Ann Thorac Surg 2003;76:921-923
© 2003 The Society of Thoracic Surgeons
Case reports
Spontaneous cardiac rupture
Chia-Hsun Lin, MDa,
Ming-Jen Lu, MDa*,
Samuel Haw-Han Chieng, MDa,
Chi-Ren Hung, MDa
a Division of Cardiovascular Surgery, Department of Surgery, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
Accepted for publication February 14, 2003.
* Address reprint requests to Dr Lu, Department of Surgery, Shin Kong Wu Ho-Su Memorial Hospital, No. 95, Wen-Chang Road, Shih-lin District 111, Taipei, Taiwan
e-mail: m000726{at}ms.skh.org.tw
 |
Abstract
|
|---|
An 83-year-old woman had a sudden onset of loss of consciousness with no detectable blood pressure. Pulseless electrical activity was present in the electrocardiogram and massive pericardial effusion was found by echocardiography. Emergent subxiphoid pericardiotomy and drainage was immediately performed to release the cardiac tamponade at bedside and was followed by rushing the patient to the operating room for exploration. As a result a ruptured hole was identified on the posterior-lateral wall of the left ventricle and the defect was successfully repaired. The patient had an uneventful postoperative recovery and received postoperative study by cardiac catheterization, which disclosed coronary artery disease.
|
Introduction
|
|---|
Cardiac rupture remains a major cause of death when encountered in the emergency room. The following tamponade of the heart happens very rapidly, resulting in a fatal fall in cardiac output and circulatory collapse. The interval between rupture and collapse may be variable, but it is usually short, even when the rupture hole is small. Most cardiac ruptures develop from penetrating or blunt trauma to the chest. Spontaneous rupture of the heart rarly occurs. We describe a case successfully salvaged from rupture of the left ventricle by a prompt diagnosis of cardiac tamponade, proper hemodynamic management, and expeditious surgical drainage and repair.
An 83-year-old woman had sudden loss of consciousness develop while chatting with neighbors and was sent to the emergency room at 2:25 PM, May 23, 2001. She had been capable of riding her bicycle to do farm work every day and had no documented medical history prior to this event. In the emergency room, the patient’s Glasgow coma scale was E1V1M3 and her blood pressure was not detected. Physical examinations revealed isocoric and reactive pupils, engorged jugular veins, very distant heart sound, course breathing sound bilaterally, and cyanotic extremities without palpable pulse. The electrocardiographic monitoring showed sinus tachycardia, which was correlated with pulseless electrical activity. The transthoracic echocardiogram was done at 2:35 PM which revealed massive pericardial effusions with diastolic compression of the right atrium and ventricle. The patient was intubated at 2:37 PM and echo-guide needle pericardiocentesis was attempted, but it failed. The blood pressure was still undetectable and bradycardia had developed, so cardiopulmonary resuscitation was started at 2:50 PM. Emergent pericardiotomy by subxiphoid approach was performed at 2:51 PM, and massive bloody pericardial effusions and clots with high pressure were drained out. The peripheral pulse presented to be 95 per minute, and the systolic blood pressure went up to 90 mm Hg. The patient was rushed into the operating room for emergent surgery after consent was obtained from her son at 3:01 PM. Under the impression of aortic dissection with rupture, cardiopulmonary bypass was first established by cannulation of the left femoral artery and vein before a median sternotomy was carried out. After the pericardium was opened, there was no tissue adhesion in the pericardial cavity. The blood clots were removed easily and a ruptured hole was found over the posterior-lateral wall of the left ventricle (Fig 1).
No typical infarction or scar tissue on the myocardium was observed. Consequently, the ascending aorta was cross clamped and cold blood cardioplegic solution was infused into the aortic root to induce cardiac arrest. The defect was closed using 3-0 Prolene pledgeted sutures (Ethicon, Somerville, NJ) on the flaccid myocardium, and the repair was reinforced with a Teflon patch (Boston Scientific, Wayne, NJ) glued to the epicardial surface of the rupture site using surgical glue. Furthermore, no other pathology or bleeder could be identified in the pericardial cavity and mediastinum. The aortic cross clamp was released, and then the heartbeat was resumed. The patient was smoothly weaned off cardiopulmonary bypass, and the femoral artery and vein were carefully reconstructed after decannulation. Wounds on the chest and left inguinal were closed in anatomic layers. The patient recovered well with no neurologic complications or any organ dysfunction. The patient was discharged home 17 days after operation.
View larger version (129K):
[in this window]
[in a new window]
|
Fig 1. The rupture hole was located in the posterior-lateral wall of the left ventricle, beside the small first obtuse marginal branch of the left circumflex coronary artery (arrowhead).
|
|
In the follow-up, the thallium myocardial perfusion scan was positive for severe ischemia of the lateral wall, and the coronary arteriography disclosed coronary artery disease. The middle of the left anterior descending artery was obstructed completely and the apical segment of the left anterior descending artery could be faintly seen reinjected by collaterals. The circumflex artery was small in size and was 90% occluded at the origin of the main branch (Fig 2).
The right coronary artery was dominant and patent. Percutaneous catheter angioplasty with balloon dilatation and coronary stenting to the left anterior descending artery was successfully accomplished. Presently the patient is doing well with normal physical activity as she was previously.
View larger version (165K):
[in this window]
[in a new window]
|
Fig 2. The left coronary arteriogram showed the lesions of left anterior descending artery (big arrowhead), and the circumflex artery (small arrowhead).
|
|
|
Comment
|
|---|
Spontaneous cardiac rupture is a rare occurrence. Most of the cases reported in the literature were caused by myocardial infarction [1, 2]. Some sporadic cases happened in mediastinitis [3], myocardial abscess [4], myocarditis [5], angiosarcoma of the heart [6], Chaga’s disease [7], and after mitral valve replacement surgery [8].
Myocardial rupture is a disastrous complication that usually leads to sudden death. The ensuing cardiac tamponade after rupture results in rapid hemodynamic breakdown. Therefore the diagnosis of rupture is usually made too late to allow salvage of the patient. A prompt and accurate diagnosis of cardiac rupture permits a fair chance of treatment and survival. Essential clinical presentations of severe hypotension accompanied by distended jugular veins, muffled heart sound, and cyanosis of the face and extremities may alert the physician to the suspicion of cardiac tamponade and myocardial rupture. In favor of the diagnosis is the finding of electromechanical dissociation or pulseless electrical activity on the electrocardiogram. Echocardiography is an easy and effective method to confirm the diagnosis by the presence of pericardial effusion with heart compression. Once the diagnosis has been established, immediate drainage to release the tamponade and proper hemodynamic management to avoid prolonged shock and surgery without delay to repair the myocardial defect could allow the patient’s survival and prevent sequelae.
The optimal surgical treatment of the ventricular lesions requires closure with Teflon pledgeted or buttressed sutures although sutureless techniques with biological glue had been used to repair a similar problem [9]. The importance of instituting cardiopulmonary bypass as a first step during the operation should be emphasized in dealing with this life-threatening situation. The cardiopulmonary bypass is essential to stabilize the hemodynamic state if active bleeding is present after opening the pericardium and to facilitate a secure repair under empty relaxed ventricular condition [10, 11]. The successful repair of cardiac rupture is usually followed by long-term survival in the majority of patients [2].
The time of rupture occurrence associated with acute myocardial infarction varies; most ruptures occur early when developing within the first 48 hours. The early form represents 40% to 50% of cases, but the true proportion is likely to be higher because it will also include patients dying suddenly before reaching the hospital [10]. Rupture of myocardium may be classified into three types [2]: (1) The blow-up rupture is one type in which a patient probably dies within minutes before arriving at the hospital; (2) the small rupture or leak through a friable aneurysm is the second type, which makes an operation possible if proper intervention is carried out within a few hours with the help of adequate hemodynamic support; and (3) the third type is the chronic rupture, which has a formation of false aneurysm.
Our patient seemed to have the second type of cardiac rupture, which was attributed to coronary artery disease, although there was no clinical history of previous ischemic heart disease or recent events that could be traced. Moreover, the rupture site was not located in the anterior territory subtended by the left anterior descending artery enduring the most severe lesions, but probably in the area with ischemia, which was caused by the effectively 90% occluded circumflex branch.
To the best of our knowledge, only a few cases of undetected myocardial infarction with rupture of the left ventricle as the first clinical presentation have been reported in the literature [12] with successful salvaging.
|
References
|
|---|
- Oblath R.W., Levenson D.C., Griffith G.C. Factors influencing rupture of the heart after myocardial infarction. JAMA 1952;149:1276-1281.[Abstract/Free Full Text]
- Bashour T., Kabbani S.S., Ellertson D.G., Crew J., Hanna E.S. Surgical salvage of heart rupture: report of two cases and review of the literature. Ann Thorac Surg 1983;36:209-213.[Abstract]
- Valla J., Staerman H., Sevray B., et al. A rare complication of mediastinitis: rupture of the right ventricle [French]. Ann Chir 1996;50(5):401-404.[Medline]
- Harris D.G., Rossouw G.J. Myocardial abscess with contained rupture: successful repair. Ann Thorac Surg 2001;71:1360-1361.[Abstract/Free Full Text]
- Ito M., Tanabe Y., Kumakura M., Kimura K., Masani F., Aizawa Y. Left ventricular free wall rupture in acute fulminant myocarditis during long-term cardiopulmonary support. Jpn Circ J 1999;63(5):397-399.[Medline]
- Bertoli F., Remon Valera J.A., Arrocha R. Angiosarcoma of the heart and its spontaneous rupture. A rare cause of effusive-constrictive pericarditis. A case report and review of the literature [Spanish]. Rev Med de Panama 1995;20(3):84-91.
- Tostes S., Jr, Lopes E.R., Chapadeiro E. Sudden death caused by the spontaneous rupture of the right ventricle in a woman with chronic Chaga’s disease [Portuguese]. Rev Soc Bras Med Trop 1990;23(4):225-228.[Medline]
- Spencer F.C., Galloway A.C., Colvin S.B. A clinical evaluation of the hypothesis that rupture of the left ventricle following mitral valve replacement can be prevented by preservation of the chordae of the mural leaflet. Ann Thorac Surg 1985;202:673-680.
- Padro J.M., Mesa J.M., Silvestre J., et al. Subacute cardiac rupture: repair with a sutureless technique. Ann Thorac Surg 1993;55:20-24.[Abstract]
- Yaku H., Fermanis G., Horton D.A., Guy D., Lvoff R. Successful repair of a ruptured postinfarct pseudoaneurysm of the left ventricle. Ann Thorac Surg 1995;60:1097-1098.[Abstract/Free Full Text]
- Figueras J., Cortadellas J., Soler-Soler J. Left ventricular free wall rupture: clinical presentation and management. Heart 2000;83:499-504.[Free Full Text]
- Mangialavori G., Bartoletti A., Mazzoni V., et al. Rupture of the free wall of the left ventricle as the first manifestation of a myocardial infarct. A clinical case operated on with success [Italian]. Giorn Ital Card 1992;22(7):863-867.
Top
Abstract
Introduction
