Coronary Artery Vasospasm Clinical Presentation

  • Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Eric H Yang, MD   more...
 
Updated: Apr 19, 2012
 

History and Physical Examination

Patients with coronary artery vasospasm typically describe anginal symptoms, including retrosternal pain or pressure with radiation to the neck, jaw, left shoulder, or arm. This may be particularly true if there is significant coexistent atherosclerosis.[27] Notably, symptoms associated with vasospastic angina often occur at rest and may exhibit a circadian pattern, with most episodes occurring in the early hours of the morning.[4] In severe cases, associated arrhythmias may be present, ranging from heart block to ventricular tachycardia.[28]

Distinguishing unstable angina pectoris related to coronary atherosclerosis from variant angina may be difficult and require special investigations for diagnosis, including coronary angiography. In some patients, the distinction may be an arbitrary one because it is likely that vasospasm is both a cause and a consequence of plaque rupture and thrombosis in patients with unstable angina pectoris.

In addition, many patients with variant angina have obstructive coronary artery disease (CAD). Indeed, in as many as 60% of cases, coronary artery vasospasm occurs at a site with preexisting coronary atherosclerosis,[15] which suggests that underlying arterial dysfunction may be a predisposing factor for spasm.

Although spasm is more likely to occur in the presence of atherosclerotic lesions, the absence of traditional risk factors for atherosclerotic CAD may make vasospastic angina more likely; the exception is cigarette smoking, which is a common risk factor for both clinical syndromes.[14] Spasm is found more often in patients with symptoms that occur at rest (55.5%) than in those with exertional angina (27.7%).[16]

A minority of patients with variant angina may have a more systemic abnormality of vasomotor tone; this may include symptoms of migraine headache and Raynaud phenomenon.[29]

No features on physical examination are specific for vasospastic angina. Signs may be absent between symptomatic episodes. During periods of angina, physical findings relating to ischemia and ventricular dysfunction may be present, including rales, jugular venous distention, peripheral edema, extra heart sounds, ectopy or other arrhythmia (eg, tachycardia or bradycardia), and murmurs (such as occur with ischemic mitral regurgitation).

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Complications

Myocardial infarction (MI) is a potential complication of variant angina, especially in the myocardial territory corresponding to the location of the electrocardiographic (ECG) changes during previous anginal attacks. The incidence of MI depends on diagnostic criteria, but has been reported to be as high as 30% in some series.

The incidence and prognosis of MI in patients with variant angina appear to be associated with the extent and severity of any underlying atherosclerotic coronary stenoses. Adverse outcomes are more likely and survival poorer in patients with multivessel atherosclerotic CAD.[23]

Arrhythmias may occur with severe vasospastic angina. Both atrioventricular conduction abnormalities and ventricular arrhythmias can cause life-threatening hemodynamic deterioration and syncope. The risk of sudden death is approximately 2% and is most common in patients with multivessel spasm[25] and prior serious arrhythmia during anginal attacks. In extreme cases, defibrillator implantation may be considered.[30]

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Contributor Information and Disclosures
Author

Stanley S Wang, MD, JD, MPH  Clinical Cardiologist, Austin Heart South; Director of Legislative Affairs, Austin Heart; Director, Sleep Disorders Center at Heart Hospital of Austin; Assistant Professor of Medicine (Adjunct), University of North Carolina School of Medicine

Stanley S Wang, MD, JD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Sleep Medicine, American College of Cardiology, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, American Stroke Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital, University of North Carolina at Chapel Hill School of Medicine

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Gregory J Dehmer, MD Director, Division of Cardiology, Scott & White Healthcare; Professor of Medicine, Texas A&M Health Science Center College of Medicine

Gregory J Dehmer, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

References

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This electrocardiogram (ECG) is from a patient who underwent urgent cardiac catheterization, which revealed diffuse severe coronary spasm (most marked in the left circumflex system) without any fixed obstructive lesions. Severe left ventricular wall motion abnormalities were present, involving the anterior and inferior segments. A question of so-called takotsubo cardiomyopathy (left ventricular apical ballooning syndrome) is also raised (see Bybee et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Int Med 2004:141:858-65). The latter is most often reported in postmenopausal, middle-aged to elderly women in the context of acute emotional stress and may cause ST elevations acutely with subsequent T wave inversions. A cocaine-induced cardiomyopathy (possibly related to coronary vasospasm) is a consideration but was excluded here. Myocarditis may also be associated with this type of ECG and the cardiomyopathic findings shown here. No fixed obstructive epicardial coronary lesions were detected by coronary arteriography. The findings in this ECG include low-amplitude QRS complexes in the limb leads (with an indeterminate QRS axis), loss of normal precordial R wave progression (leads V1-V3), and prominent anterior/lateral T wave inversions. Image courtesy of http://ecg.bidmc.harvard.edu .
 
 
 
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