Fatal cardiac rupture during stress exercise testing: case series and review of the literature.

Abstract: Mortality rates of exercise testing are low and cardiac rupture and sudden death are rare. Three cases of fatal cardiac rupture that occurred during exercise stress testing are reported. Once thought to be a fatal complication, there are increasing reports of ante-mortem diagnosis and survival. Cardiac rupture is a stuttering process with recognizable clinical symptoms that allow early recognition and treatment. Certain clinical, biochemical, ECG and hemodynamic markers may allow identification of patients likely to sustain rupture. Strategies for diagnosis, resuscitation, and definitive intervention are reviewed.

Key Words: cardiac rupture, exercise stress testing, myocardial infarction

**********

Exercise stress testing is a common procedure used in the evaluation of chest pain. It is increasingly being deployed as a risk-stratifying tool for patients presenting to hospital with acute coronary syndromes. The current guidelines for the management of unstable angina and non-ST segment elevation myocardial infarction (MI) propose initial medical therapy and then either an early invasive approach with angiography or alternatively, a conservative approach. (1), (2) The latter is for patients who are not in a high-risk category or who do not develop recurrent chest pain. Here, simple exercise treadmill testing in patients with normal electrocardiograms (ECGs) may be done or increasingly, exercise or pharmacological stress testing in conjunction with an imaging modality such as nuclear or echocardiography is used. Stress testing is also advocated in stable patients post-MI who have received thrombolytics several days before, to assess the extent of residual ischemia. A submaximal stress test is usually administered on or approximately on Days 3 to 5 while a symptom-limited stress test may be safely performed approximately 4 to 6 weeks after MI. (3) Three cases of fatal cardiac rupture during exercise testing that occurred in an exercise laboratory during an 18-month period are reported. We discuss whether certain clinical events may precede free wall myocardial rupture and allow its prediction, and review strategies for diagnosis, resuscitation, and definitive intervention.

Discussion

Depending on the prevalence of coronary artery disease in the population being tested, the mortality rates of exercise testing range from 1 in 10,000 to 1 in 50,000. (4-10) In general, when nonselect populations are tested, mortality rates of 1 in 20,000 might be expected. (11) Cardiac rupture and sudden death are rare complications with isolated reports. (12-15) Once thought to be a fatal complication, there are increasing reports of ante-mortem diagnosis and survival. It is now believed cardiac rupture is a stuttering process with recognizable clinical symptoms that allow early recognition and treatment.

The incidence of ventricular free wall rupture after MI has been consistently defined by numerous autopsy series. (16), (17) It complicates approximately 4% of myocardial infarctions and accounts for 12 to 21% of deaths after MI. Cardiac rupture usually occurs within the first week of infarction, therefore a window period of opportunity exists for diagnosis and early intervention. Certain clinical, biochemical, ECG and hemodynamic markers may allow identification of patients at risk of rupture.

Clinical features that are risk factors for cardiac rupture include increasing age, female sex, preexisting hypertension and first coronary event. (16-19) Pericarditis, repetitive unprovoked emesis, restlessness, and agitation are predictive symptoms of rupture and most patients will have two or more of this triad. (20), (21) Other risk factors include chest pain that is refractory to opiate therapy, (22), (23) and persistently elevated serum C-reactive protein levels post-MI. (24) Classic clinical features of tamponade such as hypotension, pulses paradoxus, elevated venous pressure, quiet heart sounds and bradycardia are often present.

Serial ECGs are of great importance in further predicting patients at risk. The presence of lateral infarction, especially if associated with inferior and/or posterior extension, identifies a subset of patients at increased risk. (20) Persistent, progressive or recurrent ST segment elevation, especially persistently positive T waves after 48 to 72 hours or the gradual reversal of initially inverted T waves, should increase the degree of suspicion. EMD is the most frequent form of cardiac arrest in patients dying of MI, (25) and the development of sudden EMD in patients with a first MI without overt heart failure is highly predictive of acute left ventricular wall rupture. (18), (26), (27) Sudden onset of EMD in a post-MI patient should prompt a diagnosis of tamponade and emergency pericardiocentesis should be considered.

A high index of clinical suspicion is required in the diagnosis of subacute cardiac rupture. The differential diagnosis of recurrent chest pain in patients after MI includes pericarditis and ongoing ischemia; however, these groups of patients should always be evaluated for possible mechanical complications, including cardiac rupture. Transthoracic two-dimensional echocardiography almost always confirms an antemortem diagnosis, and is an informative tool in this regard. (16) The presence of tamponade, pericardial effusion greater than 5 mm, high density intrapericardial echoes or right atrial or right ventricular wall compression is highly sensitive and specific. (28) If pericardial fluid is identified, pericardiocentesis should be considered and if blood is obtained, immediate consideration for surgery is mandatory. (20) The most common site of rupture is the anterior or lateral aspect of the ventricular free wall and rupture occurs in the infarcted area in almost all cases. (16), (19), (20) Isolated posterior infarction is uncommon and inferior wall infarction is unusual unless associated with infarction of the lateral or posterior wall.

Surgical exploration and rupture repair are the definitive diagnostic and therapeutic procedures. Often there is a time interval between clinical diagnosis and surgical repair, and temporary stabilization is necessary. Inotropic support is advocated in all cases and is of proved benefit in improving cardiac output. (29) Successful pericardiocentesis will relieve the immediate threat to life. If facilities allow, the use of partial femoral bypass may be used to achieve hemodynamic control but in practical terms it is often not possible to accomplish this with acceptable speed to be of benefit. Facilities may enable intra-aortic balloon pump support to be achieved expeditiously, but this should not be required if pericardiocentesis has been successful. Aims of surgery are to relieve tamponade with closure or repair of the ventricular wall defect. Revascularization is often considered at the same time as the majority of patients who undergo post-mortem examination have multi-vessel disease with critical stenosis of at least one major epicardial coronary artery. (16)

Conclusions

These cases highlight a catastrophic complication after routine stress testing post-MI. We draw attention to the importance of patient selection and screening before stress testing and emphasize a greater understanding of the clinical events that may precede free wall myocardial rupture. A clinician who is familiar with exercise physiology, cardiology, electrocardiology and advanced life support should supervise high-risk patients. In the event of an exercise-induced cardiac arrest, adequate provision for prompt cardiac resuscitation is mandatory. It is axiomatic that a defibrillator must be immediately available as well as a complete trolley of cardiac resuscitation equipment.

Key Points

* Three cases involving a catastrophic complication during routine stress exercise testing after myocardial infarction are reported.

* The cases highlight the importance of patient selection and screening before stress testing and emphasize a better understanding of the clinical events that may precede free wall myocardial rupture.

* A clinician who is familiar with exercise physiology, cardiology, electrocardiology and advanced life support should supervise high risk patients, and a defibrillator as well as a complete trolley of cardiac resuscitation equipment must be readily available.

Acknowledgment

We thank Andrew Bowman, consultant cardiologist, for his support and expert advice in preparing the manuscript.

From the Departments of Cardiology and Pathology, Royal Cornwall Hospital, Truro, Cornwall, England.

Reprint requests to Laurence Weinberg, BSc, MBBCh, MRCP, Unit 3, 71 Wattle Valley Road, Canterbury, Victoria 3126, Australia.

Accepted November 26, 2002.

Copyright [c] 2003 by The Southern Medical Association 0038-4348/03/9611-1151

References

1. Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA guidelines for the management of patients with unstable angina and non-ST -segment elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guide-lines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol 2000;36:970-1062.

2. British Cardiac Society Guidelines and Medical Practice Committee and Royal College of Physicians Clinical Effectiveness and Evaluation Unit. Guideline for the management of patients with acute coronary syndromes without persistent ECG ST segment elevation. Heart 2001;85:133-142.

3. Jain A, Myers GH, Sapin PM, et al. Comparison of symptom-limited and low level exercise tolerance tests early after myocardial infarction. J Am Coll Cardiol 1993;22:1816-1820.

4. Rochmis P, Blackburn H. A survey of procedures, safety, and litigation experience in approximately 170,000 tests. JAMA 1971;217:1061-1066.

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

6. Gibbons LW, Mitchell TL, Gonzalez V. The safety of exercise testing. Prim Care 1994;21:611-629.

7. Atterhog JH, Jonsson B, Samuelsson R. Exercise testing: A prospective study of complication rates. Am Heart J 1979;98:572-579.

8. Sheffield LT, Haskell W, Heiss G, et al. Safety of exercise testing volunteer subjects: The Lipid Research Clinics' Prevalence Study Experience. J Cardiol Rehab 1982;2:395-400.

9. Kaltenbach M, Scherer D, Dowinski S. Complications of exercise testing: A survey in three German-speaking countries. Eur Heart J 1982;3:199-202.

10. Wendt T, Scherer D, Kaltenbach M. Life-threatening complications in 1,741,106 cases of ergometry [in German]. Dtsch Med Wochenschr 1984;109:123-127.

11. Gibbons L, Blair SN, Kohl HW, et al. The safety of maximal exercise testing. Circulation 1989;80:846-852.

12. Hamm LF, Crow RS, Stull GA, et al. Safety and characteristics of exercise testing early after acute myocardial infarction. Am J Cardiol 1989;63:1193-1197.

13. Daniels CJ, Orsinelli DA. Cardiac rupture with dobutamine stress echocardiography. J Am Soc Echocardiogr 1997;10:979-981.

14. Juneau M, Colles P, Theroux P, et al. Symptom-limited versus low level exercise testing before hospital discharge after myocardial infarction. J Am Coll Cardiol 1992;20:927-933.

15. Carlon R, Pedon L, Maiolino P. Cardiac rupture during maximal exercise testing before hospital discharge after acute myocardial infarction [in Italian]. G Ital Cardiol 1996;26:539-544.

16. Sutherland FW, Guell FJ, Pathi VL, et al. Postinfarction ventricular free wall rupture: Strategies for diagnosis and treatment. Ann Thorac Surg 1996;61:1281-1285.

17. Reddy SG, Roberts WC. Frequency of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906-911.

18. Morpurgo M, Rietti P. Postinfarction cardiac rupture and electromechanical dissociation. Acta Cardiol 1997;52:17-23.

19. Mann JM, Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction: Analysis of 138 necropsy patients and comparison with 5 necropsy patients with acute myocardial infarction without rupture. Am J Cardiol 1988;62:847-859.

20. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: Report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22:720-726.

21. Morocutti G, Fontanelli A, Bernardi G, et al. Identification of patients at risk of post-infarction heart rupture: Clinical and therapeutic characteristics of 121 consecutive cases and review of the literature [in Italian]. Minerva Cardioangiol 1995;43:117-126.

22. Leone A, Fabiano P, Bertanelli F, et al. Postinfarction cardiac rupture in the nineties: Do we know determining factors? Singapore Med J 1992;33:282-286.

23. Herlitz J, Samuelsson SO, Richter A, et al. Prediction of rupture in acute myocardial infarction. Clin Cardiol 1988;11:63-69.

24. Ueda S, Ikeda U, Yamamoto K, et al. C-reactive protein as a predictor of cardiac rupture after acute myocardial infarction. Am Heart J 1996;131:857-860.

25. Rietti P, Marzegalli M, Schmid C, et al. Electromechanical dissociation in myocardial infarction: Anatomicoclincal study of 82 cases [in Italian]. Minerva Cardioangiol 1997;45:173-179.

26. Figueras J, Curos A, Cortadellas J, et al. Reliability of electromechanical dissociation in the diagnosis of left ventricular free wall rupture in acute myocardial infarction. Am Heart J 1996;131:861-864.

27. Nakamura F, Minamino T, Higashino Y, et al. Cardiac free wall rupture in acute myocardial infarction: Ameliorative effect of coronary reperfusion. Clin Cardiol 1992;15:244-250.

28. Lopez-Sendon J, Gonzalez A, Lopez de Sa E, et al. Diagnosis of sub-acute ventricular wall rupture after acute myocardial infarction: Sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol 1992;19:1145-1153.

29. Holt BD, Gabel M, Fowler NO. Hemodynamic efficacy of rapid saline infusion and dobutamine versus saline infusion alone in a model of cardiac rupture. J Am Coll Cardiol 1990;16:1745-1749.

RELATED ARTICLE: Case Reports

Patient 1

A 64-year-old woman with hypertension and diabetes mellitus presented with chest pain. ECGs showed Q-waves in the inferior leads with 1 mm ST -elevation and T -wave inversion in the inferolateral leads. Her pain settled with conventional medical treatment. Serial creatine kinase enzymes were normal but cardiac troponin I was 2.06 ng/ml (normal, <0.1) confirming an acute coronary event. On the third day, a submaximal Bruce exercise treadmill test was performed. After six minutes of exercise, she collapsed and had a cardiac arrest with electromechanical dissociation (EMD). Emergency pericardiocentesis revealed 65 ml blood. Resuscitation was unsuccessful. Postmortem examination showed a hemopericardium (500 ml) secondary to rupture of the posterior wall of the left ventricle in an area of acute infarction.

Patient 2

A 73-year-old man with hypertension was admitted with chest pain. Serial ECGs showed T-wave flattening in the inferolateral leads. Peak serial creatine kinase was 250 U/L. Cardiac troponin I was 28.1 ng/ml, confirming a non-ST segment elevation MI. On the third day, a Bruce exercise treadmill test was performed. After 3 minutes, without clinical or ECG warning, he had a cardiac arrest with asystole. Resuscitation was unsuccessful. Postmortem examination showed rupture of an acute posterolateral MI and a hemopericardium (450 ml).

Patient 3

A 66-year-old man with a family history of coronary artery disease was admitted with an acute ST -segment elevation inferolateral MI. Thrombolytic therapy was not performed because of late presentation. Peak serum creatine kinase level was 1,196 U/L; cardiac troponin I was 2.73 ng/ml. On the sixth day, a submaximal Bruce exercise treadmill test was performed. After 4 minutes of exercise, nonsustained ventricular ectopics were recorded. The test was terminated. Significant ST elevation in the inferior leads with ST depression in the lateral leads developed. The patient then had a cardiac arrest with EMD and asystole; resuscitation was unsuccessful. Postmortem examination showed 410 ml frank and clotted blood within the pericardial space secondary to a rupture of a MI involving the posterior and lateral aspects of the left ventricle.

Laurence Weinberg, BSC, MBBCH, MRCP, Karikalan Kandasamy, MBBS, MD, MRCP, Stephen J. Evans, MRCP, PHD, and Joseph Mathew, FMCPATH, FRCPATH, CERT THLE, PGCE, MBBS