Exercise Testing Induces Fatal Thromboembolism

Abstract

Thromboembolism is still one of the most important complications of prosthetic heart valves. Embolism to a major coronary branch is rare, but acute proximal occlusions can be fatal, even when the coronary arteries are otherwise normal and intervention is rapid. We report a fatal complication of an exercise test in a patient who had a St. Jude bileaflet mitral valve.

After an exercise test, a 42-year-old woman with a mechanical prosthetic valve had a severe hemodynamic collapse with acute ST segment changes. Coronary angiography showed a totally occluded left main coronary artery with TIMI grade 0 to 1 flow. Rapid injection of contrast material and the passage of a floppy guidewire through the thrombus restored a TIMI grade 3 flow. Angiography showed no coronary atherosclerostic involvement. Despite successful coronary reperfusion, intra-aortic balloon counterpulsation, and intensive medication, the patient died. This case demonstrates that exercise testing should be applied with great caution in patients with prosthetic valves, and only after a careful evaluation of valve function. We recommend transesophageal echocardiography prior to exercise testing in these patients. (Tex Heart Inst J 2002;29:48–50)

Coronary embolism is a rare but life-threatening complication of prosthetic heart valves. Other known causes of coronary embolism are active infective endocarditis, native left-sided valve stenosis, atrial fibrillation, left ventricular aneurysm, dilated cardiomyopathy, cardiac tumors, cardiac catheterization, and surgery. ¹ The left anterior descending coronary artery is the most frequent site of involvement. ²

The clinical manifestations of coronary embolism vary in accordance with the size of the embolus and the size of the arterial lumen in which it lodges. A small embolus can travel distally to a small coronary segment and can resolve completely without significant myocardial damage. However, if a coronary artery segment has some degree of atherosclerosis at a proximal site, even a fairly small embolus is more likely to lodge proximally. Emboli to the left main coronary artery are very rare but are usually fatal. ³ It is difficult to estimate the incidence of this situation, especially in patients with prosthetic heart valves.

Case Report

In February 1995, a 42-year-old woman with a mechanical prosthetic valve was admitted to our department for evaluation of her exercise capacity and detection of possible myocardial ischemia, by means of an exercise stress test. She had undergone a closed mitral commissurotomy in 1986, and implantation of a St. Jude 29-mm bileaflet mitral valve (St. Jude Medical; Minneapolis, Minn) in 1992.

For 3 months prior to the 1995 admission, she had experienced atypical chest pain and exercise intolerance. A transthoracic echocardiogram at the time of admission revealed normal functioning of the mechanical prosthetic valve in the mitral position, normal left ventricular function, and mild left atrial dilatation. Her prothrombin time was 24 seconds and the international normalized ratio (INR) was 2.8.

On the treadmill, our patient reached the 4th stage of the Bruce protocol with no significant problem and achieved a heart rate of 154 beats/min and a maximum METS (metabolic equivalent) of 12.9. During the recovery stage, she collapsed suddenly, with chest pain. We observed acute ST segment elevations in D₁–aVL and V₅–V_6, ST depressions in V₁–V₃ derivations (Fig. 1), and severe hypotension. Because a severe coronary embolism was suspected, we performed emergency coronary angiography, which revealed total occlusion of the left main coronary artery, with TIMI* grade 0 to 1 flow (Fig. 2A and Fig. 2B). Contrast medium was injected rapidly and the thrombus was penetrated with a 0.014-inch floppy guidewire, which restored TIMI grade 3 flow (Fig. 2C). Neither the left coronary nor the right coronary artery showed any evidence of atherosclerotic lesions. Because coronary flow was quite good and there was no visible embolic material at the distal vascular bed, thrombolytic therapy was not administered.

Fig. 1 Electrocardiographic changes in the patient: A) Acute ST elevations are seen in D₁–aVL and V₅–V₆, together with ST depressions in V₁–V₃; B) 3 minutes later, ST segments are still elevated at V₅–V₆, and QRS complexes are larger.

Fig. 2 A) The 1st coronary angiogram, at the anteroposterior position, shows a total occlusion of the left main coronary artery. B) After the 1st injection of contrast medium, the TIMI flow grade is better, but a thrombus is observed at the bifurcation of the left anterior descending and circumflex coronary arteries. C) TIMI flow 3 and a normal left coronary artery are seen at the end of the procedure. TIMI = Thrombolysis in Myocardial Infarction (clinical trial)

Despite the use of intra-aortic balloon counterpulsation, double inotropic support with dopamine and dobutamine, and heparinization, we could not restore adequate arterial blood pressure, and the patient's QRS complexes enlarged progressively. She died at the 5th hour of the event.

Discussion

It is extremely difficult to estimate the incidence of coronary embolism because of silent, subclinical microembolizations in patients with normal coronary arteries. Although acute embolism to the left main coronary artery is usually fatal, ³ there is a report of an embolism from a 22-year-old Starr-Edwards aortic ball valve that caused only unstable angina and a small myocardial infarction. ⁴ Most commonly, the source of the coronary embolism is an aortic valve (native or prosthetic), but disease of mitral valves has also been implicated. ^5,6 Known risk factors for valvular embolization are atrial arrhythmias, spontaneous contrast images at echocardiography, infective endocarditis, inadequate anticoagulation, and prosthetic valve dysfunction.

Our patient appeared to have none of these risk factors for coronary embolism. She had a prosthetic mitral valve and mild left atrial enlargement, but her anticoagulation level seemed to be adequate and her transthoracic echocardiogram was quite normal. Even so, a thrombus formed either on the mechanical valve itself or in the left atrial appendage.

The safety of the exercise stress test for this kind of patient is not well known. It is true that secondary ST changes due to chamber enlargement in valve disease usually decrease the specificity and sensitivity of exercise testing for the detection of coronary ischemia. However, there were no noteworthy secondary ST changes in this patient, and another aim of the test was to determine her exercise capacity.

Conclusion

A single case report, of course, does not provide a clear directive for the use of transesophageal echocardiography (TEE) in prosthetic-valve patients who are about to undergo exercise testing. Yet the extreme danger of this complication requires clinicians to consider any reasonable means of prevention. Evidence of a thrombus, a vegetation, or serious valve dysfunction should be excluded, to the degree possible, before the exercise test, and we think that TEE is the best means of doing this. We remain uncertain, though, of the absolute safety of exercise testing in prosthetic-valve patients, even when TEE shows the valves to be completely normal.

In sum, we have learned to proceed with great caution before subjecting prosthetic-valve patients to exercise tests. Especially if the patient has recent-onset angina, we now check every structural detail of the valve and look for evidence of inadequate anticoagulation or infection. We have not had a treadmill death since this case in 1995, but in preparation for exercise testing we have discovered valve dysfunction and rapid progression of atherosclerosis after valve implantation. In a patient with an aortic mechanical valve, TEE revealed a root aneurysm, which would not have been seen on transthoracic echocardiography (TTE). In another patient, who had recent-onset angina 3 months after replacement of a mechanical mitral valve, coronary angiography showed a newly developed proximal lesion of the left anterior descending coronary artery, after normal results on TTE and TEE.