Prinzmetal<unk>  Although<unk>  has been documented in between 2% to 10% of<unk>  patients, it can be overlooked by cardiologists who stop further evaluations after ruling out typical<unk> . Individuals who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome", and are immediately tested for elevations in their blood levels of enzymes such as creatine kinase isoenzymes or troponin that are markers for cardiac damage. They are also tested by ECG which may suggest<unk>  if it shows elevations in the ST segment or an elevated ST segment plus a widening of the R wave during symptoms that are triggered by a provocative agent (e.g. ergonovine or acetylcholine). The electrocardiogram may show depressions rather than elevations in ST segments but in all diagnosable cases clinical symptoms should be promptly relieved and ECC changes should be promptly reversed by rapidly acting sublingual or intravenous nitroglycerin. However, the gold standard for diagnosing<unk>  is to visualize coronary arteries by angiography before and after injection of a provocative agent such as ergonovine, methylergonovine or acetylcholine to precipitate an attack of<unk> sospasm. A positive test to these inducing agents is defined as a ≥90% (some experts require lesser, e.g. ≥70%) constriction of involved arteries. Typically, these constrictions are fully reversed by rapidly acting nitroglycerin. Individuals with<unk>  may have many undocumented episodes of symptom-free coronary artery spasm that are associated with poor blood flow to portions of the heart and subsequent irregular and potentially serious heart arrhythmias. Accordingly, individuals with<unk>  should be intermittently evaluated for this using long-term ambulatory cardiac monitoring.
Variant angina
Microvascular angina
Unstable angina
Coronary steal
Bundle branch block
Atopy
Palisade 
Renal angina