Ischemic Heart DiseaseIschemic Heart Disease

William J Hunter MDWilliam J Hunter MD

Types of Heart DiseaseTypes of Heart Disease

•Acquired Heart DiseaseAcquired Heart Disease

•Congenital Heart DiseaseCongenital Heart Disease

Acquired Heart DiseaseAcquired Heart Disease

• Ischemic Heart DiseaseIschemic Heart Disease

•Hypertensive Heart DiseaseHypertensive Heart Disease

•Valvular Heart DiseaseValvular Heart Disease

•Myocardial Heart DiseaseMyocardial Heart Disease

Ischemic Heart DiseaseIschemic Heart Disease

•Supply of oxygen in the coronary Supply of oxygen in the coronary arterial blood is inadequate to arterial blood is inadequate to provide for the oxygen demands of provide for the oxygen demands of the heart.the heart.

Epidemiology of ischemic Epidemiology of ischemic heart diseaseheart disease

• 500,000 die500,000 die

•Overall rate has fallen since 1980Overall rate has fallen since 1980

•Prevention - working on risk factors: Prevention - working on risk factors: smoking, hypertension, cholesterol, smoking, hypertension, cholesterol, better diabetic control, aspirin better diabetic control, aspirin prophylaxis prophylaxis

•Therapeutic advances- new medications, Therapeutic advances- new medications, coronary care units, thrombolysis, coronary care units, thrombolysis, angioplasty, stents and coronary bypass angioplasty, stents and coronary bypass surgerysurgery

Results of Ischemic HDResults of Ischemic HD•Angina Pectoris - ASVDAngina Pectoris - ASVD

•Stable anginaStable angina

•Prinzmetal’s angina - spasmPrinzmetal’s angina - spasm

•Preinfarction (unstable) angina - MIPreinfarction (unstable) angina - MI

•Myocardial Infarct- myocardial necrosisMyocardial Infarct- myocardial necrosis

•Sudden cardiac deathSudden cardiac death

•Chronic ischemic HD with heart failure- Chronic ischemic HD with heart failure- ‘focal fibrosis’ or presbycardia ‘focal fibrosis’ or presbycardia

Acute Coronary Acute Coronary SyndromesSyndromes

• The new ‘in’ word- TV adsThe new ‘in’ word- TV ads

•A spectrum -from unstable angina to A spectrum -from unstable angina to acute myocardial infarctacute myocardial infarct

•Atherosclerotic plaque disruption Atherosclerotic plaque disruption and associated platelet-fibrin and associated platelet-fibrin thrombus formationthrombus formation

•Sudden deathSudden death

Acute Acute coronary coronary SyndromeSyndrome

Etiology of Ischemic HDEtiology of Ischemic HD

• 95-98% Atherosclerotic Narrowing 95-98% Atherosclerotic Narrowing with plaqueswith plaques

•Coronary embolism (rare)Coronary embolism (rare)

•Dissecting aneurysm (rare)Dissecting aneurysm (rare)

•Arteritis (polyarteritis, rheumatoid, Arteritis (polyarteritis, rheumatoid, Kawasaki Disease) (rare)Kawasaki Disease) (rare)

•Syphilis (rare)Syphilis (rare)

•Cocaine abuseCocaine abuse

Coronary AtherosclerosisCoronary Atherosclerosis• 90% have at least one 75% occlusion- 90% have at least one 75% occlusion-

the key is acute change of the plaquethe key is acute change of the plaque

•Hemorrhage into the atheromaHemorrhage into the atheroma

•Rupture of the plaque with thrombosisRupture of the plaque with thrombosis

•Erosion or ulceration of the plaque with Erosion or ulceration of the plaque with thrombosisthrombosis

•Most have two arteries involvedMost have two arteries involved

•Most blocks are in the epicardial arteriesMost blocks are in the epicardial arteries

Atherosclerotic plaque

Hemorrhage into plaque compromises lumenHemorrhage into plaque compromises lumen

Cut section of a coronary artery with complete occlusion

Histologic section with recent thrombosis

Rupture of PlaqueRupture of Plaque

Progression of Myocardial necrosis after Progression of Myocardial necrosis after occlusionocclusion

Myocardial InfarctMyocardial Infarct

•Most have Most have

• >75% occlusion of coronary by >75% occlusion of coronary by plaqueplaque

•multi-vessel diseasemulti-vessel disease

•80% have recent thrombus80% have recent thrombus

•LAD most commonly involvedLAD most commonly involved

Typical MITypical MI

• Most have multivessel diseaseMost have multivessel disease

• Ulcerative stenotic plaque or hemorrhage Ulcerative stenotic plaque or hemorrhage into the plaqueinto the plaque

• Platelets aggregatePlatelets aggregate

• Tissue thromboplastin releasedTissue thromboplastin released

• Vasoactive amines releasedVasoactive amines released

• Thrombosis and spasm occurThrombosis and spasm occur

• Ischemic necrosisIschemic necrosis

Arteries involvedArteries involved

• LAD (40 - 50%) Anterior wall, apex, LAD (40 - 50%) Anterior wall, apex, Anterior 2/3 septumAnterior 2/3 septum

•RCA (30- 40%) Post wall, post 1/3 RCA (30- 40%) Post wall, post 1/3 septumseptum

• LCA (15- 20%) Lateral wallLCA (15- 20%) Lateral wall

Role of Hemodynamic Role of Hemodynamic ChangesChanges

•Sudden drop in BPSudden drop in BP

•Must be difference in pressure Must be difference in pressure between coronary ostia and coronary between coronary ostia and coronary sinussinus

Role of VasospasmRole of Vasospasm

•Vasospasm documented in anginaVasospasm documented in angina

•Spasm can cause rupture of plaquesSpasm can cause rupture of plaques

•Rare cases of MI after spasmRare cases of MI after spasm

Role of PlateletRole of Platelet

•Rupture of Plaques > adherenceRupture of Plaques > adherence

• The aggregation contributes to The aggregation contributes to blockageblockage

• Thromboxane, histamine, serotonin Thromboxane, histamine, serotonin => vasospasm=> vasospasm

•ASA helpsASA helps

Supply of O2 in the BloodSupply of O2 in the Blood•AnemiaAnemia

•CO and cyanideCO and cyanide

•O2 demandO2 demand

•HypertensionHypertension

•Valvular diseaseValvular disease

•HyperthyroidismHyperthyroidism

• FeverFever

•CatecholaminesCatecholamines

• (? personality types)(? personality types)

Role of acute Plaque Role of acute Plaque Change in MIChange in MI

•Hemorrhage into the atheroma - Hemorrhage into the atheroma - expanding its volumeexpanding its volume

•Rupture or fissuring, exposing the Rupture or fissuring, exposing the highly thrombogenic plaque highly thrombogenic plaque constituentconstituent

•Erosion or ulcerationErosion or ulceration

•Note that the original plaque may not Note that the original plaque may not have been a significant lesion (no have been a significant lesion (no critical stenosiscritical stenosis

Time of DayTime of Day

•Peak incidence of MI: 6am to noonPeak incidence of MI: 6am to noon

•Adrenergic stimulation of awakening Adrenergic stimulation of awakening can put more stress on the plaquecan put more stress on the plaque

•Surge of blood pressure at same Surge of blood pressure at same time frametime frame

Key Events in Ischemic Key Events in Ischemic DamageDamage

FeatureFeature TimeTime

Onset of ATP depletionOnset of ATP depletion secondssecondsLoss of contractilityLoss of contractility < 2 min< 2 min

ATP reducedATP reduced

to 50%to 50% 10 min10 min

to 10%to 10% 40 min40 min

Irreversible cell injuryIrreversible cell injury 20 -40 min20 -40 min

Microvascular injuryMicrovascular injury > 1 hr > 1 hr

Gross Changes of MIGross Changes of MI• Up to 5 hours- no changesUp to 5 hours- no changes

• 6-24 hour- pallor6-24 hour- pallor

• 24-48 hours- central pallor - hyperemia at margins24-48 hours- central pallor - hyperemia at margins

• 2-5 days - hyperemic border, yellow band, soft 2-5 days - hyperemic border, yellow band, soft dull centerdull center

• 5-10 days- broader yellow border and thin new 5-10 days- broader yellow border and thin new pink borderpink border

• 10 days-3 wks - islands of red brown tissue 10 days-3 wks - islands of red brown tissue surrounded by red-purple granulation tissuesurrounded by red-purple granulation tissue

• 3-6 weeks - fibrosis3-6 weeks - fibrosis

Acute myocardial infarct

Acute myocardial infarct

Acute MI - 4 daysAcute MI - 4 days

Acute MIAcute MI

Myocardial changesMyocardial changes

Histology of MIHistology of MI• 0-6 hours - none (? waviness)0-6 hours - none (? waviness)

• 6-24 hours- eosinophilia, loss of cross 6-24 hours- eosinophilia, loss of cross striationstriation

• 24-48 hours- coagulative necrosis, PMN24-48 hours- coagulative necrosis, PMN

• 2-5 days- phagocytosis, granulation tissue2-5 days- phagocytosis, granulation tissue

• 10 days - 3weeks increasing fibrosis, 10 days - 3weeks increasing fibrosis, PMN’s disappearPMN’s disappear

• 3-6 weeks - maturing fibrosis3-6 weeks - maturing fibrosis

Normal myocardium – note central nuclei and intercalated disks

Early ischemia- contraction bandsEarly ischemia- contraction bands

Early MI – coagulation necrosis. Pyknosis and karyolysis of nuclei

Early coagulation necrosis- loss of myocyte nuclei

MI 4daysMI 4days

Later coagulation necrosis – infiltration of neutrophils

Remote infarct – fibrous scar

Complications of MIComplications of MI•Arrhythmias (90%)Arrhythmias (90%)

•CHF 60%CHF 60%

•Cardiogenic shock 10%Cardiogenic shock 10%

•Rupture (wall, septum, PAP M.) 5-10%Rupture (wall, septum, PAP M.) 5-10%

•Mural thrombus and embolismMural thrombus and embolism

•PericarditisPericarditis

•Ventricular AneurysmsVentricular Aneurysms

•Papillary muscle dysfunctionPapillary muscle dysfunction

Complications of MI – Hemopericardium due to rupture

Rupture of myocardial infarct hemopericardium

Area of infarct

MI with ruptureMI with rupture

Rupture of myocardial infarct

Rupture of ventricularseptum– giving rise to Acute right heart failure

Rupture of papillary muscle

Infarct of papillary muscle – leading to mitral valve dysfunction

Mural thrombus

Ventricular aneurysm due to MI - with Ventricular aneurysm due to MI - with mural thrombusmural thrombus

thrombusthrombus

Diagnosis of MIDiagnosis of MI

•Symptoms and signsSymptoms and signs

• 1/2 may be silent1/2 may be silent

•EKG- New Q-wave, S-T segment and EKG- New Q-wave, S-T segment and T-wave changesT-wave changes

•Enzymes, CK, (CKMB) , TroponinsEnzymes, CK, (CKMB) , Troponins

•Drs. Lynch & Baltaro will talk more Drs. Lynch & Baltaro will talk more about thisabout this

Subendocardial Infarct- Subendocardial Infarct- non Q wave infarctnon Q wave infarct

• severe ASCDsevere ASCD

• no critical stenosisno critical stenosis

•Multifocal or bridges arterial zonesMultifocal or bridges arterial zones

• diabetesdiabetes

•DangerousDangerous

Infarct Modification After Infarct Modification After ReperfusionReperfusion

•Reperfusion early- may prevent most Reperfusion early- may prevent most necrosisnecrosis

•Hemorrhage - leaky damaged vesselsHemorrhage - leaky damaged vessels

•Necrosis with contraction bandsNecrosis with contraction bands

• Increased oxygen free radicalsIncreased oxygen free radicals

Effects of reperfusionEffects of reperfusion