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ISCHEMIC HEART DISEASE Ischemic heart disease (IHD) is the generic designation for a group of closely related syndromes

resulting from myocardial ischemiaan imbalance between the supply (perfusion) and demand of the heart for oxygenated blood. Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrient substrates and inadequate removal of metabolites Reduction or absence of blood supply to the heart 80-90% of all heart dse mortality CAUSES o Atherosclerosis (90-95%) o Vasospasm- d/t vascular phenomena o Thrombosis- Virchows Triad (hypercoagulability, endothelial damage, hemodynamic changes: stasis and turbulence) o Stenosis- d/t thrombosis or thickening of vessels o Inflammatory arteritis SYNDROMES CHRONIC ANGINA PECTORIS SUDDEN MYOCARDIAL ISCHEMIC (reversible) CARDIAC INFARCTION HEART - Sudden chest pain DEATH DISEASE Stable/typical Prinzmetal/var Unstable/cresce - permanent - postinfarctio - unexpecte angina iant angina ndo angina n myocardial d death decompensa - chest pain d/t - chest pain damage d/t from - chest pain tion (CHF) vasospasm even at total cardiac during * CHF- end pt (dec in vessel rest occlusion of causes exertion do caliber) - BV are after or bld supply of all cardiac more work partially without the heart dies-> dse increase occluded onset of coagulative an demand MORPHOLOG (preinfarct symptoms necrosis uncommon the most Y: ) - congenital pattern of - due to common form or acquired episodic Refers to a irreversible appears Heart usually - fatal angina that pattern of myocardial to be enlarged and arrhythmia occurs at pain that ischemia caused heavy, (most rest and is occurs with by the secondary to common due to progressively reduction left cause) coronary increasing of ventricular artery frequency, is - (e.g., coronary hypertrophy spasm. precipitated asystole, perfusion and dilation. with ventricular Usually there to a Invariably progressively fibrillation) is an critical there is less effort, elevated ST level by moderate to often occurs segment on chronic severe at rest, and the stenosing stenosing tends to be of electrocardi coronary atheroscleros more ogram atheroscl is of the prolonged (ECG), erosis; coronary duration. indicative of is usually arteries and transmural relieved sometimes ischemia. by rest total the anginal (thereby occlusion. attacks are decreasin unrelated to g Discrete, physical demand) gray-white activity, or scars of healed heart rate, nitroglyce infarcts are or blood rin, a usually pressure. strong present. The vasodilat mural or. endocardium is generally normal except


SY 2011-2012

Subject: Pathology Topic: Cardiac Pathology Lecturer: Dr. Cruz Date of Lecture: September 26, 2011 Transcriptionist: & The Soloist Pages: 11

for some superficial, patchy, fibrous thickenings, although mural thrombi may be present. The major microscopic findings include myocardial hypertrophy, diffuse subendocardi al vacuolization , and scars of previously healed infarcts. NOTE: In more than 90% of cases, the cause of myocardial ischemia is reduction in coronary blood flow due to atherosclerotic coronary arterial obstruction. Thus, IHD is often termed coronary artery disease (CAD) or coronary heart disease. In most cases, there is a long period (decades) of silent, slowly progressive, coronary atherosclerosis before these disorders become manifest. Thus, the syndromes of IHD are only the late manifestations of coronary atherosclerosis that probably began during childhood or adolescence

Acute myocardial infarction, unstable angina, and sudden cardiac death are sometimes referred to as acute coronary syndromes. Acute coronary syndromes are frequently initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through superficial erosion, ulceration, fissuring, rupture, or deep hemorrhage, usually with superimposed thrombosis PATHOGENESIS: The dominant influence in the causation of the IHD syndromes is diminished coronary perfusion relative to myocardial demand, owing largely to a complex and dynamic interaction among fixed atherosclerotic narrowing of the epicardial coronary arteries, intraluminal thrombosis overlying a disrupted atherosclerotic plaque, platelet aggregation, and vasospasm In summary, Acute coronary syndromesangina, acute MI, and sudden deathshare a common pathophysiologic basis in coronary atherosclerotic plaque disruption and associated intraluminal platelet-fibrin thrombus formation. The critical consequence is downstream myocardial ischemia. Stable angina results from increases in myocardial oxygen demand that outstrip the ability of markedly stenosed coronary arteries to increase oxygen delivery but is not usually associated with plaque disruption. Unstable angina derives from a sudden change in plaque morphology, which induces partially occlusive platelet aggregation or mural thrombus, and vasoconstriction leading to severe but transient reductions in coronary blood flow. In some cases, distal microinfarcts occur secondary to thromboemboli. In MI, acute plaque change induces total thrombotic occlusion. Finally, sudden cardiac death frequently involves a coronary lesion in which disrupted plaque and often partial thrombus and possibly embolus have led to regional myocardial ischemia that induces a fatal ventricular arrhythmia

* Fibrin strand- stabilizes platelet aggregates thus contributing to atheroma formation

Happens during the first decade of life Plaques inc size rupture causes severe chest pain

II. MYOCARDIAL INFARCTION produced most often by atherosclerosis leading to thrombosis ischemic coagulative necrosis of myocardial fibers with loss of normal contractile (vascular portion) and conductive (subendocardium) responses of affected myocardium microscopic examination of an infarct can be seen 3hours post infarction and some of the infarcted parts are mostly evident 6hours post infarction Epidemiology o age peak : 55-64yrs (males); 80s (females)- may be d/t estrogen o sex : 3:1, M:F o risk factors: HPN, hypercholesterolemia, cigarette smoking, diabetes melittus, sedentary lifestyle and oral contraceptive use PATHOGENESIS: In the typical case of MI, the following sequence of events can be proposed: The initial event is a sudden change in the morphology of an atheromatous plaque, that is, disruption manifest as intraplaque hemorrhage, erosion or ulceration, or rupture or fissuring. Exposed to subendothelial collagen and necrotic plaque contents, platelets undergo adhesion, aggregation, activation, and release of potent aggregators including thromboxane A2, serotonin, and platelet factors 3 and 4. Vasospasm is stimulated by platelet aggregation and the release of mediators. Other mediators activate the extrinsic pathway of coagulation, adding to the bulk of the thrombus. Frequently within minutes, the thrombus evolves to completely occlude the lumen of the coronary vessel. Pathology o common location: left ventricle (because this is the active portion of the heart) o 2 forms: Transmural infarct-

Most myocardial infarcts are transmural, in which the ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. This pattern of infarction is usually associated with coronary atherosclerosis, acute plaque change, and superimposed thrombosis

Subendocardial- inner 1/3 of the heart, mistaken for epigastric pain or heartburn

constitutes an area of ischemic necrosis limited to the inner one third or at most one half of the
ventricular wall; under some circumstances, it may extend laterally beyond the perfusion territory of a single coronary artery. The subendocardial zone is normally the least well-perfused region of myocardium and therefore is most vulnerable to any reduction in coronary flow. Distribution of arterial involvement and resultant infarction o LAD/Left anterior descending coronary artery (40% to 50%): infarct involves anterior wall of left ventricle near apex; anterior portion of ventricular septum; apex circumferentially o RAD: Right Anterior Descending (30-40%) - post. wall of LV, post 1/3 of IVS o LCA: Left Circumflex Artery (15-20%) - lateral wall of LV except at apex Location, size, morphology depends on o location, severity and rate of occlusion o size of vascular bed perfused by occluded vessel o duration of occlusion o metabolic/oxygen demands of myocardium at risk o extent of collateral blood vessels o presence, site, and severity of coronary spasm o alterations in BP, heart rate, cardiac rhythm

Collateralization o May be d/t diligent/ aerobic excercise o Is the growth of a blood vessel or several blood vessels that serve the same end organ or vascular bed as another blood vessel that cannot adequately supply that end organ or vascular bed sufficiently. (Wikipedia) Complications o cardiac arrhythmias - 75-95% of complicated cases (most common) o LV congestive heart failure - 60% o cardiogenic shock - 10-15% o rupture of free wall (cardiac tamponade), septum or papillary muscle (murmurs)- 15% o thromboembolism- 15-40% o OTHERS: pericarditis, ventricular aneurysms (portion of the heart wall is not ruptured but weakened)

Infarcted part of the heart is the pale area on the circle (d/t loss of bld supply): DxOld MI

Enlarged coronary artery - Almost 70% occlusion Cholesterol clefts -Thickening of smooth muscle -No intima

Coronary Artery Atheromatous plaque

Tigering Ischemia

Thrombus aneurysm

Cardiac enzymes r/t MI CPK (Creatine Phosphokinase) - More common is CPKMB1 and 2

III. HYPERTENSIVE HEART DISEASE Response of the heart to increased demands induced by systemic or pulmonary hypertension Causes o 95%- d/t essential HPN, idiopathic, or benign o 5%- d/t secondary HPN o Endocrine o Structural defect Systemic HHD o Minimal Criteria for Dx of HHD: LVH in the absence of other cardiovascular pathology history of hypertension

Pathologic features: concentric hypertrophy without dilatation(compensated) dilatation and thinning of wall (marks decompensation)

Concentric Hypertrophy - Global thickness of LV - Previous infarct

Pulmonary HHD (Cor Pulmonale) o right ventricular enlargement secondary to pulmonary HPN o not a primary heart condition but d/t a pulmonary dse o Acute vs Chronic o Acute cor pulmonale can follow massive pulmonary embolism. o Chronic cor pulmonale usually implies right ventricular hypertrophy (and dilation) secondary to prolonged pressure overload caused by obstruction of the pulmonary arteries or arterioles or compression or obliteration of septal capillaries (e.g., owing to primary pulmonary hypertension or emphysema). Morphology.

In acute cor pulmonale, there is marked dilation of the right ventricle without hypertrophy. On crosssection, the normal crescent shape of the right ventricle is transformed to a dilated ovoid. In chronic cor pulmonale, the right ventricular wall thickens, sometimes up to 1.0 cm or more, and may even come to approximate that of the left ventricle. More subtle stages of right ventricular hypertrophy may be observed as thickening of the muscle bundles in the outflow tract, immediately below the pulmonary valve, or of the moderator band, the muscle bundle that connects the ventricular septum to the anterior right ventricular papillary muscle. Sometimes there is secondary compression of the left ventricular chamber or tricuspid regurgitation with fibrous thickening of this valve.

Causes Obstructive Carcinoma emphysema Bronchiectasis Chronic bronchitis Cystic lung Pneumoconiosis Chronic pneumonia Fibrosis Pleural effusion Pathogenesis RV enlargement due to pulmonary hypertension caused by lung disorders COPD, DIP, atelectasis, cystic fibrosis Pulmonary embolism (acute CP), Primary Pulmonary HPN Kyphoscoliosis (structural defect) Pickwickian habitus (aka: Obesity Hypoventilation Syndrome; is a condition in which severely overweight people fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels and high blood carbon dioxide (CO2) levels. ~~ Wikipedia) metabolic acidosis, hypoxia

Saddle Pulmonary Embolism - Embolus sits on the bifurcation of the right and left pulmonary arteries occludes the RPA so bld cannot flow to the RV

IV. CONGENITAL HEART DISEASES Structural abnormality of heart present at birth May be COMPATIBLE vs. INCOMPATIBLE with life (depends on the presence of life-saving shunts) Incidence/ etiology: Affects 0.3to 1% of all livebirths/1000; 9births/1000 Frequencies o VSD- 33% (most common) o TOF- 9% o T ARTERIOSUS- 1% o ASD- 5% o AS- 8% o PDA- 10% o TA- 1% o TGA- 5% o CoA- 5% o PS- 10% o TAPVC- 1 o A-V SD- 4% Clinical effects of congenital heart disease o Cyanosis o Clubbing o Polycythemia- compensatory mech d/t poor oxygenation o pulmonary vascular disease- d/t too much bld in the pulmonary vascular bed o hypertrophic changes o stunted growth o paradoxical embolization- venous embolus becomes a systemic embolism, shunt vessel should be present o infectious endocarditis

Classification of Congenital Heart Diseases by RUBIN INITIAL LEFT TO RIGHT SHUNTS VSD - most common congenital heart defect, 30% isolated - frequently associated with other anomalies - defect is significant if greater than 1.0cm in diameter - Life- saving defect: TOF Types: a. Membranou s- close to AV bundle of HIS 90% b. Muscularbelow pulmonary valve; muscular septum c. Infracristal d. Supracristal ROGER'S DISEASE - muscular, less than 0.5cm in diameter) ASD - most common in ADULTS communicati on between atria because of abnormal opening - most common CHD in adults to be clinically apparent Major Types: a. Ostium Secundum - 90% of all ASD deficiency or fenestratio n of septum primum, deficiency of septum secundum, or both - involves the valve or limbus of the fossa ovalis b. Ostium PDA aortopulmona ry channel remains open: 85-90% isolated normally open for 1-2month after birth (closes at the end of 2mos) prematuri ty delayed closure especially if large distressed with low O2 tensiondelayed closure - Life-saving defect: TOGV and Pulmonary atresia - cyanosis of the lower extremities since after subclavian artery - Mngt: surgical TOF - results embryologicall y from anterosuperior displacement of the infundibular septum - most common form of cyanotic congenital heart disease 4 Features: 1. VSD (membrano us, size of the aortic lumen) life saving 2. OBSTRUCTI ON TO THE RIGHT VENTRICUL AR OUTFLOW TRACT (Subpulmon ary stenosis) 3. AORTA OVERRIDES THE VSD 4. RVH * remember: PROV PDA TGA

RIGHT TO LEFT SHUNTS Truncus Arteriosus development al failure of separation of the embryologic arteriosus into the aorta and pulmonary artery resulting in a single artery receiving blood from both ventricles - usually accompanied by VSD TA - complete occlusion of the tricuspid valve orifice - results from unequal distribution of the normal AV canal - associated with right ventricular hypoplasia - right to left shunt maintained thru ASD/ patent foramen ovale with VSD so communicat ion between Left and great artery from the hypoplastic right ventricle Total Anomalous Pulmonary Venous Connection - results embryologically when the common pulmonary vein fails to develop or becomes atretic causing primitive systemic venous channels from the lungs to remain patent - 50% cases drains into the innominate/ brachiocephalic vein (L) or the coronary sinus - associated with PDA or patent foramen ovale

NO SHUNTS Coarctation of aorta - constriction, narrowing of aorta - more common in MALES 2 Types: a. Pre-ductal (Infantile type) - tubular hypoplasia of the aortic arch - patency of PDA necessary for life - RVH in utero - early CHF - cyanosis of the lower half of the body b. Post-ductal (adult type) asymptomati c in early stage hypertension in the upper extremities but with weak pulses and lower BP in extremities Pulmonary stenosis - a dynamic or fixed obstruction to flow from the right ventricle of the heart to the pulmon ary artery. - usually d/t isolated valvular obstruction, but may be d/t subvalvular or supravalvul ar obstruction. - It may occur in association with more complicate d congenital heart disorders. (Wikipedia)

- AKA: Ventriculoarte rial discordance - aorta arises from the right ventricle and the pulmonary artery emanates from the left ventricle - embryologic defect is abnormal formation of the truncal and aortopulmona ry septa incompatible with life in the absence of shunts: a. VSD (35%) stable shunt b. PDA AND PATENT FORAMEN OVALE (65%)unstable - RHV and thin-walled left ventricle

Primum Defect - 5% of all ASD - occurs low and adjacent to valves, anteroinfe rior to the fossa ovalis c. Sinus Venosus Defect - 5% of all ASD - located high in the septum, posterior to fossa ovalis near the entrance of the SVC

closure, INDOMETHACI N (PG inhibitor)

Right Ventricular Hypertrophy Overriding of the aorta VSD - severity of obstruction to RV outflow determines direction of blood flow "pink tetralogy"- mild pulmonary stenosis (baby is not cyanotic but dusky looking)

- Mngt: surgery STAT

development of collateral vessels--"rib notching" 2/t enlarged internal mammary and intercostal arteries

LUTEMBACHE R'S SYNDROME - small ASD associated with mitral stenosis * Eisenmenger syndrome (or Eisenmenger's reaction)- is defined as the process in which a left-to-right shunt caused by a congenital heart defect causes increased flow through the pulmonary vasculature, causing pulmonary hypertension, which in turn, causes increased pressures in the right side of the heart and reversal of the shunt into a right-to-left shunt. (Wikipedia) * Atrioventricular Septal Defect - abnormal development of embryologic AV canal - failure of fusion of superior and inferior endocardial

cushions with incomplete closure of AV septum and inadequate formation of septal tricuspid and anterior

mitral leaflet

NOTICE TO THE PUBLIC: Guys kindly read your books, Ive tried to put some infos coming from the book but its not enough ..I think..

ASD- Secundum type

VSD- Muscular type

Transposition of the Great Arteries

~~Happy Studying! ^_^

Please read and review Netters atlas plus Robbins and Cotran Patho book..