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Coronary Artery Disease Dory Roedel Ferraro, DNP, ANP-BC, CBN College of New Rochelle Coronary Artery Disease Heart disease cause by impaired coronary blood flow Most cases are caused by atherosclerosis 1.6 million Americans have new or recurrent myocardial infarctions (MI) One third will die within 24 hours (500,000) Risk factors: smoking, HTN, dyslipidemias, diabetes, advancing age, abdominal obesity, physical inactivity Coronary Arteries Arise from the coronary sinus above the aortic valve Left coronary artery-supplies the anterior and left lateral portions of the LV Left anterior descending Circumflex Right coronary artery-supplies most of the RV and posterior part of the LV in most people Posterior descending artery Assessment of Coronary Blood Flow and Myocardial Perfusion ECG Exercise stress testing Echocardiography Used to visualize the regional distribution of bloodflow MRI and CT Tests structure and function of the heart Nuclear cardiac imaging Observes cardiac function under stress MRI quantifies the volume, mass and function of the ventricles CT assesses coronary artery calcification Cardiac catheterization Visualizes lesions within coronary arteries, determines extent of CAD Pathogenesis of CAD Fixed or stable plaque which obstructs blood flow Unstable/vulnerable plaque (high-risk plaque), which can rupture and cause platelet adhesion and thrombus formation A sudden surge of sympathetic activity can increase the risk for plaque disruption Determinates of plaque vulnerability to disruption The size of the lipid rich core The stability and thickness of its fibrous cap The presence of inflammation The lack of smooth muscle cells Acute Coronary Syndrome Unstable angina Non-ST segment elevation (non-Q-wave) MI ST segment elevation MI Subtotal or intermittent thrombotic coronary occlusion Complete coronary occlusion ECG changes T-wave inversion, ST segment elevation, development of an abnormal Q wave Unstable Angina/Non-ST-Segment MI Clinical syndrome of myocardial ischemia Ranges from stable angina to MI Dependent on severity of ischemia ECG pattern UA ST-segment depression (or transient ST elevation) and T-wave changes Degree of ST-segment deviation is important measure of ischemia and prognosis No serum markers for MI NSTEMI Serum markers are present Pathophysiology of UA/NSTEMI: 5 Phases Development of unstable plaque that ruptures or erodes with superimposed thrombosis An obstruction: spasm, constriction, dysfunction, adrenergic stimuli Sever narrowing of the coronary lumen Inflammation (inflammatory cells release cytokines) Any physiological state causing ischemia related to decreased oxygen supply (fever, hypotension) Pain of UA/NSTEMI Characterized by at least one of three features: Occurs at rest or minimal exertion and lasts for more than 20 minutes Severe and described as frank pain and of new onset (within 1 month) More severe, prolonged or frequent than previously experienced ST-Segment Elevation MI (STEMI) Ischemic death of myocardial tissue associated with atherosclerosis Extent of infarct depends on Location and extent of occlusion Amount of heart tissue supplied by the vessel Duration of the occlusion Metabolic needs of the affected tissue Extent of collateral circulation HR, BP and cardiac rhythm ST-Segment Elevation MI (STEMI) Transmural Infarct involves full thickness of the ventricle wall Involves obstruction of a single artery Subendocardial Infarct involves inner 1/3 to ½ of the ventricle wall Severely narrowed, but still patent arteries ST-Segment Elevation MI (STEMI) Conversion from aerobic to anaerobic metabolism Inadequate production of energy to sustain normal myocardial function Changes in cell structure develop within several minutes Changes are reversible if blood flow is restored Irreversible damage occurs to cells within 40 minutes Necrosis occurs after 20 to 40 minutes of severe ischemia Clinical Manifestations of STEMI Onset is usually abrupt Pain is significant symptom: severe and crushing More prolonged than angina and not relieved by NTG Women experience atypical chest discomfort GI symptoms are common Tachycardia, anxiety, restlessness and feeling of impending doom Pale cool and moist skin Management of Acute Coronary Syndrome 12-lead ECG Expeditious implementation of reperfusion therapy within 60 to 90 minutes for patients with ECG evidence of infarction Oxygen, ASA, nitrates, analgesics, antiplatelets and anticoagulants, βblockers Serum Biomarkers Triponon assays – primary biomarker tests for myocardial damage Begin to rise within 3 hours of myocardial damage May remain elevated for 7-10 days TnI-cardiac specific troponin I TnT-cardiac specific troponin T CK-MB-creatinine kinase MB Pharmacological Management of Acute Coronary Syndrome Nitroglycerin Vasodilator (preload and afterload) myocardial O2 consumption Relieves pain Morphine Anxiety and autonomic nervous system activity β-Adrenergic blockers myocardial O2 demand Alter resting membrane potentials, life-threatening ventricular arrhythmias ASA Inhibition of platelet aggregation Promote reperfusion and prevents likelihood of rethrombosis ACE inhibitors Reduces LV dysfunction CO and SV and pulmonary vascular resistance Chronic Ischemic Heart Disease Chronic stable angina Silent myocardial ischemia Variant or vasospastic angina Chronic Stable Angina Associated with a fixed coronary obstruction that produces an imbalance between coronary blood flow and metabolic demands of the heart Only half patients with coronary artery disease experience angina Usually precipitated by situations that increase the work demands of the heart: exertion, exposure to cold, emotional stress and relieved with rest or sublingual nitroglycerin (NTG) Steady constricting, squeezing or suffocating sensation in the precordial or substernal chest or back, sometimes radiating to the left shoulder, jaw or arm Silent Myocardial Ischemia Occurs in the absence of anginal pain Episodes may be shorter and involve less myocardial tissue than those producing pain Reason for painless episodes unclear Defects in pain threshold or pain transmission Autonomic neuropathy with with sensory denervation (patients with DM) Variant (Vasospastic) Angina “Prinzmetal angina” Caused by coronary artery vasospasm Usually occurs during rest, minimal exertion, or nocturnally ECG changes are transient Diagnosis and Treatment of Chronic Ischemic Heart Disease ECG, echocardiography, exercise stress testing, nuclear imaging studies, cardiac catheterization and coronary arteriography Treatment directed toward symptom reduction and prevention of MI Lifestyle modification Pharmacologic agents Nitrates (vasodilators), beta-blockers ( myocardial oxygen requirements), calcium channel blockers (coronary and peripheral artery vasodilation) Percutaneous intervention (balloon angioplasty, stents) Coronary bypass grafting Endocardial Disorders Infective Endocarditis (IE) Rare, serious, potentially life-threatening infection of the inner surface of the heart and cardiac valves Characterized by colonization or invasion of the valves and endocardium by a microbial agent leading to destruction of underlying tissue Contributing factors: Obvious (dental procedure) or occult infection (oral cavity, gut or SQ injury) Host factors (structural valvular abnormalities, neutropenia, immunosuppression, DM, ETOH) Staphylococcal infections are leading cause Manifested by fever and chills, anorexia, malaise, petechial or splinter hemorrhages under the nailbeds Rheumatic Heart Disease Cardiac manifestation of rheumatic fever (RF) RF is an immune-mediated, multisystem inflammatory disease that occurs a few weeks after a group A streptococcal throat infection Inflammation of all three layers of the heart Likely an immunological response Causes chronic deformity and impairment of heart valves Rare in developed countries Valvular Disorders Most commonly involves valves are the mitral and aortic valves Produce abnormal heart sounds (murmurs) Two types of mechanical disruption: Stenosis-narrowing of the valve which causes turbulent blood flow and increased workload in the chamber emptying through the narrowed valve Regurgitation-caused by a valve which does not close properly, thereby permitting backflow Diagnosis and Treatment of Valvular Disorders Diagnosis Cardiac auscultation Echocardiography Transesophageal echocardiography Treatment Medical management of heart failure Surgical repair or replacement Mitral Valve Disease Mitral valve stenosis Incomplete opening of the mitral valve during systole Left atrial distension and impaired filling of left ventricle pulmonary congestion Symptoms are related to pulmonary congestion (DOE, PND, palpitations, chest pain, atrial arrhythmias) Mitral regurgitation Incomplete closure of the mitral valve Eventually impairs LV function Mitral valve prolapse (1 to 2.5% of the population) Usually asymptomatic and an incidental finding Aortic Valve Disorders Aortic stenosis Usually first diagnosed by the presence of a loud, systolic ejection murmur Eventually causes angina, syncope and heart failure Aortic regurgitation Incompetent aortic valve that allows blood to flow back to the left ventricle during diastole Eventually left ventricular failure develops (exertional dyspnea, orthopnea, PND) Disorders of the Pericardium Acute Pericarditis Signs and symptoms resulting from pericardial inflammation of less than 2 weeks duration Infectious or non-infectious etiology (viral, bacterial, mycobacterial, connective tissue diseases, uremia, neoplasms, radiation, trauma, drug toxicity) Viral infection is the most common cause Chest pain, auscultatory pericardial friction rub, electrocardiographic changes Pericardial Effusion Accumulation of fluid in the pericardial cavity usually a result of an inflammatory or infectious process Small effusions or large effusions that develop slowly may not produce symptoms Sudden accumulations may raise intracardiac pressures that significantly limit venous return to the heart Diagnosed by echocardiography Treatment Phamacotherapy: diuretics, NSAIDs, corticosteroids Pericardiocentesis Cardiac Tamponade Compression of the heart due to accumulation of fluid or blood in the pericardial sac Life-threatening condition Key diagnostic finding: pulsus paradoxus (10mm or more fall in systolic BP that occurs with inspiration) Treated with closed or open pericardiocentesis Cardiomyopathies Primary Cardiomyopathies Genetic, mixed, or acquired Hypertrophic (HCM) - massively hypertrophied LV with disproportionate thickening of the ventricular septum, abnormal diastolic filling, cardiac arrhythmias, intermittent LV outflow obstruction Dilated (DCM) – characterized by progressive cardiac dilation and systolic dysfunction common cause for heart failure and leading indication for heart transplant frequently familial Restrictive – ventricular filling is restricted due to excessive rigidity Inflammatory (myocarditis)- usually caused by a viral infection Secondary Cardiomyopathies Heart muscle disease in the presence of a multisystem disorder Cardiomyopathies associated with drugs, DM, muscular dystrophy, autoimmune disorders, and cancer treatment agents Heart Disease in Infants and Children Congenital Most congenital defects arise between the 4th and 7th week of gestation when the major development of the fetal heart occurs Thought to be multifactorial: environmental, genetic and chromosomal influences 1 in 125 children are born with a congenital heart defect Acquired Kawasaki disease Cardiomyopathy Rheumatic fever Fetal and Perinatal Circulation Fetal circulation if anatomically and physiologically different from the postnatal circulation Fetus is maintained in a low oxygen state (PO2 30-35) and fetal CO is higher Oxygenation of the blood occurs: Through the placenta before birth Through the lungs after birth 40% of the blood moves from the right atrium through the foramen ovale into the left atrium 90% of the blood ejected into the pulmonary artery gets diverted through the ductus arteriosus into the into the ascending aorta Postnatal Circulation Foramen ovale closes Ductus arteriosus usually closes within 24-72 hours Factors affecting postnatal pulmonary vasculature development: Alveolar hypoxia Prematurity Lung disease Congenital heart defects Congenital Heart Defects Patent Ductus Arteriosus Persistence of the fetal ductus beyond the prenatal period Persistent patency: open > 3 months Ductal closure delayed in very premature infants and infants with congenital heart defects Contributing factors: Infant hypoxia Fall in endogenous levels of prostaglandins and adenosine Release of vasoactive substances Atrial Septal Defects Opening in the atrial septum persists as a result of improper septal formation Single or multiple Small to large Most common is the ostium secundum defect Most children are asymptomatic Ventricular Septal Defect An opening in the ventricular septum that results from incomplete separation of the ventricles during early fetal development Most common form of congenital defect Signs and symptoms range from asymptomatic murmur to congestive heart failure Approximately 1/3 small defects close spontaneously Large defects cause shunting of blood with eventual development of symptoms (tachypnea, diaphoresis and failure to thrive) Endocardial Cushion Defects 2% of all congenital heart defects Seen in 30% of children with Down syndrome Partial or complete Abnormalities similar to atrial and ventricular septal defects Pulmonary Stenosis Obstruction of blood flow from the right ventricle to the pulmonary circulation 10% of all congenital heart defects Produces some impairment of the pulmonary blood flow an dincreases workload of right side of the heart Tetralogy of Fallot Most common cyanotic congenital heart defect Four associated defects: Ventricular septal defect Dextroposition (aorta overrides the RV and is in communication with the septal defect) Obstruction or narrowing of the pulmonary outflow channel (pulmonic valve stenosis, decrease in pulmonary trunk) Hypertrophy of the RV Transposition of the Great Arteries Aorta arises from the RV Pulmonary artery arises fro the LV More common in mothers with DM Two to three times more common in boys Cyanosis is most common presenting symptom Ventricular septal defects are present in 50% of infants Coarctation of the Aorta Localized narrowing of the aorta Frequently associated with other congenital heart defects Classic sign: Disparity in pulsations and blood pressures in the arms and legs; pulsations are weak or delayed in lower extremities Functional Single Ventricle Only one functional ventricle Surgical palliation with a series of operations Long-term outcomes uncertain Kawasaki Disease Acute vasculitis with potential for involvement of the coronary arteries Occurs predominantly in young children (80% < 5 years old) Leading cause of acquired heart disease Triphasic Acute febrile phase (7-14 days): fever, conjunctivitis, redness and swelling of hands and feet, strawberry tongue Subacute phase (10-24 days): desquamation of the skin on fingers and toes, arthritis and GI manifestations Convalescent phase: until symptoms subside