Cvs Disease

Chapter

six

Cardiovascular System Disease

Section 1

Atherosclerosis (AS)

Definition Atherosclerosis is a disease of large and medium sized arteries, characterised by lipid deposition and fibrosis. fibrosis

atherosclerosis

Arteriosclerosis

arteriolosclerosis

medial calcification

Aetiology and Pathogenesis Hard risk factors 1. Abnormality of blood lipid

LDL↑

HDL↓

2. Hypertension 3. Smoking 4. Diseases which can cause secondary hyperlipemia Soft risk factors 5. obesity 6. Genetic factors 7. Less exercise and others

pathogenesis  Response

to injury hypothesis  Lipid infiltration/insudation hypothesis  Clonal proliferation hypothesis

Foam cells

Pathologic change Fatty streaks or dots

Fibrous plaque

Atheromatous plaque

Complicated lesion

Morphology Fatty streaks and dots Lipid infiltrate to intima from the plasma macroscopically, flat or slightly elevated yellow streaks or dots. Microscopically, accumulation of lipid in smooth muscle cells and macrophages——foam cells accumulation. Fatty streaks and dots usually formed in early age, although they may evolve

Fatty streaks

Fibrous plaque  Grossly

a elevated flat or round lesion (0.31.5cm) whitish-yellow or waxy white.  Microscopically, foam cells aggregate to form a plaque, with slightly central necrosis. The surface fibrous tissue proliferate to form a fibrous cap.

Fibrous plaque

Fibrous plaque Grossly a elevated flat or round lesion (0.3-1.5cm) whitish-yellow or waxy white. In large lesions, the central portion is frequently soft containing degenerated and necrotic tissue, free fat and visible cholesterol crystals. Microscopically, the cholesterol appears as clear, elongated, fusiform clefts because the crystals have been dissolved out in preparation of the section, a core of amorphous extracellular lipids. It typically is composed of a superficial fibrous cap containing smooth muscle cells , scattered leukocytes, and dense connective tissue overlying a cellular zone with smooth muscle cells, macrophages, and T lymphocytes; and a central necrotic core containing dead cells, lipid, cholesterol clefts, lipidladen foam cells (macrophages and smooth muscle cells), and plasma proteins. In the periphery are proliferating small blood vessels attempting to organize the plaque.

Atheromatous plaque (atheroma)  Grossly,

the soft yellow nodules  Microscopically, besides the aggregation of foam cells, there severe necrosis in the centre of the plaque with the formation of cholesterol crystals, which are clear, elongated, fusiform clefts. (The lipid substance was dissolved by solvents during the staining process.)

Atheromatous plaque

Atheromatous plaque

Atheromatous plaque The soft yellow nodules is an atheroma. In advanced lesions, ulceration of atheroma and superimposed thrombi may be seen. The internal elastic lamina is frayed and fragmented, and in places, it may be absent. Calcium salts become deposited in the atheromatous lesions, and form thin, brittle, calcified plates, which may crack easily. The atheromatous lesions are much more prevalent in the abdominal than in the thoracis aorta. Their distributions is patchy, at point of stress. e.g., vessels on the posterior wall of the aorta and at the point of branching of major vessles.

Complicated lesion Hemorrhage into the plaques Atheromatous ulceration Superimposed thrombi Formation of an aneurysm

Complicated lesions  Hemorrhage

into the plaque: induced by the rapture of the plaque or the damage of the trophic blood vessels.  Ulceration: rapture of the plaque, which can induce thrombosis or embolism secondarily.

Thrombosis over the plaque Producing occlusion of the lumen, or, in the case of small thrombi may organize, become incorporated into the intima, and contribute to growth of the plague. Calcification and ulceration  Formation of an aneurysm: the disordered artery dilated because of thinning and weakening of the media adjacent to the large plaque.

Narrowing of the lumen, resulting in ischemia. Obstruction of small vessels, caused by the plaque itself or one of its complications may lead to serious ischemic effects— e.g., sudden death or myocardial in farct, with involvement of the coronary arteries, infarct of the brain in cerebral atherosclerosis, and hypertension with renal arterial disease. The Leriche syndrome, occurring chiefly in men and characterized by ischemic effects in the lower limbs. Symptomatic atherosclerotic disease most often relates to the heart, brain, kidneys, lower extremities, and small intestine.

Atherosclerosis

Atheromatous ulceration

Calcification

Atherosclerosis lesions in main arteries

1. Aorto-atherosclerosis

2. Coronary

3. Carotid and Cerebral atherosclerosis

4. Renal atherosclerosis

Atherosclerotic contracted kidney

5. Artery of extremity

6. Mesenteric artery

Section 2 Coronary atherosclerosis and coronary heart disease

Coronary atherosclerotic heart disease≈ Coronary heart disease. Besides of the atherosclerosis, the vasopasm, thrombosis can also induce coronary heart disease, which usually is called ischemic heart disease, including angina pectoris, myocardial infarction, sudden cardiac death, fibrous myocardium. The left anterior descending branch, which is responsible for blood supply for anterior wall of left ventricle and 2/3 anterior part of the interventricle septum, is most frequently

Angina pectoris Angina pectoris is episodic chest pain caused by ischemia of the myocardium, which commonly radiates from the substernal and left pectoral regions to the left shoulder and medial aspect of the left arm. Typical or stable angina pectoris: a predictable angina that occurs at a fixed level of exercise, as a result of an increased demand in myocardial work. Variant angina: this is angina at rest or, some cases, awakens the patient from sleep caused by an increase in the coronary vasomotor tone Unstable angina pectoris: the frequence of the angina increases gradually.

Myocardial infarctions Myocardial necrosis result from the break of coronary blood supply

Types Subendocardial myocardial infarction Limited to the inner one third of the ventricular wall Transmural myocardial infarction Infarction of full thickness of ventricular wall Occlusion of the anterior descending branch of the left coronary artery produces an infarct of the anterior part of the interventricular septum, the apical and anterior part of the wall of the left ventricles.

Various coronary arteries

frequencies

The sites of regional infarction

Left anterior 40-50% descending coronary artery

Anterior and apical left ventricle, anterior 2/3 of the interventricular septum

Left circumflex coronary artey

15-20%

Lateral wall of left ventricle

Right coronary artery

30-40%

Posterior wall of the left ventricle Posterior 1/3 of the interventricular septum.

Pathologic change

6 hours

8~9 hours

After 4 days The necrotic muscles fibres are swollen, hyalinized, and lacking their striations and nuclei, leukocytes abundantly infiltrate the area.

After 7 days Granulation tissue formation

2-8 weeks The healing of myocardial infarcts is by scar tissue, replacing the destroyed muscle, which does not regenerate.

Complications (1) Functional disorder of papillary muscle (2) Rupture of the heart (3) Ventricular aneurysm (4) Mural thrombosis (5) Acute pericarditis

cardiogenic shock, arrhythmias

Fibrosis of the myocardium

Sudden cardiac death

Section 3

Primary Hypertension

Primary hypertension is so called because these seemed to be no primary lesion.

systolic pressure ≥140mmHg diastolic pressure ≥90mmHg

Secondary hypertension ( symptomatic hypertension)

Aetiology and Pathogenesis

1. Genetic factors 2. Diet

Na+

3. Vocation, social and psychological stress

Renin —— Angiotensin —— Aldosterone

Cases of high blood pressure commonly are divided into primary (essential) and secondary (symptomic) types. The less common secondary type is a result of renal disease (such as chronic pyelonephritis and glomerulnnephritis), renal artery stenosis , cerebral or cardiac vascular disease, or endocrine lesions, such as an adrenal or pituitary tumor. The common essential type of hypertension is so called because these seemed to be no primary lesion. It has been recognized that renal arteriolar sclerosis is an almost constant postmorten finding in essential hypertension. The arteriolar sclerosis is often a generalized change, particularly common is the spleen, pancreas, adrenal glands, and brain, but it is only in the kidneys that arteriolar sclerosis and hypertension seem to be closely associated.

Types and pathologic change

Benign hypertension 1. Dysfunctions stage spasm of arteriole

3 stages

2. Artery systemic changes Arteriolosclerosis musle arteriole elastic musclar artery

fibrosis AS

Arteriolosclerosis (Hyaline degeneration of arteriole)

3. Organs change Hypertensive heart disease

kidney of hypertension

Primary granular contracted kidney

brain change

cerebral hemorrhage Retinal change

malignant hypertension

Hyperplastic arteriosclerosis Necrotizing arteriolitis

Section 4 Rheumatism Laryngopharynx Group A beta-hemolytic streptococci

Allergic disease

Connective tissue, Aschoff body

Affects the heart, arteries, joints, skin, subcuteneous tissues and the nervous system

rheumatic fever

Aetiology and Pathogenesis

It generally is agreed that is occurs after infection with Group A beta-hemolytic streptococci. streptococci The lesions of rheumatism are not the result of direct infection by these organisms but represent an allergic or hypersensitivity reaction.

Ab-Ag crossing reaction

Pathologic change

1. Nonspecific inflammation

1. granulomatous inflammation

3 stages

Alternative and degeneration stage

proliferative stage Around the fibrinoid necrotic foci the proliferation of histocytic cells, forming a granuloma. In their charcteristic form, as may be seen in the myocardium, each of these minute nodules of proliferation inflammaties is known as an Aschoff body. body

Fibrosis or healing stage

Different organs rheumatic lesions Carditis

Rheumatic heart disease Chronic rheumatic heart disease

Endocarditis the mitral valve

vegetation

Myocarditis Aschoff bodies

Rheumatic pericarditis

Rheumatic arthritis

Erythema annullare

Subcutaneous nodules

Rheumatic arteritis

Chorea minor

Section 6

Valvular vitium of the heart

Mitral stenosis Rheumatic inflammation

Apex of heart, diastole murmur

left atrium failure → lung congestion → right heart failure → systemic congestion

X ray: pear like heart

Mitral insufficiency

Combined with mitral stenosis

Apex of heart, systole murmur

left heart failure → lung congestion → right heart failure → systemic congestion

Aortic stenosis aortic valve, ejective murmur

left atrium failure → lung congestion → right heart failure → systemic congestion

Angina pectoris, pulse pressure ↓

X ray: boot like heart

Aortic insufficiency aortic valve, diastole murmur

left atrium failure → lung congestion → right heart failure → systemic congestion

Pulse pressure ↓

water-hammer pulse, pistol shot sound

Valvular vitium of the heart result from a healed or chronic valvulitis or, occasionally, are congenital malformations. The results of imflammation in the valves are seen as thickening, adhesions, retraction, and shortening of the leaflets. There may be a narrowing of the valve opening (stenosis), or closure of the valve may be insufficient so that leakage (regurgitation) occur through it. Valvalar insufficiency and stenosis may be produced by the same deformity. Valve deformities are common on the left side of the heart (aortic and mitral) but are uncommon on the right side (tricuspid and pulmonary).

Mitral stenosis Mitral stenosis is one of commonest valve deformities and almost invariably is caused by rheumatic inflammation. Fibrous thickening, adhesions, and retraction of valve leaflets with bridging and calcification across the commissures and chordae are thickened, fused, and shortened, May produce all degrees of stenosis. The orifice may be narrowed to a tiny slit “fish mouth” or “button hole” stenosis. The rigidity and retraction usually cause some insufficiency of the valve as well. Inceased work of the left atrium will compensate for a mild mitral stenosis. A more severe uncompensated stenosis results in increased pressure and stasis in the pulmonary circulation and increases the work of the right ventricle. Thus left atrial dilatation, chronic passive congestion of the lungs, and right ventricular hypertrophy constantly accompany any great degree of mitral stenosis. In pure stenosis, the left ventricle is normal or small in size. Clinically left heart failure and right heart failure X-ray shows the heart like a pear.

6.2 Mitral insufficiency Mitral insufficiency essentially caused by rheumatic endocarditis and secondery by SBE, and occasionally by congenital heart disease. Regurgitation through the mitral valve is most often a relative insufficiency resulting from the dilatation of the mitral ring accompanying a dilatation of the left ventricle, but insufficiency also may be caused by shortening and retraction of the leaflets and chordae tendineae. If regurgitation is severe, one finds left atrial dilatation along with hypertrophy of the left and right ventricles. X-ray shows the heart like a ball.

6.3 Aortic stenosis Aortic stenosis may occur as a pure lesion, but frequently it is associated with aortic insufficiency. Noncalcific valvular sterosis ususally is caused by rheumatic fever. Congenital valvular and subaortic stenosis also occur. Bicuspid aortic valve is sometimes associated with aortic stenosis. Calcific aortic stenosis is attributed mainly to rheumatic fever. However, when it occurs in advanced age; particularly in the absence of lesions in other valves, it is ragarded as atherosclerotic in origin. Healed bacterial endocarditis, especially related to Brucella organisms, is a possible cause. Left ventricular failure, hypertrophy, and dilatation (poststenotic dilation of the aortic root) result from the stenosis. Angina pectoris appears frequently because of a reduced coronary blood flow syncope with increase risk of (in hypertrophied myocardium) sudden death and chronic heart failure. The differences of pressure pulse pressure and systemic diastolic pressure are diminishing. X –ray show the heart like boots.

Aortic insufficiency Regurgitation through the aortic valve during diastole may result from dilatation of the aortic ring or from changes in the leaflets themselves. Dilatation of the ring may accompany dilatations of the rest of the heart ,or it may result from disease such as syphilitic aortitis and Marfan syndrom. Changes in the leaflets are commonly caused by syphilitis or rheumatic fever and SBE. The leaflets may be simply affected or distorted at the commissure, but often the whole leaflets is thickened, with rounded edges and distinct shortening and retraction.

Diastolic regurgitation through the aortic valve is accompanied by a significant fall of systemic diastolic pressure and hence a high pulse pressure ( the differences between the higher pulse pressure and lower diastolic pressure are increasing). Severe hypertrophy and dilatation of the left ventricle result from the extra work. Fibrosis of the endocardium, with formation of endocardial “pockets”, caused by the regurgitating blood, is a characteristic feature. Angina pectoris may result from coronary insufficiency (related to low diastolic pressure). And an increased demand of the hypertrophied heart for more oxygen. In turn left heart failure, pulmonary atery, congestion high pressure and right heart failure . Clinically around blood vessels sign. X-ray shows that heart like a ball.