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BACKGROUND: Takotsubo syndrome (TS) is a reversible cause of heart failure; however, a minority of patients can develop serious complications, including cardiac rupture (CR). OBJECTIVES: Analyze case reports of CR related to TS, detailing patient characteristics to uncover risk factors and prognosis for this severe complication. METHODS: We conducted a systematic search of MEDLINE and Embase databases to identify case reports of patients with TS complicated by CR, from inception to October 2023. RESULTS: We included 44 subjects (40 females; 4 males) with a median age of 75 (IQR 71-82) years, of White/Caucasian (61%) or East Asian/Japanese (39%) ethnicity. An emotional trigger was present in 15 (34%) subjects and an apical ballooning pattern was observed in all cases (100%). ST-segment elevation was reported in 39 (93%) of 42 cases, with the anterior myocardial segments (37 [88%]) being the most compromised, followed by lateral (26 [62%]) and inferior (14 [33%]) segments. The median time to cardiac rupture was 48 (5-120) hours since admission, with the left ventricular free wall (25 [57%]) being the most frequent site of perforation. Surgery was attempted in 16 (36%) cases, and 28 (64%) patients did not survive. CONCLUSIONS: CR related to TS is a rare complication associated with high mortality and affecting elderly females, specially from White/Caucasian or East Asian/Japanese descent, presenting with anterior or lateral ST-segment elevation, and an apical ballooning pattern. Although data is limited and additional prospective studies are needed, the awareness of this life-threatening complication is crucial to early identify high-risk patients. CONDENSED ABSTRACT: Cardiac rupture is a rare complication of Takotsubo syndrome. We conducted a systematic review of cases complicated by cardiac rupture, and we identified 44 subjects (40 females and 4 males) with a median age of 75 (IQR 71-82) years, of White/Caucasian (61%) or East Asian/Japanese (39%) ethnicity, all with an apical ballooning pattern (100%). The median time to cardiac rupture was 48 (5-120) hours since admission, with the left ventricular free wall (25 [57%]) being the most frequent site of perforation. Surgery treatment was attempted in 16 (36%) cases, and 28 (64%) patients did not survive.

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Left ventricular free wall rupture is a lethal complication of myocardial infarction. Although emergent surgical repair is the treatment of choice, the method of repair remains highly individualized. This report presents a case of spontaneous coronary artery dissection in a patient with Turner syndrome that led to left ventricular free wall rupture and was successfully repaired on cardiopulmonary bypass using a suture-free technique with the EVARREST Fibrin Sealant Patch.

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BACKGROUND: Left ventricular free wall rupture (LVFWR) is a rare and fatal complication after acute myocardial infarction. Early recognition and aggressive treatment are recommended. METHODS: Between August 1999 and February 2023, 11 patients aged between 64 and 79 years developed LVFWR after acute myocardial infarction (mean interval, 3.5 days). Three patients had active bleeding (blowout-type LVFWR), and the other 8 patients experienced the oozing or sealed state. Eight patients were treated using a sutureless technique with Teflon felt and glue, 2 patients were treated using the primary suture closure technique, and 1 was treated using both the primary suture and the sutureless technique with Teflon felt and glue. RESULTS: One patient died in the operating room as a result of bleeding. Cardiovascular stability and hemostasis were achieved in the other 10 patients. There were 3 early deaths (all 3 cases as a result of area bleeding; 1 was treated with primary suture, 2 with sutureless glue). Three patients received percutaneous coronary intervention before discharge. All 8 remaining patients survived and were discharged. Three patients were lost to follow-up. The follow-up period ranged from 2 to 97 months, with 4 patients exhibiting New York Heart Association class I symptoms and 1 exhibiting New York Heart Association class II symptoms. CONCLUSION: Optimal surgical treatment for postinfarction LVFWR remains controversial. The sutureless technique may be a promising strategy for treating postinfarction LVFWR.

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Background: Most pericardial effusions that occur in the setting of ST-segment elevation myocardial infarction (STEMI) are small, simple, and without symptomology. However, in its most severe form, pericardial effusion can precipitate cardiac tamponade, and when untreated, can cause abrupt hemodynamic instability. Pericardial effusion may be a manifestation of left ventricular free-wall rupture, hemorrhagic pericarditis, or aortic dissection involving a coronary artery. Case Report: We describe the case of a 65-year-old male who experienced chest pain for several days prior to admission but delayed seeking care because he wished to avoid coronavirus disease 2019 exposure. Upon arrival, he was hemodynamically unstable. Electrocardiogram was consistent with anterior STEMI. Bedside echocardiogram demonstrated a hypertrophic left ventricle with preserved function and a large, complex pericardial effusion with cardiac tamponade physiology. Computed tomography of the chest identified hemopericardium but was unable to delineate etiology. The patient underwent emergent thoracotomy because of persistent shock, and during the surgery, left ventricular free-wall rupture was identified and repaired. Coronary artery bypass grafting to the patient's left anterior descending artery was also performed. The patient remained asymptomatic at 2-year follow-up. Conclusion: The differential for hemodynamic compromise in a patient with STEMI is broad, but quickly distinguishing pump failure from other life-threatening causes of shock is imperative to dictate time-sensitive management decisions. The presence of a hemorrhagic pericardial effusion in the setting of STEMI is a surrogate marker for a severe infarct and can help the bedside physician determine whether a patient will be better served in the catheterization lab for revascularization or in the operating room for surgical repair.

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INTRODUCTION AND OBJECTIVES: Mechanical complications confer a dreadful prognosis in ST-elevation myocardial infarction (STEMI). Their prevalence and prognosis are not well-defined in the current era of primary percutaneous coronary intervention (pPCI) reperfusion networks. We aimed to analyze prevalence and mortality trends of post-STEMI mechanical complications over 2 decades, before and after the establishment of pPCI networks. METHODS: Prospective, consecutive registry of STEMI patients within a region of 850 000 inhabitants over 2 decades: a pre-pPCI period (1990-2000) and a pPCI period (2007-2017). We analyzed the prevalence of mechanical complications, including ventricular septal rupture, papillary muscle rupture, and free wall rupture (FWR). Twenty eight-day and 1-year mortality trends were compared between the 2 studied decades. RESULTS: A total of 6033 STEMI patients were included (pre-pPCI period, n=2250; pPCI period, n=3783). Reperfusion was supported by thrombolysis in the pre-pPCI period (99.1%) and by pPCI in in the pPCI period (95.7%). Mechanical complications developed in 135 patients (2.2%): ventricular septal rupture in 38 patients, papillary muscle rupture in 24, and FWR in 73 patients. FWR showed a relative reduction of 60% in the pPCI period (0.8% vs 2.0%, P<.001), without significant interperiod changes in the other mechanical complications. After multivariate adjustment, FWR remained higher in the pre-pPCI period (OR, 1.93; 95%CI, 1.10-3.41; P=.023). At 28 days and 1 year, mortality showed no significant changes in all the mechanical complications studied. CONCLUSIONS: The establishment of regional pPCI networks has modified the landscape of mechanical complications in STEMI. FWR is less frequent in the pPCI era, likely due to reduced transmural infarcts.

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Objectives: Post-infarction ventricular septal defect (VSD) is one of the known complications after acute myocardial infarction. This study investigated the clinical results after surgical repair of VSD. Methods: This retrospective study included all patients undergoing surgical repair of VSD from 1996 to 2020 in Oman. Results: Out of a total of 75 patients, 62.5% were men, with a mean age of 59 years. The mean follow-up was 17.2 (7.5) years. Of the 75 patients, 34 (45.3%) patients died within 30 days. Total survival was 41.3% at 5 years, while the 10-year survival rate was 33.3%. Outcomes and predictors for 30 days mortality were the number of concomitant coronary involvement and anastomoses performed, residual postoperative shunt and postoperative dialysis. Conclusion: Even with surgical repair, early mortality of post-infarction septal defect is still considerably high. Early repair and the anatomically posterior rupture are predictors of early mortality. In patients surviving the immediate postoperative period, long-term survival is limited by pre-existing coronary artery disease, postoperative renal failure and the presence of a residual postoperative shunt.

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Background: Mechanical complications of acute myocardial infarction represent life-threatening events, including ventricular septal rupture (VSR), left ventricular free-wall rupture (LVFWR) and papillary muscle rupture (PMR). In-hospital mortality is high, even when prompt surgery can be offered. The role of concomitant coronary artery bypass grafting (CABG) in the surgical treatment of these conditions is still debated. Methods: A systematic review of the literature, from 2000 onwards, about these complications was performed, analyzing data of subjects receiving versus not-receiving concomitant CABG. Primary outcome was early mortality. Secondary outcome was late mortality for hospital survivors. Subgroup analysis for VSR, LVFWR and PMR was also performed. Results: Thirty-six studies were identified, including 4,321 patients (mostly VSR-related). Preoperative coronarography was performed in 92.2% of the cases, showing single-vessel disease in 54.3% of patients. Concomitant CABG rate was 49.0%. Early mortality was 32.6% and late mortality was 40.0% with 5.2 years of mean follow-up. The analysis showed no difference in early (OR 0.96; P=0.60) or late mortality (RR 0.91; P=0.49) between CABG and non-CABG group. In subgroup analysis, concomitant CABG was associated with significantly lower mortality at long term for PMR (RR 0.42; P=0.001), although it showed a higher, but not significant, mortality in VSR (RR 1.24; P=0.20). Conclusions: Concomitant CABG in the treatment for post-infarction mechanical complications showed no significant impact on both early and late mortality, although deserving some distinctions among different types of complication and single versus multiple vessel disease. However, larger, dedicated studies are required to provide more consistent data and evidence.

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Abstract We describe a rare case of isolated right ventricular inferior free-wall rupture and cardiogenic shock caused by occlusion of the distal left circumflex coronary artery. Our case highlights the central role of transthoracic echocardiography in identifying unexpected conditions that can guide management - in our case involving early surgical intervention, thus leading to favourable patient outcomes.

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Objective: To determine the clinical characteristics, therapeutic and in-hospital mortality of patients with mechanical complications post myocardial infarction. Materials and methods: Observational, descriptive and retrospective study. We included patients >18 years old with a diagnosis of mechanical complication post myocardial infarction hospitalized at the Instituto Nacional Cardiovascular- INCOR in Lima -Peru, from January 1, 2017 to December 31, 2021. Variables like clinical characteristics, treatments, complications, and in-hospital mortality were studied. Results: We found 37 cases, with a predominance of males (73.0%) and a median age of 73 years old. The location of the myocardial infarction was 51.4% in the anterior wall and 43.2% in the inferior wall. The patients received reperfusion therapy with fibrinolysis in 5 cases (13.5%), coronary angioplasty in 5 (13.5%), and 73% received only medical management prior to the diagnosis of mechanical complications. Of the 37 patients, 13 (35.1%) presented isolated ventricular free wall rupture, 12 (32.4%) isolated interventricular septum rupture, 10 (27.0%) the combination of ventricular free wall rupture and interventricular septum, and 2 (5.4%) papillary muscle rupture. In-hospital mortality was 51.4%. Conclusions: The ventricular free wall rupture was the most frequent complication, patients with mechanical complications after myocardial infarction still maintain high intra-hospital mortality rates, mainly in those who did not have adequate surgical treatment.

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We describe a rare case of isolated right ventricular inferior free-wall rupture and cardiogenic shock caused by occlusion of the distal left circumflex coronary artery. Our case highlights the central role of transthoracic echocardiography in identifying unexpected conditions that can guide management - in our case involving early surgical intervention, thus leading to favourable patient outcomes.

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A 79-year-old man had an out-of-hospital acute ST-segment-elevation myocardial infarction with cardiac arrest. Cardiopulmonary resuscitation performed by a bystander resulted in traumatic hemopericardium. We discuss the patient's case, highlight the challenges of managing simultaneously life-threatening thrombosis and hemorrhage, and present our conclusions regarding the patient's eventual death.

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Over the past few decades, advances in pharmacological, catheter-based, and surgical reperfusion have improved outcomes for patients with acute myocardial infarctions. However, patients with large infarcts or those who do not receive timely revascularization remain at risk for mechanical complications of acute myocardial infarction. The most commonly encountered mechanical complications are acute mitral regurgitation secondary to papillary muscle rupture, ventricular septal defect, pseudoaneurysm, and free wall rupture; each complication is associated with a significant risk of morbidity, mortality, and hospital resource utilization. The care for patients with mechanical complications is complex and requires a multidisciplinary collaboration for prompt recognition, diagnosis, hemodynamic stabilization, and decision support to assist patients and families in the selection of definitive therapies or palliation. However, because of the relatively small number of high-quality studies that exist to guide clinical practice, there is significant variability in care that mainly depends on local expertise and available resources.

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Ventricular septal rupture (VSR) represents a rare complication of acute myocardial infarction, often presenting with cardiogenic shock and associated with high in-hospital mortality despite prompt intervention. Although immediate surgery is recommended for patients who cannot be effectively stabilized, the ideal timing of intervention remains controversial. Mechanical circulatory support (MCS) may allow hemodynamic stabilization and delay definitive treatment even in critical patients. However, the interactions between MCS and VSR pathophysiology as well as potentially related adverse effects remain unclear. A systematic review was performed, from 2000 onward, to identify reports describing MCS types, effects, complications, and outcomes in the pre-operative VSR-related setting. One hundred eleven studies (2,440 patients) were included. Most patients had well-known negative predictors (e.g., cardiogenic shock, inferior infarction). Almost all patients had intra-aortic balloon pumps, with additional MCS adopted in 129 patients (77.5% being venoarterial extracorporeal membrane oxygenation). Mean MCS bridging time was 6 days (range: 0 to 23 days). In-hospital mortality was 50.4%, with the lowest mortality rate in the extracorporeal membrane oxygenation group (29.2%). MCS may enhance hemodynamic stabilization and delayed VSR treatment. However, the actual effects and interaction of the MCS-VSR association should be carefully assessed to avoid further complications or incorrect MCS-VSR coupling.

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BACKGROUND: Systemic erythematous lupus (SLE) is an autoimmune disease associated with significant cardiovascular morbidity and mortality, even in young patients. CASE SUMMARY: A young female with recently diagnosed SLE under corticotherapy developed pulmonary oedema and respiratory failure. The diagnostic workup revealed mildly elevated cardiac troponin, significantly elevated NT-proB-type natriuretic peptide (NT-proBNP) and mild pericardial effusion without other echocardiographic abnormalities. Systemic erythematous lupus-associated myocarditis was presumed, and her clinical status improved after corticotherapy intensification. However, transthoracic echocardiogram repeated days later revealed a large pericardial effusion with findings suggestive of a contained myocardial rupture originating in the inferolateral basal left ventricular (LV) segment, which was confirmed by computed tomography scan. Cardiac catheterization exhibited normal coronary arteries. The patient was submitted to cardiac surgery and the LV pseudoaneurysm was successfully repaired. DISCUSSION: Myocardial rupture with LV pseudoaneurysm formation usually occurs in the setting of acute myocardial infarction, but also in other rare contexts. Cardiac rupture is associated with an extremely high mortality unless early diagnosis and urgent surgical intervention are provided.

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INTRODUCTION: Studies have been performed to identify the association between ABO blood groups and coronary artery disease. However, data is scarce about the impact of ABO blood groups on heart rupture (HR) after acute myocardial infarction (AMI). METHODS: We conducted a retrospective case-control study that included 61 consecutive patients with HR after AMI during a period from 1 January 2012 to 1 December 2019. The controls included 600 patients who were selected randomly from 8143 AMI patients without HR in a ratio of 1:10. Univariate and multivariate logistic regression analysis were used to identify the association between ABO blood groups and HR. RESULTS: Patients with blood group A had a greater risk of HR after AMI than those with non-A blood groups (12.35% vs 7.42%, P < 0.001). After adjusting for age, gender, heart rate at admission, body mass index (BMI), and systolic blood pressure (SBP), blood group A was independently related to the increased risk of HR after AMI (OR = 2.781, 95% CI 1.174-7.198, P = 0.035), and remained as an independent risk factor of HR after AMI in different multivariate regression models. CONCLUSION: Blood group A is significantly associated with increased HR risk after AMI.

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BACKGROUND: Regulatory T cells (Tregs), traditionally recognized as potent suppressors of immune response, are increasingly attracting attention because of a second major function: residing in parenchymal tissues and maintaining local homeostasis. However, the existence, unique phenotype, and function of so-called tissue Tregs in the heart remain unclear. METHODS: In mouse models of myocardial infarction (MI), myocardial ischemia/reperfusion injury, or cardiac cryoinjury, the dynamic accumulation of Tregs in the injured myocardium was monitored. The bulk RNA sequencing was performed to analyze the transcriptomic characteristics of Tregs from the injured myocardium after MI or ischemia/reperfusion injury. Photoconversion, parabiosis, single-cell T-cell receptor sequencing, and adoptive transfer were applied to determine the source of heart Tregs. The involvement of the interleukin-33/suppression of tumorigenicity 2 axis and Sparc (secreted acidic cysteine-rich glycoprotein), a molecule upregulated in heart Tregs, was further evaluated in functional assays. RESULTS: We showed that Tregs were highly enriched in the myocardium of MI, ischemia/reperfusion injury, and cryoinjury mice. Transcriptomic data revealed that Tregs isolated from the injured hearts had plenty of differentially expressed transcripts in comparison with their lymphoid counterparts, including heart-draining lymphoid nodes, with a phenotype of promoting infarct repair, indicating a unique characteristic. The heart Tregs were accumulated mainly because of recruitment from the circulating Treg pool, whereas local proliferation also contributed to their expansion. Moreover, a remarkable case of repeatedly detected T-cell receptor of heart Tregs, more than that of spleen Tregs, suggests a model of clonal expansion. Besides, HelioshighNrp-1high phenotype proved the mainly thymic origin of heart Tregs, with a small contribution of phenotypic conversion of conventional CD4+ T cells, proved by the analysis of T-cell receptor repertoires and conventional CD4+ T cells adoptive transfer experiments. The interleukin-33/suppression of tumorigenicity 2 axis was essential for sustaining heart Treg populations. Last, we demonstrated that Sparc, which was highly expressed by heart Tregs, acted as a critical factor to protect the heart against MI by increasing collagen content and boosting maturation in the infarct zone. CONCLUSIONS: We identified and characterized a phenotypically and functionally unique population of heart Tregs that may lay the foundation to harness Tregs for cardioprotection in MI and other cardiac diseases.

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BACKGROUND: Cardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture can be accelerated by thrombolytic therapy, but the relevance of this risk factor remains controversial. METHODS: We analyzed protease-activated receptor 4 (Par4) expression in mouse hearts with MI and investigated the effects of Par4 deletion on cardiac remodeling and function after MI by echocardiography, quantitative immunohistochemistry, and flow cytometry. RESULTS: Par4 mRNA and protein levels were increased in mouse hearts after MI and in isolated cardiomyocytes in response to hypertrophic and inflammatory stimuli. Par4-deficient mice showed less myocyte apoptosis, reduced infarct size, and improved functional recovery after acute MI relative to wild-type (WT). Conversely, Par4-/- mice showed impaired cardiac function, greater rates of myocardial rupture, and increased mortality after chronic MI relative to WT. Pathological evaluation of hearts from Par4-/- mice demonstrated a greater infarct expansion, increased cardiac hemorrhage, and delayed neutrophil accumulation, which resulted in impaired post-MI healing compared with WT. Par4 deficiency also attenuated neutrophil apoptosis in vitro and after MI in vivo and impaired inflammation resolution in infarcted myocardium. Transfer of Par4-/- neutrophils, but not of Par4-/- platelets, in WT recipient mice delayed inflammation resolution, increased cardiac hemorrhage, and enhanced cardiac dysfunction. In parallel, adoptive transfer of WT neutrophils into Par4-/- mice restored inflammation resolution, reduced cardiac rupture incidence, and improved cardiac function after MI. CONCLUSIONS: These findings reveal essential roles of Par4 in neutrophil apoptosis and inflammation resolution during myocardial healing and point to Par4 inhibition as a potential therapy that should be limited to the acute phases of ischemic insult and avoided for long-term treatment after MI.

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