Case Report

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American Journal of Emergency Medicine

journal homepage: www. elsevier. com/ locate/ajem

American Journal of Emergency Medicine 34 (2016) 120.e1-120.e3

Use of intra-aortic balloon pump support for oozing-type Cardiac rupture after acute myocardial infarction

Left ventricular free wall rupture usually leads to acute hemopericardium and sudden cardiac death resulting in cardiac tamponade. Rarely, only a few patients with subacute free wall rupture such as oozing-type ventricular rupture or left ventricular false aneurysm may permit time for pericardiocentesis and surgery. We report a 63-year-old man with ST-elevation myocardial infarction who underwent primary percutaneous coronary intervention about 12 hours from the onset, and cardiac tamponade occurred on the second day. An Intra-aortic balloon pump was immediately inserted for hemodynamic support. After 100 mL of pericardial fresh blood was drained from the percardial cavity, his Hemodynamic collapse was promptly improved with IABP support. In the following 24 hours, about 600 mL of hemorrhagic pericardial fluid was drained. The most likely diagnosis was concerning for oozing-type ventricular rupture, and a conservative approach was decided. The patient survived to the acute phase under IABP support and was discharged with Complete recovery.

Left ventricular free wall rupture (LVFWR) is the most serious me- chanical complication of acute myocardial infarction (AMI) and usually presents with Rapid progression to Cardiovascular collapse, electrome- chanical dissociation, and sudden death [1]. Because LVFWR after AMI leading to hemopericardium and tamponade is often rapidly fatal, these patients usually have no chance for surgery. Rarely, patients who present with subacute ventricular rupture may permit time for pericardiocentesis and surgery. Although emergency surgical treatment is considered the criterion standard in the setting of cardiac rupture, the early mortality of cardiac operation is still very high [2,3]. We here re- port a case of oozing-type LVFWR secondary to ST-elevation AMI who survived to the acute phase under intra-aortic balloon pump (IABP) support and was discharged with complete recovery.

A 63-year-old, previously healthy man was transferred to our emer- gency department with chest pain ongoing for about 11 hours. He had a 30-year history of smoking and had no other risk factors other than dys- lipidemia. On physical examination, he was found to have a tempera- ture of 36.6?C, a heart rate of 94 beats/min, a respiratory rate of 20 breaths/min, and a blood pressure of 102/75 mm Hg. Cardiovascular and other system examinations revealed no pathologic signs. The initial electrocardiogram (ECG) showed sinus rhythm with ST-segment eleva- tion in leads I, AVL, and V₁ through V₅ (Fig. 1). Bedside transthoracic echocardiography revealed hypokinesia of anterior wall motion, a minor pericardial effusion, and left ventricular ejection fraction about 40%. The blood tests revealed a leukocyte level of 10.26 x 10^-9/L, and the serum levels of creatine kinase MB mass 781 ng/mL and troponin I of 280.826 ng/mL (reference range, 0-0.04 ng/mL). Because the chest pain was consistent with the ECG changes, ischemic echocardiography,

and the raise in cardiac enzymes, the patient was diagnosed as having acute ST-elevation anterior wall myocardial infarction and required emergency invasive intervention. He was initially managed medically with oral 300 mg aspirin, 180 mg ticagrelor, 25 mg metoprolol, and in- travenous tirofiban therapy. Forty minutes after admission, emergency coronary angiography was performed, which showed that the right cor- onary artery and left circumflex coronary artery were normal with no evidence of atherosclerosis and total occlusion of the proximal left ante- rior descending (LAD) thrombus. We performed percutaneous coronary intervention (PCI) in the LAD and a drug-eluting stent was deployed to the LAD (Fig. 2). The patient was then transferred to the cardiac care unit for Close monitoring.

On the second day, the patient complained of dyspnea and his blood pressure abruptly decreased to 74/50 mm Hg and the heart rate increased to 156 beats/min on monitor. An IABP was immediately inserted for hemodynamic support. A bedside transthoracic echocardi- ography showed massive pericardial fluid. Because the cardiac tamponade was evident and occurred later in the second day of post- PCI, LVFWR or coronary artery perforation was first suspected. Because the guide wire had not been positioned outside the arterial bed and there were no contrast extravasations during the procedure, coronary artery perforation was unlikely. In addition, there had been a small pericardial effusion before PCI. The cause of tamponade most possibly was concerning for LVFWR. Tirofiban was stopped and immediate percutaneous pericardiocentesis was performed. A 6F Pigtail catheter was introduced into the pericardium. After about 100 mL of pericardial fresh blood was drained from the percardial cavity, his hemodynamic collapse was promptly and dramatically improved with the blood- pressure increasing to 110/65 mm Hg and the heart rate decreasing to 102 beats/min under IABP support. After discussing with cardiac surgeons, a conservative approach was decided at first. Reversal of the anticoagulation was attempted with 400 mL of fresh-frozen plasma. In the following 24 hours, pericardial effusion was drained for another 5 or 6 times and about 600 mL of hemorrhagic pericardial fluid was aspi- rated from the pericardial cavity. Hemoglobin levels declined from 12.3 to 9.4 g/dL. Serial echocardiography examinations in the following 2 weeks showed a stable moderate-to-large pericardial effusion (Fig. 3), which was drained by several times. Under the IABP support, hemody- namic function was relatively stable and the most likely diagnosis was concerning for oozing-type ventricular rupture. In the third week, peri- cardial effusion was reduced and the IABP was discontinued. The patient survived to discharge from the hospital 35 days after admission without other complications.

Left ventricular free wall rupture is usually associated with large transmural myocardial infarctions and typically occurs in an area of in- farction without myocardial reperfusion. It often leads to acute

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Fig. 1. The 12-lead ECG results on admission which demonstrated sinus rhythm with ST-segment elevation in leads I, AVL, and V₁ through V₅. The diagnosis was acute anterior wall myocardial infarction.

hemopericardium and sudden cardiac death resulting in cardiac tamponade. In the present era, the overall incidence of ventricular free wall rupture ranges from 0.8% to 6.2% [2,4]. With increasing use of early thrombolysis or Primary PCI, better systolic blood pressure con- trol, ?-blockers, and angiotensin-converting enzyme inhibitors, the in- cidence of this mechanical complication has declined over the years [5]. Although reperfusion therapy decreases the overall risk of cardiac rupture, unsuccessful reperfusion or late administration of Fibrinolytic therapy may accelerate the process of cell necrosis and lead to earlier ventricular wall rupture [6]. Suzuki et al [7] suggested that the common feature to develop early myocardial rupture after PCI for ST-segment el- evation infarction is associated with severely failed reperfusion at the level of microcirculation. Okino et al [8] confirmed that thrombolysis is one of the contributing causes of free wall rupture in AMI patients un- dergoing PCI, even when PCI is successful. Thrombolysis, especially if administered late, increases the risk of intramyocardial hemorrhage and inflammatory response which may accelerate the occurrence of myocardial rupture. In our case, although the patient had treated with primary PCI, the oozing-type rupture could be associated with a large transmural infarction with delayed admission. In addition, the use of tirofiban and heparin may increase the risk of blood oozing.

Left ventricular free wall rupture can be classified into 2 types ac-

cording to morphology: oozing-type (incipient rupture) and blow-out type (true rupture). Most patients with blow-out type rupture usually develop sudden hemodynamic collapse followed by electromechanical dissociation and death. Occasionally, only a few patients with subacute

free wall rupture, such as oozing-type ventricular rupture or left ventricu- lar false aneurysm sealing of the site by thrombus formation, may permit time for pericardiocentesis and/or surgery alive. Recently, percutaneous intrapericardial fibrin-glue injection therapy has provided favorable out- comes for cases with oozing-type LVFWR [9-11]. Fibrin-glue has an ad- vantage of high biocompatibility and is biodegradable. It is absorbed without an inflammation, and there are no adverse events such as con- strictive pericarditis induced by a percutaneous intrapericardial fibrin- glue injection therapy. As one therapeutic alternative to Surgical repair, it seems to be effective and less invasive [11]. Nasir et al [12] proposed that conservative or surgical management would result in better out- comes in patients presenting with LVFWR secondary to AMI. Patients with a milder form of LVFWR, such as oozing or subacute-type rupture, can be managed conservatively, but the irony is that it is very difficult to identify these patients because even a small oozing-type ventricular rup- ture can increase in size and lead to large defect with sudden arrest and most probably death [12]. In our case, considering the patient’s clinical and hemodynamic relatively stable with IABP support and Pericardial drainage, we performed Conservative treatment strategy. The patient eventually survived to hospital discharge.

In conclusion, the present report describes a case of oozing-type LVFWR secondary to AMI using IABP support as a bridge to recovery. An IABP not only improved diastolic myocardial perfusion but also, even more important, decreased systolic afterload which reduced pres- sure inside the ventricular or wall stress. The IABP in this case had created a window for the Healing process in the setting of oozing-type rupture.

Fig. 2. A, Emergency coronary angiography revealed total occlusion of the proximal LAD. B, PCI was performed in the LAD, and a drug-eluting stent was deployed to the LAD.

Z-P. Zhang et al. / American Journal of Emergency Medicine 34 (2016) 120.e1-120.e3 120.e3

Fig. 3. transthoracic echocardiogram in Apical 4-chamber (C) and short-axis (D) views showing moderate-to-large pericardial effusion (white arrows).

Zhi-Ping Zhang, MD*

Xi Su, MD

Cheng-Wei Liu, MD Dan Song, MD Jian Peng, MD

Ming-Xiang Wu, MD Yu-Chun Yang, MD

Bo Liu, MD Cheng-Yi Xu, MD Fang Wang, MD

Department of Cardiology, Wuhan Asia Heart Hospital

Wuhan 430022, China

*Corresponding author

E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2015.05.054

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