PRINZMETAL’S ANGINA, HISTORY, DIAGNOSIS, TREATMENT.
FREE STUDY AT THE CHOLESTEROL CENTER,
JEWISH HOSPITAL, CINCINNATI OH
PHONE 513-924-8250, FAX 513-924-8273, EMAIL glueckch@healthall.com
If you have well defined Prinzmetal’s angina, we may be able to help devise a safe, case-specific medical intervention, depending on the presence or absence of two gene polymorphisms associated with arterial spasm, and a mutation associated with abnormalities in nitric oxide synthesis. You can call the Cholesterol Center (513-585-7951) to make an appointment for this entirely free study in Cincinnati, which will take about 1 hour and small blood sample. Alternatively if you cannot get to Cincinnati give your history by phone which will take about 30 minutes of your time and arrange to send a small blood sample, we can work with you through the MDL laboratory of Cincinnati (513-475-6631) to get a mailed blood sample. After talking to us and giving your history ( 513-585-7951) then call 513-475-6631 (MDL) to arrange to have your physician draw a 5 cc purple top tube of blood so that the crucial PCR tests can be done and mail it unrefrigerated in a crush-proof container, overnight or 2-day delivery to MDL, 3130 Highland Ave. Cincinnati, OH 45219.
Prinzmetal's angina, also known as variant angina or angina inversa, is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles. It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than by atherosclerosis (buildup of fatty plaque and hardening of the arteries). It was first described in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).
CURRENTLY, the initiating factor in Prinzmetals angina is not known. The hypothesis is that mutations in eNOS T-786c and stromeolysin-1 5A/6A genes can be implicated as causes for reduced synthesis of nitric oxide from endothelium leading to vasospastic episodes .The over the counter amino acid, L-arginine enhances NO synthesis, improves endothelial dilatation, decreases platelet aggregation, and reverses endothelial dysfunction, therefore will possibly improve quality of life.
Features
Symptoms typically occur at rest, rather than on exertion. 2/3 of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms.
It is associated with specific EKG changes (elevation rather than depression of the ST segment)
Diagnosis
Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome", and are generally tested for cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may show a degree of positivity, as coronary spasm too can cause myocardial damage. Echocardiography or thallium scintigraphy is often performed.
The gold standard is coronary angiography with injection of provocative agents into the coronary artery. Rarely, an active spasm can be documented angiographically (e.g. if the patient receives an angiogram with intent of performing a primary coronary intervention with angioplasty). Depending on the local protocol, provocation testing may involve substances such as ergonovine, methylergonovine or acetylcholine.
Exaggerated spasm is diagnostic of Prinzmetal angina.
EKG finding will more often show ST elevation than ST depression.
Treatment
Prinzmetal angina typically, but not always, responds to nitrates and calcium channel blockers.
If we find eNOS T786 hetero or homozygous and/or stomeolysin-1 5A6A hetero or homozygosity, then we will suggest treatment with 12g L arginine, available OTC in 1g capsule.
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