Arteriopathy in the High-Performance Athlete

Abstract

Pain occurs frequently in high-performance athletes and is most often due to musculoskeletal injury or strain. However, athletes who participate in sports that require highly frequent, repetitive limb motion can also experience pain from an underlying arteriopathy, which causes exercise-induced ischemia.

We reviewed the clinical records and follow-up care of 3 high-performance athletes (mean age, 29.3 yr; range, 16–47 yr) who were admitted consecutively to our institution from January 2002 through May 2003, each with a diagnosis of limb ischemia due to arteriopathy. The study group comprised 3 males: 2 active in competitive baseball (ages, 16 and 19 yr) and a cyclist (age, 47 yr). Provocative testing and radiologic evaluation established the diagnoses. Treatment goals included targeted resection of compressive structures, arterial reconstruction to eliminate stenosis and possible emboli, and improvement of distal perfusion.

Our successful reconstructive techniques included thoracic outlet decompression and interpositional bypass of the subclavian artery in the 16-year-old patient, pectoralis muscle and tendon decompression to relieve compression of the axillary artery in the 19-year-old, and patch angioplasty for endofibrosis affecting the external iliac artery in the 47-year-old. Each patient was asymptomatic on follow-up and had resumed participation in competitive athletics.

The recognition and anatomic definition of an arteriopathy that produces exercise-induced ischemia enables the application of precise therapy that can produce a symptom-free outcome and the ability to resume competitive athletics.

Pain occurs frequently in high-performance athletes and is most often due to musculoskeletal injury or strain. However, athletes who participate in sports that require highly frequent, repetitive limb motion can also experience pain due to an underlying arteriopathy, which causes exercise-induced ischemia. Although potentially correctable by surgical or endovascular intervention, such arteriopathy is often unrecognized during routine physical examinations. Reasons for lack of recognition include the similarity of symptoms to those caused by the more usual musculoskeletal injury, failure to consider possible medical problems in younger, highly conditioned athletes, and the challenge of eliciting abnormal vascular indings during routine physical examination without provocative testing. Herein, we review our treatments and the postoperative outcomes of 3 high-performance athletes who presented with ischemic symptoms that arose from arteriopathy.

Patients and Methods

We reviewed the clinical records and follow-up care of 3 high-performance athletes (mean age, 29.3 yr; range, 16–47 yr) who were admitted consecutively to our institution from January 2002 through May 2003 with a diagnosis of limb ischemia due to arteriopathy. The study group comprised 3 males: a 16-year-old and a 19-year-old who were active in competitive baseball, and a 47-year-old competitive cyclist (Table I).

TABLE I. Demographic, Sporting, Anatomic, and Clinical Information

In each patient, unilateral limb pain developed in an extremity subjected to highly frequent, repetitive motion arising from the demands of each sport (the baseball players, upper extremity; the cyclist, lower). Pain resulted from the sport-speciic limb motion and was relieved by rest. Each patient was initially evaluated by a team physician or a sports-medicine specialist and was treated conservatively, with a combination of rest and other measures that included nonsteroidal anti-inlammatory drugs, hydrocortisone injections, and physical therapy. In each instance, physical examination elicited no abnormal indings. Persistence of pain prompted provocative testing and radiologic evaluation of all patients (Table I). In the provocative-testing process, the vascular and neurologic portions of the physical examination were re-evaluated under stress or during maneuvers that placed the affected limb in the extreme positions of the sport-specific repetitive motion.

Patient 1

The 16-year-old patient, a baseball pitcher, had also been a football quarterback. One year before developing ischemic symptoms, he had experienced an acromioclavicular shoulder separation of his throwing arm and had undergone successful surgical repair and rehabilitation. He resumed playing baseball until he developed unilateral arm pain that was precipitated by throwing.

Provocative testing showed thoracic outlet compression (TOC) with a decreased arm–brachial index of 0.26 during arm maneuvers. Digital subtraction angiography (DSA) and ultrasonography showed a localized dissection of the subclavian artery with distal brachial artery thrombosis (Figs. 1A and 1B). The patient was treated with thoracic outlet decompression, which included division of the anterior and medial scalene muscles, division of the ibromuscular bands, and 1st-rib resection; brachial thrombectomy; resection of the affected subclavian artery; and an interpositional bypass with a reversed greater saphenous vein.

Fig. 1 Patient 1. Digital subtraction angiography shows A) localized dissection of the subclavian artery with B) distal brachial artery thrombosis.

Patient 2

On examination, the 19-year-old baseball pitcher had a normal radial pulse that was diminished at 90° of abduction and absent at 120° of abduction. Magnetic resonance imaging and DSA were initially performed with the limb in a position of adduction (Fig. 2A). Neither examination showed an anatomic abnormality. However, dynamic cineangiography from a position of adduction to 120° of abduction showed compression and occlusion of the axillary artery immediately distal to the subscapular arterial branch (Figs. 2B and 2C).

Fig. 2 Patient 2. Digital subtraction angiography shows A) normal axillary arterial flow with the right limb in a position of adduction, B) compression of the axillary artery with the right limb in a position of 90° abduction, and C) occlusion of the axillary artery with the right limb in a position of 120° abduction (hyperabduction, overhand throwing position).

The pectoralis minor muscle and tendon, the proximal third of the pectoralis major insertion, and the clavipectoral fascia, all compressing the axillary artery, were surgically decompressed.

Patient 3

The 47-year-old cyclist had a normal pulse rate and a normal ankle–brachial index of 1.06 at rest. However, the latter reading decreased to 0.26 during a treadmill test of 5 min at a 12° grade and 2 mph. Evaluation by DSA revealed mild-to-moderate narrowing of the external iliac artery, suggesting endoibrosis (Fig. 3A). Surgical management via a retroperitoneal approach included an extended patch angioplasty with an external iliac vein. Histopathologic examination of a branch vessel obtained during surgery conirmed the diagnosis of endoibrosis (Fig. 3B).

Fig. 3 Patient 3. A) Digital subtraction angiography reveals mildto-moderate narrowing of the external iliac artery, suggesting endofibrosis. B) A histopathologic operative specimen shows intimal thickening with collagen deposition, smooth-muscle-cell hypertrophy, and absence of inflammatory or atherosclerotic lesions, suggesting endofibrosis (H&E stain; high power [orig. × 450]).

Follow-Up

All 3 patients underwent clinical and noninvasive re-examination during the immediate postoperative period and at 6-month intervals thereafter. The follow-up period totaled 96 patient-months (mean, 32 months; range, 24–48 months).

Results

All patients underwent successful operative repair without morbidity. Each was asymptomatic and showed no abnormalities during postoperative provocative testing. Examinations of patients 1 and 2 showed neither a clinical pulse obliteration during arm maneuvers nor an abnormal decrease of the ipsilateral arm–brachial index during rest or during provocative, noninvasive laboratory evaluation. Patient 3's postoperative treadmill test (5 min at a 12° grade and 6 mph) produced an ankle–brachial index of 0.98 after exercise.

All 3 patients resumed competitive athletic participation with no evidence of recurrent ischemia. The lack of recurrent symptoms, the normal results of clinical examinations, and the normal results of noninvasive testing precluded the need for invasive postoperative radiologic evaluation.

Discussion

Multiple factors can individually or collectively cause arteriopathy that evokes exercise-induced ischemia. These include direct vascular compression by muscle or tendon, the cumulative effects of recurrent localized injury, variable individual autoimmune and inflammatory responses, and the additive effect of extrinsic, contact-induced trauma. Sport-speciic repetitive motion, weight training, and cross-training can result in muscular development that leads to mechanical vascular compression. This has been shown in athletes such as baseball players who use a repetitive throwing motion, and particularly in pitchers, who may develop TOC consequent to the development of the anterior and medial scalene muscles.^1–3 In the athlete who throws repetitively, TOC of arterial structures is more often due to soft-tissue (muscular) hypertrophy than to compression from a cervical rib; the latter is frequently the case in the general population.^3,4 Despite a primary muscular origin (anterior and medial scalene hypertrophy) of this type of TOC, resection of the 1st rib is usually required in the throwing athlete to provide exposure adequate to permit end-to-end anastomosis of an interpositional bypass.

Although TOC syndrome arising from compression of the subclavian artery has been documented in the proximal throwing limbs of high-performance athletes, other reports^5,6 and our study additionally noted distal arterial compromise at the level of the axillary artery. Rohrer and colleagues⁵ observed a 20-mmHg mean pressure difference of the upper extremity and radiologic compression of the axillary artery in the throwing position of baseball pitchers, position players, and a control group of non-athletes. Within that study group, pitchers experienced the highest degree of compression and occlusion during provocative maneuvers. The researchers believed that the additive effects of mechanical compression of the axillary artery due to the throwing motion itself, along with the development and hypertrophy of the pectoralis major and minor muscle groups in pitchers, accounted in part for this finding. Of the 2 muscle groups, hypertrophy of the pectoralis minor muscle and compression by its tendon were considered especially important in the compromise of axillary artery flow. This hypothesis was further supported by cadaver studies that showed direct compression of the subclavian and axillary arteries in the extremes of the throwing position.⁵

Recognizing arteriopathy as the source of exercise-induced ischemia and pain is important in directing therapy. Documenting the anatomic location of the arteriopathy is equally important in determining prognoses and applications of speciic interventions. Durham and associates⁶ concluded that most patients with TOC syndrome and a subclavian artery arteriopathy would require surgical correction and would benefit from early intervention. However, patients with arteriopathy arising from compression of the axillary artery by the pectoralis muscle or tendon and the humeral head may beneit from nonoperative therapy, including exercise modiication. Therefore, these patients would beneit from a trial of conservative management before operative intervention.

Direct mechanical compression of an artery with or without the influence of extrinsic sports-related, contact-induced trauma is one of several equally important factors that can cause arteriopathy and resultant exercise-related ischemia. The arteriopathy may occur in any limb subjected to highly frequent, repetitive motion. As we show herein, endofibrosis characterized by intimal thickening with collagen deposition, smooth-muscle-cell hypertrophy, and absence of inflammatory lesions or atherosclerosis can also cause exercise-induced ischemia^7–11 (Fig. 3B). No clear or potentially important origin of this type of arteriopathy has been suggested, beyond the interaction of autoimmune and inflammatory responses to localized trauma in limbs subjected to highly frequent, repetitive motion.^8,9 In addition, there is no consensus regarding therapeutic intervention. Scavee and associates¹⁰ recommended complete resection of an affected artery with an interpositional bypass replacement. However, we discovered that a less aggressive procedure, patch angioplasty, produced an effective, durable outcome in our patient. To our knowledge, ours is the 1st such patient to have been treated by this method.

The primary symptom of each patient in our study was pain, which is the most frequently occurring ischemic symptom in athletes who experience arteriopathy related to highly frequent, repetitive limb motion. Other ischemic symptoms have also been documented,^12–14 including numbness, weakness, and susceptibility to fatigue. When these symptoms occur without pain in the throwing arms of athletes, the clinical findings are often described as “dead-arm syndrome.”¹³ The evaluation of and the therapeutic approach to these patients and to patients who present with pain is identical.^12,14

Our results, which show successful, lasting outcomes with no symptoms and the resumption of participation in competitive athletics after surgery, attest to the importance of establishing a diagnosis in order to direct therapy precisely. In addition, the application of various surgical approaches and techniques in these patients conirms the importance of precise anatomic deinition of disease distribution in order to apply patient-speciic interventions. When athletes experience recurrent exercise-induced pain or accelerated fatigue, they may have a localized musculoskeletal injury or strain that would improve with rest and conservative treatment. The persistence of such symptoms warrants a vascular examination that includes provocative testing in order to rule out or diagnose an arteriopathy that underlies exercise-induced ischemia. Prompt intervention to correct the arteriopathy can improve distal perfusion and enable the athlete to return to optimal activity in his chosen sport.