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. 2026 Jul 18;14:100641. doi: 10.1016/j.jhlto.2026.100641

Successful combination therapy of sutureless repair and microaxial left ventricular assist device for left ventricular free wall rupture after acute myocardial infarction

Masaaki Omori 1,⁎, Masahiko Fujii 1, Manabu Sakurai 1, Yusuke Hagiwara 1, Kenji Mogi 1
PMCID: PMC13485603  PMID: 42620526

Abstract

An 81-year-old man underwent sutureless repair of a left ventricular free wall rupture (LVFWR). A major postoperative complication, cardiogenic shock (CS), occurred on postoperative day two. An Impella 5.5 SmartAssist® (Abiomed, Denver, MA, US), surgically implanting microaxial left ventricular assist device (LVAD), was applied as a mechanical circulatory support (MCS) device and LV unloading device. The hemodynamic state drastically improved after the application, without major complications related to the microaxial LVAD.

Keywords: left ventricular free wall rupture, microaxial left ventricular assisted device, mechanical circulatory support, cardiogenic shock

Case report

An 81-year-old man was diagnosed with anterior LVFWR. Due to LVFWR, his circulatory status was obstructive shock, thus we decided to undergo emergency surgery without coronary angiography (CAG). The operative findings indicated an oozing rupture of the left ventricular (LV) anterior wall with a large hematoma (Figure 1). The operative cardiopulmonary bypass was not required because the oozing rupture site was anterior LV wall. The off-pump sutureless repair was facilitated by TachoSil® (CSL Behring, King of Prussia, PA, US) and Beriplast P Adhesion® (CSL Behring) was performed. The hemodynamic state looked been improved at this time. Postoperatively, the patient was managed with deep sedation and LV unloading using an intra-aortic balloon pumping (IABP). To maintain minimal pulsatility, limited amounts of inotropic agents were administered to mitigate the risk of re-rupture.

Figure 1.

Figure 1

Intraoperative image. Rupture site was shown in the Asterisk, surrounding a large hematoma. AAo and mPA indicated the ascending aorta and main pulmonary trunk, respectively.

Nevertheless, on postoperative day two, gradual progressive LV dysfunction caused by MI resulted in CS, consistent with SCAI staging D, and congestive heart failure with 24% of LV ejection fraction (LVEF) (Figure 2A, B), under two mcg/kg/min of dobutamine (DOB) and 0.025 mcg/kg/min of norepinephrine (NAd).It was not possible to increase dosage of catecholamines any further, concerning the re-rupture, that led to requiring an upgrade of the MCS device. Given these findings, it was determined that Impella constituted a suitable MCS device that reduces repaired LV wall tension, and Impella 5.5® was selected due to increased hemodynamic support and an extended implementation period when compared to Impella CP®.

Figure 2.

Figure 2

Trans-thoracic echogram and chest X-ray on postoperative day two. (A) shows left ventricular (LV) dysfunction LV ejection fraction was 24% calculated by modified Sympson method. (B) displays cardiomegaly and congestion of bilateral lungs, consistent with decompensated heart failure.

Prior to Impella 5.5® insertion, the right axillary artery was ensured to have a sufficient diameter to allow Impella 5.5® to pass through by computed tomography. In the operation, the Impella 5.5® was inserted into the LV via the right axillary artery anastomosed with a ten millimetres Triplex Advanced® artificial graft (TERUMO, Tokyo, Japan), without complications. The IABP was surgically removed concurrently. The perioperative hemodynamic state was monitored by Oximetry CV Catheter® (Edwards Lifesciences, Irvine, CA, US). The hemodynamics were improved by P7 support level, with decreased heart rate (HR) from 112 to 64 bpm, increased systolic blood pressure (BP) by 32 mmHg, increased central venous oxygen saturation 69–83%, decreased vasoactive-inotropic score 4.5 to zero, decreased lactate 3.32–1.31 mmol/L, and increased urine amount 778–2575 cc per day. The time to event figure was also attached in Figure 3. Regarding anticoagulation protocol during microaxial LVAD support, heparin-free purge solution until six hours since the insertion to prevent bleeding complication, followed by five units per one milliliter (U/mL) heparin contained purge next six hours and subsequently increased to 20 U/mL. Then, systemic heparin continuous infusion was added to achieve activated clotting time ranging from 160 to 180 s.

Figure 3.

Figure 3

Postoperative Time Couse.

We continued the same management to prevent the re-rupture of the myocardial infarcted (MI) site; LV unloading to mitigate the risk of re-rupture for one week. Impella® support level was controlled to achieve adequate unloading LV by monitoring LV end-diastolic pressure (LVEDP) on Impella 5.5® console, aiming at zero to 10 mmHg during that time. Cardioprotective agents were titrated according to the guideline-directed medical therapy during microaxial LVAD support, especially beta-blockers. We were concerned about the risk of re-rupture after suture-less repair, so we considered cardiac interventions should be refrained. Therefore, the CAG was done on postoperative day seven. The echocardiogram LVEF was 28%. The CAG revealed total occlusion of the proximal left anterior descending artery (LAD) and significant stenosis of the other two arteries. Considering the stable hemodynamics under microaxial LVAD support, no findings of asynergy at right coronary artery (RCA) and left circumflex artery (LCx) regions on echocardiogram, and the potential risks of re-rupture after revascularization, the coronary interventions were postponed at this period. The chest tubes were kept in place to prevent cardiac tamponade and to facilitate monitoring for postoperative bleeding at least one week after LVFWR when re-rupture may occur. They were removed on day 12. Cardiac rehabilitation was commenced, and microaxial LVAD support was gradually weaned. On day 12, tracheostomy was done, the ventilation was weaned on day 15, subsequently. The PCI was performed to RCA and LCx on day 28. This angiogram revealed that the occluded LAD had been recanalized at this time, therefore our cardiologists decided not to perform PCI to LAD. At this period, the echocardiogram LVEF was improved to 43%. On the regards of weaning microaxial LVAD, we comprehensively evaluated hemodynamic parameters. On day 30, the microaxial LVAD was successfully removed with; 5 mcg/kg/min of DOB and 0.15 mcg/kg/min of NAd without recurrence of heart failure. One month later, catecholamines were discontinued, and the patient was discharged on day 69, when LVEF was 43% and he is doing well at home.

Discussion

LVFWR rarely occurs in as low as 0.01% incidence1, Reperfusion therapy for AMI had been standard way that made LVFWR incidence lower. While this lower incidence, LVFWR is a critical condition accompanied by 30-day postoperative mortality rate of up to 28.6%2. The most common postoperative major adverse event is low cardiac output syndrome (20.7%), followed by re-rupture (7.1%)2. Therefore, management of these potential complications; MCS and LV unloading, reducing LV wall tension preventing the re-rupture influences patient prognosis.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is generally considered for circulatory support in cases of CS to support systemic perfusion. However, VA-ECMO solely cannot unload the LV, potentially aggravating LV function3. IABPs have been used to prevent re-rupture by adequate unloading of the LV4. Yet IABP postoperative support did not improve mortality1. Given these previous reports, VA-ECMO and IABP may not be suitable for postoperative management of LVFWR because they cannot provide sufficient circulatory support or LV unloading. In contrast, microaxial LVAD can overcome these disadvantages, providing robust circulatory support and LV unloading, even under arrhythmia, such as atrial fibrillation. From the above and in our case, V-A ECMO was not required given right heart function was normal and hemodynamic was prominently improved with solely microaxial LVAD support.

Potential adverse events should be considered when using microaxial LVAD support. microaxial LVAD can injure the LV wall, particularly during the acute phase of MI, when the infarcted myocardium is fragile. Therefore, it is crucial to take great care to insert microaxial LVAD into the LV. A former report revealed that Impella CP® has higher incidence of LV perforation5. According to instructions for the Impella®, the inlet of Impella 5.5® should be positioned 5.0 cm below the aortic valve, whereas for the Impella CP®, it is 3.5 cm with 4.0 cm of pigtail at the tip, which unavoidably results in a prolonged insertion into the LV than the Impella 5.5®, potentially leading to injury as well as suction on the LV wall. Thus, it is speculated that implantation of the Impella 5.5® after repair of LVFWR may be safer than the Impella CP®.

Another potential adverse event of microaxial LVAD is hemolysis, which causes acute kidney injury. Previous reports noted that Impella CP® and 2.5® increased the risks of mortality, bleeding, and acute kidney injury (AKI) when compared to IABP during VA-ECMO therapy6. On the other hand, Impella 5.0 and 5.5® decreased the 40-day in-hospital mortality without the increased risk of bleeding and AKI6, which might be attributed to lower incidence of hemolysis with the Impella 5.5® due to fewer rotating motors compared to the Impella CP®. Our patient did not show hemolysis or AKI due to microaxial LVAD using Impella 5.5®. Thus, Impella 5.5® may be optimal for prolonged circulatory assistance without microaxial LVAD-related complications.

Conclusions

This is the rare case of the postoperative use of Impella 5.5® SmartAssist after LVFWR. Combined therapy with sutureless repair for LVFWR and subsequent microaxial LVAD support is effective and can potentially improve surgical outcomes for LVFWR.

Patient consent

Informed consent was obtained from the patient for publication of case report according to the written informed consent form and we explained this verbally at our hospital. The patient agreed with the nature and purpose of the case report, potential risk and alternatives to participation in the report, and assurance of confidentiality.

Declaration of Generative AI and AI-assisted technologies in the writing process

Statement: During the preparation of this work the author used ChatGPT in order to translate this manuscript Japanese to English. After using this service, the author reviewed and edited the content as needed and takes full responsibility for the content of the published article.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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