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ISCHMIC HEART DISEASE
PRESENTATION
DR . OMAR ALKASEM
Natural History of CAD : A story of remodeling
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Heart - Pathology
Heart - Pathology
Ischemic Heart Disease
75% stenosis = symptomatic ischemia induced by exercise
90% stenosis = symptomatic even at rest
Pathogenesis
↓ coronary perfusion relative to myocardial demand
Role of Acute Plaque Change
(Erosion/ulceration, Hemorrhage into the atheroma, Rupture/fissuring,
Thrombosis)
Role of Inflammation
T cell, Macrophages (MMPs), CRP
Role of Coronary Thrombus
The most dreaded complication
Role of Vasoconstriction (VC)
Platelet & Endothelial factors, VC substances
Cardiovascular Disease Risk Factors
History of CAD/PAD
Male Sex
History of TIA/CVA
Smoking
Hypertension
Diabetes Mellitus
Dyslipidemia
Low HDL < 40
Elevated LDL / TG
Family History - event in first
degree relative > 55 male,
> 65 female
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Chronic Kidney Disease
Obesity
Lack of regular physical
activity
Diet poor in fruits,
vegetables, and fiber
Age > 45 male, > 55 female
Western Lifestyle
Smoking,
Framingham Most Significant
Milestones
1960 Cigarette smoking found to increase the risk of heart disease
1961 Cholesterol level, blood pressure, and electrocardiogram
abnormalities found to increase the risk of heart disease
1967 Physical activity found to reduce the risk of heart disease and
obesity to increase the risk of heart disease
1970 High blood pressure found to increase the risk of stroke
1976 Menopause found to increase the risk of heart disease
1978 Psychosocial factors found to affect heart disease
1988 High levels of HDL cholesterol found to reduce risk of death
1994 Enlarged left ventricle (one of two lower chambers of the
heart) shown to increase the risk of stroke
1996 Progression from hypertension to heart failure described
Ischemic Cascade
Angina
Δ ECG
Stress ECG
Systolic Dysfunction
Stress Echo/MRI
Diastolic Dysfunction
Perfusion
Abnormalities
Nuclear Imaging
Duration and severity of ischemia
Heart - Pathology
Ischemic Heart Disease
Classification = mainly 4 types
Angina pectoris
Acute Coronary syndromes
Sudden cardiac death
Chronic IHD with heart failure
Angina Pectoris
At least 70% occlusion of coronary
artery resulting in pain. What
kind of pain?
Chest pain
Radiating pain to:
Left shoulder
Jaw
Left or Right arm
Usually brought on by physical
exertion as the heart is trying to
pump blood to the muscles, it
requires more blood that is not
available due to the blockage of
the coronary artery(ies)
Is self limiting usually stops
21
when exertion is ceased
Spectrum of ACS Presentations
UA
Definition
Ischemia without
necrosis
Negative Biomarkers
NSTEMI
STEMI
Necrosis
(nontransmural)
Transmural necrosis
Positive biomarkers
Positive biomarkers
Diagnosis
No ECG ST-segment elevation
Treatment
Invasive or conservative depending on risk
ECG ST-segment
elevation
Immediate reperfusion
MI –Complications
Poor prognosis in = elderly, females, DM, old case of MI, Anterior
wall infarct – worst, posterior –worse, Inferior wall – best
1. Arrhythmia = Vent. Fibrillation – MC arrhythmia lead to
sudden death in MI patients, before they reach hospital
2. pump failure – LVF, cariogenic shock, if >LV wall infarcts, lead to death (
70% of hospitalized MI patients)
3. Ventricular rupture = Free or lateral LV wall – MC site, later cause false
aneurysm,
4. True aneurysm = rupture is very rare
5. Pericarditis = Dressler’s syndrome ( Late MI complication)
6. Recurrence
Dysrhythmias
Occurs in 72-100% of AMI pts treated in
coronary care unit
PVCs are common in AMI
occur in >90% of AMI patients
Atrial premature contractions are also common
occur in up to 50% of AMI patients
not associated with increased mortality
Dysrhythmias
Early in AMI, pts often show increased
autonomic nervous system activity
sinus brady, AV block, hypotension occur from
increased vagal tone
Later, increased sympathetic activity results in
incr catecholamine release
thus creates electrical instability: PVCs, Vtach,
Vfib, accelerated idioventricular rhythms, AV
junctional tachycardia
Dysrhythmias
Hemodynamic consequences of dysrhythmias
are dependent on ventricular function
Normal hearts have a loss of 10-20% of left
ventricular output when atrial kick is eliminated
Reduced left ventricular compliance can result in
35% reduction in stroke volume when the atrial
systole is eliminated
Dysrhythmias
Persistant tachycardia is associated with poor
prognosis
due increase myocardial oxygen use
When Vtach occurs late in AMI course, usually
associated with transmural infarct and left
ventricular dysfunction
induces hemodynamic deterioration
mortality rate approaches 50%
Conduction Disturbances
First degree and Mobitz I (Wenckebach)
more common with inferior AMI
intermittent during the first 72 hrs after infarction
rarely progresses to complete block or pathologic
rhythm
Mobitz II
usually associated with anterior AMI
does progress to complete heart block
Conduction Disturbances
Complete Heart Block
occurs in setting of inferior MI
usually progresses from less AV blocks
this form is usually stable & should resolve
Mortality is 15% in absence of RV involvement &
increases to 30% when RV is affected
Complete block in setting of anterior MI results
in grave prognosis
Conduction Disturbance
New RBBB
occurs in approximately 2% of AMI pts
associated with anteroseptal AMI
associated with increased mortality because often
leads to complete AV block
Conduction Disturbance
New LBBB
occurs in 5% of pts with AMI
associated with high mortality
Left posterior hemiblock associated with higher
mortality than isolated anterior hemiblock
represents larger area of infarction
58 yo Man,
Chest pain
after lunch
on the way
to car.
Bad sushi?
Physical Examination
Not helpful in distinguishing pts with ACS from
those with non cardiac etiologies
Pts may appear deceptively will without
distress or be uncomfortable, pale, cyanotic,
and in respiratory distress.
Vital Signs
Bradycardic rhythms are more common with
inferior wall MI
in the setting of anterior wall MI, bradycardia or
heart block is very poor prognostic sign
Extremes of blood pressures are associated
with worse prognosis
Heart Sounds
S1 and S2 are often diminished due to poor myocardial
contractility
S3 is present in 15-20% of pts with AMI
implies a failing myocardium
S4 is common in pts with long standing HTN or
myocardial dysfunction
Presence of new systolic murmur is an ominous sign
signifies papillary m. dysfunction, flail leaflet of mitral
valve, or VSD
Differential Dx for ACS Chest Pain
Syndromes (beyond STEMI, NSTEMI, UA)
Aortic dissection
Pulmonary embolus
Perforating ulcer
Pericarditis
GERD (Gastroesophageal reflux disease)
Heart failure, Pneumonia, Pneumothorax
Example of ST-segment Elevation (STEMI)
J point
STE
Example of ST-segment Depression
(UA/STEMI)
STD
J point
Normal 12-lead ECG
LATERAL
ANTERIOR
LATERAL
INFERIOR
http://www.uptodate.com/contents/image?imageKey=CARD%2F1617. Accessed Aug 6.
2011.
Early-Stage Acute MI (STEMI)
ST-segment elevation
T-wave inversion
ST-segment depression
UA - NSTEMI
T-wave inversion
48 yo M, HBP with Chest pain while walking
ECG
ST segment is elevated on the initial ECG in
approximately 50% of pts with AMI
most other AMI pts will have ST depression and/or
T wave inversions
Only 1-5% of pts with AMI have an entirely
normal initial ECG
ECG
Reciprocal ST segment changes predict:
a larger infarct distribution
an increased severity of underlying CAD
more severe pump failure
a higher likelihood of cardiovascular complications
increased mortality
Difficult ECG interpretations
ST elevation in absence of AMI
early repolarization
LVH
pericarditis/myocarditis
Left ventricular aneurysm
Hypertropic cardiomyopathy
hypothermia
ventricular paced rhythms
LBBB
T wave inversions without ischemia
.persistent juvenile pattern
.seizures or Stokes Adams syncope
.post-tachycardia T wave inversion
.post-pacemaker T wave inversion
.Intracranial pathology (CNS hemorrhage)
.Mitral valve prolapse
.Pericarditis
.primary or secondary myocardial disease
T wave inversion without ischemia
PE or cor pulmonale
spontaneous PTX
myocardial contusion
LVH
ventricular paced rhythms
RBBB
LBBB
Cardiac Enzymes
Serial measurements are more sensitive and
accurate than initial single measurement
serum markers have less utility in the diagnosis
of UA, only about 50% will have elevated
troponins
Myoglobin
Rises within 2-3 hours of symptoms onset
peaks within 4 to 24 hours
more sensitive than CK and CK-MB but not
specific for cardiac muscle
there is a high false-positive rate due to its
presence in all muscle tissue
Troponin
Main regulatory protein for the actin-myosin
myofibrils
3 subunits:
inhibitory subunit (Trop I)
tropomyosin binding subunit (Trop T)
calcium binding subunit (Trop C)
Trop I has not been identified in skeletal m. during
any stage of develop therefore specific to
myocardium
Non-MI Causes of Troponin Elevation
Timing of Release of Various Biomarkers After
Acute Myocardial Infarction
Cardiac-specific troponins are
optimum biomarkers (Level IC)
For STEMI, reperfusion therapy
should be initiated as soon as
possible and is not contingent on a
biomarker assay (Level IC)
TIMI Risk Score (n=7)
TIMI Risk Score Calculator
Age ≥65 years?
Yes (+1)
≥3 Risk Factors for CAD?
Yes (+1)
Known CAD (stenosis ≥50%)?
Yes (+1)
ASA Use in Past 7d
Yes (+1)
Severe angina (≥2 episodes w/in 24 hrs)?
Yes (+1)
ST changes ≥0.5 mm?
Yes (+1)
+ Cardiac Marker?
Yes (+1)
Total Score
pts
What does TIMI RISK mean?
Increasing TIMI RISK 0/1 to
5/7 increases risk of death, MI,
urgent revascularization within
14 days 5% to 41%.
Treatment of Acute Coronary
Syndrome
Early Invasive
Initial
Conservative
Cardiovascular Diet