Successful emergency surgical intervention in acute non-ST-segment elevation myocardial infarction with rupture: A case report

Abstract

BACKGROUND

The incidence of acute myocardial infarction (AMI) is rising, with cardiac rupture accounting for approximately 2% of deaths in patients with acute ST-segment elevation myocardial infarction (STEMI). Ventricular free wall rupture (FWR) occurs in approximately 2% of AMI patients and is notably rare in patients with non-STEMI. Types of cardiac rupture include left ventricular FWR, ventricular septal rupture, and papillary muscle rupture. The FWR usually leads to acute cardiac tamponade or electromechanical dissociation, where standard resuscitation efforts may not be effective. Ventricular septal rupture and papillary muscle rupture often result in refractory heart failure, with mortality rates over 50%, even with surgical or percutaneous repair options.

CASE SUMMARY

We present a rare case of an acute non-STEMI patient who suffered sudden FWR causing cardiac tamponade and loss of consciousness immediate before undergoing coronary angiography. Prompt resuscitation and emergency open-heart repair along with coronary artery bypass grafting resulted in successful patient recovery.

CONCLUSION

This case emphasizes the risks of AMI complications, shares a successful treatment scenario, and discusses measures to prevent such complications.

Key Words: Acute non-ST segment elevation myocardial infarction; Cardiac rupture; Acute myocardial infarction; Free wall rupture; Case report

Core Tip: Acute myocardial infarction (MI) is often complicated by mechanical disruptions such as free wall rupture or ventricular septal perforation, typically associated with ST-elevation MI, but rarely encountered in non-ST-segment elevation MI. Cardiac rupture leading to acute pericardial tamponade is frequently fatal. In this report, we describe an uncommon case of successful surgical intervention in a patient with non-ST-segment elevation MI complicated by cardiac rupture.

INTRODUCTION

Acute myocardial infarction (AMI) refers to acute myocardial injury characterized by an increase and/or decrease in serum cardiac troponin, with at least one value above the upper reference limit (99^th percentile of the reference value), accompanied by clinical evidence of acute myocardial ischemia. This evidence includes: (1) Acute myocardial ischemic symptoms; (2) New ischemic electrocardiographic changes; (3) New pathological Q waves; (4) New imaging evidence of myocardial loss or regional wall motion abnormalities; and (5) Coronary angiography or intracoronary imaging, or autopsy confirming coronary artery thrombosis[1]. Based on the presence of ST-segment elevation on the patient’s electrocardiogram (ECG), AMI can be classified into ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI).

AMI complicated by cardiac rupture accounts for about 4%-20% of all-cause deaths in myocardial infarction (MI) patients, with ventricular free wall rupture (FWR) occurring in 2% of AMI patients[2]. The incidence of STEMI was significantly higher than that of NSTEMI. Depending on the location, cardiac rupture can be divided into FWR, ventricular septal rupture (VSR), and papillary muscle rupture. The probability of ventricular FWR is higher than that of VSR and papillary muscle rupture, and the incidence is higher in females than in males[3].

In recent years, there has been a steady increase in the incidence of AMI[4]. Despite advancements in reperfusion strategies such as emergency percutaneous coronary intervention and thrombolysis, the mortality rate associated with mechanical complications of AMI remains exceedingly high[5]. In particular, cardiac FWR, a rare but serious complication of AMI, has an extremely high mortality rate once it occurs[6]. This report presents a successful case of treating acute NSTEMI complicated by cardiac rupture. In this case, we emphasize the importance of recognizing early AMI complications and providing insights into effective treatment strategies.

CASE PRESENTATION

Chief complaints

A 66-year-old female was admitted to hospital due to recurrent discomfort in the precordial region for more than 10 days.

History of present illness

The patient had experienced precordial discomfort for the past 10 days, which occurred after physical activity and was accompanied by chest tightness. Each episode lasted approximately 5-10 minutes and was relieved by rest. In the past three days, the frequency of these symptoms increased, and the patient began to experience precordial discomfort even with mild exertion. Coronary computed tomography (Figure 1) angiography conducted on May 29, 2023, identified calcification and moderate to severe narrowing in the mid-to-distal section of the right coronary artery (RCA), as well as calcification with moderate narrowing in the proximal section of the left anterior descending artery. Upon further treatment at our hospital, the outpatient diagnosis included coronary artery disease, angina pectoris, and hypertension.

Figure 1 Coronary computed tomography images multiple calcifications.

History of past illness

The patient had a history of hypertension for over 10 years, which was managed with oral nifedipine extended-release tablets, resulting in a blood pressure range of 130-140 mmHg/70-80 mmHg. Additionally, the patient had undergone colon tumor surgery two years prior.

Personal and family history

There were none personal and family history of the disease.

Physical examination

Upon admission, physical examination revealed a blood pressure of 128 mmHg/72 mmHg, clear consciousness, and a fair general condition. Auscultation of the lungs revealed coarse breath sounds without rales. The heart exhibited a regular rhythm, normal heart sounds, and a heart rate of 60 beats per minute (bpm). Valvular auscultation did not reveal pathological murmurs. The abdomen was soft, non-tender, and without rebound tenderness, and no edema was observed in the lower extremities.

Laboratory examinations

Upon admission, the ECG showed sinus rhythm and a normal ECG (Figure 2). Post-admission laboratory results indicated, troponin I at 2.3 ng/mL, myoglobin at 124 ng/mL, N-terminal proBNP at 1310 pg/mL, creatine kinase at 926 U/L, creatine kinase type M and B at 28 U/L, and D-dimer at 0.3 mg/L.

Figure 2 First electrocardiogram sinus rhythm, roughly normal.

Imaging examinations

Echocardiography revealed significant findings including a left atrium diameter of 3.6 cm, a left ventricle diameter of 4.4 cm, and a left ventricular ejection fraction of 67%. Further evaluation demonstrated mild mitral and tricuspid regurgitation.

MULTIDISCIPLINARY EXPERT CONSULTATION

Consultation with the Department of Cardiology, Coronary Angiography and Internal Medicine are recommended.

FINAL DIAGNOSIS

Coronary atherosclerotic heart disease, acute NSTEMI, hypertension, and status after colon cancer surgery.

TREATMENT

Following admission, the patient received dual antiplatelet therapy (aspirin and clopidogrel) and intravenous nitrates. Coronary angiography was scheduled on the afternoon. During transfer to the catheterization room, the patient reported throat pain, loss of consciousness, and agonal respiration. Immediate cardiac monitoring revealed a heart rate of 70 bpm, sinus rhythm, and blood pressure of 80 mmHg/50 mmHg. Vasoactive drugs were administered intravenously, but the patient’s condition deteriorated with a decrease in heart rate to 30 bpm. Cardiopulmonary resuscitation was initiated, including chest compressions and endotracheal intubation was initiated. Bedside echocardiography revealed a large pericardial effusion, indicating cardiac tamponade due to cardiac rupture. Blind pericardiocentesis was performed under fluoroscopic guidance, and 10 mL of hemorrhagic fluid was aspirated from approximately 3 cm below the left nipple using a 20 mL syringe. Following this procedure, the patient’s heart rate increased to 110 bpm, and blood pressure increased to approximately 100 mmHg/60 mmHg. However, after one minute later, the heart rate decreased to 30 bpm. Subsequently, under ultrasound guidance, a puncture was made at the intersection of the left fourth and fifth intercostal spaces and left midclavicular line. A 6F pigtail catheter was inserted, and continuous negative pressure drainage was initiated using a 20 mL syringe. Additionally, 4 units of packed red blood cells were prepared for immediate transfusion.

Transfer and surgical procedure

The patient was transferred to a tertiary hospital under maintenance with dopamine at 100 μg/kg/minute and epinephrine at 20 μg/kg/minute. Upon arrival, the patient was promptly transferred to the operating room for thoracotomy to repair the cardiac rupture, followed by coronary artery bypass grafting. Challenges emerged during the procedure, particularly in draining pericardial effusion, potentially owing to coagulation abnormalities. The patient was positioned supine and underwent immediate cannulation of the superficial vein, internal jugular vein, and radial artery under general anesthesia. As the surgery progressed, the patient’s blood pressure gradually dropped, and the heart rate decreased to 40 bpm, leading to cardiac arrest. External chest compressions were promptly initiated, followed by chest and lower limb disinfection, the application of sterile drapes, and emergency thoracotomy. Median sternotomy was performed, and after opening the pericardium, approximately 100 mL of dark red blood clots were removed (Figure 3A). Upon further examination after irrigation, a 5 mm tear was identified on the diaphragmatic surface of the left ventricle, approximately 3 cm from the apex (Figure 3B), accompanied by profuse bleeding of bright red blood. Surrounding this tear was a 5 cm × 6 cm area of dark red myocardial necrosis, resulting in significantly reduced ventricular activity and fragile tissue due to necrosis. Multiple attempts to suture the tear using prolene sutures resulted in further tearing of the edges. Hepatic needle suturing with pledgets on healthy tissue edges has also proved ineffective in controlling bleeding.

Figure 3 Transfer and surgical procedure. A: Hemopericardium, dark red blood clot; B: Myocardial tear, roughly 3 cm from the apex; C: Surgical process.

The patient maintained a persistently low blood pressure throughout the procedure, with systolic pressure fluctuating between 30-50 mmHg, requiring continuous administration of high-dose vasopressor medications and blood transfusions. Subsequent attempts involved using multiple pledgeted prolene sutures in a purse-string fashion around the original suture line, resulting in a significant improvement in bleeding after tightening and knotting (Figure 3C). After repair, there was no revealed bleeding from the left ventricular tear. Coronary exploration identified plaques in various areas, particularly in the RCA with soft plaque formation in the anterior descending branch. Although no significant plaques were palpable, the patient was diagnosed with left posterior descending artery occlusion leading to cardiac rupture based on preoperative coronary computed tomography angiography and intraoperative findings. This diagnosis prompted consideration of aortic-RCA bypass. Utilizing the left great saphenous vein with the assistance of a cardiac stabilizer, an aortic-RCA bypass was successfully performed without the need to stop the heart. Following the procedure, there was a gradual stabilization of blood pressure and heart rhythm. The wound closure process involved meticulous hemostasis, which was reinforced by titanium wire sutures weaving through both sides of the sternum. Upon inspection of the anastomotic sites and wounds, no evidence of active bleeding was observed. The pericardium was intermittently closed, and drainage tubes were placed in the right pleural cavity and mediastinum. The instruments and materials were thoroughly checked for accuracy, and the sternum was secured and reinforced using four titanium wires and one titanium cable. The chest was closed in sequence, and incisions in the lower limbs were sutured.

OUTCOME AND FOLLOW-UP

The endotracheal tube was removed on postoperative day 5, and the patient showed improvement during the one-month hospitalization. After a six-month follow-up, the patient’s general condition continued to be favorable, leading to discharge.

DISCUSSION

Ventricular FWR, which occurs in approximately 2% of AMI patients and is notably rare in NSTEMI[7]. In this study, we present a rare case of an acute NSTEMI patient who suffered sudden FWR causing to cardiac tamponade and loss of consciousness immediately before undergoing coronary angiography. Prompt resuscitation and emergency open-heart repair along with coronary artery bypass grafting resulted in successful patient recovery. This case emphasizes the risk of AMI complications, shares a successful treatment scenario, and discusses measures to prevent such complications.

The incidence of cardiac rupture peaks within 24 hours after AMI[8], with a second peak occurring between days 3-5 post-AMI[9-11]. FWR often leads to acute cardiac tamponade or electromechanical dissociation, posing challenges for the current rescue techniques[12]. Studies by Roberts[13] and Shoji et al[14] revealed majority cases of cardiac rupture identified, all of which were STEMI patients. Cardiac rupture is extremely rare in NSTEMI patients, with a 100% mortality rate for FWR and an average survival period of less than one day[15]. Reported risk factors for cardiac rupture include emotional stress, straining during bowel movements, elevated blood pressure, and inappropriate use of positive inotropic agents[16]. Studies have linked cardiac rupture occurrence to factors such as the location and size of MI, intracardiac pressures, myocardial contractility, lipid profile, cardiac afterload, age, sex, time of presentation, and treatment modalities[17]. Elderly MI patients often present with characteristics that increase susceptibility to mechanical complications, such as multivessel disease, extensive myocardial involvement, thinning ventricular walls, increased fat infiltration, decreased ventricular compliance, and poor fibrous repair capability post-MI[18].

Anterior wall MI, especially STEMI, is associated with a higher risk of cardiac FWR. However, this patient did not exhibit obvious ST-segment elevation on the ECG from admission to resuscitation which is a highly unusual occurrence. The current guidelines for STEMI recommend immediate surgical repair in patients with cardiac rupture (Class I recommendation). Surgical intervention is advised for ventricular FWR, whereas percutaneous closure is suggested for VSR. In this particular case, successful management of cardiac FWR involved the following: (1) Early identification of sudden Aschoff’s syndrome and hypotension, leading to consideration of cardiac etiology; (2) Timely pericardiocentesis following confirmation of pericardial effusion via ultrasound, with immediate blind pericardiocentesis using a 20 mL syringe to relieve pericardial pressure and allow for subsequent catheter placement; (3) Continuous negative pressure drainage with a 20 mL syringe after connecting the pericardial drainage tube without a collection bag to prevent recurrent pericardial tamponade; (4) Prompt intubation for respiratory support and transfusion of packed red blood cells for supportive therapy; and (5) Efficient coordination with a tertiary hospital for swift transfer and definitive open-chest surgical treatment.

CONCLUSION

In conclusion, based on our findings, the prevention of cardiac rupture in AMI is crucial. Patients should follow strict bed rest protocols, avoiding strenuous activities such as turning over, coughing, defecation, and urination which can increase cardiac load. Furthermore, enhanced education and heightened awareness among healthcare professionals are essential to effectively preventing and manage such complications.

ACKNOWLEDGEMENTS

We would like to express our deepest gratitude to all those who contributed to the successful completion of this case report. First and foremost, we extend our heartfelt thanks to the patient and their family for their cooperation and trust in our medical team during such a critical and challenging time. Their courage and resilience throughout the entire process were truly inspiring.

We are particularly grateful to the surgical team, nurses, and support staff in the cardiology and emergency departments, whose swift and professional actions were instrumental in the successful management of this case. Their commitment to providing high-quality care ensured a positive outcome, and we sincerely appreciate their tireless dedication. Special thanks to the hospital administration for their continued support, as well as to the editorial team of this journal for their guidance throughout the submission process. Lastly, we are grateful to our families for their understanding and encouragement, which enabled us to devote the necessary time and energy to this project. Without their unwavering support, this work would not have been possible. Thank you all for your invaluable contributions.