Coronary Atherosclerotic Heart Disease
Definition
A multi factorial metabolic disorder of the arteries of the heart leading to development of varying degrees of stenosis including closure of the lumen of the artery. It is the leading cause of morbidity and mortality in North America and Western Europe.
History
Symptoms: A pressure, band, vice like, burning or crushing sensation most likely in the midsternal region. Frequently associated with radiation of the discomfort to the back, scapula, shoulder, arm, neck or epigastric regions. May have slight to severe nausea, shortness of breath, diaphoresis, or vomiting.
General: Symptoms occur when the myocardial oxygen demand exceeds supply. Symptoms are most likely to occur during exertion but may occur at rest.
Age: Any; however, the risk is increased with advancing age, usually after age 40.
Onset: The onset of the disease is slow and gradual but the symptoms may be acute. Twenty five percent of initial symptoms occur shortly before death.
Intensity: Vary from a mild nagging sensation to severe crushing pain. Location of the lesion in the vascular tree and the severity of the lesion can playa role in the severity of symptoms.
Aggravating Factors: Any condition producing increased myocardial oxygen demand such as emotional upset, cold temperature, eating a large meal, exertion, and underlying medical conditions.
Alleviating Factors: Any measure that equilibrates supply and demand of the myocardium such as rest, relief of emotional stress, or correction of underlying metabolic abnormality.
Associated Factor: Genetic predispostion, hypertension elevated lipids male gender tobacco use obesity, sedentary life-style and personality factors.
Physical Examination
Cardiovascular: Auscultate for murmurs, gallops, S3 ,or signs of congestive heart failure (CHF) that may indicate myocardial dysfunction.
Pulmonary: Auscultate for rales that may suggest CHF.
General: The physical examination plays a relatively small role in the diagnosis of coronary atherosclerotic heart disease (CASHD) and myocardial infarction. Pulse rate usually rapid, but bradycardia is possible. Low grade temperature may be associated with myocardial infarction. Blood pressure may be elevated or depressed. Hypotension is an ominous sign.
Pathophysiology
CASHD is a progressive disease beginning in childhood with clinical signs and symptoms occurring in mid-to late adulthood. Multi factorial process that requires extensive proliferation of smooth muscle within the intima of the affected artery along with an accumulation of macrophages and smooth muscle cells that form a matrix of connective tissue. There is an accumulation of lipids within muscle cells and surrounding connective tissue giving rise to lesions of variable composition within the vascular tree, primarily at bifurcations of major branches.
Diagnostic Studies
Laboratory: There is no specific laboratory test to diagnose CASHD. Creatinine phosphokinase, SGOT, and lactic dehydrogenase isoenzymes have a staged peak elevation with myocardial infarction. Creatinine phosphokinase rises within 3 to 4 hours and peaks in 12 to 16 hours. SGOT peaks at 24 to 48 hours and lactic dehydrogenase rises at 36 to 48 hours and peaks at 4 to 7 days. Creatinine phosphokinase-MB is an isoenzyme specific for cardiac muscle.
Radiology CXR: Nonspecific for CASHD or angina. Aorta or coronary arteries may be calcified.
Coronary artery angiography: Will show the presence or absence of lesions within the coronary arteries. It also allows measurement of left ventricular end-diastolic pressure and left ventricular function.
Other
ECG: Resting ECG is normal in 50 to 75 percent of patients. Q waves may be present in old or new myocardial infarctions. S-T elevation suggests acute myocardial infarction. S-T segment depression suggests ischemia and T-wave inversion suggests subendocardial injury in the corresponding area of the heart represented by the ECG leads.
Exercise stress test: Low risk test that evaluates the heart under increased myocardial oxygen demand. The test is limited by the patient’s ability to achieve a target heart rate during progressive increments of workload, heart rate limiting drugs, and the presence of left bundle branch block. The test is considered positive with S-T segment changes, hypotensive episodes during exercise, development of left bundle branch block, arrhythmias, or other untoward changes during exercise (e.g., shortness of breath, diaphoresis, chest pain, or early fatigue). Test may involve the administration of thallium or other isotopes that are injected during peak exercise periods and will define perfused versus unperfused areas of myocardium. The test may also involve the administration of persantine that acts to increase oxygen demand pharmacologically and used for patients who are unable to reach their target heart rate through exercise.
Differential Diagnosis
Traumatic
Musculoskeletal: Pain is exacerbated or produced with any tension on the chest, bones, or muscles of the chest. Traumatic aortic dissection: History of blunt chest trauma or deceleration injury. Infectious
Acute pericarditis: Pain usually occurs in a younger patient population and is of sudden onset, severe, persistent, and is intensified with valsalva. Usually relived by leaning forward and/or sitting up. Friction rub may be present on physical examination. ECG may show widespread S-T elevation.
Pneumonia: Produces a pleural type pain that will increase with cough or movement. Physical examination demonstrates a pleural rub or rales. Infiltrate may be seen on CXR. Sputum cultures may be positive for causative organism.
Metabolic
platelet hypercoagulation: Various etiologies may cause coronary artery occlusion by clumping of the platelets.
Anemias: Decreased myocardial oxygen supply due to decreased hemoglobin. Hyperthrombosis: Various etiologies cause coronary artery occlusion by thrombus of red blood cells.
Neoplastic: Tumor that produces pressure, inflammation, or invasion of pericardial, pleural, muscular or skeletal surfaces. May cause chest pain. Seen on computed tomography (CT) scan or CXR
Vascular Coronary artery spasm: Transient, nonfixed total or partial occlusion of the coronary artery lumen secondary to spasm of the smooth muscle in the coronary artery wall.
Coronary artery emboli: Due to endocarditis, prosthetic valve, or left ventricular thrombus.
Pulmonary artery emboli: Secondary to thrombus from the left side of the heart, vegetative valves of the left side of the heart, or from aortic disease.
Aortic dissection: Due to a combination of atheromatous plaque and hypertension. Associated with a sudden onset of pain described as a “ripping or tearing” pain that radiates to the chest or abdomen. Pulmonary hypertension: Multiple etiologies. Pain is due to pressure on the vascular bed.
Arteriovenous fistula: Deep in the coronary vasculature causes a distal vascular steal.
Congenital: Anomalous origins of the coronary arteries, arteriovenous fistula, hypoplastic, or a plastic coronary arteries. Congenital abnormalities are usually discovered early in life and rarely cause chest pain in the elderly population.
Treatment
The goal of therapy is to alleviate immediate discomfort, limit the amount of myocardial damage, prevent further damage, and manage long-term problems.
Acute Myocardial Infarction
Sedation with anxiolytics. Relieve discomfort with morphine or other analgesics. Use with caution in hypotensive patients (mean arterial pressure <65). Recannalize the artery with angioplasty, atherectomy, throbolytic agents (e.g., tissue plasminogen activator, streptokinase) or surgery. Treat secondary conditions such as hypo tension, CHF, arrhythmias, or arterial or ventricular rupture.
Pediatric Considerations
True angina pectoris is rare in the pediatric population. However, it is common to encounter pediatric patients with the complaint of chest pain. Distinguishing cardiac from non cardiac chest pain in this age group may be difficult. If myocardial chest pain is suspected by history, consideration should be given to familial hyperlipoproteinemia, pericarditis, Kawasaki disease with coronary artery involvement, anomalous origin of the coronary arteries, arrhythmias, and obstructive cardiac lesions. Myocardial infarction is extremely rare, but may occur with the aforementioned anomalies, embolisms secondary to endocarditis, or after surgical disruption of the coronary arteries. ECG findings may differ in children. Initially, the findings include ST segment elevation and abnormally large Q waves that may persist for several years (Q waves may be normal). Over a period of 2 to 3 weeks the S-T segment will gradually return to normal. During this time, the T wave inay become inverted. Once the diagnosis is confirmed, a thorough search for the etiology is performed so that effective therapy can commence.
Unstable or Stable Angina
Relieve discomfort with analgesics (e.g., opiates). Administer nitrates (intravenous, sublingual, transdermal, or oral), calcium channel blockers, beta blockers, or angiotensin converting enzyme inhibitors to reequilibrate the supply and demand of oxygen. The goal of therapy is to keep the mean arterial pressure greater than 65 and less than 70, maintain the heart rate at 70 to 80 bpm, and prevent coronary artery spasm. Consider intravenous heparin to (1000 ml/hour after 5000 ml bolus) with or without ECG changes. Consider long term, low dose aspirin (baby aspirin) every day to reduce platelet aggregation. Educate the patient regarding diet, exercise, and risk factors for prevention of further events.
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