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Date posted: November 29, 2011

Dr Meera Narendran BHMS,MD(Hom)
The coronary circulation
The arterial supply of heart is derived from right and left coronary arteries. The left main coronary artery divides into the left anterior descending artery and the circumflex artery.

Left anterior descending artery

  • Gives branches to supply the
  • Anterior left vetricle
  • The apex
  • The anterior part of the septum

Left circumflex artery

  • Gives marginal branches to supply the
  • Posterior left ventricle
  • Inferior Surface

The right coronary artery

  • Gives branches to supply the
  • Right atrium
  • Right ventricle
  • Infero-posterior aspects of the left ventricle.

The SA node is supplied by the right coronary artery in 60% of individuals, and AV node in 90%.
So abrupt occlusion of the

  • 1. RCA Causes infarction of the inferior part of the left ventricle and right ventricle.
  • 2. LAD or LCX Infrarction in the corresponding territory.
  • 3. Occlusion of left main artery is usually fatal

Ischaemic heart disease or (coronary heart disese)
Ischaemic heart disese is defined as the accute or chronic form of cardiac disability arising from inbalance between the myocardial supply and demand for oxygenated blood.

Etiopathogenesis
IHD is invariably caused by disease affecting the coronary arteries, the most prevalent is atheroscleresis account for about 90% cases. So etiology of IHD can be consider under 3 headings.
1. Coronary atherosclerosis
2. Superadded changes in coronary atheresclerosis
3. Non-atherosclerotic causes

I. Coronary atherosclerosis
Coronary atherosclerosis resulting in fixed obstruction is the major cause of IHD in more than 90% cases.
Atherosclerotic leisions are distributed in one or more of the three coronary arterial trunks, the highest incidence in the descending branch of the left coronary followed by the right coronary artery and still less in circumflex branch of the left coronary. About 1/3 of cases have single vessel disease, most often in left anterior descending arterial involvement.
The atheroscerotic plaques in the coronary are more often eccentrically located bulging into the lumen from one side. The area of severest involvement is about 3 to 4 cm. from the coronary ostia more often at or near the bifurcation of the arteries. Significant stenotic leisions that my produce chronic myocardial ischamia show more than 75% reduction in the cross – sectional area of a coronary artery or its branch. Complication like calcification, coronary thrombosis, ulceration, haemarahage, rupture and aneurysm formation can occur in these vessels.

II. Superadded changes in coronary atherosclerosis
The attacks of acute coronary syndromes namely acute myocardial infraction, unstable angina and sudden ischemic death are precipitated by certain changes superimposed on a pre-existing fixed coronary atheromatous plaque.
1. Acute changes
Such as plaque haemarrhage fissuring or ulceration that result in embolisation of atheromatous debris.
2. Coronary artery thrombosis
Transmural acute myocardial infraction is often precipitated by partial coronary thrombosis. It occurs due to surface ulceration of fixed atheromatous plaque, ultimately causing complete luminal occlusion. The lipid core of plaque is highly thrombogenic

III. Non-atherosclerotic causes
A number of other leisions may cause IHD in less than 10% of cases.
1. Vasopasm
2. Stenosis of coronary ostia:- From extension of syphilitic aortitis or from aortic atherosclerotic plaques.
3. Arteritis - Like in rheumatic arteritis, polyarteritis nodosa, TAO etc.
4. Embolism - Embolism from elsewhere, which occurarely
5. Thrombotic disease - Eg:- Hypercoagulability of the blood.
6. Trauma
7. Aneurysm -Extension of dissecting aneurysm from aorta
8. Compression -By a primary or secondary tumour.

Effects of myocardial ischamia
Depending upon the suddenness of onset, degree, duration, location and extent of the area affected by myocardial ischamia, there can be two types of ischamic manifestations.
a. Myocardial infarction
b. Non-infract effects of myocardial ischamia which include.
Angina pectoris
Chronic ischamic heart disease
Sudden cardiac death

Major risk factors for coronary artery disease
Fixed Modifiable
1. Age 1. Smoking
2. Male Sex 2. Hypertension
3. Family history 3. Lipid dlisorder
4. Diabetes Mellitus
5. Haemostatic variables
6. Sedentary life style
7. Obesity
8. Dietary deficiencies of antioxidant ,vitamins and polyunsaturated fatty acids.

Myocardial infarction
Acute myocardial infarction is the most important consequence of coronary artery disease.
Incidence
The incidence of Myocardial infarction correlates well with the incidence of atherosclerosis in a geographic area.
Age:- Occur in all ages incidence is higher in the elderly
Sex:- Males have an increased risk. After menopause sex difference gradually declines.
Etiopathogenesis
In 90% cases of MI, serve atherosclerosis (more than 75% compromise of lumen) of one or more of the the three major coronary arteries is the etiology.

1. Machanism of myocordial ischamia can be due to
a. Diminised coronary bood flow.
b. Increased myocardial demand.
c. Hypertrophy of the heart without simultaneous increase of coronary blood flow.

2. Role of platelets
Rupture of an atherosclerotic plaque exposes the subendothelial collegen to platelets which undergo aggregation, activation and release reaction and there will be production and release of thromboxane – A2 (local vosoconstrictor). The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of ruptured plaque, thus fibrin is formed from fibrinogen. The coronary artery eventually becomes occluded by a thrombus containing platelets aggregates and fibrin threads.

3. Complicated plaques
Two important complications in coronary atherosclerotic plaques are coronary thrombosis and haemarrhage.

4. Non-atherosclerotic causes
Like vasospasm, arteritis, embolism etc.

Types of infarcts
Infarcts have been classified in a number of ways.
1. According to the anatomic region of the left ventricle involved, they are called

  • Anterior
  • Posterior (inferior)
  • Lateral
  • Septal
  • Circumferential
  • and they can be Anterolateral
  • Posterolateral (inferolateral)
  • Anteroseptal

2. According to the degree of thickness of the ventricular wall involved infarates are of 2 types.

  • Transmural or full-thickness
  • When they involve – the entire thickness of the ventricular wall.
  • Subendocardial or laminar
  • When they involve the inner subendocardial half of the myocardium.

3. According to the age of infarcts, they are of 2 types.

  • Acute, recent or fresh infarcts
  • Healed or organised infarcts
  • Location of infarcts
  • Infarcts are most frequently located in the left ventricle. Right ventricle is less suceeptible. Atrial infarcts whenever present are more often in the right atrium. Left artium is protected because it is supplied by the oxygenated blood in the left atrial chamber.

There are three main regions of myocardial infarction
1. Stenosis of the left anterior descending artery (40-50%)

  • Infarction is seen in the
  • Anterior part of the left ventricle, including the apex
  • Anterior 2/3 of the interventricular septum.

2. Stenosis of the right coronary artery (30-40%)

  • It involves the
  • Posterior part of the left ventricle
  • Posterior 1/3 of the interventricular septum

3. Stenosis of left circumflex coronary artery (15-20%)

  • Lateral wall of the left ventricle
  • The early infacts (3 to 6 hours old) can be detected by histochemical staining for dehydrogenases by triphenyl tetrazolium chloride which imparts red brown colour to the normal heart muscle, while the area of infarcted muscle fails to stain due to lack of dehydrogenases.
  • The gross and microscopic changes in the myocardial infarction vary according to the age of the infarct and therefore described sequentially.

Sequential pathologic changes in myocardial infarction
Time Gross changes Light microscopy

First week

  • 0 – 6 hours No change or Pale No change. Stretehing and waviness of fibre
  • 6 – 12 hours No change or Pale coagulative necrosis begins. Neutrophilic in filtration. Oedema and haemarrhage
  • 24 hours cyanotic red-purple area of coagulative necrosis complete neatrophilic infiltrate well devel haemarrhage oped.
  • 4th day well defined yellow border prominent neutrophilic infiltrate some undergoing degeneration
  • 7th day Bright yellow to yellow green Being of resorption of necrosed fibres by macrophages onset of soft fibrovascular response neutrophils gradually disappear.

Second week
10th day Red-purple periphery Most of the necrosed muscle in a small infarct removed fibrovascular reaction more prominent. Pigmented macrophages, eosinophils, lymphocytes, plasma cells are present.
14th day Red-purple periphery Necrosed muscle mostly removed, neutrophils disappear fibrocollagenic tissue at the periphary.

Third week
Red-purple periphery Necrosed muscles from larger infarcts removed more in growth of fibrocollagenic tissue.
4th to 6th week Thin, grey-white, hard, shrunken fibrous scar. Increased fibrocollagenic tissue. decreased vascularity fewer pigmented macrophages lymphocytes and plasma cells.
By special techniques like electron microscopy chemical and histochemical studies, changes can be demonstrated in early infarcts before detectable light microscopic alterations appear. Injury become irreversible unless the blood flow is restored within 20-30 minutes.

1. Electron microscopic changes
They are evident in less than half an hour on onset of infarction.
a. Disappearance of perinuclear glycogen granules within 5 minutes of ischamia
b. swelling of mitochondria in 20 to 30 minutes
c. Disurption of sarcolemma
d. Nuclear alternations like peripheral clumping of nuclear chromation.
2. Chemical and histochemical changes
a. Glycogen depletion in myocardial fibres within 30 to 60 minutes of infarction.
b. Increase in lactic acid in the myocardial fibres.
c. Loss K+ from the ischaemic fibres
d. Increase of Na+ in the ischaemic cells
e. Influx of Ca++ into the cells causing irreversible cell injury

Diagnosis
The diagnosis of acute MI is made by
1. clinical features
2. ECG changes
3. Serum-enzymes

1. Clinical features
In upto half of cases, a pericipitating factor appears to be present such as vigorous physical exercise, emotional stress or a medical or surgical illness. Mostly it is seen in the morning within a few hours of awakening, due to a combination of an increase in sympathetic tone and an increased tendency to thrombosis between 6 AM and 12 Noon.
a. Pain
Describe it as heavy, squeezing and crushing. Typically involves the central portion of the chest or the epigastrium and occasionaly it radiates to the arm. Less common sites of radiation include abdomen, back, lower jaw and neck. Pain is often accompained by weakness, sweating, nausea, vomiting and anxiety.
It can also be presented as indigestion, apprehension, shock, oliguria, low grade fever and acute pulmonary oedema
b. The combination of substernal chest pain persisting for more-than 30 mts. and diaphoresis strongly suggest AMI.

2. ECG changes
ST – elevation is the earliest change. There will be Q – wave MI & Non – Q wave MI in ECG. Most patients initially presenting with ST Segment elevation evolve Q waves on the ECG and diagnased as Q – wave MI.
A small proportion may show non – Q wave MI. When the obstructing thrombus is not totally occlusive, obstruction is transient or if a rich collateral network is present, S.T – elevation will be absent ECG changes are best seen in the leads which face the infarcted area.
If the infarction is in the
1. Anteroseptal area changes in leads V1 to V4
2. Anterolateral area changes from V4 to V6, AVL and lead 1.
3. Inferior area Lead II, III and AVF while lead I, a VL and anterior chest leads show reciprocal changes that is ST depression.
4. Posterior wall of the left ventricle Reciprocal changes of ST depression and a tall
R wave inleads V1 – V4.

3. Serum cardiac markeres
1. Creatine Phosphokinase
There are 3 forms of CPK of them CPK – MB is specific for heart muscles. CPK – MB has further 2 forms CPK – MBI and CPK – MB2. CPK – MB2 is the myocardial form. A ratio of CPK – MB2 : CK – MB1 above 1.5 is highly sensitive for the diagnosis of acute MI after 4-6 hours of onest of myocardial ischamia. It disappear from blood b4 48 hours.
2. Cardiac – Specific troponins (CTn)
Immunoassay CTn is more specific for MI. Troponins are contractile muscle proteins presents in human cardiac & skeletal muscle but cardiac troponins are specific for myocardium. There are 2 types of CTn.
a. Cardiac troponin T (CTnT)
b. Cardiac troponin I (CTnI)
Both CTnT and CTnI are not found in blood normally, but after myocardial injury, their levels rise very high around the same time, when CK – MB is elevated in after 4-6 hrs. Both troponin levels remains high for much longer duration.
CTnI for 7-10 days and CTnT for 10-14 days.
3. Lactic dehydrogenase (LDH)
Lacks specificity. LDH-I is myocardial specific. Estimation of ratio of LHD-I : LDH-2 above I is helpful in making a diagnosis.
LDH levels begins to rise after 24 hrs., reach peak in 3-6 days and return to normal in 14 days.
4. AST
AST starts to rise about 12 hrs. after infarction and reaches a peak on the first of second day returning to normal within 3 or 4 days.
5. Myoglobin
Though myoglobin is the first eardiac marker to become elevated after myocardial infarction, it lacks cardiac specificity and is excreated in the urine rapidly. Its levels, thus return to normal within 24 hrs. of attack of acute MI.

Complications

  • 1. Arrhythmias
  • 2. Cogestive heart failure
  • 3. Cardiogenic shock
  • 4. Conduction defects
  • 5. Mural thrombosis and thromboembolism
  • 6. Papillary muscle dysfunction
  • 7. Ventricular aneurysm
  • 8. Repture of the interventricular septum
  • 9. Repture of the left ventricular free wall
  • 10. Shoulder – hand dystrophy
  • 11. Pericarditis
  • 12. Post myocardial infarction (Dressler’s Syndrome)
  • 13.Persistent fever, pericarditis and pleurisy

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