Cardiolite

We report a case of a marathon runner who presented with chest tightness, ST-segment depression, and ventricular fibrillation following treadmill exercise testing. At cardiac catheterization, the patient was found to have an isolated lesion in the left anterior descending (LAD) artery that was hemodynamically insignificant by accepted angiographic and coronary flow reserve standards. Ventricular fibrillation was thought to be idiopathic, and an implantable cardioverter defibrillator was placed. Chest pain and ST-segment depression followed by ventricular fibrillation was reproduced during follow-up treadmill testing, prompting reconsideration of the original diagnostic hypothesis. A coronary stent was deployed in the LAD artery. The patient has been asymptomatic and arrhythmia free during follow-up treadmill testing and recreational running. (CHEST 2000; 118:249-252)

Key words: exercise testing; marathon runner; ventricular fibrillation

Abbreviations: CAD = coronary artery disease; CFR = coronary flow reserve; ICD = implantable cardioverter defibrillator; LAD = left anterior descending; VF = ventricular fibrillation

Ventricular fibrillation (VF) is the most common manifestation of electrical instability associated with sudden cardiac death. When VF occurs, it is usually associated with severe coronary artery disease (CAD). Exercise-induced VF is rare in healthy subjects without a history of CAD; however, there are reports of sudden arrhythmic death associated with vigorous physical exertion in persons with occult CAD.[1,2] Asymptomatic myocardial ischemia during peak or symptom-limited exercise testing can precipitate threatening ventricular arrhythmias in patients with CAD.[3] Coronary lesions [is less than or equal to] 70% diameter stenosis and/or with coronary flow reserve (CFR) [is greater than] 2.0 are generally considered to be hemodynamically insignificant. In this report, we describe a marathon runner with an isolated left anterior descending (LAD) coronary artery lesion of [is less than] 70% and CFR of 2.7, who experienced VF during maximal treadmill testing. A defibrillator was implanted for presumed idiopathic exercise-induced VF. VF was subsequently reproduced with maximal exercise testing, terminated by the defibrillator, and finally prevented by successful percutaneous transluminal coronary angioplasty to the mid LAD coronary artery.

CASE REPORT

A 59-year-old male marathon runner with no significant medical history presented with mild chest tightness after running 4 to 5 miles. He had no associated difficulty in breathing, palpitations, diaphoresis, nausea, lightheadedness, dizziness, or syncope. Based on his age and symptoms, the patient was classified at an intermediate-to-high probability of having significant CAD.[4] Baseline resting ECG showed normal sinus rhythm with a normal QT interval and no ST-segment or T-wave abnormalities. He underwent a conventional treadmill exercise test during which he exercised for 13 rain (Bruce protocol[5]) and achieved 106% of his age-predicted maximal heart rate. During stage V (5.0 miles/h, 18% grade), he developed mild left-sided chest tightness and the test was terminated. The ECG at peak exercise showed 1.5 to 2.0 mm ST-segment depression in the inferolateral leads (Fig 1). During recovery, the patient developed a junctional rhythm that deteriorated to VF (Fig 2) and was promptly defibrillated with 200 J. He was admitted to the hospital for surveillance and further management.

[Figures 1-2 ILLUSTRATION OMITTED]

The patient had no personal or family history of CAD, diabetes mellitus, hypertension, hypercholesteremia, cigarette smoking, alcohol abuse, or IV drug use. He was physically active. His training included running 8 to 10 miles, 3 to 4 times per week. Moreover, he did not take any medications at the time.

His physical examination revealed a resting BP of 160/90 mm Hg and heart rate of 82 beats/min. He was alert and oriented and was in no acute distress. Neck examination showed normal jugular venous pressure without carotid bruits. Lungs were clear bilaterally. Results of heart examination were normal without murmur or gallop. Extremities showed no edema, and he had good pulses bilaterally.

Laboratory evaluation revealed normal electrolyte, calcium, and magnesium values. Cardiac enzyme measurements were negative (creatinine kinase-MB fraction [is less than] 5% of total creatine kinase). Cardiac catheterization revealed a 50% eccentric lesion in the mid LAD coronary artery. The remaining coronaries were angiographically normal. Left ventriculography showed normal left ventricular function (ejection fraction, 60%). Doppler ultrasound coronary flow reserve indicated the LAD lesion to be hemodynamically insignificant (CFR, 2.7). A two-dimensional echocardiogram confirmed normal left ventricular function and the absence of valvular diseases.

The patient received an implantable cardioverter defibrillator (ICD) for presumed idiopathic VF. He was started on metoprolol tartrate, which was discontinued because of severe fatigue, and he was referred to the outpatient cardiac rehabilitation program for ECG-monitored exercise prior to returning to endurance training. A repeat exercise test with concomitant myocardial perfusion imaging (Cardiolite; Dupont Pharmaceuticals; Wilmington, DE) was performed. He exercised for 13 min on the Bruce protocols and achieved 102% of his age-predicted maximal heart rate. Once again, the ECG showed 1.5 to 2.0-mm horizontal-to-upsloping ST-segment depression in inferior and lateral leads associated with mild chest tightness. The test was stopped due to fatigue. Four minutes into recovery, the patient developed VF, which was promptly terminated by the defibrillator. Nuclear imaging revealed a subtle anterior reversible defect.

The patient underwent repeat coronary angiography with intravascular ultrasound that demonstrated a 60 to 70% eccentric stenosis in the mid LAD coronary artery. Angioplasty was performed with placement of a 4.0 x 16.0-mm stent (NIR; Boston Scientific, Boston, MA) to the mid LAD artery. The region of stenosis was eliminated (Fig 3, top and bottom). Repeat intravascular ultrasound demonstrated excellent luminal enlargement, stent symmetry, and apposition. After 4 weeks, the patient underwent a third treadmill exercise test. He exercised for 11 min and achieved 99% of his age-predicted maximal heart rate. There were no ischemic ECG changes or symptoms. He was enrolled in a phase II cardiac rehabilitation program and completed 18 ECG telemetry-monitored sessions without symptoms or threatening arrhythmias. He has subsequently resumed long-distance running.

[Figure 3 ILLUSTRATION OMITTED]

DISCUSSION

VF during exercise treadmill testing is rare. In one widely quoted study,[6] involving 170,000 exercise stress tests performed in 73 medical centers, the mortality rate was one death per 10,000 tests (0.01%), and the combined morbidity/mortality rate was 4/10,000 (0.04%). A 1980 survey[7] of 518,448 exercise stress tests conducted at 1,375 centers revealed a 50% lower mortality rate, 0.5 deaths/10,000 tests (0.005%), but a higher combined complication rate 8.86/10,000 tests (0.09%). Another review[8] of the complication rates of exercise testing involving 11 reports from 1969 to 1995 revealed average morbidity and mortality rates of 0.028% and 0.005%, respectively.

The prevalence of exertion-related sudden cardiac death in athletes is similarly low. In a study of 215,413 marathon runners participating in US Marine Corps or civilian marathons over a 19-year period, the prevalence of sudden death during or immediately following a marathon was 0.002% (1 in 50,000).[9] Although the incidence of sudden cardiac death among marathon runners is low (one death in 215,000 h), it is higher than for other types of exercise such as noncompetitive running (one death per 396,000 h), cross country skiing (one death per 607,000 h), or noncompetitive exercise (one death per 375,000 h).[10-12]

Out-of-hospital VF occurs predominantly in three clinical settings. One is as a complication of acute myocardial infarction; another is as a manifestation of transient myocardial ischemia, especially during or after vigorous physical exertion; and a third is as an event that appears to be unassociated with overt ischemia, for example, during inactivity. The latter often occurs in the setting of advanced CAD and, in all probability, shares an ischemic etiology at the cellular level. Myocardial ischemia is clearly the most common trigger for ventricular tachycardia, VF, or both.[13] In this case, myocardial ischemia was suspected clinically on the basis of exertional symptoms and exercise-induced ST-segment depression. However, angiographic findings did not support this hypothesis.

Pathophysiologic evidence suggests that vigorous physical exertion may, by increasing myocardial oxygen consumption and simultaneously shortening coronary perfusion time, evoke myocardial ischemia, which can precipitate ventricular tachycardia or VF. The sympathetic stimulation associated with strenuous exercise can cause regional variations in coronary blood flow and oxygen delivery and hence dyshomogeneity of the electrophysiologic milieu even in the absence of a compromised coronary circulation.[14,15] In addition to symptomatic or silent ischemia,[16] sodium-potassium shifts, increased catecholamine excretion, and circulating free fatty acids may be arrhythmogenic (Fig 4).

[Figure 4 ILLUSTRATION OMITTED]

The present case illustrates the limitations of coronary angiography and CFR standards in assessing lesion severity in highly trained endurance athletes. Although lesions with diameter stenoses [is less than] 70% and/or CFR [is greater than] 2.0 are generally considered hemodynamically insignificant, the present case suggests that mild-to-moderate coronary obstruction can elicit myocardial ischemia and associated sequelae at supra normal exercise levels, resulting in VF.

The decision to employ an ICD in a 59-year-old patient in whom myocardial ischemia is suspected but not proven is difficult. When chest pain and ischemic ST-segment depression precede VF and a clear target vessel is identified, correction of the underlying coronary lesion is often sufficient therapy. In this case, the failure of the coronary lesion to meet accepted angiographic and CFR standards for hemodynamic significance led to the conclusion that the exercise-induced VF would not be prevented by revascularization and an ICD was placed. Although this management approach proved erroneous, it was prudent nevertheless. The fallacious belief that exercise-induced VF could be successfully treated by primary angioplasty to an "insignificant" coronary lesion without ICD is more likely to result in tragedy than the scenario described here.

CONCLUSION

The present case is unique in that a hemodynamically insignificant coronary lesion by accepted angiographic criteria and coronary blood flow measurements reproducibly caused myocardial ischemia and VF after physical exertion. VF was presumed idiopathic on the basis of the angiography and CFR, and the patient underwent cardioverter-defibrillator implantation. The reproduction of ST-segment depression, chest pain, and VF during exercise testing prompted reconsideration of the idiopathic VF hypothesis and led to an ultimately successful albeit unconventional intervention (ie, coronary angioplasty of a 60 to 70% lesion).

REFERENCES

[1] Waller BF, Roberts WC. Sudden death while running in conditioned runners age 40 years or over. Am J Cardiol 1980; 45:1292-1300

[2] Thompson PD, Stern MP, Williams P, et al. Deaths during jogging or running: a study of 18 cases. JAMA 1979; 242: 1265-1267

[3] Hong RA, Bhandari AK, McKay CR, et al. Life threatening ventricular tachycardia and fibrillation induced by painless myocardial ischemia during exercise testing. JAMA 1987; 257:1937-1940

[4] Gibbons RA, Balady GJ, Beasely JW, et al. ACC/AHA guidelines for exercise testing. J Am Coll Cardiol 1997; 30:260-315

[5] Brace RA, Kusumi F, Hosmer D. Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J 1973; 85:546-562

[6] Rochmis P, Blackburn H. Exercise tests: a survey of procedures, safety, and litigation experience in approximately 170,000 tests. JAMA 1971; 217:1061-1066

[7] Stuart RJ Jr, Ellestad MH. National survey of exercise stress testing facilities. Chest 1980; 77:94-97

[8] Franklin BA, Gordon S, Timmis GC, et al. Is direct physician supervision of exercise stress testing routinely necessary? Chest 1997; 111:262-265

[9] Maron BJ, Poliac LC, Roberts WO. Risk of sudden cardiac death associated with marathon running. J Am Coll Cardiol 1996; 28:428-431

[10] Hillis WS, McIntyre PD, Maclean J, et al. Sudden death in sport. Br Med J 1994; 309:657-660

[11] Thompson PD, Funk E J, Carleton RA, et al. Incidence of death during jogging in Rhode Island from 1975 through 1980. JAMA 1982; 247:2535-2538

[12] Cobb LA, Weaver WD. Exercise: a risk factor for sudden death in patients with coronary heart disease. J Am Coll Cardiol 1986; 7:215-219

[13] Coggins DL, Flynn AE, Austin RE, et al. Nonuniform loss of regional flow reserve during myocardial ischemia in dogs. Circ Res 1990; 67:253-264

[14] Hirsh PD, Hillis LD, Campbell WB, et al. Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease. N Engl J Med 1981; 304:685-691

[15] Podrid PJ. Role of higher nervous activity in ventricular arrhythmia and sudden cardiac death: implications for alternate antiarrhythmic therapy. Ann NY Acad Sci 1984; 432: 296-313

[16] Hoberg E, Schuler G, Kunze B, et al. Silent myocardial ischemia as a potential link between lack of premonitoring symptoms and increased risk of cardiac arrest during physical stress. Am J Cardiol 1990; 65:583-589

(*) From the William Beaumont Hospital, Division of Cardiology, Royal Oak, MI.

Manuscript received October 20, 1999; accepted October 21, 1999.

Correspondence to: Sreenivasulu R. Gangasani, MD, William Beaumont Hospital, Division of Cardiology, 3601 West Thirteen Mile Rd, Royal Oak, MI 48073; e-mail: Gangasanisr@hotmail.com

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