Acute coronary syndrome

Acute coronary syndrome

Acute coronary syndrome is a myocardial ischemia due to : 1- myocardial infarction (NSTEMI or STEMI) 2- unstable angina

NSTEMI = non-ST elevation myocardial infarction STEMI = ST elevation myocardial infarction

• Unstable angina : is defined as angina at rest, new onset exertional angina

(<2 months), recent acceleration of angina (<2 months), or post revascularization angina.

Acute myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Myocardial infarction occurs when myocardial ischemia, a diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis. Ischemia at this critical threshold level for

an extended period results in irreversible myocardial cell damage or death.

(Critical imbalance between oxygen supply and demand to the myocardium)

Classification

1 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)

Anatomic or morphologic

Transmural= Full thickness

Non-transmural= Partial thickness

ECG

Q wave MI

Non Q wave MI

Does not distinguish transmural from a non-transmural MI .

DEFINITION:

Myocardial infarction ((acute, evolving, recent))

Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following:

– a) Ischemic symptoms;

– b) Development of pathologic Q waves on the ECG;

– c) ECG changes indicative of ischemia (ST segment elevation or depression);( dynamic T wave changes) or

– d) Coronary artery intervention (e.g., coronary angio-plasty).

NSTEMI is an acute process of myocardial ischemia with sufficient severity and duration to result in myocardial necrosis.

– The initial ECG in patients with NSTEMI does not show ST-segment elevation.

– NSTEMI is distinguished from UA by the detection of cardiac markers indicative of myocardial necrosis in NSTEMI .


Unstable angina—an acute process of myocardial ischemia that is not of

sufficient severity and duration to result in myocardial necrosis.

Prevalence

Incidence of 600 per 100,000 people

The survival rate for U.S. pts hospitalized with MI is approximately 90%

This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.

Increase in the proportion of NSTEMI compared to STEMI

Approximately 500,000 to 700,000 deaths are caused by heart disease annually in the United States.

PATHOPHYSIOLOGY:

The severity of an MI depends on three factors: 1.the level of the occlusion in the coronary artery 2. the length of time of the occlusion, and 3. the presence or absence of collateral circulation.

Generally, the more proximal the coronary occlusion, the more extensive the amount of myocardium that will be at risk of necrosis. The larger the myocardial infarction, the greater the chance of death because of a mechanical complication or pump failure. The longer the period of vessel occlusion, the greater the chances of irreversible myocardial damage distal to the occlusion.

STEMI is usually the result of complete coronary occlusion after plaque rupture. This arises most often from a plaque that previously caused less than 50%

occlusion of the lumen. NSTEMI is usually associated with greater plaque burden without complete occlusion. This difference contributes to the increased early mortality seen in STEMI and the eventual equalization of mortality between STEMI and NSTEMI after 1 year.


Most myocardial infarctions are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists for more than 20 minutes, irreversible myocardial cell damage and cell death will occur.

The atherosclerotic plaque occurs over a period of years to decades. The plaque has a fibromuscular cap and an underlying lipid-rich core. Plaque erosion can occur because of the actions of matrix metalloproteases and the release of other collagenases and proteases in the plaque, which result in thinning of the overlying fibromuscular cap. The action of proteases, in addition to hemodynamic forces applied to the arterial segment, can lead to a disruption of the endothelium and fissuring or rupture of the fibromuscular cap. The loss of structural stability of a plaque often occurs at the juncture of the fibromuscular cap and the vessel wall, a site otherwise known as the shoulder region. Disruption of the endothelial surface can cause the formation of thrombus via platelet-mediated activation of the coagulation cascade. If a thrombus is large enough to occlude coronary blood flow, an MI can result.

Risk factors for atherosclerosis:


Age

Male gender

Smoking

Hypercholesterolemia and triglyceridemia

Diabetes Mellitus

Poorly controlled hypertensionFamily HistorySedentary lifestyleType A personality

Signs and symptoms:

The history is critical in making the diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation.

Acute MI can have unique manifestations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. An asymptomatic MI is not necessarily less severe than a symptomatic event, but patients who experience asymptomatic MIs ((SILENT)) are more likely to be diabetic. Despite the diversity of manifesting symptoms of MI, there are some characteristic symptoms.

TYPICAL SYMPTOM-chest pain or discomfort. You have to ask the patient about onset as the vascular insult is acute and ask about duration , aggravating or relieving symptoms ,site , character, radiation, severity ,course and association.

ONSET-all of a sudden , for first time in most of cases , awake pt

SITE-anterior precordium , central , right or left sided ,interscapular

DURATION- minutes to hours to days according to severity.


CHARACTER- pressure sensation, fullness, or squeezing in the midportion of the thorax, burning , heaviness, stabbing , piercing, heart burn, pins and needles, colicky, tightness ,ANY TYPE .

RADIATION-may radiate to jaw OR teeth, tip of shoulder, arm to the inner sit of the upper limb more left or both limbs, and/or back ,anterior neck and epigastrium up and down to the jaw.

AGGREVATING FACTORS- 60% no factors, others can be related to stressful event or exercise or heavy work or walking in windy weather or sudden heavy work or bad news.

ASSOCITED SYMPTOMS Nausea with and without vomiting Diaphoresis or sweating Syncope or near syncope Dyspnea- angina equivalent, poor LV function Nausea

SEVERITY-awake the patient from sleeping , fear of death, abstinence from work , can’t sleep or eat , interfere with daily activities , chest discomfort that is not relieved in any posture.

ATYPICAL SYMPTOMS

As many as half of MI are clinically silent((DIABETICS AND ELDERY))

Epigastric discomfort with or without nausea and vomiting.All of sudden epigastric pain in a patient above 40years wither heart burn or colicy abdominal pain or radiating up to the neck.Sudden dyspnea with out lung diseases.Syncope or near syncope without other causePalpitation all of sudden with fear of death in elder pt.Impairment of cognitive function without other cause.Profuse sweating all of sudden in diabetic with out hypoglycemia.Jaw pain all of sudden in elder patient.Fatigability al of sudden

MI can occur at any time of the day, but most appear to be clustered around the early hours of the morning or are associated with demanding physical activity, or both.


Physical signs:

Most of the patients has no signs on presentation(completely normal).

Others , they may present with left ventricular failure (dyspnea) or sweating and cold extremities in others.

The physical exam can often be unremarkable

Hypertension , Hypotension

Tachycardia , bradycardia.

Sweating , dyspnea , apprehensive

Acute valvular dysfunction may be present

Rales on chest examination

Neck vein distention

Third heart sound may be present

A fourth heart sound--- poor LV compliance

Dysrhythmias

Low grade fever( fever in MI develop after a day of MI).

CAUSES OF MI OTHER THAN PLAQUE:

Coronary artery vasospasm

Ventricular hypertrophy

Hypoxia

Coronary artery emboli

Cocaine


Arteries

Coronary anomalies

Aortic dissection

Pediatrics Kawasaki disease, Takayasu arteritis

Increased afterload which increases myocardial demand

Acute coronary syndromes can also be due to secondary causes: – Thyrotoxicosis – Anemia – Tachycardia – Hypotension – Hypoxemia – Arterial inflammation (infection, arteritis)

Differentials

4 IMPORTANT LIFE SAVING DIAGNOSIS NOT TO BE MISSED:

1.Acute coronary syndrome2.Pulmonary embolism3.Aortic Dissection4.Pneumothorax

Other D/D

Endocarditis Myocarditis Pericarditis

Anxiety Aortic stenosis Asthma

Cholecystitis and biliary colic Cholethiasis

Esophagitis Pneumonia COPD


DiagnosisDx of acute coronary syndrome is based on

1- History, 2- Physical exam, 3- ECG, 4- Cardiac enzymes


INVESTIGATION:

2 OF 3 ARE DIAGNOSTIC FOR MI:

1.CHEST PAIN2.ECG3.CARDIAC ENZYMES

1.Complete blood count:

CBC is indicated if anemia is suspected as precipitant

Leukocytosis may be observed within several hours after myocardial injury and returns to levels within the reference range within one week.

2.Renal function test and electrolytes:

Potassium and magnesium levels should be monitored and corrected ( rhythmogenic).

Decrease cardiac output may lead to renal impairment .

Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization

3. Electrocardiogram

A normal ECG does not exclude ACS

The first diagnostic test is electrocardiography (ECG), which may demonstrate that a MI is in progress or has already occurred

High probability include ST segment elevation in two contiguous leads or presence of q waves

Intermediate probability ST depression


In addition to ST-segment elevation, 81% of electrocardiograms during STEMI demonstrate reciprocal ST-segment depression as well.

T wave inversions are less specific in NSTEMI

Localization of MI

ST elevation only

Inferior wall- II, III, aVF Lateral wall_ I, aVL, V4-V6 Anteroseptal- V1-V3 Anterolateral- V1-V6 Right ventricular- RV4, RV5 Posterior- R/S ratio >1 in V1 and T wave

inversion4. Cardiac Biomarkers

Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle .

Living myocardial cells contain enzymes and proteins (e.g., creatine kinase, troponin I and T, myoglobin) associated with specialized cellular functions. When a myocardial cell dies, cellular membranes lose integrity, and intracellular enzymes and proteins slowly leak into the blood stream. These enzymes and proteins can be detected by a blood sample analysis. These values vary depending on the assay used in each laboratory. Given the acuity of a STEMI and the need for urgent intervention, the laboratory tests are usually not available at the time of diagnosis. Thus, good history taking and an ECG are used to initiate therapy in the appropriate situations.


Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury

These biomarkers have a characteristic rise and fall pattern.

a. Troponin T and I

• These isoforms are very specific for cardiac injury.

• Preferred markers for detecting myocardial cell injury.

• Rise 2-6 hours after injury

• Peak in 12-16 hours• Stay elevated for 5-14 days

b. Creatinine Kinase ( CK-MB)

Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB)

Increased in over 90% of myocardial infraction

However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions

Time sequence after myocardial infarction

Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days

MB2 released from heart muscle and converted to MB1.

A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury


c. Myoglobin

Damage to skeletal or cardiac muscle release myoglobin into circulation.

Time sequence after infarction

Rises fast 2hours Peaks at 6-8 hours

Returns to normal in 20-36 hours

Have false positives with skeletal muscle injury and renal failure

5. Chest X-Ray

Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax)


Chest radiography also reveals complications of myocardial infarction such as heart failure(CONGESTED LUNG-WHITE).

5.Echocardiography Use 2-dimentional and M mode echocardiography

when evaluating overall ventricular function and wall motion abnormalities, intracardiac thrombus.

Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)

The presence of wall motion abnormalities on the ECHO may be the result of an acute MI or previous (old) MI or other myopathic processes, limiting its overall diagnostic utility.

Complications of MI:

Arrhythmic Complications of MIAbout 90% of patients who have an acute myocardial infarction (AMI) develop some form of cardiac arrhythmia during or immediately after the event. In 25% of patients, such rhythm abnormalities manifest within the first 24 hours. In this group of patients, the risk of serious arrhythmias, such as ventricular fibrillation, is greatest in the first hour and declines thereafter. The incidence of arrhythmia is higher with an ST-elevation myocardial infarction (STEMI) and lower with a non–ST-elevation myocardial infarction.

The clinician must be aware of these arrhythmias, in addition to reperfusion strategies, and must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise. Most peri-infarct arrhythmias are benign and self-limited. However, those that result in hypotension, increase myocardial oxygen requirements, and/or predispose the patient to develop additional malignant ventricular arrhythmias should be aggressively monitored and treated.

Pathophysiology of arrhythmic complications

AMI is characterized by generalized autonomic dysfunction that results in enhanced automaticity of the myocardium and conduction system. Electrolyte


imbalances (eg, hypokalemia and hypomagnesemia) and hypoxia further contribute to the development of cardiac arrhythmia.

The damaged myocardium acts as substrate for re-entrant circuits, due to changes in tissue refractoriness.

Enhanced efferent sympathetic activity, increased concentrations of circulating catecholamines, and local release of catecholamines from nerve endings in the heart muscle itself have been proposed to play roles in the development of peri-infarction arrhythmias. Furthermore, transmural infarction can interrupt afferent and efferent limbs of the sympathetic nervous system that innervates myocardium distal to the area of infarction. The net result of this autonomic imbalance is the promotion of arrhythmias.

Classification of peri-infarction arrhythmias

Supraventricular tachyarrhythmias, including sinus tachycardia, premature atrial contractions, paroxysmal supraventricular tachycardia, atrial flutter, and atrial fibrillation

Accelerated junctional rhythms Bradyarrhythmias, including sinus bradycardia and junctional bradycardia Atrioventricular (AV) blocks, including first-degree AV block, second-

degree AV block, and third-degree AV block Intraventricular blocks, including left anterior fascicular block, right

bundle branch block (RBBB), and left bundle branch block (LBBB) Ventricular arrhythmias, including premature ventricular contractions

(PVCs), accelerated idioventricular rhythm, ventricular tachycardia, and ventricular fibrillation

Reperfusion arrhythmias

Mechanical Complications of MI:Left ventricular failure due to

1. Ventricular free wall rupture (VFWR)

2.ventricular septal rupture (VSR)


http://emedicine.medscape.com/article/428240-overview

3. papillary muscle rupture with severe mitral regurgitation (MR).

4.RV infarction

5.Infarct expansion, aneurysm, LV remodeling

6. Intracardiac Thrombus

Treatment of ACS:The goals of therapy in acute MI are 1. the expedient restoration of normal coronary blood flow and 2. the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient's failure to recognize MI symptoms quickly and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals. “Time is muscle” guides the management decisions in acute STEMI, and an early invasive approach is the standard of care for acute NSTEMI

Treatment of STEMI ((6A))ADMISSION & CANNULAASSURANCEANALGESIAANGESIEDASPIRIN 600MG CRUSHEDAIR- OXYGENTHROMBOLYSIS FOR STEMI & LBBB/NG &HEPARIN FOR NSTEMI• ASA• NTG (consider MSO4 if pain not relieved)• Beta Blocker• Heparin/LMWH• ACE-I after 24 hrs• +/-Clopidogrel • +/- Statin• Activate the Cath Lab!!!

Pain Control

Pain from MI is often intense and requires prompt and adequate analgesia. The agent of choice is morphine sulfate, IV at 5 to 15 minute intervals at doses of 2 to 4 mg OR pethidine 50mg-150mg. Reduction in myocardial


http://emedicine.medscape.com/article/155618-overview

ischemia also serves to reduce pain, so oxygen therapy, nitrates, and beta blockers remain the mainstay of therapy.

Fibrinolytics

Restoration of coronary blood flow in MI patients can be accomplished pharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy is indicated for patients who present with a STEMI within 12 hours of symptom onset without a contraindication. These are streptokinase. Metalase , tissue plasminogen activator.

Absolute contraindications to fibrinolytic therapy

1. Allergy to thrombolysis 2. History of intracranial hemorrhage3. Ischemic stroke or closed head injury within the past 3 months4. Presence of an intracranial malignancy5. Signs of an aortic dissection6. Active bleeding(duodenal ulcer,varices, haemophylia).

Fibrinolytic therapy is primarily used at facilities without access to an experienced interventionalist within 90 minutes of presentation.

Cautions/Relative Contraindications

■ Severe uncontrolled hypertension on presentation (BP >180/110 mm Hg)

■ History of prior cerebrovascular accident or known intracerebral disease not covered in contraindications

■ Current use of anticoagulants in therapeutic doses (international normalized ratio [INR] ≥2:3); known bleeding diathesis

■ Recent trauma (within 2–4 weeks), including head trauma

or traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation (CPR) or major surgery (<3 weeks)


As a class, the plasminogen activators have been shown to restore normal coronary blood flow in 50% to 60% of STEMI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective within the first hour of symptom onset and when the door-to-needle time is 30 minutes or less

Supplemental Oxygen

Oxygen should be administered to patients with symptoms or signs of pulmonary edema or with pulse oximetry less than 90% saturation. AIM- the erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissues may be diminished. In some cases, elevated pulmonary capillary pressure and pulmonary edema can decrease oxygen uptake as a result of impaired pulmonary alveolar-capillary diffusion. Supplemental oxygen increases the driving gradient for oxygen uptake.

Arterial blood that is at its maximum oxygen-carrying capacity can potentially deliver oxygen to myocardium in jeopardy during an MI via collateral coronary circulation. The recommended duration of supplemental oxygen administration in a MI is 2 to 6 hours, longer if congestive heart failure occurs or arterial oxygen saturation is less than 90%

Aspirin• Aspirin is an antiplatelet agent that initiates the irreversible inhibition of

cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregation

• Administration of ASA in ACS reduces cardiac endpoints The nidus of an occlusive coronary thrombus is the adhesion of activated

platelets at the site of intimal disruption in an unstable atherosclerotic plaque. Its beneficial effect is observed early in therapy and persists for years with

continued use. The long-term benefit is sustained, even at doses as low as 75 mg/day

ACC/AHA Guidelines for Aspirin Therapy Aspirin should be given in a dose of 75-325 mg/day

to all patients with ACS unless there is a


contraindication (in which case, clopidogrel should be given)

Nitrates

Nitroglycerin is considered a cornerstone of anti-anginal therapy, despite little objective evidence for its benefit.

Mechanism of Action -Relaxes vascular smooth muscle

- Benefit is thought to occur via reduction in myocardial O2 demand

secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reduction.

Titrate to relief of chest pain; chest pain = death of myocardial cellsNo documented mortality benefitContraindications :

1.BP<100mm Hg

2.Pt. Has already taken maximum dose of three doses (1.2mg)

Dose

– .4mg sublingual Tablet or Metered-dose Spray

– .4mg Trans-dermal patch May repeat at 5 minute intervals up to 3 .

If tablet form - Protect potencyStore in original brown bottle,Keep tightly sealed Protect from light, air, heat, Secure new supply every 4 - 6 months

Intravenous nitroglycerin in patients with persistent chest pain after three sublingual nitroglycerin tablets, as well as in patients with

hypertension or HF. However, nitrates must be used with caution or avoided in settings in which hypotension is likely or could result in serious hemodynamic decompensation, such as right ventricular infarction or severe aortic stenosis. In addition, nitrates are contraindicated in patients


who have taken a phosphodiesterase inhibitor for erectile dysfunction (or pulmonary hypertension) within the previous 24 hours

Beta Blockers • Beta Blockers reduce myocardial oxygen demand by reducing heart rate, contractility, and ventricular wall tension

• Administration of beta blockers in ACS reduces cardiac endpoints

AHA/ACC Guidelines for Beta Blocker Therapy

• Intravenous beta blockers should be used initially in all patients (without contraindication) followed by oral beta blockers with the goal being decrease in heart rate to 60 beats per minute

• A combination of beta blockers and nitrates can be viewed as first line therapy in all patients with ACS

Heparin • Heparin (unfractionated heparin or UFH) has traditionally been the mainstay of therapy in acute coronary syndromes as its efficacy has been documented in several large, randomized trials

LMWH • More recent studies indicate that low molecular weight heparin is also effective in the reduction of end points such as myocardial infarction

or death, DVT ,INTRACARDIAC THROMBUS OR PE.• Some studies report that LMWH, when used in combination with ASA, may be superior to continuous infusion of Heparin.

ACC/AHA Guidelines for Heparin Therapy• All patients with acute coronary syndromes should

be treated with a combination of ASA (325 mg/day)


and low molecular weight heparin unless one of the drugs is contraindicated

Enoxaparin 1mg/Kg bd

• UFH if primary PCI• After thrombolysis continue until hospital discharge?

ACE-I To reduce ventricular remodeling over days to weeks after myocardial

damage. However, there is data that a mortality benefit exists when

these agents are used early in the course of ACS.

• Administration of ACE-I in ACS reduces cardiac endpoints

AHA/ACC Guidelines for ACE-I Therapy • ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension

and other clear cut contraindications are absentStatins • Statins may be of benefit in ACS• Mechanisms ---plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation.

IIBIIIA Inhibitors

• More potent inhibition of platelet aggregation may be of importance in patients with ACS that is associated with unstable coronary lesion and thrombus formation.

This can be achieved by the use of GP IIBIIIA inhibitors• Administration of IIBIIIA inhibitors reduces cardiac endpoints


AHA/ACC Guidelines for use of IIBIIIA inhibitors • A IIBIIIA inhibitor should be administered to all patients in whom a

percutaneous intervention is planned (in addition to heparin/ASA) • Eptifibatide or Tirofiban should be administered to patients with

ACS in whom PCI is not planned if other high risk features are present (TIMI risk score >3)

TIMI Risk Score• Age >65 yrs• Daily ASA Therapy (>7 days prior to event)• Symptoms of Unstable Angina• Documented CAD (stenosis > 50%)• 3 or more traditional cardiac risk factors• Elevated cardiac enzymes• ECG changes

Score of 3 or less = low risk Score of 4-5 = intermediate risk (use IIBIIIA)

Score of 6-7 = high risk (use IIBIIIA)

Clopidogrel • Clopidogrel is a potent antiplatelet agent• It should be administered to all patients who cannot take ASA• The CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin in

patients going for PCI,STEMI ,NSTEMI.• Give 300 mg loading dose followed by 75mg/day

AHA/ACC Guidelines for Clopidogrel

• Clopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intolerance• In hospitalized patients in whom an early, noninterventional approach is


planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months.

Do not use clopidogrel if there is any possibility patient may be candidate for CABG

Emergent Revascularization • In the setting of STEMI primary PCI is associated with better outcomes than

thrombolysis

• Emergent PCI is also indicated in the setting of a new LBBB PCI = percutaneous coronary intervention AHA/ACC Guidelines for Primary PCI

• Primary PCI is indicated as an alternative to thrombolysis when the following criteria are met: – STEMI or new LBBB – Can undergo PCI within 12 hours of the onset of symptoms – The MD doing the intervention does more than 75 PCI’s/yr

– The procedure is done in a center that does more than 200 PCI’s/yr and has surgical backup

Treatment of NSTEMI/USA• ASA• NTG (consider MSO4 if pain not relieved)• Beta Blocker• Heparin/LMWH• ACE-I• +/- Statin• +/- Clopidogrel (don’t give if CABG is a possibility)• +/- IIBIIIA inhibitors (based on TIMI risk score)

ANTIAARYTHMIC FOR ARRTHMIA AND DIURETIC FOR FAILUREDILTIAZEM (CCB) FOR CORONARY SPASM


Acute coronary syndrome

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