1 Pathophysiology & Clinical Presentations Acute Coronary Syndromes

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Pathophysiology & Pathophysiology & Clinical PresentationsClinical Presentations

Acute Coronary SyndromesAcute Coronary Syndromes

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Ischemic Heart Disease - OverviewIschemic Heart Disease - Overview

Atherosclerosis

Atherothrombosis

Pathophysiology

Clinical Presentations

Silent ischemia

Stable angina Acute Coronary Syndromes

ParametersAnatomy: Atheroma / Atherothrombosis

Subjective: Angina

Objective: EKG T wave ST seg changes

Chemistry: Cardiac serum biomarkers:

CPK, CK-MB, Troponins

Epicardial & Microvascular Spam

Prevalence & severity of stenosis

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Events During AtherogenesisEvents During Atherogenesis

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P x r

2hWall Stress =

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ISCHEMIC CASCADEISCHEMIC CASCADE

Predictable sequence of Predictable sequence of pathophysiologic events post pathophysiologic events post

myocardial supply/demand imbalancemyocardial supply/demand imbalance

•Biochemical metabolic actions

•Flow Maldistribution

•Hypoperfusion

•(Rales)

Angina / SI

• Compliance

• Contractility

• EF

• LVEDP

•(S4)Nuclear

Echo

EKG

TIME FROM ONSET OF ISCHEMIA

± 45 sec.

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Effect of Fixed Stenosis on Myocardial Blood Flow

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Progression of coronary plaque over time Clinical FindingsProgression of coronary plaque over time Clinical Findings

Acute Coronary SyndromesSudden Cardiac Death

Acute silent occlusive process

Angina pectoris

Thrombogenicrisk factors

Atherogenic risk factors

Endothelial dysfunction

20 years 60 yearsAge

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IHD – Clinical SpectrumIHD – Clinical SpectrumChronicChronic

Stable AnginaStable AnginaSilent IschemiaSilent IschemiaMixed AnginaMixed AnginaMicrovascular Angina Microvascular Angina

(Syndrome X)(Syndrome X)Stunned & HibernatingStunned & Hibernating

Acute Acute Unstable AnginaUnstable AnginaAcute Myocardial Acute Myocardial

Infarction (NSTEMI, Infarction (NSTEMI, STEMI)STEMI)

Sudden Cardiac DeathSudden Cardiac DeathPrinzmetal AnginaPrinzmetal Angina

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Clinical Classification of Chest PainClinical Classification of Chest PainTypical angina (defineTypical angina (define))1.1.Substernal chest discomfort with a characteristic Substernal chest discomfort with a characteristic

quality and duration that isquality and duration that is2.2.Provoked by exertion or emotional stress andProvoked by exertion or emotional stress and3.3.Relieved by rest or nitroglycerinRelieved by rest or nitroglycerinAtypical angina ( probable)Atypical angina ( probable) Meets 2 of the above characteristicsMeets 2 of the above characteristicsNoncardiac chest painNoncardiac chest pain Meets one or none of the typical angina Meets one or none of the typical angina

characteristicscharacteristicsDIFFERENTIAL DIAGNOSIS OF CHEST PAINDIFFERENTIAL DIAGNOSIS OF CHEST PAIN1.1.Cardiovascular: Pericarditis, Aortic Valve Disease, Cardiovascular: Pericarditis, Aortic Valve Disease,

Aortic Dissection, Pulmonary Embolism, Mitral Aortic Dissection, Pulmonary Embolism, Mitral Valve ProlapseValve Prolapse

2.2.Gastrointestinal: Esophageal, Biliary, Peptic ulcer, Gastrointestinal: Esophageal, Biliary, Peptic ulcer, PancreatitisPancreatitis

3.3.Pulmonary: Pneumothorax, Pneumonia, PleuritisPulmonary: Pneumothorax, Pneumonia, PleuritisChest Wall: Costochondritis, Rib fracture, Herpes Chest Wall: Costochondritis, Rib fracture, Herpes

zosterzosterPsychological: Anxiety disordersPsychological: Anxiety disorders

ClasClasss

ActivActivity ity evokingevoking

angianginana

LimitLimits to s to normalnormal

activactivityity

II ProlProlonged onged exertionexertion

NoneNone

IIII WalkWalking > 2 ing > 2 blocksblocks

SlighSlightt

IIIIII WalkWalking < 2 ing < 2 blocksblocks

MarkMarkeded

IVIV MiniMinimal or mal or restrest

SeveSeverere

Canadian Cardiovascular Society Classification ( CCSC)

*CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II*CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV

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CAD - Clinical SpectrumCAD - Clinical SpectrumChronic ischemic heart diseaseChronic ischemic heart disease Ischemia precipitated by increased myocardial oxygen demand Ischemia precipitated by increased myocardial oxygen demand in the setting of a fixed, not vulnerable atherosclerotic lesion. It is in the setting of a fixed, not vulnerable atherosclerotic lesion. It is called called Stable AnginaStable Angina when the clinical characteristics (Angina when the clinical characteristics (Angina attacks) do not change in frequency, duration, precipitating attacks) do not change in frequency, duration, precipitating causes, or easy with the angina is relieved, for at least 60 days.causes, or easy with the angina is relieved, for at least 60 days.

--Silent Ischemia, -Mixed Angina -Syndome X -Silent Ischemia, -Mixed Angina -Syndome X -Stunning & Hibernating.Stunning & Hibernating.Acute Coronary Syndromes (ACS)Acute Coronary Syndromes (ACS) Ischemia or infarction are caused from a primary reduction in Ischemia or infarction are caused from a primary reduction in coronary flow, precipitated by plaque disruption and subsequent coronary flow, precipitated by plaque disruption and subsequent thrombus formation:thrombus formation:

Unstable Angina, NSTEMI, STEMIUnstable Angina, NSTEMI, STEMI Prinzmetal AnginaPrinzmetal Angina

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Stable Plaque Vulnerable Plaque

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UA NSTEMI STEMI

+ S. Markers

Plaque DisruptionPlaque Disruption

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Distinguishing Features of Acute Coronary Syndromes

STEMISTEMINSTEMINSTEMI

Positive (+)Positive (+)Positive (+)Positive (+)Negative (-)Negative (-)Cardiac Cardiac Serum Serum BiomarkersBiomarkers

ST elevation ST elevation ( and Q waves ( and Q waves later)later)

ST depression ST depression and/pr T Wave and/pr T Wave inversioninversion

Dynamic, transiet < 24 hours

T-wave inversion and/or ST seg

depression

EKC initial EKC initial findingsfindings

Prolonged ( > 30 min ) Prolonged ( > 30 min ) crushing, strangling crushing, strangling

chest pain more severe chest pain more severe and wider radiation than and wider radiation than

usual anginausual angina

•Rest anginaRest angina - Rest or nocturnal - Rest or nocturnal Angina ≥ 20 minutes occurring Angina ≥ 20 minutes occurring within a week of presentation.within a week of presentation.•New onset anginaNew onset angina - ( < 2 months ) - ( < 2 months ) exertional angina progressing to exertional angina progressing to CCSA IIICCSA III•Crescendo anginaCrescendo angina - < 2 moths - < 2 moths acceleration of previously stable acceleration of previously stable angina to at least CCSA III.angina to at least CCSA III.•Within 30 day post MI, PCI or Within 30 day post MI, PCI or CABGCABG

Anginal Anginal PresentationPresentationss

Myocardial InfarctionMyocardial InfarctionUnstable AnginaUnstable Angina

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Acute Coronary Syndromes Acute Coronary Syndromes Coronary AtherothrombosisCoronary Atherothrombosis

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-RCA, 1yr. Before of the acute MI (B)

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

•Ischemic symptoms

•EKG changes indicative of ischemia (ST-seg elevation or depression)

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T-wave ∆

ST-seg ∆

Path. Q waves

Zone of ischemia

Zone of injury

Zone of necrosis

Lateral AnteriorSeptal

Inferior

T Wave – ST seg. changes

>0.03 seconds

>1/3 the total of QRS

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2020

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“ Time is muscle”

Myocardial Infarction is a true emergency in cardiac care.

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If the clinical picture is consistent with acute STEMI (including True Posterior MI) or new left bundle branch block (LBBB) is present in EKG, select and implement reperfusion therapy, Fibrinolysis or PCI as quickly as possible within 12 hours of symptoms onset to obtain and sustain optimal flow in the infarct-related artery (IRA). Do not wait for serum cardiac biomarkers result before implementing reperfusion strategy !

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ACS Treatment ACS Treatment

RevascularizationRevascularizationMechanical: PCI, CABGMechanical: PCI, CABGPharmacologic: ThrombolyticsPharmacologic: Thrombolytics

Stabilization of Vulnerable Plaque AspirinStabilization of Vulnerable Plaque AspirinAntithromboticsAntithromboticsBeta-BlockersBeta-BlockersACE-InhibitorsACE-InhibitorsLipid-Lowering Agents (+stantins)Lipid-Lowering Agents (+stantins)AntioxidantsAntioxidantsAggressive Risk Factors ModificationsAggressive Risk Factors Modifications

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Complications of Ml

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COMPLICATIONS OF INFARCTION

Ventricular Septal RupturePapillary Muscle Rupture

Ventricular Free Wall Rupture

Left Ventricular Thrombus