Myocardial Infarction
No Results
No Results
processing….
Myocardial infarction (MI) (ie, heart attack) is the irreversible death (necrosis) of heart muscle secondary to prolonged lack of oxygen supply (ischemia). Approximately 1.5 million cases of MI occur annually in the United States. See the images below.
See Are You Missing Subtle MI Clues on ECGs? Test Your Skills, a Critical Images slideshow, to help identify a variety of electrocardiographic abnormalities.
Patients with typical MI may have the following symptoms in the days or even weeks preceding the event (although typical STEMI may occur suddenly, without warning):
Fatigue
Chest discomfort
Malaise
Typical chest pain in acute MI has the following characteristics:
Intense and unremitting for 30-60 minutes
Substernal, and often radiates up to the neck, shoulder, and jaw, and down the left arm
Usually described as a substernal pressure sensation that also may be characterized as squeezing, aching, burning, or even sharp
In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas
The patient’s vital signs may demonstrate the following in MI:
The patient’s heart rate is often increased (tachycardic) secondary to a high sympathoadrenal discharge
The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias; bradyarrhythmias may be present
In general, the patient’s blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction
However, with right ventricular MI or severe left ventricular dysfunction, hypotension and cardiogenic shock can be seen
The respiratory rate may be increased in response to pulmonary congestion or anxiety
Coughing, wheezing, and the production of frothy sputum may occur
See Clinical Presentation for more detail.
Laboratory studies
Laboratory tests used in the diagnosis of MI include the following:
Cardiac biomarkers/enzymes: The American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) guidelines recommend that cardiac biomarkers should be measured at presentation in patients with suspected MI, and that the only biomarker that is recommended to be used for the diagnosis of acute MI at this time is cardiac troponin due to its superior sensitivity and accuracy. [1, 2, 3, 4]
Troponin levels: Troponin is a contractile protein that normally is not found in serum; it is released only when myocardial necrosis occurs
Complete blood cell count
Comprehensive metabolic panel
Lipid profile
Electrocardiography
The ECG is the most important tool in the initial evaluation and triage of patients in whom an acute coronary syndrome (ACS), such as MI, is suspected. It is confirmatory of the diagnosis in approximately 80% of cases.
Cardiac imaging
For individuals with highly probable or confirmed acute MI, coronary angiography can be used to definitively diagnose or rule out coronary artery disease.
See Workup for more detail.
Prehospital care
For patients with chest pain, prehospital care includes the following:
Intravenous access, supplemental oxygen if SaO2 is less than 90%, pulse oximetry
Immediate administration of nonenteric-coated chewable aspirin
Nitroglycerin for active chest pain, given sublingually or by spray
Telemetry and prehospital ECG, if available
Emergency department and inpatient care
Initial stabilization of patients with suspected MI and ongoing acute chest pain should include administration of sublingual nitroglycerin if patients have no contraindications to it.
The American Heart Association (AHA) recommends the initiation of beta blockers to all patients with STEMI (unless beta blockers are contraindicated). [1, 2]
If STEMI is present and the patient is within 90 minutes of a PCI-capable facility, the patient should undergo emergent coronary angiography and primary PCI. If the patient is longer than 120 minutes from a PCI-capable facility, fibrinolysis should be considered. [2]
Although patients presenting without ST-segment elevation (non-STE-ACS) are not candidates for immediate administration of thrombolytic agents, they should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission.
Coronary care units have reduced early mortality rates from acute MI by approximately 50% by providing immediate defibrillation and by facilitating the implementation of beneficial interventions. These interventions include the administration of intravenous (IV) medications and therapy designed to do the following:
Limit the extent of MI
Salvage jeopardized ischemic myocardium
Recanalize infarct-related arteries
See Treatment and Medication for more detail.
Myocardial infarction (MI) usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium. (See Etiology for details.)
The electrocardiographic (ECG) results of an acute MI are seen below.
Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with MI, many events are either “silent” or are not clinically recognized by patients, families, and health care providers. (See Presentation.) The appearance of cardiac biomarkers in the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis. (See Workup.)
MI is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–ST-segment elevation MI (NSTEMI)—collectively referred to as non–ST-segment acute coronary syndrome (NSTE ACS)—and ST-segment elevation MI (STEMI). Patients with ischemic discomfort may or may not have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST elevations seen on the ECG reflect active and ongoing transmural myocardial injury. Without immediate reperfusion therapy, most patients with STEMI develop Q waves, reflecting a dead zone of myocardium that has undergone irreversible damage and death.
Those without ST elevations are diagnosed either with unstable angina or NSTEMI―differentiated by the presence of cardiac enzymes. Both these conditions may or may not have changes on the surface ECG, including ST-segment depressions or T-wave morphological changes.
MI may lead to impairment of systolic or diastolic function and to increased predisposition to arrhythmias and other long-term complications.
Coronary thrombolysis and mechanical revascularization have revolutionized the primary treatment of acute MI, largely because they allow salvage of the myocardium when implemented early after the onset of ischemia. (See Treatment.)
The modest prognostic benefit of an opened infarct-related artery may be realized even when recanalization is induced only 6 hours or more after the onset of symptoms; that is, when the salvage of substantial amounts of jeopardized ischemic myocardium is no longer likely. The opening of an infarct-related artery may improve ventricular function and collateral blood flow; prevent ventricular remodeling, as well as decrease infarct expansion, ventricular aneurysm formation, and left ventricular dilatation; and reduce late arrhythmia associated with ventricular aneurysms, and mortality. [5, 6, 7]
Evidence suggests a benefit from the use of beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and statins.
The American College of Cardiology (ACC)/American Heart Association (AHA)/European Society of Cardiology/World Heart Federation released the Observations From the TRITON-TIMI 38 Trial (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis in Myocardial Infarction 38), which better outlines a universal definition of MI, along with a classification system and risk factors for cardiovascular death. [8]
(See Treatment for more details.)
Myocardial infarction (MI), commonly known as a heart attack, is defined pathologically as the irreversible death of myocardial cells caused by ischemia. Clinically, MI is a syndrome that can be recognized by a set of symptoms, chest pain being the hallmark of these symptoms in most cases, supported by biochemical laboratory changes, electrocardiographic (ECG) changes, or findings on imaging modalities able to detect myocardial injury and necrosis.
According to the third universal definition of MI, implemented by a joint task force from the European Society of Cardiology (ESC), American College of Cardiology (ACC) Foundation, American Heart Association (AHA), and the World Heart Federation (WHF), MI is diagnosed when either of the following two criteria are met. [9]
1. Detection of an increase or decrease in cardiac biomarker values (preferably using cardiac troponin [cTn]) with at least one value above the 99th percentile of the upper reference limit (URL) and with at least one of the following findings:
2. Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic changes or injury or new BBB on ECG, but death occurred before cardiac biomarker levles were obtained, or before cardiac biomarker values would be increased.
Types of MI
The Joint ESC/ACCF/AHA/WHF Task Force further classified MI into 5 types on the basis of the underlying cause [7] :
The term “acute coronary syndrome” (ACS) refers to a spectrum of conditions that occur due to acute myocardial ischemia and/or infarction as a result of an abrupt reduction in blood flow through the coronary artery circulation.
ACS is divided into two main categories, non–ST elevation (NSTE) ACS and ST-elevation MI (STEMI)
NSTE ACS
NSTE ACS is further divided into unstable angina (UA) and non–ST-elevation myocardial infraction (NSTEMI). These two conditions resemble each other very closely. UA is distinguished from NSTEMI by the absence of an elevation of cardiac biomarker levels. [1]
STEMI
The major discriminating feature of STEMI is the presence of symptoms of myocardial ischemia/injury along with persistent ECG ST-segment elevation in addition to the presence of cardiac biomarkers. [2]
Myocardial injury and myocardial cell death
For the normal heart to continue to function and to steadily pump blood efficiently to meet the demands of the body, it needs to have a constant supply of oxygen and nutrients provided mainly by the coronary circulation. A condition called myocardial ischemia happens if blood supply to the myocardium does not meet the demand. If this imbalance persists, it triggers a cascade of cellular, inflammatory and biochemical events, leading eventually to the irreversible death of heart muscle cells, resulting in MI.
Evolution of MI and ventricular remodeling
The spectrum of myocardial injury depends not only on the intensity of impaired myocardial perfusion but also on the duration and the level of metabolic demand at the time of the event. Severe loss of the ability of the heart muscle cell to contract can be observed as early as within 60 seconds. Persistence of oxygen deprivation to the myocardium through the cessation of blood supply will lead to irreversible myocardial injury within 20 to 40 minutes and up to several hours, depending on several factors including the existing metabolic state of the body and presence of coronary collateral blood flow. [10]
Typical MI initially manifests as coagulation necrosis that is ultimately followed by a healing process characterized by formation of myocardial scarring, known as myocardial fibrosis. This mechanism allows significant architectural changes to the composition, shape and contractile function of the myocardium, especially in the left ventricle, which is the major contributor to the contractile function of the heart. Eventually the left ventricle dilates and changes to a more spherical shape, in a process known as ventricular remodeling. Despite being an irreversible process, ventricular remodeling is a regulated process, therefore, specific treatment strategies and agents should be used in acute MI management in order to reduce the occurrence and severity of ventricular remodeling. [11]
Reperfusion injury
In some occasions, restoration of blood flow to the damaged myocardium triggers further ischemic cellular damage, this paradoxical effect is known as reperfusion injury. This process involves a complex interaction between oxygen free radicals and intracellular calcium, leading to acceleration of myocardial damage and death, microvascular dysfunction and fatal arrhythmias. The role of nitric oxide (an endothelium-derived relaxing factor) as a cardioprotective agent against reperfusion injury, has been demonstrated, as nitric oxide works to inactivate oxygen free radicals, therefore, ameliorating the process of reperfusion injury. [12] Despite the improved understanding of the process of reperfusion injury, there are no specific therapies to prevent it.
Stunned and hibernating myocardium
Stunned myocardium is a condition of transient left ventricular dysfunction following an ischemic event to the myocardium. It occurs if coronary blood flow was impaired for a brief period of time (5 to 15 minutes). Usually, stunned myocardium persists for hours or days following the re-establishment of coronary blood flow.
However, prolonged exposure of the myocardium to an ischemic state, results in an impairment of its contractile function, which can be partial or complete, this is known as myocardial hibernation, and is reversible with revascularization.
Both myocardial stunning and hibernation occur because of loss of essential metabolites required for normal myocardial contractility, such as adenosine, which is needed for adenosine triphosphate (ATP)-dependent contraction. [13]
The atheromatous plaque responsible for acute MI develops in a dynamic process in multiple stages. Starting with arterial intimal thickening, which consists of vascular smooth muscles with very minimal or no inflammatory cells, this process can be observed soon after birth. Subsequently, the formation of fibrous cap atheroma occurs, which has a lipid-rich necrotic core that is surrounded by fibrous tissue. Eventually, a thin-cap fibroatheroma develops, this is also known as a vulnerable plaque which is composed mainly of a large necrotic core separated from the vascular lumen by a thin fibrous cap that is infiltrated by inflammatory cells and is deficient of smooth muscle cells, making it vulnerable to rupture. [14, 15]
The process of acute coronary thrombosis leading to ACS involves the pathogenic mechanism of plaque rupture, and less frequently plaque erosion.
The Brasilia Heart Study Group indicates that changes in high-density lipoprotein (HDL) during an MI may alter the antiatherogenic function of HDL to transport lipids from arterial walls. [16] The investigators noted a simultaneous decrease in lipid transfer to HDL and in the capacity of HDL to efflux cholesterol from cells occurs in the acute period after an MI.
In a nested case-control study that evaluated the associations of plasma metabolic markers with the risks of incident MI, ischemic stroke, and intracerebral hemorrhage, investigators found positive associations of lipoproteins and lipids with MI and ischemic stroke but not with intracerebral hemorrohage, as well as positive associations between triglyceride concentrations and MI. [17] Except for small HDL, there was also an inverse association of HDL particles with MI, and an inverse association of cholesterol in large HDL with MI and ischemic stroke. The study cohort included 912 patients with MI, 1146 with ischemic stroke, 1138 with intracerebral hemorrhage, and 1466 control subjects. [17]
Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS) cases. Approximately 90% of myocardial infarctions (MIs) result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the major triggers for coronary thrombosis. Following plaque erosion or rupture, platelet activation and aggregation, coagulation pathway activation, and endothelial vasoconstriction occur, leading to coronary thrombosis and occlusion.
Within the coronary vasculature, flow dynamics and endothelial shear stress are implicated in the pathogenesis of vulnerable plaque formation. [18] A large body of evidence indicates that in numerous cases, culprit lesions are stenoses of less than 70% and are located proximally within the coronary tree. [19, 20] Coronary atherosclerosis is especially prominent near branching points of vessels. [21] Culprit lesions that are particularly prone to rupture are atheromas containing abundant macrophages, a large lipid-rich core surrounded by a thinned fibrous cap.
Nonmodifiable risk factors for atherosclerosis include the following:
Age
Sex
Family history of premature coronary heart disease
Male-pattern baldness
Modifiable risk factors for atherosclerosis include the following [22] :
Smoking or other tobacco use
Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders
Dyslipidemia
Diabetes mellitus
Hypertension
Obesity (abdominal obesity)
Psychosocial stress
Sedentary lifestyle and/or lack of exercise
Reduced consumption of fruits and vegetables
Poor oral hygiene
Type A personality
Elevated homocysteine levels
Presence of peripheral vascular disease
MI can also occur for causes other than atherosclerosis. Nonatherosclerotic causes of MI include the following:
Coronary occlusion secondary to vasculitis
Ventricular hypertrophy (eg, left ventricular hypertrophy, hypertrophic cardiomyopathy)
Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
Coronary trauma
Primary coronary vasospasm (variant angina)
Drug use (eg, cocaine, amphetamines, ephedrine)
Arteritis
Coronary anomalies, including aneurysms of coronary arteries
Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
Factors that decrease oxygen delivery, such as hypoxemia of severe anemia
Aortic dissection, with retrograde involvement of the coronary arteries
Respiratory infections, particularly influenza [23, 24]
In addition, MI can result from hypoxia due to carbon monoxide poisoning or acute pulmonary disorders.
Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis.
Acute MI is rare in childhood and adolescence. Although adults acquire coronary artery disease from lifelong deposition of atheroma and plaque, which causes coronary artery spasm and thrombosis, children with acute MI usually have either an acute inflammatory condition of the coronary arteries or an anomalous origin of the left coronary artery. Intrauterine MI also does occur, often in association with coronary artery stenosis. [25]
Coronary artery disease (CAD) is the leading cause of death in the United States; approximately 500,000-700,000 deaths related to CAD occur each year, making it the cause of death in an estimated one third of all deaths in the population for those older than 35 years.
Approximately 1.5 million cases of myocardial infarction (MI) occur annually in the United States; the yearly incidence rate is approximately 600 cases per 100,000 people. The proportion of patients diagnosed with non–ST-elevation MI (NSTEMI) compared with ST-elevation MI (STEMI) has progressively increased. Despite an impressive decline in age-adjusted death rates attributable to acute MI since the mid-1970s, the total number of MI-related deaths in the United States has not declined. [26]
The death rate related to acute MI is approximately three times higher in men than in women. It is more frequent in black patients compared to white patientss, an excess that disappears by age 75 years. Among the Hispanic population, coronary mortality is not as high as it is among black individuals and white persons. [27]
CAD is also the number one cause of death in European countries.
In the European Union, death rates related to CAD dropped by almost 30% between the mid 1960s to the mid and late 1990s; however, within Eastern European countries, there was an increase in death rates related to acute MI in the early1990s, followed by a subsequent decline. In the Russian Federation, cardiovascular mortality remained the same. [28]
An analysis of death certificates from the World Health Organization (WHO) database demonstrated that CAD mortality in Japan was significantly lower than in the United States and Europe, and it was further reduced by about 30% by the mid 1990s. [28]
In China, there has been a significant increase in mortality related to CAD, this is most likely attributed to the increase in cardiovascular disease risk factors, predominantly smoking and dyslipidemia. [29]
The incidence of CAD and related mortality is expected to rise dramatically in other developing countries including India, Latin America, the Middle East and Sub-Saharan Africa, with an estimated 80% increase, from approximately 9 million in 1990 to a projected 20 million by 2020. [30, 31]
It is believed that these international trends in the incidence of CAD and subsequent acute MI are largely related to consequences of social and economic changes in these countries, resulting in better healthcare access and increases in life expectancy, in addition to adoption of westernized diets, reduction in physical activity, and higher rates of smoking.
A major Canadian-led global study (INTERHEART trial) in 52 countries across Africa, Asia, Australia, Europe, the Middle East, and North and South America, has identified 9 easily measured risk factors (smoking, abnormal blood lipid levels, hypertension, diabetes, obesity, diet, physical activity, alcohol consumption, and psychosocial factors) that account for over 90% of the risk for acute MI. [22] The INTERHEART investigators found that these risk factors are the same in almost every geographic region and every racial/ethnic group worldwide, and they are consistent in men and women. The INTERHEART trial showed that smoking 1-5 cigarettes daily increased the risk of an acute MI by 40%, and the risk increased with the amount of tobacco smoked per day. It also concluded that all forms of tobacco, including filtered and nonfiltered cigarettes, pipes and cigars, and chewing tobacco, are harmful, and that abdominal obesity is a greater risk factor than body-mass index (BMI), indicating that measurement of waist-to-hip ratio could replace BMI as an indicator of obesity. [22, 31, 32]
Acute myocardial infarction (MI) is associated with a 30% mortality rate; about 50% of the deaths occur prior to arrival at the hospital. An additional 5-10% of survivors die within the first year after their myocardial infarction. Approximately half of all patients with an MI are rehospitalized within 1 year of their index event.
Overall, prognosis is highly variable and depends largely on the extent of the infarct, the residual left ventricular function, and whether the patient underwent revascularization.
Better prognosis is associated with the following factors:
Successful early reperfusion (ST-elevation MI [STEMI] goals: patient arrival to fibrinolysis infusion within 30 minutes OR patient arrival to percutaneous coronary intervention [PCI] within 90 minutes)
Preserved left ventricular function
Short-term and long-term treatment with beta-blockers, aspirin, and angiotensin-converting enzyme (ACE) inhibitors
Poorer prognosis is associated with the following factors:
Advanced age
Diabetes mellitus
Previous vascular disease (eg, cerebrovascular disease or peripheral vascular disease)
Elevated thrombolysis in MI (TIMI) risk score for unstable angina/non–ST elevation acute coronary syndrome (NSTE-ACS) (TIMI risk score includes 7 factors: age ≥65 y, ≥3 risk factors for cardiac disease, previous coronary disease, ST-segment deviation ≥0.5 mm, ≥2 episodes of angina in last 24 hours, aspirin use within prior week, and elevated cardiac enzyme levels) [1, 3, 33]
Delayed or unsuccessful reperfusion
Poorly preserved left ventricular function (the strongest predictor of outcome)
Evidence of congestive heart failure (Killip classification ≥II) [34] or frank pulmonary edema (Killip classification ≥III) [35]
Elevated B-type natriuretic peptide (BNP) levels [36, 37, 38]
Elevated high sensitive C-reactive protein (hs-CRP), a nonspecific inflammatory marker [39]
Involvement of electrocardiograph (ECG) lead aVR [40, 41]
Depression
It has been shown that five baseline parameters at presentation of patients with acute MI account for over 90% of the prognostic predictors of 30-day mortality from acute MI. These parameters include age, systolic blood pressure on presentation, Killip classification, heart rate, and anatomic location of the MI.
The Killip classification is widely used in patients presenting with acute MI for the purpose of risk stratification, as follows [42] :
Patients with active symptoms of acute coronary syndrome (ACS) should be instructed to call emergency services (eg, 911 in the United States), and they should be transported by emergency medical services personnel, not by themselves, family, or friends. Patients should be instructed to go to the emergency department immediately if the suspected ACS symptoms last longer than 20 minutes at rest or are associated with near syncope/syncope or hemodynamic instability.
If nitroglycerin is prescribed to a patient with suspected ACS, the patient should be instructed to take a dose if symptoms arise. If no relief is experienced 5 minutes after the first dose, the patient should contact emergency services. If relief is experienced within 5 minutes of the first nitroglycerin dose, repeated doses can be given every 5 minutes for a maximum of 3 doses total. If by then the symptoms have not yet fully resolved, the patient, a family member, or a caregiver should contact emergency services. [1]
Diet plays an important role in the development of coronary artery disease (CAD). Educate post–myocardial infarction (MI) patients about the role of a low-cholesterol and low-salt diet. A dietitian should see and evaluate all patients prior to discharge from the hospital. Additionally, emphasis on exercise training should be made, because current evidence demonstrates that cardiac rehabilitation after MI results in lower rates of recurrent cardiovascular events. [43]
All patients should be educated regarding the critical role of smoking in the development of CAD. Smoking cessation classes should be offered to help patients avoid smoking after their MI.
For patient education resources, see the Heart Health Center and Cholesterol Center, as well as High Cholesterol, Cholesterol Charts (What the Numbers Mean), Lifestyle Cholesterol Management, Chest Pain, Coronary Heart Disease, Heart Attack, Angina Pectoris, Cholesterol-Lowering Medications, and Statins for Cholesterol.
[Guideline] Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Dec 23. 130 (25):e344-426. [Medline]. [Full Text].
[Guideline] O’Gara PT, Kushner FG, Ascheim DD, et al. American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Jan 29. 127 (4):e362-425. [Medline]. [Full Text].
[Guideline] Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016 Jan 14. 37 (3):267-315. [Medline]. [Full Text].
[Guideline] Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC); Steg PG, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012 Oct. 33 (20):2569-619. [Medline]. [Full Text].
Costa e Silva R, Pellanda L, Portal V, Maciel P, Furquim A, Schaan B. Transdisciplinary approach to the follow-up of patients after myocardial infarction. Clinics (Sao Paulo). 2008 Aug. 63 (4):489-96. [Medline].
Rathore SS, Gersh BJ, Weinfurt KP, Oetgen WJ, Schulman KA, Solomon AJ. The role of reperfusion therapy in paced patients with acute myocardial infarction. Am Heart J. 2001 Sep. 142(3):516-9. [Medline].
Jaffe AS. Third universal definition of myocardial infarction. Clin Biochem. 2013 Jan. 46 (1-2):1-4. [Medline].
Bonaca MP, Wiviott SD, Braunwald E, et al. American College of Cardiology/American Heart Association/European Society of Cardiology/World Heart Federation Universal definition of myocardial infarction classification system and the risk of cardiovascular death: observations from the TRITON-TIMI 38 Trial (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis in Myocardial Infarction 38). Circulation. 2012 Jan 31. 125(4):577-83. [Medline].
Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012 Oct 16. 60 (16):1581-98. [Medline].
Fujita M, Nakae I, Kihara Y, et al. Determinants of collateral development in patients with acute myocardial infarction. Clin Cardiol. 1999 Sep. 22 (9):595-9. [Medline].
Burchfield JS, Xie M, Hill JA. Pathological ventricular remodeling: mechanisms: part 1 of 2. Circulation. 2013 Jul 23. 128 (4):388-400. [Medline].
Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007 Sep 13. 357 (11):1121-35. [Medline].
Marban E. Myocardial stunning and hibernation. The physiology behind the colloquialisms. Circulation. 1991 Feb. 83 (2):681-8. [Medline].
McGill HC Jr, McMahan CA, Zieske AW, et al. Associations of coronary heart disease risk factors with the intermediate lesion of atherosclerosis in youth. The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. Arterioscler Thromb Vasc Biol. 2000 Aug. 20 (8):1998-2004. [Medline].
Kolodgie FD, Virmani R, Burke AP, et al. Pathologic assessment of the vulnerable human coronary plaque. Heart. 2004 Dec. 90 (12):1385-91. [Medline].
Soares AAS, Tavoni TM, de Faria EC, Remalay AT, Maranhao RC, Sposito AC, et al. HDL acceptor capacities for cholesterol efflux from macrophages and lipid transfer are both acutely reduced after myocardial infarction. Clin Chim Acta. 2018 Mar. 478:51-6. [Medline].
Holmes MV, Millwood IY, Kartsonaki C, et al, for the China Kadoorie Biobank Collaborative Group. Lipids, lipoproteins, and metabolites and risk of myocardial infarction and stroke. J Am Coll Cardiol. 2018 Feb 13. 71 (6):620-32. [Medline]. [Full Text].
Chatzizisis YS, Coskun AU, Jonas M, Edelman ER, Feldman CL, Stone PH. Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior. J Am Coll Cardiol. 2007 Jun 26. 49(25):2379-93. [Medline].
Wang JC, Normand SL, Mauri L, Kuntz RE. Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation. 2004 Jul 20. 110(3):278-84. [Medline].
Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995 Aug 1. 92(3):657-71. [Medline].
McDaniel MC, Willis P, Walker B, et al. Plaque necrotic core content is greater immediately distal to bifurcations compared to bifurcations in the proximal lad of patients with CAD. Am J Cardiol. 2008. 102(8):242i.
Yusuf S, Hawken S, Ounpuu S, et al, for the INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004 Sep 11-17. 364 (9438):937-52. [Medline].
Macintyre CR, Heywood AE, Kovoor P, et al. Ischaemic heart disease, influenza and influenza vaccination: a prospective case control study. Heart. 2013 Dec. 99 (24):1843-8. [Medline].
Kwong JC, Schwartz KL, Campitelli MA, et al. Acute myocardial infarction after laboratory-confirmed influenza infection. N Engl J Med. 2018 Jan 25. 378 (4):345-53. [Medline]. [Full Text].
Concheiro-Guisan A, Sousa-Rouco C, Fernandez-Santamarina I, Gonzalez-Carrero J. Intrauterine myocardial infarction: unsuspected diagnosis in the delivery room. Fetal Pediatr Pathol. 2006 Jul-Aug. 25(4):179-84. [Medline].
Rogers WJ, Frederick PD, Stoehr E, et al. Trends in presenting characteristics and hospital mortality among patients with ST elevation and non-ST elevation myocardial infarction in the National Registry of Myocardial Infarction from 1990 to 2006. Am Heart J. 2008 Dec. 156 (6):1026-34. [Medline].
Lloyd-Jones D, Adams RJ, Brown TM, et al, for the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Executive summary: heart disease and stroke statistics–2010 update: a report from the American Heart Association. Circulation. 2010 Feb 23. 121 (7):948-54. [Medline].
Levi F, Lucchini F, Negri E, La Vecchia C. Trends in mortality from cardiovascular and cerebrovascular diseases in Europe and other areas of the world. Heart. 2002 Aug. 88 (2):119-24. [Medline].
Critchley J, Liu J, Zhao D, Wei W, Capewell S. Explaining the increase in coronary heart disease mortality in Beijing between 1984 and 1999. Circulation. 2004 Sep 7. 110 (10):1236-44. [Medline].
Reddy KS. Cardiovascular disease in non-Western countries. N Engl J Med. 2004 Jun 10. 350 (24):2438-40. [Medline].
Okrainec K, Banerjee DK, Eisenberg MJ. Coronary artery disease in the developing world. Am Heart J. 2004 Jul. 148 (1):7-15. [Medline].
Ezzati M. How can cross-country research on health risks strengthen interventions? Lessons from INTERHEART. Lancet. 2004 Sep 11-17. 364 (9438):912-4. [Medline].
Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T, Papuchis G. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000 Aug 16. 284(7):835-42. [Medline].
Jaber WA, Prior DL, Marso SP, Houghtaling PL, Menon V, Harrington RA. CHF on presentation is associated with markedly worse outcomes among patients with acute coronary syndromes: PURSUIT trial findings. Circulation 1999:100(suppl I):I-433 .
Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol. 1967 Oct. 20(4):457-64. [Medline].
James SK, Lindahl B, Siegbahn A, et al. N-terminal pro-brain natriuretic peptide and other risk markers for the separate prediction of mortality and subsequent myocardial infarction in patients with unstable coronary artery disease: a Global Utilization of Strategies To Open occluded arteries (GUSTO)-IV substudy. Circulation. 2003 Jul 22. 108 (3):275-81. [Medline].
de Lemos JA, Morrow DA, Bentley JH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes. N Engl J Med. 2001 Oct 4. 345 (14):1014-21. [Medline].
Haaf P, Reichlin T, Corson N, et al. B-type natriuretic peptide in the early diagnosis and risk stratification of acute chest pain. Am J Med. 2011 May. 124 (5):444-52. [Medline].
Morrow DA, Rifai N, Antman EM, et al. C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI 11A substudy. Thrombolysis in Myocardial Infarction. J Am Coll Cardiol. 1998 Jun. 31 (7):1460-5. [Medline].
Boggs W. Worse Prognosis for Myocardial Infarction Patients With ST-Deviation in AVR. Medscape. Jul 11 2013. [Full Text].
Alherbish A, Westerhout CM, Fu Y, et al. The forgotten lead: does aVR ST-deviation add insight into the outcomes of ST-elevation myocardial infarction patients?. Am Heart J. Jul 3 2013. [Full Text].
Lee KL, Woodlief LH, Topol EJ, et al, for the GUSTO-I investigators. 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. 1995 Mar 15. 91 (6):1659-68. [Medline].
[Guideline] Smith SC Jr, Allen J, Blair SN, et al,. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update: endorsed by the National Heart, Lung, and Blood Institute. Circulation. 2006 May 16. 113 (19):2363-72. [Medline]. [Full Text].
Mann DL, Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 10th ed. Philadelphia, PA: Elsevier Saunders; 2015.
Wijnbergen I, Van’t Veer M, Pijls NH, Tijssen J. Circadian and weekly variation and the influence of environmental variables in acute myocardial infarction. Neth Heart J. 2012 Sep. 20 (9):354-9. [Medline].
Kundi H, Kiziltunc E, Korkmaz A, Cicek G, Ornek E, Ileri M. A novel risk scoring system to predict cardiovascular death in patients with acute myocardial infarction: CHA2DS2-VASc-CF score. Clin Appl Thromb Hemost. 2018 Mar. 24 (2):273-8. [Medline].
Kacprzak M, Kidawa M, Zielińska M. Fever in myocardial infarction: is it still common, is it still predictive?. Cardiol J. 2012. 19 (4):369-73. [Medline].
Risøe C, Kirkeby OJ, Grøttum P, Sederholm M, Kjekshus JK. Fever after acute myocardial infarction in patients treated with intravenous timolol or placebo. Br Heart J. 1987 Jan. 57 (1):28-31. [Medline].
Patel MR, Mahaffey KW, Armstrong PW, Weaver WD, Tasissa G, Hochman JS, et al. Prognostic usefulness of white blood cell count and temperature in acute myocardial infarction (from the CARDINAL Trial). Am J Cardiol. 2005 Mar 1. 95 (5):614-8. [Medline].
Lee-Lewandrowski E, Januzzi JL Jr, Grisson R, Mohammed AA, Lewandrowski G, Lewandrowski K. Evaluation of first-draw whole blood, point-of-care cardiac markers in the context of the universal definition of myocardial infarction: a comparison of a multimarker panel to troponin alone and to testing in the central laboratory. Arch Pathol Lab Med. 2011 Apr. 135 (4):459-63. [Medline].
Apple FS. A new season for cardiac troponin assays: it’s time to keep a scorecard. Clin Chem. 2009 Jul. 55 (7):1303-6. [Medline].
Diercks DB, Peacock WF 4th, Hollander JE, et al. Diagnostic accuracy of a point-of-care troponin I assay for acute myocardial infarction within 3 hours after presentation in early presenters to the emergency department with chest pain. Am Heart J. 2012 Jan. 163 (1):74-80.e4. [Medline].
Takakuwa KM, Ou FS, Peterson ED, et al. The usage patterns of cardiac bedside markers employing point-of-care testing for troponin in non-ST-segment elevation acute coronary syndrome: results from CRUSADE. Clin Cardiol. 2009 Sep. 32 (9):498-505. [Medline].
Mueller C. Biomarkers and acute coronary syndromes: an update. Eur Heart J. 2014 Mar. 35 (9):552-6. [Medline].
Anderson JL, Adams CD, Antman EM, et al, for the ACC, AHA Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the management of patients with unstable angina/NSTEMI, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction): developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interv… Circulation. 2007 Aug 14. 116 (7):e148-304. [Medline].
Reichlin T, Irfan A, Twerenbold R, et al. Utility of absolute and relative changes in cardiac troponin concentrations in the early diagnosis of acute myocardial infarction. Circulation. 2011 Jul 12. 124(2):136-45. [Medline].
Storrow AB, Nowak RM, Diercks DB, et al. Absolute and relative changes (delta) in troponin I for early diagnosis of myocardial infarction: Results of a prospective multicenter trial. Clin Biochem. 2015 Mar. 48 (4-5):260-7. [Medline].
Storrow AB, Christenson RH, Nowak RM, et al. Diagnostic performance of cardiac troponin I for early rule-in and rule-out of acute myocardial infarction: Results of a prospective multicenter trial. Clin Biochem. 2015 Mar. 48 (4-5):254-9. [Medline].
Cullen L, Parsonage WA, Greenslade J, et al. Delta troponin for the early diagnosis of AMI in emergency patients with chest pain. Int J Cardiol. 2013 Oct 3. 168 (3):2602-8. [Medline].
Thygesen K, Mair J, Mueller C, et al, for the Study Group on Biomarkers in Cardiology of the ESC Working Group on Acute Cardiac Care. Recommendations for the use of natriuretic peptides in acute cardiac care: a position statement from the Study Group on Biomarkers in Cardiology of the ESC Working Group on Acute Cardiac Care. Eur Heart J. 2012 Aug. 33 (16):2001-6. [Medline].
Goldstein JA, Chinnaiyan KM, Abidov A, et al, for the CT-STAT Investigators. The CT-STAT (Coronary Computed Tomographic Angiography for Systematic Triage of Acute Chest Pain Patients to Treatment) trial. J Am Coll Cardiol. 2011 Sep 27. 58 (14):1414-22. [Medline].
Samad Z, Hakeem A, Mahmood SS, et al. A meta-analysis and systematic review of computed tomography angiography as a diagnostic triage tool for patients with chest pain presenting to the emergency department. J Nucl Cardiol. 2012 Apr. 19 (2):364-76. [Medline].
Cremer PC, Khalaf S, Agarwal S, et al. Myocardial perfusion imaging in emergency department patients with negative cardiac biomarkers: yield for detecting ischemia, short-term events, and impact of downstream revascularization on mortality. Circ Cardiovasc Imaging. 2014 Nov. 7 (6):912-9. [Medline].
Amgen Inc. FDA approves Amgen’s Repatha (evolocumab) to prevent heart attack and stroke [press release]. Available at https://www.amgen.com/media/news-releases/2017/12/fda-approves-amgens-repatha-evolocumab-to-prevent-heart-attack-and-stroke/. December 1, 2017; Accessed: December 7, 2017.
Sabatine MS, Giugliano RP, Keech AC, et al, for the FOURIER Steering Committee and Investigators. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017 May 4. 376 (18):1713-22. [Medline]. [Full Text].
Becker L, Larsen MP, Eisenberg MS. Incidence of cardiac arrest during self-transport for chest pain. Ann Emerg Med. 1996 Dec. 28 (6):612-6. [Medline].
Mathews R, Peterson ED, Li S, et al. Use of emergency medical service transport among patients with ST-segment-elevation myocardial infarction: findings from the National Cardiovascular Data Registry Acute Coronary Treatment Intervention Outcomes Network Registry-Get With The Guidelines. Circulation. 2011 Jul 12. 124 (2):154-63. [Medline].
[Guideline] Jneid H, Addison D, Bhatt DL, et al. 2017 AHA/ACC clinical performance and quality measures for adults with ST-elevation and non-ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures. J Am Coll Cardiol. 2017 Oct 17. 70 (16):2048-90. [Medline].
Wendling P. AHA/ACC issue new performance, quality measures for MI. Medscape Medical News. Available at https://www.medscape.com/viewarticle/886075. September 22, 2017; Accessed: March 26, 2018.
[Guideline] Ibanez B, James S, Agewall S, et al, for the ESC Scientific Document Group . 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2018 Jan 7. 39 (2):119-77. [Medline]. [Full Text].
Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev. 2013 Aug 21. 8:CD007160. [Medline].
Gislason GH, Jacobsen S, Rasmussen JN, et al. Risk of death or reinfarction associated with the use of selective cyclooxygenase-2 inhibitors and nonselective nonsteroidal antiinflammatory drugs after acute myocardial infarction. Circulation. 2006 Jun 27. 113 (25):2906-13. [Medline].
Luepker RV, Raczynski JM, Osganian S, et al. Effect of a community intervention on patient delay and emergency medical service use in acute coronary heart disease: The Rapid Early Action for Coronary Treatment (REACT) Trial. JAMA. 2000 Jul 5. 284 (1):60-7. [Medline].
De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time delay to treatment and mortality in primary angioplasty for acute myocardial infarction: every minute of delay counts. Circulation. 2004 Mar 16. 109 (10):1223-5. [Medline].
Armstrong PW, Westerhout CM, Welsh RC. Duration of symptoms is the key modulator of the choice of reperfusion for ST-elevation myocardial infarction. Circulation. 2009 Mar 10. 119 (9):1293-303. [Medline].
Bates ER, Nallamothu BK. Commentary: the role of percutaneous coronary intervention in ST-segment-elevation myocardial infarction. Circulation. 2008 Jul 29. 118 (5):567-73. [Medline].
Ellis SG, Armstrong P, Betriu A, et al, for the Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events Investigators. Facilitated percutaneous coronary intervention versus primary percutaneous coronary intervention: design and rationale of the Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events (FINESSE) trial. Am Heart J. 2004 Apr. 147 (4):E16. [Medline].
Andersen HR, Nielsen TT, Rasmussen K, et al, for the DANAMI-2 Investigators. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med. 2003 Aug 21. 349 (8):733-42. [Medline].
Widimsky P, Budesínsky T, Vorac D, et al, for the ‘PRAGUE’ Study Group Investigators. Long distance transport for primary angioplasty vs immediate thrombolysis in acute myocardial infarction. Final results of the randomized national multicentre trial–PRAGUE-2. Eur Heart J. 2003 Jan. 24 (1):94-104. [Medline].
Vaidya SR, Qamar A, Arora S, Devarapally SR, Kondur A, Kaul P. Culprit versus multivessel coronary intervention in ST-segment elevation myocardial infarction: a meta-analysis of randomized trials. Coron Artery Dis. 2018 Mar. 29 (2):151-60. [Medline].
Spitaleri G, Brugaletta S, Scalone G, et al. Role of ST-segment resolution in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention (from the 5-year outcomes of the EXAMINATION Trial) [in press]. Am J Cardiol. 7 Feb 2018. [Full Text].
Rencuzogullari I, Cagdas M, Karabag Y, et al. Association of the SYNTAX Score II with cardiac rupture in patients with ST-segment elevation myocardial infarction undergoing a primary percutaneous coronary intervention. Coron Artery Dis. 2018 Mar. 29 (2):97-103. [Medline].
Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. 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. Lancet. 1994 Feb 5. 343 (8893):311-22. [Medline].
White HD. Thrombolytic therapy in the elderly. Lancet. 2000 Dec 16. 356 (9247):2028-30. [Medline].
Van de Werf F, Barron HV, Armstrong PW, et al, for the ASSENT-2 Investigators. Assessment of the Safety and Efficacy of a New Thrombolytic. Incidence and predictors of bleeding events after fibrinolytic therapy with fibrin-specific agents: a comparison of TNK-tPA and rt-PA. Eur Heart J. 2001 Dec. 22 (24):2253-61. [Medline].
Kodumuri V, Balasubramanian S, Vig A, et al. A meta-analysis comparing percutaneous coronary intervention with drug eluting stents versus coronary artery bypass grafting in unprotected left main disease [in press]. Am J Cardiol. 5 Feb 2018. [Full Text].
Yusuf S, Mehta SR, Chrolavicius S, et al, for the OASIS-6 Trial Group. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA. 2006 Apr 5. 295 (13):1519-30. [Medline].
Giraldez RR, Nicolau JC, Corbalan R, et al. Enoxaparin is superior to unfractionated heparin in patients with ST elevation myocardial infarction undergoing fibrinolysis regardless of the choice of lytic: an ExTRACT-TIMI 25 analysis. Eur Heart J. 2007 Jul. 28 (13):1566-73. [Medline].
Wallentin L, Goldstein P, Armstrong PW, et al. Efficacy and safety of tenecteplase in combination with the low-molecular-weight heparin enoxaparin or unfractionated heparin in the prehospital setting: the Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT)-3 PLUS randomized trial in acute myocardial infarction. Circulation. 2003 Jul 15. 108 (2):135-42. [Medline].
Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT)-3 Investigators. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction. Lancet. 2001 Aug 25. 358 (9282):605-13. [Medline].
White H, Hirulog and Early Reperfusion or Occlusion (HERO)-2 Trial Investigators. Thrombin-specific anticoagulation with bivalirudin versus heparin in patients receiving fibrinolytic therapy for acute myocardial infarction: the HERO-2 randomised trial. Lancet. 2001 Dec 1. 358 (9296):1855-63. [Medline].
Wiviott SD, Braunwald E, McCabe CH, et al, for the TRITON-TIMI 38 Investigators. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007 Nov 15. 357 (20):2001-15. [Medline].
Tcheng JE, Mackay SM. Prasugrel versus clopidogrel antiplatelet therapy after acute coronary syndrome: matching treatments with patients. Am J Cardiovasc Drugs. 2012 Apr 1. 12 (2):83-91. [Medline].
Schnapf AJ. Prasugrel versus clopidogrel: new management strategies for acute coronary syndrome. J Cardiovasc Nurs. 2013 Sep-Oct. 28 (5):483-94. [Medline].
Ryan TJ. Percutaneous coronary intervention in st-elevation myocardial infarction. Curr Cardiol Rep. 2001 Jul. 3(4):273-9. [Medline].
Berger JS, Sallum RH, Katona B, et al. Is there an association between aspirin dosing and cardiac and bleeding events after treatment of acute coronary syndrome? A systematic review of the literature. Am Heart J. 2012 Aug. 164 (2):153-162.e5. [Medline].
CURRENT-OASIS 7 Investigators, Mehta SR, Bassand JP, Chrolavicius S, et al. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes. N Engl J Med. 2010 Sep 2. 363 (10):930-42. [Medline].
CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet. 1996 Nov 16. 348 (9038):1329-39. [Medline].
Wallentin L, Becker RC, Budaj A,et al, for the PLATO Investigators. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009 Sep 10. 361 (11):1045-57. [Medline].
Storey RF, Becker RC, Harrington RA, et al. Characterization of dyspnoea in PLATO study patients treated with ticagrelor or clopidogrel and its association with clinical outcomes. Eur Heart J. 2011 Dec. 32 (23):2945-53. [Medline].
The PURSUIT Trial Investigators. Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients with acute coronary syndromes. Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy. N Engl J Med. 1998 Aug 13. 339 (7):436-43. [Medline].
Gibson CM, Goel M, Cohen DJ, et al. Six-month angiographic and clinical follow-up of patients prospectively randomized to receive either tirofiban or placebo during angioplasty in the RESTORE trial. Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis. J Am Coll Cardiol. 1998 Jul. 32 (1):28-34. [Medline].
Goodman SG, Cohen M, Bigonzi F, et al. Randomized trial of low molecular weight heparin (enoxaparin) versus unfractionated heparin for unstable coronary artery disease: one-year results of the ESSENCE Study. Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q Wave Coronary Events. J Am Coll Cardiol. 2000 Sep. 36 (3):693-8. [Medline].
Petersen JL, Mahaffey KW, Hasselblad V, et al. Efficacy and bleeding complications among patients randomized to enoxaparin or unfractionated heparin for antithrombin therapy in non-ST-Segment elevation acute coronary syndromes: a systematic overview. JAMA. 2004 Jul 7. 292 (1):89-96. [Medline].
White HD, Kleiman NS, Mahaffey KW, et al. Efficacy and safety of enoxaparin compared with unfractionated heparin in high-risk patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention in the Superior Yield of the New Strategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors (SYNERGY) trial. Am Heart J. 2006 Dec. 152 (6):1042-50. [Medline].
Stone GW, McLaurin BT, Cox DA, et al, for the ACUITY Investigators. Bivalirudin for patients with acute coronary syndromes. N Engl J Med. 2006 Nov 23. 355 (21):2203-16. [Medline].
Goto K, Lansky AJ, Fahy M, et al. Predictors of outcomes in medically treated patients with acute coronary syndromes after angiographic triage: an Acute Catheterization And Urgent Intervention Triage Strategy (ACUITY) substudy. Circulation. 2010 Feb 23. 121 (7):853-62. [Medline].
FUTURA/OASIS-8 Trial Group, Steg PG, Jolly SS, Mehta SR, et al. Low-dose vs standard-dose unfractionated heparin for percutaneous coronary intervention in acute coronary syndromes treated with fondaparinux: the FUTURA/OASIS-8 randomized trial. JAMA. 2010 Sep 22. 304 (12):1339-49. [Medline].
Jolly SS, Faxon DP, Fox KA, et al. Efficacy and safety of fondaparinux versus enoxaparin in patients with acute coronary syndromes treated with glycoprotein IIb/IIIa inhibitors or thienopyridines: results from the OASIS 5 (Fifth Organization to Assess Strategies in Ischemic Syndromes) trial. J Am Coll Cardiol. 2009 Jul 28. 54 (5):468-76. [Medline].
Garg R, Yusuf S. Overview of randomized trials of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. Collaborative Group on ACE Inhibitor Trials. JAMA. 1995 May 10. 273 (18):1450-6. [Medline].
Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000 Jan 20. 342 (3):145-53. [Medline].
ONTARGET Investigators, Yusuf S, Teo KK, Pogue J, et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med. 2008 Apr 10. 358 (15):1547-59. [Medline].
Pitt B, Remme W, Zannad F, et al, for the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003 Apr 3. 348 (14):1309-21. [Medline].
Lopez-Jimenez F, Simha V, Thomas RJ, et al. A summary and critical assessment of the 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular disease risk in adults: filling the gaps. Mayo Clin Proc. 2014 Sep. 89 (9):1257-78. [Medline].
Schwartz GG, Olsson AG, Ezekowitz MD, Ganz P, Oliver MF, Waters D, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA. 2001 Apr 4. 285(13):1711-8. [Medline].
Patti G, Barczi G, Orlic D, et al. Outcome comparison of 600- and 300-mg loading doses of clopidogrel in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: results from the ARMYDA-6 MI (Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty-Myocardial Infarction) randomized study. J Am Coll Cardiol. 2011 Oct 4. 58 (15):1592-9. [Medline].
[Guideline] Eckel RH, Jakicic JM, Ard JD, et al. American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Jun 24. 129 (25 Suppl 2):S76-99. [Medline]. [Full Text].
David TE. Operative management of postinfarction ventricular septal defect. Semin Thorac Cardiovasc Surg. 1995 Oct. 7(4):208-13. [Medline].
Gaudiani VA, Miller DG, Stinson EB, Oyer PE, Reitz BA, Moreno-Cabral RJ, et al. Postinfarction ventricular septal defect: an argument for early operation. Surgery. 1981 Jan. 89(1):48-55. [Medline].
Daggett WM, Buckley MJ, Akins CW, Leinbach RC, Gold HK, Block PC, et al. Improved results of surgical management of postinfarction ventricular septal rupture. Ann Surg. 1982 Sep. 196(3):269-77. [Medline]. [Full Text].
Fish KM, Ishikawa K, Hajjar RJ. Stem cell therapy for acute myocardial infarction: on the horizon or still a dream?. Coron Artery Dis. 2018 Mar. 29 (2):89-91. [Medline].
Schachinger V, Erbs S, Elsasser A, et al, for the REPAIR-AMI Investigators. Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction. N Engl J Med. 2006 Sep 21. 355 (12):1210-21. [Medline].
Traverse JH, Henry TD, Ellis SG, et al. Effect of intracoronary delivery of autologous bone marrow mononuclear cells 2 to 3 weeks following acute myocardial infarction on left ventricular function: the LateTIME randomized trial. JAMA. 2011 Nov 16. 306(19):2110-9. [Medline].
[Guideline] Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J. 2014 Oct 1. 35 (37):2541-619. [Medline]. [Full Text].
[Guideline] Levine GN, Bates ER, Blankenship JC, et al. 2015 ACC/AHA/SCAI focused update on primary percutaneous coronary intervention for patients with ST-elevation myocardial infarction: an update of the 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention and the 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation. 2016 Mar 15. 133 (11):1135-47. [Medline]. [Full Text].
[Guideline] Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation. 2011 Dec 6. 124 (23):e574-651. [Medline]. [Full Text].
[Guideline] Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA guideline for coronary artery bypass graft surgery: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011 Dec 6. 124 (23):e652-735. [Medline]. [Full Text].
[Guideline] Kulik A, Ruel M, Jneid H, et al, for the American Heart Association Council on Cardiovascular Surgery and Anesthesia. Secondary prevention after coronary artery bypass graft surgery: a scientific statement from the American Heart Association. Circulation. 2015 Mar 10. 131 (10):927-64. [Medline]. [Full Text].
[Guideline] Rihal CS, Naidu SS, Givertz MM, et al. 2015 SCAI/ACC/HFSA/STS clinical expert consensus statement on the use of percutaneous mechanical circulatory support devices in cardiovascular care: endorsed by the American Heart Assocation, the Cardiological Society of India, and Sociedad Latino Americana de Cardiologia Intervencion; affirmation of Value by the Canadian Association of Interventional Cardiology-Association Canadienne de Cardiologie d’intervention. J Am Coll Cardiol. 2015 May 19. 65 (19):e7-e26. [Medline]. [Full Text].
[Guideline] Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation Guidelines for mechanical circulatory support: executive summary. J Heart Lung Transplant. 2013 Feb. 32 (2):157-87. [Medline]. [Full Text].
[Guideline] Levine GN, Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines: an update of the 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention, 2011 ACCF/AHA guideline for coronary artery bypass graft surgery, 2012 ACC/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable isc… Circulation. 2016 Sep 6. 134 (10):e123-55. [Medline]. [Full Text].
Modi KA, Nylk TM, Sheridan FM. Medical management of acute ST elevation myocardial infarction. J La State Med Soc. 2001 Jun. 153(6):284-90. [Medline].
Ohman EM, Harrington RA, Cannon CP, Agnelli G, Cairns JA, Kennedy JW. Intravenous thrombolysis in acute myocardial infarction. Chest. 2001 Jan. 119(1 Suppl):253S-277S. [Medline].
Chou R, for the High Value Care Task Force of the American College of Physicians. Cardiac screening with electrocardiography, stress echocardiography, or myocardial perfusion imaging: advice for high-value care from the American College of Physicians. Ann Intern Med. 2015 Mar 17. 162 (6):438-47. [Medline].
Ferencik M. High-risk coronary plaque predicts acute coronary syndrome independently of >50% coronary stenosis and cardiovascular risk factors in patients with acute chest pain: results from ROMICAT II trial (abstract 109). Presented at: Society of Cardiovascular Computed Tomography 2014 Annual Scientific Meeting; July 11, 2014; San Diego, California.
Busko M. High-risk plaque predicts ACS in ER patients with chest pain. Heartwire. July 18, 2014. [Full Text].
Diaz-Zamudio M. Quantitative plaque burden from coronary CT angiography noninvasively predict lesion-specific ischemia in intermediate coronary lesions (abstract 231). Presented at: Society of Cardiovascular Computed Tomography 2014 Annual Scientific Meeting; July 12, 2014; San Diego, California.
Than M, Cullen L, Reid CM, Lim SH, et al. A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study. Lancet. 2011 Mar 26. 377 (9771):1077-84. [Medline].
Innocenti F, Lazzeretti D, Conti A, Zanobetti M, Vicidomini S, Pini R. Stress echocardiography in the ED: diagnostic performance in high-risk subgroups. Am J Emerg Med. 2013 Jul 1. [Medline].
Boggs W. Stress Echo Rules out Myocardial Ischemia in the ED. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/808919. Accessed: August 12, 2013.
Terkelsen CJ, Sorensen JT, Maeng M, et al. System delay and mortality among patients with STEMI treated with primary percutaneous coronary intervention. JAMA. 2010 Aug 18. 304 (7):763-71. [Medline].
Jeffrey S. AVOID Oxygen? Evidence of Harm in MI. Medscape. Nov 21 2014. [Full Text].
Nainggolan L. New US STEMI Guidelines Are More User Friendly. Medscape News Dec 18, 2012. Available at http://www.medscape.com/viewarticle/776325. Accessed: February 6, 2013.
Niccoli G, Rigattieri S, De Vita MR, et al. Open-label, randomized, placebo-controlled evaluation of intracoronary adenosine or nitroprusside after thrombus aspiration during primary percutaneous coronary intervention for the prevention of microvascular obstruction in acute myocardial infarction: the REOPEN-AMI study (Intracoronary Nitroprusside Versus Adenosine in Acute Myocardial Infarction). JACC Cardiovasc Interv. 2013 Jun. 6 (6):580-9. [Medline].
Montalescot G, Zeymer U, Silvain J, et al. Intravenous enoxaparin or unfractionated heparin in primary percutaneous coronary intervention for ST-elevation myocardial infarction: the international randomised open-label ATOLL trial. Lancet. 2011 Aug 20. 378(9792):693-703. [Medline].
Stone GW, Witzenbichler B, Guagliumi G, et al. Heparin plus a glycoprotein IIb/IIIa inhibitor versus bivalirudin monotherapy and paclitaxel-eluting stents versus bare-metal stents in acute myocardial infarction (HORIZONS-AMI): final 3-year results from a multicentre, randomised controlled trial. Lancet. 2011 Jun 25. 377(9784):2193-204. [Medline].
Charlot M, Grove EL, Hansen PR, et al. Proton pump inhibitor use and risk of adverse cardiovascular events in aspirin treated patients with first time myocardial infarction: nationwide propensity score matched study. BMJ. 2011 May 11. 342:d2690. [Medline]. [Full Text].
AstraZeneca. US FDA approves expanded indication for BRILINTA to include long-term use in patients with a history of heart attack [news release]. Available at http://www.astrazeneca.com/Media/Press-releases/Article/20150903. September 3, 2015; Accessed: September 15, 2015.
Bonaca MP, Bhatt DL, Cohen M, Steg PG, Storey RF, Jensen EC, et al. Long-term use of ticagrelor in patients with prior myocardial infarction. N Engl J Med. 2015 May 7. 372 (19):1791-800. [Medline].
Cuzick J, Thorat MA, Bosetti C, et al. Estimates of benefits and harms of prophylactic use of aspirin in the general population. Ann Oncol. 2014 Aug 5. [Medline].
Bankhead C. Benefits add up for regular aspirin use. MedPage Today. August 5, 2014. [Full Text].
Stiles S. L-Carnitine Retakes Spotlight, Hints at Survival Benefit in Acute MI: Meta-analysis. Medscape Medical News. Available at http://www.medscape.com/viewarticle/782488. Accessed: May 2, 2013.
DiNicolantonio JJ, Lavie CJ, Fares H, Menezes AR, O’Keefe JH. L-carnitine in the secondary prevention of cardiovascular disease: systematic review and meta-analysis. Mayo Clin Proc. 2013 Jun. 88 (6):544-51. [Medline].
Reuters Health Information. Prophylactic Lidocaine for Out-of-Hospital Cardiac Arrest Seen Helpful. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/805805. Accessed: June 30, 2013.
Kudenchuk PJ, Newell C, White L, Fahrenbruch C, Rea T, Eisenberg M. Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest. Resuscitation. 2013 Jun 3. [Medline].
Boggs W. Aspiration thrombectomy may improve angioplasty after acute MI. Medscape Medical News. May 13, 2013. [Full Text].
Kumbhani DJ, Bavry AA, Desai MY, Bangalore S, Bhatt DL. Role of aspiration and mechanical thrombectomy in patients with acute myocardial infarction undergoing primary angioplasty: An updated meta-analysis of randomized trials. J Am Coll Cardiol. 2013 May 8. [Medline].
Zaman S, Narayan A, Thiagalingam A, et al. Long-term arrhythmia-free survival in patients with severe left ventricular dysfunction and no inducible ventricular tachycardia post myocardial infarction. Circulation. 2013 Dec 31. [Medline].
O’Riordan M. Positive EP test helps ID post-MI patients for ICDs. Heartwire. January 2, 2014. [Full Text].
Wood S. FDA Review Finds No Increased Risk of MI With Dabigatran (Pradaxa). Medscape Medical News. Available at http://www.medscape.com/viewarticle/825080. Accessed: May 27, 2014.
FDA. FDA study of Medicare patients finds risks lower for stroke and death but higher for gastrointestinal bleeding with Pradaxa (dabigatran) compared to warfarin. Available at http://www.fda.gov/Drugs/DrugSafety/ucm396470.htm. Accessed: May 27, 2014.
O’Riordan M. A shot in arm, a boost for the heart: flu vaccination reduces AMI risk. Medscape Medical News. August 26, 2013. [Full Text].
Rao KK, Enriquez JR, de Lemos JA, Alexander KP, Chen AY, McGuire DK, et al. Use of aldosterone antagonists at discharge after myocardial infarction: Results from the National Cardiovascular Data Registry Acute Coronary Treatment and Intervention Outcomes Network (ACTION) Registry-Get with the Guidelines (GWTG). Am Heart J. 2013 Oct. 166(4):709-715. [Medline].
Stiles, S. Even With CKD, Warfarin Safely Cuts Events in AF After MI, Study Finds. Medscape Medical News. Available at http://www.medscape.com/viewarticle/821444. Accessed: March 12, 2014.
Carrero JJ, Evans M, Szummer K, Spaak J, Lindhagen L, Edfors R, et al. Warfarin, kidney dysfunction, and outcomes following acute myocardial infarction in patients with atrial fibrillation. JAMA. 2014 Mar 5. 311(9):919-28. [Medline].
FDA approves Zontivity to reduce the risk of heart attacks and stroke in high-risk patients. US Food and Drug Administration. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm396585.htm. Accessed: May 12, 2014.
Finkle WD, Greenland S, Ridgeway GK, et al. Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men. PLoS One. 2014. 9(1):e85805. [Medline]. [Full Text].
Freiberg MS, Chang CC, Kuller LH, Skanderson M, Lowy E, Kraemer KL, et al. HIV infection and the risk of acute myocardial infarction. JAMA Intern Med. 2013 Mar 4. 1-9. [Medline].
O’Riordan M. Another study links testosterone therapy to MI risk. Heartwire. January 30, 2014. [Full Text].
Quinn T, Johnsen S, Gale CP, Snooks H, McLean S, Woollard M, et al. Effects of prehospital 12-lead ECG on processes of care and mortality in acute coronary syndrome: a linked cohort study from the Myocardial Ischaemia National Audit Project. Heart. 2014 Apr 14. [Medline].
Stiles S. Prehospital ECG Cuts Mortality in STEMI and NSTEMI: UK Study. Medscape Medical News. Available at http://www.medscape.com/viewarticle/823754. Accessed: April 19, 2014.
Chughtai H, Ratner D, Pozo M, et al. Prehospital delay and its impact on time to treatment in ST-elevation myocardial infarction. Am J Emerg Med. 2011 May. 29 (4):396-400. [Medline].
Xiang L, Zhong A, You T, Chen J, Xu W, Shi M. Prognostic significance of right bundle branch block for patients with acute myocardial infarction: a systematic review and meta-analysis. Med Sci Monit. 2016 Mar 27. 22:998-1004. [Medline].
Kim KH, Jeon KN, Kang MG, et al. Prognostic value of computed tomographic coronary angiography and exercise electrocardiography for cardiovascular events. Korean J Intern Med. 2016 Mar 25. [Medline].
Hussain MA, Bin-Ayeed SA, Saeed OQ, Verma S, Al-Omran M. Impact of diabetes on carotid artery revascularization. J Vasc Surg. 2016 Apr. 63 (4):1099-1107.e4. [Medline].
Stetler J, Karatasakis A, Christakopoulos GE, et al. Impact of crossing technique on the incidence of periprocedural myocardial infarction during chronic total occlusion percutaneous coronary intervention. Catheter Cardiovasc Interv. 2016 Jul. 88 (1):1-6. [Medline].
Mizuno S, Kunisawa S, Sasaki N, Fushimi K, Imanaka Y. Effects of night-time and weekend admissions on in-hospital mortality in acute myocardial infarction patients in Japan. PLoS One. 2018. 13 (1):e0191460. [Medline]. [Full Text].
Brooks M. FDA approves evolocumab (Repatha) to prevent CV events. Medscape Medical News. Available at https://www.medscape.com/viewarticle/889513. December 1, 2017; Accessed: December 7., 2017.
CPR = cardiopulmonary resuscitation; INR = international normalized ratio; STEMI = ST-elevation myocardial infarction; US = United States of America.
Table modified from 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. [2]
Fibrinolytic Agent
Dose
Fibrin Specificity
Antigenic
Patency Rate
Non-fibrin specific
Streptokinase (no longer marketed in the US)
1.5 million units IV given over 30–60 min
No
Yes
60%–68%
Fibrin specific
Tenecteplase
(TNK-tPA)
30 mg for weight < 60 kg
35 mg for 60–69 kg
40 mg for 70–79 kg
45 mg for 80–89 kg
50 mg for >90 kg
++++
No
85%
Reteplase (rPA)
10-U IV boluses given 30 min apart
++
No
84%
Alteplase (tPA)
Bolus 15 mg followed by infusion 0.75 mg/kg for 30 min (maximum 50 mg), then 0.5 mg/kg (maximum 35 mg) over the next 60 min; total dose not to exceed 100 mg.
++
No
73%-84%
IV = intravenous; rPA = recombinant human tissue plasminogen activator; STEMI = ST-elevation myocardial infarction; tPA = tissue plasminogen activator; US = United States of America.
Table modified from 2013 ACCF/AHA guidelines for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. [2]
A Maziar Zafari, MD, PhD Professor of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center
A Maziar Zafari, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American Heart Association, American Society of Echocardiography, Association of Professors of Medicine
Disclosure: Nothing to disclose.
Mahmoud H Abdou, MD Fellow, Division of Cardiology, Emory University School of Medicine
Mahmoud H Abdou, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, Libyan Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Yasmine S Ali, MD, FACC, FACP, MSCI President, Nashville Preventive Cardiology, PLLC; Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine
Yasmine S Ali, MD, FACC, FACP, MSCI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, National Lipid Association, Tennessee Medical Association
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: MCG Health, LLC.
Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona
Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.
Samer M Garas, MD, FACC, FSCAI Interventional Cardiologist, President, St Vincent’s Health System Cardiovascular Council
Samer M Garas, MD, FACC, FSCAI is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.
Ahmad M Jeroudi, MD Fellow in Cardiovascular Disease, Division of Cardiology, Emory University School of Medicine
Disclosure: Nothing to disclose.
Shilpa V Reddy, MD Fellow in Cardiovascular Disease, Division of Cardiology, Emory University School of Medicine
Shilpa V Reddy, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.
David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Drew Evan Fenton, MD, FAAEM Private Practice
Disclosure: Nothing to disclose.
Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Eric Vanderbush, MD, FACC Chief, Department of Internal Medicine, Division of Cardiology, Harlem Hospital Center; Clinical Assistant Professor of Cardiology, Columbia University College of Physicians and Surgeons
Eric Vanderbush, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association
Disclosure: Nothing to disclose.
Myocardial Infarction
Research & References of Myocardial Infarction|A&C Accounting And Tax Services
Source
0 Comments