Coronary vasospasm
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For information about Prinzmetal's angina, click here
For information about PCI-induced coronary vasospasm, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Lakshmi Gopalakrishnan, M.B.B.S.; Alexander Morss, M.D.; Brian Bigelow, M.D.; David Lorenz, M.D.; Jason Choi, M.D.; Felipe Chaparro M.D.
Synonyms and keywords: Coronary vasoconstriction, coronary artery spasm, vasospastic angina, variant angina , focal coronary artery vasospasm, dynamic coronary obstruction
Overview
Coronary vasospasm is a multi-factorial, transient, and abrupt reduction of luminal diameter of an epicardial coronary artery due to inappropriate constriction of coronary smooth muscle that can generate distal ischemia. This may occur spontaneously or in the context of angioplasty, particularly if denudation of the endothelium or dissection occurs. In addition, the vasospasm can either be focal or multifocal (which compromises more than one vessel).
Classification
Classification by Location
Coronary artery spasm can be classified according to the location of vasoconstriction:
Focal coronary spasm
Focal coronary spasm is limited to a localized segment of the coronary artery.
Multifocal coronary spasm
Multifocal coronary spasm involves several localized segments of the same coronary artery.
Multivessel coronary spasm
Multivessel coronary spasm involves several coronary arteries.[1][2]
Classification by Clinical Syndrome
Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.
Spontaneous
- A subtype of epicardial coronary artery spasm is known as Prinzmetal's angina. Prinzmetal's angina is characterized by the sudden onset of chest pain at rest with ST elevation on ECG. Click here for more information about Prinzmetal's angina.
Iatrogenic
- Coronary vasospasm can be secondary to PCI. Click here for more information about PCI-induced coronary vasospasm.
Pathophysiology
- The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known.
- Coronary spasm can be explained by a hyperreactivity to vasoconstrictor stimuli that results from endothelial dysfunction or primary hyperreactivity of smooth muscle cells. Vasoconstrictor stimuli include changes in the autonomic nervous system, inflammation, and calcium availability in the myocardium.[3][4] Dysfunction of the autonomic nervous system and endothelial dysfunction can lead to chronic intermittent vasospasm, which usually occurs where a fixed, non-calcified stenosis is located.
- A significant group of patients with variant angina have underlying obstructive coronary artery disease.[5]
- Occasionally, coronary vasospasm can be induced by angioplasty (PCI-induced), which occurs secondary to endothelial denudation and nitric oxide loss. Some cases are catheter-induced which is caused by a contact of a catheter without balloon deployment. Catheter-induced coronary vasospasm is usually short-lived. Catheter-induced coronary vasospasm is most prone to occur at the ostium of the right coronary artery (RCA). The left main is less susceptible to ostial spasm.
Causes
Causes in Alphabetical Order
- Acute pericarditis
- Angina pectoris
- Anxiety disorders
- Cocaine toxicity
- Coronary dissection can mimic and can cause spasm
- Drugs- Naratriptan, Sumatriptan
- Esophageal motility disorders
- Esophageal spasm
- Gastroesophageal reflux disease
- Isolated coronary artery anomalies
- Myocardial infarction
- Myocardial ischemia
- Panic disorder
- Coronary thrombosis can mimic and can cause spasm
- Unstable angina
Epidemiology and Demographics
- Young patients with fewer cardiovascular risk factors (with the exception of smoking) are at a higher risk for coronary vasospasm, as are noncalcified lesions and eccentric plaques.
- Rotoblator cases are more prone to coronary vasospasm. The reported incidence of rotoblater cases with coronary vasospasm ranges anywhere from 4 to 36%.
Risk Factors
- Autoimmune diseases
- Cocaine use
- Cold exposure
- Hyperventilation
- Insulin resistance
- Japanese descent
- Smoking
Coronary Vasospasm in Japanese Patients
A discrepancy in the prevalence of coronary artery spasm exists across different ethnicities; in particular, the Japanese population has been reported to have a greater prevalence of this condition compared to Caucasians.[6] In fact, according to a study involving 2251 patients, coronary artery spasm has been estimated to account for approximately 41% of Japanese patients with angina pectoris who underwent angiography.[7] In addition, coronary spasm in Japanese is characterized by a diffuse hyperreactivity as manifested by a segmental pattern of spasm as well as by a multivessel involvement compared to focal involvement in other populations.[8] Moreover, following the administration of acetylcholine early after myocardial infarction for provocation of spasm, there has been three fold higher incidence of coronary spasm and a higher incidence of multivessel spasm among Japanese compared to Caucasians.[9] These findings highlight that the vasomotor reactivity of coronary artery is not homogeneous across the different populations and is most likely related to genetic and environmental factors. Since endothelial dysfunction and enhanced vasoconstriction are part of the multifactorial pathophysiology of coronary spasm, it has been suggested that gene polymorphism of NO synthase, angiotensin converting enzyme, angiotensin receptor type 1 as well as other enzymes and susceptibility genes can explain the predisposition of the Japanese population to coronary spasm.[6]
Treatment
- The main goals of treating coronary vasospasm are to:
- Reverse the spontaneous abrupt luminal diameter reduction
- Reverse PTCA-induced vasospasm
- Stabilize chronic intermittent vasospasm.
- Calcium channel blockers and nitrates are the mainstay of chronic therapy for coronary vasospasm.
- Atropine has also been used to treat the condition.[10]
Contraindicated medications
Coronary artery vasospasm is considered an absolute contraindication to the use of the following medications:
References
- ↑ Ahooja V, Thatai D (2007). "Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease". J Invasive Cardiol. 19 (7): E178–81. PMID 17620681. Unknown parameter
|month=ignored (help) - ↑ Miwa K, Ishii K, Makita T, Okuda N (2004). "Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis". Circ. J. 68 (5): 483–7. PMID 15118293. Unknown parameter
|month=ignored (help) - ↑ Lanza GA, Careri G, Crea F (2011). "Mechanisms of coronary artery spasm". Circulation. 124 (16): 1774–82. doi:10.1161/CIRCULATIONAHA.111.037283. PMID 22007100.
- ↑ Mahemuti A, Abudureheman K, Schiele F, Ecarnot F, Abudureyimu S, Tang B; et al. (2014). "Association between inflammatory markers, hemostatic markers, and traditional risk factors on coronary artery spasm in patients with normal coronary angiography". J Interv Cardiol. 27 (1): 29–35. doi:10.1111/joic.12086. PMID 24345233.
- ↑ Maseri A, Severi S, Nes MD, L'Abbate A, Chierchia S, Marzilli M et al. (1978) "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol 42 (6):1019-35. PMID: 727129
- ↑ 6.0 6.1 Murase Y, Yamada Y, Hirashiki A, Ichihara S, Kanda H, Watarai M; et al. (2004). "Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women". Eur Heart J. 25 (11): 970–7. doi:10.1016/j.ehj.2004.02.020. PMID 15172469.
- ↑ Yasue H, Sasayama S, Kikuchi K, Okumura K, Matsubara T, Miwa K, et al. The study on the role of coronary spasm in ischemic heart disease. In: Annual report of the research on cardiovascular diseases. Osaka: National Cardiovascular Center; 2000. p. 96–7 (in Japanese).
- ↑ Beltrame JF, Sasayama S, Maseri A (1999). "Racial heterogeneity in coronary artery vasomotor reactivity: differences between Japanese and Caucasian patients". J Am Coll Cardiol. 33 (6): 1442–52. PMID 10334407.
- ↑ Pristipino C, Beltrame JF, Finocchiaro ML, Hattori R, Fujita M, Mongiardo R; et al. (2000). "Major racial differences in coronary constrictor response between japanese and caucasians with recent myocardial infarction". Circulation. 101 (10): 1102–8. PMID 10715255.
- ↑ Turkoglu S, Arpag U, Timurkaynak T (2007). "Spontaneous coronary vasospasm in the catheterisation laboratory: prompt resolution after atropine injection". Heart. 93 (2): 215. doi:10.1136/hrt.2006.093187. PMID 17228071. Unknown parameter
|month=ignored (help)