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

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 Ischemic Heart Disease - Overview
Pathophysiology
Parameters
Anatomy: Atheroma / Atherothrombosis

Atherosclerosis Subjective: Angina

Epicardial & Objective: EKG T wave ST seg
Microvascular Spam changes
Atherothrombosis Chemistry: Cardiac serum
biomarkers:
CPK, CK-MB,
Troponins

Silent ischemia

Stable angina Acute Coronary Prevalence & severity of

Syndromes
stenosis
Clinical Presentations 2
Events During Atherogenesis

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 Pxr
Wall Stress =
2h

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 ISCHEMIC CASCADE

TIME FROM ONSET OF ISCHEMIA

•Flow Maldistribution

•Biochemical metabolic actions

•Hypoperfusion
Nuclear
• Compliance •(S4)

• LVEDP •(Rales)

Echo • Contractility

• EF
Predictable sequence of
pathophysiologic events post
myocardial supply/demand imbalance
EKG
± 45 sec.

Angina / SI 5
Effect of Fixed Stenosis on Myocardial Blood Flow

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Progression of coronary plaque over time Clinical Findings

Acute Coronary Syndromes

Sudden Cardiac Death

Acute silent
Angina occlusive
pectoris process
Endothelial dysfunction
Atherogenic Thrombogenic
risk factors risk factors
Age
20 years 60 years
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IHD – Clinical Spectrum
Chronic
 Stable Angina
 Silent Ischemia
 Mixed Angina
 Microvascular Angina
(Syndrome X)
 Stunned & Hibernating
Acute
 Unstable Angina
 Acute Myocardial
Infarction (NSTEMI,
STEMI)
 Sudden Cardiac Death
Prinzmetal Angina
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 Clinical Classification of Chest Pain
Typical angina (define) Canadian Cardiovascular
1. Substernal chest discomfort with a Society Classification ( CCSC)
characteristic quality and duration that is
Class Activity Limits
2. Provoked by exertion or emotional stress and evoking to
3. Relieved by rest or nitroglycerin normal
angina
Atypical angina ( probable) activity
Meets 2 of the above characteristics I Prolong None
Noncardiac chest pain ed
Meets one or none of the typical angina exertion
characteristics
II Walking Slight
DIFFERENTIAL DIAGNOSIS OF CHEST PAIN >2
 Cardiovascular: Pericarditis, Aortic Valve blocks
Disease, Aortic Dissection, Pulmonary
Embolism, Mitral Valve Prolapse III Walking Marked
 Gastrointestinal: Esophageal, Biliary, Peptic <2
ulcer, Pancreatitis blocks
 Pulmonary: Pneumothorax, Pneumonia, IV Minimal Severe
Pleuritis or rest
 Chest Wall: Costochondritis, Rib fracture,
Herpes zoster
 Psychological: Anxiety disorders
*CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II
ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV 9
 CAD - Clinical Spectrum
 Chronic ischemic heart disease
Ischemia precipitated by increased myocardial oxygen
demand in the setting of a fixed, not vulnerable atherosclerotic
lesion. It is called Stable Angina when the clinical
characteristics (Angina attacks) do not change in frequency,
duration, precipitating causes, or easy with the angina is
relieved, for at least 60 days.
-Silent Ischemia, -Mixed Angina -Syndome X
-Stunning & Hibernating.
 Acute Coronary Syndromes (ACS)
Ischemia or infarction are caused from a primary reduction in
coronary flow, precipitated by plaque disruption and
subsequent thrombus formation:
Unstable Angina, NSTEMI, STEMI
Prinzmetal Angina 10
Stable Plaque Vulnerable Plaque

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 Plaque Disruption

UA NSTEMI STEMI

+ S. Markers

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 Distinguishing Features of Acute Coronary Syndromes

Unstable Angina Myocardial Infarction

NSTEMI STEMI
Anginal •Rest angina - Rest or nocturnal Prolonged ( > 30 min )
Presentatio Angina ≥ 20 minutes occurring
ns within a week of presentation. crushing, strangling
•New onset angina - ( < 2 months ) chest pain more severe
exertional angina progressing to and wider radiation than
CCSA III
•Crescendo angina - < 2 moths usual angina
acceleration of previously stable
angina to at least CCSA III.
•Within 30 day post MI, PCI or
CABG
EKC initial Dynamic, transiet < 24 hours ST depression ST elevation
findings T-wave inversion and/or ST seg and/pr T Wave ( and Q waves
depression inversion later)
Cardiac Negative (-) Positive (+) Positive (+)
Serum
Biomarkers 13
Acute Coronary Syndromes
Coronary Atherothrombosis

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

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 Acute MI
Typical 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. changes
T-wave ∆

ST-seg ∆

Zone of ischemia
Path. Q waves
Zone of injury

Zone of necrosis
>0.03 seconds
Lateral
Septal Anterior
>1/3 the total of
QRS

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Inferior
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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
 Revascularization
 Mechanical: PCI, CABG
 Pharmacologic: Thrombolytics
 Stabilization of Vulnerable Plaque Aspirin
 Antithrombotics
 Beta-Blockers
 ACE-Inhibitors
 Lipid-Lowering Agents (+stantins)
 Antioxidants
 Aggressive Risk Factors Modifications

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 Complications of Ml

Deaths from MI

21%

Prehospital
24 hours, in-hospital
8% 52% 48 hours, in-hospital
30 Days

19%

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 COMPLICATIONS OF INFARCTION

Papillary Muscle Rupture Left Ventricular Thrombus Ventricular Septal Rupture

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Ventricular Free Wall Rupture