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DEFINITIONAcute myocardial infarction can be defined from a number of different perspectives related to clinical, electrocardiographic (ECG), bio-chemical, and pathological characteristics.The present guidelines pertain to patients presenting with ischaemic symptoms and persistent ST-segment elevation on the ECG (STEMI). The great majority of these patients will show a typical rise of biomarkers of myocardial necrosis and progress to Q-wave myocardial infarction. Separate guidelines patients presenting with ischaemic symptoms but withoutpersistent ST-segment elevation.

2012 by the European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, Inc., and the World Heart Federation1. Typical rise and/or fall of biochemical markers of myocardial necrosis with at least one of the following :a. Ischemic symptomsb. Development of pathologic Q waves in the ECGc. Electrocardiographic changes indicative of ischemia (ST-segment elevation or depression)d.Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality 2. Pathologic findings of an acute myocardial infarction

Criteria for Acute, Evolving, or Recent MI Either of the following criteria satisfies the diagnosis for acute, evolving, or recent MI:

2012 by the European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, Inc., and the World Heart FederationEPIDEMIOLOGIPATHOGENESISThe hallmark is the sudden imbalance between myocardial oxygen consumption (MVO2) and demand,which is usually the result of coronary artery obstruction. The imbalance may also be caused by other conditions, including excessive myocardial oxygen demand in the setting of a stable flow-limiting lesion; acute coronary insufficiency due to other causes (e.g., vasospastic, angina, coronary embolism, coronary arteritis);Noncoronary causes of myocardial oxygen supply-demand mismatch (e.g. hypotension, severe anemia, hypertension, tachycardia, hypertrophic cardiomyopathy, severe aortic stenosis);Nonischemic myocardial injury (e.g., myocarditis, cardiac contusion, cardiotoxic drugs); and multifactorialCauses that are not mutually exclusive (e.g., stress cardiomyopathy ,pulmonary embolism, severe heart failure [HF], sepsis).Expanding Risk FactorsSmokingHypertensionDiabetes MellitusDyslipidemiaLow HDL < 40Elevated LDL / TGFamily Historyevent in first degree relative >55 male/65 femaleAge-- > 45 for male/55 for femaleChronic Kidney DiseaseLack of regular physical activityObesityLack of Etoh intakeLack of diet rich in fruit, veggies, fiber

Type Miocardial Infarction

2012 by the European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, Inc., and the World Heart Federation

2012 by the European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, Inc., and the World Heart Federation

2012 by the European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, Inc., and the World Heart FederationCLINICAL PRESENTATIONChest pain is the usual symptom which brings these patients to medical attention. Pain is severe, diffuse, retrosternal and radiates to arms or from jaws to umbilicus. Pain does not get relieved with sublingual nitrates or usual pain killers. It is often associated with eructations and retrosternal burning.

Commonly patients mistake it for acid peptic symptoms and waste precious time with antacids. It is accompanied with vomiting, sweating and breathlessness. About 15-20% of infarcts can be painless specially in elderly and diabetics. Equal number may have less characteristic pain than described above. The pain needs to be distinguished from other causes of acute severe chest pain which can bring patients to emergency room.

Pandey et al, 2011Thus, although pain of myocardial infarction is quite distinctive it may be mimicked by other conditions. A good short history of type of pain, duration, accompanying symptoms, risk factors and preceding activities before the pain can be useful. Examination of pulse and blood pressure and respiratory rate help greatly in risk stratification of these patients. Palpation and auscultation are also helpful in these acutely distressed individuals. In the hurry to do an early ECG these things should not be missed.

Pandey et al, 2011ElectrocardiographyECG is generally the first investigation available for making a diagnosis in a patient presenting with acute severe chest pain.Tall T waves and ST elevation are the hallmarks of early presentation within minutes of onset of pain.The third change appearance of Q waves, is delayed and seen after 6 hours of onset. Q waves denote significant myocardial necrosis.The initial changes of upright and tall T wave with concave upward ST segment elevation subsequently, gives way to T wave inversion and ST coving with convexity upwards over one day to one week.

Pandey et al, 2011Shortly after occlusion of a coronary artery, serial ECG changes are detected by leads facing the ischemic zoneFirst, the T waves become tall, symmetrical, and peaked (grade 1 ischemia). Second, there is ST elevation (grade 2 ischemia) without distortion of the terminal portion of the QRS. Third, changes in the terminal portion of the QRS complex may appear (grade 3 ischemia).The changes in the terminal portion of the QRSare explained by prolongation of the electrical conduction in the Purkinje fibers in the ischemic region.

Pandey et al, 2011EchocardiographyEchocardiography is helpful in the evaluation of chest pain, especially during active chest pain. The absence of LV wall motion abnormalities during chest pain usually but not always excludes myocardial ischemia or infarction, and the presence of regional wall motion abnormalities helps in confirming the diagnosis

Pandey et al, 2011CARDIAC BIOMARKERSCardiac biomarkers have conventionally being used for diagnosis of acute myocardial infarction.These have also been used in patients with NSTEMI and unstable angina for finding high risk individuals. Elevation of CPK, CPK-MB and Troponins I and T occurs in all patients with myocardial necrosis that is seen in myocardial infarction. Serial CK-MB estimations were done earlier for estimation of infarct size before echocardiography.

Pandey et al, 2011Cardiac markersTroponin ( T, I)

Very specific and more sensitive than CKRises 4-8 hours after injuryMay remain elevated for up to two weeksCan provide prognostic informationTroponin T may be elevated with renal dz, poly/dermatomyositis

CK-MB isoenzyme

Rises 4-6 hours after injury and peaks at 24 hoursRemains elevated 36-48 hoursPositive if CK/MB > 5% of total CK and 2 times normalElevation can be predictive of mortalityFalse positives with exercise, trauma, DM,History, PhysicalEKGChest PainSTEMIUA/NSTEMI/High RiskMod RiskLow RiskDefinite Non-CardiacInitial Risk Stratification SchemeRisk Stratification UA or NSTEMI- Evaluate for Invasive vs. conservative treatment- Directed medical therapyBased on initialEvaluation, ECG, andCardiac markers- Assess for reperfusion- Select & implement reperfusion therapy- Directed medical therapySTEMI Patient?YESNOSTEMI cardiac care STEP 1: AssessmentTime since onset of symptoms90 min for PCI / 12 hours for fibrinolysis

Is this high risk STEMI?KILLIP classificationIf higher risk may manage with more invasive rx

Determine if fibrinolysis candidateMeets criteria with no contraindications

Determine if PCI candidateBased on availability and time to balloon rx

2008 by the European Society of Cardiology,STEMI cardiac careSTEP 2: Determine preferred reperfusion strategy Fibrinolysis preferred if: 90mindoor to balloon minus door to needle > 1hrDoor to needle goal 3 hrHigh risk STEMIKillup 3 or higherSTEMI dx in doubt

2008 by the European Society of Cardiology,Medical Therapy

Morphine AnalgesiaReduce pain/anxietydecrease sympathetic tone, systemic vascular resistance and oxygen demandCareful with hypotension, hypovolemia, respiratory depression

Oxygen Up to 70% of ACS patient demonstrate hypoxemiaMay limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation

2008 by the European Society of Cardiology,Nitroglycerin Analgesiatitrate infusion to keep patient pain freeDilates coronary vesselsincrease blood flowReduces systemic vascular resistance and preloadCareful with recent ED (erectile dysfunction) meds, hypotension, bradycardia, tachycardia, RV infarction

Aspirin (160-325mg chewed & swallowed) Irreversible inhibition of platelet aggregationStabilize plaque and arrest thrombusReduce mortality in patients with STEMICareful with active gastrointestinal bleeding, hypersensitivity, bleeding disorders 2008 by the European Society of Cardiology,Beta-Blockers 14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMIApproximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptomsBe aware of contraindications (CHF, Heart block, Hypotension)Reassess for therapy as contraindications resolve

ACE-Inhibitors / ARB Start in patients with anterior MI, pulmonary congestion, LVEF < 40% in absence of contraindication/hypotensionStart in first 24 hoursARB as substitute for patients unable to use ACE-I 2008 by the European Society of Cardiology,Heparin LMWH or UFH (max 4000u bolus, 1000u/hr)Indirect inhibitor of thrombin less supporting evidence of benefit in era of reperfusionAdjunct to surgical revascularization and thrombolytic / PCI reperfusion24-48 hours of treatmentCoordinate with PCI team Used in combo with aspirin and/or other platelet inhibitorsChanging from one to the other not recommended

2008 by the European Society of Cardiology,Additional medication therapyClopidodrel Irreversible inhibition of platelet aggregationUsed in support of cath / PCI intervention or if unable to take aspirin3 to 12 month duration depending on scenario

Glycoprotein IIb/IIIa inhibitors Inhibition of platelet aggregation at final common pathwayIn support of PCI intervention as early as possible prior to PCI 2008 by the European Society of Cardiology,Unstable angina/NSTEMI cardiac careEvaluate for conservative vs. invasive therapy based upon:Risk of actual ACSTIMI risk scoreACS risk categories per AHA guidelines

LowIntermediateHighAssessmentFindings indicating HIGH likelihood of ACSFindings indicating INTERMEDIATE likelihood of ACS in absence of high-likelihood findingsFindings indicating LOW likelihood of ACS in absence of high- or intermediate-likelihood findingsHistoryChest or left arm pain or discomfort as chief symptomReproduction of previous documented anginaKnown history of coronary artery disease, including myocardial infarctionChest or left arm pain or discomfort as chief symptomAge > 50 yearsProbable ischemic symptomsRecent cocaine usePhysical examinationNew transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or ralesExtracardiac vascular diseaseChest discomfort reproduced by palpationECGNew or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptomsFixed Q wavesAbnormal ST segments or T waves not documented to be newT-wave flattening or inversion of T waves in leads with dominant R wavesNormal ECGSerum cardiac markersElevated cardiac troponin T or I, or elevated CK-MBNormal Normal Risk Stratification to Determine the Likelihood of Acute Coronary SyndromeACS risk criteriaLow Risk ACS

No intermediate or high risk factors

10 minutes rest pain, now resolved

T-wave inversion > 2mm

Slightly elevated cardiac markers

High Risk ACS

Elevated cardiac markersNew or presumed new ST depressionRecurrent ischemia despite therapyRecurrent ischemia with heart failureHigh risk findings on non-invasive stress testDepressed systolic left ventricular functionHemodynamic instabilitySustained Ventricular tachycardiaPCI with 6 monthsPrior Bypass surgery

Conservative therapyInvasive therapyChest Pain centerLOW RISKINTERMEDIATE RISKHIGH RISKConservative Therapy for UA/NSTEMIEarly revascularization or PCI not plannedMONA + Anticoagulant ClopidogrelGlycoprotein IIb/IIIa inhibitorsOnly in certain circumstances (planning PCI, elevated TnI/T)Surveillence in hospitalSerial ECGsSerial MarkersInvasive therapy option UA/NSTEMICoronary angiography and revascularization within 12 to 48 hours after sign and symptomFor high risk ACS (class I, level A)MONA + AnticoagulantClopidogrel20% reduction death/MI/Stroke 1 month minimum duration and possibly up to 9 monthsGlycoprotein IIb/IIIa inhibitors