Bems Kiran presentation1

INTRODUCTIONIschemic heart disease also designated

as coronary artery disease refers to a group of closely related syndromes caused by an imbalance between myocardial oxygen demand and blood supply.

ETIOLOGYThe most common cause of imbalance

between need and supply of oxygen is atherosclerotic narrowing of the coronary arteries producing ischemia.

RISK FACTORS FOR ATHEROSCLEROSIS

Fixed Risk FactorsAgeMale SexFamily History

MODIFIABLE RISK FACTORS

STRONG ASSOCIATIONHyperlipidemiaHypertensionCigarette SmokingDiabetes Mellitus

OTHER ASSOCIATIONS

ObesityLack of exerciseHeavy alcoholismDietary factorsOral contraceptivesGoutHigh level of coagulation factor vii &

fibrinogenAnxiety & depression

PATHOGENESIS

Defective Oxygen DeliveryIncreased Oxygen DemandIHD becomes symptomatic when there is 75% or more reduction of the lumen of one or more coronary arteries by atherosclerotic plaque.

Superimposed Lesions Acute changes in plaque morphology

Local platelet aggregation Coronary artery spasm Coronary artery thrombosis

CLASSIFICATION OF IHD

Stable anginaUnstable anginaMyocardial infarctionSudden cardiac death

WHAT IS ANGINA?

Angina is a clinical syndrome characterized by intermittent chest pain caused by reversible myocardial ischemia.

The pain is usually substernal or precordial radiating to the shoulder and arm or to the jaw.

It lasts for several minutes.

TYPES OF ANGINA

STABLE ANGINAVARIANT ANGINA

UNSTABLE ANGINA

STABLE ANGINAIt occurs due to increased myocardial

oxygen demand during exertion in a patient of narrow coronary arteries.

VARIANT ANGINAIt occurs at rest and produced by the

reduction of the myocardial blood supply due to coronary artery spasm.

UNSTABLE ANGINAIn this type of angina, frequency, severity

and duration of episodes are progressively increased. It occurs at rest due to thrombus formation and coronary artery spasm.

DIFFERENCE B/W STABLE & UNSTABLE ANGINA

STABLE ANGINA

Due to fixed stenosis

Demand-led ischemia

Related to effort

Symptoms over long term

UNSTABLE ANGINA

Due to dynamic stenosis

Supply-led ischemia

Symptoms at rest

Symptoms over short term

INVESTIGATIONS

ECGETTThallium scanCT AngiographyEchocardiography Coronary Angiography

ECG

During pain ECG showsST –segment depression with or without T

wave inversion that reverses after ischemia disappears.

Elevation of ST segment in variant angina.The resting ECG may be normal b/w

attacks however it may show old MI, heart block or left ventricular hypertrophy.

ETT

When history is suggestive of angina but ECG normal ETT is performed for diagnosis.

Positive test is one in which ST segment is depressed by 1 mm.

MYOCARDIAL INFARCTION

INTRODUCTION•MI is death or necrosis of myocardial cells.

Myocardial infarction (MI or AMI for acute myocardial infarction), commonly known as a heart attack, occurs when the blood supply to part of the heart is interrupted.

ETIOLOGY Commonly caused due to occlusion of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, in the wall of an artery. The resulting ischaemia and hypoxia, if left untreated for a sufficient period, can cause damage and or death (infarction) of heart muscle tissue.

ETIOPATHOGENESIS1. Mechanism of MI i) Diminished coronary blood flow ii) Increased myocardial demand iii) Cardiac hypertrophy without se of

coronary blood flow

2. Role of Platelets - rupture of atherosclerotic plaque exposes

subendothelial collagen to platelets - aggregation, activation, release of platelets

3. Complicated Plaques i) Superimposed coronary thrombosis ii) Intramural haemorrhage

4. Non-atherosclerotic causes - coronary vasospasm - arteritis - embolism - thrombotic diseases - trauma

5. Transmural versus subendocardial infarcts

Transmural infarcts- involve full thickness of

ventricular wall subendocardial (laminar) infarcts- affecting inner subendocardial one-third to one-half.

Classical symptoms of acute myocardial

infarction

Sudden chest pain Shortness of breath Nausea Vomiting Palpitations Sweating Anxiety

Risk factors for myocardial infarction

1. Older age 2. Sex (males) 3. Tobacco smoking 4. Hypercholesterolemia 5. Diabetes 6. Hypertension 7. Obesity 8. Stress

Pathological Changes

Vary according to the age of the infarct

Most infarcts occur singly (very less multifocal), 4-10 cm size

Most often in left ventricle

Subendocardial infarcts produce less well-defined infarcts gross changes than the transmural infarcts.

CLINICAL DIAGNOSIS

Clinical diagnosis is based on Symptoms ECG changesElevation of specific serum enzymes

SYMPTOMS

Onset is sudden with severe constricting, crushing, burning substernal or precordial pain that radiates to the left shoulder and arm or jaw.

Pain is accompanied by sweating, nausea, vomiting or dyspnea.

Cardiogenic shock.

ECG Changes

ST Segment elevation, follwed by abnormal new Q waves and inverted T wave.

Serum EnzymesCreatinine phosphokinaseLactic dehydrogenaseCardiac troponin I & Troponin T.

CHRONIC ISCHEMIC HEART DISEASE

Chronic IHD some times called ischemic cardiomyopathy is used to describe the development of progressive CHF.

It is characterized by multifocal areas of myocardial atrophy and fibrosis secondary to slowly developing coronary atherosclerosis leading to dilatation of cardiac chambers.

CLINICAL FEATURES

Usually it remains asymptomatic and progressively CHF develops.

Cardiac arrhythmias may occur when scarring involves conduction system.

Angina, MI

TYPES OF HEART FAILURE

ACUTE HEART FAILURE CHRONIC HEART FAILURE RIGHT AND LEFT HEART FAILURE CONGESTIVE HEART FAILURE FARWARD HEART FAILURE BACKWARD HEART FAILURE CARDIAC ARREST

ACUTE HEART FAILURE

Sudden onset of heart failure without previous symptoms of ischemia or MI.

CHRONIC HEART FAILURE

Gradual onset of heart failure with symptoms of ischemia or MI.

CONGESTIVE CARDIAC FAILURE

Bi ventricular heart failure.

CARDIAC ARREST

Complete cessation of heart function.

Conductive system of heart completely block.