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Lifes battles dont go always to the stronger or

faster man,

But sooner or later, The man who wins is the man


who thinks he can
ISCHEMIC HEART
DISEASE
ISCHEMIC (CORONARY) HEART DISEASE
(IHD/CHD/CAD)
Closely related syndromes caused by an imbalance between myocardial
O2 demand and blood supply. The most common cause (90%) is
atherosclerosis of the coronary arteries.

1. Angina Pectoris (stable/variant/unstable)


2. Acute Myocardial Infarction (MI)
3. Sudden Cardiac Death
4. Chronic Ischemia Heart Disease with CHF

Acute Coronary Syndromes


Unstable angina, acute MI & Sudden cardiac death having common
pathogenesis
ANGINA PECTORIS
Paroxysmal and usually recurrent attacks of substernal or precordial chest
discomfort and radiating to left shoulder (15 sec-15 min)

VARIANTS
STABLE OR TYPICAL ANGINA
Exertional, emotional excitement or any cause leading to increased
cardiac workload (> 75% stenosis)

PRINZMETAL VARIANT ANGINA


Episodic angina occurring at rest, and due to coronary artery spasm.

UNSTABLE OR CRESCENDO ANGINA (Pre-infarction angina)


Progressive, increasing frequency, precipitated with progressively less
effort and even at rest & of prolonged duration (plaque rupture with
mural thrombosis/thromboembolism or vasospasm or both)
MYOCARDIAL INFARCTION
It is coagulative necrosis of discrete part of myocardium due to abrupt
decrease in coronary blood flow following a complete thrombotic occlusion
of a coronary artery previously narrowed by atherosclerosis.

CHRONIC ISCHEMIC HEART DISEASE WITH CHF


This is insidious development of CHF most often in elderly patients as a
consequence of ischemic myocardial damage. History of angina and usually
prior MI is positive

SUDDEN CARDIAC DEATH


Defined as unexpected death from cardiac causes early after or without
onset of symptoms. Mostly it is complication and often first clinical
manifestation of IHD (mechanism of death is almost always a lethal
arrhythmia)
IHD - Epidemiology
Peak incidence: Males >60y/o Females >70y/o
Men > Women
Risk factors - Increased risk:
Hypertension Smoking
Diabetes Mellitus Stress
High LDL/Cholesterol/ non-fasting triglycerides/Lp(a)

Risk factors - Decreased risk: 100


90 85.9

Regular Exercise Folate (homocystinemia)


79.3

Percent of Population
80 73.3 72.6
70

ETOH/Red Wine High HDL


60
50
37.9 38.5

Estrogen
40
30
20 15.9
7.8
10
0
20-39 40-59 60-79 80+

Men Women

AMI leading single cause of death in industrialized nations


In USA, 1.5 million have AMI annually - 500,000 fatalities
DISTRIBUTION OF MYOCARDIAL INFARCTION IN
RELATION TO BLOOD SUPPLY

LEFT ANTERIOR DESCENDING CORONARY ARTERY (40-50%)


Most common artery to occlude. Results in an anterior infarct: (anterior wall,
anterior two thirds of septum & entire apex of heart, circumferentially)

LEFT CIRCUMFLEX CORONARY ARTERY (15-20%)


Occlusion leads to a posterolateral infarct (posterior & lateral left aspect of heart)

RIGHT CORONARY ARTERY (30-40%)


Occlusion results in a posterior 1/3 of septal infarct, inferior and posterior wall of
left ventricle & posterior right ventricular free wall
Left Coronary Artery.
Anterior Descending (LAD) LCx
Left Circumflex (LCx)
Right Coronary Artery. (RCA)

LAD
RCA
Infarction of the Right Ventricle is rare, because the right side has far less
demand for oxygen. Right Ventricular infarcts are usually extensions of
posterior septal infarcts caused by occlusion of the Right Coronary Artery.

GRADES
Coronary atherosclerosis or stenosis is graded as follows.

GRADE 1: 0-25% OCCLUSION -- asymptomatic and common


GRADE 2: 25-50% OCCLUSION -- possible stable angina
GRADE 3: 50-75% OCCLUSION -- stable angina
GRADE 4: 75%+ OCCLUSION -- unstable angina, impending MI and thrombosis.
PATHOGENESIS OF ACUTE CORONARY SYNDROMES

Advanced stenosing coronary atherosclerosis (fixed obstruction)

Erosion/ulceration, Rupture/fissuring of or Hemorrhage into atheromatous plaque

Abrupt changes in configuration of plaque

Activation of thrombosis (partial/total), coagulation, vasoconstriction & embolism


(Platelet adherence, activation and aggregation)

Acute coronary occlusion Myocardial Infarction


(2/3 rupturing plaques have occlusion of 50% or less & 85% <70%)

10% cases of transmural acute MI are unassociated with atherosclerotic thrombosis


(vasospam, emboli, vasculitis, vascular disection, shock)
Role of inflammation in atherosclerosis & weakening fibrous cap is also important
Characteristics of Unstable & Stable Plaque

Unstable Stable
Lack of
Inflammatory inflammatory
cells cells
Thin Thick
Few fibrous cap More fibrous cap
SMCs SMCs

Intact
Eroded endothelium
endothelium
Activated
macrophages Foam cells

Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with permission from Cannon CP.
Atherothrombosis slide compendium. Available at: www.theheart.org.
Coronary Atherosclerosis

Coronary Atherosclerosis with


Thrombosis
THROMBOSIS

It is the process of formation of solid mass in


circulation from the constituents of flowing blood
(within a blood vessel or cardiac chamber, in a living
organism (always formed ante-mortem). The mass
itself is called Thrombus.

Blood clot: mass of coagulated blood formed in vitro or in stagnant column of blood
Hematoma: extravasular accumulation of blood clot into tissues.
Hemostatic plugs: simplest form of thrombus formed in healthy individuals at the site
of bleeding
COMPOSITION OF THROMBUS

Fibrin, Platelets, RBC's


(Hemostatic plug formation: endothelial injury, platelet aggregation, fibrin meshwork )

LOCATION OF THROMBI
Arteries, veins, heart chambers, heart valves

TYPES OF THROMBI
Arterial vs. venous;
bland vs. septic
PATHOGENESIS OF THROMBOSIS
(Predisposing Factors)

Virchows Triad
Endothelial injury (in atherosclerosis)
Stasis or turbulence of blood flow
Blood hypercoagulability
MYOCARDIAL RESPONS
Early biochemical changes (CPK & ATP) within seconds loss of contractility within
60 Sec.
Irreversible cell injury20-40 min
Microvascular injury>1 hr
Permanent damage to the heart occurs when the perfusion of the myocardium is
severely reduced for an extended interval (usually at least 2 to 4 hours)

Factors affecting the extent of MI


Location, severity and rate of development of coronary atherosclerotic obstruction
Size of vascular bed perfused by obstructed vessels
Duration of occlusion
Metabolic / O2 need of myocardium at risk
Extent of collateral circulation
Presence, site, and severity of coronary arterial spasm
Change in BP, heart rate & cardiac rhythm
PROGRESSION OF ISCHEMIC NECROSIS IN MYOCARDIUM
Ischemic necrosis starts in subendocardial zone-wave front of cell death moves
through myocardium (transmural thickness)
TYPES OF INFARCTS

TRANSMURAL INFARCT
Infarct extending from epicardium to endocardium (full or nearly
full thickness of ventricular wall,
(caused by occlusion of major coronary epicardial trunk or major secondary
epicardial branches)

SUBENDOCARDIAL INFARCT
Diffuse, circumferential infarct, around the subendocardium
limited to inner 1/3 or at most of ventricular wall
(caused by shock, CHF, hypotension, or anything that results in inadequate blood
supply to the coronary arteries or lysed coronary thrombus )
RECOGNITION OF ACUTE MYOCARDIAL INFARCTION
BY PATHOLOGIC METHODS

The gross and microscopic appearance of an infarct depends on the


duration of survival of the patient following the MI

ULTRASTRUCTURAL FEATURES OF IRREVERSIBLE DAMAGE (20-40 min)


WAVY FIBERS (1-3 hr.)
STAINING DEFECT WITH TRI-PHENYL TETRAZOLIUM CHLORIDE DYE (2-3 hr.)

CLASSIC HISTOLOGIC FEATURES OF NECROSIS (6-12 hr.)

GROSS ALTERATION (12-24 hr.)


Following infarction, macroscopic changes evolve
over time

Time from Onset Gross Morphologic Finding

12 - 24 Hours Red blue hue (mottling) Pallor


24 - 72 Hours Pallor with some hyperaemia
3 - 7 Days Central yellowing with hyperaemic border
10 - 21 Days Very yellow with vascular margins, soft
7 weeks Firm, greyish white (fibrosis)

(timing depends on size - larger infarct may develop slower)


AMI - Microscopic Morphology

Coagulation Necrosis & Inflammation (1-3 days)

Demolition/Resorption of Necrotic Debris (3-7 days)

Granulation Tissue (1-2 weeks)

Organization & Scar (by the end of 6 weeks)

(Efficiency of repair depends on the size of the original lesion)


INFARCT MODIFICATION BY REPERFUSION

Removal of thrombus to re-establishes flow through the occluded coronary artery


Early reperfusion can salvage myocardium & limit infarct size & improve function & survival
Reperfusion is most effective in first 3-4 hours (salvage part of damaged myocardium)
Reperfused myocardium reveals hemorrhage (leaky vasculature damaged at time of ischemia) &
necrosis with contraction bands (accentuation of disintegration in lethally damaged
myocardium)
Salvages reversibly injured cells and changes morphology of cells already lethally injured.

Reperfusion injury by generation of O2 free radicals , infiltrating WBC & calcium overload can
cause some small amount of new cellular damage due to prominent apoptosis, and can induce
microvascular injury can cause hemorrhage & endothelial cell swelling that occludes capillaries
& prevent local reperfusion to areas of critically injured myocardium. It may induce arrhythmia
& hibernation.

Salvaged part may show stunned myocardium (prolonged postischemic ventricular dysfunction)
In any moment of decision the best thing you
can do is the right thing, the next best thing is
the wrong thing, and the worst thing you can
do is nothing.
CLINICAL PRESENTATION
SYMPTOMS
PAIN
(deep, visceral) heavy squeezing, crushing, stabbing or burning, more severe than
angina pectoris and lasts longer, typically it is in central portion of chest and/or
epigastrium and on occasion it radiates to arm, neck, jaw & shoulder, not relieved by
NTG.
(D/D acute pericarditis, pulmonary embolism, acute aortic dissection,
costochondritis etc.)
Painless infarction is seen in elderly and in patients with diabetes mellitus-(Silent or
asymptomatic infarction- 10-15%)
DYSPNEA
ANXIETY
NAUSEA & VOMITING
WEAKNESS
COLLAPSE & SYNCOPE
SUDDEN DEATH
SIGNS
SYMPATHETIC ACTIVATION
Tachycardia, hypertension, sweating, pallor
PARASYMPATHETIC ACTIVATION
Bradycardia, hypotension, nausea, vomiting.

IMPAIRED MYOCARDIAL FUNCTION


Hypotension, oliguria, cold peripheries, narrow pulse pressure, raised JVP, 3 rd & 4
th heart sound, diffuse apical impulse, decreased intensity of heart sound and
paradoxical splitting of heart sound, transient apical systolic murmur, pericardial
friction rub, carotid pulse often decreased in volume breathlessness & lung
crepitation
TISSUE DAMAGE
Fever
50% have precipitating factors like vigorous physical exercise, emotional stress or
a medical or surgical illness. Most commonly it occurs in the morning within a few
hours of awakening.
LABORATORY FINDINGS

ECG
SERUM CARDIAC MARKERS
CARDIAC IMMAGING
NON-SPECIFIC INDICES OF TISSUE NECROSIS &
INFLAMMATION
ECG

Transmural infarction shows Q waves or loss of R waves


Non transmural infarction shows transient ST -segment & T wave changes

Acute anterior myocardial infarction:


ST elevation in the anterior leads V1 - 6, I and aVL reciprocal ST depression
in the inferior leads

Acute inferior myocardial infarction: ST elevation in the inferior leads II, III
and aVF reciprocal ST depression in the anterior leads

Acute posterior myocardial infarction: Hyperacute- the mirror image of


acute injury in leads V1 3, Fully evolved- tall R wave, tall upright T wave
in leads V1 -3 usually associated with inferior and/or lateral wall MI
Common serum markers used to detect AMI

Marker Initial Mean time to Time to return to


elevation peak elevation baseline after AMI
after AMI after AMI
Myoglobin 1-4h 6h 18 - 24 h
CK-MB 2-4h 10 - 24 h 48 - 72 h
MB-isoform 1-6h 4 - 12 h 38 h
cTnI 2-4h 24 - 48 h 5 - 10 days
cTnT 2-4h 24 - 48 h 5 - 14 days
Suggested testing schedule for cardiac markers

Marker <6h 6 - 12 h 12 - 24 h 24 - 48 h > 48 h


Myoglobin +++ + - - -
Troponin I + ++ +++ +++ +++
Troponin T + ++ +++ +++ +++
CK-MB + ++ +++ - -
MB- isoforms ++ +++ + - -
CARDIAC IMMAGING

Chest x-ray
Echocardiogram
Computed tomography (CT) scan
Magnetic resonance imaging (MRI)
Magnetic resonance angiography (MRA)
Nuclear imaging (MUGA scan, Thallium stress test, SPECT & PET test)
Other imaging tests

Trans-esophageal echocardiogram (T.E.E.)


Cardiac catheterization (Cath') - also known as coronary angiography
Treatment of Coronary Thrombosis

Thrombolytic Enzymes (tPA)


Percutaneous Coronary Angioplasty PTCA with or without stent
Coronary Arterial Bypass Graft (CABG)
COMPLICATIONS

BEFORE REACHING HOSPITAL


Sudden cardiac death (SCD) in 25% of patient

IN HOSPITAL
Uncomplicated cases (10-20%)
Complicated cases (80-90%)
Cardiac arrhythmia (75-95%)
LVF & Mild to moderate pulmonary edema (60%)
Cardiogenic Shock (10%)
Rupture of free wall, septum or papillary muscles (4-8%)
Thromboembolism (15-49%)
OTHER COMPLICATIONS

RECURRENT CHEST DISCOMFORT


Develops in about >25% of patients hospitalized for MI. Recurrent or
persistent ischemia may lead to extension of the original infarct or re-
infarction in a new myocardial zone. Repeat thrombolysis, prompt
coronary angiography and mechanical revascularization is recommended.

PERICARDITIS
Fibrinous or fibrino-hemorrhagic type is encountered in patient with acute
transmural MI on 2 nd or 3 rd day, responds to aspirin
DRESSLER SYNDROME (postmyocardial syndrome)
It is a delayed autoimmune pericarditis, pleuritis and/or pneumonitis that
occurs following cardiac surgery or myocardial infarction. It is
characterized by pleuro-pericardial chest pain and fever. Develops within
few days to 6 weeks. Respond to aspirin

THROMBOEMBOLISM
Observed in15-49% of cases, occur in association with large infarct, hear
failure and left ventricular thrombosis. Results due to abnormality in the
contractility with endocardial damage.
Treatment: systemic anticoagulant

LEFT VENTRICULAR ANEURYSM


Late complication. Commonly due to large anteroseptal transmural infarct
healing into thin scar. Complicated by congestive heart failure, arterial
embolism and arrhythmias.
INFARCT EXTENSION
New necrosis may occur adjacent to an existing infarct. Commonly results from
retrograde propagation of thrombus, more proximal vasospasm, impaired
cardiac contractility or appearance of arrhythmia.

INFARCT EXPANSION
It is disproportionate stretching, thinning and dilatation of the infarcted region
(especially with anteroseptal infarcts), which is often associated with mural
thrombosis. Early MI expansion likely provides the substrate for scar thinning
and late aneurysm formation.

Progressive late heart failure (chronic IHD)


Propensity towards specific complications & prognosis after MI depend on
myocardial infarct size, site and transmural extent
Large transmural infarcts lead to cardiogenic shock, arrhythmia and late
congestive heart failure
Anterior infarcts are commonly complicated by regional dilatation, mural
thrombi & rupture
Posterior/inferior infarcts are accompanied by serious conduction blocks
Subendocardial infarcts are rarely complicated by pericarditis, rupture and
ventricular aneurysm
Right ventricular infarction is characterized by jugular venous distension,
Kassmaul s sign & hepatomegaly (with or without hypotension).

VENTRICULAR REMODELING

Over all mortality within first year is 30%


After one year 3-4% year
CHRONIC ISCHEMIC HEART DISEASE
(ISCHEMIC CARDIOMYOPATHY)

Progressive CHF as a consequence of long-term ischemic myocardial injury.


Many cases are associated with angina pectoris and may be preceded by AMI,
some are asymptomatic.

Morphology
Moderate to severe coronary atherosclerosis
Cardiomegaly
Myocardial hypertrophy
Dilation of all cardiac chambers
Myocardial fibrosis
Myocytolysis
Cause of Death
Arrhythmia, CHF,MI
SUDDEN CARDIAC DEATH

Defined as unexpected death from cardiac causes in individuals without


symptomatic heart disease or early after symptoms onset (usually
within 1 hour)

Most common cause of sudden cardiac death is ischemic heart disease,


usually in the form of ventricular arrhythmias.

Sudden death accounts for 50% of all cardiac deaths.


Sudden Cardiac Death

Morphology

Marked Coronary atherosclerosis: one or more 3 coronaries > 75% occlusion is present in
80-90%
50% show acute placque disruption & 25% show MI
Most die of ischemic malignant Ventricular Arrhythmia

Scars of previous MI & subendothelial myocyte vacoulization indicate severe chronic


ischemia

Morphology may be elusive


Conduction disorders

(channelopathies, long QT syndrome, short QT syndrome, WPW syndrome, Sick sinus syndrome )
PERICARDITIS
INFECTIOUS AGENTS
ACUTE Viruses
<6 WEEKS Pyogenic becteria
Tuberculosis
Fungi
Other parasites

PRESUMABLY IMMUNOLOGICALLY MEDIATED


Rheumatic fever
SUBACUTE Systemic lupus erythematosus
6 WEEKS TO 6 MONTHS Scleroderma
Postcardiotomy
Postmyocardial infarction (Dressler) syndrome
Drug hypersensitivity reaction

MISCELLANEOUS
Myocardial infarction
Uremia
Following cardiac surgery
CHRONIC Neoplasia
>6 MONTHS Trauma
Radiation

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