Coronary vasospasm: Difference between revisions
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**Removal of interventional hardware with guide wire in place to minimize mechanical provocation. This strategy may minimize distal vessel spasm. | **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. | **Repeat prolonged (2-5 min) PTCA at low pressure (1-4 atmospheres). May mechanically "break" vasospasm. | ||
**Stenting. This | **Stenting. This 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=== | ===Treatments for chronic vasospasm=== | ||
Revision as of 17:11, 22 June 2010
| Coronary vasospasm | |
| ICD-9 | 413.1 |
|---|---|
| DiseasesDB | 13727 |
| MedlinePlus | 000159 |
| eMedicine | med/447 |
| MeSH | D003329 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Synonyms and related key words: 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. Also, the vasospasm can either be focal or multifocal (which compromises more than one vessel).
Subtypes of Vasospasm
A subtype of epicardial coronary artery spasm is known as Prinzmetal's angina. In this subtype of epicardial coronary artery vasospasm, symptoms typically occur at rest, rather than on exertion (thus attacks usually occur at night). Two-thirds of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms. Prinzmetal's angina is typically associated with specific EKG changes (elevation rather than depression of the ST segment).
(Cardiac) syndrome X is angina (chest pain) with signs associated with decreased blood flow to heart tissue but with normal coronary arteries. It is thought to involve the coronary microvasculature rather than the large epicardial arteries. It occurs more often in young women. Some studies have found increased risk of other vasospastic disorders in syndrome X patients, such as migraine and Raynaud's phenomenon. It is treated with calcium channel blockers, such as nifedipine, and usually carries a favorable prognosis. This is a distinct diagnosis from Prinzmetal's angina which involves spasm of the main epicardial coronary arteries. Syndrome X involves spasm of the downstream microvasculature.
Coronary vasospasm can occur in either a single epicardial coronary artery or in multiple epicardial coronary arteryies. [1][2] When it does occur in multiple vessels, the prognosis is worse as it may result in ventricular tachycardia or ventricular fibrillation. The patient with multivessel spasm may benefit from dual calcium channel blockade.
Pathophysiology
The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known. Sometimes coronary vasospasm is induced by angioplasty (PCI-induced), which occurs secondary to endothelial denudation and nitric oxide loss. Others are catheter-induced, which is caused by a contact of a catheter without balloon deployment. Catheter-induced coronary vasospasms are usually short-lived. They are most prone to occur at the ostium of the right coronary artery (RCA), and the left main is less susceptible to ostial spasm. Additionally, the autonomic nervous system and endothelial dysfunction can lead to chronic intermittent vasospasm, which usually occurs where a fixed, noncalcified stenosis is located.
Epidemiology
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. Also, rotoblator cases are more prone to coronary vasospasm, with a 4-36% incidence.
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.
Differential Diagnosis of Underlying Causes of Coronary Vasospasm
(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
Treatment
The main goals of treating coronary vasospasm are to reverse the spontaneous, abrupt luminal diameter reduction, reverse PTCA-induced vasospasm, and to 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.[3]
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 5-10mg
- 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 10mg sublingual
- Atropine 0.5mg 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. This 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. 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. A patient who has suffered VT/VF due to spontaneous vasospasm (not due to acute infarction) should also likely undergo ICD placement.
- Diltiazem 240-360mg PO qd
- Verapamil 240-480mg PO qd
- Nifedipine XL 60-120mg PO qd
- Nicardipine 40-160mg PO qd
- Long-acting nitrates
- Isosorbide mononitrate (Imdur) 60-240mg PO qd
- Isosorbide dinitrate (Isordil) 20-40mg PO tid
- Statins
- Fluvastatin 30mg 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. It lowers future event rates of vasospasm and acute coronary syndromes.
- PTCA/stenting
- 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 is reserved only for the most refractory cases.
One Sequence of Treatment Choices to Manage PCI-Induced Vasospasm
Therapeutic treatment of PCI-induced vasospasm should be performed in this order:
- Intracoronary vasodilators (either nitroglycerin or calcium channel blockers may be given first
- Combined therapy of intracoronary nitroglycerine and calcium channel blockers
- Removal of hardware with guidewire in place
- Repeat PTCA
- Stenting if above measures have failed. Refractory vasospasm may be indicative of dissection, which is also an indication for stenting.
How To Know if Treatment of PCI-Induced Vasospam is Working
Therapies for vasospasm will usually take effect within seconds to one minute.
- Repeat angiography
- Resolution of ECG changes (ST depression or elevation)
- Resolution of symptoms, if present
Pathological Findings
-
Coronary artery: Intramural Left Anterior Descending Artery: Micro, low mag, morphologically normal artery 72 years old female who developed anterior myocardial infarction after cholecystectomy -
Coronary artery: Intramural Left Anterior Descending Artery: Micro, med mag, trichrome, abnormal media with fibrous tissue, 72 years old female who developed anterior myocardial infarction after cholecystectomy, There is no sign of atherosclerosis, but left anterior descending artery is intramural.
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) - ↑ 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)
Further reading
- Hibino H, Kurachi Y (2006). "A new insight into the pathogenesis of coronary vasospasm". Circ. Res. 98 (5): 579–81. doi:10.1161/01.RES.0000215571.12500.ab. PMID 16543506. Unknown parameter
|month=ignored (help)