Repaired Left Ventricular Free Wall Rupture After Acute Myocardial Infarction by Percutaneous Intrapericardial Fibrin-Glue Injection Therapy

ABSTRACT: Left ventricular free wall rupture is a rare, but occasionally lethal, complication after acute myocardial infarction (AMI). This case report describes a patient who presented with cardiogenic shock due to oozing-type rupture secondary to AMI and successfully underwent percutaneous intrapericardial fibrin-glue injection therapy. Cardiac magnetic resonance imaging demonstrated the thin layer of fibrin that covered the ruptured infarct myocardium immediately after fibrin-glue injection and its disappearance without any complications at 6 months.

J INVASIVE CARDIOL 2013;25(9):E186-E187

Key words: cardiac rupture, acute myocardial infarction, magnetic resonance imaging

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Left ventricular free wall rupture (LVFWR) rarely occurs in patients after acute myocardial infarction (AMI), but is occasionally a lethal complication after AMI.^1,2 Although surgical treatment for LVFWR after AMI is considered the gold standard, operative mortality is still high.^3-5 Percutaneous intrapericardial fibrin-glue injection therapy (PIFIT) is a new therapeutic alternative to surgical repair for cases with oozing-type LVFWR.^6-8 Herein, we demonstrate a patient with oozing-type LVFWR who was successfully treated by PIFIT and show the covering and disappearance of injected fibrin-glue on the ruptured myocardium using cardiac magnetic resonance imaging (CMR).

Case Report. A 63-year-old man with a history of hypertension was transferred to the emergency department in our hospital due to loss of consciousness after prolonged chest pain of over 12 hours. On arrival, his systolic blood pressure was 60 mm Hg. A 12-lead electrocardiogram showed a sinus rhythm, abnormal Q-wave and negative T in I aVL, tall R-wave in V1-2, ST elevation in leads I aVL V6 and ST depression in leads V1-V5. Plasma creatine kinase (normal range, 50-230 U/L) and MB fraction (normal range, 8-17 IU/L) levels were elevated (2953 U/L and 257 IU/L, respectively), but level of C-reactive protein was within normal range at admission. Echocardiography showed severe hypokinesis of the posterior-lateral wall and massive pericardial echo-free space. Computed tomography showed no contrast enhancement of the posterior-lateral wall and massive pericardial fluid (the average Hounsfield density was 73.2 HU), but no aortic dissection (Figures 1A and 1B). A 6 Fr pigtail catheter was immediately introduced into the pericardial space and percutaneous drainage was performed due to cardiogenic shock. After 70 mL of pericardial fresh blood was drained, vital signs were stabilized. Emergency coronary angiography revealed total occlusion of the proximal left circumflex artery with thrombus (Figures 1C and 1D). Coronary intervention was not performed, and PIFIT was initiated. The fibrin-glue was injected into the pericardial space from a 6 Fr pigtail catheter as described in a previous report.1 The catheter was clamped for several hours and then removed without resistance. Serial echocardiography was carefully observed and it demonstrated no reappearance of the pericardial effusion. CMR demonstrated the thin layer of fibrin-glue that covered the ruptured infarct myocardium immediately after PIFIT (Figures 2A and 2B). At 2 weeks post AMI, the patient was discharged from the hospital without any other complications related to PIFIT or AMI. CMR at 6 months post PIFIT revealed the disappearance of the thin layer of fibrin-glue, no reappearance of the pericardial effusion, and no development of pseudoaneurysm formation (Figures 2C and 2D). In addition, the Doppler pattern of mitral in-flow by echocardiography at 6 months post PITIF demonstrated no early increased diastolic filling velocity followed by a rapid deceleration and no dynamic changes with respiration, meaning no constrictive pericarditis. 

Discussion. LVFWR occurs in approximately 0.8%-6% of　patients after AMI. LVFWR is still a lethal complication after AMI.^2,3 LVFWR was categorized into either oozing-type (incipient rupture) or blow-out type (true rupture). Patients with LVFWR in cardiogenic shock or in cardiopulmonary arrest need to receive circulatory support under resuscitation and to undergo surgery on an emergency basis. Surgical treatment for LVFWR after AMI is the gold standard, but operative mortality is still high.^4-6 PIFIT is one therapeutic alternative to surgical repair and is less invasive. It seems to be effective and has provided favorable outcomes for cases with oozing-type LVFWR.^1,7,8

Fibrin-glue used by a PIFIT has an advantage of high biocompatibility and is biodegradable. Hattori et al estimated the pharmacokinetics of fibrin-glue in the pericardial space in an animal model and demonstrated that a fibrin network formed within 1 day after intrapericardial fibrin-glue injection was eliminated within 1 week.⁹ Murata et al found no inflammatory adhesion of epicardium to the pericardium in a postmortem heart after a PIFIT.⁷ These findings suggest that fibrin-glue in the pericardial space is absorbed without an inflammation, and adverse events such as constrictive pericarditis are not induced by a PIFIT. Interestingly, it has also been reported that fibrin-glue facilitates the wound-healing process.^10,11 Therefore, PIFIT is one therapeutic alternative option for patients with oozing-type LVFWR secondary to AMI. In addition, CMR is a useful modality for patient assessment after PIFIT.

References

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