponin in Patients Attending Emergency Departments. | journal=Am J Med | year= 2019 | volume= 132 | issue= 1 | pages= 110.e8-110.e21 | pmid=30580773 | doi=10.1016/j.amjmed.2018.10.002 | pmc=6310691 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30580773 }} </ref><ref name="pmid29114078">{{cite journal| author=Shah ASV, Sandoval Y, Noaman A, Sexter A, Vaswani A, Smith SW et al.| title=Patient selection for high sensitivity cardiac troponin testing and diagnosis of myocardial infarction: prospective cohort study. | journal=BMJ | year= 2017 | volume= 359 | issue= | pages= j4788 | pmid=29114078 | doi=10.1136/bmj.j4788 | pmc=5683043 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29114078 }} </ref>. | High sensitivity troponin levels have reduced predictive value when prevalence is low<ref name="pmid30580773">{{cite journal| author=Lee KK, Noaman A, Vaswani A, Gibbins M, Griffiths M, Chapman AR et al.| title=Prevalence, Determinants, and Clinical Associations of High-Sensitivity Cardiac Troponin in Patients Attending Emergency Departments. | journal=Am J Med | year= 2019 | volume= 132 | issue= 1 | pages= 110.e8-110.e21 | pmid=30580773 | doi=10.1016/j.amjmed.2018.10.002 | pmc=6310691 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30580773 }} </ref><ref name="pmid29114078">{{cite journal| author=Shah ASV, Sandoval Y, Noaman A, Sexter A, Vaswani A, Smith SW et al.| title=Patient selection for high sensitivity cardiac troponin testing and diagnosis of myocardial infarction: prospective cohort study. | journal=BMJ | year= 2017 | volume= 359 | issue= | pages= j4788 | pmid=29114078 | doi=10.1136/bmj.j4788 | pmc=5683043 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29114078 }} </ref>. | ||
===Clinical | ===Clinical Prediction Rules=== | ||
[[Clinical prediction rule]]s can help diagnose<ref name="pmid29622596">{{cite journal| author=Reaney PDW, Elliott HI, Noman A, Cooper JG| title=Risk stratifying chest pain patients in the emergency department using HEART, GRACE and TIMI scores, with a single contemporary troponin result, to predict major adverse cardiac events. | journal=Emerg Med J | year= 2018 | volume= 35 | issue= 7 | pages= 420-427 | pmid=29622596 | doi=10.1136/emermed-2017-207172 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29622596 }} </ref>: | [[Clinical prediction rule]]s can help diagnose<ref name="pmid29622596">{{cite journal| author=Reaney PDW, Elliott HI, Noman A, Cooper JG| title=Risk stratifying chest pain patients in the emergency department using HEART, GRACE and TIMI scores, with a single contemporary troponin result, to predict major adverse cardiac events. | journal=Emerg Med J | year= 2018 | volume= 35 | issue= 7 | pages= 420-427 | pmid=29622596 | doi=10.1136/emermed-2017-207172 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29622596 }} </ref>: | ||
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*In the setting of NSTEMI, the [[The GRACE risk score|GRACE risk score]] may best predict complications according to a [[cohort study]]<ref name="pmid15764619">{{cite journal| author=de Araújo Gonçalves P, Ferreira J, Aguiar C, Seabra-Gomes R| title=TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interaction with revascularization in NSTE-ACS. | journal=Eur Heart J | year= 2005 | volume= 26 | issue= 9 | pages= 865-72 | pmid=15764619 | doi=10.1093/eurheartj/ehi187 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15764619 }} </ref>. However, the HEART risk score was not assessed in this cohort. | *In the setting of NSTEMI, the [[The GRACE risk score|GRACE risk score]] may best predict complications according to a [[cohort study]]<ref name="pmid15764619">{{cite journal| author=de Araújo Gonçalves P, Ferreira J, Aguiar C, Seabra-Gomes R| title=TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interaction with revascularization in NSTE-ACS. | journal=Eur Heart J | year= 2005 | volume= 26 | issue= 9 | pages= 865-72 | pmid=15764619 | doi=10.1093/eurheartj/ehi187 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15764619 }} </ref>. However, the HEART risk score was not assessed in this cohort. | ||
===Diagnostic | ===Diagnostic Pathways=== | ||
Clinical diagnostic pathways may help<ref name="pmid29138293">{{cite journal| author=Than MP, Pickering JW, Dryden JM, Lord SJ, Aitken SA, Aldous SJ et al.| title=ICare-ACS (Improving Care Processes for Patients With Suspected Acute Coronary Syndrome): A Study of Cross-System Implementation of a National Clinical Pathway. | journal=Circulation | year= 2017 | volume= | issue= | pages= | pmid=29138293 | doi=10.1161/CIRCULATIONAHA.117.031984 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29138293 }} </ref>. The European Society of Cardiology recommends two pathways<ref name="pmid26320110">{{cite journal| author=Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F et al.| title=2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). | journal=Eur Heart J | year= 2016 | volume= 37 | issue= 3 | pages= 267-315 | pmid=26320110 | doi=10.1093/eurheartj/ehv320 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26320110 }} </ref>: | Clinical diagnostic pathways may help<ref name="pmid29138293">{{cite journal| author=Than MP, Pickering JW, Dryden JM, Lord SJ, Aitken SA, Aldous SJ et al.| title=ICare-ACS (Improving Care Processes for Patients With Suspected Acute Coronary Syndrome): A Study of Cross-System Implementation of a National Clinical Pathway. | journal=Circulation | year= 2017 | volume= | issue= | pages= | pmid=29138293 | doi=10.1161/CIRCULATIONAHA.117.031984 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29138293 }} </ref>. The European Society of Cardiology recommends two pathways<ref name="pmid26320110">{{cite journal| author=Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F et al.| title=2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). | journal=Eur Heart J | year= 2016 | volume= 37 | issue= 3 | pages= 267-315 | pmid=26320110 | doi=10.1093/eurheartj/ehv320 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26320110 }} </ref>: | ||
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==Treatment== | ==Treatment== | ||
===Coronary | ===Coronary Angiography=== | ||
Coronary angiography within 12 hours likely benefits high risk (elevated cardiac biomarkers at baseline or diabetes or a [[GRACE score]]<ref name="pmid28893843">{{cite journal| author=Deharo P, Ducrocq G, Bode C, Cohen M, Cuisset T, Mehta SR et al.| title=Timing of Angiography and Outcomes in High-Risk Patients With Non-ST-Segment-Elevation Myocardial Infarction Managed Invasively: Insights From the TAO Trial (Treatment of Acute Coronary Syndrome With Otamixaban). | journal=Circulation | year= 2017 | volume= 136 | issue= 20 | pages= 1895-1907 | pmid=28893843 | doi=10.1161/CIRCULATIONAHA.117.029779 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28893843 }} </ref> | [[Coronary angiography]] within 12 hours likely benefits high risk (elevated [[cardiac biomarkers]] at baseline or [[diabetes]] or a [[GRACE score]] more than 140) [[Patient|patients]].<ref name="pmid28893843">{{cite journal| author=Deharo P, Ducrocq G, Bode C, Cohen M, Cuisset T, Mehta SR et al.| title=Timing of Angiography and Outcomes in High-Risk Patients With Non-ST-Segment-Elevation Myocardial Infarction Managed Invasively: Insights From the TAO Trial (Treatment of Acute Coronary Syndrome With Otamixaban). | journal=Circulation | year= 2017 | volume= 136 | issue= 20 | pages= 1895-1907 | pmid=28893843 | doi=10.1161/CIRCULATIONAHA.117.029779 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28893843 }} </ref><ref name="pmid28778541">{{cite journal| author=Jobs A, Mehta SR, Montalescot G, Vicaut E, Van't Hof AWJ, Badings EA et al.| title=Optimal timing of an invasive strategy in patients with non-ST-elevation acute coronary syndrome: a meta-analysis of randomised trials. | journal=Lancet | year= 2017 | volume= 390 | issue= 10096 | pages= 737-746 | pmid=28778541 | doi=10.1016/S0140-6736(17)31490-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28778541 }} [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=29170158 Review in: Evid Based Med. 2017 Dec;22(6):227] </ref> | ||
==Prevention== | ==Prevention== | ||
'''Primary | '''Primary Prevention''' | ||
The primary prevention strategies include:<ref name="ACS">Acute Coronary Syndrome https://medlineplus.gov/ency/article/007639.htm (2016) Accessed on November 17, 2016 </ref> | The [[Prevention (medical)|primary prevention]] strategies include:<ref name="ACS">Acute Coronary Syndrome https://medlineplus.gov/ency/article/007639.htm (2016) Accessed on November 17, 2016 </ref> | ||
*Dietary modifications: | *Dietary modifications: | ||
:*High consumption of fruits, vegetables, whole grains and lean meats | |||
:*High consumption of [[Fruit|fruits]], [[Vegetable|vegetables]], [[whole grains]] and lean meats | |||
:*Limit foods high in [[cholesterol]] and [[saturated fats]] | :*Limit foods high in [[cholesterol]] and [[saturated fats]] | ||
*Physical exercise | *Physical exercise | ||
Line 888: | Line 889: | ||
*Regular [[blood pressure]], [[blood sugar]] and [[cholesterol]] check | *Regular [[blood pressure]], [[blood sugar]] and [[cholesterol]] check | ||
'''Secondary | '''Secondary Prevention''' | ||
The secondary prevention strategies include:<ref name="pmid18439049">{{cite journal| author=Lee HY, Cooke CE, Robertson TA| title=Use of secondary prevention drug therapy in patients with acute coronary syndrome after hospital discharge. | journal=J Manag Care Pharm | year= 2008 | volume= 14 | issue= 3 | pages= 271-80 | pmid=18439049 | doi=10.18553/jmcp.2008.14.3.271 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18439049 }} </ref><ref name="pmid26152179">{{cite journal| author=Diamantis E, Troupis T, Mazarakis A, Kyriakos G, Diamanti S, Troupis G et al.| title=Primary and Secondary Prevention of Acute Coronary Syndromes: The Role of the Statins. | journal=Recent Adv Cardiovasc Drug Discov | year= 2014 | volume= 9 | issue= 2 | pages= 97-105 | pmid=26152179 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26152179 }} </ref><ref name="pmid20224426">{{cite journal| author=Islam AM, Patel PM| title=Preventing serious sequelae after an acute coronary syndrome: the consequences of thrombosis versus bleeding with antiplatelet therapy. | journal=J Cardiovasc Pharmacol | year= 2010 | volume= 55 | issue= 6 | pages= 585-94 | pmid=20224426 | doi=10.1097/FJC.0b013e3181d9f81f | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20224426 }} </ref> | The [[Prevention (medical)|secondary prevention]] strategies include:<ref name="pmid18439049">{{cite journal| author=Lee HY, Cooke CE, Robertson TA| title=Use of secondary prevention drug therapy in patients with acute coronary syndrome after hospital discharge. | journal=J Manag Care Pharm | year= 2008 | volume= 14 | issue= 3 | pages= 271-80 | pmid=18439049 | doi=10.18553/jmcp.2008.14.3.271 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18439049 }} </ref><ref name="pmid26152179">{{cite journal| author=Diamantis E, Troupis T, Mazarakis A, Kyriakos G, Diamanti S, Troupis G et al.| title=Primary and Secondary Prevention of Acute Coronary Syndromes: The Role of the Statins. | journal=Recent Adv Cardiovasc Drug Discov | year= 2014 | volume= 9 | issue= 2 | pages= 97-105 | pmid=26152179 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26152179 }} </ref><ref name="pmid20224426">{{cite journal| author=Islam AM, Patel PM| title=Preventing serious sequelae after an acute coronary syndrome: the consequences of thrombosis versus bleeding with antiplatelet therapy. | journal=J Cardiovasc Pharmacol | year= 2010 | volume= 55 | issue= 6 | pages= 585-94 | pmid=20224426 | doi=10.1097/FJC.0b013e3181d9f81f | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20224426 }} </ref> | ||
*Dietary modifications | *Dietary modifications | ||
*Regular [[blood pressure]], [[blood sugar]] and [[cholesterol]] check | *Regular [[blood pressure]], [[blood sugar]] and [[cholesterol]] check | ||
*Compliance with therapy for post acute coronary syndrome event | *Compliance with [[therapy]] for post acute coronary syndrome event | ||
*[[Cardiac rehabilitation]] programs | *[[Cardiac rehabilitation]] programs | ||
Revision as of 21:58, 7 February 2020
Resident Survival Guide |
Acute Coronary Syndrome Chapters |
AHA/ACC Guidelines for Acute Coronary Syndrome |
---|
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]; Tarek Nafee, M.D. [3]
Synonyms and keywords: ACS
Overview
Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary arteries. The most common symptom prompting diagnosis of ACS is chest pain, often radiating of the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST-elevation myocardial infarction (30%), non ST-elevation myocardial infarction (25%), or unstable angina (38%).[1] These types are named according to the appearance of the electrocardiogram.[2] There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome.
ACS should be distinguished from stable angina, which is chest pain which develops during exertion and resolves at rest. New onset angina however should be considered as a part of acute coronary syndrome, since it suggests a new problem in a coronary artery.Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use.[3] Cardiac chest pain can also be precipitated by anemia, bradycardias or tachycardias.
Classification
Acute coronary syndrome may be classified as follows:
Symptoms
The signs and symptoms of acute coronary syndrome include:[4]
- Substernal chest pain
- Occurs at rest or exertion
- Radiation to neck, jaw, left shoulder and left arm
- Aggravated by physical activity and emotional stress
- Relieved by rest, nitroglycerin or both
- Chest discomfort described crushing, squeezing, burning, choking, tightness or aching
- Dyspnea
- Diaphoresis
- Nausea and vomiting
- Fatigue
- Syncope
Pathophysiology
For more information on atherosclerotic plaque, click here
The pathophysiology of acute coronary syndromes depends on coronary atherosclerotic plaque which includes:[5][6]
Initiation and Progression of Coronary Atherosclerotic Plaque
- The endothelium of coronary arteries are damaged by the risk factors resulting in endothelial dysfunction, leading to the formation of atherosclerotic plaque.
- The macrophages in the atherosclerotic plaque release matrix metalloproteinases, leading to plaque disruption. [7]
- The balance between smooth muscle cells and macrophages in the plaque plays a major role in plaque vulnerability and the propensity to rupture.
Plaque Vulnerability
The plaque vulnerability depends on the following factors:[8][9][10][10][11]
- Inflammation (A high density of macrophages and T-lymphocytes are marker of unstable atherosclerotic plaque)
- Large lipid core
- Locally increased matrix metalloproteinases that degrade collagen
- Thin fibrous cap
- Relative paucity of smooth muscle cells
- Increase in plaque neovascularity and plaque hemorrhage
- Eccentric outward remodelling
Pathogenesis
The pathogenesis of acute coronary syndrome depends on:[12][13][14][15]
- Endothelial integrity
- Inflammation
- Thrombogenicity of the blood
Following plaque rupture or endothelial erosion, the subendothelial matrix is exposed to the circulating platelets, which get activated leading to thrombus formation. Two types of thrombi can form:
- White clots: Platelet-rich clots which partially occludes the artery
- Red clots: Fibrin rich clots superimposed on white clots and cause total occlusion of the artery
Risk Factors
Common risk factors in the development of acute coronary syndrome are:[5]
- Age (men >45 and women >55)
- Diabetes mellitus
- Hypercholesterolemia
- Hypertension
- Smoking
- Obesity
- Lack of physical activity
- Family history of heart disease
- History of HTN, DM and pre-eclampsia during pregnancy
Diagnosis
High-sensitivity Cardiac Troponin (hs-cTn)
99th percentile of a healthy reference population (recommended cut-off)[16] |
Turnaround time | Name and manufacturer | FDA Approval? | |
---|---|---|---|---|
Troponin T hs-cTnT |
14 ng/L[17][18] | 18 minutes[19] | Elecsys (Roche Diagnostics) |
|
Troponin I hs-cTnI |
26.2 ng/L[17][20] | ARCHITECTSTAT (Abbott Laboratories) |
High sensitivity troponin assays are available:
- Troponin T: Elecsys by Roche Diagnostics[19]
- Troponin I: ARCHITECTSTAT by Abbott Laboratories
When both tests have sensitivity of > 99%, cTnT can exclude infarction in more patients with a sensitivity of 90% according to meta-analysis[21][22][17].
The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9)[17].
High sensitivity troponin levels have reduced predictive value when prevalence is low[23][24].
Clinical Prediction Rules
Clinical prediction rules can help diagnose[25]:
- HEART risk score (History, EKG, Age, Risk factors, and troponin) is the only one of these three prediction rules designed for use prior to diagnosis[26]
- GRACE risk score incorporates 8 findings[27]
- TIMI risk score[28]
Regarding the comparative performance of the prediction rules:
- In the setting of acute chest pain, the HEART score may best predict complications according to a cohort study[29].
- In the setting of NSTEMI, the GRACE risk score may best predict complications according to a cohort study[30]. However, the HEART risk score was not assessed in this cohort.
Diagnostic Pathways
Clinical diagnostic pathways may help[31]. The European Society of Cardiology recommends two pathways[16]:
The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA[32].
More recent strategies include:
- Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection[33].
- Single cTnI measurement, combined with low-risk clinical prediction rule[25]
Differential Diagnosis
Diagnosis of ACS is initiated by a clinical suspicion based on a thorough history of the patient's symptoms. Subsequently, confirmatory tests should be ordered to confirm the diagnosis, identify the specific cause of ACS, or to rule out other possible differentials. In some circumstances, utilizing a clinical prediction tool may be beneficial in guiding the clinician's diagnosis. View the page on diagnosis using the clinical prediction rule for ACS for more detail.[34][35] Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows:[36][37][38][39][40][41][42][43][44][45][46][47][48][49][50]
Organ System | Diseases | Presentation | Diagnostic Tests | Past Medical History | Other Findings | |||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Chest Pain | GI Symptoms | Pulmonary | Neck | |||||||||||||||||||||
On Palpation | On inspiration | Radiating to Extremeties | Radiating to Back | With Movement | Nausea or Vomitting | Epigastric Pain | Odynophagia or Dysphagia | Shortness of Breath | Jugular
Distention |
Cardiac Biomarkers | CBC Findings | ESR | D-Dimer | EKG
Findings |
CXR Findings | DM | Hyperlipidemia | Obesity | Trauma | Inxn* | Htn | |||
Cardiovascular | Acute Coronary Syndrome | + | + | + | + | + | + | + | + | + | + | + | •Palpitations | |||||||||||
Aortic Dissection | + | + | + | - | + | + | - | + | •Pain maximal upon onset •Pain difficult to treat with opiates
•Weak pulse in one arm compared to other •Symptoms similar to stroke | |||||||||||||||
Brugada Syndrome | No chest pain | + | •Syncope
•ST-segment elevation •F/H of sudden cardiac death | |||||||||||||||||||||
Takotsubo carditis | Sudden onset of chest pain mimicking myocardial infarction | + | + | + | + | + | - | •Extreme emotional or physical stress•syncope
•Women>men •ST segment elevation •Left ventricular apical ballooning on echo •Normal coronary arteries | ||||||||||||||||
Pericarditis | + | + | + | •Relieving factor: Sitting up and leaning forward
•Aggravating factor: Lying down and breathing deep |
+ | + | + | + | + | + | + | •Other causes:Malignancy, autoimmune disorders, chest trauma | ||||||||||||
Organ System | Diseases | Presentation | Diagnostic Tests | Past Medical History | Other Findings | |||||||||||||||||||
Chest Pain | GI Symptoms | Pulmonary | Neck | |||||||||||||||||||||
On Palpation | On inspiration | Radiating to Extremeties | Radiating to Back | With Movement | Nausea or Vomitting | Epigastric Pain | Odynophagia or Dysphagia | Shortness of Breath | Jugular
Distention |
Cardiac Biomarkers | CBC Findings | ESR | D-Dimer | EKG
Findings |
CXR Findings | DM | Hyperlipidemia | Obesity | Trauma | Inxn* | Htn | |||
Pulmonary | Pleuritis (pleurisy) |
+ | + | + | + | •Aggravating factor: Deep breathing | + | + | + | + | + | + | •Other causesPulmonary embolism, malignancy, autoimmune diseases | |||||||||||
Pulmonary Embolism | + | •Aggravating factors: Deep breathing, coughing, eating, bending and stooping | + | + | + | •Other causes: Immobility, pregnancy, oral contraceptive pills | ||||||||||||||||||
Pneumonia | + | + | + | + | + | + | •Complications: Sepsis, ARDS, Lung abscess | |||||||||||||||||
Gastrointestinal | GERD | + | + | + | •Other symptoms: Hoarseness, Dry cough at night, Sensation of lump in throat etc | |||||||||||||||||||
Esophageal Spasms | + | + | + | + | + | + | + | • Risk factors: Anxiety or depression and drinking wine, very hot or cold foods | ||||||||||||||||
Esophagitis | + | + | + | + | + | + | + | • Causes: Hiatal hernia, infection, medications, radiation therapy | ||||||||||||||||
Gastritis | + | + | + | + | + | + | + | • Causes: H.pylori infection, bile reflux, alcohol use, alcohol use | ||||||||||||||||
Organ System | Diseases | Presentation | Diagnostic Tests | Past Medical History | Other Findings | |||||||||||||||||||
Chest Pain | GI Symptoms | Pulmonary | Neck | |||||||||||||||||||||
On Palpation | On inspiration | Radiating to Extremeties | Radiating to Back | With Movement | Nausea or Vomitting | Epigastric Pain | Odynophagia or Dysphagia | Shortness of Breath | Jugular
Distention |
Cardiac Biomarkers | CBC Findings | ESR | D-Dimer | EKG
Findings |
CXR Findings | DM | Hyperlipidemia | Obesity | Trauma | Inxn* | Htn | |||
Musculoskeletal | Muscle sprain/Spasm | + | + | + | + | • Causes: Over use, dehydration, electrolyte abnormalities | ||||||||||||||||||
Costochondritis | + | + | + | + | + | + | + | + | + | + | + | • Risk factors: Rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome | ||||||||||||
Rib fracture/Trauma | + | + | + | + | + | + | + | + | + | + | • Complications: Pneumothorax, hemothorax, surgical emphysema | |||||||||||||
Psychiatry | Anxiety (Panic Attack) | Chest tightness | + | + | • Other symptoms: Palpitations, trembling, sweating, choking, light headed, hot or cold flashes. |
The following table summarizes the significant history, and diagnostic test findings that will help differentiate the acute coronary syndromes from one another, as well as from other coronary artery diseases:[51][52][53][54][55][56]
Acute Coronary Syndromes | History and Symptoms | Pathology | Diagnostic tests | Treatment | Complications | Prognosis | |||||
---|---|---|---|---|---|---|---|---|---|---|---|
Chest pain | Duration of Chest pain | Coronary Artery | Plaque | Cardiac Biomarkers (e.g.CK-MB, Troponins) |
EKG Findings | Medical Therapy | Reperfusion (e.g. PCI, CABG, or Medical) | ||||
At Rest | Exertion | ||||||||||
Unstable Angina | + | + | <30 minutes | Partial occlusion | Erosion
or (39%) |
Normal | •Normal EKG findings (some cases)
|
+ | •Arrhythmias
•MI •Sudden death |
•1 year mortality rate is 1.7% | |
NSTEMI | + | + | >30 minutes | Partial or complete occlusion | Rupture
(56%) or Erosion |
Elevated | •No EKG findings (some cases)
|
+ | + | •Arrhythmias
•Sudden death |
•1 year mortality rate is 24.4%
•30 day mortality rate is about 2% |
STEMI | + | + | >30 minutes | Complete occlusion | Rupture
(50%-75%) or Erosion |
Elevated | •ST elevation in at least 2
contiguous leads in V2-V3
two precordial leads V1-V4
leads plus ST elevation in lead aVR (suggestive of occlusion of the left main or proximal LAD artery)
|
+ | + | •Reinfarction
interventricular septum and LV free wall •Sudden death |
•30 day mortality rate is
1.1% in <45 yrs and 20.4% in >75 yrs patients |
Other Coronary Artery Diseases | |||||||||||
Chronic stable angina | - | + | ≤ 5 minutes | Severely narrowed | Stable plaque | Normal | •Normal EKG in 50% of cases
•Down sloping, up sloping or horizontal ST segment depression •T wave inversion |
+ | •Heart failure | •Estimated annual mortality rate is 0.9%-1.4%
•Annual incidence of non-fatal MI between 0.5%-2.6% •1 year mortality rate is 1.3% | |
Prinzmetal's angina | •Occur at rest
(Mid night to early morning) •Not associated with exertion |
5-30 minutes | Coronary artery vasospasm | - | Normal | •Transient ST segment elevation | + | •Arrhythmias
•MI |
•5 year survival is excellent (90%-95%) |
Treatment
Coronary Angiography
Coronary angiography within 12 hours likely benefits high risk (elevated cardiac biomarkers at baseline or diabetes or a GRACE score more than 140) patients.[57][58]
Prevention
Primary Prevention
The primary prevention strategies include:[59]
- Dietary modifications:
- High consumption of fruits, vegetables, whole grains and lean meats
- Limit foods high in cholesterol and saturated fats
- Physical exercise
- 30 minutes of moderate exercise
- Weight loss
- Smoking cessation
- Regular blood pressure, blood sugar and cholesterol check
Secondary Prevention
The secondary prevention strategies include:[60][61][62]
- Dietary modifications
- Regular blood pressure, blood sugar and cholesterol check
- Compliance with therapy for post acute coronary syndrome event
- Cardiac rehabilitation programs
References
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|month=
ignored (help) - ↑ Grech ED, Ramsdale DR (2003). "Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction". BMJ. 326 (7401): 1259–61. doi:10.1136/bmj.326.7401.1259. PMC 1126130. PMID 12791748. Unknown parameter
|month=
ignored (help) - ↑ Achar SA, Kundu S, Norcross WA (2005). "Diagnosis of acute coronary syndrome". Am Fam Physician. 72 (1): 119–26. PMID 16035692.
- ↑ Abidov A, Rozanski A, Hachamovitch R, Hayes SW, Aboul-Enein F, Cohen I; et al. (2005). "Prognostic significance of dyspnea in patients referred for cardiac stress testing". N Engl J Med. 353 (18): 1889–98. doi:10.1056/NEJMoa042741. PMID 16267320. Review in: Evid Based Med. 2006 Jun;11(3):91
- ↑ 5.0 5.1 Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ, Chesebro J (1988). "Insights into the pathogenesis of acute ischemic syndromes". Circulation. 77 (6): 1213–20. PMID 3286036.
- ↑ Libby P (2001). "Current concepts of the pathogenesis of the acute coronary syndromes". Circulation. 104 (3): 365–72. PMID 11457759.
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- ↑ Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT (1994). "Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture". Circulation. 90 (2): 775–8. PMID 8044947.
- ↑ Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J (1993). "Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content". Br Heart J. 69 (5): 377–81. PMC 1025095. PMID 8518056.
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- ↑ Herman MP, Sukhova GK, Libby P, Gerdes N, Tang N, Horton DB; et al. (2001). "Expression of neutrophil collagenase (matrix metalloproteinase-8) in human atheroma: a novel collagenolytic pathway suggested by transcriptional profiling". Circulation. 104 (16): 1899–904. PMID 11602491.
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- ↑ Moreno PR, Bernardi VH, López-Cuéllar J, Murcia AM, Palacios IF, Gold HK; et al. (1996). "Macrophages, smooth muscle cells, and tissue factor in unstable angina. Implications for cell-mediated thrombogenicity in acute coronary syndromes". Circulation. 94 (12): 3090–7. PMID 8989114.
- ↑ Weiss EJ, Bray PF, Tayback M, Schulman SP, Kickler TS, Becker LC; et al. (1996). "A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis". N Engl J Med. 334 (17): 1090–4. doi:10.1056/NEJM199604253341703. PMID 8598867.
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- ↑ Koerbin G, Tate J, Potter JM, Cavanaugh J, Glasgow N, Hickman PE (2012). "Characterisation of a highly sensitive troponin I assay and its application to a cardio-healthy population". Clin Chem Lab Med. 50 (5): 871–8. doi:10.1515/cclm-2011-0540. PMID 22628331.
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