Smooth Muscle Hypercontractility
At a cellular level, pathways that lead to enhanced myosin light chain phosphorylation promote vasoconstriction. Increased activity of Rho-kinase leading to enhanced myosin light chain phosphorylation has been implicated in the pathogenesis of coronary vasospasm. Diagnosis
There are no set criteria to diagnose coronary vasospasm. Thorough history taking by a clinician can assist in the diagnosis of coronary vasospasm. In cases where symptoms of chest pain are present, identifying features that distinguish episodes of vasospastic angina from traditional angina can aid in the diagnosis. Features such as chest pain at rest, a diurnal variation in tolerance for exercise with a reduction in tolerance for exercise in the morning, and responsiveness of chest pain to calcium channel blockers as opposed to beta blockers can be important clues.EKG can occasionally be used to diagnose episodes of coronary vasospasm. However, relying on EKG is not always possible due to the transient nature of coronary vasospasm episodes. Due to the challenge of capturing episodes of coronary vasospasm spontaneously, provocative testing to induce coronary vasospasm during coronary catheterization can be used to make the diagnosis. Provocative testing relies upon the use of pharmacological agents that promote or trigger episodes of vasospasm. Agents commonly administered include ergonovine and acetylcholine. Both pharmacological agents have vasoconstrictive effects on coronary arteries. However, in the clinical setting, provocative testing is not routinely performed. The reason for this is due to the adverse effects of these pharmacological agents.
Etymology
The signs and symptoms of DiGeorge syndrome are so varied that different groupings of its features were once regarded as separate conditions. These original classifications included velocardiofacial syndrome, Shprintzen syndrome, DiGeorge sequence/syndrome, Sedlackova syndrome, and conotruncal anomaly face syndrome. All are now understood to be presentations of a single syndrome. ICD-10 2015 version mentions DiGeorge syndrome using two codes:  D82.1 (Di George syndrome) and Q93.81 (Velo-cardio-facial syndrome). The ICD-11 Beta Draft discusses the syndrome under “LD50.P1 CATCH 22 phenotype". However, since this syndrome is caused by the deletion of a small piece of chromosome 22, some recommend that the name "22q11.2 deletion syndrome (22q11.2DS)" be used. Some experts support changing the name of both DiGeorge and velocardiofacial syndromes to CATCH-22. The International 22q11.2 Foundation, through its "Same Name Campaign", advocates for the name 22q11.2 deletion syndrome. See also
References
This article incorporates public domain text from The U.S. National Library of Medicine

External links

DiGeorge syndrome at Curlie
McDonald-McGinn DM, Emanuel BS, Zackai EH (December 16, 2005). "22q11.2 Deletion Syndrome". In Pagon RA, Bird TD, Dolan CR, Stephens K (eds.). GeneReviews. University of Washington, Seattle. PMID 20301696. NBK1523. Firth HV (February 17, 2009). "22q11.2 Duplication". In Pagon RA, Bird TD, Dolan CR, Stephens K (eds.). GeneReviews. University of Washington, Seattle. PMID 20301749. NBK3823.