3.2. Medicine_Acute Coronary Syndromes 2014A

November 12, 2012 Acute Coronary Syndromes Dr. Uy o NQMI (Non-Q-wave MI): there is increased myocardial necrosis but no Q wave  incomplete (note: both UA and NQMI are called Non-STEMI ACS) o STEMI: at bigger area  complete obstruction o ACI (acute coronary insufficiency): prolonged chest pain > 20mins, with (+) ST changes and enzyme/ biomarker elevation o ST-elevation MI (STEMI): prolonged chest paon (>20 mins), persisting ST elevation despite NTG. The ST elevation is at least 1mm in 2 adjacent leads, or at least 2 mm in 2 adjacent precordial leads. o Left Bundle Branch Block (recent)

OUTLINE I. a. b. c. d. e. f. g. II. III. IV.

Acute Coronary Syndromes Clinical Data Signs Initial Investigation Subsequent Investigation ECG Changes Biomarkers Assessment and Treatment of ACS Complications of MI Coronary Artery Disease Unstable Angina/ NSTEMI

ACUTE CORONARY SYNDROMES  Represent a dynamic spectrum of similar disease process, being part of a continuum of ischemic coronary disease  Each syndrome is associated with specific strategies in prognosis and management

Figure 1. Spectrum of Acute Coronary Syndromes  Composed of patients with Acute Myocardial Infarction with STsegment Elevation (STEMI), Non-ST-segment Elevation MI (NSTEMI) and Unstable Angina, All present with chest pain  Biomarkers for MI- Troponin T, Troponin I, CPK

Figure 4. Course of Myocardial Hypoxia

CLINICAL DATA  Chest pain o Typical chest pain, severe but prolonged and sense of impending death (Angor Animi) o Nausea, vomiting, sweating, dizziness, extreme weakness and dyspnea  Symptoms of complications 
 o Dyspnea, PND, irritability, palpitation  Silent – painless myocardial infarction (but with other symptoms like dyspnea, paroxysmal nocturnal dyspnea irritability or palpitation)  Common in diabetics and stroke patients because sensation and perception maybe altered and they cannot complain of pain.

Figure 2. Sequelae of Coronary Thrombus

Figure 3. Thrombus formation and ACS.

 Starts with thrombus formation then becomes either: o Unstable Angina: plaque with a small fissure  sudden formation of small clot (dark red) cause sudden decrease of blood flow  sudden ischemic episode  unstable angina

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SIGNS         

Anxious patient Signs of cardiogenic shock if present Cold sweats Peripheral cyanosis Hypotension, thready pulse Oliguria Pulse: Arrhythmias may be detected Low grade fever due to necrosis & inflammation Auscultation: o First heart sound (S1) is weak because contractility is impaired o Pulmonary components of S2 may be accentuated resulting to pulmonary HTN o Third heart sound (S3 gallop) o Pericardial frictioin rub if pericarditis occurs o Murmur of mitral regurgitation or VSD if complications occur o Moist rales may be heard at the base of the lungs Note: In some cases, auscultation may reveal no abnormality

INITIAL INVESTIGATIONS  Immediate ECG o ECG is sole test required to select patients for emergency reperfusion. (thrombolysis is indicated for cases of STE-MI and none for non- STEMI)

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 Blood Test o Serum troponin I or T levels (or CK-MB if troponin not available) o Full blood count o Serum creatinine (eGFR) and electrolyte levels o Serum creatinine kinase (CK) level o Serum lipid levels within 24 hours o Blood glucose level (to rule out co-morbidities)  Chest Xray o Useful, but should not delay reperfusion treatment where indicated (can be useful if there is congestion, patient can go on heart failure; or presence of wide mediastinum indicating a dissecting aneurysm)  Caridac Biomarker: Troponin level (Cardiac Troponin I or T) o On arrival; + if pain is >3 hours (Not repeated if positive) o Repeat after 8 hours after last episode of pain or other symptoms of coronary insufficiency if initially negative, then if 2nd test is still (-), send patient home unless there is strong sign that patient has MI. o Serial troponin measurements in patients with NSTEACS suspected to be at high risk  Total CK Level o Serial measurements performed for 48 hours in patients with MI. Can be remeasured to confirm a second event if reinfarction is suspected later  CK-MB Level o Measure in all patients with an ACS if troponin assay unavailable o Troponin: goes up 24 hrs remains elevated up to 7 days CKMB: rise and fall within 24 hrs 


INVESTIGATION (SUBSEQUENT)  Echocardiography o Although acute STEMI cannot be distinguished from an old myocardial scar or from acute severe ischemia by echocardiography, the ease and safety of the procedure make its use appealing as a screening tool in the Emergency Department setting. o Echocardiographic estimation of left ventricular function is useful prognostically  Radionuclide Scintigraphy o Myocardial perfusion imaging with 201Tl or 
99mTc-sestamibi, which are distributed in proportion to myocardial blood flow and concentrated by viable myocardium, reveal a defect ("cold spot") in most patients during the first few hours after development of a transmural infarct. o Used less often than echocardiography because they are more complicated and lack sensitivity and specificity in many clinical circumstances  Cardiac Catheterization  Cardiac MRI o Myocardial infarction can be detected accurately with high resolution cardiac magnetic resonance imaging using a technique referred to as late enhancement o A standard imaging agent (gadolinium) is administered and images are obtained after a 10-min delay.

ECG CHANGES IN ACS

Figure 5. ECG changes/ injury pattern in MI: Q-wave remains permanent. When a patient has a Q-wave, it can be said that there was a previous MI  Ischemia (1-2 hours) o Abnormal Q waves >2mm wide or > 25% height of R wave in that lead  Unstable Angina/ NSTEMI o ST-segment depression o T-wave inversion in 30-50% of patients  ST-Elevation MI o ST-segment elevation O.o o Pathologic Q wave o Inversion of T wave

Figure 6. NSTEMI: Again, NSTEMI include MI’s with T-wave inversion or ST Depression

BIOMARKERS

Figure 7. Biomarkers of MI. The Troponins are the biomarker of choice after 4 days, as they remain elevated for up to 10 days, whereas CPK would have already gone down by Day 2). CPK goes up within a few hours after an MI, peaks in 24 hours, and normalizes in 2 days. Application: A patient comes in with ischemia that eventually resolved. 5 days later, he had chest pain. What would you test for? CPK! Troponin would still be up from the previous attack and will not say anything about the recent one.

ASSESSMENT AND TREATMENT OF ACS  Initial Assessment o Rapid but detailed inquiry o Vital signs and PE o 12-Lead ECG and Serial ECG o Chest X-ray o Enzymatic Assessment  Initial General Treatment (MONA) o Morphine: pain killer 2-4mg/ 5-10 min; SubQ o Oxygen: 4L/min o Nitroglycerin: Sublingual or IV o Aspirin: 160 – 325 mg (Chew) 
 Note: Today, Statins are also used to establish pleopmorphic effect because they have anti-oxidant effect which can fight against free radicals produced by inflammatory processes.

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COMPLICATIONS OF THROMBOLYTIC USE  Allergic Reactions  Hemorrhage  Hemorrhagic Stroke

OTHER TREATMENTS OF ACS  Conjunctive therapy: combined with thrombolytic agents o Aspirin o Heparin o Clopidogrel, potent antiplatelet agent  Adjunctive therapies - Agents given instead of or in addition to thrombolytic agents: o IV Nitroglycerin o Beta blockers o ACE inhibitors - especially in: Large infarction, Heart failure and Hypertension

COMPLICATIONS OF ACUTE MI Figure 8. Treatment of ACS. Antiplatelets and anticoagulants are important! When a patient comes in acutely complaining of chest pain, we can be aggressive with treatment by opening up the coronary a. to prevent further necrosis of cardiac cells- do a Primary Percutaneous Coronary Intervention (PPCI), preferably within 90 mins! (For details about PCI, check out Ischemia trans)

SPECIFIC TREATMENT  Reperfusion therapy: only for patients with ST segment elevation or new Left Bundle Branch Block  Thrombolytic agents: (door-to-neddle time < 30 mins); for reperfusion therapy  Kinases (e.g. Streptokinase) - dissolves thrombus unlike anticoagulants that only prevents thrombus formation. Acts by promoting the conversion of plasminogen to plasmin which subsequently lyses fibrin thrombi.  Primary Percutaneous Transluminal Coronary Angioplasty (door-todilatation time < 60 mins) o Effective in restoring perfusion in STEMI when carried out on an emergency basis in the first few hours of Mi
 o It has the advantage of being applicable to patients who have contraindications to fibrinolytic therapy.

 Early o Arrhythmias o Acute Heart Failure o Cardiogenic Shock o Acute Mitral Regurgitation o Ventricular Septal Rupture or Free Wall Rupture o Acute Pericarditis o Mural thrombosis o Sudden Death  Late o Dressler’s syndrome (fever, joint pain, pleurisy, pericarditis) – has a dramatic response to Indomethacin or corticosteroids) o Myocardial aneurysm and thrombus o Ischemic cardiomyopathy o Ventricular Fibrillation

CONTRAINDICATIONS TO USE OF THROMBOLYTICS A. Absolute Contraindications     

History of Cerebrovascular Hemorrhage or CVA Non-hemorrhagic stroke or cerebrovascular event within the past year Marked hypertension (systolic > 180 mmHg and/or diastolic >110 mmHg) Suspicion of aortic dissection Active internal bleeding (including menstruation)

Figure 9. Complications of Myocardial Infarction

CORONARY ARTERY DISEASE

B. Relative Contraindications      

Current use of anticoagulants A recent (10 min) cardiopulmonary resuscitation Known bleeding diathesis, pregnancy, a hemorrhagic Ophthalmic condition (e.g., hemorrhagic diabetic retinopathy) Active peptic ulcer disease History of severe hypertension that is currently adequately controlled.

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Figure 10. Course of Atherosclerosis. End-result is Coronary Thrombosis  Initiated by rupture of an unstable plaque which leads to Coronary a. Occlusion o Intermittent Occlusion= Unstable Angina o Complete occlusion= Acute MI  3 I’s of coronary artery event: Ischemia, Injury, Infarction

UNSTABLE ANGINA/ NSTEMI  Most commonly caused by a reduction in oxygen supply and/ or by an increase in myocardial oxygen demand superimposed on an atherosclerotic coronary plaque, with varying degrees of obstruction.  Four pathologic processes that may contribute to the development of UA/NSTEMI: o Plaque rupture or erosion with superimposed non-occlusive thronmbus (most common cause) o Dynamic obstruction (eg. coronary spasm, as in Prinzmetal’s/ variant angina) o Progressive mechanical obstruction (rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention) o Secondary UA related to increased myocardial oxygen demand and/or decreased supply (eg. tachycardia, anemia)  Progressioin of Myocardial Infarction o Acute Stage: First few hours to 7 days o Healing Stage: 7-28 days o Healed Stage: >29 days

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