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

Thank You

10-02-2012

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Health & Medicine

Acute Coronary Syndrome