Spasmodic Intermittent Constriction of the Brachial Artery Causing Upper Extremity Claudication
Umer Malik, MD1 â— M. Habeeb Ahmed, MD, FABHP, RVT2 â— Robert Dieter, MD, RVT, FACC3 â— Aravinda Nanjundappa, MD, FACC, FSCAI, RVT4
From the 1Department of Internal Medicine, San Joaquin General Hospital; 2Department of Vascular Medicine, Regional Medical Center; 3Department of Interventional Cardiology and Vascular and Endovascular Medicine, Loyola University Health System; 4Department of Medicine, West Virginia University.
Disclosure The authors have no affiliations with any commercial entity that may represent a conflict of interest with the content of this article.
Intermittent dynamic constriction of the arteries has been well known to involve different arterial beds.1-4 We report an unusual case of a patient presenting with such severe intermittent vasospastic constriction of the brachial artery that it resulted in symptoms of decreased blood supply. Angiography of the subclavian territory revealed 99% obliteration of the lumen of the brachial artery during systole, with complete resolution at end diastole. To our knowledge, this is the first reported case of dynamic intermittent vasospasm of the brachial artery.
A 74-year-old woman presented to the outpatient clinic with pain, tingling, and numbness of the left upper extremity that worsened upon exertion. She noted experiencing intermittent weakness of the left upper extremity. Her medical history was significant for hypertension, hyperlipidemia, chronic obstructive pulmonary disease, asthma, hypothyroidism, arthritis, gangrene of the left leg, varicose veins, and peripheral vascular disease. Her surgical history included a hysterectomy and skin grafting. She was an ex-smoker, with a 30-pack-year history of smoking, and she drank occasionally. The patient’s medication included thyroid supplements, an ipratropium inhaler, angiotensin-receptor blockers, and calcium supplements.
The physical examination was notable for different blood pressures in both arms, with a reading of 166/80mm Hg in the right arm and 111/74 mm Hg in the left. Pulses were 2+ in the right upper extremity and 1+ in the left brachial and radial artery. Other significant findings included a 1/6 ejection systolic murmur at the aortic area, a left carotid bruit, and trace edema of the lower limbs. The remainder of the physical examination was normal.
The patient’s different blood pressures and low upthrust of pulses in the left extremity led to suspicion of an underlying vascular problem, and angiography of the subclavian, carotid, and vertebral territory was performed. Severe stenosis of the left brachial artery with almost 99% stenosis during systole (Figure 1) and complete resolution of constriction at end diastole was found (Figure 2). Other angiographic findings included mild-to-moderate left subclavian artery stenosis and mild left vertebral artery stenosis. The patient was started on calcium channel blockers to control her blood pressure and treat the vasospasm of the brachial artery. At the follow-up examination, she was doing well on pharmacotherapy.
In the late 1950s, Myron Prinzmetal first described a “variant” form of angina that was characterized by episodes of cardiac chest pain associated with discernable changes on electrocardiography.4 Today, variant angina is a very well-known entity, characterized by transient reduction in the luminal diameter of the coronaries due to vasospasm, rather than by static obstruction of the lumen (atherosclerosis). Intermittent dynamic contraction has been documented for different vascular beds, including the retinal artery, leading to amaurosis fugax; digital vessels, resulting in Raynaud’s phenomena; and the cerebral vessels, causing cortical migraine and cerebral artery vasospasm after subarachnoid hemorrhage.5,6 A case of vasospasm of the cerebral vessels leading to cerebral infarction was documented by Kuzumoto and colleagues.2 Another report documented dynamic unilateral subclavian artery obstruction due to respiratory variation.7
The brachial artery is a continuation of the axillary artery, which begins at the lower margin of the teres major tendon and terminates by dividing into its two branches, the radial and ulnar arteries. The brachial artery and its branches is the major source of blood supply to the upper extremities; thus, any obstruction of blood flow in these vessels would, at least theoretically, result in signs and symptoms of vascular insufficiency in the entire upper extremity, ranging from numbness and tingling to weakness and pain (especially upon exertion).
Our patient presented with nonspecific signs of vascular ischemia, including claudication, weakness, tingling, and numbness of the left upper extremity; however, her physical examination was more consistent with obstruction of blood flow, demonstrated by unilateral low blood pressure and decreased upthrust of pulses in one the left arm. Angiography was performed to resolve the mystery, which revealed complete constriction of the brachial artery during systole, with almost 99% obliteration of the lumen, and complete resolution during diastole. Nontraumatic obstruction of blood flow is a very rare phenomenon, and while this may be recognized to occur in some arterial beds, there are no other reports in the literature of this occurring in the territory of the brachial artery, as was found in our patient.
Calcium channel blockers have been shown to help resolve vasospastic episodes of the vascular bed,8-11 which is why we used this medication in our patient. The treatment appeared to be effective, and during her follow-up examination. The patient noted improvement in the weakness and numbness of the left upper extremity.
With increasing use of angiographic interventions to visualize the peripheral vascular bed, the likelihood is high that more cases of spastic vascular insufficiency of different vascular beds will be uncovered. Physicians should consider evaluating patients who have pain in the upper extremities for underlying vasospastic constriction of the brachial artery once common causes of upper extremity pain are ruled out. It is certainly possible that brachial artery constriction is a common but unrecognized entity.
1. Heckmann JG, Gaul C, Neundörfer B, Harazny J, Michelson G. Vasospastic amaurosis fugax. J Neurol Neurosurg Psychiatry. 2003;74(2):149.
2. Kuzumoto Y, Mitsui Y, Ueda H, Kusunoki S. Vasospastic cerebral infarction induced by smoking: a case report [in Japanese]. No To Shinkei. 2005;57(1):33-36.
3. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris. I. A variant form of angina pectoris; preliminary report. Am J Med. 1959;27:375-388.
4. Maseri A, Chierchia S. Coronary artery spasm: demonstration, definition, diagnosis, and consequences. Prog Cardiovasc Dis. 1982;25(3):169-192.
5. Burger SK, Saul RF, Selhorst JB, Thurston SE. Transient monocular blindness caused by vasospasm. N Engl J Med. 1991;325(12):870-873.
6. Winterkorn JM, Kupersmith MJ, Wirtschafter JD, Forman S. Brief report: treatment of vasospastic amaurosis fugax with calcium-channel blockers. N Engl J Med. 1993;329(6):396-398.
7. Dieter RS, Morshedi-Meibodi A, Ahmed MH, et al. Description of a new angiographic sign: dynamic left subclavian artery obstruction. Vasc Dis Manag. 2006;3(5):334-336.
8 Miller FW, Santoro TJ. Nifedipine in the treatment of migraine headache and amaurosis fugax in patients with systemic lupus erythematosus. N Engl J Med. 1984;311(14):921.
9. Rodeheffer RJ, Rommer JA, Wigley F, Smith CR. Controlled double-blind trial of nifedipine in the treatment of Raynaud’s phenomenon. N Engl J Med. 1983;308(15):880-883.
10. Hillis LD, Braunwald E. Coronary-artery spasm. N Engl J Med. 1978;299(13):695-702.
11. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298(6674):636-642.
Figure 1—Angiography of the left brachial artery showing almost 99% stenosis during systole.
Figure 2—Angiography of the left brachial artery showing complete resolution of constriction at end diastole.