| Myocardial Infarction |
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Acute myocardial infarction ('''AMI''' or '''MI'''), more commonly known as a '''heart attack''', is a medical condition that occurs when the Blood Supply to a part of the Heart is interrupted. The resulting Ischemia or Oxygen Shortage causes damage and potential death of heart tissue. It is a Medical Emergency , and the leading cause of death for both men and women all over the world.1 Important Risk Factor s are a previous history of vascular disease such as Atherosclerotic Coronary Heart Disease and/or Angina , a previous heart attack or Stroke , any previous episodes of abnormal heart rhythms or Syncope , older age—especially men over 40 and women over 50, Smoking , excessive alcohol consumption, the abuse of certain illicit drugs, high triglyceride levels, high LDL ("Low-density lipoprotein") and low HDL ("High density lipoprotein"), Diabetes , High Blood Pressure , Obesity , and chronically high levels of stress in certain persons. The term ''myocardial infarction'' is derived from '' Myocardium '' (the heart muscle) and '' Infarction '' (tissue death due to oxygen starvation). The phrase "heart attack" is sometimes used incorrectly to describe Sudden Cardiac Death , which may or may not be the result of acute myocardial infarction. Classical symptoms of acute myocardial infarction include Chest Pain (typically radiating to the left arm), Shortness Of Breath , Nausea , Vomiting , Palpitation s, Sweating , and Anxiety or a feeling of impending doom. Patients frequently feel suddenly ill. Women often experience different symptoms from men. The most common symptoms of MI in women include shortness of breath, weakness, and Fatigue . Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms. Immediate treatment for suspected acute myocardial infarction includes Oxygen , Aspirin , Glyceryl Trinitrate and Pain Relief , usually Morphine Sulfate . The patient will receive a number of diagnostic tests, such as an Electrocardiogram (ECG, EKG), a chest X-ray and Blood Test s to detect elevated Creatine Kinase or Troponin levels (these are chemical markers released by damaged tissues, especially the myocardium). Further treatment may include either Medication s to Break Down Blood Clots that block the blood flow to the heart, or mechanically restoring the flow by Dilatation or Bypass Surgery of the blocked coronary artery. Coronary Care Unit admission allows rapid and safe treatment of complications such as Abnormal Heart Rhythms . EPIDEMIOLOGY Myocardial infarction is a common presentation of Ischemic Heart Disease . The WHO estimated that in 2002, 12.6 percent of deaths worldwide were from ischemic heart disease. Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and Lower Respiratory Infection s in developing countries.2 In the United States , Diseases Of The Heart are the Leading Cause Of Death , causing a higher Mortality than Cancer ( Malignant Neoplasms ).3 Coronary Heart Disease is responsible for 1 in 5 deaths in the U.S.. Some 7,200,000 men and 6,000,000 women are living with some form of coronary heart disease. 1,200,000 people suffer a (new or recurrent) coronary attack every year, and about 40% of them die as a result of the attack.4 This means that roughly every 65 seconds, an American dies of a coronary event. Risk factors Risk factors for Atherosclerosis are generally risk factors for myocardial infarction:
Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.7 Non-modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a Genetic Predisposition . Socioeconomic factors such as a shorter Education and lower Income (particularly in women), and Living With A Partner may also contribute to the risk of MI.8 To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and Marital Status . Women who use Combined Oral Contraceptive Pill s have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.9 Inflammation is known to be an important step in the process of Atherosclerotic Plaque formation.10 C-reactive Protein (CRP) is a sensitive but non-specific Marker for Inflammation . Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as Stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high sensitivity CRP assays as a means of Screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known Coronary Artery Disease .11 Whether CRP plays a direct role in atherosclerosis remains uncertain. Inflammation in Periodontal disease may be linked coronary heart disease, and since Periodontitis is very common, this could have great consequences for Public Health .12 Serological studies measuring Antibody levels against typical periodontitis-causing Bacteria found that such antibodies were more present in subjects with coronary heart disease.13 Periodontitis tends to increase blood levels of CRP, Fibrinogen and Cytokines ;14 thus, periodontitis may mediate its effect on MI risk via other risk factors.15 Preclinical Research suggests that periodontal bacteria can promote aggregation of Platelets and promote the formation of Foam Cell s.1617 A role for specific periodontal bacteria has been suggested but remains to be established.18 Baldness , Hair Greying , a diagonal Earlobe Crease 19 and possibly other Skin features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.20 PATHOPHYSIOLOGY Plaque slowly builds up in the inner lining of a Coronary Artery and then suddenly ruptures, totally occluding the artery and preventing blood flow downstream.]] See Also: Acute coronary syndrome Acute myocardial infarction is a type of Acute Coronary Syndrome , which is most frequently (but not always) a manifestation of Coronary Artery Disease . The most common triggering event is the disruption of an Atherosclerotic Plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of Cholesterol and fibrous tissue in plaques in the wall of Arteries (in this case, the Coronary Arteries ), typically over decades. Blood stream column irregularities visible on angiographies reflect artery Lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a Thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium). If impaired blood flow to the heart lasts long enough, it triggers a process called the Ischemic Cascade ; the heart cells die (chiefly through Necrosis ) and do not grow back. A Collagen Scar forms in its place. Recent studies indicate that another form of cell death called Apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.21 As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias. Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger Re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is Ventricular Fibrillation (''V-Fib''/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is Ventricular Tachycardia (''V-Tach''/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac Output and Blood Pressure may fall to dangerous levels, which is particularly bad for the patient experiencing acute myocardial infarction. The Cardiac Defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect " Reboot ing" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest. TRIGGERS Heart attack rates are higher in association with intense exertion, be it , increases mechanical "shear stress" on Atheroma s and the likelihood of plaque rupture.Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. " Prediction of coronary heart disease using risk factor categories ". ''Circulation'' 1998; 97(18): 1837-47. PMID 9603539 Acute severe infection, such as Pneumonia , can trigger myocardial infarction. A more controversial link is that between '' Chlamydophila Pneumoniae '' infection and atherosclerosis.22 While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.23 Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.24 CLASSIFICATION s.25]] Acute myocardial infarction is a type of Acute Coronary Syndrome , which is most frequently (but not always) a manifestation of Coronary Artery Disease . The acute coronary syndromes include ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and Unstable Angina (UA). Depending on the location of the obstruction in the Coronary Circulation , different zones of the heart can become injured. Using the Anatomical Terms Of Location , one can describe anterior, inferior, lateral, apical and septal infarctions (and combinations, such as anteroinferior, anterolateral, and so on).26 For example, an occlusion of the Left Anterior Descending Coronary Artery will result in an anterior wall myocardial infarct.27 Another distinction is whether a MI is subendocardial, affecting only the inner third to one half of the heart muscle, or transmural, damaging (almost) the entire wall of the heart.28 The inner part of the heart muscle is more vulnerable to oxygen shortage, because the coronary arteries run inward from the Epicardium to the Endocardium , and because the blood flow through the heart muscle is hindered by the Heart Contraction . The phrases transmural and subendocardial infarction used to be considered synonymous with Q-wave and non-Q-wave myocardial infarction respectively, based on the presence or absence of Q waves on the ECG. It has since been shown that there is no clear Correlation between the presence of Q waves with a transmural infarction and the absence of Q waves with a subendocardial infarction,29 but Q waves are associated with larger infarctions, while the lack of Q waves is associated with smaller infarctions. The presence or absence of Q-waves also has clinical importance,30 with improved outcomes associated with a lack of Q waves.31 The phrase "massive attack" is not a recognized medical term. SYMPTOMS The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.. Retrieved November 25, 2006. Other conditions such as Aortic Dissection or Pulmonary Embolism may present with chest pain and must be considered in the Differential Diagnosis . Shortness of breath ( Dyspnea ) occurs when the damage to the heart limits the Output of the Left Ventricle , causing Left Ventricular Failure and consequent Pulmonary Edema . Other symptoms include Diaphoresis (an excessive form of Sweating ), weakness, Light-headedness , Nausea , Vomiting , and Palpitation s. Loss Of Consciousness and even Sudden Death can occur in myocardial infarctions. Women often experience markedly different symptoms than men. The most common symptoms of MI in women include dyspnea, weakness, and Fatigue . Fatigue, sleep disturbances, and Dyspnea have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, Chest Pain may be less predictive of coronary Ischemia than in men.32 Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction.D Lee, D Kulick, J Marks. Heart Attack (Myocardial Infarction) by MedicineNet.com . Retrieved November 28, 2006. Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms.33 These cases can be discovered later on electrocardiograms or at autopsy without a prior history of related complaints. A silent course is more common in the Elderly , in patients with Diabetes Mellitus 34 and after Heart Transplantation , probably because the Donor heart is not connected to nerves of the host.35 In diabetics, differences in Pain Threshold , Autonomic Neuropathy , and Psychological factors have been cited as possible explanations for the lack of symptoms. DIAGNOSIS The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with , retrieved November 27, 2006. A Coronary Angiogram allows to visualize narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At Autopsy , a Pathologist can diagnose a myocardial infarction based on Anatomopathological findings. A . Retrieved November 27, 2006. Technetium is used in a MUGA Scan . Diagnostic criteria WHO criteriaGillum RF, Fortmann SP, Prineas RJ, Kottke TE. International diagnostic criteria for acute myocardial infarction and acute stroke. ''Am Heart J'' 1984;108:150-8. PMID 6731265 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied: # Clinical history of ischaemic type chest pain lasting for more than 20 minutes # Changes in serial ECG tracings # Rise and fall of serum cardiac biomarkers such as Creatine Kinase , Troponin I, and Lactate Dehydrogenase Isozyme s specific for the heart. The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac Troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI. Physical examination The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased . Retrieved November 22, 2006.Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. ''Harrison's Principles of Internal Medicine''. p. 1444. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1. If heart failure ensues, elevated Jugular Venous Pressure and Hepatojugular Reflux , or swelling of the legs due to peripheral Edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on Precordial Examination . Various abnormalities can be found on Auscultation , such as a third and fourth Heart Sound , Systolic Murmurs , paradoxical splitting of the second heart sound, a Pericardial friction rub and Rales over the lung.Kasper DL, ''et al.'' ''Harrison's Principles of Internal Medicine''. p. 1450. (ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST segment elevation in leads II, III, and aVF along with reciprocal ST segment depression in leads I and aVL.]] Electrocardiogram The primary purpose of the does not directly examine the Right Ventricle , and does a relatively poor job of examining the posterior basal and lateral walls of the Left Ventricle . In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG . The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.Masoudi FA, Magid DJ, Vinson DR et al."Implications of the Failure to Identify High-Risk Electrocardiogram Findings for the Quality of Care of Patients With Acute Myocardial Infarction." ''Circulation'' 2006; 114: 1565-1571. The 12 lead ECG is used to classify patients into one of three groups: :1. those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with Thrombolytics or primary PCI ), :2. those with ST segment depression or T wave inversion (suspicious for ischemia), and :3. those with a so-called non-diagnostic or normal ECG."2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." ''Circulation'' 2005; 112: IV-89 - IV-110. A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation.Somers MP, Brady WJ, Perron AD, Mattu A. "The prominent T wave: electrocardiographic differential diagnosis." ''Am J Emerg Med'' 2002; 20(3): 243-51. PMID 11992348 In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction.Smith SW, Whitwam W. "Acute Coronary Syndromes." ''Emerg Med Clin N Am'' 2006; '''24(1)''': 53-89. PMID 16308113 Hyperacute T waves need to be distinguished from the peaked T waves associated with , Left Bundle Branch Block , Paced Rhythm , benign early repolarization, Pericarditis , Hyperkalemia , and ventricular aneurysm.Brady WJ, Chan TC, Pollack M. "Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy." ''J Emerg Med'' 2000; '''18(1)''': 71-8. PMID 10645842"Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians." ''Acad Emerg Med'' 2001; '''8(4)''': 349-60. PMID 11282670"ST-segment elevation in conditions other than acute myocardial infarction." ''New Engl J Med'' 2003; '''349(22)''': 2128-35. PMID 14645641 Left Bundle Branch Block and Pacing can interfere with the electrocardiographic diagnosis of acute myocadial infarction. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads.Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, Wagner GS. "Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block." ''N Engl J Med'' 1996; 334 (8): 481-7. PMID 8559200 The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction."Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment." ''Acad Emerg Med'' 2001; '''8(10)''': 961-7. PMID 11581081 The constellation of leads with ST segment elevation enables the clinician to identify what area of the heart is injured, which in turn helps predict the so-called culprit artery. As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction.36'' Full text '' Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred. Cardiac markers See Also: Cardiac marker Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood. These proteins are released into the bloodstream when damage to the heart occurs, as in the case of a myocardial infarction. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Then it was found that disproportional elevation of the ''MB'' subtype of the enzyme Creatine Kinase (CK) was very specific for myocardial injury. Current guidelines are generally in favor of Troponin sub-units I or T, which are very specific for the heart muscle and are thought to rise before permanent injury develops.37 Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future.38. Summary for laymen The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why Blood Test s for them are taken over a 24 hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.39 Angiography of the coronary arteries.]] See Also: Coronary catheterization In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary Angiography can be performed. A Catheter is inserted into an artery (usually the Femoral Artery ) and pushed to the vessels supplying the heart. Obstructed or narrowed arteries can be identified, and Angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by Interventional Cardiologists . Histopathology ) from autopsy specimen of myocardial infarct (7 days post-infarction).]] Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative Necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.40 Although earlier changes can be discerned using s, then with Lymphocyte s and Macrophage s, who Phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by Granulation Tissue , which will replace the infarct with a fibrous ( Collagen ous) Scar (which are typical steps in Wound Healing ). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with Red Blood Cell s. These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.41 FIRST AID As myocardial infarction is a common medical emergency, the signs are often part of First Aid courses. The Emergency Action Principles also apply in the case of myocardial infarction. Immediate care When symptoms of myocardial infarction occur, people wait an average of three hours, instead of doing what is recommended: . Retrieved December 13, 2006. Acting immediately by calling the emergency services can prevent sustained damage to the heart ("time is muscle"). TIME IS MUSCLE TIME WASTED IS MUSCLE LOST . Early Heart Attack Care, St. Agnes Healthcare. Retrieved November 29, 2006. Certain positions allow the patient to rest in a position which minimizes breathing difficulties. A half-sitting position with knees bent is often recommended. Access to more oxygen can be given by opening the window and widening the collar for easier breathing. Aspirin can be given quickly (if the patient is not Allergic to aspirin); but taking aspirin before calling the Emergency Medical Services may be associated with unwanted delay.42 Aspirin has an Antiplatelet effect which inhibits formation of further Thrombi (blood clots) that clog arteries. Non-enteric Coated or soluble preparations are preferred. If chewed or dissolved, respectively, they can be Absorbed by the body even quicker. If the patient cannot swallow, the aspirin can be used sublingually. U.S. guidelines recommend a dose of 162 – 325 mg.43 Australian guidelines recommend a dose of 150 – 300 mg.Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3. Glyceryl Trinitrate (nitroglycerin) Sublingual ly (under the tongue) can be given if it has been prescribed for the patient. If an Automated External Defibrillator (AED) is available the rescuer should immediately bring the AED to the patient's side and be prepared to follow its instructions should the victim lose consciousness. If possible the rescuer should obtain basic information from the victim, in case the patient is unable to answer questions once Emergency Medical Technicians arrive (if the patient becomes unconscious). The victim's name and any information regarding the nature of the victims pain will useful to health care providers. Also the exact time that these symptoms started, what the patient was doing at the onset of symptoms, and anything else that might give clues to the pathology of the chest pain. It is also very important to relay any actions that have been taken, such as the number or dose of aspirin or nitroglycerin given, to the EMS personnel. Other general first aid principles include monitoring pulse, breathing, level of consciousness and, if possible, the blood pressure of the patient. In case of Cardiac Arrest , Cardiopulmonary Resuscitation (CPR) can be administered. Automatic external defibrillation (AED) Since the publication of data showing that the availability of Automated External Defibrillator s (AEDs) in public places may significantly increase chances of survival, many of these have been installed in public buildings, Public Transport facilities, and in non-ambulance emergency vehicles (e.g. Police Car s and Fire Engine s). AEDs analyze the heart's rhythm and determine whether the rhythm is amenable to Defibrillation ("shockable"), as in Ventricular Tachycardia and Ventricular Fibrillation . Emergency services is promoted by a 9-1-1 system currently available to 90% of the population in the United States. Most are capable of providing Oxygen , IV access, sublingual Nitroglycerine , Morphine , and Aspirin . Some are capable of providing Thrombolytic Therapy in the prehospital setting.Morrow, Antman, Sayah, et al. "Evaluation of the time saved by prehospital initiation of reteplase for ST-elevation myocardial infarction: results of The Early Retavase-Thrombolysis in Myocardial Infarction (ER-TIMI) 19 trial." ''J Am Coll Cardiol'' 2002;40(1):71-7. PMID 1210325844 With is not staffed 24 hours a day.Rokos I. and Bouthillet T., "The emergency medical systems-to-balloon (E2B) challenge: building on the foundations of the D2B Alliance," ''STEMI Systems'', Issue Two, May 2007. Accessed June 16, 2007. Even in the absence of a formal alerting program, prehospital 12 lead ECGs are independently associated with reduced door to treatment intervals in the emergency department.Cannon CP at al. ''Management of Acute Coronary Syndromes''. p. 176. New Jersey: Humana Press, 1999. ISBN 0-89603-552-2. Wilderness first aid In Wilderness First Aid , a possible heart attack justifies Evacuation by the fastest available means, including MEDEVAC , even in the earliest or precursor stages. The patient will rapidly be incapable of further exertion and have to be carried out. Air travel Certified personnel traveling by commercial aircraft may be able to assist an MI patient by using the on-board First Aid Kit , which may contain some cardiac drugs (such as Glyceryl Trinitrate spray, Aspirin , or Opioid painkillers) and Oxygen . Pilots may divert the flight to land at a nearby airport. Cardiac Monitors are being introduced by some airlines, and they can be used by both on-board and ground-based physicians.Dowdall N. "'Is there a doctor on the aircraft?' Top 10 in-flight medical emergencies." ''BMJ'' 2000; 321(7272):1336-7. PMID 11090520. TREATMENT A heart attack is a Medical Emergency which demands both immediate attention and activation of the Emergency Medical Services . The ultimate goal of the management in the acute phase of the disease is to salvage as much myocardium as possible and prevent further complications. As time passes, the risk of damage to the heart muscle increases; hence the phrase that in myocardial infarction, "time is muscle," and time wasted is muscle lost. The treatments itself may have complications. If attempts to restore the blood flow are initiated after a critical period of only a few hours, the result is . First line Oxygen , Aspirin , Glyceryl Trinitrate (nitroglycerin) and Analgesia (usually Morphine , hence the popular Mnemonic ''MONA'', ''morphine, oxygen, nitro, aspirin'') are administered as soon as possible. In many areas, first responders can be trained to administer these prior to arrival at the hospital. Morphine is the preferred pain relief drug due to its ability to dilate blood vessels, which aids in blood flow to the heart as well as its pain relief properties. Of the first line agents, only aspirin has been proven to decrease Mortality .46 Once the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often given. These include Beta Blocker s,4748 anticoagulation (typically with Heparin ), and possibly additional antiplatelet agents such as Clopidogrel . These agents are typically not started until the patient is evaluated by an emergency room physician or under the direction of a cardiologist. These agents can be used regardless of the reperfusion strategy that is to be employed. While these agents can decrease mortality in the setting of an acute myocardial infarction, they can lead to complications and potentially death if used in the wrong setting. Reperfusion The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era.Lee KL, Woodlief LH, Topol EJ, et al. "Predictors of 30-Day Mortality in the Era of Reperfusion for Acute Myocardial Infarction." ''Circulation'' 1995; 91: 1659-1668. PMID 7882472Stone GW, Grines CL, Browne KF, et al. "Predictors of in-hospital and 6-month outcome after acute myocardial infarction in the reperfusion era: the Primary Angioplasty in Myocardial Infarction (PAMI) trail." ''J Am Coll Cardiol'' 1995; '''25''': 370-377. PMID 14645641 Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with Thrombolytic Therapy , Percutaneous Coronary Intervention (PCI) or when these therapies are unsuccessful, Bypass Surgery . Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with Antiplatelet Drug s and Anticoagulated . If their condition remains ( Hemodynamically ) stable, they can be offered either late Coronary Angiography with subsequent restoration of blood flow (revascularization), or Non-invasive Stress Testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however."Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group." ''Lancet'' 1994; 343(8893): 311-22. PMID 7905143 The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding. At least 10% of patients with STEMI don't develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted.Verheugt FW, Gersh BJ, Armstrong PW. "Aborted myocardial infarction: a new target for reperfusion therapy." ''Eur Heart J'' 2006; 27(8): 901-4. PMID 16543251 Thrombolytic therapy See Also: Thrombolysis Thrombolytic therapy is indicated for the treatment of STEMI if the drug can be administered within 12 hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and primary PCI is not immediately available. The effectiveness of Thombolytic Therapy is highest in the first 2 hours. After 12 hours, the risk associated with thrombolytic therapy outweighs any benefit.Boersma E, Maas AC, Deckers JW, Simoons ML. "Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour." ''Lancet'' 1996; 348 (9030): 771-5. PMID 8813982 Because irreversible injury occurs within 2–4 hours of the infarction, there is a limited window of time available for reperfusion to work. Thrombolytic drugs are contraindicated for the treatment of unstable angina and NSTEMI"Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction. Results of the TIMI IIIB Trial. Thrombolysis in Myocardial Ischemia." ''Circulation'' 1994; 89 (4): 1545-56. PMID 8149520 and for the treatment of individuals with evidence of Cardiogenic Shock .49 Although no perfect thrombolytic agent exists, an ideal thrombolytic drug would lead to rapid reperfusion, have a high sustained patency rate, be specific for recent thrombi, be easily and rapidly administered, create a low risk for intra-cerebral and systemic bleeding, have no antigenicity, adverse hemodynamic effects, or clinically significant drug interactions, and be cost effective.White HD, Van de Werf FJ. "Thrombolysis for acute myocardial infarction.." ''Circulation'' 1998; 97 (16): 1632-46. PMID 9593569 Currently available thrombolytic agents include Streptokinase , Urokinase , and Alteplase (recombinant Tissue Plasminogen Activator , rtPA). More recently, thrombolytic agents similar in structure to rtPA such as Reteplase and Tenecteplase have been used. These newer agents boast efficacy at least as good as rtPA with significantly easier administration. The thrombolytic agent used in a particular individual is based on institution preference and the age of the patient. Depending on the thrombolytic agent being used, Adjuvant anticoagulation with Heparin or Low Molecular Weight Heparin may be of benefit.5051 With tPA and related agents (reteplase and tenecteplase), heparin is needed to maintain coronary artery patency. Because of the anticoagulant effect of fibrinogen depletion with streptokinase52 and urokinase535455 treatment, it is less necessary there. Intracranial bleeding (ICB) and subsequent Cerebrovascular Accident (CVA) is a serious side effect of thrombolytic use. The risk of ICB is dependent on a number of factors, including a previous episode of intracranial bleed, age of the individual, and the thrombolytic regimen that is being used. In general, the risk of ICB due to thrombolytic use for the treatment of an acute myocardial infarction is between 0.5 and 1 percent. Thrombolytic therapy to abort a myocardial infarction is not always effective. The degree of effectiveness of a thrombolytic agent is dependent on the time since the myocardial infarction began, with the best results occurring if the thrombolytic agent is used within two hours of the onset of symptoms.56 If the individual presents more than 12 hours after symptoms commenced, the risk of intracranial bleed are considered higher than the benefits of the thrombolytic agent.57 Failure rates of thrombolytics can be as high as 20% or higher.58 In cases of failure of the thrombolytic agent to open the infarct-related coronary artery, the patient is then either treated conservatively with anticoagulants and allowed to "complete the infarction" or Percutaneous Coronary Intervention (PCI, see below) is then performed. Percutaneous coronary intervention in this setting is known as "rescue PCI" or "salvage PCI". Complications, particularly bleeding, are significantly higher with rescue PCI than with primary PCI due to the action of the thrombolytic agent. Percutaneous coronary intervention See Also: Percutaneous coronary intervention material (in a cup, upper left corner) removed from a coronary artery during a Percutaneous Coronary Intervention to abort a myocardial infarction. Five pieces of thrombus are shown (arrow heads).]] The benefit of prompt, expertly performed primary percutaneous coronary intervention over thrombolytic therapy for acute ST elevation myocardial infarction is now well established.596061 Logistic and economic obstacles seem to hinder a more widespread application of time. Few hospitals can provide PCI within the 90 minute interval,Bradley EH, Herrin J, Wang Y, Barton BA, Webster TR, Mattera JA, Roumanis SA, Curtis JP, Nallamothu BK, Magid DJ, McNamara RL, Parkosewich J, Loeb JM, Krumholz HM. "Strategies for reducing the door-to-balloon time in acute myocardial infarction." ''N Engl J Med'' 2006; 355(22): 2308-20. PMID 17101617 which prompted the American College of Cardiology (ACC) to launch a national Door to Balloon (D2B) Initiative in November of 2006. Over 800 hospitals have joined the D2B Alliance as of March 16, 2007.62 The current guidelines in the United States restrict primary PCI to hospitals with available emergency bypass surgery as a backup, but this is not the case in other parts of the world.63 Primary PCI involves performing a coronary Angiogram to determine the anatomical location of the infarcting vessel, followed by balloon Angioplasty (and frequently deployment of an intracoronary stent) of the thrombosed arterial segment. In some settings, an extraction catheter may be used to attempt to aspirate (remove) the thrombus prior to balloon angioplasty. While the use of intracoronary Stent s do not improve the short term outcomes in primary PCI, the use of stents is widespread because of the decreased rates of procedures to treat restenosis compared to balloon angioplasty.64 Adjuvant therapy during primary PCI include intravenous Heparin , Aspirin , and Clopidogrel . The use of Glycoprotein IIb/IIIa Inhibitor s are often used in the setting of primary PCI to reduce the risk of ischemic complications during the procedure.6566 Due to the number of antiplatelet agents and anticoagulants used during primary PCI, the risk of bleeding associated with the procedure are higher than during an elective PCI. Coronary artery bypass surgery See Also: Coronary artery bypass graft surgery from its surrounding tissue, Adipose Tissue (yellow). The tube visible at the bottom is the aortic cannula (returns blood from the HLM ). The tube above it (obscured by the Surgeon on the right) is the venous cannula (receives blood from the body). The patient's Heart is stopped and the Aorta is cross-clamped. The patient's head (not seen) is at the bottom.]] Despite the guidelines, emergency bypass surgery for the treatment of an acute myocardial infarction (MI) is less common then PCI or medical management. In an analysis of patients in the U.S. National Registry Of Myocardial Infarction (NRMI) from January 1995 to May 2004, the percentage of patients with Cardiogenic Shock treated with primary PCI rose from 27.4% to 54.4%, while the increase in CABG treatment was only from 2.1% to 3.2%.Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS; NRMI Investigators. "Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock." ''JAMA'' 2005; 294(4): 448-54. PMID 16046651 Emergency coronary artery bypass graft surgery (CABG) is usually undertaken to simultaneously treat a mechanical complication, such as a ruptured papillary muscle, or a ventricular septal defect, with ensueing cardiogenic shock.67 In uncomplicated MI, the .Creswell LL, Moulton MJ, Cox JL, Rosenbloom M. "Revascularization after acute myocardial infarction." ''Ann Thorac Surg'' 1995; 60(1): 19-26. PMID 7598589 In patients developing cardiogenic shock after a myocardial infarction, both PCI and CABG are satisfactory treatment options, with similar survival rates.White HD, Assmann SF, Sanborn TA, Jacobs AK, Webb JG, Sleeper LA, Wong CK, Stewart JT, Aylward PE, Wong SC, Hochman JS. "Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock: results from the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial." ''Circulation'' 2005; '''112(13)''': 1992-2001. PMID 1618643668 Coronary artery bypass surgery involves an artery or vein from the patient being implanted to bypass initially but bears less risk of recurrent procedures (but these may be again Minimally Invasive ). Monitoring for arrhythmias Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a Coronary Care Unit and protocolised administration of Antiarrhythmic Agent s. Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the Ventricular Ectopy that is often seen after a myocardial infarction.697071 Rehabilitation . Retrieved December 2, 2006. , updated March 2005. Retrieved December 4, 2006. Secondary prevention The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly Smoking Cessation , regular Exercise , a sensible Diet For Patients With Heart Disease , and Limitation Of Alcohol Intake . Patients are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, Congestive Heart Failure or Cerebrovascular Accident (CVA). Unless contraindicated, such medications may include:Smith A, Aylward P, Campbell T, ''et al.'' Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. ISSN 1327-9513
New therapies under investigation Patients who receive Stem Cell Treatment by Coronary Artery injections of Stem Cells derived from their own Bone Marrow after a myocardial infarction (MI) show improvements in left ventricular Ejection Fraction and End-diastolic Volume not seen with Placebo . The larger the initial infarct size, the greater the effect of the infusion. Clinical Trial s of Progenitor Cell infusion as a treatment approach to ST elevation MI are proceeding.83 There are currently 3 Biomaterial and Tissue Engineering approaches for the treatment of MI, but these are in an even earlier stage of Medical Research , so many questions and issues need to be addressed before they can be applied to patients. The first involves Polymer ic left ventricular restraints in the prevention of Heart Failure . The second utilizes '' In Vitro '' engineered cardiac tissue, which is subsequently implanted '' In Vivo ''. The final approach entails injecting cells and/or a scaffold into the myocardium to create '' In Situ '' engineered cardiac tissue.Christman KL, Lee RJ. "Biomaterials for the Treatment of Myocardial Infarction". ''J Am Coll Cardiol'' 2006; 48(5): 907-13. PMID 16949479 COMPLICATIONS Complications may occur immediately following the heart attack (in the Acute phase), or may need time to develop (a Chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. Congestive heart failure See Also: Congestive heart failure A myocardial infarction may compromise the function of the heart as a pump for the Circulation , a state called Heart Failure . There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as Mitral Regurgitation in the case of left-sided MI. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies.84 Myocardial rupture See Also: Myocardial rupture Myocardial Rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later. In the modern era of early revascularization and intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs.85 This may occur in the free walls of the ventricles, the Septum between them, the Papillary Muscles , or less commonly the Atria . Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular Aneurysm , a localized dilation or ballooning of the heart chamber. Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction. In addition, the risk of rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI.8687 The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.88 Rupture is usually a catastrophic event that may result a life-threatening process known as Cardiac Tamponade , in which blood accumulates within the Pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a Ventricular Septal Defect with Shunting of blood through the defect from the left side of the heart to the right side of the heart. Rupture of the papillary muscle may also lead to acute Mitral Regurgitation and subsequent Pulmonary Edema and possibly even Cardiogenic Shock . Life-threatening arrhythmia showing ventricular tachycardia.]] Since the electrical characteristics of the infarcted tissue change (see Pathophysiology Section ), Arrhythmias are a frequent complication. The re-entry phenomenon may cause too fast heart rates ( Ventricular Tachycardia and even Ventricular Fibrillation ), and ischemia in the Electrical Conduction System Of The Heart may cause a Complete Heart Block (when the impulse from the Sinoatrial Node , the normal cardiac pacemaker, doesn't reach the heart chambers any more). Pericarditis See Also: Pericarditis As a reaction to the damage of the heart muscle, Inflammatory cells are attracted. The inflammation may reach out and affect the heart sac. This is called Pericarditis . In Dressler's Syndrome , this occurs several weeks after the initial event. Cardiogenic shock A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is Cardiogenic Shock . Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a Cardiac Output to supply an adequate amount of oxygenated blood to the tissues of the body. While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an Intra-aortic Balloon Pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor. PROGNOSIS The prognosis for patients with myocardial infarction varies greatly, depending on the patient, the condition itself and the given treatment. Using simple Variable s which are immediately available in the Emergency Room , patients with a higher risk of adverse outcome can be identified. For example, one study found that 0.4% of patients with a low risk profile had died after 90 days, whereas the Mortality Rate in high risk patients was 21.1%.Lopez de Sa E, Lopez-Sendon J, Anguera I, Bethencourt A, Bosch X; Proyecto de Estudio del Pronostico de la Angina (PEPA) Investigators. "Prognostic value of clinical variables at presentation in patients with non-ST-segment elevation acute coronary syndromes: results of the Proyecto de Estudio del Pronostico de la Angina (PEPA)." ''Medicine (Baltimore)'' 2002; 81(6): 434-42. PMID 12441900 Although studies differ in the identified variables, some of the more Reproduced risk stratifiers include age, Hemodynamic parameters (such as Heart Failure , Cardiac Arrest on admission, Systolic Blood Pressure , or Killip Class of two or greater), ST-segment deviation, Diabetes , Serum Creatinine concentration, Peripheral Vascular Disease and elevation of cardiac markers.Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F, Avezum A, Goodman SG, Flather MD, Anderson FA Jr, Granger CB. "Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE)." ''BMJ'' 2006; 333(7578):1091. PMID 1703269189 Assesment of Left Ventricular Ejection Fraction may increase the predictive power of some risk stratification models.90 The prognostic importance of Q-waves is debated.91 Prognosis is significantly worsened if a mechanical complication ( Papillary Muscle rupture, myocardial free wall rupture, and so on) were to occur. There is evidence that case fatality of myocardial infarction has been improving over the years in all ethnicities.92 LEGAL IMPLICATIONS At s may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car, taxi or airplane. SEE ALSO
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