Acute coronary syndrome

Last updated

Acute coronary syndrome
Heart attack diagram.png
Blockage of a coronary artery
Specialty Cardiology

Acute coronary syndrome (ACS) is a syndrome (a set of signs and symptoms) due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. [1] The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder [2] or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus. [3]

Contents

Acute coronary syndrome is subdivided in three scenarios depending primarily on the presence of electrocardiogram (ECG) changes and blood test results (a change in cardiac biomarkers such as troponin levels): [4] ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), or unstable angina. [5] STEMI is characterised by complete blockage of a coronary artery resulting in necrosis of part of the heart muscle indicated by ST elevation on ECG, NSTEMI is characterised by a partially blocked coronary artery resulting in necrosis of part of the heart muscle that may be indicated by ECG changes, and unstable angina is characterised by ischemia of the heart muscle that does not result in cell injury or necrosis. [6] [7]

ACS should be distinguished from stable angina, which develops during physical activity or stress and resolves at rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or with minimal exertion, or at lesser degrees of exertion than the individual's previous angina ("crescendo angina"). New-onset angina is also considered unstable angina, since it suggests a new problem in a coronary artery. [8]

Signs and symptoms

Symptoms of the acute coronary syndromes are similar. [8] The cardinal symptom of critically decreased blood flow to the heart is chest pain, experienced as tightness, pressure, or burning. [9] Localisation is most commonly around or over the chest and may radiate or be located to the arm, shoulder, neck, back, upper abdomen, or jaw. [9] This may be associated with sweating, nausea, or shortness of breath. [8] [9] Previously, the word "atypical" was used to describe chest pain not typically heart-related, however this word is not recommended and has been replaced by "noncardiac" to describe chest pain that indicate a low likelihood of heart-related pain. [9]

In unstable angina, symptoms may appear on rest or on minimal exertion. [6] The symptoms can last longer than those in stable angina, can be resistant to rest or medicine, and can get worse over time. [8] [10]

Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. [11] Chest pain with features characteristic of cardiac origin (angina) can also be precipitated by profound anemia, brady- or tachycardia (excessively slow or rapid heart rate), low or high blood pressure, severe aortic valve stenosis (narrowing of the valve at the beginning of the aorta), pulmonary artery hypertension and a number of other conditions. [12]

Pathophysiology

In those who have ACS, atheroma rupture is most commonly found 60% when compared to atheroma erosion (30%), thus causes the formation of thrombus which block the coronary arteries. Plaque rupture is responsible for 60% in ST elevated myocardial infarction (STEMI) while plaque erosion is responsible for 30% of the STEMI and vice versa for Non ST elevated myocardial infarction (NSTEMI). In plaque rupture, the content of the plaque is lipid rich, collagen poor, with abundant inflammation which is macrophage predominant, and covered with a thin fibrous cap. Meanwhile, in plaque erosion, the plaque is rich with extracellular matrix, proteoglycan, glycoaminoglycan, but without fibrous caps, no inflammatory cells, and no large lipid core. After the coronary arteries are unblocked, there is a risk of reperfusion injury due spreading inflammatory mediators throughout the body. Investigations is still underway on the role of cyclophilin D in reducing the reperfusion injury. [13]

Other, less common, causes of acute coronary syndrome include spontaneous coronary artery dissection, [14] ischemia in the absence of obstructive coronary artery disease (INOCA), and myocardial infarction in the absence of obstructive coronary artery disease (MINOCA). [15]

Diagnosis

Classification of acute coronary syndromes. ACS scheme.jpg
Classification of acute coronary syndromes.

Electrocardiogram

In the setting of acute chest pain, the electrocardiogram (ECG or EKG) is the investigation that most reliably distinguishes between various causes. [17] The ECG should be done as early as practicable, including in the ambulance if possible. [18] ECG changes indicating acute heart damage include: ST elevation, new left bundle branch block and ST depression amongst others. The absence of ECG changes does not immediately distinguish between unstable angina and NSTEMI. [6]

Blood tests

Change in levels of cardiac biomarkers, such as troponin I and troponin T, are indicative of myocardial infarction including both STEMI and NSTEMI, however their levels are not affected in unstable angina. [6]

Prediction scores

A combination of cardiac biomarkers and risk scores, such as HEART score and TIMI score, can help assess the possibility of myocardial infarction in the emergency setting. [19] [13]

Prevention

Acute coronary syndrome often reflects a degree of damage to the coronaries by atherosclerosis. Primary prevention of atherosclerosis is controlling the risk factors: healthy eating, exercise, treatment for hypertension and diabetes, avoiding smoking and controlling cholesterol levels; in patients with significant risk factors, aspirin has been shown to reduce the risk of cardiovascular events. Secondary prevention is discussed in myocardial infarction. [20]

After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17% reduction in hospital admissions for acute coronary syndrome. 67% of the decrease occurred in non-smokers. [21]

Treatment

People with presumed ACS are typically treated with aspirin, clopidogrel or ticagrelor, nitroglycerin, and if the chest discomfort persists morphine. [22] Other analgesics such as nitrous oxide are of unknown benefit. [22] Angiography is recommended in those who have either new ST elevation or a new left or right bundle branch block on their ECG. [1] Unless the person has low oxygen levels additional oxygen does not appear to be useful. [23]

STEMI

If the ECG confirms changes suggestive of myocardial infarction (ST elevation in specific leads, a new left bundle branch block or a true posterior MI pattern), thrombolytics may be administered or percutaneous coronary intervention may be performed. In the former, medication is injected that stimulates fibrinolysis, destroying blood clots obstructing the coronary arteries. In the latter, a flexible catheter is passed via the femoral or radial artery and advanced to the heart to identify blockages in the coronary arteries. When occlusions are found, they can be intervened upon mechanically with angioplasty and usually stent deployment if a lesion, termed the culprit lesion, is thought to be causing myocardial damage. Data suggest that rapid triage, transfer and treatment is essential. [24] The time frame for door-to-needle thrombolytic administration according to American College of Cardiology (ACC) guidelines should be within 30 minutes, whereas the door-to-balloon percutaneous coronary intervention (PCI) time should be less than 90 minutes. It was found that thrombolysis is more likely to be delivered within the established ACC guidelines among patients with STEMI as compared to PCI according to a 2009 case control study. [25]

NSTEMI and NSTE-ACS

If the ECG does not show typical changes consistent with STEMI, the term "non-ST segment elevation ACS" (NSTE-ACS) may be used and encompasses "non-ST elevation MI" (NSTEMI) and unstable angina.

The accepted management of unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, a second platelet inhibitor such as clopidogrel, prasugrel or ticagrelor, and heparin (usually a low-molecular weight heparin), with intravenous nitroglycerin and opioids if the pain persists. The heparin-like drug known as fondaparinux appears to be better than enoxaparin. [26]

If there is no evidence of ST segment elevation on the electrocardiogram, delaying urgent angioplasty until the next morning is not inferior to doing so immediately. [27] Using statins in the first 14 days after ACS reduces the risk of further ACS. [28]

Cocaine-associated ACS should be managed in a manner similar to other patients with acute coronary syndrome except beta blockers should not be used and benzodiazepines should be administered early. [29]

Prognosis

Prediction scores

The TIMI risk score can identify high risk patients in ST-elevation and non-ST segment elevation MI ACS [30] [31] and has been independently validated. [32] [33]

Based on a global registry of 102,341 patients, the GRACE risk scoreestimates in-hospital, 6 months, 1 year, and 3-year mortality risk after a heart attack. [34] It takes into account clinical (blood pressure, heart rate, EKG findings) and medical history. [34] Nowadays, GRACE risk score is also used within non-ST elevation ACS patients as a high-risk criteria(GRACE score > 140), which may favor early invasive strategy within 24 hours of the heart attack. [35]

Biomarkers

The aim of prognostic markers is to reflect different components of pathophysiology of ACS. For example:[ citation needed ]

Coronary CT angiography combined with troponin levels is also helpful to triage those who are susceptible to ACS. F-fluoride positron emission tomography is also helpful in identifying those with high risk, lipid-rich coronary plaques. [13]

Day of admission

Studies have shown that for ACS patients, weekend admission is associated with higher mortality and lower utilization of invasive cardiac procedures, and those who did undergo these interventions had higher rates of mortality and complications than their weekday counterparts. This data leads to the possible conclusion that access to diagnostic/interventional procedures may be contingent upon the day of admission, which may impact mortality. [36] [37] This phenomenon is described as weekend effect.

See also

Related Research Articles

<span class="mw-page-title-main">Coronary artery disease</span> Reduction of blood flow to the heart

Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the cardiac muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, and myocardial infarction.

<span class="mw-page-title-main">Angina</span> Chest discomfort that is generally brought on by inadequate blood flow to the cardiac muscle

Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease.

<span class="mw-page-title-main">Chest pain</span> Discomfort or pain in the chest as a medical symptom

Chest pain is pain or discomfort in the chest, typically the front of the chest. It may be described as sharp, dull, pressure, heaviness or squeezing. Associated symptoms may include pain in the shoulder, arm, upper abdomen, or jaw, along with nausea, sweating, or shortness of breath. It can be divided into heart-related and non-heart-related pain. Pain due to insufficient blood flow to the heart is also called angina pectoris. Those with diabetes or the elderly may have less clear symptoms.

<span class="mw-page-title-main">Cardiac stress test</span> Measures the hearts ability to respond to external stress in a controlled clinical environment

A cardiac stress test is a cardiological examination that evaluates the cardiovascular system's response to external stress within a controlled clinical setting. This stress response can be induced through physical exercise or intravenous pharmacological stimulation of heart rate.

<span class="mw-page-title-main">Variant angina</span> Medical condition

Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.

<span class="mw-page-title-main">Unstable angina</span> Medical condition

Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.

P2Y<sub>12</sub> Protein-coding gene in the species Homo sapiens

P2Y12 is a chemoreceptor for adenosine diphosphate (ADP) that belongs to the Gi class of a group of G protein-coupled (GPCR) purinergic receptors. This P2Y receptor family has several receptor subtypes with different pharmacological selectivity, which overlaps in some cases, for various adenosine and uridine nucleotides. The P2Y12 receptor is involved in platelet aggregation and is thus a biological target for the treatment of thromboembolisms and other clotting disorders. Two transcript variants encoding the same isoform have been identified for this gene.

<span class="mw-page-title-main">Bivalirudin</span> Anticoagulant drug

Bivalirudin, sold under the brand names Angiomax and Angiox, among others, is a specific and reversible direct thrombin inhibitor (DTI). Chemically, it is a synthetic congener of the naturally occurring drug hirudin, found in the saliva of the medicinal leech Hirudo medicinalis. It is manufactured by The Medicines Company.

Door-to-balloon is a time measurement in emergency cardiac care (ECC), specifically in the treatment of ST segment elevation myocardial infarction. The interval starts with the patient's arrival in the emergency department, and ends when a catheter guidewire crosses the culprit lesion in the cardiac cath lab. Because of the adage that "time is muscle", meaning that delays in treating a myocardial infarction increase the likelihood and amount of cardiac muscle damage due to localised hypoxia, ACC/AHA guidelines recommend a door-to-balloon interval of no more than 90 minutes. As of 2006 in the United States, fewer than half of STEMI patients received reperfusion with primary percutaneous coronary intervention (PCI) within the guideline-recommended timeframe. It has become a core quality measure for the Joint Commission on Accreditation of Healthcare Organizations (TJC).

The Thrombolysis In Myocardial Infarction (TIMI) Study Group, is an academic research organization (ARO) affiliated with Brigham and Women's Hospital and Harvard Medical School with a focus in the field of cardiovascular disease. The group has its headquarters in Boston, Massachusetts.

<span class="mw-page-title-main">Wellens' syndrome</span> Medical condition

Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in people with unstable angina. Originally thought of as two separate types, A and B, it is now considered an evolving wave form, initially of biphasic T wave inversions and later becoming symmetrical, often deep, T wave inversions in the anterior precordial leads.

<span class="mw-page-title-main">Coronary ischemia</span> Medical condition

Coronary ischemia, myocardial ischemia, or cardiac ischemia, is a medical term for a reduced blood flow in the coronary circulation through the coronary arteries. Coronary ischemia is linked to heart disease, and heart attacks. Coronary arteries deliver oxygen-rich blood to the heart muscle. Reduced blood flow to the heart associated with coronary ischemia can result in inadequate oxygen supply to the heart muscle. When oxygen supply to the heart is unable to keep up with oxygen demand from the muscle, the result is the characteristic symptoms of coronary ischemia, the most common of which is chest pain. Chest pain due to coronary ischemia commonly radiates to the arm or neck. Certain individuals such as women, diabetics, and the elderly may present with more varied symptoms. If blood flow through the coronary arteries is stopped completely, cardiac muscle cells may die, known as a myocardial infarction, or heart attack.

<span class="mw-page-title-main">Myocardial infarction</span> Interruption of blood supply to a part of the heart

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often such pain occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn.

<span class="mw-page-title-main">Reperfusion therapy</span> Restoring blood flow post-heart attack

Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack. Reperfusion therapy includes drugs and surgery. The drugs are thrombolytics and fibrinolytics used in a process called thrombolysis. Surgeries performed may be minimally-invasive endovascular procedures such as a percutaneous coronary intervention (PCI), which involves coronary angioplasty. The angioplasty uses the insertion of a balloon and/or stents to open up the artery. Other surgeries performed are the more invasive bypass surgeries that graft arteries around blockages.

<span class="mw-page-title-main">Electrocardiography in myocardial infarction</span>

Electrocardiography in suspected myocardial infarction has the main purpose of detecting ischemia or acute coronary injury in emergency department populations coming for symptoms of myocardial infarction (MI). Also, it can distinguish clinically different types of myocardial infarction.

<span class="mw-page-title-main">Francis M. Fesmire</span> American emergency physician (1969–2014)

Francis Miller Fesmire was an American emergency physician and a nationally recognized expert in myocardial infarction. He authored numerous academic articles and assisted in the development of clinical guidelines on the standard of care in treating patients with suspected myocardial infarction by the American College of Emergency Physicians and the American Heart Association/American College of Cardiology. He performed numerous research investigations in chest pain patients, reporting the usefulness of continuous 12-lead ECG monitoring, two-hour delta cardiac marker testing, and nuclear cardiac stress testing in the emergency department. The culmination of his studies was The Erlanger Chest Pain Evaluation Protocol published in the Annals of Emergency Medicine in 2002. In 2011 he published a novel Nashville Skyline that received a 5 star review by ForeWord Reviews. His most recent research involved the risk stratification of chest pain patients in the emergency department.

A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers. A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

<span class="mw-page-title-main">Management of acute coronary syndrome</span>

Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.

Kounis syndrome is defined as acute coronary syndrome caused by an allergic reaction or a strong immune reaction to a drug or other substance. It is a rare syndrome with authentic cases reported in 130 males and 45 females, as reviewed in 2017; however, the disorder is suspected of being commonly overlooked and therefore much more prevalent. Mast cell activation and release of inflammatory cytokines as well as other inflammatory agents from the reaction leads to spasm of the arteries leading to the heart muscle or a plaque breaking free and blocking one or more of those arteries.

Professor Aly Saad, is a professor of cardiology at Zagazig University and a member of the higher committee of promotion of professors and assistant professors of cardiovascular diseases and critical care subspecialty in Egypt.

References

  1. 1 2 Amsterdam, E. A.; Wenger, N. K.; Brindis, R. G.; Casey, D. E.; Ganiats, T. G.; Holmes, D. R.; Jaffe, A. S.; Jneid, H.; Kelly, R. F.; Kontos, M. C.; Levine, G. N.; Liebson, P. R.; Mukherjee, D.; Peterson, E. D.; Sabatine, M. S.; Smalling, R. W.; Zieman, S. J. (23 September 2014). "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. 130 (25): e344–e426. doi: 10.1161/CIR.0000000000000134 . PMID   25249585.
  2. ↑ Goodacre S, Pett P, Arnold J, Chawla A, Hollingsworth J, Roe D, Crowder S, Mann C, Pitcher D, Brett C (November 2009). "Clinical diagnosis of acute coronary syndrome in patients with chest pain and a normal or non-diagnostic electrocardiogram". Emergency Medicine Journal. 26 (12): 866–870. doi: 10.1136/emj.2008.064428 . PMID   19934131. Archived from the original on 5 April 2017.
  3. ↑ Canto JG, Shlipak MG, Rogers WJ (June 2000). "Prevalence, Clinical Characteristics, and Mortality among Patients with Acute Myocardial Infarction Presenting Without Chest Pain". JAMA. 283 (24): 3223–3229, vi. doi: 10.1001/jama.283.24.3223 . PMID   10866870.
  4. ↑ Grech ED, Ramsdale DR (June 2003). "Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction". BMJ. 326 (7401): 1259–61. doi:10.1136/bmj.326.7401.1259. PMC   1126130 . PMID   12791748.
  5. ↑ Torres M, Moayedi S (May 2007). "Evaluation of the acutely dyspneic elderly patient". Clin. Geriatr. Med. 23 (2): 307–25, vi. doi:10.1016/j.cger.2007.01.007. PMID   17462519.
  6. 1 2 3 4 Collet, Jean-Philippe; Thiele, Holger; Barbato, Emanuele; Barthélémy, Olivier; Bauersachs, Johann; et al. (7 April 2021). "2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation". European Heart Journal. 42 (14): 1289–1367. doi: 10.1093/eurheartj/ehaa575 . ISSN   1522-9645. PMID   32860058. Unstable angina is defined as myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis. [...] Compared with NSTEMI patients, individuals with unstable angina do not experience acute cardiomyocyte injury/necrosis.
  7. ↑ Barthélémy, Olivier; Jobs, Alexander; Meliga, Emanuele; et al. (7 April 2021). "Questions and answers on workup diagnosis and risk stratification: a companion document of the 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation". European Heart Journal. 42 (14): 1379–1386. doi: 10.1093/eurheartj/ehaa602 . ISSN   1522-9645. PMC   8026278 . PMID   32860030. NSTEMI is characterized by ischaemic symptoms associated with acute cardiomyocyte injury (=rise and/or fall in cardiac troponin T/I), while ischaemic symptoms at rest (or minimal effort) in the absence of acute cardiomyocyte injury define unstable angina. This translates into an increased risk of death in NSTEMI patients, while unstable angina patients are at relatively low short-term risk of death.
  8. 1 2 3 4 "Acute Coronary Syndromes (Heart Attack; Myocardial Infarction; Unstable Angina) - Heart and Blood Vessel Disorders". MSD Manual Consumer Version. Retrieved 12 February 2023.
  9. 1 2 3 4 Gulati, Martha; Levy, Phillip D.; Mukherjee, Debabrata; Amsterdam, Ezra; Bhatt, Deepak L.; et al. (30 November 2021). "2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 144 (22): e368–e454. doi: 10.1161/CIR.0000000000001029 . ISSN   0009-7322. PMID   34709879.
  10. ↑ "Unstable Angina".
  11. ↑ Achar SA, Kundu S, Norcross WA (2005). "Diagnosis of acute coronary syndrome". Am Fam Physician. 72 (1): 119–26. PMID   16035692. Archived from the original on 9 October 2007.
  12. ↑ "Chest Pain in the Emergency Department: Differential Diagnosis". The Cardiology Advisor. 20 January 2019. Retrieved 25 July 2019.
  13. 1 2 3 Eisen, Alon; Giugliano, Robert P; Braunwald, Eugene (20 July 2016). "Updates on acute coronary syndrome: A review". JAMA Cardiology. 1 (16): 718–730. doi:10.1001/jamacardio.2016.2049. PMID   27438381.
  14. ↑ Franke, Kyle B; Wong, Dennis TL; Baumann, Angus; Nicholls, Stephen J; Gulati, Rajiv; Psaltis, Peter J (4 April 2019). "Current state-of-play in spontaneous coronary artery dissection". Cardiovascular Diagnosis and Therapy. 9 (3): 281–298. doi: 10.21037/cdt.2019.04.03 . PMC   6603494 . PMID   31275818.
  15. ↑ Tamis-Holland, JE (27 March 2019). "Diagnosis and Management of MINOCA Patients". Circulation. 139 (18): 891–908. doi: 10.1161/CIR.0000000000000670 . PMID   30913893.
  16. ↑ Alpert JS, Thygesen K, Antman E, Bassand JP (2000). "Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction". J Am Coll Cardiol. 36 (3): 959–69. doi: 10.1016/S0735-1097(00)00804-4 . PMID   10987628.
  17. ↑ Chun AA, McGee SR (2004). "Bedside diagnosis of coronary artery disease: a systematic review". Am. J. Med. 117 (5): 334–43. doi:10.1016/j.amjmed.2004.03.021. PMID   15336583.
  18. ↑ Neumar, RW; Shuster, M; Callaway, CW; Gent, LM; Atkins, DL; Bhanji, F; Brooks, SC; de Caen, AR; Donnino, MW; Ferrer, JM; Kleinman, ME; Kronick, SL; Lavonas, EJ; Link, MS; Mancini, ME; Morrison, LJ; O'Connor, RE; Samson, RA; Schexnayder, SM; Singletary, EM; Sinz, EH; Travers, AH; Wyckoff, MH; Hazinski, MF (3 November 2015). "Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 132 (18 Suppl 2): S315–67. doi: 10.1161/cir.0000000000000252 . PMID   26472989.
  19. ↑ Fanaroff, Alexander C.; Rymer, Jennifer A.; Goldstein, Sarah A.; Simel, David L.; Newby, L. Kristin (10 November 2015). "Does This Patient With Chest Pain Have Acute Coronary Syndrome?: The Rational Clinical Examination Systematic Review". JAMA. 314 (18): 1955–1965. doi:10.1001/jama.2015.12735. ISSN   1538-3598. PMID   26547467.
  20. ↑ Grundy, Scott M.; Stone, Neil J.; Bailey, Alison L.; Beam, Craig; Birtcher, Kim K.; Blumenthal, Roger S.; Braun, Lynne T.; de Ferranti, Sarah; Faiella-Tommasino, Joseph; Forman, Daniel E.; Goldberg, Ronald; Heidenreich, Paul A.; Hlatky, Mark A.; Jones, Daniel W.; Lloyd-Jones, Donald (25 June 2019). "2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines". Journal of the American College of Cardiology. 73 (24): 3168–3209. doi: 10.1016/j.jacc.2018.11.002 . ISSN   0735-1097. PMID   30423391.
  21. ↑ Pell JP, Haw S, Cobbe S, et al. (2008). "Smoke-free Legislation and Hospitalizations for Acute Coronary Syndrome" (PDF). New England Journal of Medicine. 359 (5): 482–91. doi:10.1056/NEJMsa0706740. hdl: 1893/16659 . PMID   18669427.
  22. 1 2 O'Connor RE, Brady W, Brooks SC, et al. (November 2010). "Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18 Suppl 3): S787–817. doi: 10.1161/CIRCULATIONAHA.110.971028 . PMID   20956226.
  23. ↑ Neumar, RW; Shuster, M; Callaway, CW; Gent, LM; Atkins, DL; Bhanji, F; Brooks, SC; de Caen, AR; Donnino, MW; Ferrer, JM; Kleinman, ME; Kronick, SL; Lavonas, EJ; Link, MS; Mancini, ME; Morrison, LJ; O'Connor, RE; Samson, RA; Schexnayder, SM; Singletary, EM; Sinz, EH; Travers, AH; Wyckoff, MH; Hazinski, MF (3 November 2015). "Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 132 (18 Suppl 2): S315–67. doi: 10.1161/cir.0000000000000252 . PMID   26472989.
  24. ↑ Blankenship JC, Skelding KA (2008). "Rapid Triage, Transfer, and Treatment with Percutaneous Coronary Intervention for Patients with ST-Segment Elevation Myocardial Infarction". Acute Coronary Syndromes. 9 (2): 59–65. Archived from the original on 15 July 2011.
  25. ↑ Janda, SP; Tan, N (2009). "Thrombolysis versus primary percutaneous coronary intervention for ST elevation myocardial infarctions at Chilliwack General Hospital". The Canadian Journal of Cardiology. 25 (11): e382–4. doi:10.1016/S0828-282X(09)70165-5. PMC   2776568 . PMID   19898701.
  26. ↑ Bundhun, PK; Shaik, M; Yuan, J (8 May 2017). "Choosing between Enoxaparin and Fondaparinux for the management of patients with acute coronary syndrome: A systematic review and meta-analysis". BMC Cardiovascular Disorders. 17 (1): 116. doi: 10.1186/s12872-017-0552-z . PMC   5422952 . PMID   28482804.
  27. ↑ Montalescot G, Cayla G, Collet JP, Elhadad S, Beygui F, Le Breton H, et al. (2009). "Immediate vs delayed intervention for acute coronary syndromes: a randomized clinical trial". JAMA. 302 (9): 947–54. doi:10.1001/jama.2009.1267. PMID   19724041.
  28. ↑ Vale, N; Nordmann, AJ; Schwartz, GG; de Lemos, J; Colivicchi, F; den Hartog, F; Ostadal, P; Macin, SM; Liem, AH; Mills, EJ; Bhatnagar, N; Bucher, HC; Briel, M (1 September 2014). "Statins for acute coronary syndrome". The Cochrane Database of Systematic Reviews. 9 (9): CD006870. doi:10.1002/14651858.CD006870.pub3. PMID   25178118.
  29. ↑ McCord J, Jneid H, Hollander JE, et al. (April 2008). "Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology". Circulation. 117 (14): 1897–907. doi: 10.1161/CIRCULATIONAHA.107.188950 . PMID   18347214.
  30. ↑ Morrow, D. A.; Antman, E. M.; Charlesworth, A.; Cairns, R.; Murphy, S. A.; de Lemos, J. A.; Giugliano, R. P.; McCabe, C. H.; Braunwald, E. (24 October 2000). "TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy". Circulation. 102 (17): 2031–2037. doi:10.1161/01.cir.102.17.2031. ISSN   1524-4539. PMID   11044416.
  31. ↑ Antman EM, Cohen M, Bernink PJ, et al. (2000). "The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making". JAMA. 284 (7): 835–42. doi:10.1001/jama.284.7.835. PMID   10938172.
  32. ↑ Pollack CV, Sites FD, Shofer FS, Sease KL, Hollander JE (2006). "Application of the TIMI risk score for unstable angina and non-ST elevation acute coronary syndrome to an unselected emergency department chest pain population". Academic Emergency Medicine. 13 (1): 13–8. doi:10.1197/j.aem.2005.06.031. PMID   16365321.
  33. ↑ Chase M, Robey JL, Zogby KE, Sease KL, Shofer FS, Hollander JE (2006). "Prospective validation of the Thrombolysis in Myocardial Infarction Risk Score in the emergency department chest pain population". Annals of Emergency Medicine. 48 (3): 252–9. doi:10.1016/j.annemergmed.2006.01.032. PMID   16934646.
  34. 1 2 Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F, Avezum A, Goodman SG, Flather MD, Anderson FA Jr, Granger CB (2006). "Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE)". BMJ. 333 (7578): 1091. doi:10.1136/bmj.38985.646481.55. PMC   1661748 . PMID   17032691.
  35. ↑ "2023 ESC Guidelines for the management of acute coronary syndromes". www.escardio.org. Retrieved 13 February 2024.
  36. ↑ Khoshchehreh M, Groves EM, Tehrani D, Amin A, Patel PM, Malik S (2016). "Changes in mortality on weekend versus weekday admissions for Acute Coronary Syndrome in the United States over the past decade". Int J Cardiol. 210: 164–172. doi:10.1016/j.ijcard.2016.02.087. PMC   4801736 . PMID   26950171.
  37. ↑ Kostis W.J.; Demissie K.; Marcella S.W.; Shao Y.-H.; Wilson A.C.; Moreyra A.E. (2007). "Weekend versus weekday admission and mortality from myocardial infarction". N Engl J Med. 356 (11): 1099–1109. doi: 10.1056/nejmoa063355 . PMID   17360988.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.