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ACS-3.pptx
1. Presenter : Dr Mulusew (IMR1 )
Moderator : Dr Dereje (Consultant
Internist)
Approach to acute coronary
Syndrome I
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Approach to ACS
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2. Outline
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• Introduction
• Epidemiology
• Pathophysiology
• Risk factors
• Clinical presentation
• Investigation
• Risk stratification
• Management
• Take Home Messages
3. Introduction
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Acute chest pain remains one of the most common
reasons for seeking care in the ED ,in US
2nd most common complaint
10% of 100 million nontraumatic visits
4. CAUSES OF ACUTE CHEST PAIN
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About 10% to 15% patients being evaluated for
acute chest pain in EDs have ACS
A small percentage has other life- threatening
problems, such as PE or acute aortic dissection
Most leave the ED without a diagnosis or with a
diagnosis of a non–cardiac- related condition
15. ACS
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• Patients with ACS are classified into two groups to
facilitate evaluation and management
• STEMI
• NSTE-ACS
• NSTEMI
• UA
16. Epidemiology
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• The incidence of NSTEMI is rising whereas the
incidence of STEMI is declining
wider use of preventive measures
aging of the population
wider use of cTn assays with higher sensitivity
wider implementation of the universal definition of MI
18. Pathophysiology
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The pathogenesis of NSTE- ACS involves five
processes operating singly or in various
combinations:
(1) disruption of an unstable atheromatous plaque
(2) erosion of an atheromatous plaque
(3) coronary arterial vasoconstriction
(4) gradual intraluminal narrowing
(5) oxygen supply- demand mismatch
21. Features of vulnerable plaque
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Thin fibrous cup
Lipid rich necrotic core
Increased inflammatory cells
Neovascularization
Intraplaque hemorrhage
Microcalcification
Decreased number of smooth muscle cells
22. Angiography Study in NSTE-ACS
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10% have stenosis of the left main coronary artery
35% have three-vessel coronary artery disease
20% have two-vessel disease
20% have singlevessel disease
15% have no apparent critical epicardial coronary
artery stenosis
25. CLINICAL PRESENTATION
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Typically, chest discomfort is severe and has at
least one of three features
occurrence at rest or with minimal exertion lasting >10 min
relatively recent onset within the prior 2 weeks
crescendo pattern more severe, prolonged, or frequent than
previous episodes
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The chest discomfort is typically located in the
substernal region and radiates to
the left arm
left shoulder
neck
jaw
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Approach to ACS
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Anginal equivalents such as dyspnea, epigastric
discomfort, nausea, or weakness may occur instead of
chest discomfort
These equivalents are more frequent in women, the
elderly, and patients with diabetes mellitus
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Approach to ACS
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The physical examination may be unremarkable
If the patient has a large NSTEMI
Diaphoresis
sinus tachycardia
a third and/or fourth heart sound
basilar rales
hypotension
30. Electrocardiogram
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The first-line diagnostic tool in the assessment of
patients with suspected ACS
Should be done within 10 min of the patient’s
arrival in the emergency room
At first contact with EMS in the pre-hospital setting
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ECG in the setting of NSTE-ACS may be normal in
>30% of patients, characteristic abnormalities
include
ST-segment depression
transient ST-segment elevation
T-wave changes
left circumflex artery occlusion may be detected
only in V7-V9
34. Cardiac Biomarkers
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complement clinical assessment and 12-lead ECG
in the
diagnosis, risk stratification, and treatment of
patients with suspected NSTE-ACS
Measurement of a biomarker of cardiomyocyte
injury, preferably hs-cTn, is mandatory in all
patients with suspected NSTEACS
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In patients with NSTEMI, there is a characteristic
temporal rise of the plasma concentration
There is a direct relationship between the degree of
elevation and mortality
The 1-h rapid rule-out MI algorithm has been
recommended by recent practice guidelines
40. Risk assessment and outcomes
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Biomarkers
Add prognostic information in terms of short and long-
term mortality to clinical and ECG variables
While hs-cTn T and I have comparable diagnostic
accuracy, hs-cTn T has greater prognostic accuracy
The higher the hs-cTn levels, the greater the risk of
death
Scr and eGFR should also be determined in all patients
41. Clinical scores for risk assessment
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• A number of prognostic models that aim to
estimate the future risk of all-cause mortality or the
combined risk of all-cause mortality or MI
• These models have been formulated into clinical
risk scores and, among these, the GRACE risk
score offers the best discriminative performance
42. GRACE
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Age
HR
SBP
Initial serum creatinine
Killip Class
Cardiac arrest at admission
Presence of initial cardiac biomarker
ST segment deviation
44. Ischemic and bleeding risk
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Major bleeding events affect prognosis in a similar
way to spontaneous ischemic complications
PRECISE-DAPT scores have been designed to
guide and inform decision making on DAPT
duration
none of these risk prediction models have been
prospectively tested in RCTs
45. Management
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low likelihood of ischemia can be managed in an
ED or a dedicated “chest pain unit”
clinical monitoring for recurrent ischemic
discomfort
Bed rest with continuous ECG monitoring
stress testing to detect and grade ischemia
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Patients who “rule-in” for NSTE-ACS should be
admitted to the hospital
bed rest with continuous ECG monitoring,
preferably on a specialized cardiac unit
Ambulation if no recurrence of ischemia and does
not develop an elevation of cTn for 24 h
48. ANTITHROMBOTIC THERAPY
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Antithrombotic therapy consisting of antiplatelet
and anticoagulant drugs represents the second
major cornerstone of treatment
64. LONG-TERM MANAGEMENT
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Risk factor modification is key
importance of smoking cessation
following an appropriate diet
achieving and maintaining optimal weight
daily exercise
blood pressure control
control of hyperglycemia (in diabetic patients)
67. Top 10 Take Home Messages
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68. REFERENCE
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1,Harrison principle of internal medicine 21st edition
2,Braunwalds heart disease 12th edition
3, 2020 ESC Guidelines for the management of acute
coronary syndromes in patients presenting without
persistent ST-segment elevation
4, 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR
Guideline for the Evaluation and Diagnosis of
Chest Pain
Among unselected patients presenting with acute chest pain to the emergency department, disease prevalence can be expected to be the following: 5-10% STEMI, 15-20% NSTEMI, 10% unstable angina, 15% other cardiac conditions, and 50% non-cardiac diseases.
After injuries, chest pain is the second most common reason for adults to present to the emergency department (ED) in the United States and accounts for >6.5 million visits, which is 4.7% of all ED visits.1 Chest pain also leads to nearly 4 million outpatient visits annually in the United States.2 Chest pain remains a diagnostic challenge in the ED and outpatient setting and requires thorough clinical evaluation.
the leading cause of death for men and women, accounting for >365 000 deaths annually.3 Distinguishing between serious and benign causes of chest pain is imperative. The lifetime prevalence of chest pain in the United States is 20% to 40%,4 and women experience this symptom more often than men.5 Of all ED patients with chest pain, only 5.1% will have an acute coronary syndrome(ACS), and more than half will ultimately be found to have a noncardiac cause.6 Nonetheless, chest pain is the most common symptom of CAD in both men and women.
Figure 2. Index of Suspicion That Chest “Pain” Is Ischemic in Origin on the Basis of Commonly Used Descriptors
Chest pain should be considered acute when it is new onset or involves a change in pattern, intensity, or duration compared with previous episodes in a patient with recurrent symptoms
Chest pain should be considered stable when symptoms are chronic and associated with consistent precipitants such as exertion or emotional stress
The choice of imaging depends on the clinical question of importance, to either a) ascertain the diagnosis of CAD and define coronary anatomy or b) assess ischemia severity among patients with an expected higher likelihood of ischemia with an abnormal resting ECG or those incapable of performing maximal exercise
Evaluation Algorithm for Patients With Suspected ACS at Intermediate Risk With No Known CAD Test choice should be guided by local availability and expertise. *Recent negative test: normal CCTA ≤2 years (no plaque/no stenosis) OR negative stress test ≤1 year, given adequate stress. †High-risk CAD means left main stenosis ≥ 50%; anatomically significant 3-vessel disease (≥70% stenosis). ‡For FFR-CT, turnaround times may impact prompt clinical care decisions. However, the use of FFR-CT does not require additional testing, as would be the case when adding stress testing. CAD indicates coronary artery disease; CCTA, coronary CT angiography; CMR, cardiovascular magnetic resonance imaging; CT, computed tomography; FFR-CT, fractional flow reserve with CT; GDMT, guideline-directed medical therapy; ICA, invasive coronary angiography; INOCA, ischemia and no obstructive coronary artery disease; PET, positron emission tomography; and SPECT, single-photon emission CT
Patients with acute coronary syndrome (ACS) are commonly classified into two groups to facilitate evaluation and management, namely patients with acute myocardial infarction (MI) with ST-segment elevation (STEMI) on their presenting electrocardiogram (ECG)(Chap. 275) and those with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) The latter include patients with non-ST segment elevation MI (NSTEMI), who, by definition, have evidence of myocyte necrosis, and those with unstable angina (UA), who do not
The incidence of NSTEMI is rising due to the increasing burden of obesity, diabetes, and chronic kidney disease in an aging population and the increasing detection of myocardial necrosis by troponin (see below), whereas the incidence of STEMI is declining due to greater use of aspirin, statins, and less smoking. Among patients with NSTE-ACS, the proportion with NSTEMI is increasing while that with UA is falling because of the wider use of highly sensitive troponin (hsTn) assays (see below) with enhanced detection of myocyte necrosis, thereby reclassifying UA to NSTEMI.
The pathogenesis of NSTE- ACS involves five processes operating singly or in various combinations: (1) disruption of an unstable atheromatous plaque, (2) erosion of an atheromatous plaque (3) coronary arterial vasoconstriction, (4) gradual intraluminal narrowing of an epicardial coronary artery caused by progressive atherosclerosis or restenosis after percutaneous coronary intervention (PCI), and (5) oxygen supply- demand mismatch
Comparison of the characteristics of human atheromata complicated by thrombosis and causing acute coronary syndrome. The column on the left highlights some of the characteristics demonstrated by analyses of human coronary arterial lesions that have undergone thrombosis by these two diverse mechanisms. NETs, neutrophil extracellular traps
Among patients with NSTE-ACS studied at angiography, ~10% have stenosis of the left main coronary artery, 35% have three-vessel coronary artery disease, 20% have two-vessel disease, 20% have singlevessel disease, and 15% have no apparent critical epicardial coronary artery stenosis; some of the latter may have obstruction of the coronary microcirculation and/or spasm of the epicardial vessels.
Male predominance
More common in elderly pts and also high mortality rate
Common identified CV risk factors :Hypertension, type 2 diabetes, abnormal lipid profiles, obesity, smoking, advanced age, male gender, family history of CVD (first degree relative: male 45 years, female 55 years),previous MI,PCI and coronary artery bypass
Age (men >45 years; women >55 years) Family history of premature coronary artery disease (CAD) or myocardial infarction (MI) in first-degree relative: Men <55 years; women <65 years
Typically, chest discomfort is severe and has at least one of three features: (1) occurrence at rest (or with minimal exertion), lasting >10 min; (2) of relatively recent onset (i.e., within the prior 2 weeks); and/or (3) a crescendo pattern, i.e., distinctly more severe, prolonged, or frequent than previous episodes.
The chest discomfort is typically located in the substernal region and radiates to the left arm, left shoulder, and/or superiorly to the neck and jaw. Anginal equivalents such as dyspnea, epigastric discomfort, nausea, or weakness may occur instead of chest discomfort. These equivalents are more frequent in women, the elderly, and patients with diabetes mellitus.
The diagnosis of NSTEMI is established if a patient with any of these features (without electrocardiographic ST-segment elevations) develops evidence of myocardial necrosis, as reflected in abnormally elevated levels of circulating troponin, in the absence of another explanation
The physical examination resembles that in patients with stable angina and may be unremarkable. However, if the patient has a large area of myocardial ischemia or a large NSTEMI, the physical findings can include diaphoresis; pale, cool skin; sinus tachycardia; a third and/or fourth heart sound; basilar rales; and hypotension
Electrocardiogram New ST-segment depression occurs in about one-third of patients with NSTE-ACS. It may be transient but can persist for as long as several days following NSTEMI. T-wave changes are more common but are a less specific sign of ischemia, unless they are new and deep T-wave inversions (≥0.3 mV)
Cardiac Biomarkers Patients with NSTEMI have elevated biomarkers of necrosis, such as cardiac troponin (cTn) I or T (cTnI or cTnT) cTns are sensitive, relatively specific, and the preferred markers of myocardial necrosis. Elevated levels of cTn with a dynamic early change distinguish patients with NSTEMI from those with UA
The resting 12-lead ECG is the first-line diagnostic tool in the assessment of patients with suspected ACS. It is recommended to perform it within 10 min of the patient’s arrival in the emergency room or, ideally, at first contact with the emergency medical services in the pre-hospital setting and to have it immediately interpreted by a qualified physician
complement clinical assessment and 12-lead ECG in the diagnosis, risk stratification, and treatment of patients with suspected NSTE-ACS. Measurement of a biomarker of cardiomyocyte injury, preferably hs-cTn, is mandatory in all patients with suspected NSTEACS
In patients with NSTEMI, there is a characteristic temporal rise of the plasma concentration, peaking at 12–24 h after onset of symptoms and gradually decreasing thereafter. There is a direct relationship between the degree of elevation and mortality. The 1-h rapid rule-out MI algorithm (no abnormal elevation of hsTn at 0 or 1 hour after presentation) has been recommended by recent practice guidelines. It is important to distinguish myocardial injury from myocardial necrosis; the former is defined by elevations of cTn >99th percentile of the upper reference limit in patients without a clear clinical history or electrocardiographic features of acute myocardial ischemia. Myocardial injury may be caused by a variety of noncardiac and cardiac conditions other than MI
Assessment of risk can be accomplished by one of several clinical risk scoring systems, including those developed from the Thrombolysis in Myocardial Infarction (TIMI) Trials, the Global Registry of Acute Coronary Event (GRACE), and the HEART (history, electrocardiogram, age, risk factors, troponin) score. Multibiomarker strategies are now gaining favor, both to define more fully the pathophysiologic mechanisms underlying a patient’s presentation and to stratify the patient’s risk further. Early risk assessment is useful in identifying patients who would derive the greatest benefit from an early invasive strategy
Patients with a low likelihood of ischemia can usually be managed in an emergency department or a dedicated “chest pain unit”
Evaluation of such patients includes clinical monitoring for recurrent ischemic discomfort and continuous monitoring of ECGs, stress testing to detect and grade ischemia
CCTA to assess epicardial coronary artery obstruction, and serum troponin
Medical therapy consists of an acute phase focused on the clinical symptoms and stabilization of the culprit lesion(s) and a longer-term phase that involves therapies directed at the prevention of disease progression and future recurrent NSTE-ACS
Patients who “rule-in” for NSTE-ACS by clinical features, cTn, or ST-T-wave changes on the ECG should be admitted to the hospital
Patients should be placed on bed rest with continuous ECG monitoring for ST-segment deviation and cardiac arrhythmias, preferably on a specialized cardiac unit
Ambulation is permitted if the patient shows no recurrence of ischemia (symptoms or ECG changes) and does not develop an elevation of cTn for 24 h
The time of hospital discharge is a “teachable moment” for the patient with NSTE-ACS, when the caregiver can review and optimize the medical regimen. Risk factor modification is key, and the importance of smoking cessation, following an appropriate diet, achieving and maintaining optimal weight, daily exercise, blood pressure control, and control of hyperglycemia (in diabetic patients) should be emphasized
