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3- Ischemic heart diseases & Cardiomyopathy . Dr Tarek atia. Ischaemic Heart Disease (IHD). Common Health problem. High Mortality & Morbidity . Etiology: Commonly Atherosclerosis Two major types: Angina & Myocardial Infarction . Risk factors : Hypertension
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3- Ischemic heart diseases & Cardiomyopathy Dr Tarek atia
Ischaemic Heart Disease (IHD) • Common Health problem. • High Mortality & Morbidity. • Etiology: Commonly Atherosclerosis • Two major types: Angina & Myocardial Infarction. • Risk factors : • Hypertension • Abnormal Blood Lipids • LDL Cholesterol (low density lipoprotein) • HDL Cholesterol (high density lipoprotein) • Diabetes Smoking, • Genetic. Life style, Diet,
Ischemic Heart Disease • Imbalance between Myocardial oxygen supply and demand = Myocardial hypoxia and accumulation of waste metabolites due to atherosclerotic disease of coronary arteries
Patterns of IHD • Myocardial Infarction • Angina Pectoris • Sudden cardiac death
Pathogenesis • Obstruction of the blood flow due to: • Atheroma, Thrombosis, Embolism • Diminished coronary perfusion resulting in: • Ischemia : Angina • Infarction : Necrosis
Myocardial Infarction-MI Avascular necrosis (Coagulative necrosis) of the myocardium “Death of heart tissue due to lack of blood supply” Etiology: Atherosclerosis is the common cause. Clinically: Severe chest pain, dyspnea & sweating Complications: Cardiogenic shock, Heart failure or Death.
MyocardialInfarctions Apical infarct Posterolateral infarct
Recent infarction: white patches of Coagulative necrosis of the myocardium Wavy fibers; is a diagnostic sign of recent myocardial infarct.
Wavy fibers are another sign of an early infarct. Coagulative necrosis, interstitial bleeding, and a few inflammatory cells. Coagulative necrosis with neutrophils and nuclear debris (2-3 day old infarct). MI 2-4 weeks - resorption, fibrosis
Complications • Ventricular aneurysm • Arrhythmias • Heart failure • Cardiogenic shock ------- death • Myocardial wall rupture
Angina Pectoris • Paroxysmal attacks of acute chest pain • Substernal or precordial • Due to myocardial ischemia
2- Variant Angina • Chest pain occurs at rest • Reversible spasm 3- Unstable Angina • Prolonged chest pain or pain at rest 4- Sudden cardiac death • Unexpected death within one hour of heart attack • Commonly with high grade coronary stenosis • Ventricular electrical instability 1- Stable Angina • Pain related to exertion • Relieved by rest or vasodilators
Signs & Symptoms of Angina • Dyspnea, nausea, chest pain or discomfort • Angina is a diffuse sensation rather than discrete
Diagnostic Tests • Blood tests: include serum lipids, fasting blood sugar, Hematocrit, thyroid hormonal assay (Anemia and hyperthyroidism can exacerbate myocardial ischemia). • Exercise Stress Test: used to confirm diagnosis of angina • Other Diagnostic Tests: • Radionuclide studies • Myocardial perfusion scintigraphy • Exercise radionuclide ventriculography • Echocardiography • Ambulatory ECG monitoring • Coronary arteriography
Cardiomyopathy Any disease affects the cardiac muscle is called Cardiomyopathy
1- Myocarditis Etiology: Viral – coxsackie A, influenza Bacteria – diphtheria, TB, streptococci Fungal & protozoa – trypanosomes Chlamydia and rickettsia Hypersensitivity – SLE, RHD, drugs Physical agents – radiation Idiopathic – giant cell myocarditis
Morphology Dilated heart in myocarditis Gross:dilated, flabby heart, pale patches with hemorrhage Microscopic:interstitial inflammatory infiltrate with myocyte necrosis, fibrosis Mononuclear cells:idiopathic or viral Neutrophils:bacterial Eosinophils:hypersensitivity Granulomatous:TB
2- Giant Cell Myocarditis Giant Cell Myocarditis Myocyte necrosis Multinucleated giant cells Lymphocytes, plasma cells, macrophages, eosinophils, and neutrophils Rapid progression to death
3- Dilated Cardiomyopathy Cardiomyopathy – loss of myofibrils Gross:increased weight, dilatation, endocardial fibrosis, normal valves and coronary arteries Microscopic:myocyte hypertrophy, myofibrillar loss and interstitial fibrosis Etiology:viral, genetic, toxins Clinical significance:heart failure & death
4- Hypertrophic cardiomyopathy Hypertrophy of ventricular septum (95%) Disarray of myofibers (100%) Volume reduction of ventricles (90%) Endocardial thickening of LV (75%) Mitral valve leaflet thickening (75%) Dilated atria (100%) Abnormal intramural coronaries (50%)
Etiology:hereditary, can appear sporadically Clinical significance:syncope, arrhythmias and sudden death with a risk of 2-6% per year Cannot equate with hypertrophy alone! There is variation in heart size without disease.
Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy – myofiber dysarray – not all fibers are pulling the same direction. Thus the contraction is ineffective.
Notes to Heart Physiology • Essential functions of the heart • To cover metabolic needs of all tissues by adequate bloodsupply. • To receive all blood coming back from the tissue to the heart. • Essential conditions for fulfilling these functions • Normal structure and functions of the heart. • Adequate filling of the heart by blood.
Heart Failure: • A state that develops when the heart fails to maintain an adequate cardiac output to meet the metabolic demands of the body.
HF is characterized by: • Decreased cardiac output (forward failure) • Decreased venous return (backward failure), • Both
Pathophysiology • The onset of HF is preceded by Cardiac hypertrophy:compensatory response of the myocardium to increase mechanical workincrease the mass & the size of the heart.
Normal heart Pressure – overload Hypertrophy Volume – overload hypertrophy
Effects of Heart Failure:-Enlarged heartTachycardia Left Side Heart Failure • Hypoxia • Dyspnea Right Side Heart Failure • Venous congestions • Edema
A- Left Sided Heart Failure • Progressive obstructing of the blood within the pulmonary circulation and the consequences of diminished peripheral blood pressure and blood flow. • Causes : • Ischemic Heart Diseases • Systemic hypertension, • Valvular disease,
Morphology of the heart: • Depends on the cause of the disease process. • Left ventricle is usually hypertrophied and dilated. • Secondary enlargement of the left atrium with resultant AF.
Lung alveoli filed with fluid and HF cells Pulmonary changes: • A perivascular and interstitial transudation, particularly in the interlobular septa. • Accumulation of oedema fluid in the alveolar spaces. • Heart failure cells (alveolar macrophage eating RBCS). Heart Failure cells
Clinical Manifestation • Dyspnea (breathlessness): • Exaggeration of the normal breathlessness that follows exertion. • Orthopnea: • Dyspnea on lying down that is relieved by sitting or standing. • Paroxysmal nocturnal dyspnea: • An extension of orthopnea with attacks of extreme dyspnoea, usually occurring at night. • Coughwith Blood tinged sputum
B. Right Sided Heart Failure Causes of Rt. HF • Usually as a consequences of left sided heart failure. • Chronic pulmonary hypertension due to increased resistance within the pulmonary circulation. • Other causes : multiple pulmonary emboli, valvular diseases.
Clinical Manifestations 1- HEART: • Hypertrophy and dilation are generally confined to right ventricle and atrium. 2- LIVER AND PORTAL SYSTEM: • Congestive hepatomegaly • Passive congestion • Centrilobular necrosis. • long standing Right failure -cardiac cirrhosis
3- SPLEEN: • Congestive splenomegaly. 4- GIT: • Ascites: accumulation of transudate in the peritoneal cavity. 5- KIDNEYS: • Congestion is more marked than in left sided HF. • Increases fluid retention ---- Peripheral edema
Heart Failure LHF RHF Absence of respiratory symptoms/insignificant. Systemic (and portal) venous congestive. Hepato-splenomegaly Peripheral oedema Pleural effusion Ascites. • Pulmonary congestion and oedema. • Cough • Dyspnoea • Orthopnea