Myocardial InfarctionMyocardial Infarction

Khaled Dajani, MD, MBAKhaled Dajani, MD, MBA

Division of CardiologyDivision of Cardiology

BackgroundBackground

Myocardial Infarction if the rapid Myocardial Infarction if the rapid development of myocardial necrosis by a development of myocardial necrosis by a critical imbalance between oxygen supply critical imbalance between oxygen supply and demand to the myocardiumand demand to the myocardium

ClassificationClassification

Acute coronary syndromes includeAcute coronary syndromes include

ST-elevation MI (STEMI)ST-elevation MI (STEMI)

Non ST-elevation MI ( NSTEMI)Non ST-elevation MI ( NSTEMI)

Unstable AnginaUnstable Angina

Cardiac markers in circulation indicates Cardiac markers in circulation indicates myocardial infarction and help categorize myocardial infarction and help categorize MI and is a useful adjunct to diagnosisMI and is a useful adjunct to diagnosis

ClassificationClassification

Anatomic or morphologicAnatomic or morphologic

Transmural= Full thicknessTransmural= Full thickness

Non-transmural= Partial thicknessNon-transmural= Partial thickness

ECGECG

Q wave MIQ wave MI

Non Q wave MINon Q wave MI

Does not distinguish transmural from a non-Does not distinguish transmural from a non-transmural MI as determined by pathologytransmural MI as determined by pathology

PrevalencePrevalence

In the US, 1.3 million cases of nonfatal MI In the US, 1.3 million cases of nonfatal MI were reported in 2006were reported in 2006

Incidence of 600 per 100,000 peopleIncidence of 600 per 100,000 people

Increase in the proportion of NSTEMI Increase in the proportion of NSTEMI compared to STEMIcompared to STEMI

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

HistoryHistory

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

HistoryHistory

Chest Pain- anterior precordium tightnessChest Pain- anterior precordium tightness

Pain may radiate to jaw, neck and Pain may radiate to jaw, neck and epigastriumepigastrium

Dyspnea- angina equivalent, poor LV Dyspnea- angina equivalent, poor LV functionfunction

Nausea/abdominal pain with posterior MINausea/abdominal pain with posterior MI

AnxietyAnxiety

HistoryHistory

Nausea with and without vomitingNausea with and without vomiting

Diaphoresis or sweatingDiaphoresis or sweating

Syncope or near syncopeSyncope or near syncope

Elderly present with MS changes, fatigue, Elderly present with MS changes, fatigue, syncope or weaknesssyncope or weakness

As many as half of MI are clinically silentAs many as half of MI are clinically silent

PhysicalPhysical

The physical exam can often be The physical exam can often be unremarkableunremarkable

HypertensionHypertension

HypotensionHypotension

Acute valvular dysfunction may be presentAcute valvular dysfunction may be present

RalesRales

Neck vein distentionNeck vein distention

PhysicalPhysical

Third heart sound may be presentThird heart sound may be present

A fourth heart sound poor LV complianceA fourth heart sound poor LV compliance

DysrhythmiasDysrhythmias

Low grade feverLow grade fever

CausesCauses

Most frequent cause is rupture of an Most frequent cause is rupture of an atherosclerotic lesion within coronary wall atherosclerotic lesion within coronary wall with subsequent spasm and thrombus with subsequent spasm and thrombus formationformation

Coronary artery vasospasmCoronary artery vasospasm

Ventricular hypertrophyVentricular hypertrophy

HypoxiaHypoxia

Coronary artery emboliCoronary artery emboli

CausesCauses

CocaineCocaine

ArteriesArteries

Coronary anomaliesCoronary anomalies

Aortic dissectionAortic dissection

Pediatrics Kawasaki disease, Takayasu Pediatrics Kawasaki disease, Takayasu arteritisarteritis

Increased afterload which increases Increased afterload which increases myocardial demandmyocardial demand

Risk factors for atherosclerosisRisk factors for atherosclerosis

AgeAge

Male genderMale gender

SmokingSmoking

Hypercholesterolemia and triglyceridemiaHypercholesterolemia and triglyceridemia

Diabetes MellitusDiabetes Mellitus

Poorly controlled hypertensionPoorly controlled hypertension

Type A personalityType A personality

Risk factors for atherosclerosisRisk factors for atherosclerosis

Family HistoryFamily History

Sedentary lifestyleSedentary lifestyle

DifferentialsDifferentials

Acute coronary syndromeAcute coronary syndrome

AnxietyAnxiety

Aortic stenosisAortic stenosis

AsthmaAsthma

Cholecystitis and biliary colicCholecystitis and biliary colic

CholethiasisCholethiasis

COPDCOPD

DifferentialsDifferentials

Aortic DissectionAortic Dissection

EndocarditisEndocarditis

EsophagitisEsophagitis

ShockShock

MyocarditisMyocarditis

PericarditisPericarditis

Pulmonary embolismPulmonary embolism

Mechanisms of Myocardial damageMechanisms of Myocardial damage

The severity of an MI is dependent of three The severity of an MI is dependent of three factorsfactors

The level of the occlusion in the coronaryThe level of the occlusion in the coronary

The length of time of the occlusionThe length of time of the occlusion

The presence or absence of collateral The presence or absence of collateral circulationcirculation

Cardiac BiomarkersCardiac Biomarkers

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

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

These biomarkers have a characteristic These biomarkers have a characteristic rise and fall pattern rise and fall pattern

Troponin T and ITroponin T and I

These isoforms are very specific for These isoforms are very specific for cardiac injurycardiac injury

Preferred markers for detecting myocardial Preferred markers for detecting myocardial cell injurycell injury

Rise 2-6 hours after injuryRise 2-6 hours after injury

Peak in 12-16 hoursPeak in 12-16 hours

Stay elevated for 5-14 daysStay elevated for 5-14 days

Creatinine Kinase ( CK-MB)Creatinine Kinase ( CK-MB)

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

Increased in over 90% of myocardial Increased in over 90% of myocardial infractioninfraction

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

Creatine Kinase (MB)Creatine Kinase (MB)

Time sequence after myocardial infarctionTime sequence after myocardial infarction

Begins to rise 4-6 hoursBegins to rise 4-6 hours

Peaks 24 hoursPeaks 24 hours

returns to normal in 2 daysreturns to normal in 2 days

MB2 released from heart muscle and MB2 released from heart muscle and converted to MB1.converted to MB1.

A level of MB2 > or = 1 and a ratio of A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injuryMB2/MB1 > 1.5 indicates myocardial injury

MyoglobinMyoglobin

Damage to skeletal or cardiac muscle Damage to skeletal or cardiac muscle release myoglobin into circulationrelease myoglobin into circulation

Time sequence after infarctionTime sequence after infarction

Rises fast 2hoursRises fast 2hours

Peaks at 6-8 hoursPeaks at 6-8 hours

Returns to normal in 20-36 hoursReturns to normal in 20-36 hours

Have false positives with skeletal muscle Have false positives with skeletal muscle injury and renal failureinjury and renal failure

Renal Failure and Renal Renal Failure and Renal TransplantationTransplantation

Diagnostic accuracy of serum markers of Diagnostic accuracy of serum markers of cardiac injury are altered in patients with cardiac injury are altered in patients with renal failurerenal failureCardiac troponins decreased diagnostic Cardiac troponins decreased diagnostic sensitivity and specificity in patients sensitivity and specificity in patients receiving renal replacement therapyreceiving renal replacement therapyCurrent data show levels of troponin I are Current data show levels of troponin I are unaltered while levels of troponin T may unaltered while levels of troponin T may be elevatedbe elevated

CBCCBC

CBC is indicated if anemia is suspected as CBC is indicated if anemia is suspected as precipitantprecipitant

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

Chemistry ProfileChemistry Profile

Potassium and magnesium levels should Potassium and magnesium levels should be monitored and corrected be monitored and corrected

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

C-reactive Protein (CRP)C-reactive Protein (CRP)

C- reactive protein is a marker of acute C- reactive protein is a marker of acute inflammationinflammation

Patients without evidence of myocardial Patients without evidence of myocardial necrosis but with elevated CRP are at necrosis but with elevated CRP are at increased risk of an eventincreased risk of an event

Chest X-RayChest X-Ray

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

Chest radiography also reveals Chest radiography also reveals complications of myocardial infarction complications of myocardial infarction such as heart failuresuch as heart failure

EchocardiographyEchocardiography

Use 2-dimentional and M mode Use 2-dimentional and M mode echocardiography when evaluating overall echocardiography when evaluating overall ventricular function and wall motion ventricular function and wall motion abnormalitiesabnormalities

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

ElectrocardiogramElectrocardiogram

A normal ECG does not exclude ACSA normal ECG does not exclude ACS

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

Intermediate probability ST depressionIntermediate probability ST depression

T wave inversions are less specificT wave inversions are less specific

Localization of MILocalization of MI

ST elevation onlyST elevation onlyInferior wall- II, III, aVFInferior wall- II, III, aVFLateral wall_ I, aVL, V4-V6Lateral wall_ I, aVL, V4-V6Anteroseptal- V1-V3Anteroseptal- V1-V3Anterolateral- V1-V6Anterolateral- V1-V6Right ventricular- RV4, RV5Right ventricular- RV4, RV5Posterior- R/S ratio >1 in V1 and T wave Posterior- R/S ratio >1 in V1 and T wave inversioninversion

TherapyTherapy

The goals of therapy in AMI The goals of therapy in AMI are the expedient restoration are the expedient restoration of normal coronary flow and of normal coronary flow and the maximum salvage of the maximum salvage of functional myocardiumfunctional myocardium

Antiplatelet AgentsAntiplatelet Agents

Aspirin at lease 160mg immediately Aspirin at lease 160mg immediately

Interferes with function of cyclooxygenase Interferes with function of cyclooxygenase and inhibits the formation of thromboxaneand inhibits the formation of thromboxane

ASA alone has one of the greatest impact ASA alone has one of the greatest impact on the reduction of MI mortality.on the reduction of MI mortality.

Clopidogrel, ticlopidine, have not been Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior shown in any large scal trail to be superior to Aspirin in acute MIto Aspirin in acute MI

Supplemental OxygenSupplemental Oxygen

Because MI impairs the circulatory Because MI impairs the circulatory function of the heart, oxygen extraction by function of the heart, oxygen extraction by the heart and other tissues may be the heart and other tissues may be diminished diminished

Supplemental oxygen should be Supplemental oxygen should be administered to patient with symptoms and administered to patient with symptoms and or signs of pulmonary edema or pulse or signs of pulmonary edema or pulse oximetry readings less than 90%.oximetry readings less than 90%.

NitratesNitrates

IV nitrates to all patients with MI and IV nitrates to all patients with MI and congestive heart failure, persistent congestive heart failure, persistent ischemia, hypertension, or large anterior ischemia, hypertension, or large anterior wall MIwall MIPrimary benefit vasodilator effectPrimary benefit vasodilator effectMetabolized to nitric oxide in the vascular Metabolized to nitric oxide in the vascular endothelium, relaxes endotheliumendothelium, relaxes endotheliumVasodilatation reduces myocardial oxygen Vasodilatation reduces myocardial oxygen demand and preload and afterloaddemand and preload and afterload

Beta-blockersBeta-blockers

Recommended within 12 hours of MI Recommended within 12 hours of MI symptoms and continued indefinitelysymptoms and continued indefinitely

Reduces Myocardial mortality by Reduces Myocardial mortality by decreasing arrythmogenic deathdecreasing arrythmogenic death

Decrease the rate and force of myocardial Decrease the rate and force of myocardial contraction and decreases overall oxygen contraction and decreases overall oxygen demanddemand

Unfractionated heparinUnfractionated heparin

Forms a chemical complex with Forms a chemical complex with antithrombin III inactivates both free antithrombin III inactivates both free thrombin and factor Xathrombin and factor Xa

Recommended in patients with MI who Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with undergo PTCA or fibrinolytic therapy with alteplasealteplase

Low-molecular weight heparinLow-molecular weight heparin

Direct activity against factors Xa and IIaDirect activity against factors Xa and IIaProven to be effective in treating ACS that Proven to be effective in treating ACS that are characterized by unstable angina or are characterized by unstable angina or non ST- elevation MInon ST- elevation MITheir fixed doses are easy to administer Their fixed doses are easy to administer and laboratory testing to measure their and laboratory testing to measure their therapeutic effect is not necessary makes therapeutic effect is not necessary makes them attractive alternative of un-them attractive alternative of un-fractionated heparinfractionated heparin

ThrombolyticsThrombolytics

Indicated with MI and ST segment Indicated with MI and ST segment elevation greater than 0.1mV in 2 elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset contiguous ECG leads, or new onset LBBB, who present less than 12 hours but LBBB, who present less than 12 hours but not more than 24 hours after symptom not more than 24 hours after symptom onsetonsetThe most critical variable in achieving The most critical variable in achieving successful fibrinolysis is time form successful fibrinolysis is time form symptom onset to drug administrationsymptom onset to drug administration

ThrombolyticsThrombolytics

As a class the plasminogen activators have As a class the plasminogen activators have been shown to restore coronary blood flow in 50-been shown to restore coronary blood flow in 50-80% of patients80% of patients

Contraindication active intracranial bleeding, Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, CVA 2months, CNS neoplasm, HTN, coagulopathycoagulopathy

Retaplase slightly higher angiographic patency Retaplase slightly higher angiographic patency but did not translate into survival benefitbut did not translate into survival benefit

Intracranial bleed risk major drawbackIntracranial bleed risk major drawback

Glycoprotein IIb/IIIa AntagonistsGlycoprotein IIb/IIIa Antagonists

Potent inhibitors of platelet aggregationPotent inhibitors of platelet aggregation

Use during PCI and in patients with high Use during PCI and in patients with high risk features ACS have been shown to risk features ACS have been shown to reduce the composite end points of death, reduce the composite end points of death, reinfraction and the need for target lesionreinfraction and the need for target lesion

Percutanous Coronary InterventionPercutanous Coronary Intervention

Alternative if performed by skilled operator Alternative if performed by skilled operator in an experienced centerin an experienced centerStandard is a “ door to balloon” time of 90 Standard is a “ door to balloon” time of 90 minutesminutesPCI can successfully restore coronary PCI can successfully restore coronary blood flow in 90 to 95% of MI patientsblood flow in 90 to 95% of MI patientsPCI definitive survival advantage over PCI definitive survival advantage over fibrinolytics for MI patients who are in fibrinolytics for MI patients who are in cardiogenic shockcardiogenic shock

Surgical RevascularizationSurgical Revascularization

Emergent or surgical revascularization in Emergent or surgical revascularization in setting of failed PTCA in patients with setting of failed PTCA in patients with hemodynamic instability and coronary hemodynamic instability and coronary anatomy amendable to surgical graftinganatomy amendable to surgical graftingAlso indicated of mechanical Also indicated of mechanical complications of MI including VSD, free complications of MI including VSD, free wall rupture, or acute MRwall rupture, or acute MRCarries a higher risk of perioperative Carries a higher risk of perioperative mortality than elective CABGmortality than elective CABG

Lipid ManagementLipid Management

All post MI patients should be on AMA All post MI patients should be on AMA step II diet ( < 7% of calories from step II diet ( < 7% of calories from saturated fats)saturated fats)Post MI patients with LDL > 100 mg/dl are Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try recommended to be on drug therapy to try to lower levels to <100 mg/dlto lower levels to <100 mg/dlRecent data indicate that all MI patients Recent data indicate that all MI patients should be on statin therapy, regardless of should be on statin therapy, regardless of lipid levels or diet lipid levels or diet

Long term MedicationsLong term Medications

Most oral medications instituted in the Most oral medications instituted in the hospital at the time of MI are continued hospital at the time of MI are continued long termlong term

Aspirin, beta blockers and statin are Aspirin, beta blockers and statin are continued indefinitelycontinued indefinitely

ACEI indefinitely in patients with CHF, ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or ejection fraction <.40, hypertension, or diabetesdiabetes

Thank You!Thank You!