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Chest pain

MedGen UID:
2992
Concept ID:
C0008031
Sign or Symptom
Synonyms: Chest Pain; Chest Pains; Pain, Chest; Pains, Chest
SNOMED CT: Chest pain (29857009)
 
HPO: HP:0100749

Definition

An unpleasant sensation characterized by physical discomfort (such as pricking, throbbing, or aching) localized to the chest. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVChest pain

Conditions with this feature

Chinese restaurant syndrome
MedGen UID:
891
Concept ID:
C0008127
Disease or Syndrome
Multiple endocrine neoplasia type 2A
MedGen UID:
9958
Concept ID:
C0025268
Neoplastic Process
Multiple endocrine neoplasia type 2 (MEN2) includes the following phenotypes: MEN2A, FMTC (familial medullary thyroid carcinoma, which may be a variant of MEN2A), and MEN2B. All three phenotypes involve high risk for development of medullary carcinoma of the thyroid (MTC); MEN2A and MEN2B involve an increased risk for pheochromocytoma; MEN2A involves an increased risk for parathyroid adenoma or hyperplasia. Additional features in MEN2B include mucosal neuromas of the lips and tongue, distinctive facies with enlarged lips, ganglioneuromatosis of the gastrointestinal tract, and a marfanoid habitus. MTC typically occurs in early childhood in MEN2B, early adulthood in MEN2A, and middle age in FMTC.
Familial Mediterranean fever
MedGen UID:
45811
Concept ID:
C0031069
Disease or Syndrome
Familial Mediterranean fever (FMF) is divided into two phenotypes: type 1 and type 2. FMF type 1 is characterized by recurrent short episodes of inflammation and serositis including fever, peritonitis, synovitis, pleuritis, and, rarely, pericarditis and meningitis. The symptoms and severity vary among affected individuals, sometimes even among members of the same family. Amyloidosis, which can lead to renal failure, is the most severe complication, if untreated. FMF type 2 is characterized by amyloidosis as the first clinical manifestation of FMF in an otherwise asymptomatic individual.
Ehlers-Danlos syndrome, type 4
MedGen UID:
82790
Concept ID:
C0268338
Disease or Syndrome
Vascular Ehlers-Danlos syndrome (vEDS) is characterized by arterial, intestinal, and/or uterine fragility; thin, translucent skin; easy bruising; characteristic facial appearance (thin vermilion of the lips, micrognathia, narrow nose, prominent eyes); and an aged appearance to the extremities, particularly the hands. Vascular dissection or rupture, gastrointestinal perforation, or organ rupture are the presenting signs in most adults with vEDS. Arterial rupture may be preceded by aneurysm, arteriovenous fistulae, or dissection but also may occur spontaneously. The majority (60%) of individuals with vEDS who are diagnosed before age 18 years are identified because of a positive family history. Neonates may present with clubfoot, hip dislocation, limb deficiency, and/or amniotic bands. Approximately half of children tested for vEDS in the absence of a positive family history present with a major complication at an average age of 11 years. Four minor diagnostic features – distal joint hypermobility, easy bruising, thin skin, and clubfeet – are most often present in those children ascertained without a major complication.
Anti-glomerular basement membrane disease
MedGen UID:
140788
Concept ID:
C0403529
Disease or Syndrome
A rare, fulminant small vessel vasculitis that affects the capillary beds of the kidneys and lungs and characterized by the presence of anti-glomerular basement membrane (GBM) and, in its full-blown form, anti-alveolar basement membrane (ABM) antibodies. Consequently, it may manifest as a rapidly progressive, isolated glomerulonephritis (anti-GBM nephritis) or as a pulmonary-renal syndrome with severe lung hemorrhage.
Hypertrophic cardiomyopathy 6
MedGen UID:
331466
Concept ID:
C1833236
Disease or Syndrome
Mutations in the PRKAG2 gene (602743) give rise to a moderate, essentially heart-specific, nonlysosomal glycogenosis with clinical onset typically in late adolescence or in the third decade of life, ventricular pre-excitation predisposing to supraventricular arrhythmias, mild to severe cardiac hypertrophy, enhanced risk of sudden cardiac death in midlife, and autosomal dominant inheritance with full penetrance (summary by Burwinkel et al., 2005).
Hypertrophic cardiomyopathy 10
MedGen UID:
331754
Concept ID:
C1834460
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the MYL2 gene.
Coronary artery disease, autosomal dominant, 1
MedGen UID:
330802
Concept ID:
C1842247
Disease or Syndrome
Coronary artery disease (CAD) and its most important complication, acute myocardial infarction (MI), are leading causes of death and disability in the developed world. Multiple risk factors for CAD/MI have been identified, including family history, hypertension, hypercholesterolemia, obesity, smoking, and diabetes. Several genomewide scans of affected sib pairs have identified susceptibility loci for CAD, e.g., 607339 and 300464.
Familial Mediterranean fever, autosomal dominant
MedGen UID:
341987
Concept ID:
C1851347
Disease or Syndrome
Familial Mediterranean fever (FMF) is divided into two phenotypes: type 1 and type 2. FMF type 1 is characterized by recurrent short episodes of inflammation and serositis including fever, peritonitis, synovitis, pleuritis, and, rarely, pericarditis and meningitis. The symptoms and severity vary among affected individuals, sometimes even among members of the same family. Amyloidosis, which can lead to renal failure, is the most severe complication, if untreated. FMF type 2 is characterized by amyloidosis as the first clinical manifestation of FMF in an otherwise asymptomatic individual.
Arrhythmogenic right ventricular dysplasia 10
MedGen UID:
347543
Concept ID:
C1857777
Disease or Syndrome
Arrhythmogenic right ventricular cardiomyopathy (ARVC) – previously referred to as arrhythmogenic right ventricular dysplasia (ARVD) – is characterized by progressive fibrofatty replacement of the myocardium that predisposes to ventricular tachycardia and sudden death in young individuals and athletes. It primarily affects the right ventricle, and it may also involve the left ventricle. The presentation of disease is highly variable even within families, and some affected individuals may not meet established clinical criteria. The mean age at diagnosis is 31 years (±13; range: 4-64 years).
Arrhythmogenic right ventricular dysplasia 5
MedGen UID:
346805
Concept ID:
C1858379
Disease or Syndrome
Arrhythmogenic right ventricular cardiomyopathy (ARVC) – previously referred to as arrhythmogenic right ventricular dysplasia (ARVD) – is characterized by progressive fibrofatty replacement of the myocardium that predisposes to ventricular tachycardia and sudden death in young individuals and athletes. It primarily affects the right ventricle, and it may also involve the left ventricle. The presentation of disease is highly variable even within families, and some affected individuals may not meet established clinical criteria. The mean age at diagnosis is 31 years (±13; range: 4-64 years).
Hypertrophic cardiomyopathy 4
MedGen UID:
350526
Concept ID:
C1861862
Disease or Syndrome
While most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nHypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. 
Autoimmune pulmonary alveolar proteinosis
MedGen UID:
410079
Concept ID:
C1970472
Disease or Syndrome
Pulmonary alveolar proteinosis is a pathologic entity characterized by intraalveolar surfactant accumulation. There are 3 clinically distinct forms: hereditary (usually congenital), secondary, and acquired. The acquired form of pulmonary alveolar proteinosis is the most common form, accounting for approximately 90% of cases. The mean age at diagnosis is 39 years and it is associated with smoking in 72% of cases. The estimated incidence and prevalence are 0.36 and 3.70 cases per million, respectively (Trapnell et al., 2003; Seymour and Presneill, 2002). Secondary pulmonary alveolar proteinosis develops in association with conditions involving functional impairment or reduced numbers of alveolar macrophages. Such conditions include some hematologic cancers, pharmacologic immunosuppression, inhalation of inorganic dust or toxic fumes, and certain infections. Congenital pulmonary alveolar proteinosis is a rare, severe, often fatal disorder of newborns associated with pulmonary surfactant metabolism dysfunction caused by mutations in genes involved in surfactant metabolism (see, e.g., SMDP1, 265120) (Trapnell et al., 2003). See 300770 for information on congenital PAP due to CSF2RA (306250) deficiency.
Sarcoidosis, susceptibility to, 2
MedGen UID:
436694
Concept ID:
C2676468
Finding
Any sarcoidosis in which the cause of the disease is a mutation in the BTNL2 gene.
Hypertrophic cardiomyopathy 11
MedGen UID:
436962
Concept ID:
C2677506
Disease or Syndrome
An autosomal dominant subtype of familial hypertrophic cardiomyopathy caused by mutation(s) in the ACTC1 gene, encoding actin, alpha cardiac muscle 1.
Long QT syndrome 9
MedGen UID:
395635
Concept ID:
C2678485
Disease or Syndrome
Long QT syndrome (LQTS) is a cardiac electrophysiologic disorder, characterized by QT prolongation and T-wave abnormalities on the EKG that are associated with tachyarrhythmias, typically the ventricular tachycardia torsade de pointes (TdP). TdP is usually self-terminating, thus causing a syncopal event, the most common symptom in individuals with LQTS. Such cardiac events typically occur during exercise and emotional stress, less frequently during sleep, and usually without warning. In some instances, TdP degenerates to ventricular fibrillation and causes aborted cardiac arrest (if the individual is defibrillated) or sudden death. Approximately 50% of untreated individuals with a pathogenic variant in one of the genes associated with LQTS have symptoms, usually one to a few syncopal events. While cardiac events may occur from infancy through middle age, they are most common from the preteen years through the 20s. Some types of LQTS are associated with a phenotype extending beyond cardiac arrhythmia. In addition to the prolonged QT interval, associations include muscle weakness and facial dysmorphism in Andersen-Tawil syndrome (LQTS type 7); hand/foot, facial, and neurodevelopmental features in Timothy syndrome (LQTS type 8); and profound sensorineural hearing loss in Jervell and Lange-Nielson syndrome.
Sarcoidosis, susceptibility to, 1
MedGen UID:
394568
Concept ID:
C2697310
Finding
Any sarcoidosis in which the cause of the disease is a mutation in the HLA-DRB1 gene.
Hypertrophic cardiomyopathy 13
MedGen UID:
442487
Concept ID:
C2750472
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the TNNC1 gene.
Hypertrophic cardiomyopathy 18
MedGen UID:
462615
Concept ID:
C3151265
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the PLN gene.
Yao syndrome
MedGen UID:
934587
Concept ID:
C4310620
Disease or Syndrome
Yao syndrome (YAOS) is an autoinflammatory disease characterized by periodic fever, dermatitis, arthritis, and swelling of the distal extremities, as well as gastrointestinal and sicca-like symptoms. The disorder is associated with specific NOD2 variants (and Shen, 2017).
Sudden cardiac failure, alcohol-induced
MedGen UID:
934630
Concept ID:
C4310663
Disease or Syndrome
Telangiectasia, hereditary hemorrhagic, type 1
MedGen UID:
1643786
Concept ID:
C4551861
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are characteristically found on the lips, tongue, buccal and gastrointestinal (GI) mucosa, face, and fingers. The appearance of telangiectases is generally later than epistaxis but may be during childhood. Large AVMs occur most often in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. A minority of individuals with HHT have GI bleeding, which is rarely seen before age 50 years.
Arrhythmogenic right ventricular dysplasia, familial, 14
MedGen UID:
1712001
Concept ID:
C5394505
Disease or Syndrome
Arrhythmogenic right ventricular cardiomyopathy/dysplasia-14 (ARVD14) is characterized by palpitations, chest pain, and presyncope. Electrocardiography shows epsilon waves, T-wave inversion across anterior leads, premature ventricular contractions, ventricular tachycardia, and left bundle branch block. Dilation of the right ventricle with hypokinesia and aneurysmal changes are seen on echocardiography. Cardiac MRI may show fibrofatty infiltration, which has been confirmed by endocardial biopsy in some patients. Sudden death may occur (Mayosi et al., 2017). For a discussion of genetic heterogeneity of ARVD, see ARVD1 (107970).
Cardiac valvular dysplasia 2
MedGen UID:
1823999
Concept ID:
C5774226
Disease or Syndrome
Cardiac valvular dysplasia-2 (CVDP2) is characterized primarily by congenital stenosis and insufficiency of the semilunar valves, although mild insufficiency of the atrioventricular valves has been observed as well. Other features include subaortic stenosis and dilation of the ascending aorta and/or pulmonary artery in some patients (Wunnemann et al., 2020; Massadeh et al., 2020). For a discussion of genetic heterogeneity of CVDP, see CVDP1 (212093).
Hyper-IgE recurrent infection syndrome 1, autosomal dominant
MedGen UID:
1846538
Concept ID:
CN031130
Disease or Syndrome
STAT3 hyper IgE syndrome (STAT3-HIES) is a primary immune deficiency syndrome characterized by elevated serum IgE, eczema, and recurrent skin and respiratory tract infections, together with several nonimmune features. This disorder typically manifests in the newborn period with a rash (often diagnosed as eosinophilic pustulosis) that subsequently evolves into an eczematoid dermatitis. Recurrent staphylococcal skin boils and bacterial pneumonias usually manifest in the first years of life. Pneumatoceles and bronchiectasis often result from aberrant healing of pneumonias. Mucocutaneous candidiasis is common. Nonimmune features may include retained primary teeth, scoliosis, bone fractures following minimal trauma, joint hyperextensibility, and characteristic facial appearance, which typically emerges in adolescence. Vascular abnormalities have been described and include middle-sized artery tortuosity and aneurysms, with infrequent clinical sequelae of myocardial infarction and subarachnoid hemorrhage. Gastrointestinal (GI) manifestations include gastroesophageal reflux disease, esophageal dysmotility, and spontaneous intestinal perforations (some of which are associated with diverticuli). Fungal infections of the GI tract (typically histoplasmosis, Cryptococcus, and Coccidioides) also occur infrequently. Survival is typically into adulthood, with most individuals now living into or past the sixth decade. Most deaths are associated with gram-negative (Pseudomonas) or filamentous fungal pneumonias resulting in hemoptysis. Lymphomas occur at an increased frequency.

Professional guidelines

PubMed

Ammirati E, Moslehi JJ
JAMA 2023 Apr 4;329(13):1098-1113. doi: 10.1001/jama.2023.3371. PMID: 37014337
Bhatt DL, Lopes RD, Harrington RA
JAMA 2022 Feb 15;327(7):662-675. doi: 10.1001/jama.2022.0358. PMID: 35166796
Yadlapati R, Gyawali CP, Pandolfino JE; CGIT GERD Consensus Conference Participants
Clin Gastroenterol Hepatol 2022 May;20(5):984-994.e1. Epub 2022 Feb 2 doi: 10.1016/j.cgh.2022.01.025. PMID: 35123084Free PMC Article

Recent clinical studies

Etiology

Dawson LP, Smith K, Cullen L, Nehme Z, Lefkovits J, Taylor AJ, Stub D
J Am Coll Cardiol 2022 Jun 14;79(23):2333-2348. doi: 10.1016/j.jacc.2022.03.380. PMID: 35680185
Cutugno C
Am J Nurs 2022 May 1;122(5):56-58. doi: 10.1097/01.NAJ.0000830768.27347.ca. PMID: 35447656
Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
Circulation 2021 Nov 30;144(22):e368-e454. Epub 2021 Oct 28 doi: 10.1161/CIR.0000000000001030. PMID: 34709928
Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
Circulation 2021 Nov 30;144(22):e368-e454. Epub 2021 Oct 28 doi: 10.1161/CIR.0000000000001029. PMID: 34709879
Cayley WE Jr
Am Fam Physician 2005 Nov 15;72(10):2012-21. PMID: 16342831

Diagnosis

Writing Committee, Kontos MC, de Lemos JA, Deitelzweig SB, Diercks DB, Gore MO, Hess EP, McCarthy CP, McCord JK, Musey PI Jr, Villines TC, Wright LJ
J Am Coll Cardiol 2022 Nov 15;80(20):1925-1960. Epub 2022 Oct 11 doi: 10.1016/j.jacc.2022.08.750. PMID: 36241466Free PMC Article
Dawson LP, Smith K, Cullen L, Nehme Z, Lefkovits J, Taylor AJ, Stub D
J Am Coll Cardiol 2022 Jun 14;79(23):2333-2348. doi: 10.1016/j.jacc.2022.03.380. PMID: 35680185
Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
Circulation 2021 Nov 30;144(22):e368-e454. Epub 2021 Oct 28 doi: 10.1161/CIR.0000000000001030. PMID: 34709928
Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
Circulation 2021 Nov 30;144(22):e368-e454. Epub 2021 Oct 28 doi: 10.1161/CIR.0000000000001029. PMID: 34709879
Rushton S, Carman MJ
Nurs Clin North Am 2018 Sep;53(3):421-431. Epub 2018 Jul 11 doi: 10.1016/j.cnur.2018.04.009. PMID: 30100007

Therapy

Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
Circulation 2021 Nov 30;144(22):e368-e454. Epub 2021 Oct 28 doi: 10.1161/CIR.0000000000001030. PMID: 34709928
Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
Circulation 2021 Nov 30;144(22):e368-e454. Epub 2021 Oct 28 doi: 10.1161/CIR.0000000000001029. PMID: 34709879
Akbarialiabad H, Taghrir MH, Abdollahi A, Ghahramani N, Kumar M, Paydar S, Razani B, Mwangi J, Asadi-Pooya AA, Malekmakan L, Bastani B
Infection 2021 Dec;49(6):1163-1186. Epub 2021 Jul 28 doi: 10.1007/s15010-021-01666-x. PMID: 34319569Free PMC Article
Hartmann-Boyce J, Chepkin SC, Ye W, Bullen C, Lancaster T
Cochrane Database Syst Rev 2018 May 31;5(5):CD000146. doi: 10.1002/14651858.CD000146.pub5. PMID: 29852054Free PMC Article
Imazio M, Gaita F, LeWinter M
JAMA 2015 Oct 13;314(14):1498-506. doi: 10.1001/jama.2015.12763. PMID: 26461998

Prognosis

SCOT-HEART Investigators, Newby DE, Adamson PD, Berry C, Boon NA, Dweck MR, Flather M, Forbes J, Hunter A, Lewis S, MacLean S, Mills NL, Norrie J, Roditi G, Shah ASV, Timmis AD, van Beek EJR, Williams MC
N Engl J Med 2018 Sep 6;379(10):924-933. Epub 2018 Aug 25 doi: 10.1056/NEJMoa1805971. PMID: 30145934
Douglas PS, Hoffmann U, Patel MR, Mark DB, Al-Khalidi HR, Cavanaugh B, Cole J, Dolor RJ, Fordyce CB, Huang M, Khan MA, Kosinski AS, Krucoff MW, Malhotra V, Picard MH, Udelson JE, Velazquez EJ, Yow E, Cooper LS, Lee KL; PROMISE Investigators
N Engl J Med 2015 Apr 2;372(14):1291-300. Epub 2015 Mar 14 doi: 10.1056/NEJMoa1415516. PMID: 25773919Free PMC Article
Backus BE, Six AJ, Kelder JC, Bosschaert MA, Mast EG, Mosterd A, Veldkamp RF, Wardeh AJ, Tio R, Braam R, Monnink SH, van Tooren R, Mast TP, van den Akker F, Cramer MJ, Poldervaart JM, Hoes AW, Doevendans PA
Int J Cardiol 2013 Oct 3;168(3):2153-8. Epub 2013 Mar 7 doi: 10.1016/j.ijcard.2013.01.255. PMID: 23465250
Gulalp B, Karagun O, Tekin A, Benli S
J Emerg Med 2013 Jan;44(1):58-60. Epub 2012 Feb 1 doi: 10.1016/j.jemermed.2011.06.128. PMID: 22305150
Prisant LM, Nalamolu VR
J Clin Hypertens (Greenwich) 2005 Jun;7(6):367-71. doi: 10.1111/j.1524-6175.2005.04116.x. PMID: 16088302Free PMC Article

Clinical prediction guides

Writing Committee Members, Gulati M, Levy PD, Mukherjee D, Amsterdam E, Bhatt DL, Birtcher KK, Blankstein R, Boyd J, Bullock-Palmer RP, Conejo T, Diercks DB, Gentile F, Greenwood JP, Hess EP, Hollenberg SM, Jaber WA, Jneid H, Joglar JA, Morrow DA, O'Connor RE, Ross MA, Shaw LJ
J Cardiovasc Comput Tomogr 2022 Jan-Feb;16(1):54-122. Epub 2021 Dec 1 doi: 10.1016/j.jcct.2021.11.009. PMID: 34955448
Dinh A, Miertschin S, Young A, Mohanty SD
BMC Med Inform Decis Mak 2019 Nov 6;19(1):211. doi: 10.1186/s12911-019-0918-5. PMID: 31694707Free PMC Article
Zhang L, McMahon CJ, Shah S, Wu JS, Eisenberg RL, Kung JW
Curr Probl Diagn Radiol 2018 Mar-Apr;47(2):94-97. Epub 2017 May 30 doi: 10.1067/j.cpradiol.2017.05.011. PMID: 28716296
Poldervaart JM, Langedijk M, Backus BE, Dekker IMC, Six AJ, Doevendans PA, Hoes AW, Reitsma JB
Int J Cardiol 2017 Jan 15;227:656-661. Epub 2016 Oct 30 doi: 10.1016/j.ijcard.2016.10.080. PMID: 27810290
Chen YY, Su WP, Fang HY
Gastroenterology 2015 May;148(5):e7-9. Epub 2015 Mar 28 doi: 10.1053/j.gastro.2014.10.048. PMID: 25824358

Recent systematic reviews

Akbarialiabad H, Taghrir MH, Abdollahi A, Ghahramani N, Kumar M, Paydar S, Razani B, Mwangi J, Asadi-Pooya AA, Malekmakan L, Bastani B
Infection 2021 Dec;49(6):1163-1186. Epub 2021 Jul 28 doi: 10.1007/s15010-021-01666-x. PMID: 34319569Free PMC Article
Richards JR, Hollander JE, Ramoska EA, Fareed FN, Sand IC, Izquierdo Gómez MM, Lange RA
J Cardiovasc Pharmacol Ther 2017 May;22(3):239-249. Epub 2016 Dec 14 doi: 10.1177/1074248416681644. PMID: 28399647
Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA
JAMA 2016 Aug 16;316(7):754-63. doi: 10.1001/jama.2016.10026. PMID: 27533160
Fanaroff AC, Rymer JA, Goldstein SA, Simel DL, Newby LK
JAMA 2015 Nov 10;314(18):1955-65. doi: 10.1001/jama.2015.12735. PMID: 26547467
Imazio M, Gaita F, LeWinter M
JAMA 2015 Oct 13;314(14):1498-506. doi: 10.1001/jama.2015.12763. PMID: 26461998

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