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Coronary heart disease
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Atherosclerosis
- The commonestarterial diseasecharacterized by
formation of fibrofatty plaques,formed of a deepersoft part and a hard
sclerotic fibrous cap
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Epidemiology a. Most common cause of morbidity causedby vascular disease.
b. Highest incidence in Finland, WesternEurope, USA and Canada.
c. Increased incidence with advanced age.d. More in males than females up to theage of menopause.
Atherosclerosis
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Risk factors
- Constitutional risk factors.
- Hard risk factors
- Soft risk factors
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Nonmodifiable:Age…The number and severity ofatheromatous lesions increase with
age.Sex…More common in males thanfemales up to the age of 55 years.Estrogen has a protective effect ??
Familial predisposition…Familialhyperlipidemia (hypercholestrolemia)is associated with increased risk ofatherosclerosis.
Risk factors
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Modifiable: - Hyperlipidemia…Increased level of
cholesterol and LDL is associated with
increased risk of atherosclerosis.On the contrary, HDL has a protectiveeffect against atherosclerosis.
- Hypertension- Diabetes mellitus…due to associated
hyperlipidemia - Cigarette smoking
Risk factors
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Modifiable: - Exercise… Reduces the incidence of
atherosclerosis and death from
ischemic heart diseases - Overweight….Atherogenic diet high in
animal saturated fatty acids and
cholesterol.. High complex sugars in diet.. Low vegetables and fish.
- Stress and personality…Personality A
Risk factors
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Reaction to injury formulation
Injury (or dysfunction) of endotheliumleads to…
Entry of monocytes and lipids to
subendothelim.T cells located in the arterial wall
produce cytokines such as TNF, IL-6 and
IFN-γ that stimulate endothelial cellsand activate macrophages.
Platelet adhesion and aggregation.
Pathogenesis of Atherosclerosis
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Pathogenesis of AtherosclerosisRelease of mitogenic factors from
platelets andmacrophages…..proliferation andmigration of smooth muscle fibers.
Monocytes and smooth muscle cellsengulf lipid and cause lipid depositioninto the lesion.
At later stages, macrophages secretemetalloproteinases that digest collagenat the fibrous cap causing weakness and
rupture of the plaque.
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Pathogenesis of Atherosclerosis
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Pathology of atherosclerosisSites….
* Aorta, especially descending* Coronaries and cerebrals* Femoral , renal, superior mesenteric
and internal carotids.Grossly….- Multiple irregular patches more aroundostea of branches.
- Color ranges from yellow to whiteaccording to relative amount of fat andfibrous tissue.- Covered by glistening intima (if notcomplicated)
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• The plaques are formed of
• 1- Central core of cholesterol and cholesterol
esters, lipid laden macrophages (foam cells),necrotic debris and calcification.2- Subendothelial fibrous cap formed ofproliferated smooth muscle cells, foam cells
and extra cellular matrix
Pathology of atherosclerosis
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Complications of atherosclerosis
1- Narrowing of vascular lumen…chronicischemia.2- Superimposed thrombosis…acute
ischemia.3- Ulceration with liberation of fatty
core … acute ischemia, fat emboli, DIC. 4- Pressure atrophy of the media with
fibrosis….weakening of the wall ….Aneurysmal dilatation.
5- Dystrophic calcification.
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Complicated atheromas
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Ischemic heart disease (IHD)
Is a group of closely relatedsyndromes resulting from
myocardial ischemia withimbalance between thesupply (perfusion) and
demand of the heart foroxygenated blood.
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IHD
*Ischemia is not only insufficiencyof oxygen, but also reducedavailability of nutrient substrates
and inadequate removal ofmetabolites
*In more than 90% of cases, the
cause of ischemia is reduction incoronary blood flow due toatherosclerotic coronary arterial
obstruction .
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Clinical manifestations of IHD
Myocardial infarction: the most
important form of IHD, in which theduration and severity of ischemia issufficient to cause death of heart
muscle Angina pectoris: in which the
ischemia is less severe and does not
cause death of cardiac muscle . Chronic IHD with heart failure
Sudden cardiac death
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Pathogenesis of IHD
Acute Change on top of atheromatousPlaque
Disruption, Thrombosis, vascular spasm
Coronary Thrombosis*luminal obstruction by thrombosis isusually incomplete (mural thrombus).
* thrombus superimposed on partiallystenotic plaque converts it to a totalocclusion.
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Pathogenesis of IHDVasoconstriction (vasospasm)
Vasoconstriction compromises lumen, and, byincreasing mechanical forces, can potentiateplaque disruption. Vasoconstriction at sitesof atheroma is stimulated by:
(1) circulating adrenergic agonists.(2) locally released platelet contents.(3) Imbalance between endothelial cell
relaxing factors and contracting factors(e.g., endothelin) due to atheroma-associated endothelial dysfunction.
(4) Mediators released from perivascularinflammatory cells.
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Angina Pectoris
Paroxysmal and usually recurrent attacksof substernal or precardial chestdiscomfort (variously described asconstricting, squeezing, choking, orknifelike) caused by transient (15seconds to 15 minutes) myocardialischemia that falls short of inducing the
cellular necrosis that defines infarction .
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There are three overlapping patterns ofangina pectoris:
(1) Stable or typical angina.
(2) Prinzmetal or variant angina.
(3) Unstable or crescendo angina.
Angina Pectoris
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They are caused by varying combinationsof increased myocardial demand anddecreased myocardial perfusion, owingto fixed stenosing plaques, disruptedplaques, vasospasm, thrombosis, plateletaggregation, and embolization.
Angina Pectoris
St bl i
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Stable angina The most common form (typical) appears
to be caused by the reduction ofcoronary perfusion to a critical level bychronic stenosing coronaryatherosclerosis.
The attacks are provoked by physicalactivity, emotional excitement, or anyother cause of increased cardiac
workload.Typical angina pectoris is usually relievedby rest (decrease demand) ornitroglycerin, a strong vasodilator.
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Prinzmetal angina
An uncommon pattern of episodic anginaoccurs at rest and is due to coronaryartery spasm. Although individualswith this form of angina may well havesignificant coronary atherosclerosis,the anginal attacks are unrelated to
physical activity, heart rate, or bloodpressure.
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Unstable angina
Progressively increasing pain frequency,is precipitated with progressively lesseffort, often occurs at rest, and tendsto be of more prolonged duration .
It is induced by disruption of anatherosclerotic plaque withsuperimposed partial (mural)
thrombosis and possibly embolization orvasospasm or both.
It is referred to as preinfarction angina
and in the spectrum of IHD
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Myocardial Infarction
1-Transmural Infarction
Most myocardial infarcts are
transmural ,in which the ischemic
necrosis involves the full or nearly fullthickness of the ventricular wall in thedistribution of a single coronary artery.This pattern of infarction is usuallyassociated with coronaryatherosclerosis, acute plaque change,and superimposed thrombosis
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2- Subendocardial (nontransmural)infarct: It constitutes an area of ischemic
necrosis limited to the inner one third
or at most one half of the ventricularwall.It occurs as a result of a plaque
disruption followed by coronary
thrombus that becomes lysed beforemyocardial necrosis extends across themajor thickness of the wall
Myocardial Infarction
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(MI) Incidence and Risk FactorsMI occurs at any age, but the frequency
rises progressively with increasing ageand when predispositions toatherosclerosis are present ,such as
Hypertension,
Cigarette smoking, Diabetes mellitus,
Genetic hypercholesterolemia, Causes of hyperlipoproteinemia. Nearly 10% of myocardial infarcts occurin people under age 40, and 45% occurin eo le under a e 65.
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Blacks and whites are equally affected.Throughout life, men are at significantly
greater risk of MI than women withprogressively declines with advancingage
IHD is the overwhelming cause of deathin elderly women. Moreover, recent
epidemiologic evidence suggests thatpostmenopausal hormone replacementtherapy does not protect women againstMI
(MI) Incidence and Risk Factors
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Before 6-12 hours, MI is inapparantonly by histochemical techniques.
By 18-24 hours, infarcted tissueappear pale to cyanotic area.
In the 1st week, lesions areprogressively more define, yellow andsoft.
7-10th day, hyperaemic granulationtissue fill the are
6th week, white fibrous scar.
(MI) Morphology, Gross
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Within 1hour,there is intracellularedema. Myocyte at the paripherybecomes wavy and contracted.
By 12-72 hours, dead myocyte becomes
hyperesinophilic with loss of nuclei(coagulative necrosis).
From 3 -7 days, dead myocyte are
digested by invading macrophages.7-10th day, granulation tissue replaces
necrotic tissue leading to dense fibrousscar .
(MI) Morphology, Microscopic
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Acute MI
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Acute MI
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Acute MI
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Neutrophilic infiltrate along with areas ofnecrosis, diffuse interstitial edema and palemyocytes with fading nuclei and decreased
striations
Acute MI
ld M
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Old MI
Old M
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Old MI
Old MI
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Old MI
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MI with mural thrombus
(MI) i
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The location and severity of development of
myocardial infarction depends on:The size of the vascular bed perfused by
the obstructed vesselsThe duration of the occlusionThe metabolic/oxygen needs of the
myocardium at riskThe extent of collateral blood vessels
The presence, site and severity ofcoronary arterial spasm
Other factors, such as alterations in bloodpressure, heart rate, and cardiac rhythm.
(MI) severity
(MI) Cli i l F
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Typical symptoms, biochemical evidence,
and by the ECG pattern
Laboratory evaluation is based onmeasuring the blood levels of intracellular
macromolecules that leak out of fatallyinjured myocardial cells through damagedcell membranes; include myoglobin, cardiactroponins T and I, creatine kinase (CK),lactate dehydrogenase, and many others.they do not reflect its mechanism Troponinlevels remain elevated for 7 to 10 days after
the acute event.
(MI) Clinical Features
(MI) C li i
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o Arrhythmias
o Myocardial ruptureo Pericarditiso Right ventricular infarction
o Infarct extensiono Infarct expansiono Mural thrombus
o Ventricular aneurysmo Papillary muscle dysfunctiono Progressive late heart failureo Contractile dysfunction
(MI) Complications
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Chronic Ischemic Heart Disease
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Chronic Ischemic Heart Disease(CIHD)
Progressive heart failure as aconsequence of ischemic myocardialdamage.
The term ischemic cardiomyopathy isoften used by clinicians to describeCIHD.
In most instances, there has beenprior MI and sometimes previouscoronary arterial bypass graft surgeryor other interventions.
Chronic Ischemic Heart Disease
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Morphology: Hearts are usually enlarged and heavy,secondary to left ventricular hypertrophy anddilation.
Discrete, gray-white scars of healed infarctsare usually present. The mural endocardium is
generally normal except for some superficial,patchy, fibrous thickenings, although mural
thrombi may be present.The major microscopic findings includemyocardial hypertrophy, diffuse subendocardialvacuolization, and scars of previously healed
infarcts.
Chronic Ischemic Heart Disease(CIHD)
S dd C di D th
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Sudden Cardiac Death
unexpected death from cardiac causes
early after symptom onset (usually within 1hour) or without the onset of symptoms.In many adults, SCD is a complication andoften the first clinical manifestation ofIHD.Increased cardiac mass is an independentrisk factor for cardiac death; thus, some
young patients who die suddenly, includingathletes, have hypertensive hypertrophy orunexplained increased cardiac mass as theonly finding.
Sudden Cardiac Death
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With decreasing age of the victim, the followingnonatherosclerotic causes of SCD becomeincreasingly probable: Congenital structural or coronary arterialabnormalities
Aortic valve stenosisMitral valve prolapseMyocarditisDilated or hypertrophic cardiomyopathy
Pulmonary hypertensionHereditary or acquired abnormalities of thecardiac conduction systemIsolated hypertrophy, hypertensive or unknown.
Sudden Cardiac Death
Sudden Cardiac Death
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The ultimate mechanism of SCD is most
often a lethal arrhythmia (e.g., asystole,ventricular fibrillation) triggered byelectrical irritability of myocardium
induced by ischemia.The prognosis of patients risky forSCD, is markedly improved by
implantation of an automatic cardioverterdefibrillator, which senses andelectrically counteracts an episode ofventricular fibrillation.
Sudden Cardiac Death
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Thank
you