a b s t r a c t

Left ventricular free wall rupture (LVFWR) is a rare and fatal mechanical complication following an acute myo- cardial infarction (AMI). Cases of survival after LVFWR due to ST-segment elevation myocardial infarction treated with a conservative treatment strategy are extremely rare. In this case, a 55-year-old male pa- tient with several Cardiovascular risk factors presented to the emergency department with symptoms of ongo- ing chest pain and syncope. The patient’s electrocardiogram was in sinus rhythm with ST-elevation on I, aVL, and V4-6 leads. His myoglobin and Troponin I levels were elevated. Due to the unstable hemodynamic state of the patient, Bedside echocardiography was performed. The echocardiography indicated LVFWR after AMI. Pericardiocentesis was used to restore a satisfactory hemodynamic state in the patient. Following the initial treatment, the patient opted for a conservative treatment strategy and was uneventfully discharged after 19 days.

(C) 2020 The Author(s). This is an open access article under the CC BY-NC-ND license

(http://creativecommons.org/licenses/by-nc-nd/4.0/).

Introduction

Cardiac rupture is a rare but fatal complication of AMI. It accounts for approximately 20% of STEMI patient in-hospital deaths [1]. The three types of cardiac rupture are ventricular septal rupture, free-wall rup- ture, and Papillary muscle rupture. Treatment of LVFWR is challenging due to the limited time available to administer emergent therapeutic in- tervention after onset. The survival rate of AMI patients with conserva- tively treated LVFWR was reported to be only 10% [2]. Recently, we encountered a case in which the patient survived an LVFWR after STEMI with conservative treatment.

Case

A 55-year-old male with no history of myocardial infarction was transferred to the emergency department due to ongoing chest pain (duration: two days) and syncope prior to arrival. He had a history of hypertension and smoking. His vital signs were as follows: temperature

Abbreviations: AMI, Acute myocardial infarction; STEMI, ST-segment elevation myo- cardial infarction; LVFWR, left ventricular free wall rupture; PPCI, Primary percutaneous coronary intervention; CAG, coronary angiogram; IABP, intra-aortic balloon pump.

* Corresponding author at: Department of Cardiology, The First Affiliated Hospital of Soochow University, No.188, Shizi Road, Suzhou 215006, Jiangsu, China.

E-mail address: [email protected] (X. Zhao).

¹Liyuan Yan and Haipeng Wang contributed equally to this work and should be considered

as co-first authors.

36.2 ?C, heart rate 120 beats/min, respiratory rate 18 breaths/min, and blood pressure 63/55 mmHg. An electrocardiogram showed sinus rhythm with an elevation of ST segments on I, aVL, and V4-6 leads (Fig. 1), indicating acute anterolateral myocardial infarction. He had el- evated myoglobin (574 ng/ml) and troponin I (310 pg/ml) levels. He was diagnosed with STEMI and given aspirin (300 mg) and ticagrelor (180 mg). Dopamine and norepinephrine were administered to main- tain blood pressure. The patient was transferred to the cardiac catheter- ization laboratory for a Primary percutaneous coronary intervention ; however, the patient’s hemodynamics worsened and a bedside echocardiography was performed. The bedside echocardiography re- vealed regional left ventricular wall motion abnormalities and pericar- dial effusion, indicating LVFWR (Fig. 2). Pericardiocentesis with ultrasound guidance was performed, and 180 ml of hemorrhagic peri- cardial effusion was aspirated. After drainage of the pericardial effusion, the patient’s hemodynamic state improved. His blood pressure was 110/70 mmHg and his heart rate was 90 beats/min. A coronary angio- gram (CAG) showed an occluded diagonal branch (Fig. 3). We recom- mended that the patient receive Surgical repair of the rupture. However, the patient and his family chose to maintain Conservative therapy. His drug regimen included Dual antiplatelet therapy with aspi- rin and clopidogrel, statin, beta-blocker, Calcium-channel blocker, and angiotensin-converting enzyme inhibitor. Following no fluid drainage two weeks later, the pericardium catheter was removed. The patient was discharged 19 days after admission following no further events. His condition remained stable one month after discharge.

22 L. Yan et al. / American Journal of Emergency Medicine 39 (2021) 21-23

Fig. 1. Electrocardiogram revealing anterolateral ST-segment elevation.

Fig. 2. Echocardiogram showing pericardial effusion (white arrow). AO, aorta; RV, right ventricle.

This study was approved by the Ethics Committee of the First Affili- ated Hospital of Soochow University. Written consent for the case re- port was obtained from the patient.

Discussion

During the era of thrombolytic therapy, or the no reperfusion era, the incidence of cardiac rupture after STEMI was 6% [3]. In recent years, the incidence of cardiac rupture after AMI has decreased to less than 2% with the widespread use of PPCI [4]. Among in-hospital deaths due to AMI, cardiac rupture is a common cause [5]. The mortality rate for free-wall rupture is 75% to 90%, and the mortality rate for ventricular septal rupture is 40% to 75% [6].

Timely diagnosis and an emergent treatment strategy are essential for saving patients’ lives. The median time of death following LVFWR is 8 h [7]. Risk factors for cardiac rupture include advanced age, Female gender, absence of prior angina, history of hypertension, no history of myocardial infarction, anterior infarct, absence of PPCI, Single-vessel disease without collateral circulation, anemia, and elevated heart rate

Fig. 3. Coronary angiography revealing an occluded diagonal branch (white arrow). LAD, left anterior descending artery; D1, the first diagonal branch.

[4,6,8]. The clinical manifestations of LVFWR range from hemodynamic instability to sudden cardiac death. Echocardiography is the most criti- cal tool for a timely diagnosis with a sensitivity and specificity of more than 90% [7]. echocardiographic findings of LVFWR range from a peri- cardial collection of blood or thrombus to overt cardiac tamponade [9]. Pericardiocentesis, which confirms hemorrhagic pericardial effu- sion, further supports an LVFWR diagnosis. Surgery can help to confirm the location of the cardiac rupture. In this case, the patient did not re- ceive surgical repair.

After an LVFWR diagnosis, the first step of treatment is to restore a satisfactory hemodynamic state using pericardiocentesis, an intra- aortic balloon pump (IABP), intravenous fluid, and inotropic support

L. Yan et al. / American Journal of Emergency Medicine 39 (2021) 21-23 23

[10]. Due to the poor prognosis of conservative strategies [2], surgical repair is typically the cornerstone of the treatment strategy. A prompt CAG before surgical repair will reveal the condition of the coronary ar- teries, which may help surgeons design the most appropriate Surgical strategy [11]. Conservative management includes maintaining hemody- namic stability, prolonged bed rest, strict blood pressure control, and in- sertion of an IABP [10].

In conclusion, LVFWR is a rare but often lethal complication after AMI. Timely diagnosis is key to successful emergent interventions that save patients’ lives. Bedside echocardiography is the most important tool for diagnosing LVFWR after AMI and has high diagnostic levels of sensitivity and specificity. The development of LVFWR surgical repair has improved the prognosis of AMI patients with LVFWR; however, as seen in this case, a conservative treatment strategy is a substitution for surgical repair when patients are unwilling to undergo surgery.

Funding sources

This research did not receive any specific grants from funding agen- cies in the public, commercial, or not-for-profit sectors.

Declaration of Competing Interest

None.

Acknowledgements

None.

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