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Angina pectoris

MedGen UID:
1929
Concept ID:
C0002962
Sign or Symptom
Synonyms: Angina Pectoris; Angor Pectoris; Stenocardia; Stenocardias
SNOMED CT: Angina (194828000); Cardiac angina (194828000); Angina pectoris (194828000); Stenocardia (194828000); Anginal syndrome (194828000); AP - Angina pectoris (194828000); Ischemic heart disease - angina (194828000); Ischemic chest pain (225566008)
 
HPO: HP:0001681

Definition

Paroxysmal chest pain that occurs with exertion or stress and is related to myocardial ischemia. [from HPO]

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease is the most common of the lysosomal storage disorders and results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A), leading to progressive lysosomal deposition of globotriaosylceramide and its derivatives in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesia), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhidrosis, hypohidrosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, females may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, late-onset forms occur in males with greater than 1% a-Gal A activity. Clinical manifestations include cardiac disease, which usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy, arrhythmia, and proteinuria; renal failure, associated with ESRD but without the skin lesions or pain; or cerebrovascular disease presenting as stroke or transient ischemic attack.
Hutchinson-Gilford syndrome
MedGen UID:
46123
Concept ID:
C0033300
Disease or Syndrome
Hutchinson-Gilford progeria syndrome (HGPS) is characterized by clinical features that typically develop in childhood and resemble some features of accelerated aging. Children with HGPS usually appear normal at birth. Profound failure to thrive occurs during the first year. Characteristic facial features include head that is disproportionately large for the face, narrow nasal ridge, narrow nasal tip, thin vermilion of the upper and lower lips, small mouth, and retro- and micrognathia. Common features include loss of subcutaneous fat, delayed eruption and loss of primary teeth, abnormal skin with small outpouchings over the abdomen and upper thighs, alopecia, nail dystrophy, coxa valga, and progressive joint contractures. Later findings include low-frequency conductive hearing loss, dental crowding, and partial lack of secondary tooth eruption. Motor and mental development is normal. Death occurs as a result of complications of severe atherosclerosis, either cardiac disease (myocardial infarction or heart failure) or cerebrovascular disease (stroke), generally between ages six and 20 years. Average life span is approximately 14.5 years.
Cholestanol storage disease
MedGen UID:
116041
Concept ID:
C0238052
Disease or Syndrome
Cerebrotendinous xanthomatosis (CTX) is a lipid storage disease characterized by infantile-onset diarrhea, childhood-onset cataract, adolescent- to young adult-onset tendon xanthomas, and adult-onset progressive neurologic dysfunction (dementia, psychiatric disturbances, pyramidal and/or cerebellar signs, dystonia, atypical parkinsonism, peripheral neuropathy, and seizures). Chronic diarrhea from infancy and/or neonatal cholestasis may be the earliest clinical manifestation. In approximately 75% of affected individuals, cataracts are the first finding, often appearing in the first decade of life. Xanthomas appear in the second or third decade; they occur on the Achilles tendon, the extensor tendons of the elbow and hand, the patellar tendon, and the neck tendons. Xanthomas have been reported in the lung, bones, and central nervous system. Some individuals show cognitive impairment from early infancy, whereas the majority have normal or only slightly impaired intellectual function until puberty; dementia with slow deterioration in intellectual abilities occurs in the third decade in more than 50% of individuals. Neuropsychiatric symptoms such as behavioral changes, hallucinations, agitation, aggression, depression, and suicide attempts may be prominent. Pyramidal signs (i.e., spasticity) and/or cerebellar signs almost invariably become evident between ages 20 and 30 years. The biochemical abnormalities that distinguish CTX from other conditions with xanthomas include high plasma and tissue cholestanol concentration, normal-to-low plasma cholesterol concentration, decreased chenodeoxycholic acid (CDCA), increased concentration of bile alcohols and their glyconjugates, and increased concentrations of cholestanol and apolipoprotein B in cerebrospinal fluid.
Autosomal recessive inherited pseudoxanthoma elasticum
MedGen UID:
698415
Concept ID:
C1275116
Disease or Syndrome
Pseudoxanthoma elasticum (PXE) is a systemic disorder that affects the elastic tissue of the skin, the eye, and vascular system. Individuals most commonly present with angioid streaks of the retina found on routine eye examination or associated with retinal hemorrhage and/or characteristic papules in the skin. The most frequent cause of morbidity and disability in PXE is reduced vision due to complications of subretinal neovascularizations and macular atrophy. Other manifestations include premature gastrointestinal angina and/or bleeding, intermittent claudication of arm and leg muscles, stroke, renovascular hypertension, and cardiovascular complications (angina/myocardial infarction). Most affected individuals live a normal life span.
Hypertrophic cardiomyopathy 2
MedGen UID:
349383
Concept ID:
C1861864
Disease or Syndrome
Hypertrophic 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. \n\nWhile 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\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\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.
Pseudoxanthoma elasticum, forme fruste
MedGen UID:
357280
Concept ID:
C1867450
Disease or Syndrome
Pseudoxanthoma elasticum (PXE) is a systemic disorder that affects the elastic tissue of the skin, the eye, and vascular system. Individuals most commonly present with angioid streaks of the retina found on routine eye examination or associated with retinal hemorrhage and/or characteristic papules in the skin. The most frequent cause of morbidity and disability in PXE is reduced vision due to complications of subretinal neovascularizations and macular atrophy. Other manifestations include premature gastrointestinal angina and/or bleeding, intermittent claudication of arm and leg muscles, stroke, renovascular hypertension, and cardiovascular complications (angina/myocardial infarction). Most affected individuals live a normal life span.
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.
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 17
MedGen UID:
462614
Concept ID:
C3151264
Disease or Syndrome
An autosomal dominant subtype of familial hypertrophic cardiomyopathy caused by mutation(s) in the JPH2 gene, encoding junctophilin-2.
Hyperlipidemia due to hepatic triglyceride lipase deficiency
MedGen UID:
462816
Concept ID:
C3151466
Disease or Syndrome
Hepatic lipase deficiency is characterized by premature atherosclerosis, elevated total cholesterol, triglycerides (TG), and very low density lipoprotein (VLDL), as well as TG-rich low density lipoprotein (LDL) and HDL subfractions (summary by Hegele et al., 1991).
Pulmonary hypertension, primary, autosomal recessive
MedGen UID:
1802382
Concept ID:
C5676877
Disease or Syndrome
Primary pulmonary hypertension-5 (PPH5) is an autosomal recessive disorder characterized by the onset of pulmonary arterial hypertension in infancy, resulting in right heart dysfunction and ultimately right heart failure. Death in early childhood is common (Machado et al., 2022). For a discussion of genetic heterogeneity of primary pulmonary hypertension, see PPH1 (178600).

Professional guidelines

PubMed

Ullrich-Daub H, Daub S, Olschewski M, Münzel T, Gori T
Dtsch Arztebl Int 2023 Nov 3;120(44):739-746. doi: 10.3238/arztebl.m2023.0205. PMID: 37721132Free PMC Article
Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, Prescott E, Storey RF, Deaton C, Cuisset T, Agewall S, Dickstein K, Edvardsen T, Escaned J, Gersh BJ, Svitil P, Gilard M, Hasdai D, Hatala R, Mahfoud F, Masip J, Muneretto C, Valgimigli M, Achenbach S, Bax JJ; ESC Scientific Document Group
Eur Heart J 2020 Jan 14;41(3):407-477. doi: 10.1093/eurheartj/ehz425. PMID: 31504439
Kloner RA, Chaitman B
J Cardiovasc Pharmacol Ther 2017 May;22(3):199-209. Epub 2016 Dec 14 doi: 10.1177/1074248416679733. PMID: 28196437

Curated

UK NICE guideline NG185, Acute coronary syndromes, 2020

Recent clinical studies

Etiology

Ullrich-Daub H, Daub S, Olschewski M, Münzel T, Gori T
Dtsch Arztebl Int 2023 Nov 3;120(44):739-746. doi: 10.3238/arztebl.m2023.0205. PMID: 37721132Free PMC Article
Makowski M, Makowska JS, Zielińska M
Cardiol Clin 2020 Nov;38(4):629-637. Epub 2020 Sep 17 doi: 10.1016/j.ccl.2020.07.009. PMID: 33036723
Picard F, Sayah N, Spagnoli V, Adjedj J, Varenne O
Arch Cardiovasc Dis 2019 Jan;112(1):44-55. Epub 2018 Sep 7 doi: 10.1016/j.acvd.2018.08.002. PMID: 30197243
Ong P, Athanasiadis A, Sechtem U
Cardiovasc Drugs Ther 2016 Aug;30(4):351-356. doi: 10.1007/s10557-016-6676-z. PMID: 27358172
Kloner RA, Henderson L
Am J Cardiol 2013 Jun 1;111(11):1671-6. Epub 2013 Apr 2 doi: 10.1016/j.amjcard.2013.02.009. PMID: 23558039

Diagnosis

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J Cardiovasc Med (Hagerstown) 2023 Mar 1;24(3):219-220. Epub 2023 Jan 24 doi: 10.2459/JCM.0000000000001428. PMID: 36724392
Nguyen TH, Ong GJ, Girolamo OC, De Menezes Caceres' V, Muminovic A, Chirkov YY, Horowitz JD
Expert Rev Cardiovasc Ther 2021 Oct;19(10):917-927. Epub 2021 Oct 28 doi: 10.1080/14779072.2021.1991314. PMID: 34633245
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Therapy

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Prognosis

Jia RF, Li L, Li H, Cao XJ, Ruan Y, Meng S, Wang JY, Jin ZN
Am J Cardiol 2020 Apr 1;125(7):1039-1045. Epub 2020 Jan 8 doi: 10.1016/j.amjcard.2020.01.005. PMID: 32014245
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Cochrane Database Syst Rev 2017 Feb 8;2(2):CD011747. doi: 10.1002/14651858.CD011747.pub2. PMID: 28178363Free PMC Article
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Clinical prediction guides

Feldman DI, Latina J, Lovell J, Blumenthal RS, Arbab-Zadeh A
Trends Cardiovasc Med 2022 Oct;32(7):421-428. Epub 2021 Aug 25 doi: 10.1016/j.tcm.2021.08.009. PMID: 34454051
Gong Y, Zheng B, Yi T, Yang F, Hong T, Liu Z, Huo Y, Li J, Huo Y
Catheter Cardiovasc Interv 2022 Feb;99(3):763-771. Epub 2021 Feb 15 doi: 10.1002/ccd.29558. PMID: 33590679
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JACC Cardiovasc Interv 2020 Jan 13;13(1):33-45. Epub 2019 Nov 11 doi: 10.1016/j.jcin.2019.11.001. PMID: 31709984Free PMC Article
Picard F, Sayah N, Spagnoli V, Adjedj J, Varenne O
Arch Cardiovasc Dis 2019 Jan;112(1):44-55. Epub 2018 Sep 7 doi: 10.1016/j.acvd.2018.08.002. PMID: 30197243
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Recent systematic reviews

Xie W, Wang Y, Xiao S, Qiu L, Yu Y, Zhang Z
BMJ 2022 Sep 21;378:e070244. doi: 10.1136/bmj-2022-070244. PMID: 36130740Free PMC Article
Dibben G, Faulkner J, Oldridge N, Rees K, Thompson DR, Zwisler AD, Taylor RS
Cochrane Database Syst Rev 2021 Nov 6;11(11):CD001800. doi: 10.1002/14651858.CD001800.pub4. PMID: 34741536Free PMC Article
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Anderson L, Thompson DR, Oldridge N, Zwisler AD, Rees K, Martin N, Taylor RS
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    Curated

    • NICE, 2020
      UK NICE guideline NG185, Acute coronary syndromes, 2020

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