Ventricular double rupture following myocardial infarction: a case report and literature review

Abstract

Background

The frequency of mechanical complications related to transmural myocardial infarction (MI) has decreased due to the widespread implementation of reperfusion therapies. However, mortality related to these complications remains high, requiring prompt intervention by a Heart Team. Ventricular double rupture (VDR) is a particularly rare and fatal MI complication.

Case presentation

A 58-year-old female patient presenting with 3 days of chest pain was diagnosed with ST-elevation MI. She underwent primary percutaneous coronary intervention of the left anterior descending artery. Transthoracic echocardiogram revealed an apical ventricular septum rupture and a mild pericardial effusion suggestive of free wall rupture. Emergent surgical repair included ventricular septal defect closure with a heterologous pericardial patch and repair of the free wall rupture with Dacron patch placement. Perioperative intraaortic balloon pump support was utilized. The patient had a favorable clinical course and was asymptomatic at her cardiology follow-up.

Conclusions

VDR is the combination of two types of mechanical complications of MI. High clinical suspicion is necessary in hemodynamically unstable patients and those with risk factors for myocardial rupture, warranting echocardiographic evaluation for its diagnosis and characterization. Treatment of VDR is primarily surgical and may involve mechanical circulatory support (MCS). Despite advances in reperfusion therapies and surgical techniques, the prognosis of VDR remains poor. Our patient had a favorable outcome highlighting the importance of a multidisciplinary approach.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12245-025-00907-2.

Background

The leading cause of death globally is ischemic heart disease, accountable for 13% of the total deaths of the world in 2021 [1]. Mechanical complications related to acute myocardial infarction (MI) occur in 0.27–0.91% of patients following ST-elevation MI [2–4]. Reperfusion therapies have reduced the frequency of mechanical complications. However, mortality related to these complications has not significatively decreased, and they remain a determinant factor in the clinical evolution after MI [5]. Here we report a patient presenting with a ST-elevation MI complicated with a double left ventricular rupture which was successfully treated with surgical ventricular repair using a heterologous pericardial patch.

Case presentation

A 58-year-old female patient with no relevant medical history presented with oppressive retrosternal pain radiating to the back with onset 3 days prior to admission, with a progressive intensity reaching of 8 out of 10 on the numeric rating scale, triggered by physical activity and associated to progressive dyspnea until rest. She had a delayed presentation attributed to pandemic-related barriers to care. At physical examination the patient was tachycardic, tachypneic, with respiratory distress, requiring supplementary oxygen with a non-rebreather mask, with normal blood pressure and temperature. On auscultation, heart sounds were rhythmic and bilateral rales were heard. Rapid sequence intubation was performed. The electrocardiogram (ECG) showed sinus tachycardia, right bundle branch block and ST segment elevation in V2 to V6 leads. Chest x-ray was suggestive of pulmonary edema and bilateral pleural effusion (Fig. 1). Initial laboratory evaluation demonstrated leukocytosis with neutrophilia, suggestive of a systemic inflammatory response. In addition, mild elevation of lactate, metabolic acidosis with partial respiratory compensation and hyperkalemia were consistent with tissue hypoperfusion. These findings reflected a critical clinical state warranting urgent intervention. Detailed laboratory results are provided in Table 1.

Fig. 1.

Chest x-ray. Perihilar haze, upper lobe pulmonary venous diversion, septal lines, bilateral diffuse opacities, bilateral blunting of costophrenic angles, cardiomegaly. Centrally placed endotracheal tube, right subclavian central venous catheter with distal end projecting into the right atrium

Table 1.

Laboratory results on admission

Test	Patient value	Reference value	Unit
Leukocyte count	12,470	3980–10,040	/µL
Neutrophil count	11,270	1560–6130	/µL
Hemoglobin	11.6	12–15.7	g/dL
Platelets	180,000	182,000–369,000	/µL
Creatinine	0.87	0.51–0.95	mg/dL
Blood urea nitrogen	24.5	6–20	mg/dL
Sodium	134.3	135–145	mmol/L
Potassium	6.02	3.5–5.1	mmol/L
Lactate	2.34	0.5–2.2	mmol/L
Arterial blood gases
pH	7.29	7.35–7.45
FiO2	0.4
PO2	104.7	83–108	mmHg
PO2/FiO2 ratio	261.7		mmHg
PCO2	29.2	35–48	mmHg
HCO3	13.8	21–28	mmol/L
BE	−11.5		mmol/L

FiO2 Fraction of inspired oxygen, PO2 Partial pressure of oxygen, PCO2 Partial pressure of carbon dioxide, HCO3 Bicarbonate, BE Base excess

Following guideline-directed management for ST-elevation MI, the patient was urgently taken to the catheterization laboratory for primary percutaneous coronary intervention. A coronary angiogram revealed diffuse calcified disease and critical stenosis in the middle third of the left anterior descending artery (LAD) and 90% stenosis in the middle segment of the posterior descending artery (PDA) (Fig. 2). Ventriculography was not performed to minimize delays in revascularization. Angioplasty and insertion of a drug-eluting stent in the mid-LAD was performed (see Supplementary file Video 1).

Fig. 2.

Coronary angiogram. A Critical stenosis of the middle third of the left anterior descending artery. B 90% stenosis of the middle third of the posterior descending artery

After the procedure, the patient was admitted to the intensive care unit requiring invasive mechanical ventilation and inotropic support with dobutamine. Transthoracic echocardiography (TTE) showed a mildly reduced left ventricular ejection fraction (LVEF) of 45%, with anterior wall akinesia and apical akinesia and ballooning, findings consistent with a recent extensive anterior infarction. A loss of myocardial wall continuity was observed between the mid and apical segments of the interventricular septum, consistent with an apical ventricular septal defect (VSD) measuring up to 14 mm in diameter. Color Doppler imaging revealed turbulent flow across the defect, indicative of a left-to-right shunt with an interventricular peak gradient of 35 mmHg. The right ventricle was dilated and exhibited systolic dysfunction, likely due to volume overload and pulmonary hypertension, with an estimated pulmonary artery systolic pressure of 70 mmHg. Additional findings included mild tricuspid regurgitation, biatrial enlargement and inferior vena cava dilatation. Of particular concern was a mild pericardial effusion containing multiple echogenic images compatible with fresh thrombi, raising suspicion for an evolving free wall rupture (FWR), without signs of cardiac tamponade. The precise location of the FWR could not be clearly delineated on transthoracic imaging (Fig. 3; see Supplementary Video 2).

Fig. 3.

Transthoracic echocardiogram. A Apical four-chamber view. Apical ventricular septal defect. Small pericardial effusion. Apical epicardial thrombus. B Color Doppler imaging: Left-to-right shunt through the VSD

The patient was taken to emergent surgery (Fig. 4) following pre-procedural insertion of an intra-aortic balloon pump (IABP). The surgical intervention was initiated under general intravenous anesthesia with orotracheal intubation, followed by an intraoperative transesophageal echocardiogram (TEE). Invasive hemodynamic monitoring was established using a Swan-Ganz catheter, central venous line, arterial line and IABP. The patient had a previous right saphenectomy. A left saphenectomy was performed for PDA revascularization; however, the graft was of poor quality. Internal mammary artery grafting was not pursued to avoid prolonging the surgical time, given the patient’s critical condition. After systemic heparinization, cardiopulmonary bypass (CPB) was initiated via aortic and bicaval cannulation. Myocardial protection was achieved with antegrade blood cardioplegia (Chaux solution, 120 cc), complemented by Custodiol (1,000 cc). Moderate hypothermia to 34 °C was induced to enhance myocardial protection during aortic cross-clamping, which lasted 80 min, with a total CPB time of 123 min.

Fig. 4.

Intraoperative photographic record. A The free wall rupture has been extended longitudinally to allow complete exposure of the interventricular defect. A bovine pericardial patch is used to close the ventricular septal defect with circumferential 3 − 0 polypropylene sutures. B A Dacron patch is used to repair the myocardial wall with interrupted, pledget-reinforced polypropylene sutures

An apical thrombus was removed, uncovering an apical FWR, from which a 4 cm longitudinal ventriculotomy was created 2 cm lateral to the LAD, revealing a septal defect with a maximum diameter of 25 mm. Daggett’s technique was used to repair the defect (Figs. 4 and 5). Necrotic tissue surrounding the VSD was debrided, and the defect was closed using a heterologous pericardial patch secured with interrupted 3 − 0 polypropylene sutures with pledget reinforcement, avoiding necrotic tissue. A Dacron patch was used to close the ventriculotomy, also reinforced with pledget sutures. Fibrin glue was applied over the suture line to enhance sealing. During weaning from CPB with gradual rewarming, spontaneous sinus rhythm was restored. However, significant bleeding at the ventriculotomy suture was observed, requiring reinforcement with additional interrupted stitches and a continuous polypropylene suture.

Fig. 5.

Schematic representation of Daggett’s technique. A Exposure of the ventricular septal defect (VSD) through a ventriculotomy and placement of a pericardial patch to close the defect. B Closure of the VSD with a bovine pericardial patch and the ventriculotomy with a Dacron patch. C Closure of the ventriculotomy

Hemostasis was supported by transfusion of blood products (2 units of fresh frozen plasma, 12 units of cryoprecipitate, 2 apheresis platelet units, and 3 packed red blood cell units), as well as administration of Octaplex (factors II, VII, IX, X, and proteins S and C) and topical hemostatic agents. IABP support was maintained to reduce left ventricular afterload and preserve coronary perfusion pressures. To further decrease left ventricular wall stress, nitroglycerin was administered. Dobutamine was discontinued due to tachycardia.

Post-bypass, the patient developed severe ventricular bleeding and signs of coagulopathy. Vasopressor support with norepinephrine (0.05 mcg/kg/min) and vasopressin was administered. The post-bypass intraoperative TEE confirmed correct patch positioning and adequate ventricular function. Due to persistent bleeding, the sternum was left open with packing and a vacuum-assisted closure (VAC) system, and the patient was transferred to the intensive care unit in critical condition for advanced management.

Twenty-four hours later, a second surgical intervention was performed. Intraoperative TEE revealed a LVEF of 30% and no residual shunts. The VAC system was removed, the cavity was irrigated, and mediastinal and left chest tubes were inserted. The chest wall was closed.

Postoperatively, the patient had a favorable clinical course. She was weaned from the IABP within 24 h without need for inotropic or vasopressor support. She was extubated 48 h after the surgery and required parenteral nitroglycerin for blood pressure control over the following seven days. The Heart Team decided not to pursue PDA revascularization, opting instead to continue medical management. The patient did not report chest pain or dyspnea, her physical examination was normal and she was discharged on dual antiplatelet therapy, a high-intensity statin and guideline-directed heart failure treatment. At follow-up, she was asymptomatic, with adequate blood pressure control and no signs of heart failure. Control echocardiogram showed a left ventricle with normal dimensions, a 45% ejection fraction and apical akinesia, right ventricle had normal dimensions and systolic function, there was no evidence of shunts and valvular function was preserved. The timeline of events is summarized in Fig. 6.

Fig. 6.

Timeline of clinical events

Discussion

Mechanical complications of MI include VSR, FWR and papillary muscle rupture (PMR). Ventricular double rupture (VDR) is the combination of two the previously mentioned. It is an infrequent and usually late presentation, that may not be diagnosed until surgical intervention and is associated with high mortality rates despite advances in reperfusion therapies [6], owing to the complex nature of the injury and the high risk of cardiac tamponade and cardiogenic shock. In a case series [7] VDR was observed in 0.3% of all MI cases, in 3% of those with FWR and in 16.1% of VSR. Of the 10 VDR cases, both VSR and FWR were apical in 8 patients, as was in our case. The survival rate was 20%.

Mann [8] classified VDR according to finding in pathology specimens into true double rupture and junctional rupture. In the true double rupture, separate tears are observed in the ventricular septum and free wall. In the junctional type, a single rupture involving the junction between the septum and the free wall is seen. Surgical findings in this case revealed a true double rupture.

Ventricular rupture should be suspected in any hemodynamically unstable patient or one who presents with signs of cardiac tamponade, especially in relation to unsuccessful or late reperfusion [5]. Risk factors for myocardial rupture include ST elevation or Q wave in the ECG at admission, anterior wall involvement, late or unsuccessful reperfusion, no history of angina, MI or diabetes and female sex [9, 10]. It has been proposed that patients who lack some cardiovascular risk factors and consequently have less burden of coronary artery disease, are less likely to have developed collateral circulation, leading to necrosis and rupture of the involved tissue. Socioeconomic factors also play an important role, impacting on access to early specialized medical evaluation and reperfusion therapy [5]. In regard to the mentioned risk factors, our patient was a female presenting three days after the onset of chest pain, with no prior history of cardiovascular disease or diabetes, and showed anterior wall ST-segment elevation on the admission ECG.

An early echocardiogram is essential for the detection of mechanical complications of MI, leading to timely intervention. In hemodynamically unstable patients, bedside echocardiography is increasingly relevant. TTE findings include a ventricular septal defect with left-to-right shunt in VSR; mitral regurgitation with leaflet flail and visualization of a ruptured papillary muscle in PMR; and varied findings of FWR including the loss of continuity of the myocardial wall with flow across the defect, pericardial effusion, cardiac tamponade physiology and epicardial clots. Cardiac magnetic resonance imaging can also be useful in the detection and characterization of a VDR, particularly in cases of contained rupture or an irregularly shaped VSR [11, 12]. In this case, echocardiographic assessment revealed a VSR and indirect signs of a FWR, prompting intervention.

Hemodynamically unstable patients may benefit from intravenous fluids, inotropic support, mechanical circulatory support (MCS) or pericardiocentesis, in which the finding of hemopericardium is highly suggestive of a FWR [2]. The definitive treatment for VDR is surgical management, which solves cardiac tamponade, closes the defect and prevents recurrent rupture or pseudoaneurysm formation. Given the life-threatening nature of this mechanical complication, particularly due to FWR-related hemopericardium, most patients require urgent or emergent surgical repair. Stabilization with mechanical circulatory support devices may allow brief postponement of surgery to optimize patient condition [13]. Although delayed intervention has been associated with improved outcomes in isolated VSR — allowing time for fibrosis of the initially friable myocardial tissue — [14] such an approach is rarely feasible in VDR. In this scenario, surgical timing is most often dictated by the urgency of the clinical presentation rather than by optimal tissue conditions.

Surgery is guided by findings and available materials, with a sutured or sutureless approach. Sutured repair includes linear closure, infartectomy and closure, and patch covering. Sutureless repair attaches a patch onto the myocardial surface with surgical glue, which is ineffective in presence of active bleeding [11]. In the presented case, Daggett’s direct septal closure technique was used, which involves placing two prosthetic patches for closing the VSD and the ventriculotomy [15], the latter being an extension of the apical FWR in our patient. Bleeding from the left ventriculotomy suture line was a complication of the procedure [16] despite administration of human prothrombin complex and the use of IABP to reduce left ventricular afterload and wall stress. David’s infarct exclusion method was not feasible due to difficulty in closing the ventriculotomy without a patch [17]. Performing myocardial revascularization along with the correction of ventricular rupture is associated with improved survival. However, postoperative mortality can exceed 40% [6, 7]. Patients with prohibitive surgical risk or those who cannot access emergent repair receive medical treatment, with notably high mortality rates reaching 90% [18].

The role of MCS in the management of MI mechanical complications has been explored in several studies with mixed outcomes, its impact on long-term survival remains uncertain. Pre-operative use of MCS serves as a bridge to surgical treatment in patients with cardiogenic shock and post-operative support may help weaning from cardiopulmonary bypass as it can reduce left intra-ventricular pressure and increase coronary blood flow. However, a meta-analysis of randomized trials found no significant reduction in 6-month mortality (regardless of the device used) and increased major bleeding and vascular complications in patients with infarct-related cardiogenic shock (AMICS) [13]. IABP is the most frequently used MCS device. In a comparative study, the Impella device was associated with higher in-hospital mortality and increased costs compared to IABP in patients with AMICS [19].

Our patient was treated with percutaneous LAD reperfusion, surgical ventricular repair with a patch covering approach and perioperative IABP support, leading to a satisfactory clinical course. Mechanical complications are determinants of clinical outcomes and survival after MI. Despite the decrease in their incidence with early reperfusion therapies, no significant reduction in related mortality has been observed. High clinical suspicion and echocardiographic evaluation can be decisive in identifying mechanical complications, leading to prompt surgical intervention. Perioperative medical management and MCS play a significant role in the care of patients with mechanical MI complications.

Abbreviations

AMI

Acute Myocardial Infarction

AMICS

Acute Myocardial Infarction-Related Cardiogenic Shock

BE

Base Excess

COVID-19

Coronavirus Disease 2019

CPB

Cardiopulmonary bypass

ECG

Electrocardiogram

FiO₂

Fraction of Inspired Oxygen

FWR

Free Wall Rupture

HCO₃

Bicarbonate

IABP

Intra-Aortic Balloon Pump

ICU

Intensive Care Unit

LAD

Left Anterior Descending Artery

LVEF

Left Ventricular Ejection Fraction

MCS

Mechanical Circulatory Support

PDA

Posterior Descending Artery

PMR

Papillary Muscle Rupture

PO₂

Partial Pressure of Oxygen

PCO₂

Partial Pressure of Carbon Dioxide

TEE

Transesophageal Echocardiography

TTE

Transthoracic Echocardiogram

VAC

Vacuum-Assisted Closure

VDR

Ventricular Double Rupture

VSD

Ventricular Septal Defect

VSR

Ventricular Septal Rupture

Authors' contributions

C.A.C., P.O. and M.J.R. conceptualized the case report, reviewed the literature and drafted the manuscript. J.A.Z. and J.S. selected the diagnostic imaging figures, helped interpret the imaging findings and contributed insights with their expertise on the field. A.D.P., C.E.V. and G.A.C. led the clinical management of the patient, reviewed the manuscript and provided critical input on the clinical aspects of the case.

Funding

This study was not supported by any external funding.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

This case report was reviewed and approved by the Institutional Review Board (IRB) of Fundación Valle del Lili, Cali, Colombia. The patient provided informed consent for the use and publication of their medical information, and all identifying details have been anonymized to ensure confidentiality.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.