Download - Acute Coronary Syndrome
ACS (Acute Coronary Syndrome)
By Dr. Ahmed Azhad
ACS
(Acute Coronary Syndrome)
ACS
(Acute Coronary Syndrome)
Coronary Arteries
UA/NSTEMI - Definition
UA diagnosis is mainly clinical:
Chest pain or discomfort:
Occurring at rest or minimal exertion (>10 minutes)
Severe and of new onset (within past 4-6 weeks)
Crescendo pattern
NSTEMI:
C/F of UA + Evidence of myocardial necrosis (elevated biomarkers)
UA/NSTEMI - Pathophysiology
Reduction in oxygen supply OR
Increase in myocardial oxygen demand superimposed on an atherosclerotic plague with varying degrees of obstruction
Contributors to the above are:
Plague rupture or erosion with superimposed non-occlusive thrombus (most common cause)
UA/NSTEMI Pathophysiology
(continued)
Dynamic obstruction (coronary spasm)
Progressive mechanical obstruction (rapidly advancing coronary atherosclerosis or restenosis following PCI)
Secondary UA related to increased myocardial oxygen demand or decreased supply (anemia/tachcardia)
UA/NSTEMI Clinical features
History and Examination:
Chest pain in substernal region or epigastrium, radiating to neck, left shoulder, and left arm
Diaphoresis
Pale cool skin
Sinus tachycardia
3rd and 4th heart sounds on auscultation
Basilar rales
Hypotension
UA/NSTEMI Investigations
ECG:
UA : ST-segment depression , transient ST-elevation and/or T-wave inversion (30-50%)
C/F + new ST-segment deviation of 0.05mV is an important predictor of adverse outcome
T-wave changes are sensitive for ischaemia but less specific (exception: new, deep T-wave inversions 0.3 mV
UA/NSTEMI ECG
UA/NSTEMI Investigations (2)
Cardiac Biomarkers:
CK-MB, Troponin-T
Direct relationship between degree of Troponin-T and mortality (not available in IGMH)
Patients without clinical history of ischemia: minor troponin elevations can be caused by:
Congestive heart failure
Myocarditis
Pulmonary embolism
False-positive readings
Unclear history + small troponin elevations = not diagnostic of ACS
UA/NSTEMI Enzyme assays
UA/NSTEMI Diagnosis
AHA 2010 Algorithm
High-likelihood of ACS:
H/o typical ischemic discomfort
Established CAD by angiography
Prior MI
Congestive heart failure
New ECG changes
Elevated cardiac biomarkers
UA/NSTEMI Diagnosis (2)
Intermediate-likelihood of ACS:
Age > 70 years
Male gender
Diabetes Mellitus
Peripheral arterial disease / Cerebrovascular disease
Old ECG abnormalities
UA/NSTEMI Diagnosis (3)
ED Evaluation of Chest Pain Rule Out MI
UA/NSTEMI Treatment
Bed Rest with continuous ECG monitoring for ST-deviation and cardiac rhythm
Ambulation allowed when no recurrence of ischemia and non-elevation of biomarkers 12-24 hours
Rx: anti-ischemic + anti-thrombotic therapy
UA/NSTEMI Rx anti-ischemic
Nitrates (upto 3 doses, 5 minutes apart; then IV nitroglycerin 5-10 g/min with non-absorbing tubing, can be increased 10 g/min every 3-5 minutes
Until symptoms relieved OR
Systolic BP < 100 mm Hg
Contraindications: 1) Hypotension 2) Sildenafil use within past 24 hours
blockers
ACE inhibitors
Statins
Morphine if pain not responding to nitroglycerin and -blockers
UA/NSTEMI Rx anti-thrombotic
Aspirin 162 325 mg loading, then 75 162 mg/d
Clopidogrel 300mg loading, then 75mg/day
IV antiplatelet therapy: Abciximab, Eptifibatide, Tirofiban
Heparins: UFH 60-70 U/kg (max: 5000 U), then 12-15 U/kg/hr (init. Max: 1000 U/hr titrated to a PTT 50-70s)
Enoxaparin 1mg/kg s.c. Q12h, first dose preceded by 30mg iv-bolus. (If CC < 30 cc/min, 1mg/kg OD)
Fondiparinux, Bivalirudin
UA/NSTEMI Rx Additional
High-risk patients (multiple risk factors, ST-segment deviation and/or postive biomarkers)
Coronary ateriography within 48 hours of admission followed by coronary revascularisation (PCI or CABG)
Low-risk patients: Watchful waiting; arteriography if:
Rest pain
ST segment changes
Evidence of ischemia on stress test
UA/NSTEMI Prognosis
Wide spectrum:
30 day risk of Death: 1-10%
30 day risk of new or recurrent infarct: 3-10%
TIMI Trials:
7 independent risk factors
CRP and BNP (marker of increased myocardial wall tension) correlate independently with increased mortality
UA/NSTEMI Discharge
Teachable moment
Risk-factor modification: smoking cessation, optimal weight, daily exercise, diet, BP control, control of hyperglycemia, lipid management
Drugs: beta blockers, statins, ACE inhibitors, aspirin + clopidogrel 9-12 months, then aspirin alone thereafter
STEMI
Occurs when there is thrombotic occlusion of a coronary artery.
Thrombus develops rapidly.
Cardiac biomarkers can be used to distinguish UA from NSTEMI and to assess the magnitude of STEMI.
STEMI - Pathophysiology
Thrombotic occlusion of a coronary artery previously affected by atherosclerosis.
Occurs due to rapid development of a thrombus at the site of vascular injury.
Facilitating factors:
Cigarette smoking
Hypertension
Lipid accumulation
STEMI - Pathophysiology
STEMI Pathophysiology (2)
Occurs when the surface of an atherosclerotic plaque becomes disrupted and conditions favour thrombogenesis
Coronary artery gets occluded by a thrombus
Rarely by coronary emboli, congenital abnormalities, coronary spasm, inflammatory diseases
STEMI Clinical Features
Half of the cases have a precipitating factor:
Vigourous physical exercise
Emotional stress
Medical or Surgical illness
Usually in the morning / within a few hours of waking up but can occur anytime
C/o:
Pain deep, heavy, squeezing, crushing, stabbing or burning
STEMI Clinical Features (2)
Similar to angina pectoris, but is usually more severe and lasts longer
Central portion of the chest and/or epigastrium
Radiation upto occipital area but not below umblicus
Associated with weakness, sweating, nausea, vomiting, anxiety and a sense of impending doom
Does not subside with rest
STEMI DD of chest pain
Acute pericarditis (radiation of pain to trapezius)
Pulmonary embolism
Acute aortic dissection
Costochondritis
Gastrointestinal disorders
STEMI Other presentations
STEMI in Diabetes painless
STEMI in elderly - sudden-onset breathlessness pulmonary edema
Others with or without pain:
Sudden loss of consciousness, sudden profound weakness, arrhythmia, unexplained drop in arterial pressure
STEMI Physical findings
Anxious, restlessness
Pallor
Pain > 30 minutes + diaphoresis -> STEMI
BP/Pulse: can be normal or increased (sympathetic hyperactivity); decreased in inferior infarcts
3rd and 4th heart sounds
Mid-systolic or late systolic murmur
STEMI - Investigations
ECG ST elevation, Q waves (ideal time: within 10 minutes)
Cardiac biomarkers:
Troponin-T (preffered) lasts till 7-10 days after STEMI
CK/CK-MB: Rises within 4-8 hours, returns to normal in 48-72 hours (can also rise due to cardiac surgery, myocarditis, electrical cardioversion). CKMB mass:CK 2.5 suggestive of cardiac muscle damage.
Should be noted that recanalisation would cause earlier and higher peak of enzymes.
3. TLC rise: 12,000 15,000/L. Few hours upto 3-7 days.
4. ESR rise peaking in 1st week, raised for upto 2 weeks.
STEMI ECG (1)
ST-segment elevation or presumed new LBBB
ST-segment elevation in 2 or more contiguous leads = STEMI
Threshold values:
Men 40 yrs : J-point elevation (V2 and V3) - 0.2 mV : and 0.1mV in all other leads
Men < 40 yrs : J-point elevation (V2 and V3) - 0.25 mV : and 0.1mV in all other leads
Women: L-point elevation (V2 and V3) 0.15 mV : and 0.1mV in all other leads
STEMI ECG (2)
Ischemic ST-segment depression > 0.05mV or dynamic T-wave inversion with pain or discomfort = UA/NSTEMI
Non-persistent/transient ST-elevation 0.5mm for < 20 minutes is also included in this category.
Threshold values: J-point depression 0.05mV in leads V2 and V3, and 0.1mV in all other leads (men and women)
STEMI ECG (3)
Non-diagnostic ECG with non-specific ST-segment or T-wave changes = non-conclusive for ischemia
Threshold values:
Normal ECGs
ST-segment deviation < 0.5mm, T-wave inversions 0.2 mm
STEMI Other Investigations
2-D Echo wall motion abnormalities
Radio-nuclide imaging with 99m-Tc labelled blood red cells
STEMI Initial Rx
Prehospital care
Management in the Emergency Department
Goals:
Control of cardiac discomfort
Rapid identification of patients for reperfusion
Avoidance of inappropriate discharge of patients with STEMI
Rx:
Aspirin 160 325 mg chewable tablets
O2 at 2-4L/min for hypoxemic patients
STEMI Initial Rx (2)
Control of discomfort
Sublingual nitroglycerin 0.4mg at 5-min intervals
Abolishes chest pain
Decreases myocardial oxygen demand (by lowering preload)
Increases myocardial oxygen supply (by dilating coronary vessels)
If chest discomfort returns, consider IV nitroglycerin
Avoid nitrates in patients with systolic BP 60, SBP > 100mm Hg. After this 50mg Q6H oral x 48 hrs, then 100mg Q12H.
STEMI - Rx
Limiting infarct size:
Primary PCI (Door-balloon time 90 minutes)
Thrombolysis (Door-needle time 30 minutes)
Tissue plasminogen activator
Streptokinase (1.5 MU over 60 minutes)
Tenecteplase
Reteplase
Contraindications: Active internal bleeding, Recent CVA, Intraspinal or intracranial surgery, intracranial neoplasm, severe uncontrolled hypertension
Complications: Hemorrhagic stroke (0.5 0.9%)
STEMI Post reperfusion
Pharmacotherapy:
Antiplatelet + Antithrombotic therapy
Aspirin
Clopidogrel
Heparin
Beta blockers
ACE Inhibitors
References
Harrisons Principles of Internal Medicine 17th Edition
Circulation (journal of AHA)
http://circ.ahajournals.org/content/122/18_suppl_3/S787
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