Ischemia, Infarction

ICHEMIC HEART DIHEART DISEASE

Mr.Alfrin Antony Asst Lecturer Department of pathology +919738289032

DEFINITION:- Ischemic hear disease is defined as acute or chronic form of cardiac disability arising from the imbalance between myocardial supply and demand for oxygenated blood. ETIOPATHOGENISIS 1). Coronary atherosclerosis 2). Super added changes in coronary atherosclerosis a). Acute changes in chronic atheomatous plaque b). Coronary artory thrombosis c). Local plate let aggregation and coronary artory spasam 3). Nonathero sclerotic causes a). Vasospasam b). Stenosis of coronary artory c). Arteritis d). Embolism f). Thrombotic disease g). Trauma h). Aneurysms i). Compression EFFECTS MYOCARDIAL ISCHEMIA 1). Myocardial infarction 2). Non-Infract effect of ischemia a). Angina pectoris b). Chronic ischemic heart disease c). Sudden cardiac death

MYOCARDIAL INFARCTION DEFINITION:-Myocardial infarction is a life threatening condition characterized by the formation of necrotic areas with in the myocardium ETIOPATHOGENISIS 1). MECHANISAM OF MYOCARDIAL ISCHEMIA It happened by one or of th following mechanisms a). Diminished coronary blood flow b). Increased myocardial demand c). Hypertrophy of the heart without simultaneous ivrease of coronary blood flow 2). ROLE OF PLATELETS:- Rupture of atherosclerotic plaque exposes subendothelial collagen to platelets which undergo aggregation, activation and release reaction. These events contribute to the build up of the platelet mass that may give rise emboli or initiate thrombosis 3). COMPLICATED PLAQUES:a). Coronary Thrombosis (50% of acute MI) b). Intra mural hemorrhage (33%of acute MI)

Hemorrhage and thrombosis may occur in some cases 4). Non atherosclerotic Causees (10%) 5). TRANSMURAL VERSUS SUBENDOCARDIAL INFARCTS. SL NO

FEATURE

1

Definition

TRANSMURAL INFARCT Full thickness, Solid

SUBENDOCARDIAL INFARCT Inner third to half, patchy

2.

Frequency

Most frequent (95%)

Less frequent

3.

Distribution

Circumfeential

4.

Pathogenisis

Specific area of coronary supply >75% coronary stenosis

5.

Coronary Thrombosis

Common

Rare

6.

Epicarditis

Common

None

Hypoperfusion of myocardium

TYPES OF INFARCTS 1). According to anatomic region of the left ventricle involved a).Anterior b).Posterior c). Inferior d).Lateral e).Septal f).Circumferential g).Antroseptal h).Antrolateral i).Infrolateral 2).According to the degree of thickness of ventricular Wall involved a). Full thickness or transmural b). Subendocardial or laminar 3). According to the age of Infarcts a). Newly-formed infarcts are called acute, recent or fresh b). Advanced Infarcts are called old, healed or organized LOCATION OF INFARCTS -Left ventricle > Right ventricle (bcz of thin wall, less metabolic requirement, adequately nourished by thebesian vessels) -Right atrial infarct accompanying the infarct of the left ventricle. > Left atrium (protected by oxygenated blood in the myocardium) The region of infarction depends upon the area of obstructed there are three coronary arterial trunks.

1). Stenosis of the left anterior descending coronary artery (40-50) :- The region of infarction is the anterior part of the left ventricle including apex and the anterior 2/3 of intervetricular septum 2). Stenosis of the right coronary (30-40%):- Posterior part of the left ventricle and the posterior 1/3 rd interventricular septum 3). Stenosis of the left circumflex coronary artory (15-20%):- Lateral wall of the left ventricle TIME FIRST WEEK 0-6 hours 6-12 hours

GROSS CHANGES

LIGHT MICROSCOPY

No changes ,TTC negative in infracted area -do-

No changes , Stretching and waviness of fibres Coagulative necrosis begins; neutrophilic inflammation begins; edema and hemorrhages present. Coagulative necrosis progresses; marginal neutrophilic infiltrate. Coagulative necrosis complete, neutrophilic infiltrate developed. Prominent neutrophilic infiltrate, Some undergoing degeneration. Beginning of resorption of necrosed fibers by macrophages , onset of fibro vascular response, neutrophils gradually disappear.

24 hrs

Cyanotic red-purple area of hemorrhage

48-72 hours

Pale, hyperaemic

4th day

Well defined yellow border

7th day

Bright yellow to yellow-green

Second week 10th day

Red-purple periphery

14th day

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Third week

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Most of the necrosed muscle in a small infarct removed ; fibrovascular reaction more prominent; pigmented macrophages, eosinophils, lymphocytes, plasma cells present Necrosed cells mostly removed; neutrophils disappear, fibrocolagenic tissue at the periphery Necrosed muscle fibes from larger infracts removed , more in growth of fibrocollagenic tissue

Fourth to sixth week

Thin ,gray-white, hard, shrunken fibrous scar

Increased fibrocollagenic tissue, decreased vascularity, fever pigmented macrophages, lymphocytes and plasma cells

COMPLICATIONS  Arrhythmias  Congestive heart failure  Cardiogenic shock  Mural thrombosis and thombembolism  Rupture  Cardiac aneurysm  Pericaditis  Post-myocardial infarction syndrome

ANGINA PECTORIS (Greek ankhon ("strangling") Latin pectus ("chest") = "a strangling feeling in the chest".) Angina pectoris is severe chest pain due to ischemia of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries It is not common to equate severity of angina with risk of fatal cardiac events. There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle (i.e. there can be severe pain with little or no risk of a heart attack, and a heart attack can occur without pain). TYPES:a).STABLE ANGINA This refers to the more common understanding of angina related to myocardial ischemia. Typical presentations of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc) with minimal or nonexistent symptoms at rest. Symptoms typically abate several minutes following cessation of precipitating activities and resume when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms.

b).UNSTABLE ANGINA (“CRESCENDO”) Unstable angina (UA) is defined as angina pectoris that changes or worsens. [1] It has at least one of these three features: 1. it occurs at rest (or with minimal exertion), usually lasting >10 min; 2. it is severe and of new onset (i.e., within the prior 4-6 weeks); and/or 3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously). UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina (other than symptoms) is the pathophysiology of the atherosclerosis. In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity. c).PRINZMETAL’S ANGINA A variant form of angina (Prinzmetal's angina) occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women. ETIOPATHOGENISIS: 1. a reduction of blood flow to the heart that can be caused by stenosis, spasm, or acute occlusion (by an embolus) of the heart's arteries 2. resistance of the blood vessels 3. reduced oxygen-carrying capacity of the blood. Myocardial fibrosis respesents healing of minute infarcts involving small scattered groups of myocardial fibers PATHOLOGIC CHANGES GROSSLY Normal or hypertrophy of heart, gray white fibrosis of brown myocardium (left ventricle), previous scars of MI may be present, valves may be calcified distorted or calcified, moderate to severe atherosclerosis (coronary artery)

MICROSCOPICALLY Scattered areas of diffuse myocardial fibrosis, especially around small blood vessels in interstitial tissue of myocardium. Variation in fiber size and foci of myocytolysis Areas of brown atrophy myocardium may

present Coronary arteries show atherosclerotic plagues and may have complicated lesions in the form of superimposed thrombosis CLINICAlL MANIFESTATION Most patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen), back, neck, jaw, or shoulders, following skin dermatomes. Typical locations for radiation of pain are arms (often inner left arm), shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating and nausea in some cases. It usually lasts for about 3 to 5 minutes, and is relieved by rest or specific anti-angina medication. Chest pain lasting only a few seconds is normally not angina. Myocardial ischemia comes about when the myocardia (the heart muscles) receive insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardia or by decreased supply to the myocardia. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients is directly correlated to blocked or narrowed blood vessels. Some experience "autonomic symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting and pallor. SUDDEN CARDIAC DEATH Sudden cardiac death is defined as sudden death with in 24 hr of onset of cardiac symptoms. Causes:  IHD  Coronary vasospasm  Calcific aortic stenosis  Myocarditis  Hypetrophic cadiomyopathy  Mitral valve prolapse  Endocarditis  Heriditory and acquired defects of the conduction system The mechanisam of sudden death by myocardial ischemia is always by fatel arrhythmias, chiefly ventricular asystole or fibrilation.