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Angina pectoris

MedGen UID:
1929
Concept ID:
C0002962
Finding; Finding
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

Angina is chest pain or discomfort you feel when there is not enough blood flow to your heart muscle. Your heart muscle needs the oxygen that the blood carries. Angina may feel like pressure or a squeezing pain in your chest. It may feel like indigestion. You may also feel pain in your shoulders, arms, neck, jaw, or back. . Angina is a symptom of coronary artery disease (CAD), the most common heart disease. CAD happens when a sticky substance called plaque builds up in the arteries that supply blood to the heart, reducing blood flow. There are three types of angina:. -Stable angina is the most common type. It happens when the heart is working harder than usual. Stable angina has a regular pattern. Rest and medicines usually help. -Unstable angina is the most dangerous. It does not follow a pattern and can happen without physical exertion. It does not go away with rest or medicine. It is a sign that you could have a heart attack soon. -Variant angina is rare. It happens when you are resting. Medicines can help. Not all chest pain or discomfort is angina. If you have chest pain, you should see your health care provider. NIH: National Heart, Lung, and Blood Institute.  [from MedlinePlus]

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A) and progressive lysosomal deposition of globotriaosylceramide (GL-3) 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, they 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, males with greater than 1% a-Gal A activity may have: (1) a cardiac variant phenotype that usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy and arrhythmia, and proteinuria, but without ESRD; or (2) a renal variant phenotype, associated with ESRD but without the skin lesions or pain; or (3) cerebrovascular disease presenting as stroke or transient ischemic attack.
Familial type 3 hyperlipoproteinemia
MedGen UID:
9364
Concept ID:
C0020479
Disease or Syndrome
Hyperlipoproteinemia type III, also called dysbetalipoproteinemia, is characterized by hyperlipidemia due to accumulation of remnants of the triglyceride (TG)-rich lipoproteins (TGRL), very low density lipoporteins (VLDL), and chylomicrons (CM), in response to dysfunctional genetic variants of apolipolipoprotein E or absence of apoE (summary by Blum, 2016).
Hutchinson-Gilford syndrome
MedGen UID:
46123
Concept ID:
C0033300
Disease or Syndrome
Hutchinson-Gilford progeria syndrome encompasses a spectrum of clinical features that typically develop in childhood and resemble some features of accelerated aging. Although signs and symptoms vary in age of onset and severity, they are remarkably consistent overall. Children with Hutchinson-Gilford progeria syndrome (HGPS) usually appear normal at birth. Profound failure to thrive occurs during the first year. Characteristic facies, with receding mandible, narrow nasal bridge and pointed nasal tip develop. During the first to third year the following usually become apparent: partial alopecia progressing to total alopecia, loss of subcutaneous fat, progressive joint contractures, bone changes, nail dystrophy, and abnormal tightness and/or small soft outpouchings of the skin over the abdomen and upper thighs, and delayed primary tooth eruption. Later findings include low-frequency conductive hearing loss, dental crowding, and partial lack of secondary tooth eruption. Additional findings present in some but not all affected individuals include photophobia, excessive ocular tearing, exposure keratitis, and Raynaud phenomenon. Motor and mental development is normal. Death occurs as a result of complications of severe atherosclerosis, either cardiac disease (myocardial infarction) or cerebrovascular disease (stroke), generally between ages six and 20 years. Average life span is approximately 14.6 years.
Pseudoxanthoma elasticum
MedGen UID:
18733
Concept ID:
C0033847
Disease or Syndrome
Pseudoxanthoma elasticum (PXE) is a systemic disorder that affects the elastic tissue of the skin, the eye, and the cardiovascular and gastrointestinal systems. Individuals most commonly present with papules in the skin and/or with angioid streaks of the retina found on routine eye examination or associated with retinal hemorrhage. Rarely, individuals may present with vascular signs and symptoms, such as gastrointestinal bleeding, angina, or intermittent claudication. The most frequent cause of morbidity and disability in PXE is reduced vision from macular hemorrhage and disciform scarring of the macula. Most affected individuals live a normal life span.
Sea-blue histiocyte syndrome
MedGen UID:
19908
Concept ID:
C0036489
Disease or Syndrome
APOE p.Leu167del is a rare genetic variant described in 38 cases in the literature with a range of clinical phenotypes. Three phenotypes can be associated with the APOE p.Leu167del variant: Inherited lipemic splenomegaly (also known as sea-blue histiocytosis) characterized by hypertriglyceridemia and splenomegaly. Variable manifestations include thrombocytopenia, liver function abnormalities, and cardiovascular disease. Autosomal dominant hypercholesterolemia (ADH) characterized by markedly elevated LDL cholesterol levels that leads to premature morbidity and mortality from atherosclerotic cardiovascular disease (ASCVD). Familial combined hyperlipidemia (FCHL) characterized by variable elevations of total cholesterol, triglycerides, or LDL cholesterol and a high risk of premature ASCVD. It has been suggested that the phenotype associated with the APOE p.Leu167del variant may depend on multiple factors, including sex, APOE genotype, control of hyperlipidemia, gene-gene interactions, gene-environment interactions, or perhaps epigenetic and other non-Mendelian effects.
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 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 20s 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, increased concentration of bile alcohols and their glyconjugates, and increased concentrations of cholestanol and apolipoprotein B in cerebrospinal fluid.
MYOCARDIAL INFARCTION, SUSCEPTIBILITY TO
MedGen UID:
318680
Concept ID:
C1832662
Finding
Pulmonary hypertension, primary, autosomal recessive
MedGen UID:
340354
Concept ID:
C1849552
Disease or Syndrome
Apolipoprotein E, Deficiency or Defect of
MedGen UID:
350700
Concept ID:
C1862556
Disease or Syndrome
Dysbetalipoproteinemia due to Defect in Apolipoprotein E-d
MedGen UID:
350701
Concept ID:
C1862557
Disease or Syndrome
Familial Hyperbeta- and Prebetalipoproteinemia
MedGen UID:
400080
Concept ID:
C1862558
Disease or Syndrome
Hyperlipemia with Familial Hypercholesterolemic Xanthomatosis
MedGen UID:
354777
Concept ID:
C1862560
Disease or Syndrome
Broad-Betalipoproteinemia
MedGen UID:
400081
Concept ID:
C1862561
Disease or Syndrome
Floating-Betalipoproteinemia
MedGen UID:
350702
Concept ID:
C1862562
Disease or Syndrome
Coronary artery disease, severe, susceptibility to
MedGen UID:
349546
Concept ID:
C1862591
Finding
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 the cardiovascular and gastrointestinal systems. Individuals most commonly present with papules in the skin and/or with angioid streaks of the retina found on routine eye examination or associated with retinal hemorrhage. Rarely, individuals may present with vascular signs and symptoms, such as gastrointestinal bleeding, angina, or intermittent claudication. The most frequent cause of morbidity and disability in PXE is reduced vision from macular hemorrhage and disciform scarring of the macula. Most affected individuals live a normal life span.
Lipoprotein glomerulopathy
MedGen UID:
382034
Concept ID:
C2673196
Disease or Syndrome
Lipoprotein glomerulopathy is an uncommon kidney disease characterized by proteinuria, progressive kidney failure, and distinctive lipoprotein thrombi in glomerular capillaries (Saito et al., 2006). It mainly affects people of Japanese and Chinese origin; in these populations, it is associated with mutations in the gene that encodes apolipoprotein E (APOE; 107741). The disorder had rarely been described in Caucasians.
LOW DENSITY LIPOPROTEIN CHOLESTEROL LEVEL QUANTITATIVE TRAIT LOCUS 5
MedGen UID:
390957
Concept ID:
C2676098
Gene or Genome
Hepatic lipase deficiency
MedGen UID:
462816
Concept ID:
C3151466
Disease or Syndrome
Hepatic lipase deficiency is a disorder that affects the body's ability to break down fats (lipids). People with this disorder have increased amounts of certain fats, known as triglycerides and cholesterol, in the blood. These individuals also have increased amounts of molecules known as high-density lipoproteins (HDLs) and decreased amounts of molecules called low-density lipoproteins (LDL). These molecules transport triglycerides and cholesterol throughout the body. In people with hepatic lipase deficiency, the LDL molecules are often abnormally large.Normally, high levels of HDL (known as "good cholesterol") and low levels of LDL (known as "bad cholesterol") are protective against an accumulation of fatty deposits on the artery walls (atherosclerosis) and heart disease. However, some individuals with hepatic lipase deficiency, who have this imbalance of HDL and LDL, develop atherosclerosis and heart disease in mid-adulthood, while others do not. It is unknown whether people with hepatic lipase deficiency have a greater risk of developing atherosclerosis or heart disease than individuals in the general population. Similarly, it is unclear how increased blood triglycerides and cholesterol levels affect the risk of atherosclerosis and heart disease in people with hepatic lipase deficiency.
APOE4(-)-FREIBURG PHENOTYPE
MedGen UID:
854548
Concept ID:
C3887714
Finding
APOE2 ISOFORMS
MedGen UID:
864295
Concept ID:
C4015858
Finding
HYPERLIPOPROTEINEMIA AND ATHEROSCLEROSIS ASSOCIATED WITH APOE5
MedGen UID:
864296
Concept ID:
C4015859
Finding
HYPERLIPOPROTEINEMIA, TYPE III, DUE TO APOE2-CHRISTCHURCH
MedGen UID:
864297
Concept ID:
C4015860
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE2
MedGen UID:
864298
Concept ID:
C4015861
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE DEFICIENCY
MedGen UID:
864299
Concept ID:
C4015862
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE LEIDEN
MedGen UID:
864300
Concept ID:
C4015863
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE7
MedGen UID:
864301
Concept ID:
C4015864
Finding
HYPERLIPOPROTEINEMIA, TYPE III, AUTOSOMAL DOMINANT
MedGen UID:
864302
Concept ID:
C4015865
Finding
APOLIPOPROTEINEMIA E1
MedGen UID:
864303
Concept ID:
C4015866
Finding
HYPERLIPOPROTEINEMIA, TYPE III, DUE TO APOE1-HARRISBURG
MedGen UID:
864304
Concept ID:
C4015867
Finding
Dysbetalipoproteinemia due to apoe2
MedGen UID:
864305
Concept ID:
C4015868
Finding
APOE2-DUNEDIN PHENOTYPE
MedGen UID:
864306
Concept ID:
C4015869
Finding
HYPERLIPOPROTEINEMIA, TYPE III, DUE TO APOE4-PHILADELPHIA
MedGen UID:
864307
Concept ID:
C4015870
Finding
APOE3 ISOFORM
MedGen UID:
864308
Concept ID:
C4015871
Finding
ALZHEIMER DISEASE 2, DUE TO APOE4 ISOFORM
MedGen UID:
864309
Concept ID:
C4015872
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE DEFICIENCY, AUTOSOMAL RECESSIVE
MedGen UID:
864310
Concept ID:
C4015873
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE2-FUKUOKA
MedGen UID:
864311
Concept ID:
C4015874
Finding
Hypercholesterolemia and hypertriglyceridemia, type III
MedGen UID:
864312
Concept ID:
C4015875
Finding
HYPERLIPOPROTEINEMIA, TYPE III, ASSOCIATED WITH APOE4
MedGen UID:
864313
Concept ID:
C4015876
Finding
APOE3(-)-FREIBURG PHENOTYPE
MedGen UID:
864314
Concept ID:
C4015877
Finding
APOE4 VARIANT PHENOTYPE
MedGen UID:
864315
Concept ID:
C4015878
Finding
APOE3 VARIANT PHENOTYPE
MedGen UID:
864316
Concept ID:
C4015879
Finding
APOE2 VARIANT PHENOTYPE
MedGen UID:
864317
Concept ID:
C4015880
Finding
APOE4(+) PHENOTYPE
MedGen UID:
864318
Concept ID:
C4015881
Finding
HYPERLIPOPROTEINEMIA, TYPE III, AUTOSOMAL RECESSIVE
MedGen UID:
865858
Concept ID:
C4017421
Finding
APOE-SUITA PHENOTYPE
MedGen UID:
865859
Concept ID:
C4017422
Finding
APOE3-WASHINGTON PHENOTYPE
MedGen UID:
865860
Concept ID:
C4017423
Finding
APOE3(-)-KOCHI PHENOTYPE
MedGen UID:
865861
Concept ID:
C4017424
Finding
APOE2-FUKUOKA PHENOTYPE
MedGen UID:
865862
Concept ID:
C4017425
Finding
APOE SENDAI PHENOTYPE
MedGen UID:
865863
Concept ID:
C4017426
Finding
APOE KYOTO PHENOTYPE
MedGen UID:
865864
Concept ID:
C4017427
Finding

Recent clinical studies

Etiology

Giavarini A, de Silva R
Cardiovasc Drugs Ther 2016 Aug;30(4):407-17. doi: 10.1007/s10557-016-6678-x. PMID: 27475447Free PMC Article
Won H, Her AY, Kim BK, Kim YH, Shin DH, Kim JS, Ko YG, Choi D, Kwon HM, Jang Y, Hong MK
Yonsei Med J 2016 Mar;57(2):382-7. doi: 10.3349/ymj.2016.57.2.382. PMID: 26847290Free PMC Article
Xu DP, Wu HL, Lan TH, Wang X, Sheng XG, Lin Y, Li S, Zheng CY
Chin J Integr Med 2015 Jun;21(6):408-16. Epub 2015 Jun 11 doi: 10.1007/s11655-015-2040-6. PMID: 26063318
Peng S, Zhao M, Wan J, Fang Q, Fang D, Li K
Int J Cardiol 2014 Dec 20;177(3):780-5. Epub 2014 Oct 24 doi: 10.1016/j.ijcard.2014.10.149. PMID: 25466565
Xu X, Zhang W, Zhou Y, Zhao Y, Liu Y, Shi D, Zhou Z, Ma H, Wang Z, Yu M, Ma Q, Gao F, Shen H, Zhang J
Clin Drug Investig 2014 Apr;34(4):251-8. doi: 10.1007/s40261-014-0170-9. PMID: 24470342

Diagnosis

Holland LC, Navaratnarajah M, Taggart DP
Interact Cardiovasc Thorac Surg 2016 Apr;22(4):488-92. Epub 2016 Jan 18 doi: 10.1093/icvts/ivv386. PMID: 26787727
Shao H, Zhao L, Chen F, Zeng S, Liu S, Li J
Med Sci Monit 2015 Nov 29;21:3704-15. PMID: 26615387Free PMC Article
May O, Lynggaard V, Mortensen JC, Malczynski J
Scand Cardiovasc J 2015 Feb;49(1):1-6. Epub 2015 Jan 22 doi: 10.3109/14017431.2014.994028. PMID: 25471629
Peng S, Zhao M, Wan J, Fang Q, Fang D, Li K
Int J Cardiol 2014 Dec 20;177(3):780-5. Epub 2014 Oct 24 doi: 10.1016/j.ijcard.2014.10.149. PMID: 25466565
Kong D, Wang Y, Liu Y, Zhang Z, Liu G, Qi W, Xiao L, Yuan D, Yang G
Complement Ther Med 2014 Aug;22(4):801-13. Epub 2014 May 27 doi: 10.1016/j.ctim.2014.05.008. PMID: 25146084

Therapy

Giavarini A, de Silva R
Cardiovasc Drugs Ther 2016 Aug;30(4):407-17. doi: 10.1007/s10557-016-6678-x. PMID: 27475447Free PMC Article
Won H, Her AY, Kim BK, Kim YH, Shin DH, Kim JS, Ko YG, Choi D, Kwon HM, Jang Y, Hong MK
Yonsei Med J 2016 Mar;57(2):382-7. doi: 10.3349/ymj.2016.57.2.382. PMID: 26847290Free PMC Article
Xu DP, Wu HL, Lan TH, Wang X, Sheng XG, Lin Y, Li S, Zheng CY
Chin J Integr Med 2015 Jun;21(6):408-16. Epub 2015 Jun 11 doi: 10.1007/s11655-015-2040-6. PMID: 26063318
Xiong XJ, Wang Z, Wang J
Curr Vasc Pharmacol 2015;13(4):540-53. PMID: 25360837
Peng S, Zhao M, Wan J, Fang Q, Fang D, Li K
Int J Cardiol 2014 Dec 20;177(3):780-5. Epub 2014 Oct 24 doi: 10.1016/j.ijcard.2014.10.149. PMID: 25466565

Prognosis

Giavarini A, de Silva R
Cardiovasc Drugs Ther 2016 Aug;30(4):407-17. doi: 10.1007/s10557-016-6678-x. PMID: 27475447Free PMC Article
Lee WC, Fang CY, Chen HC, Hsueh SK, Chen CJ, Yang CH, Yip HK, Hang CL, Wu CJ, Fang HY
Medicine (Baltimore) 2016 Apr;95(17):e3426. doi: 10.1097/MD.0000000000003426. PMID: 27124029Free PMC Article
Park SH, Rha SW, Choi BG, Park JY, Jeon U, Seo HS, Kim EJ, Na JO, Choi CU, Kim JW, Lim HE, Park CG, Oh DJ
Clin Exp Pharmacol Physiol 2015 Jun;42(6):588-95. doi: 10.1111/1440-1681.12396. PMID: 25865336
Xu X, Zhang W, Zhou Y, Zhao Y, Liu Y, Shi D, Zhou Z, Ma H, Wang Z, Yu M, Ma Q, Gao F, Shen H, Zhang J
Clin Drug Investig 2014 Apr;34(4):251-8. doi: 10.1007/s40261-014-0170-9. PMID: 24470342
Ling H, Packard KA, Burns TL, Hilleman DE
Am J Cardiovasc Drugs 2013 Dec;13(6):407-12. doi: 10.1007/s40256-013-0038-z. PMID: 23873327

Clinical prediction guides

Lee WC, Fang CY, Chen HC, Hsueh SK, Chen CJ, Yang CH, Yip HK, Hang CL, Wu CJ, Fang HY
Medicine (Baltimore) 2016 Apr;95(17):e3426. doi: 10.1097/MD.0000000000003426. PMID: 27124029Free PMC Article
Shao H, Zhao L, Chen F, Zeng S, Liu S, Li J
Med Sci Monit 2015 Nov 29;21:3704-15. PMID: 26615387Free PMC Article
Xu DP, Wu HL, Lan TH, Wang X, Sheng XG, Lin Y, Li S, Zheng CY
Chin J Integr Med 2015 Jun;21(6):408-16. Epub 2015 Jun 11 doi: 10.1007/s11655-015-2040-6. PMID: 26063318
Peng S, Zhao M, Wan J, Fang Q, Fang D, Li K
Int J Cardiol 2014 Dec 20;177(3):780-5. Epub 2014 Oct 24 doi: 10.1016/j.ijcard.2014.10.149. PMID: 25466565
Ling H, Packard KA, Burns TL, Hilleman DE
Am J Cardiovasc Drugs 2013 Dec;13(6):407-12. doi: 10.1007/s40256-013-0038-z. PMID: 23873327

Recent systematic reviews

Holland LC, Navaratnarajah M, Taggart DP
Interact Cardiovasc Thorac Surg 2016 Apr;22(4):488-92. Epub 2016 Jan 18 doi: 10.1093/icvts/ivv386. PMID: 26787727
Shao H, Zhao L, Chen F, Zeng S, Liu S, Li J
Med Sci Monit 2015 Nov 29;21:3704-15. PMID: 26615387Free PMC Article
Sun T, Wang X, Xu H
Chin J Integr Med 2015 Jul;21(7):542-50. Epub 2015 Mar 6 doi: 10.1007/s11655-015-2070-0. PMID: 25749902
Peng S, Zhao M, Wan J, Fang Q, Fang D, Li K
Int J Cardiol 2014 Dec 20;177(3):780-5. Epub 2014 Oct 24 doi: 10.1016/j.ijcard.2014.10.149. PMID: 25466565
Kong D, Wang Y, Liu Y, Zhang Z, Liu G, Qi W, Xiao L, Yuan D, Yang G
Complement Ther Med 2014 Aug;22(4):801-13. Epub 2014 May 27 doi: 10.1016/j.ctim.2014.05.008. PMID: 25146084

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