Guidelines Applied to
Practice (GAP)
American College of Cardiology,
Puerto Rico Chapter
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Guidelines Applied in Practice
(GAP)
Chronic Coronary
Syndromes
(Chronic Stable Angina)
INTRODUCTION
San Juan : Hotel Intercontinental, Feb. 6, 2007 - Jorge Ortega Gil, MD
Mayagüez : Casa del Médico, Feb. 7, 2007 – Marcos Velázquez, MD
Ponce : Casa del Médico, Feb. 8, 2007 – José Gómez Rivera, MD
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Ischemic Heart Disease in the United States
The Magnitude of the Health Problem
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Despite the well documented recent decline in
cardiovascular mortality, IHD remains the leading cause of
death
The initial clinical presentation is about the same for both
chronic and acute coronary syndromes (50% each)
About 1.5 million myocardial infarctions occur each year,
one third to one half are fatal
 200,000 have silent infarctions
16 million people have symptomatic CAD
Approximately 2.5 % of totally asymptomatic middle-aged
men have silent myocardial ischemia
One million each PCI and CABG are performed each year
Annual cost in 2004 was about $368 billion
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The ACC/AHA Guideline Classifications
Class I: Evidence and / or agreement that treatment is
effective
Class IIa: Weight of evidence favors use
Class IIb: Usefulness less well established
Class III: Evidence and/ or agreement that treatment is
not effective
Level of evidence:
A (high rank) – Based on large randomized trials
B (Intermediate rank) Based on smaller trials or
careful analyses
C (low rank) – Based on expert consensus
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Chronic Coronary Syndromes
(Chronic Stable Angina)
GAP
Pathophysiology &
Clinical Presentations
San Juan : Hotel Intercontinental, Feb. 6, 2007 - Jorge Ortega Gil, MD
Mayagüez : Casa del Médico, Feb. 7, 2007 – Marcos Velázquez, MD
Ponce : Casa del Médico, Feb. 8, 2007 – José Gómez Rivera, MD
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Ischemic Heart Disease - Overview
Parameters
Pathophysiology
Anatomy: Atheroma / Atherothrombosis
Atherosclerosis
Epicardial &
Microvascular Spam
Atherothrombosis
Subjective: Angina
Objective:
EKG T wave ST seg
changes
Chemistry:
Cardiac serum
biomarkers:
CPK, CK-MB,
Troponins
Silent ischemia
Stable angina
Acute Coronary
Syndromes
Clinical Presentations
Prevalence & severity of
stenosis
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Events During Atherogenesis
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Wall Stress =
Pxr
2h
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ISCHEMIC CASCADE
•Biochemical metabolic actions
Nuclear
•Hypoperfusion
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Compliance
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Echo
Predictable sequence
of pathophysiologic
events post myocardial
supply/demand
imbalance
•(S4)
LVEDP •(Rales)
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Contractility
•
EF
EKG
TIME FROM ONSET OF ISCHEMIA
•Flow Maldistribution
± 45 sec.
Angina / SI
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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
Endothelial dysfunction
Atherogenic
risk factors
Acute silent
occlusive
process
Angina
pectoris
Thrombogenic
risk factors
Age
20 years
60 years
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IHD – Clinical Spectrum
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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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ANGINA PECTORIS
Canadian Cardiovascular
Society Classification ( CCSC)
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Location: Usually Substernal, Jaw & Epigastrium
Quality: Sensation of Pain / Discomfort, Oppression,
Pressure, Burning, Tightness, Crushing or Squeezing. Can
Resemble Ïndigestion”
 Radiation: Radiates To Left Or Right Arm Or Shoulder, Jaw
or Epigastrium.
 Assocatie Symptoms:. Dyspnea, Diaphoresis, Weakness,
Nausea, Vomiting, and/or Feeling of Anxiety Or Impending
Doom
 Duration: 2 Min. – 30 Min. - To Several Hours
 - Relieved By TNG In 1-10 Min or Rest
 Related To: Exercise, Cold, Meals, Emotion, Coitus. Rest.
DIFFERENTIAL DIAGNOSIS OF CHEST PAIN
 Cardiovascular: Pericarditis, Aortic Valve Disease, Aortic
Dissection, Pulmonary Embolism, Mitral Valve Prolapse
 Gastrointestinal: Esophageal, Biliary, Peptic ulcer,
Pancreatitis
 Pulmonary: Pneumothorax, Pneumonia, Pleuritis
 Chest Wall: Costochondritis, Rib fracture, Herpes zoster
 Psychological: Anxiety disorders
Class
Activity
evoking
angina
Limits
to
normal
activity
I
Prolong None
ed
exertion
II
Walking
>2
blocks
Slight
III
Walking
<2
blocks
Marked
IV
Minimal
or rest
Severe
Typical angina (define) : Substernal chest discomfort with a characteristic quality
and duration that is Provoked by exertion or emotional stress and
Relieved by rest or nitroglycerin
Atypical angina ( probable): Meets 2 of the above characteristics
Noncardiac chest pain : Meets one or none of the typical angina characteristics
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CAD - Clinical Spectrum
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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
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Silent Ischemia
ST seg. depression
Is the objective
evidence-ST
segment shifts- of
myocardial
ischemia which is
not associated with
angina or angina
equivalents.
Iceberg’s sign
Angina
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Mixed Angina
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Exertional Angina Plus Angina at Rest or Coldinduced Angina or Emotion-Induced Angina.
 Angina at Variable Thresholds of Exercise.
Classic
Angina
Transient ST seg
depression
Prinzmetal Angina
Transient ST seg
elevation
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(positive stress testing)
Pathophysiology: Dynamic small vessel constriction (vasospasm)
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PRINZMETAL OR
VARIANT ANGINA
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Prolonged bouts of chest pain at
rest with EKG ST seg. elevation.
Pathophysiology: profound spasm of one of
the three major epicardial coronary arteries.
A = Marked transitory ST Elevation during a bout of severe
chest pain
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B = Thirty min. after A (Normal EKG)
Post-ischemic LV Dysfunction
Impaired LV contractility despite the presence of viable myocytes
Acute phenomenon – The
LV dysfunction is due to
short periods of coronary
occlusion, and persists for
minutes, hours or even days
after blood flow has been
restored. This process is
reversible spontaneously.
Chronic phenomenon –
The LV dysfunction is the
result of months or years of
chronic ischemia. This
process requires
revascularization ( PCI,
CABG) in order to restore
contractility.
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Chronic Coronary Syndromes
Treatment
 Pharmacologic
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Antithrombotics
Beta-Blockers
ACE-Inhibitors
Lipid-Lowering Agents (+stantins)
Aggressive Risk Factors Modifications
Influenza Vaccine
 Revascularization
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Mechanical: PCI, CABG
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Treatment of Chronic Ischemic Heart Disease
I. Medical
A) Antianginal and Anti-ischemic therapy
b - Blockers; Calcium antagonists;Nitroglycerin and Nitrates
B) Pharmacotherapy to prevent Myocardial Infarction and Death
Antiplatelet / Antithrombotic agents
Lipid – Lowering agents
Angiotensin – converting enzymes inhibition (ACE-I)
b – Blockers
C) Risk Factor Modification
Smoking cessation; Blood pressure control
D) Influenza Vaccine
II. Mechanical Revascularization
A) Percutaneous coronary intervenntion (PCI):
Conventional Angioplasty (PTCA)
Stents implantation: Bare metal & drug - eluting stents
B) Surgical - Coronary artery bypass graft (CABG)
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Guidelines Applied to
Practice (GAP)
American College of Cardiology,
Puerto Rico Chapter
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Holter
* EBCT *MRI
/
LVG
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