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Ischaemic Heart Disease Coronary Heart Disease

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Ischaemic Heart Disease.

Coronary Heart Disease.

 Atheroma of the coronary arteries:

 The commonest cause of changes in the luminal diameter of the

coronary arteries is the presence of atheromatous plaques.

 The lesions may encircle an artery or may be eccentric ;they may

be discrete and localised or involve the greater length of the

vessel.

 Acute changes in the plaques may account for unstable

angina,myocardial infarction and sudden death.,because

expansion of the lesion occurs when the endothelial cells

rupture,allowing haemorrhage into the plaque and platelet

aggregation on the endothelial surface.

Clinical feasture:



 Symptoms:





 The cardinal symptom is angina pectoris. This is a chest discomfort

precipited by exertion and relieved by rest. It is often descriped as

a pressing or constricting feeling.



 The patient may hold a clenched fist in front of the sternum to

indicate the squeezing nature of the pain,and may describe

radiating discomfort in the left arm and jaw,or even a choking

sensation in the throat.

 Dyspnoea frequently accompanies angina.

 There is usually rapid relief of the symptom with sublingual

nitrate tablets.

 The pain of myocardial infarction may be similar, but

generally begins at rest ,does not respond so well to nitrates,

lasts longer than 20 minutes and is often associated with

feeling of impending death,nausea,sweating and collapse.

 Unfortunately, in many patients with I H D ,the first

manifestation of disease may be sudden death. Prevention of

atheroma is necessary to reduce this.

 Signs :



 There are few physical findings in uncomplicated I H D.



 There may be evidence of hypertension or hyperlipidaemia

.

 Cardiac dilatation,hypertrophy ,and failure are all late features and are

non-specific.



 .Auscultation may reveals a fourth and third heart sounds over the apex

in Pt complicated with Lt vent .faliure.

 Orthopnoea,and fine basal crackles are present in Pt developing

pulmonary oedema.



 Some individuals have significant ischaemic episodes without

symptoms.This may discovered by routine ECG.

Other anginal syndromes

 The previous is a desciption of typical angina.Several other anginal

syndromes occur which are less common.



1-Crescendo angina and unstable angina:

 Both represent a state of preinfarction.In crescendo angina, a

history of increasingly frequent attacks of angina with ever-

diminishing levels of exertion is obtained.Unstable angina includes

situations where episodes of pain are frequent,may occure without

obvious cause and at rest.

 Decubitus angina is angina occuring at rest in bed.

 2-Vasospastic angina:





 Some degree of arterial spasm is probably present in most

episodes of angina, but spasm on normal coronary can

occur(rarely),this spasm can be sever enough to cause

infarction.



 In Prinzmetal’s syndrome,rest pain is associated with acute

ST segment elevation which resolves to normal with

cessation of pain.



 This condition is rare and almost involves coronary

vasospasm.

Differential Diagnosis of Angina:

 With all causes of chest pain:



 1-Angina pectoris.



 2-Angina due to Aortic valve stenosis.



 3-Acute Myocardial infarction.



 4-Aortic dissection.



 5-Acute pericarditis.



 6-Oesophageal spasm.

Chest Pain

 1-Cardiac ischemic pain:

 In a typical case the discomfort associated with myocardial

ischemia is described as a compression or tightness in the

chest which may also be felt in the throat, producing the

choking feeling being called angina pectoris.

 Site:retrosternal.

 Radiation:left side ,jaw ,arm,and forearm.

 The precipitating causes are typically those which will increase

myocardial oxygen demand beyond the coronary .Excersion

,Emotional upsets ,Cold .

 What increase:Emotions,stress,cold.

 What decrease:Rest,Nitroglycerin GTN.

 Duration:less than 10 minutes.

 Special types of angina:Unstable angina it is more

sever form of angina,if untreated can lead to myocardial

infarction.

 Myocardial infarction:



 It causes pain similar to angina in site,radiation and character but it is

usually more sever and prolonged and persists despite taking glycerin

trinitrate.



 Autonomic symptoms usually in association ,sweating

,irritability,palpitation ,nausea,and ,vomiting are common

,particularly in inferior wall infarction. Pt. may also be

breathless,restless with sensation of impending death.



 With acute anterior infarction,tendency for sympathetic activity to

dominate,--tachycardia,cool pale periphery and normal or even

slightly high Bl.pressure in early minutes.This contrasts with acute

inferior infarction,which associated with massive vagal discharge

,producing a cold sweaty periphery,bradycardia,hypotension,nausea

and vomiting.

 Painless or silent myocardial infarction is not

uncommon,particularly in diabetic patient and the elderly.



 This patients may present later with complications from their

infarct such as cardiac faliure or an arrhythmia , diagnosis may be

made retrospectively from routine electrocardiogram (ECG).

 Pericardial pain:





 Chest pain is usually more localized than ischemic pain.

 Site :retrosternal,may radiate to Lt shoulder.

 Prodroma:may be preceded by viral illness.

 Nature:stabbing and sharp.

 Made worse by :change in posture,respiration.

 Helped by :analgesics.,and NSAIDS.

 Accompanied by :pericardial rub.

 Aortic dissection:





 The sudden development of a linear tear in the wall of the aorta is

called acute dissection.

 The length of aorta affected varies from a few centimetres to the

whole vessel.

 Site:retrosternal.

 Onset:sudden.

 Nature:very sever ,tearing pain.

 Relived by:No ,tend to persist.

 Accompanied by :Hypertension,Syncope.sweating,.

 Risk factors for coronary Ht disease:

 1-Age :increased in older age due to atherosclerosis.

 2-Male sex .

 3-Postive family history of IHD.

 4-Hypertension.

 5-Hyperlipidaemia.

 6-Diabetes mellitus.

 7-Obesity.

 8-Lack of exercise.

Investigations:1-in angina:

 1-Resting ECG:

Recording the electrical activity of the heart ,usually normal

in between attacks ,in attack it may show ST segment

depression,T wave inversion.

 2-Excerise ECG :

It is recorded whilst the patient walks or run on motorized

treadmill or cycles.If there is +ve history of chest pain and –

ve resting ECG you can do stress ECG,it will be very useful

to confirm the diagnosis.

 3-Cardiac scintigraphy:Or Nuclear imaging:

 Myocardial perfusion scan at rest and with exercise,using

contrast like thallium,

 (Th -201) is rapidly taken immediately after IV

injection,reflects the distribution of blood flow to the

myocardium--areas of decreased myocardial perfusion means

ischemia.(receive less thallium).



 4-Echocardiography:Use echoes of ultrasound waves to map

the heart and study its functions.This can be used to assess

ventricular wall involvement..and vent.function,

 Regional wall motion abnormalities at rest reflect previous

ventricular damage.



 5-Coronary angiography:

 This is occasionally usefull in Pt with chest pain and the diagnosis

is un clear.This can be done through cardiac catheterisation.



 Coronary angiography is performed using catheters designed to

select Lt and Rt coronary artery,inject X- ray contrast

medium.,then the coronaries can be visualized.



 it is usefull because it shows the exact coronary affected ,with

narrowing or obstruction .

Normal coronary angiography.

Coronary narrowing.

Treatement of angina:

 1-Treatment of risk factors:





Hypertension ,DM,Obesity,stop smoking.Hyperlipidemia.



 2-Medical treatement :

1- Vasodilators:Nitrates

.Glyceryl trinitrate(GTN)-tablets,and,skin patches.

Isosorbide dinitrate(oral,short acting+sustained release)

Isosorbide mononitrates-(oral some SR)

2- Beta blockers.

Atenolol(B1-selective)

Propranolol(non-selective.both tacken orally..

3- Calcium channel blockers.Nifedipin,Diltiazem,Verapamil.



3-Surgical :Coronary artery bypass grafting and angioplasty.

Treatment of unstable angin

 1-ICU admission.

 2-Bed rest and light sedation.

 3-Oxygen.

 4-Low dose aspirin.antiplatlet aggregator.

 5-Heparin IV ,to minimise thrombus formation.

 6-Nitrates (buccal or iv)

 7-Close monitoring of blood pressure during nitrate infusion.care

about hypotension.

 8-B-blockers and Ca antagonists may be added when needed.

 In vasospastic or prinzmetal angina,the aim of treatment is to

prevent the powerful vasoconstriction:

 Combination therapy using long acting isosorbide

mononitrate,+calcium antagonists.

 Beta-blockers may have to be added to counteract the reflex

tachycardia and reduce the intensity of angina by reducing 02

demand during the attack.

 Investigations in acute MI:



1-ECG: Q-wave ,and riased ST segment in affected leads.



2-Cardiac enzymes:



 Creatinin kinase CK --CK-MB(cardiac specific).increased withen few

hours,and decreased in 24-48 hours.



 Cardiac-specific troponins :Troponin I .,are regulatory proteins,increased in

cardiac injury.



 Lactate dehydrogenase ( LDH):appers withen 12-24 hours,and disappered late.



3-A raised polymorphonuclear leucocyte count and elevated (ESR) are non specific

companiments of acute MI.

Treatment of acute MI:

 Acute management:



 Analgesia and oxygen,+bed rest.

.

 If acute MI diagnosed ,Thrombolysis must be done with out delay .Six

hours is the time limit withen which it is possible that measures to restore

Bl.supply.



 Thrombolytic treatement can achieve reperfusion in 50%-70% of

patients,and usually reduces the extent of ventricular damage and mortality

rate.



 Streptokinase (1.5 million units over one hour) is the agent most

commonly used.





.

Asiprin ,as an antiplateletes,150 mg chewed.



Heparin.





Nitrates,by infusion early ,later on we can use skin patches.



B-blockers,-decreased the rate of cardiac deathes.



Follow up.

Complications of acute MI;

 Acute complications:

1-Very early after infarction,all kinds of cardiac arrhythmia can

occur like:

Ventricular extrasystoles

Ventricular tachycardia

Ventricular fibrillation.

Atrial fibrillation.

Sinus tachy or bradycardia.

Conduction disturbance.

 2-Cardiac failure.





 3-Cardiogenic shock.





 4-Thromboembolism ,due to Lt ventricular mural thrombus may

form on the endocardial surface of the infarcted region.



 5-Acute ventricular septal rupture and ruptured papillary

muscle.Treatment is early surgery for both.

 Late complications:





1-Pericarditis:can occure after MI as an early complication;occur days after

infarction,clinically: sharp chest pain aggrevated by movement.



2-Post myocardial infarction syndrome(Dressler syndrome):

Late complication:It is an autoimmune pericarditis ,(antibodies aginst

cardiac myocytes were detected) occur weaks or months after infarction

consists of pericarditis, fever,high ESR, and pericardial effusion.,treated

by NSAIDs,and corticosteroids.Prognosis is good.



3-Left ventricular aneurysm .



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