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ISCHEMIC HEART DISEASE is generic designation as a result of an imbalance between the supply (perfusion) and demand of the heart for oxygenated blood. It comprises not only insufficiency of oxygen, but also reduced availability of nutrient and inadequate removal of metabolites. Reduction in coronary blood flow due to ATHEROSCLEROSIS in coronary trunk. So designated as CORONARY ARTERIAL DISEASE. ( C.A.D. ) The syndrome of IHD are Late Manifestation of CAD which began during first decades of life. * CLINICAL MANIFESTATION OF IHD.

* Divide in to 4 syndromes * 1 ANGINA PECTORIS ;- Ischemia less sever. Duration and severity is sufficient cause death of cardiac muscle. * EPIDEMIOLOGY * I.H.D. in its various forms is the leading cause of * Death for both M & F . * Reduced the incidence of IHD as a results of recent * Technical achievements in diagnosis, prevention, and * treatments * Prevention achieved by modification of determination * Of risk factors such as smoking , hypercholesterolemia, hypertension and sedentary lifestyle. * Diagnostic and therapeutic advances * Earlier , more effective , and safer treatments, * Coronary care units * Thrombolytic therapy for M. i. * Per coetaneous transluminal coronary angioplasty, ( PTCA) * Endovascular stent , * Coronary arterial by pass graft .

( CABG ) * Control of diabetes mellitus in pt. * Control of Arrythemias. * ETIO -PATHOGENESIS. * Etiology of IHD under five broad headings. * Coronary Atherosclerosis, * Role of Acute Plaque Changes, * Role of coronary thrombosis . * Role of vasoconstriction.

* Non atherosclerotic causes are * Embolism ;- Originate any where in body. * CORONARY ATHEROSCLEROSIS. * It is the major cause of IHD in > 90 % of cases. * Progressive enchroachment of lumen leading to  stenosis ( FIXED OBSTRUCTION) or to ACUTE Disruption with thrombosis. * Sudden obstruction cause ACUTE ISCHEMIC ATTACK  Or sudden death. While dynamic slowly developing obstruction may stimulate * Dynamic interaction among FIXED Atherosclerosis.

Narrowing of the epicardial coronary arteries. Platelets clumps & vasospasm. * DISTRIBUTION AND LOCATION. * One or more of the major coronary arteries are involved. * All are involved in descending order. So the single vessel or two or three vessels are involved in IHD.

Left heart is more involved due to the atherosclerosis are very common & sever in LEFT rather than RIGHT coronary artery. * ROLE OF ACUTE PLAQUE CHANGES. * All most complications are precipited as a result of Plaque changes followed by THROMBOSIS, Rupture, Fissuring, Erosion/ Ulceration and highly THROMBOGENIC at Sub-Endothelial Level. * Hemorrhage in Atheroma. * Plaque disruption lead to Platelets aggragation and Thromogenesis are common . Repetative and silent complication of Atheroma .

* Platelets release granules and vaso spasmic mediatores which is responsible for  VASO-SPASM. . PRODUCE STABLE ANGINA. * ROLE OF CORONARY THROMBUS. * Previous only partialy stenotic plaque gradually * Become large in size and convert in to total occlusion * lead to SUDDEN DEATH. * The mural thrombus in coronary artery * Lead to micro or macro emboli formation * Produce micro or macro infarct of    myocardium.

* UNSTABLE ANGINA OR SUDDEN DEATH. . * ROLE OF VASO CONSTRICTIONS . * VACONSTRICTION COMPROMISES THE LUMEN SIZE OF VESSELES AND * ANGINA PECTORIS. * It is a symptoms complex of IHD charecterized by *,PAROXYSMAL AND RECURRENT ATTACKS OF SUB-STERNAL OR PRECORDIAL DISCOMFART. ( AS – CONSTRICTING.

SQEEZING. HOKING OR KNIFELIKE) As a result of TRANSIENT ( 15 seconds to 15 minutes) MYOCARDIAL ISCHEMIA OR NECROSIS (INFARCT). * STABLE OR TYPICAL ANGINA PECTORIS. * Most common form as a result of reduction of coronary perfusion to a critical level by chronic stenosis of cor. Arteries. * Charecterised by attack of pain following physical exertion or emotional excitement ,relieved by rest * Local vasospasm may contribute to the imbalance * between supply and demand.

* There is depression of ST-segment in ECG due to poor perfusion of the sub-endocardial region of LT * side of heart. * But no elevation of cardiac enzymes in the blood. a * PRENZMENTAL OR VARIEN ANGINA. * Uncommon pattern of episodic angina as a result of sudden vasospasm of coronary trunk. * Characterized by attack of pain occurs at REST. * There is elevated ST-segment as a result of THANSMURAL ischemia.

* The angina attacks are unrelated to physical activity , heart rate or blood pressure. * Generally responds promptly to vasodilators, * such as Nitroglycerin and calcium channel blockers. * But no elevation of cardiac enzymes in the blood. * UNSTABLE OR CRESENDO ANGINA. * It is referred to as acute insufficiency & most serious patteren of angina. * The pain is precipitated with progressively less effort often occur at rest with prolonged duration.

* Induced by disruption of an atherosclerotic plaque with superimposed by thrombus & embolus * The ischemia that occures in unstable angina to inducing clinically detectable INFARCTION. * Unstable angina lies intermediate between stable angina on the one hand & M.I. on the other. * ACUTE MYOCARDIAL INFARCTION. M.I. * DEF. ;- Death of cardiac muscle due to ISCHEMIA * A significant factor that may prevent of diminish the myocardial damage is the development of collateral circulation through anastamotic channels over a period of time. * Epidemiology ;- Leading cause of death all over the world.

About 1. 5 mill. Person suffer an acute M.I. annually & 33 % die. * At least 15 % sufferer die before they reach the hospital. Incidence ratio is 10 % before 40 yrs age & 50 – 60 % under 65 yrs of age. * Female are less sufferer then male due to ostrogen.

* ETIO – PATHOGENESIS. * About 90 % of cases due to sever cor. Atheroscle. * MACHANISM OF M.I. ;- * 1) Diminished coronary blood flow in one or more * than one coronary arterial trunk ( C.A.D.) * 2) Myocardial demand for blood. (Exercise       Emotion) * 3) Hyperthrophy of heart with out simultaneous *          of blood supply ( Hypertesion & valular      heart disease. * SEQUENCE OF EVENTS OF M.I. * SEQUECE OF EVENTS CONT.

* Loss of blood supply * Cessation of aerobic & anaerobic glycolysis. * Lead to inadequate production of CKP & ADP. * Striking loss of contractibility. * Precipitating acute heart failure long before myocardial cell death. * This early changes are potentially reversible. * Ischemia lasting < 20 min.

lead to irreversible necrosis. * Produce electrical instability – arrythemia – Death. * APPROXIMATE TIME OF ONSET OF KEY  EVENTS IN ISCHEMIC CARDIAC MYOCYTES. * FEATURE * A.T.P.Depletion. * Loss of contractility * ATP Reduced * To 50 % of normal. * To 10 % of normal.

* Irreversible cell injury. * Micro vascular injury. * TIME * Seconds. * < 2 minute. * 10 minutes * 40 minutes * 20 – 40 minnutes * > 1 hour. * Classified by the panel of cardiologist & pathologist * 1) Accorging to anatomical region of Lt.

Ventricle. * ( Anterior , Posterior(inferior) , Lateral , Septal , * Circumferential or combination of any two . ) * 2) According to the demage of thickness of the * ventricular wall involved. * 3) According to the age of INFARCTS. * Acute or Recent or Fresh demages. * Old or Healed or Organised .

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