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==Treatment of ST Elevation Myocardial Infarction== | ==Treatment of ST Elevation Myocardial Infarction== | ||
Immediate treatment for suspected [[acute myocardial infarction]] includes [[ST elevation myocardial infarction oxygen therapy|oxygen]], full dose non-enteric coated [[ST elevation myocardial infarction aspirin therapy|aspirin]], [[ST elevation myocardial infarction nitrate therapy|nitroglycerin (also known as glyceryl trinitrate)]] and [[ST elevation myocardial infarction analgesic therapy|pain relief]], using an analgesic agent such [[ST elevation myocardial infarction analgesic therapy|morphine sulfate]]. Among patients who do not have signs or symptoms of [[cardiogenic shock]], [[ST elevation myocardial infarction beta blocker therapy|beta blocker administration]] has been associated with improved clinical outcomes among patients with ST elevation myocardial infarction. <ref>CAPRICORN: The Capricorn Investigators: Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction. Lancet 2001;357:1385.</ref> These agents exert | Immediate treatment for suspected [[acute myocardial infarction]] includes [[ST elevation myocardial infarction oxygen therapy|oxygen]], full dose non-enteric coated [[ST elevation myocardial infarction aspirin therapy|aspirin]], [[ST elevation myocardial infarction nitrate therapy|nitroglycerin (also known as glyceryl trinitrate)]] and [[ST elevation myocardial infarction analgesic therapy|pain relief]], using an analgesic agent such [[ST elevation myocardial infarction analgesic therapy|morphine sulfate]]. Among patients who do not have signs or symptoms of [[cardiogenic shock]], [[ST elevation myocardial infarction beta blocker therapy|beta blocker administration]] has been associated with improved clinical outcomes among patients with ST elevation myocardial infarction. <ref>CAPRICORN: The Capricorn Investigators: Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction. Lancet 2001;357:1385.</ref> These agents exert their benefit via several mechanisms: They reduce myocardial oxygen demands; they reduce contractility which in turn reduces the risk of mechanical complications; they reduce the risk of lethal [[ventricular arrhythmias]]. | ||
A cornerstone in the management of STEMI is reperfusion or opening of the closed epicardial coronary artery. This can be achieved with either drugs such as a [[fibrinolytic]] agent, or mechanically with inflation of a balloon to puch the clot aside (percutaneous coronary intervention or PCI). A decade of expereince has shown that if it can be accomplished in a timely manner (a [[door-to-balloon]] time < 90 minutes), then PCI offers superior outcomes to [[fibrinolytic]] administration. | A cornerstone in the management of STEMI is reperfusion or opening of the closed epicardial coronary artery. This can be achieved with either drugs such as a [[fibrinolytic]] agent, or mechanically with inflation of a balloon to puch the clot aside (percutaneous coronary intervention or PCI). A decade of expereince has shown that if it can be accomplished in a timely manner (a [[door-to-balloon]] time < 90 minutes), then PCI offers superior outcomes to [[fibrinolytic]] administration. | ||
In under 5% of patients, [[Coronary artery bypass surgery|bypass surgery]] may be required given the extent of disease. | In under 5% of patients, [[Coronary artery bypass surgery|bypass surgery]] may be required given the extent of disease. A common practice is to perform urgent conventional balloon angioplasty of the culprit vessel as a bridge to a more definitive CABG operation. | ||
==Monitoring of the Patient to Reduce post MI Complications== | ==Monitoring of the Patient to Reduce post MI Complications== | ||
Revision as of 20:43, 7 February 2009
| Myocardial infarction | |
| ICD-10 | I21-I22 |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Keywords and synonyms: AMI, STEMI, heart attack, MI, myocardial infarct, acute MI, coronary, coronary thrombosis
Overview
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 muscle or myocardium is interrupted. The resulting ischemia or oxygen shortage causes damage and / or irreversible death (necrosis) of the myocardium (heart muscle). It is a medical emergency, and the leading cause of death for both men and women worldwide, particularly in developed countries.[1] 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.
There are two types of acute MI: ST elevation myocardial infarction (STEMI), the topic of this chapter and non ST elevation MI (NSTEMI) which is discussed in another chapter of WikiDoc. ST elevation myocardial infarction refers to an electrocardiographic pattern in which the ST segments are elevated reflecting complete epicardial vessel occlusion. Once the vessel is opened by percutaneous coronary angioplasty, the ST segments can remain elevated due to absence of perfusion or flow into the myocardium itself. At this point in the evolution of the ST elevation MI, the epicardial artery is open, but the capillary network is occluded due to swelling, embolization, and / or vasospasm.
Non ST elevation myocardial infarction refers to a disease state in which the epicardial artery is open, but there is inadequate blood flow to the myocardium which results in an electrocardiographic pattern of ST segment depression. While ST elevation reflects transmural injury, ST depression may reflect ongoing subendocardial ischemia. Inadequate blood flow to the muscle may be due to embolization of material downstream into the myocardium or a restriction of blood flow due to severe narrowing of the epicardial artery. [2] [3] [4]
Edpidemiology and Demographics of ST Elevation MI
Myocardial infarction is a common presentation of ischemic heart disease. The World Heart Organization (WHO) estimated in 2002 that, 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 infections in developing countries.[5] Although it is difficult to ascertain the true incidence of ST elevation myocardial infarction (STEMI), according to the ACC/AHA guidelines, a conservative estimate is that approximately 500,000 patients suffer STEMI each year [6]. The incidence of STEMI has decreased over time. In an observational study of 5,832 metropolitan patients spanning from 1975 to 1997, the incidence of STEMI decreased from 171/100,000 to 101/100,000 [7]
Risk Factors for ST Elevation Myocardial Infarction
Important ST elevation myocardial infarction risk factors are a previous history of vascular disease such as atherosclerotic coronary heart disease and/or angina, a previous heart attack or stroke, advanced age, smoking, the abuse of certain illicit drugs such as cocaine, high LDL ("Low-density lipoprotein") and low HDL ("High density lipoprotein"), diabetes, high blood pressure, obesity and family history of coronary artery disease.[8] [9]
Triggers of ST Elevation Myocardial Infarction
A trigger is an activity or environmental condition that produces short-term physiological changes that may lead directly to onset of STEMI. ST elevation myocardial infarction triggers include physical exertion, psychological stress, sexual activity, diurnal (daily) variations in cortisol and platelet aggregation and circannual (yearly) variations in lipids and infectious etiologies, exposure to pollution and or particulate matter, cocaine and ingestion of a recent fatty meal. [10]
Symptoms of ST Elevation Myocardial Infarction
One third of patients who experience ST Segment Elevation Myocardial Infarction (STEMI) will die within 24 hours of the onset of ischemia, and many of the survivors will suffer significant morbidity. Morbidity and mortality from STEMI can be reduced significantly if patients and bystanders recognize symptoms early, activate the EMS, and thereby shorten the time to definitive treatment.
Classical symptoms of acute myocardial infarction include chest pain (which in some patients may radiate to the left arm), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety or a feeling of impending doom.
Many patients will state that there was no chest pain, but rather a sense of chest discomfort that they may describe as a squeezing sensation or a sense of chest heaviness or fullness.
Patients frequently feel suddenly ill. Women may experience different symptoms from men. Common associated symptoms of MI in women include shortness of breath, weakness, and fatigue.
Serial electrocardiographic studies from the Framingham study have shown that approximately one quarter of all myocardial infarctions (the appearance of new pathologic q waves) are silent, without chest pain or other symptoms.[11] The prognosis of patients with a silent MI was as bad as those with a symptomatic MI.
Diagnostic Studies in ST Elevation Myocardial Infarction
A new clinical evidence based classification system has been jointly introduced by the American College of Cardiology (ACC), American Heart Association (AHA), European Society of Cardiology (ESC), and the World Heart Federation (WHF).[12] The primary diagnostic tests include the electrocardiogram (ECG, EKG) and blood tests to detect elevated creatine kinase or troponin levels (these are chemical markers released by damaged tissues, especially the myocardium).
Treatment of ST Elevation Myocardial Infarction
Immediate treatment for suspected acute myocardial infarction includes oxygen, full dose non-enteric coated aspirin, nitroglycerin (also known as glyceryl trinitrate) and pain relief, using an analgesic agent such morphine sulfate. Among patients who do not have signs or symptoms of cardiogenic shock, beta blocker administration has been associated with improved clinical outcomes among patients with ST elevation myocardial infarction. [13] These agents exert their benefit via several mechanisms: They reduce myocardial oxygen demands; they reduce contractility which in turn reduces the risk of mechanical complications; they reduce the risk of lethal ventricular arrhythmias.
A cornerstone in the management of STEMI is reperfusion or opening of the closed epicardial coronary artery. This can be achieved with either drugs such as a fibrinolytic agent, or mechanically with inflation of a balloon to puch the clot aside (percutaneous coronary intervention or PCI). A decade of expereince has shown that if it can be accomplished in a timely manner (a door-to-balloon time < 90 minutes), then PCI offers superior outcomes to fibrinolytic administration. In under 5% of patients, bypass surgery may be required given the extent of disease. A common practice is to perform urgent conventional balloon angioplasty of the culprit vessel as a bridge to a more definitive CABG operation.
Monitoring of the Patient to Reduce post MI Complications
Admission of patients to the modern coronary care unit has been associated with rapid treatment of and reduced complications from fatal arrhythmias such as ventricular tachycardia or ventricular fibrillation.
Other complications of STEMI include reinfarction, infarct extension, postinfarction angina,rupture of the ventricular septum causing a ventricular septal defect, acute mitral regurgitation, myocardial rupture, development of a pseudoaneurysm, development of cardiogenic shock.
Prognosis
Despite advances in modern pharmacotherapy and device-based therapy, the short term mortality remains high in modern registry series (15%-20%).
References
- ↑ The World Health Report 2004 - Changing History (PDF). World Health Organization. 2004. pp. 120–4. ISBN 92-4-156265-X.
- ↑ Hurst’s The Heart, Fuster V, 12th edition, 2008
- ↑ Topol’s Textbook of Cardiovascular Medicine, Topol E, 3rd edition, 2007
- ↑ Mayo Textbook of Cardiology, 2007
- ↑ "Cause of Death - UC Atlas of Global Inequality". Center for Global, International and Regional Studies (CGIRS) at the University of California Santa Cruz. Unknown parameter
|accessyear=ignored (|access-date=suggested) (help); Unknown parameter|accessmonthday=ignored (help) - ↑ ACC/AHA guidelines for the management of patients with ST elevation myocardial infarction; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:E1-E211.
- ↑ Furman MI, Dauerman HL, Goldberg RJ, Yarzebski J, Lessard D, Gore JM. Twenty-two year (1975 to 1997) trends in the incidence, in-hospital and long-term case fatality rates from initial Q-wave and non-Q-wave myocardial infarction: a multi-hospital, community-wide perspective. J Am Coll Cardiol 2001; 37:1571-80.
- ↑ Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation 2004; 110:588–636.
- ↑ Antman E.M., Hant M., Armstrong P.W., et. al., 2007 Focused updates of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation published online Dec 10, 2007; DOI: 10.1161/CIRCULATION AHA.107.188209.
- ↑ Muller JE, Abela GS, Nesto RW, Tofler GH. Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier. J Am Coll Cardiol. 1994;23:809–813.
- ↑ Kannel WB (1986). "Silent myocardial ischemia and infarction: insights from the Framingham Study". Cardiol Clin. 4 (4): 583–91. PMID 3779719. Unknown parameter
|month=ignored (help) - ↑ Thygesen K, Alpert JS, White HD (2007). "Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction Joint ESC/ACCF/AHA/WHF". Circulation. 2007: 2634–2653. PMID 17951284.
- ↑ CAPRICORN: The Capricorn Investigators: Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction. Lancet 2001;357:1385.
External links
- Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute
- Heart Attack - overview of resources from MedlinePlus.
- Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada
- Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI
- STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
- American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.
- American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack.
- The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research
- Clinical Trial Results: An up to dated resource of Cardiovascular Research