Coronary vasospasm: Difference between revisions
Jump to navigation
Jump to search
Rim Halaby (talk | contribs) |
Rim Halaby (talk | contribs) No edit summary |
||
| Line 16: | Line 16: | ||
* Focal coronary spasm: Focal coronary spasm is limited to a localized segment of the [[coronary artery]]. | * Focal coronary spasm: Focal coronary spasm is limited to a localized segment of the [[coronary artery]]. | ||
* Multifocalocal coronary spasm: Multifocal coronary spasm involves several localized segments of the same [[coronary artery]]. | * Multifocalocal coronary spasm: Multifocal coronary spasm involves several localized segments of the same [[coronary artery]]. | ||
* Multivessel coronary spasm: Multivessel coronary spasm involves several coronary arteries. | * Multivessel coronary spasm: Multivessel coronary spasm involves several coronary arteries.<ref name="pmid17620681">{{cite journal |author=Ahooja V, Thatai D |title=Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease |journal=J Invasive Cardiol |volume=19 |issue=7 |pages=E178–81 |year=2007 |month=July |pmid=17620681 |doi= |url=http://www.digitaljic.com/nxtbooks/hmp/jic0707/index.php?startpage=54}}</ref><ref name="pmid15118293">{{cite journal |author=Miwa K, Ishii K, Makita T, Okuda N |title=Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis |journal=Circ. J. |volume=68 |issue=5 |pages=483–7 |year=2004 |month=May |pmid=15118293 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/circj/68.483?from=PubMed}}</ref> | ||
===Classification by Clinical Syndrome=== | ===Classification by Clinical Syndrome=== | ||
Coronary artery vasospasm can be classified into either spontaneous or iatrogenic. | 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]] | |||
====Iatrogenic==== | |||
* Coronary vasospasm can be secondary to [[PCI]]. | |||
* A subtype of epicardial coronary artery spasm is known as [[prinzmetal's angina]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
| Line 75: | Line 66: | ||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
* The prognosis of vasospastic angina depends on the extent of underlying [[coronary artery disease| coronary artery disease (CAD)]]. | * The prognosis of vasospastic angina depends on the extent of underlying [[coronary artery disease| coronary artery disease (CAD)]]. | ||
* When it does occur in multiple vessels, the prognosis is worse as it may result in [[ventricular tachycardia]] or [[ventricular fibrillation]]. | |||
==Diagnosis== | ==Diagnosis== | ||
Revision as of 18:56, 2 May 2014
|
Chronic stable angina Microchapters | ||
|
Classification | ||
|---|---|---|
| ||
| ||
|
Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
|
Diagnosis | ||
|
Alternative Therapies for Refractory Angina | ||
|
Discharge Care | ||
|
Guidelines for Asymptomatic Patients | ||
|
Case Studies | ||
|
Coronary vasospasm On the Web | ||
For patient information, 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, prinzmetal angina, prinzmetal's 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.
- Multifocalocal 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
Iatrogenic
- Coronary vasospasm can be secondary to PCI.
Pathophysiology
- The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known.
- 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.[3]
- 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
- 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.[4] 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.[5] 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.[6] 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.[7] 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.[4]
Natural History, Complications and Prognosis
- The prognosis of vasospastic angina depends on the extent of underlying coronary artery disease (CAD).
- When it does occur in multiple vessels, the prognosis is worse as it may result in ventricular tachycardia or ventricular fibrillation.
Diagnosis
- Physicians should suspect vasospasm if ST segment elevation is detected in patients experiencing angina, and if the ECG completely returns to baseline upon resolution of symptoms.
- Once detected, aggressive management of coronary vasospasm is necessary, as vasospasm can provoke fatal arrhythmias or myocardial infarction.
- The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven to be reversible.
- Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary vasodilators.
- The differential diagnosis of coronary spasm during percutaneous coronary intervention includes:
- Abrupt closure due to dissection or thrombus formation
- ST elevation classically observed on ECG during an episode of vasospasm.
- Intracoronary acetylcholine or ergonovine provocation test used to diagnose vasospasm.
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.[8]
Treatment of PCI-Induced Vasospasm
- Intracoronary vasodilators should be given slowly through guiding catheters with side holes to maximize the delivery into the artery with minimal dispersal through the catheter side holes.
- Intracoronary nitroglycerin 100-300 mcg. Generally well tolerated and have an additive effect.
- Intracoronary calcium channel blockers. Generally well tolerated, have an additive effect, and have a small risk of transient heart block.
- Diltiazem 0.5-2.5 mg/min, up to 5-10 mg
- Verapamil 100 mcg/min, up to 1.0-1.5 mg
- Nicardipine 100-300 mcg
- Nifedipine 10 mg sublingual (SL)
- Intracoronary nitroprusside 100-300 mcg
- Systemic vasodilators
- Nifedipine 10 mg sublingual
- Atropine 0.5 mg IV. Particularly useful in the setting of hypotension or bradycardia.
- Device related treatments
- Removal of interventional hardware with guide wire in place to minimize mechanical provocation. This strategy may minimize distal vessel spasm.
- Repeat prolonged (2-5 min) PTCA at low pressure (1-4 atmospheres). May mechanically "break" vasospasm.
- Stenting. May improve focal spasm, but may simply propagate the site of spasm to a location proximal or distal to the stent within the vessel, so it should be avoided if possible.
Treatments for Chronic Vasospasm
- Calcium channel blockers: Generally, well tolerated and can aid with hypertension control. A combination of dihyropyridine and non-dihydropyridine calcium channel blockers should be used in patients with refractory coronary vasospasm, particularly if it has resulted in ventricular arrhythmia. Multiple calcium channel blockers may be required in patients with refractory or multivessel spasm. A patient who has suffered VT/VF due to spontaneous vasospasm (not due to acute infarction) should also likely undergo ICD placement.
- Diltiazem 240-360 mg PO qd
- Verapamil 240-480 mg PO qd
- Nifedipine XL 60-120 mg PO qd
- Nicardipine 40-160 mg PO qd
- Long-acting nitrates: Generally, well tolerated and can aid with hypertension control.
- Isosorbide mononitrate (Imdur) 60-240 mg PO qd
- Isosorbide dinitrate (Isordil) 20-40 mg PO tid
- Statins: May improve endothelial dysfunction and lower inflammation. A small, randomized control trial showed that fluvastatin 30 mg daily reduced rates of vasospasm. Statins also provide benefits of LDL lowering and plaque stabilization.
- Fluvastatin 30 mg PO qd
- Hormone replacement therapy: This remains controversial, particularly due to the risk of concern of increased cardiac events.
- Smoking cessation: Should be emphasized in all patients, as it contains non-cardiac benefits as well. It lowers future event rates of vasospasm and acute coronary syndromes.
- PTCA/stenting: While resolution occurs following PTCA/stenting in some cases, spasm can propagate to a new location, proximal or distal to the stented site.
- ICD placement: As described above for patients with VT/VF due to spontaneous coronary vasospasm without other provocation that may be treated.
- Surgical autonomic denervation/plexectomy: Can be useful in cases that are refractory to medical therapy or percutaneous intervention. It's reserved only for the most refractory cases.
Making a Selection
PCI-Induced Vasospasm
- Therapeutic treatment of PCI-induced vasospasm should be performed in this order (step-wise fashion):
- Initial step is intracoronary vasodilatation with IC calcium channel blockers and/or nitrates, which should be given slowly when using guiding catheters with side holes to avoid dispersal of the drug through the holes instead of into the coronary artery.
- If one agent is unsuccessful, combined therapy should be implemented as these medications have an additive effect. Be mindful for heart block with CCB therapy.
- IV atropine can be useful if there is associated hypotension of bradycardia.
- Should medical therapy fail, remove all hardware and leave the guide wire in place to maintain position. This may minimize distal vessel spasm.
- Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres).
- Stenting should be a last ditch option, and used if above measures have failed, as it may lead to propagation of spasm to a new location. Refractory vasospasm may be indicative of dissection, which is also an indication for stenting.
Chronic Vasospasm
- Treatment of chronic vasospasm should be performed in this order (step-wise fashion): medical therapy, percutaneous intervention, and then, surgery.
Medical Therapy
- Risk factor modification (smoking cessation, lipid control) is recommended for all patients.
- Begin pharmacologic therapy with oral calcium channel blockers (diltiazem, verapamil, nifedipine) and/or nitrates. If monotherapy is ineffective, begin combination therapy which is generally well tolerated (10% of patients may require 2 calcium channel blockers). If refractory or multi-vessel spasm is present, multiple CCBs are likely necessary, as these patients are at high risk for ventricular arrhythmias. Alpha blockers may also be useful if there is incomplete response to CCB and nitrates.
- Due to their ability to improve endothelial function, statins should be considered for vasospasm.
- Certain medications should be avoided: nonselective beta blockers, aspirin, and sumatriptan can exacerbate vasospasm. Hormone replacement therapy (estrogen-progestin) have been associated with an increase in cardiac events (HERS-II and WHI trials) and should also be avoided.
Percutaneous Intervention (PCI)
- If vasospasm has a clearly definable area that is associated with coronary artery disease and refractory to medical therapy, stenting may be an effective strategy. However, stenting may simply propagate the spasm to a proximal or distal location in the vessel.
- Following any PCI, adjunctive medical therapy must be continued.
- Resolution of symptoms, ECG changes, and angiographic vasospasm is usually apparent within one minute post-procedure.
- Refractory spasm occurring during PCI is likely secondary to dissection, which requires stenting unless the artery is small and the patient is clinically stable.
- The role of revascularization in the setting of multivessel vasospasm is uncertain.
Surgery
- In the rare circumstance that a patient is refractory to pharmacologic and percutaneous therapy, surgical denervation and plexectomy have been effective.
How To Know if Treatment of PCI-Induced Vasospam is Working
Therapies for vasospasm will usually take effect within seconds to one minute. Anticipated outcomes include:
- Resolution of acute or chronic coronary vasospasm
- Resolution of ECG changes (ST depression or elevation)
- Resolution of symptomatic angina and other symptoms, if present
- Repeat angiography
Other Concerns
There are several additional factors that doctors should mindful of when considering coronary vasospasm treatments, complications, and outcomes.
- Coronary vasospasm can lead to life-threatening arrhythmias, depending on the vessel that is involved. Specifically, right coronary artery spasm can lead to sinus arrest or complete heart block, while left anterior descending artery spasm can lead to ventricular tachycardia or fibrillation. Multivessel spasm can also lead to ventricular arrhythmias.
- The right coronary artery ostium is prone to catheter-induced spasm, giving the appearance of an ostial lesion on angiography. Pre-treatment with 200 mcg of IC nitroglycerin should be administered prior to intervention of this area.
- Patients who have coronary artery disease in addition to coronary vasospasm have an overall worse prognosis.
ESC Guidelines for Diagnostic Tests in Suspected Vasospastic Angina (DO NOT EDIT)[9]
| Class I |
| "1. ECG during angina if possible. (Level of Evidence: B)" |
| "2. Coronary arteriography in patients with characteristic episodic chest pain and ST-segment changes that resolve with nitrates and/or calcium channel blockers to determine the extent of underlying coronary disease. (Level of Evidence: B)" |
| Class IIa |
| "1. Intracoronary provocative testing to identify coronary spasm in patients with normal findings or nonobstructive lesions on coronary arteriography and the clinical picture of coronary spasm. (Level of Evidence: B)" |
| "2. Ambulatory ST Segment Monitoring to identify ST-deviation. (Level of Evidence: C)" |
ESC Guidelines for Pharmacological Therapy of Vasospastic Angina (DO NOT EDIT)[9]
| Class I |
| "1. Treatment with calcium channel blocker and if necessary nitrates in patients whose coronary arteriogram is normal or shows only non-obstructive lesions. (Level of Evidence: B)" |
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) - ↑ 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
- ↑ 4.0 4.1 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) - ↑ 9.0 9.1 Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F; et al. (2006). "Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology". Eur Heart J. 27 (11): 1341–81. doi:10.1093/eurheartj/ehl001. PMID 16735367.