3. heart patghology; ischemic heart diseases
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Heart - PathologyHeart - PathologyIschemic Heart Disease
Hypoxemia (diminished transport of oxygen by the blood) less deleterious than ischemia
Also called coronary artery disease (CAD) or coronary heart disease
IHD =Syndromes late manifestations of coronary
atherosclerosis Cause => 90% of cases, coronary
atherosclerotic arterial obstruction
Ischemic Heart DiseaseHypoxemia (diminished transport of oxygen by
the blood) less deleterious than ischemiaAlso called coronary artery disease (CAD) or
coronary heart diseaseIHD =Syndromes
late manifestations of coronary atherosclerosis
Cause => 90% of cases, coronary atherosclerotic arterial obstruction
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Heart - PathologyHeart - PathologyIschemic Heart Disease
Classification = mainly 4 typesMyocardial infarction (MI)Sudden cardiac deathAngina pectorisChronic IHD with heart failure
Acute Coronary syndromesimportant predisposing factor -Plaque
disruption or Acute plaque changeAcute myocardial infarctionUnstable anginaSudden cardiac death
Ischemic Heart DiseaseClassification = mainly 4 types
Myocardial infarction (MI)Sudden cardiac deathAngina pectorisChronic IHD with heart failure
Acute Coronary syndromesimportant predisposing factor -Plaque
disruption or Acute plaque changeAcute myocardial infarctionUnstable anginaSudden cardiac death
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Heart - PathologyHeart - PathologyIschemic Heart Disease
75% stenosis = symptomatic ischemia induced by exercise
90% stenosis = symptomatic even at rest Pathogenesis
↓ coronary perfusion relative to myocardial demandRole of Acute Plaque Change
(Erosion/ulceration, Hemorrhage into the atheroma, Rupture/fissuring, Thrombosis)
Role of InflammationT cell, Macrophages (MMPs), CRP
Role of Coronary ThrombusThe most dreaded complication
Role of Vasoconstriction (VC)Platelet & Endothelial factors, VC substances
Ischemic Heart Disease 75% stenosis = symptomatic ischemia induced by
exercise 90% stenosis = symptomatic even at rest Pathogenesis
↓ coronary perfusion relative to myocardial demandRole of Acute Plaque Change
(Erosion/ulceration, Hemorrhage into the atheroma, Rupture/fissuring, Thrombosis)
Role of InflammationT cell, Macrophages (MMPs), CRP
Role of Coronary ThrombusThe most dreaded complication
Role of Vasoconstriction (VC)Platelet & Endothelial factors, VC substances
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Heart - PathologyHeart - Pathology
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Heart - PathologyHeart - Pathology
Syndrome StenosesPlaque
Disruption Plaque-Associated Thrombus
Stable angina >75% No No
Unstable angina Variable Frequent Non-occlusive
Transmural MI Variable Frequent Occlusive
Subendocardial MI
Variable Variable Widely variable
Sudden death severe Frequent Often small
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Heart - PathologyHeart - PathologyIschemic Heart Disease
Angina PectorisChest discomfort = prolonged, recurrent, different qualities
Cause = transient myocardial ischemia( seconds to minutes)
PatternsStable = 75% vessel block, transient ( <15 minutes),
aggravated by exertion, relived by rest & Nitroglycerin (VD)
Prinzmetal = coronary spasm, episodic, Typical EKG change – ST elevation, Relived by VD but not rest
Unstable = 90% vessel block or Acute plaque change ( superimposed thrombus), prolonged ( >15 min.), not relived by rest, VD, Pre-infarction Angina
Ischemic Heart Disease Angina Pectoris
Chest discomfort = prolonged, recurrent, different qualities
Cause = transient myocardial ischemia( seconds to minutes)
PatternsStable = 75% vessel block, transient ( <15 minutes),
aggravated by exertion, relived by rest & Nitroglycerin (VD)
Prinzmetal = coronary spasm, episodic, Typical EKG change – ST elevation, Relived by VD but not rest
Unstable = 90% vessel block or Acute plaque change ( superimposed thrombus), prolonged ( >15 min.), not relived by rest, VD, Pre-infarction Angina
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MI - TypesMI - Types
Transmural Full thickness
Superimposed thrombus in atherosclerosis
Focal damage
Transmural Full thickness
Superimposed thrombus in atherosclerosis
Focal damage
Sub-endocardial Inner 1/3 to half of
ventricular wall Decreased circulating blood
volume( shock, Hypotension, Lysed thrombus)
Circumferential
Sub-endocardial Inner 1/3 to half of
ventricular wall Decreased circulating blood
volume( shock, Hypotension, Lysed thrombus)
Circumferential
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Heart - PathologyHeart - PathologyIschemic Heart Disease
MI= Also called Heart attackIncidence = disease of old
elderly (45% in 65 yrs. old) young ( 10% in 40yrs. Old),
Sex = Male > FemaleEthnic = same in African & AmericanRisk factors
Major modifiable- DM, HTN, Smoking, Hypercholesterolemia
HRT for Postmenopausal females – will not protect the heart
Ischemic Heart DiseaseMI= Also called Heart attackIncidence = disease of old
elderly (45% in 65 yrs. old) young ( 10% in 40yrs. Old),
Sex = Male > FemaleEthnic = same in African & AmericanRisk factors
Major modifiable- DM, HTN, Smoking, Hypercholesterolemia
HRT for Postmenopausal females – will not protect the heart
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Heart - PathologyHeart - PathologyIschemic Heart Disease
MI Pathogenesis
Coronary vessel occlusionAtherosclerosis with thrombus = MC cause ( 90% cases)Others = vasospasm (10%)
Most important mechanism = dynamic changes in the plaque (rather than plaque size),
Plaque disruption PLTS aggregation thrombus and VC (happens in minutes)
Irreversible changes = after 30 minutes of ischemia ATP < 10% of normal
Mechanism of cell death = necrosis ( Coagulative)
Ischemic Heart Disease MI Pathogenesis
Coronary vessel occlusionAtherosclerosis with thrombus = MC cause ( 90% cases)Others = vasospasm (10%)
Most important mechanism = dynamic changes in the plaque (rather than plaque size),
Plaque disruption PLTS aggregation thrombus and VC (happens in minutes)
Irreversible changes = after 30 minutes of ischemia ATP < 10% of normal
Mechanism of cell death = necrosis ( Coagulative)
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Heart - PathologyHeart - PathologyIschemic Heart Disease
TTCIschemic Heart Disease
TTC
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Heart - PathologyHeart - PathologyIschemic Heart Disease
MI -Morphology light microscopy
First 12 hrs. after MI – no changeUp to 3 days = Coagulative necrosis, neutrophils1-2 weeks = Granulation tissue≥ 3 weeks = fine scar≥ 2 months = dense scar
EM – membrane disruption and Mitochondrial densities Special stain = TTC ( Triphenyl Tetrazolium chloride),
Detects and stains Mahogany brown with Lactate dehydrogenaseUnstained area = infarctionMahogany brown = viableWhite, glistening= scar
Most common and nonspecific change in ischemia = sub-endocardial myocyte vacuolization
Ischemic Heart Disease MI -Morphology
light microscopyFirst 12 hrs. after MI – no changeUp to 3 days = Coagulative necrosis, neutrophils1-2 weeks = Granulation tissue≥ 3 weeks = fine scar≥ 2 months = dense scar
EM – membrane disruption and Mitochondrial densities Special stain = TTC ( Triphenyl Tetrazolium chloride),
Detects and stains Mahogany brown with Lactate dehydrogenaseUnstained area = infarctionMahogany brown = viableWhite, glistening= scar
Most common and nonspecific change in ischemia = sub-endocardial myocyte vacuolization
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MI- Microscopic featuresMI- Microscopic features
One-day-old infarct
coagulative necrosis
wavy fibers
Up to 3 days duration
Neutrophilic infiltrate
1 -2 weeks
Granulation tissue
>3 weeks
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Heart - PathologyHeart - PathologyIschemic Heart Disease
MI –Reperfusion Mechanisms
Intrinsic Extrinsic =
Thrombolytic drugs = < 1hr. After onset of MIPTCA/CABG = > 1hr. After onset of MI
Target = clot lysis and restoration of blood flow
Post- reperfusion changes = Contraction bands = hyper contracting myocytes, Stunned myocardium = transient, protective dysfunction Reperfusion damage = mostly apoptosis by free radicals
( unlike MI)
Ischemic Heart Disease MI –Reperfusion Mechanisms
Intrinsic Extrinsic =
Thrombolytic drugs = < 1hr. After onset of MIPTCA/CABG = > 1hr. After onset of MI
Target = clot lysis and restoration of blood flow
Post- reperfusion changes = Contraction bands = hyper contracting myocytes, Stunned myocardium = transient, protective dysfunction Reperfusion damage = mostly apoptosis by free radicals
( unlike MI)Dr. Krishna Tadepalli, MD, www.mletips.com
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Heart - PathologyHeart - PathologyIschemic Heart DiseaseIschemic Heart Disease
Dr. Krishna Tadepalli, MD, www.mletips.com
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Heart - PathologyHeart - PathologyIschemic Heart Disease
MI = Clinical Silent MI = DM, Elderly, Cardiac transplantation
recipients, Typical features = Rapid, weak pulse and sweating
profusely (diaphoretic), Dyspnea, chest pain Lab=
Diagnostic Best markers = Troponins ( T & I), both sensitive and
cardio – specificNext best – CK-MB
PredictiveCRP- >3mg/l – highest risk
Ischemic Heart Disease MI = Clinical Silent MI = DM, Elderly, Cardiac transplantation
recipients, Typical features = Rapid, weak pulse and sweating
profusely (diaphoretic), Dyspnea, chest pain Lab=
Diagnostic Best markers = Troponins ( T & I), both sensitive and
cardio – specificNext best – CK-MB
PredictiveCRP- >3mg/l – highest risk
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Heart - PathologyHeart - PathologyIschemic Heart Disease
MI –Complications In 75% of Patients with MI Poor prognosis in = elderly, females, DM, old case of MI, Anterior
wall infarct – worst, posterior –worse, Inferior wall – best 1. Arrhythmia = Ventr. 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
Ischemic Heart Disease
MI –Complications In 75% of Patients with MI Poor prognosis in = elderly, females, DM, old case of MI, Anterior
wall infarct – worst, posterior –worse, Inferior wall – best 1. Arrhythmia = Ventr. 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
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Heart - PathologyHeart - PathologyIschemic Heart Disease
Sudden cardiac death = unexpected death in one hour due to cardiac causes with or without clinical symptoms
Cause – Atherosclerosis ( 90%), others (10%)Romano- Ward syndrome – Long Q-T syndrome
( K+, Na+ channel defects) Mechanism- Most likely due to arrhythmias ( VF) Patients – young athletes, with Pul. HTN, IHD Morphology
Prominent finding – increased heart massVacuolations in Sub – endocardial myocardium
Ischemic Heart Disease Sudden cardiac death = unexpected death in one hour
due to cardiac causes with or without clinical symptoms Cause – Atherosclerosis ( 90%), others (10%)
Romano- Ward syndrome – Long Q-T syndrome
( K+, Na+ channel defects) Mechanism- Most likely due to arrhythmias ( VF) Patients – young athletes, with Pul. HTN, IHD Morphology
Prominent finding – increased heart massVacuolations in Sub – endocardial myocardium
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Heart - PathologyHeart - Pathology
Ischemic Heart Disease Chronic IHD = also called ischemic cardiomyopathy Patients = post heart transplant receipts, previous MI or
CABG pts Cause =compromised ventricular function Morphology =vacuoles, Myocyte Hypertrophy Diagnosis= by exclusion
Ischemic Heart Disease Chronic IHD = also called ischemic cardiomyopathy Patients = post heart transplant receipts, previous MI or
CABG pts Cause =compromised ventricular function Morphology =vacuoles, Myocyte Hypertrophy Diagnosis= by exclusion
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Heart - PathologyHeart - PathologyWhat is it?What is it?
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Heart - PathologyHeart - PathologyWhat are these?What are these?
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