3.2. Medicine_Acute Coronary Syndromes 2014A

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JMA-1, JMA-2, Telma | Claveria Page 1 of4

November 12, 2012

Acute Coronary SyndromesDr. Uy

OUTLINE

I. Acute Coronary Syndromesa. Clinical Datab. Signsc. Initial Investigationd. Subsequent Investigatione. ECG Changesf. Biomarkersg. Assessment and Treatment of ACS

II. Complications of MIIII. Coronary Artery DiseaseIV. Unstable Angina/ NSTEMI

ACUTE CORONARY SYNDROMES

Represent a dynamic spectrum of similar disease process, beingpart of a continuum of ischemic coronary disease

Each syndrome is associated with specific strategies in prognosisand management

Figure 1. Spectrum of Acute Coronary Syndromes

Composed of patients with Acute Myocardial Infarction with ST-segment 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 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

o NQMI (Non-Q-wave MI): there is increased myocardial necrosis but noQ wave incomplete (note: both UA and NQMI are called Non-STEM

ACS)

o STEMI: at bigger area complete obstructiono ACI (acute coronary insufficiency): prolonged chest pain > 20mins, with

(+) ST changes and enzyme/ biomarker elevationo ST-elevation MI (STEMI): prolonged chest paon (>20 mins), persisting ST

elevation despite NTG. The ST elevation is at least 1mm in 2 adjacen

leads, or at least 2 mm in 2 adjacent precordial leads.

oLeft Bundle Branch Block (recent)

Figure 4. Course of Myocardial Hypoxia

CLINICAL DATA Chest paino 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 likedyspnea, paroxysmal nocturnal dyspnea irritability or palpitation)

Common in diabetics and stroke patients because sensation andperception maybe altered and they cannot complain of pain.

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 impairedo Pulmonary components of S2 may be accentuated resulting to

pulmonary HTN

o Third heart sound (S3 gallop)o Pericardial frictioin rub if pericarditis occurso Murmur of mitral regurgitation or VSD if complications occuro Moist rales may be heard at the base of the lungs

Note: In some cases, auscultation may reveal no abnormality

INITIAL INVESTIGATIONS Immediate ECGo ECG is sole test required to select patients for emergency reperfusion

(thrombolysis is indicated for cases of STE-MI and none for non- STE

MI)


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Blood Testo Serum troponin I or T levels (or CK-MB if troponin not available)o Full blood counto Serum creatinine (eGFR) and electrolyte levelso Serum creatinine kinase (CK) levelo Serum lipid levels within 24 hourso Blood glucose level (to rule out co-morbidities)

Chest Xrayo Useful, but should not delay reperfusion treatment where indicated

(can be useful if there is congestion, patient can go on heart failure; orpresence 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 tobe at high risk

Total CK Levelo 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 Levelo Measure in all patients with an ACS if troponin assay unavailableo Troponin: goes up 24 hrs remains elevated up to 7 days CKMB: rise and

fall within 24 hrsINVESTIGATION (SUBSEQUENT)

Echocardiographyo 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 usefulprognostically

Radionuclide Scintigraphyo 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 MRIo 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 areobtained 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)oAbnormal Q waves >2mm wide or > 25% height of R wave in that lead

Unstable Angina/ NSTEMIoST-segment depressionoT-wave inversion in 30-50% of patients

ST-Elevation MIoST-segment elevation O.ooPathologic Q waveo Inversion of T wave

Figure 6. NSTEMI:Again, NSTEMI include MIs 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 Assessmento Rapid but detailed inquiryo Vital signs and PEo 12-Lead ECG and Serial ECGo Chest X-rayo Enzymatic Assessment

Initial General Treatment (MONA)o Morphine: pain killer 2-4mg/ 5-10 min; SubQo Oxygen: 4L/mino Nitroglycerin: Sublingual or IVo 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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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 PrimaryPercutaneous 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 reperfusiontherapy

Kinases (e.g. Streptokinase) - dissolves thrombus unlike anticoagulantsthat only prevents thrombus formation. Acts by promoting the conversion

of plasminogen to plasmin which subsequently lyses fibrin thrombi.

Primary Percutaneous Transluminal Coronary Angioplasty (door-to-dilatation time < 60 mins)

o Effective in restoring perfusion in STEMI when carried out on anemergency basis in the first few hours of Mi

o It has the advantage of being applicable to patients who havecontraindications to fibrinolytic therapy.

CONTRAINDICATIONS TO USE OF THROMBOLYTICSA. 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 >110mmHg)

Suspicion of aortic dissection Active internal bleeding (including menstruation)

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.

COMPLICATIONS OF THROMBOLYTIC USE Allergic Reactions Hemorrhage Hemorrhagic StrokeOTHER TREATMENTS OF ACS Conjunctive therapy: combined with thrombolytic agentso Aspirino Heparino Clopidogrel, potent antiplatelet agent

Adjunctive therapies - Agents given instead of or in addition tothrombolytic agents:

o IV Nitroglycerino Beta blockerso ACE inhibitors - especially in: Large infarction, Heart failure and

Hypertension

COMPLICATIONS OF ACUTE MI Earlyo Arrhythmiaso Acute Heart Failureo Cardiogenic Shocko Acute Mitral Regurgitationo Ventricular Septal Rupture or Free Wall Ruptureo Acute Pericarditiso Mural thrombosiso Sudden Death

Lateo Dresslers syndrome (fever, joint pain, pleurisy, pericarditis ) has a

dramatic response to Indomethacin or corticosteroids)

o Myocardial aneurysm and thrombuso Ischemic cardiomyopathyo Ventricular Fibrillation

Figure 9. Complications of Myocardial Infarction

CORONARY ARTERY DISEASE


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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.Occlusiono Intermittent Occlusion= Unstable AnginaoComplete occlusion= Acute MI

3 Is of coronary artery event: Ischemia, Injury, InfarctionUNSTABLE ANGINA/ NSTEMI

Most commonly caused by a reduction in oxygen supply and/ or by anincrease in myocardial oxygen demand superimposed on an

atherosclerotic coronary plaque, with varying degrees of obstruction.

Four pathologic processes that may contribute to the development ofUA/NSTEMI:

o Plaque rupture or erosion with superimposed non-occlusive thronmbus(most common cause)

o Dynamic obstruction (eg. coronary spasm, as in Prinzmetals/ variantangina)

o Progressive mechanical obstruction (rapidly advancing coronaryatherosclerosis or restenosis following percutaneous coronary

intervention)

o Secondary UA related to increased myocardial oxygen demand and/ordecreased supply (eg. tachycardia, anemia)

Progressioin of Myocardial Infarctiono Acute Stage: First few hours to 7 dayso Healing Stage: 7-28 dayso Healed Stage: >29 days

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