Novel Presentation of Acute Pericarditis in an Ironman Triathlete

Introduction Nonsteroidal anti-inflammatory drugs (NSAIDs) are ubiquitous, with roughly 100 million taken in the United States every day. Although certainly beneficial to athletes, and others with acute pain, they are not without side effects. Each year in the United States about 16,000 people suffer a fatal gastrointestinal hemorrhage, roughly equal to the number of those who die from AIDS. Other serious side effects include acute renal failure, often precipitated by dehydration and hepatic injury. The effect of NSAIDs on the distal renal tubule, mediated by cyclo-oxygenase-2, inhibits the clearance of free water, and may lead to the development of exercise-associated hyponatremia (EAH) [1]. Recently it has also been shown that NSAIDs interfere with the cardioprotective effect of aspirin if taken concurrently [2]. Anti-inflammatory loading is a technique practiced by some marathon runners and triathletes, who routinely damage muscles through training and racing. Ibuprofen and other NSAIDs, taken regularly the week before an event, are thought to establish a therapeutic blood level that will prevent inflammation as it develops. The rationale for taking them during training, but not on race day, is to hopefully prevent renal injury and EAH. This case is somewhat unusual, in that the religious use of ibuprofen may have masked the symptoms of acute pericarditis. The athlete's experience and interaction with the medical community is both interesting and informative. Case Report The Ironman triathlon is a grueling challenge, combining a 2.4-mile swim, a 112-mile bicycle ride, and a 26.2-mile (marathon) run. Professional athletes can complete the course in 8 to 8.5 hours, and many top amateurs finish within 30 to 60 minutes of the winning time. Although training schedules vary by individual, most competitors swim 3 to 5 miles, cycle 150 to 250 miles, and run 40 to 45 miles each week, for the 2 months prior to an event. NSAIDs are commonly used by endurance athletes during training and racing. Recent accounts of some competitors suffering from acute renal failure or EAH, have led others to load NSAIDs during the week preceding a race, and then avoid them on race day. The inaugural Ironman Coeur d'Alene in 2004 saw 1800 competitors lined up at water's edge on race morning. This case report involves an accomplished 44-year-old man who had completed Ironman Canada in 2002 and 2003, with a best time of 10 hours and 22 minutes. He lived on a lake in Canada, and trained seriously. Each year he developed seasonal rhinitis when swimming, presumably due to water-borne pollens. He generally preferred to tolerate the symptoms of nasal congestion and itching eyes, rather than experience the way decongestants and antihistamines made him feel. He arrived in Coeur d'Alene, Idaho, 8 days before the race, to familiarize himself with the course and acclimatize to the environmental conditions. A coach had recommended anti-inflammatory loading, so he was taking two 200-mg ibuprofen tablets three times a day, with food (1200 mg total dose). His allergies were in full bloom, and he was symptomatic on each of the six practice swims he completed. While running, 2 days before the race, he noticed labored breathing for the easy pace he had set. His training partner noticed it as well, but they both ignored the symptom. Race morning he had a good swim the first lap, but soon after starting his second noticed tightness in the chest, expiratory wheezing, and confusion. Out of the water, he coughed and hacked through the transition area, then passed right by his wife without acknowledging her presence. He had trouble finding his bicycle, although it was near the front row, and then had difficulty mounting-up. His confusion cleared about 15 miles into the cycling segment, but he remembers having no power in his legs. On a tough climb that was relatively easy 3 weeks earlier, he was now gasping for air, with a heart rate of only 135 to 140 beats/min. Nausea prevented him from taking much in the way of fuel or fluids, and he recalls shivering, despite the sunny day with warm temperatures. After 70 miles, he began coughing up blood, and dropped out of the race. The desk clerk at his hotel was so concerned about his appearance that she called a doctor to evaluate him. He was diagnosed with EAH and a ruptured blood vessel in his throat from coughing. He was directed to the medical tent, but on arrival felt better and didn't want to wait for assistance. Upon returning home he consulted his physician, and together they decided this must have been a case of exercise-induced asthma. Referral to a specialist revealed normal pulmonary function testing. An electrocardiogram (ECG) was said to show cardiac injury, but results of all of his blood tests were normal. After 2 weeks of rest, a repeat ECG was read as normal and an echocardiogram revealed only an enlarged heart, which is normal for endurance athletes. It was felt that he had suffered cardiac injury and swelling from the fluid retention that commonly accompanies the use of NSAIDs. Once cleared to resume training, he went on to a personal best at Ironman Canada, finishing in 10 hours and 15 minutes. This qualified him for the Ironman Triathlon World Championship in Hawaii, and he has raced many times since then, with no similar symptoms. Discussion Acute pericarditis is usually mild, and uncomplicated cases resolve in a few weeks without sequelae. It is defined as an inflammatory condition of the pericardial sac, and origins of the great vessels. The disease process usually results in 100- to 200-mL of serous fluid, containing inflammatory cells and fibrin, accumulating in the pericardial sac. Purulent effusion is seen in immunocompromised patients with HIV, and rarely tuberculosis. The most common etiology is a viral infection (usually coxsackievirus), but it can also be caused by bacteria, mycobacteria, and fungi. Noninfectious causes of pericarditis include myocardial infarction (MI), renal failure, malignancy, medications, autoimmune disease, and trauma (Table 1).Table 1: Causes of pericarditisThe typical presentation involves central, pleuritic chest pain, with radiation to the left shoulder, and characteristically the trapezius region. Pain is made worse by deep inspiration or lying down, and relieved by leaning forward. Clinically the signs are subtle, and may include a pericardial friction rub, except with large effusions. In more severe cases, patients may present with tachycardia, hypotension, pulsus paradoxus, and distended neck veins. Diagnosis requires a high index of suspicion, and confirmatory tests, including an ECG, chest radiograph, and echocardiogram [3]. The ECG certainly provides the highest yield with regard to diagnostic tests. It is easily obtainable, cost effective, and the results are often diagnostic. Echocardiogram is not as readily available (except in a hospital setting), and a pericardial effusion must reach 250 mL before cardiac enlargement is demonstrated on chest radiograph. ECG changes are similar to those of acute MI, therefore the clinician must be able to distinguish between the two conditions. In pericarditis, the ST segment is elevated in nearly all leads, with upward concavity, often referred to as a “smiling face.” The pattern is not focal as with an acute MI, and there is no reciprocal ST depression, or T-wave inversion. Conversely, PR depression may be present. Acute MI usually occurs in anatomically contiguous leads, for example II, III, and aVF with inferior injury. The elevated ST segments demonstrate upward convexity (“sad face”), and often ST depression in the reciprocal leads. There may be T-wave inversion, but no PR depression. Early repolarization involves similar findings, but is often seen in asymptomatic athletes, and on routine electrocardiograms [4]. Other laboratory tests including complete blood count, cardiac enzymes, erythrocyte sedimentation rate, and serum chemistries are sometimes useful in distinguishing between these three conditions. Treatment includes time, rest, and use of NSAIDs. Patients not responding to these may benefit from a brief course of corticosteroids. For those who cannot tolerate either NSAIDs or corticosteroids, colchicine has been shown to be an effective alternative. Two potentially serious complications include cardiac tamponade and chronic, constrictive pericarditis. When an effusion accumulates rapidly and exceeds 250 mL, cardiac output is compromised and can be improved by urgent pericardiocentesis. Constrictive pericarditis results when purulent or persistent fibrinous effusions organize and even calcify, restricting cardiac filling. Both are fortunately uncommon complications of this condition. Although the diagnosis was never made, I believe this athlete demonstrated a case of acute viral pericarditis. He had competed at a high level before and after this event with no similar symptoms, making allergy or exercise-induced asthma unlikely. There was a preceding viral infection or concurrent allergic reaction that may have masked those symptoms. He had significant cardiac decompensation, as evidenced by the difficulty breathing, and inability to perform at a previously demonstrated functional level. Coughing of blood may have represented pulmonary edema, which would also account for the difficulty breathing. Chest pain, the hallmark symptom of pericarditis, was likely masked by regular use of NSAIDs. His ECG, unfortunately obtained a week after the event, still demonstrated changes consistent with pericarditis. There was ST segment elevation in leads V2 to V6, with upward concavity, and no reciprocal ST depression. The PR interval demonstrated some depression, and there were no T-wave inversions (Fig. 1). Within 2 weeks, the ECG findings returned to normal, except for signs of “early repolarization” (Fig. 2).Figure 2: Electrocardiogram after 2 weeks, showing normal results.Figure 1: Electrocardiographic changes of evolving pericarditis.Although pericarditis is not uncommon, I was unable to find a similar case in which a patient not only continued to exercise with this condition, but actually competed in the Ironman Triathlon. I believe this athlete had acute pericarditis, presumably from a viral upper respiratory infection, and developed a pericardial effusion. Assuming this was simply an allergy attack he continued to train and compete. Although he was asymptomatic at rest, the increased oxygen demands of exercise produced acute cardiac decompensation, and eventually lead to pulmonary edema. That he was able to race at all is a testament to the incredible conditioning of these athletes. To recover completely and race again at a high level demonstrates the tremendous resiliency of the myocardium.