Ischaemic heart diseases

ISCHEMIC HEART DISEASE

Tapeshwar Yadav(Lecturer)BMLT, DNHE, M.Sc. Medical Biochemistry

INTRODUCTION Coronary artery Disease [CAD] is the most

common , serious, chronic life threatening diseases in the USA.

More than 11 million Persons have CAD in USA.

Myocardial Ischemia [Reduced blood & oxygen supply to Heart Muscle ], Caused by

Lack of oxygen due to Inadequate perfusion which result from an Imbalance

Between oxygen supply & Demand.

Most common cause of MI is Atherosclerotic disease of Epicardial coronary Arteries. Atherosclerosis causes an decrease blood supply in the Heart at Basal Level.

Epicardial coronary Arteries are major site of Atherosclerotic disease. Risk factors for for Atherosclerosis ,

1) Increased LDL 2) Decreased HDL 3) Smoking 4) Hypertension 5) Diabetes mellitus .

These are common causes to disturb the normal functions

of the vascular Endothelium.

physiological vasomotion ,pathological spasm & small platelet plugs can upset balance between oxygen supply & demand , this causes Myocardial Ischemia.

Disturbance in oxygen supply & Demand will lead to damage of cardiac muscle, Damage is Reversible OR Permanent with subsequent

Myocardial necrosis Myocardial infarction

Coronary blood flow can be reduced by Arterial thrombi, spasm & rarely Coronary Emboli .

congenital abnormalities such as anomalous origin of left anterior descending coronary from pulmonary Artery may cause Myocardial Ischemia & Infarction in Infancy, but this cause is very rare in Adults.

Myocardial ischemia can occur due to

severe left ventricular Hypertrophy, Increased in oxygen demand due to left ventricular hypertrophy & Reduction in oxygen supply due to coronary atherosclerosis such combination leads to clinical manifestations of Myocardial ischemia.

ANGINA

Abnormal constriction OR Failure of Normal dilatation of Coronary vessels can cause ischemia to heart , it is called ‘ANGINA’.

1) STABLE ANGINA, 2) UNSTABLE ANGINA. - STABLE ANGINA– It is due to transient myocardial

ischemia.

COMPLAINTS

1) Heaviness of chest, 2) Squeezing, 3) choking, 4) chest discomfort.

This symptom is lost with in 5 to 10 mts. ANGINA Can Radiate to left shoulder & to both Arms, and especially to the Ulnar surface of form Arm & Hand.

Episodes of Angina caused by Exertion, Emotion are relieved Rest [ stable angina], pain may occur at Rest [Un stable angina],

Pain may occur at night is Recumbent [Angina-decubitus]. Stable angina may Exacerbate & Remit over days, weeks OR months & can be seasonal.

- ECG is normal is more than half of patients of Angina ,but there may be signs of an Old myocardial infarction.

prolonged & Fleeting chest pain , dull-aches are due to Angina.

-Types of depressions of ST Segments in MI.-

SQUARE WAVE, OR PLAUTEAU , FLATT or

DOWN SLOPING. Up sloping ST Changes are not

considered characteristic of ISCHEMIA. Stable angina can be treated by

Antacids & sorbitrates.

UNSTABLE ANGINA

3 group patients may be said to have Unstable Angina

1) patients with New onset [ below 2 Months] Angina that is severe and Frequent More or Less 3 episodes per Day.

2) patients with Accelerating pain, that is more frequent, severe & prolonged.

3) pain at Rest.

Unstable Angina is characterized by Rest pain with ST Changes on ECG. Or occurs in the post infarction state, it is relatively high risk of Death.

-No Myocardial necrosis in Unstable angina. -Acute myocardial infarction can be Ruled

out by changes in ECG and Measurement of cardiac Enzymes from Unstable Angina.

ACUTE MYOCARDIAL INFARCTION Gross necrosis of the myocardium

as a result of interruption of blood supply to an Area of the cardiac muscle .It is caused by Atherosclerosis of coronary arteries & coronary thrombosis.

- ECG evidence of Ischemia do not diminish with in 24 to 48hrs of the medical treatment with Drugs , then cardiac catheterization & coronary Angioplasty should be performed. If Angioplasty [PTCA] can not be done, coronary artery by pass- grafting[CABG] Should be done to relieve symptoms & preventing myocardial damage .

RISK FOCTORS FOR IHD

SERUM CHOLESTEROL - The value should be below 200 mg/dl, value around 220 mg/dl will have moderate risk & value above 240 mg/dl indicate active Treatment.

LDL- CHOLESTEROL- Blood levels under 130/mg are desirable, Between 130 & 159 mg/dl are borderline, while above 160 mg/dl carry definite risk. Hence LDL is Bad cholesterol.

HDL -cholesterol

It is good cholesterol, Above 60 mg/dl protects against Heart diseases . A level below 35 mg/dl increases the risk of IHD. For every mg of drop in HDL , risk of heard disease rises 3% , The Ratio of Total cholesterol/HDL is more than 3.5, It is Dangerous . Similarly , LDL:HDL ratio more than 2.5 is also more Dangerous.

Apo-protein level

Maintenance of A-I ; A-II ratio is 3:1 ensures influx of cholesterol from cells to Liver. Apo-I is a measure of HDL & Apo-B measures LDL. APO- I is the most reliable index with predictive value in IHD Patients.

LP ‘a’

It inhibits Fibrinolysis . Lp ‘a’

levels more than 30 mg/dl increases the risk 3 times,& when increased LP ‘a’ with LDL the the risk is increased 6 times. Lp’a’ is an indipendant risk factor for the genesis of IHD in younger age.

CIGARETTE SMOKING There is a definite dose related link

between cigarette smoking & CAD. This relation is strongest in young individual.

BLOOD PRESSURE Systolic BP more than 160 further

increases the risk of IHD. DIABETIS MELLITUS It is reportedly doubles the risk of

Atherosclerotic CAD in Men. In women below 50 yrs of age the risk increases 3-4 Fold.

SERUM TRIGLYCERIDES

Blood level more than 50- 150 mg/dl is injurious to Health.

HOMOCYSTEIN LEVELS Plasma level of

Homocystein above 15 micro moles/litt is known to increase the risk of IHD & Stroke at younger Age.

Sedentary life style& Obesity IT increases risk in IHD, People ‘APPLE TYPE’ Of

Obesity are more prone to get MI. High sensitivity C- Reactive

protein. It is Demonstrated that hs- CRP is

a predictor of future events among apparently healthy persons.

SEX

The Disease is more common among Men compare to pre-menopausal women in a ratio of 25: 1. However in post-menopausal women there is a rapid rise in the incidence of Atherosclerosis. Oestrogen may have a protective effect against Atherosclerosis & IHD. HEREDITY.

A Family history of Atherosclerotic IHD is an important risk factor.

CARDIAC ENZYMES CPK Starts to rise with in 6hrs, peaks at

18hrs , & Comes to Normal by 72hrs. CK (MB) is more specific.

LDH Starts to rise at 24 hrs, peaks at 48-72hrs & Reaches to normal in 10-14 days, LDH -I - isozyme is more specific.

Cardiac troponin– Starts to rise after 4-6 hrs, Returns to normal with in 7 to 10 days.

Myoglobin- It is the first cardiac marker to elevated after MI, Reaches normal after 24 hrs of MI.

Complications

1) ARRYTHMIAS , 2) CHF , 3) CARDIOGENIC SHOCK, 4) THRAMBO- EMBOLISM, 5) CARDIAC- RUPTURE, 6) ANEURYSM, 7) PERICARDITIS, 8) POST

MYOCARDIAL INFARCTION SYNDROME.

MANAGEMENT 1) To Access the vital signs, 2) Monitor ECG, 3) O2 inhalation, if patient is hypoxic, 4) Administration of sorbitrate, 5) Administration of Morphine &

Nitroglycerine for pain relief, 6) Administration of Thrombolytic agents, [ streptokinase, Urokinase ,Tissue plasminogen

activater, & Apsac]. 7) Administration of Beta-

blockers[ contraindicated in CHF, Severe Bradycardia] , 8) Symptomatic treatment for other complications.

8) Percutaneous trans luminal coronaryAngioplasty [PTCA] & Coronary Artery Bypass Grafting [CABG].