ST elevation myocardial infarction overview

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Overview

Pathophysiology

Pathophysiology of Vessel Occlusion
Pathophysiology of Reperfusion
Gross Pathology
Histopathology

Causes

Differentiating ST elevation myocardial infarction from other Diseases

Epidemiology and Demographics

Risk Factors

Triggers

Natural History and Complications

Risk Stratification and Prognosis

Pregnancy

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

EKG Examples

Chest X Ray

Cardiac MRI

Echocardiography

Coronary Angiography

Treatment

Pre-Hospital Care

Initial Care

Oxygen
Nitrates
Analgesics
Aspirin
Beta Blockers
Antithrombins
The coronary care unit
The step down unit
STEMI and Out-of-Hospital Cardiac Arrest
Pharmacologic Reperfusion
Reperfusion Therapy (Overview of Fibrinolysis and Primary PCI)
Fibrinolysis
Reperfusion at a Non–PCI-Capable Hospital:Recommendations
Mechanical Reperfusion
The importance of reducing Door-to-Balloon times
Primary PCI
Adjunctive and Rescue PCI
Rescue PCI
Facilitated PCI
Adjunctive PCI
CABG
Management of Patients Who Were Not Reperfused
Assessing Success of Reperfusion
Antithrombin Therapy
Antithrombin therapy
Unfractionated heparin
Low Molecular Weight Heparinoid Therapy
Direct Thrombin Inhibitor Therapy
Factor Xa Inhibition
DVT prophylaxis
Long term anticoagulation
Antiplatelet Agents
Aspirin
Thienopyridine Therapy
Glycoprotein IIbIIIa Inhibition
Other Initial Therapy
Inhibition of the Renin-Angiotensin-Aldosterone System
Magnesium Therapy
Glucose Control
Calcium Channel Blocker Therapy
Lipid Management

Pre-Discharge Care

Recommendations for Perioperative Management–Timing of Elective Noncardiac Surgery in Patients Treated With PCI and DAPT

Post Hospitalization Plan of Care

Long-Term Medical Therapy and Secondary Prevention

Overview
Inhibition of the Renin-Angiotensin-Aldosterone System
Cardiac Rehabilitation
Pacemaker Implantation
Long Term Anticoagulation
Implantable Cardioverter Defibrillator
ICD implantation within 40 days of myocardial infarction
ICD within 90 days of revascularization

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Acute myocardial infarction, 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 termmyocardial 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]

Epidemiology and Demographics

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

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]

Risk Stratification

Two main risk-stratification scores are used when assessing a patient with ST elevation MI and acute coronary syndromes; the TIMI Risk Score (for MI), and the GRACE risk score (for acute coronary syndrome.

Triggers

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]

Natural History, Complications and Prognosis

The natural progression of ST elevation myocardial infarction depends on epicardial artery patency and the risk for early vessel reocclusion. Without treatment, ST elevation myocardial infarction can prove deadly.

Prognosis

Despite advances in modern pharmacotherapy and device-based therapy, the short term mortality remains high in modern registry series (15%-20%). The prognosis for patients with myocardial infarction varies greatly depending upon simple demographic variables like age, the presence of signs and symptoms of heart failure, the duration of symptoms, and comorbidities that are present. Several risk stratification tools have been developed to predict a patient's mortality. Most of these risk scores are based upon clinical data obtained at the time of admission rather than at the time of discharge.

While we as physicians often labor under the impression that we can dramatically change a patient's prognosis, it is noteworthy that 90% of the predictive information regarding 30 day mortality is contained in the following 5 baseline variables that can be modified to only a limited degree: [11]

  1. Advanced age
  2. Sinus tachycardia
  3. Reduced systolic blood pressure
  4. Heart failure or Killip class of two or greater
  5. Anterior myocardial infarction location

Sinus tachycardia, hypotension, Killip class, and anterior MI are all essentially markers of poor pump function on admission. These risk factors for 30 day mortality have been well validated in a multivariate analysis of 41,020 patients in the GUSTO-I trial. Advanced age was the most significant factor associated with higher 30-day mortality. The rate was only 1.1% in the youngest decile (< 45 years) and climbed to 20.5% in patients > 75 (adjusted chi 2 = 717, P < .0001). Other variables most closely associated with an increased risk of mortality were lower systolic blood pressure at randomizaiton (chi 2 = 550, P < .0001), higher Killip class (chi 2 = 350, P < .0001), elevated heart rate (chi 2 = 275, P < .0001), and the presence of an anterior infarction (chi 2 = 143, P < .0001). When taken together, these five baseline characteristics contained 90% of the prognostic information. Other significant though less important factors included previous myocardial infarction, height, time to treatment, diabetes, weight, smoking status, type of thrombolytic, previous bypass surgery,hypertension, and prior cerebrovascular disease. When these variables were combined, a validated model was created which stratified patients according to their mortality risk and accurately estimated the likelihood of death.

Various risk tools such as the GRACE risk score have been developed to risk stratify patients.

Pregnancy

Physiological changes during pregnancy may increase the woman's risk of developing a myocardial infarction (MI). MI during the antepartum period is usually caused by an atherosclotic plaque rupture, whereas MI during the peripartum and postpartum period is usually caused by coronary artery dissection (commonly in the LAD). Diagnosis of MI among pregnant women is similar to that in the general population and requires clinical suspiccion, as well as ECG changes and troponin elevation. In contrast, elevated CK-MB concentration is unreliable, since CK-MB may normally increase during labor and post-delivery due to non-cardiac causes, namely placental and uterine leaks. During an MI, echocardiography is safe and may be performed to evaluate wall motion abnormalities, and fetal monitoring is recommended. Treatment is usually by percutaneous coronary intervention. If spontaneous coronary artery dissection occurs, a more thorough investigation for connective tissue diseases and vasculitis is warranted.

Diagnosis

Diagnostic Criteria

The diagnosis of acute MI is based upon the occurence of clinical symptoms such as substernal chest pain, EKG changes such as ST elevation and a rise in the release of very specific biomarkers into the bloodstream that are normally only found in side the heart muscle cell (the myocyte).

The diagnosis can be confirmed at the time of autopsy or at the time of angiography if a closed artery is seen. A new clinical evidence based diagnostic and classification system has been introduced by Thygesen K, Alpert JS, White HD, et al. and jointly sponsored by the American College of Cardiology (ACC), American Heart Association (AHA), European Society of Cardiology (ESC), and the World Heart Federation (WHF).[12]

History and Symptoms

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 includeshortness 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.[13] The prognosis of patients with a silent MI was as bad as those with a symptomatic MI.

Physical Examination

The physical examination in patients who have suspected acute myocardial infarction may reveal arrhythmia, evidence of heart failure, a new murmur, or cardiovascular compromise and shock. A systems focused examination is probably most appropriate at the time of presentation so as to not delay decisions regarding and implementation of reperfusion therapy. Following these initial stages of management, a more through examination is then warranted. Throughout the patient's course, detailed serial examinations should be performed in an effort to remain vigilant for the development of mechanical complications of acute MI. The approach to the physical examination in the patient with ST elevation MI is divided into two phases: The initial physical examination and then the more thorough examination of the patient after the initial assessment and treatment of the patient.

Laboratory Findings

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)[14]. 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).

Electrocardiogram

A primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. Common EKG findings in STEMI include ST segment elevation, new LBBB pattern and hyperacute T waves.

Imaging

Coronary Angiography

The goal of coronary angiography in STEMI patients is to identify the obstructed culprit artery and to open it as quickly as possible. The goal is to achieve a door to balloon time in under 90 minutes. This is the time from when a patient arrives at the door of the emergency room until the time that the first device is activated in the coronary artery.

Treatment

Medical Therapy

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[15]. 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.

Antiplatelet therapy is a mainstay of STEMI management. Aspirin is a cornerstone of STEMI management. Given that the majority of patients undergoing primary PCI are treated with an intracoronary stent, thienopyridine therapy is also essential. Depending upon a variety of factors, glycoprotein IIbIIIa inhibition is administered in approximately 70% of STEMI patients undergoing primary PCI.

Likewise, antithrombin therapy is also a mainstay of STEMI management. Frequent choices among patients treated with fibrinolytic agents include unfractionated heparin in the United States, and enoxaparin and fondaparinux in other countries. Among patients undergoing primary PCI, frequent choices include bivalirudin and unfractionated heparin.

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, development of a ventricular aneurysm, embolic complications, and pericarditis.

References

  1. The World Health Report 2004 - Changing History (PDF). World Health Organization. 2004. pp. 120–4. ISBN 92-4-156265-X. 
  2. Hurst’s The Heart, Fuster V, 12th edition, 2008
  3. Topol’s Textbook of Cardiovascular Medicine, Topol E, 3rd edition, 2007
  4. Mayo Textbook of Cardiology, 2007
  5. "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)
  6. Antman EM, Anbe DT, Armstrong PW; et al. (2004). "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. 44 (3): E1–E211. PMID 15358047. doi:10.1016/j.jacc.2004.07.014.  Unknown parameter |month= ignored (help)
  7. Furman MI, Dauerman HL, Goldberg RJ, Yarzebski J, Lessard D, Gore JM (2001). "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. 37 (6): 1571–80. PMID 11345367.  Unknown parameter |month= ignored (help)
  8. Antman EM, Anbe DT, Armstrong PW; et al. (2004). "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. 110 (5): 588–636. PMID 15289388. doi:10.1161/01.CIR.0000134791.68010.FA.  Unknown parameter |month= ignored (help)
  9. Antman EM, Hand M, Armstrong PW; et al. (2008). "2007 focused update 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". J. Am. Coll. Cardiol. 51 (2): 210–47. PMID 18191746. doi:10.1016/j.jacc.2007.10.001.  Unknown parameter |month= ignored (help)
  10. Muller JE, Abela GS, Nesto RW, Tofler GH (1994). "Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier". J. Am. Coll. Cardiol. 23 (3): 809–13. PMID 8113568.  Unknown parameter |month= ignored (help)
  11. Lee KL, Woodlief LH, Topol EJ; et al. (1995). "Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators". Circulation. 91 (6): 1659–68. PMID 7882472.  Unknown parameter |month= ignored (help)
  12. Thygesen K, Alpert JS, White HD; et al. (2007). "Universal definition of myocardial infarction". Circulation. 116 (22): 2634–53. PMID 17951284. doi:10.1161/CIRCULATIONAHA.107.187397.  Unknown parameter |month= ignored (help)
  13. 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)
  14. 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. 
  15. Dargie HJ (2001). "Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial". Lancet. 357 (9266): 1385–90. PMID 11356434.  Unknown parameter |month= ignored (help)

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