pathophysiology & clinical presentations

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1 Pathophysiology & Pathophysiology & Clinical Clinical Presentations Presentations Acute Coronary Syndromes Acute Coronary Syndromes GAP GAP San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MD Ortega Gil, MD Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MD Velázquez, MD Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD

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Acute Coronary Syndromes. GAP. Pathophysiology & Clinical Presentations. San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MD Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD. - PowerPoint PPT Presentation

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Page 1: Pathophysiology &  Clinical Presentations

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Pathophysiology & Pathophysiology & Clinical PresentationsClinical Presentations

Acute Coronary SyndromesAcute Coronary Syndromes

GAPGAP

San Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MDSan Juan : Hotel Intercontinental, Dec. 12, 2006 - Jorge Ortega Gil, MD Mayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MDMayagüez : Casa del Médico, Dec. 13, 2006 – Marcos Velázquez, MD

Ponce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MDPonce : Casa del Médico, Dec. 14, 2006 – José Acevedo, MD

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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

TIM

E F

RO

M O

NS

ET

OF

ISC

HE

MIA

± 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 Angina Silent IschemiaSilent Ischemia Mixed AnginaMixed Angina Microvascular Angina Microvascular Angina

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

Acute Acute Unstable AnginaUnstable Angina Acute 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 Substernal chest discomfort with a

characteristic quality and duration that ischaracteristic quality 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 PAIN Cardiovascular: Pericarditis, Aortic Valve Cardiovascular: Pericarditis, Aortic Valve

Disease, Aortic Dissection, Pulmonary Disease, Aortic Dissection, Pulmonary Embolism, Mitral Valve ProlapseEmbolism, Mitral Valve Prolapse

Gastrointestinal: Esophageal, Biliary, Peptic Gastrointestinal: Esophageal, Biliary, Peptic ulcer, Pancreatitisulcer, Pancreatitis

Pulmonary: Pneumothorax, Pneumonia, Pulmonary: Pneumothorax, Pneumonia, PleuritisPleuritis

Chest Wall: Costochondritis, Rib fracture, Chest Wall: Costochondritis, Rib fracture, Herpes zosterHerpes zoster

Psychological: Anxiety disordersPsychological: Anxiety disorders

ClassClass Activity Activity evokingevoking

anginaangina

Limits Limits to to normalnormal

activityactivity

II ProlongProlonged ed exertionexertion

NoneNone

IIII Walking Walking > 2 > 2 blocksblocks

SlightSlight

IIIIII Walking Walking < 2 < 2 blocksblocks

MarkedMarked

IVIV Minimal Minimal or restor rest

SevereSevere

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 Spectrum Chronic ischemic heart diseaseChronic ischemic heart disease Ischemia precipitated by increased myocardial oxygen Ischemia precipitated by increased myocardial oxygen

demand in the setting of a fixed, not vulnerable atherosclerotic demand in the setting of a fixed, not vulnerable atherosclerotic lesion. It is called lesion. It is called Stable AnginaStable Angina when the clinical when the clinical characteristics (Angina attacks) do not change in frequency, characteristics (Angina attacks) do not change in frequency, duration, precipitating causes, or easy with the angina is duration, precipitating causes, or easy with the angina is relieved, for at least 60 days.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 coronary flow, precipitated by plaque disruption and subsequent thrombus formation:subsequent 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

Unstable AnginaUnstable Angina Myocardial InfarctionMyocardial Infarction

NSTEMINSTEMI STEMISTEMI

Anginal Anginal PresentatioPresentationsns

•Rest anginaRest angina - Rest or nocturnal - Rest or nocturnal Angina Angina ≥ 20 ≥ 20 minutes occurring 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

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

EKC initial EKC initial findingsfindings

Dynamic, transiet < 24 hours

T-wave inversion and/or ST seg

depression

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

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

Cardiac Cardiac Serum Serum BiomarkersBiomarkers

Negative (-)Negative (-) Positive (+)Positive (+) Positive (+)Positive (+)

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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

RevascularizationRevascularization Mechanical: PCI, CABGMechanical: PCI, CABG Pharmacologic: ThrombolyticsPharmacologic: Thrombolytics

Stabilization of Vulnerable Plaque AspirinStabilization of Vulnerable Plaque Aspirin AntithromboticsAntithrombotics Beta-BlockersBeta-Blockers ACE-InhibitorsACE-Inhibitors Lipid-Lowering Agents (+stantins)Lipid-Lowering Agents (+stantins) AntioxidantsAntioxidants Aggressive Risk Factors ModificationsAggressive Risk Factors Modifications

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Complications of Ml

Deaths from MI

52%

19%

8%

21%

Prehospital

24 hours, in-hospital

48 hours, in-hospital

30 Days

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COMPLICATIONS OF INFARCTION

Ventricular Septal RupturePapillary Muscle Rupture

Ventricular Free Wall Rupture

Left Ventricular Thrombus