Phys Review -- MI .pdf

Acute Myocardial Infarction Disease summary ○ Definition: Acute myocardial infarction (AMI) is defined as a medical emergency characterized by rapid (i.e., acute) development of cellular death of a segment of cardiac muscle caused by a prolonged (30 minutes) im...

Acute Myocardial Infarction Disease summary ○ Definition: Acute myocardial infarction (AMI) is defined as a medical emergency characterized by rapid (i.e., acute) development of cellular death of a segment of cardiac muscle caused by a prolonged (30 minutes) imbalance between the oxygen supply and demands of the myocardium ○ AMI is most commonly due to obstruction in one of the coronary arteries by a ruptured atherosclerotic plaque with rapid development of an overlying thrombus (i.e., intravascular blood clot) Prevalence ○ According to data released in 2008 by the American heart association (AHA), approximately 8.1 million Americans are living today with an MI ○ Another 9.1 million Americans are susceptible to AMI, having been diagnosed with chest pain from poor coronary artery blood flow ○ In the United States, approximately 1.4 million AMIs occur each year ○ Approximately 770,000 episodes are first-time, symptomatic heart attacks, while nearly 430,000 are recurrent AMIs ○ It has been estimated with an additional 190,000 “silent” (i.e., asymptomatic) first AMIs occur each year ○ Although AMI may occur at any age, frequency increases with advancing age and most cases occur after age 45 ○ The average age of first AMI is 64.5 years for men and 70.4 years for women ○ However, certain subpopulations younger than 45 years are also at risk, particularly cocain users, people with insulin-dependent mellitus or an abnormal lipid profile, and those with a positive family history for early coronary artery disease ○ Male predilection exists in persons aged 40-70 years ○ It has been estimated that American Males have greater than one in five probability of sustaining an AMI before the age of 65 ○ Furthermore, males younger than 45 years have a 6-fold greater risk for AMI than females of the same age ○ After menopause, the rate of AMI in women approaches that of men and becomes equal by age 80 Causes and risk factors ○ AMI is most commonly caused by an obstruction in one of the coronary arteries, leading to myocardial ischemia (i.e., decreased blood flow to a segment of the heart) and a critical imbalance between oxygen supply and demand within the heart ○ The most common cause of obstruction is a ruptured plaque with subsequent rapid development of spasm of the involved blood vessel and a thrombus that together result in partial or total occlusion of one of the coronary arteries ○ Plaques build up over years within the walls of arteries from a slowly progressive, inflammatory diseases known as atherosclerosis ○ Poorly controlled hypertension ○ Positive family history of atherosclerosis ○ High levels of serum homocystein  ○ A positive family history includes any first-degree male relative age 45 years or younger or any first-degree female relative aged 55 years or younger who experienced an AMI ○ The metabolic syndrome, also recognized as a major contributor tp risk for AMI, has been increasing in prevalence at an alarming rate ○ The metabolic syndrome is defined as a constellation of three or more of the following: Abdominal obesity Serum triglyceride concentration 150 mg/dL HDL cholesterol level 40 mg/dL for men and 50 mg/dL for women Fasting blood glucose concentration 110 mg/dL Hypertension ○ As of arteries that furnish blood to the brain can lead to dementia (i.e., mental deterioration due to gradual death of brain tissue) or stroke (sudden death of brain tissue) ○ In many people, AS remains silent and causes no symptoms for decades ○ Although the disease can begin as early as the adolescent years, symptoms usually do not appear until late adulthood when arterial narrowing becomes severe ○ The most initiating event of AMI is a sudden change in the structure of an atherosclerotic plaque (usually due to rupture or fracture) with exposure of underlying collagen to elements within the blood ○ Although heart attacks can occur at any time of day, most occur between 4am-10am ○ The combination of developing thrombus and vasospasm results in partial or total obstruction of the artery and subsequent myocardial ischemia to cells downstream ○ Total occlusion of the blood vessel for more than 4 hours can result irreversible cell injury and cell death within the heart ○ Re-establishment of blood flow (i.e., reperfusion) within this period can salvage myocardial tissue and reduce both morbidity and mortality ○ The precise location and extent of cell death within the heart depends primarily on the following factors: Precise location and extent (partial or total) obstruction Presence of additional plaques that further reduce blood flow Duration of the obstruction Adequacy of collateral blood vessels that bypass the site of obstruction In an anteroseptal MI, noted on ECG are ST segment elevations in leads V1-V4 which is due to an occlusion of the left coronary artery; left anterior descending artery ○ Septal leads =V1-2 ○ Anterior leads = V3-V4 ○ Lateral leads = V5-V6 ○ The different infarct patterns are named according to the leads with maximal ST elevation: Septal = V1-V2 Anterior = V2-V5 Anteroseptal = V1-4 Anterolateral= V3-6, I + aVL Extensive anterior/anterolateral= V1-6, I + aVL ○ Hyperacute Anteroseptal STEMI: ST elevation and hyperacute T waves in V2-4 ST elevation in I and aVL with reciprocal ST depression in lead III Q waves are present in the septal leads V1-2 ○ With a typical AMI, approximately 20% of the cells die from the process of necrosis and the remaining 80% succumb to apoptosis (i.e., genetically programmed cell death) ○ The “superimposed thrombus theory) of AMI was controversial for many years because only half of all persons dying from an AMI had a demonstrable thrombus at autopsy ○ Then, cardiologists showed that approximately 90% of persons diagnosed with AMI had an intracoronary thrombus within 4 hours of the onset of symptoms but only 60% had thrombi 12-24 hours later ○ The observation suggested that, in many cases, thrombi are quickly lysed (i.e., broken up) by natural physiologic mechanisms that degrade fibrin, a protein that serves as “glue” for the thrombus and causes platelets and red blood cells to stick together ○ The chest pain of AMI is substernal, often described as “crushing,” “excruciating,” or “squeezing” and may radiate to the arms,shoulders, neck, jaw, upper back, or into the teeth. ○ This latter phenomenon is known as referred pain ○ The left arm is affected more than the right arm ○ In some cases, however, patients complain of chest discomfort that feels like “gas”, “pressure” or “tightness” ○ Patients may break out in a cold sweat, feel weak and anxious and move about seeking a position of comfort ○ Light-headedness, pallor, shortness of breath, cough, wheezing, nausea, and vomiting may be present individually or in any combination ○ In some instances, however, AMI is entirely asymptomatic (i.e., silent AMI) and may be detected with ECG at a later date ○ Up to ⅓ of patients with AMI present without chest pain ○ Atrial gallops (S4) are the rule, whereas ventricular gallops (S3) are less common and indicate significant left ventricular dysfunction. ○ Mitral valve regurgitation murmurs usually indicate papillary muscle dysfunction. ○ Approximately one half of patients who have experienced an AMI show diagnostic abnormalities on their initial ECG. ○ The classic evolution of ECG changes occurs from a few hours after onset of symptoms to several days and progresses from peaked T waves to ST segment elevations to Q wave development to T wave inversions. ○ The evolution of new Q waves is diagnostic for AMI; ○ However, Q waves are not seen in as many as half of all AMIs. ○ A single assay has a sensitivity of only 34%, but serial sampling over 24 hours increases sensitivity to near 100%. ○ The cardiac troponins are the most specific indicators and have become the criterion standard for diagnosing AMI. ○ For earlier detection of AMI, sensitivity of troponin I is superior to that of CK-MB.  ○ Troponin I is elevated in serum as early as 3 hours after onset and its concentration may remain elevated for as long as 14 days. ○ The kinetics and specificity for AMI of troponin T is similar to that of troponin I; however, troponin T is less sensitive than troponin I within the first 6 hours. Appropriate therapy ○ The primary goal of treatment is to quickly restore blood flow to the heart muscle, a process known as reperfusion, which minimizes the extent of heart muscle damage. ○ Optimal benefit is obtained if reperfusion can be established within the first 6 hours. ○ The amount of healthy heart muscle remaining after a heart attack is the most important determinant of future quality of life and longevity. ○ All patients with definite or suspected AMI should receive aspirin at a dose of 162–325 mg immediately following the onset of chest pain and regardless of whether thrombolytic therapy is being considered or the patient has been taking aspirin previously. ○ Major bleeding complications occur in up to 5% of patients, the most serious of which is intracranial hemorrhage. ○ In the United States, the most commonly used thrombolytic agents (aka clot-buster drugs) are alteplase, reteplase, and tenecteplase. ○ These medications are all biosynthetic forms of the naturally occurring enzyme, human tissue type plasminogen activator. ○ In contrast to anticoagulants, like heparin, which prevent the propagation or buildup of thrombi, thrombolytic agents promote the breakdown of thrombi by converting plasminogen to plasmin, a protease that can degrade fibrin within a thrombus.