Acute coronary syndromes: Difference between revisions
/* Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes{{cite journal|last1=Roffi|first1=Marco|last2=Patrono|first2=Carlo|last3=Collet|first3=Jean-Philippe|last4=Mueller|first4=Christian|last5=Valgimig... |
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==Overview== | ==Overview== | ||
Acute coronary syndrome (ACS) refers to any group of [[Symptom|symptoms]] attributed to obstruction of the [[coronary artery|coronary arteries]]. The most common [[symptom]] prompting [[diagnosis]] of ACS is [[chest pain]], often radiating | Acute coronary syndrome (ACS) refers to any group of [[Symptom|symptoms]] attributed to obstruction of the [[coronary artery|coronary arteries]]. The most common [[symptom]] prompting [[diagnosis]] of ACS is [[chest pain]], often radiating to the [[Arm|left arm]] or [[Jaw|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%). These types are named according to the appearance of the [[electrocardiogram]]. There can be some variation as to which forms of [[myocardial infarction]] (MI) are classified under acute coronary syndrome. | ||
ACS should be distinguished from [[Chronic stable angina|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 arteries|coronary artery]].Though ACS is usually associated with [[coronary thrombosis]], it can also be associated with [[cocaine]] use. | ACS should be distinguished from [[Chronic stable angina|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 arteries|coronary artery]].Though ACS is usually associated with [[coronary thrombosis]], it can also be associated with [[cocaine]] use. Cardiac chest pain can also be precipitated by [[anemia]], [[bradycardia]]s or [[tachycardia]]s. | ||
==Classification== | ==Classification== | ||
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* [[ST Elevation Myocardial Infarction]] | * [[ST Elevation Myocardial Infarction]] | ||
==Symptoms== | ==Symptoms== | ||
The signs and symptoms of acute coronary syndrome include: | The signs and symptoms of acute coronary syndrome include: | ||
*[[Chest pain]] | *[[Chest pain]] | ||
:*[[Chest pain|Substernal chest pain]] | :*[[Chest pain|Substernal chest pain]] | ||
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For more information on atherosclerotic plaque, click [[Atherosclerosis |here]]. | For more information on atherosclerotic plaque, click [[Atherosclerosis |here]]. | ||
The pathophysiology of acute coronary syndromes depends on [[atherosclerosis|coronary atherosclerotic plaque]] which includes: | The pathophysiology of acute coronary syndromes depends on [[atherosclerosis|coronary atherosclerotic plaque]] which includes: | ||
'''Initiation and Progression of Coronary Atherosclerotic Plaque''' | '''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. | *The [[macrophages]] in the atherosclerotic plaque release matrix [[metalloproteinases]], leading to plaque disruption. | ||
*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 Vulnerability''' | '''Plaque Vulnerability''' | ||
The plaque vulnerability depends on the following factors: | The plaque vulnerability depends on the following factors:<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> | ||
*[[Inflammation]] (A high density of [[macrophages]] and [[T-lymphocytes]] are marker of unstable [[atherosclerotic plaque]]) | *[[Inflammation]] (A high density of [[macrophages]] and [[T-lymphocytes]] are marker of unstable [[atherosclerotic plaque]]) | ||
*Large [[lipid]] core | *Large [[lipid]] core | ||
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===Pathogenesis=== | ===Pathogenesis=== | ||
The pathogenesis of acute coronary syndrome depends on: | The pathogenesis of acute coronary syndrome depends on: | ||
*[[Endothelium|Endothelial integrity]] | *[[Endothelium|Endothelial integrity]] | ||
*[[Inflammation]] | *[[Inflammation]] | ||
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! | ! | ||
! 99th percentile of a healthy reference population<br/>(recommended cut-off) | ! 99th percentile of a healthy reference population<br/>(recommended cut-off) | ||
! Turnaround time | ! Turnaround time | ||
! Name and manufacturer | ! Name and manufacturer | ||
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|- | |- | ||
! Troponin T<br />hs-cTnT | ! Troponin T<br />hs-cTnT | ||
| 14 ng/L<ref name="pmid29691270" / | | 14 ng/L<ref name="pmid29691270" /> | ||
| 18 minutes<ref name="pmid25646632" /> | | 18 minutes<ref name="pmid25646632" /> | ||
| Elecsys<br/>(Roche Diagnostics) | | Elecsys<br/>(Roche Diagnostics) | ||
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|- | |- | ||
! Troponin I<br />hs-cTnI | ! Troponin I<br />hs-cTnI | ||
| 26.2 ng/L<ref name="pmid29691270" / | | 26.2 ng/L<ref name="pmid29691270" /> | ||
| | | | ||
| ARCHITECT''STAT''<br/>(Abbott Laboratories) | | ARCHITECT''STAT''<br/>(Abbott Laboratories) | ||
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|} | |} | ||
=== Clinical Implications of High-sensitivity Cardiac Troponin Assays | === Clinical Implications of High-sensitivity Cardiac Troponin Assays === | ||
{| class="wikitable" | {| class="wikitable" | ||
|+ | |+ | ||
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Available high sensitivity troponin assays: | Available high sensitivity troponin assays: | ||
* Troponin T: Elecsys by Roche Diagnostics | * Troponin T: Elecsys by Roche Diagnostics | ||
* Troponin I: ARCHITECT''STAT'' by Abbott Laboratories | * Troponin I: ARCHITECT''STAT'' 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 | When both tests have sensitivity of > 99%, cTnT can exclude infarction in more patients with a sensitivity of 90% according to meta-analysis. | ||
The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9)<ref name="pmid29691270">{{cite journal| author=van der Linden N, Wildi K, Twerenbold R, Pickering JW, Than M, Cullen L et al.| title=Combining High-Sensitivity Cardiac Troponin I and Cardiac Troponin T in the Early Diagnosis of Acute Myocardial Infarction. | journal=Circulation | year= 2018 | volume= 138 | issue= 10 | pages= 989-999 | pmid=29691270 | doi=10.1161/CIRCULATIONAHA.117.032003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29691270 }} </ref>. | The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9)<ref name="pmid29691270">{{cite journal| author=van der Linden N, Wildi K, Twerenbold R, Pickering JW, Than M, Cullen L et al.| title=Combining High-Sensitivity Cardiac Troponin I and Cardiac Troponin T in the Early Diagnosis of Acute Myocardial Infarction. | journal=Circulation | year= 2018 | volume= 138 | issue= 10 | pages= 989-999 | pmid=29691270 | doi=10.1161/CIRCULATIONAHA.117.032003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29691270 }} </ref>. | ||
High sensitivity troponin levels have reduced predictive value when prevalence is low | High sensitivity troponin levels have reduced predictive value when prevalence is low. | ||
===Clinical Prediction Rules=== | ===Clinical Prediction Rules=== | ||
[[Clinical prediction rule]]s can help diagnose | [[Clinical prediction rule]]s can help diagnose: | ||
* 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 | * 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 | ||
* [[The GRACE risk score|GRACE risk score]] incorporates 8 findings | * [[The GRACE risk score|GRACE risk score]] incorporates 8 findings | ||
* [[TIMI risk score]] | * [[TIMI risk score]] | ||
Regarding the comparative performance of the prediction rules: | 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]] | * In the setting of acute chest pain, the HEART score may best predict complications according to a [[cohort study]]. | ||
*In the setting of NSTEMI, the [[The GRACE risk score|GRACE risk score]] may best predict complications according to a [[cohort study]] | *In the setting of NSTEMI, the [[The GRACE risk score|GRACE risk score]] may best predict complications according to a [[cohort study]]. However, the HEART risk score was not assessed in this cohort. | ||
===Diagnostic Pathways=== | ===Diagnostic Pathways=== | ||
Clinical diagnostic pathways may help | Clinical diagnostic pathways may help. 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>: | ||
* 0 h/3 h | * 0 h/3 h | ||
* 0 h/1 h<ref name="pmid30071991">{{cite journal| author=Twerenbold R, Neumann JT, Sörensen NA, Ojeda F, Karakas M, Boeddinghaus J et al.| title=Prospective Validation of the 0/1-h Algorithm for Early Diagnosis of Myocardial Infarction. | journal=J Am Coll Cardiol | year= 2018 | volume= 72 | issue= 6 | pages= 620-632 | pmid=30071991 | doi=10.1016/j.jacc.2018.05.040 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30071991 }} </ref><ref name="pmid27754881">{{cite journal| author=Pickering JW, Greenslade JH, Cullen L, Flaws D, Parsonage W, Aldous S et al.| title=Assessment of the European Society of Cardiology 0-Hour/1-Hour Algorithm to Rule-Out and Rule-In Acute Myocardial Infarction. | journal=Circulation | year= 2016 | volume= 134 | issue= 20 | pages= 1532-1541 | pmid=27754881 | doi=10.1161/CIRCULATIONAHA.116.022677 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27754881 }} </ref> | * 0 h/1 h<ref name="pmid30071991">{{cite journal| author=Twerenbold R, Neumann JT, Sörensen NA, Ojeda F, Karakas M, Boeddinghaus J et al.| title=Prospective Validation of the 0/1-h Algorithm for Early Diagnosis of Myocardial Infarction. | journal=J Am Coll Cardiol | year= 2018 | volume= 72 | issue= 6 | pages= 620-632 | pmid=30071991 | doi=10.1016/j.jacc.2018.05.040 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30071991 }} </ref><ref name="pmid27754881">{{cite journal| author=Pickering JW, Greenslade JH, Cullen L, Flaws D, Parsonage W, Aldous S et al.| title=Assessment of the European Society of Cardiology 0-Hour/1-Hour Algorithm to Rule-Out and Rule-In Acute Myocardial Infarction. | journal=Circulation | year= 2016 | volume= 134 | issue= 20 | pages= 1532-1541 | pmid=27754881 | doi=10.1161/CIRCULATIONAHA.116.022677 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27754881 }} </ref> | ||
The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA | The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA. | ||
More recent strategies include: | More recent strategies include: | ||
* Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection | * Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection. | ||
* Single cTnI measurement, combined with low-risk clinical prediction rule<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> | * Single cTnI measurement, combined with low-risk clinical prediction rule<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> | ||
==Differential Diagnosis== | ==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 [[Clinical prediction rule#Acute MI / Unstable Angina|diagnosis using the clinical prediction rule]] for ACS for more detail. | 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 [[Clinical prediction rule#Acute MI / Unstable Angina|diagnosis using the clinical prediction rule]] for ACS for more detail. | ||
Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows: | Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows: | ||
{| | {| | ||
|-style="background: #4479BA; color: #FFFFFF; text-align: center;" | |-style="background: #4479BA; color: #FFFFFF; text-align: center;" | ||
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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: | 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: | ||
{| | {| | ||
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|}<br /> | |}<br /> | ||
=== Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain | === Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain === | ||
<br /> | <br /> | ||
{| class="wikitable" | {| class="wikitable" | ||
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===Coronary Angiography=== | ===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) [[Patient|patients]]. | [[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]]. | ||
=== Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes | === Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes=== | ||
{| class="wikitable" | {| class="wikitable" | ||
|+ | |+ | ||
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|Early initiation of beta-blocker treatment is recommended | |Early initiation of beta-blocker treatment is recommended | ||
in patients with ongoing ischemic symptoms and without contraindications. | in patients with ongoing ischemic symptoms and without contraindications. | ||
!style="background:green; color:white"|I | !style="background:green; color:white"|I | ||
!style="background:blue; color:white"|B | !style="background:blue; color:white"|B | ||
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|It is recommended to continue chronic beta-blocker therapy, | |It is recommended to continue chronic beta-blocker therapy, | ||
unless the patient is in Killip class III or higher. | unless the patient is in Killip class III or higher. | ||
!style="background:green; color:white"|I | !style="background:green; color:white"|I | ||
!style="background:blue; color:white"|B | !style="background:blue; color:white"|B | ||
Line 1,011: | Line 1,011: | ||
|In patients with suspected/confirmed vasospastic angina, calcium channel blockers and | |In patients with suspected/confirmed vasospastic angina, calcium channel blockers and | ||
nitrates should be considered and beta-blockers avoided. | nitrates should be considered and beta-blockers avoided. | ||
!style="background:orange; color:white"|IIa | !style="background:orange; color:white"|IIa | ||
!style="background:blue; color:white"|B | !style="background:blue; color:white"|B | ||
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'''Primary Prevention''' | '''Primary Prevention''' | ||
The [[Prevention (medical)|primary prevention]] strategies include: | The [[Prevention (medical)|primary prevention]] strategies include: | ||
*Dietary modifications: | *Dietary modifications: | ||
:* | :*Regular 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 1,035: | Line 1,035: | ||
'''Secondary Prevention''' | '''Secondary Prevention''' | ||
The [[Prevention (medical)|secondary prevention]] strategies include: | The [[Prevention (medical)|secondary prevention]] strategies include: | ||
*Dietary modifications | *Dietary modifications | ||
*Regular [[blood pressure]], [[blood sugar]] and [[cholesterol]] check | *Regular [[blood pressure]], [[blood sugar]] and [[cholesterol]] check | ||
Line 1,049: | Line 1,049: | ||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
<references /> |
Revision as of 19:31, 18 August 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]; Sabawoon Mirwais, M.B.B.S, M.D.[4]
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 to 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%). These types are named according to the appearance of the electrocardiogram. 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. 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:
- 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:
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.
- 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:[1]
- 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:
- 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:[2]
- 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) |
Turnaround time | Name and manufacturer | FDA Approval? | |
---|---|---|---|---|
Troponin T hs-cTnT |
14 ng/L[3] | 18 minutes[4] | Elecsys (Roche Diagnostics) |
|
Troponin I hs-cTnI |
26.2 ng/L[3] | ARCHITECTSTAT (Abbott Laboratories) |
Clinical Implications of High-sensitivity Cardiac Troponin Assays
Compared with standard cardiac troponin assays, high-sensitivity assays: |
---|
Have higher negative predictive value for acute MI. |
Reduce the “troponin-blind” interval leading to earlier detection of acute MI. |
Reduce the “troponin-blind” interval leading to earlier detection of acute MI. |
Are associated with a 2-fold increase in the detection of type 2 MI. |
Levels of high-sensitivity cardiac troponin should be interpreted as quantitative markers of cardiomyocyte damage
(i.e. the higher the level, the greater the likelihood of MI): |
Elevations beyond 5-fold the upper reference limit have high (>90%) positive predictive value for acute type 1 MI. |
Elevations up to 3-fold the upper reference limit have only limited (50–60%) positive predictive value for acute MI
and may be associated with a broad spectrum of conditions. |
It is common to detect circulating levels of cardiac troponin in healthy individuals. |
Rising and/or falling cardiac troponin levels differentiate acute from chronic cardiomyocyte damage
(the more pronounced the change, the higher the likelihood of acute MI). |
Adapted from European Heart Journal (2016) 37, 267–315 |
Available high sensitivity troponin assays:
- Troponin T: Elecsys by Roche Diagnostics
- 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.
The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9)[3].
High sensitivity troponin levels have reduced predictive value when prevalence is low.
Clinical Prediction Rules
Clinical prediction rules can help diagnose:
- 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
- GRACE risk score incorporates 8 findings
- TIMI risk score
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.
- In the setting of NSTEMI, the GRACE risk score may best predict complications according to a cohort study. However, the HEART risk score was not assessed in this cohort.
Diagnostic Pathways
Clinical diagnostic pathways may help. The European Society of Cardiology recommends two pathways[5]:
The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA.
More recent strategies include:
- Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection.
- Single cTnI measurement, combined with low-risk clinical prediction rule[8]
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. Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows:
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:
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%) |
Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain
Cardiac | Pulmonary | Vascular | Gastrointestinal | Orthopedic | Other |
---|---|---|---|---|---|
Myopericarditis
Cardiomyopathiesa |
Pulmonary embolism | Aortic dissection | Esophagitis, reflex or spasm | Musculoskeletal disorders | Anxiety disorders |
Tachyarrhythmias | (Tension)-Pneumothorax | Symptomatic aortic aneurysm | Peptic ulcer, gastritis | Chest trauma | Herpes zoster |
Acute heart failure | Bronchitis, pneumonia | Stroke | Pancreatitis | Muscle injury/inflammation | Anemia |
Hypertensive emergencies | Pleuritis | Cholecystitis | Costochondritis | ||
Aortic valve stenosis | Cervical spine pathologies | ||||
Tako-Tsubo cardiomyopathy | |||||
Coronary spasm | |||||
Cardiac trauma | |||||
Bold = Common and/or important differential diagnoses
aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort |
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.
Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes
Recommendations | Class
of Recommendations |
Level
of Evidence |
---|---|---|
Early initiation of beta-blocker treatment is recommended
in patients with ongoing ischemic symptoms and without contraindications. |
I | B |
It is recommended to continue chronic beta-blocker therapy,
unless the patient is in Killip class III or higher. |
I | B |
Sublingual or i.v. nitrates are recommended to relieve angina;a intravenous treatment is recommended
in patients with recurrent angina, uncontrolled hypertension or signs of heart failure. |
I | C |
In patients with suspected/confirmed vasospastic angina, calcium channel blockers and
nitrates should be considered and beta-blockers avoided. |
IIa | B |
aShould not be administered in patients with recent intake of sildenafil or vardenafil (< 24 h) or tadalafil (< 48 h). |
Prevention
Primary Prevention
The primary prevention strategies include:
- Dietary modifications:
- Regular 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:
- Dietary modifications
- Regular blood pressure, blood sugar and cholesterol check
- Compliance with therapy for post acute coronary syndrome event
- Cardiac rehabilitation programs
References
- ↑ Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC; et al. (1999). "Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques". Circulation. 99 (19): 2503–9. PMID 10330380.
- ↑ 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.
- ↑ 3.0 3.1 3.2 van der Linden N, Wildi K, Twerenbold R, Pickering JW, Than M, Cullen L; et al. (2018). "Combining High-Sensitivity Cardiac Troponin I and Cardiac Troponin T in the Early Diagnosis of Acute Myocardial Infarction". Circulation. 138 (10): 989–999. doi:10.1161/CIRCULATIONAHA.117.032003. PMID 29691270.
- ↑ Invalid
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- ↑ Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F; et al. (2016). "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)". Eur Heart J. 37 (3): 267–315. doi:10.1093/eurheartj/ehv320. PMID 26320110.
- ↑ Twerenbold R, Neumann JT, Sörensen NA, Ojeda F, Karakas M, Boeddinghaus J; et al. (2018). "Prospective Validation of the 0/1-h Algorithm for Early Diagnosis of Myocardial Infarction". J Am Coll Cardiol. 72 (6): 620–632. doi:10.1016/j.jacc.2018.05.040. PMID 30071991.
- ↑ Pickering JW, Greenslade JH, Cullen L, Flaws D, Parsonage W, Aldous S; et al. (2016). "Assessment of the European Society of Cardiology 0-Hour/1-Hour Algorithm to Rule-Out and Rule-In Acute Myocardial Infarction". Circulation. 134 (20): 1532–1541. doi:10.1161/CIRCULATIONAHA.116.022677. PMID 27754881.
- ↑ Reaney PDW, Elliott HI, Noman A, Cooper JG (2018). "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". Emerg Med J. 35 (7): 420–427. doi:10.1136/emermed-2017-207172. PMID 29622596.