Pathology of Coronary Heart Disease 2009

8/14/2019 Pathology of Coronary Heart Disease 2009

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Coronary heart disease

Atherosclerosis

- The commonestarterial diseasecharacterized by

formation of fibrofatty plaques,formed of a deepersoft part and a hard

sclerotic fibrous cap

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

Risk factors

- Constitutional risk factors.

- Hard risk factors

- Soft risk factors

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

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

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

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

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.

Pathogenesis of Atherosclerosis

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)

• 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

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.

Complicated atheromas

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.

*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 .

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

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.

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.

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 .

There are three overlapping patterns ofangina pectoris:

(1) Stable or typical angina.

(2) Prinzmetal or variant angina.

(3) Unstable or crescendo angina.

Angina Pectoris

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

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.

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.

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

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

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

(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.

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

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

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

Acute MI

Neutrophilic infiltrate along with areas ofnecrosis, diffuse interstitial edema and palemyocytes with fading nuclei and decreased

striations

Acute MI

Old MI

MI with mural thrombus

(MI) i

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

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

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

Chronic Ischemic Heart Disease

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

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

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.

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.

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.

Pathology of Coronary Heart Disease 2009

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