Left ventricular free wall rupture caused by myocardial ischemia without treatable atherosclerotic coronary disease: a case series.

BACKGROUND: The clinical presentation of left ventricular free wall rupture (LVFWR) varies ranging from uneventful condition to congestive heart failure. Here we report two cases of LVFWR with different clinical presentation and notable outcome. A 53-year-old male presenting emergently with signs of myocardial infarction received immediate coronary angiography and thoracic CT-scan showing occlusion of the first marginal coronary branch without possibility of revascularization and minimal pericardial extravasation. Under ICU surveillance, LVFWR occurred 24 h later and was treated by pericardiocentesis and ECMO support followed by immediate uncomplicated surgical repair. Postoperative therapy-refractory vasoplegia and electromechanical dissociation caused fulminant deterioration and the early death of the patient. The second case is a 76-year old male brought to the emergency room after sudden syncope, clinical sings of pericardial tamponade and suspicion of a type A acute aortic dissection. Immediate CT-angiography excluded aortic dissection and revealed massive pericardial effusion and a hypoperfused myocardial area on the territory of the first marginal branch. Immediate sternotomy under mechanical resuscitation enabled removal of the massive intrapericardial clot and revealed LVFWR. After an uncomplicated surgical repair, an uneventful postoperative course, the patient was discharged with sinus rhythm and good biventricular function. One year after the operation, he is living at home, symptom free. DISCUSSION: Whereas the younger patient, who was clinically stable at hospital admission received delayed surgery and did not survive treatment, the older patient, clinically unstable at presentation, went into immediate surgery and had a flawless postoperative course. Thus, early surgical repair of LVFWR leads to best outcome and treating LVFWR as a high emergency regardless of the symptoms improve survival.

Successful Suture-Free Repair of Left Ventricular Rupture Using the EVARREST Patch.

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.

Severe tricuspid regurgitation with chordae tendinae rupture in CABG surgery.

A 58-year-old male patient was admitted with chest pain and was diagnosed with coronary heart disease. He was scheduled for coronary artery bypass grafting (CABG) under cardiopulmonary bypass (CPB). Intraoperative real-time transesophageal echocardiography (TEE) showed that the tricuspid valves were well-aligned and subtle regurgitation. Real-time TEE after separation from CPB showed severe tricuspid regurgitation and prolapsed chordae tendineae. The tricuspid chordae tendineae rupture due to a right atrial venous return cannula. The use of negative pressure to improve venous drainage during CPB may result in the tricuspid valve being adsorbed to the cannula, increasing the likelihood of injury to the tricuspid valve.

Up against the wall - emergency double myocardial rupture repair.

BACKGROUND: Left ventricular free wall rupture (LVFWR) and interventricular septal rupture (VSR) are potentially catastrophic mechanical complications after acute myocardial infarction (AMI). When they occur together, "double myocardial rupture" (DMR), survival is unlikely. DMR is seen in only 0.3% of all AMIs. With or without surgical intervention, the odds are against the patient. CASE PRESENTATION: A 57-year-old male self-referred to the emergency department of a remote hospital 5 days after first experiencing chest pain. Investigations in ED confirmed an inferior ST-segment elevation myocardial infarction (STEMI) complicated by DMR. Coronary angiography revealed a mid-course total occlusion of the right coronary artery (RCA). He was rapidly transferred to our regional cardiac surgical unit, arriving straight into the operating theatre, in cardiogenic shock. He was briefly conscious, before arresting prior to intubation and being massaged onto bypass. Not only did he survive the all-night operation, requiring a mitral valve replacement in the process, but he survived multiple postoperative complications to be eventually transferred on postoperative day 66, neurologically intact, to a peripheral unit to complete his rehabilitation. He was subsequently discharged home 88 days after the operation and was able to ambulate with a walking frame into his first postoperative follow-up clinic appointment. CONCLUSIONS: Our patient, against all odds, has survived DMR and multiple postoperative complications. We present the details of his case and the literature surrounding the condition. The patient's mental fortitude and his supportive family played a significant role, along with excellent multidisciplinary team work, in assuring his survival.

Surgical Outcome of Postinfarction Left Ventricular Free Wall Rupture.

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.

Male adolescent with cardiac rupture after blunt thoracic trauma.

Blunt cardiac injury, including a rupture of the atria or ventricle, is most commonly caused by motor vehicle collisions and falls from great heights. A rupture of a cardiac chamber is an extremely rare diagnosis with a high mortality rate. The best chance at survival can only be accomplished with timely intervention.To raise awareness of this potentially life-threatening injury, we describe the case of a male adolescent with cardiac rupture after blunt thoracic trauma. While the focused assessment with sonography in trauma (FAST) examination was negative, an additional CT showed pericardial effusion. During the operation a rupture of the right ventricle was observed.Even though the physical recovery of our patient is remarkable, the traumatic event still affects his mental well-being and activities in daily life. This case emphasises the need of a multidisciplinary approach to achieve the best possible physical and psychological recovery in multitrauma patients.

Sutureless repair with Hydrofit® and bovine pericardial patch for oozing-type postinfarction cardiac rupture.

Left ventricular free wall rupture is a fatal complication of myocardial infarction for which infarctectomy and reconstruction of the left ventricle using a prosthetic patch under cardiopulmonary bypass are performed. However, these surgical treatments remain challenging. Left ventricular free wall rupture secondary to acute myocardial infarction was diagnosed in an 86-year-old man. We performed sutureless repair of the left ventricular free wall rupture without cardiopulmonary bypass. During the operation, a pre-gluing bovine pericardial patch with Hydrofit® was placed twice on the ruptured site and manually pressed to provide complete hemostasis. The postoperative course was uneventful. This sutureless technique has the benefit of avoiding sutures in the fragile infarcted myocardium and might be effective for left ventricular free wall rupture treatment.

GDF5 deficiency prevents cardiac rupture following acute myocardial infarction in mice.

BACKGROUND: We previously showed that growth differentiation factor 5 (GDF5) limits infarct expansion post-myocardial infarction (MI). We now examine the acute post-MI role of GDF5 in cardiac rupture. METHODS AND RESULTS: Following permanent ligation of the left anterior descending artery, GDF5 deficiency (i.e., GDF5 knockout mice) reduced the incidence of cardiac rupture (4/24 vs. 17/24; P < .05), and improved survival over 28-d compared to wild-type (WT) mice (79% vs. 25%; P < .0001). Moreover, at 3-d post-MI, GDF5-deficient mice manifest: (a) reduced heart weight/body weight ratio (P < .0001) without differences in infarct size or cardiomyocyte size; (b) increased infarct zone expression of Col1a1 (P < .05) and Col3a1 (P < .01), suggesting increased myocardial fibrosis; and (c) reduced aortic and left ventricular peak systolic pressures (P ≤ .05), suggesting reduced afterload. Despite dysregulated inflammatory markers and reduced circulating monocytes in GDF5-deficient mice at 3-d post-MI, reciprocal bone marrow transplantation (BMT) failed to implicate GDF5 in BM-derived cells, suggesting the involvement of tissue-resident GDF5 expression in cardiac rupture. CONCLUSIONS: Loss of GDF5 reduces cardiac rupture post-MI with increased myocardial fibrosis and lower afterload, albeit at the cost of chronic adverse remodeling.

[Successful Treatment of Blow-out Type Left Ventricular Free Wall Rupture Using Sutureless Technique].

Blow-out type left ventricular free wall rupture is a serious complication of acute myocardial infarction, that carries high hospital mortality rates and poor surgical outcome. We report the case of an 88-year-old woman who developed cardiac tamponade following percutaneous coronary angioplasty for acute myocardial infarction. She was diagnosed with left ventricular free wall rupture, and rupture type was proved to be blow out after median sternotomy. To address this critical condition, we opted for the sutureless technique for its minimally invasive nature and ability to preserve left ventricular function. The patient was discharged from the hospital without any complications 22 days after surgery. Considering favorable, encouraging outcomes of this case, sutureless technique could be regarded as a viable option for blow-out type left ventricular free wall rupture.

Successful conservative treatment for left ventricular free wall rupture after acute myocardial infarction.

Left ventricular free wall rupture (LVFWR) is a rare but fatal complication of acute myocardial infarction (AMI). An 81-year-old female patient with several cardiovascular risk factors presented to the emergency department with symptoms of developing a chronic stomachache and cold sweat. An echocardiograph showed wall motion abnormalities from the lateral to posterior wall, as well as pericardial effusion containing clots of up to 17 mm in the posterior wall that indicated LVFWR after AMI. Although she was conscious after being brought to the initial care unit, she suddenly lost consciousness and fell into electromechanical dissociation (EMD). Endotracheal intubation was immediately initiated and her pericardial drainage and intra aortic balloon pump (IABP) placement, and hemodynamics recovered. Although she had 100% obstruction in the left circumflex artery (LCX) #12 on coronary angiography (CAG), she was discharged to the Intensive Care Unit (ICU) without percutaneous coronary intervention (PCI). Conservative treatment such as intubation, sedation, pericardiocentesis and strict blood pressure management as well as treatment by IABP long-term support led to the patient being uneventfully discharged after 60 days.

Risk of cardiac rupture among elderly patients with diabetes presenting with first acute myocardial infarction.

Objective: We aimed to analyze the risk of cardiac rupture (CR) in aged diabetic patients with acute ST-segment elevated myocardial infarction (STEMI) who were followed up for one month, and analyze its independent risk factors. Methods: A total of 3063 aged patients with first onset STEMI admitted to Beijing Anzhen Hospital from January 2001 to December 2020 were retrospectively included. There were 2020 patients without diabetes mellitus (DM) and 1043 patients with DM. We used propensity scores matching (PSM) method to balance baseline exposure factors between patients with or without DM, and all were divided the DM group (1043 cases) and the non-DM group (1043 cases) after the PSM. The primary outcome was CR (the composite rate of papillary muscle rupture, ventricular septum perforation, free wall rupture), which was diagnosed based on clinical manifestations and/or echocardiographic findings. Kaplan-meier survival analyses and log-rank test was used to evaluate the risk of CR between the two groups, and Cox regression analysis was used to evaluate the independent risk factors for CR. Results: After PSM, the baseline clinical data were similar between the DM and non-DM group (all P>0.05). However, level of glycated hemoglobin was significantly higher in the DM group (P<0.05). During 1 month of follow-up, there were 55 (2.64%) cases of CR, most occurred within 48h after admission (40 cases). Among the 55 cases, 11(0.53%) had papillary muscle rupture, 18(0.86%) had ventricular septum perforation, and 26(1.25%) had free wall rupture. Kaplan-meier survival analyses detected that the DM group was associated with significantly increased risk of CR (3.36% vs. 1.92%, HR=1.532, 95% CI: 1.054-2.346, P=0.030), ventricular septum perforation (1.05% vs. 0.67%, HR=1.464, 95% CI: 1.021-2.099, P=0.038) and free wall rupture (1.63% vs. 0.86%, HR=1.861, 95% CI: 1.074-3.225, P=0.027) than those in the non-DM group. Among the 2031 aged STEMI patients without CR, 144 cases (6.90%, 144/2086) died; and among the 55 patients with CR, 37 cases (1.77%, 37/2086) died due to CR. Therefore, twenty percent (20.44%, 37/181) of death was due to CR. Multivariate Cox regression analysis indicated that DM (HR=1.532, 95%CI: 1.054-2.346), age (HR=1.390, 95%CI: 1.079-1.791), female (HR=1.183, 95%CI: 1.049-1.334), troponin I (HR=1.364, 95%CI: 1.108-1.679), brain natriuretic peptide (HR=1.512, 95%CI: 1.069-2.139), revascularization (HR=0.827, 95%CI: 0.731-0.936) and ß-receptor blocker (HR=0.849, 95%CI: 0.760-0.948) were independent risk factors of CR (all P<0.05). Conclusion: DM as well as a few other factors, are independent determinants of CR. CR is not a rare event among the aged STEMI patients and twenty percent of deaths are due to CR. However, large sample-sized studies are warranted to confirm these findings.

Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarction.

Despite the high prevalence of heart failure in the western world, there are few effective treatments. Fibulin-3 is a protein involved in extracellular matrix (ECM) structural integrity, however its role in the heart is unknown. We have demonstrated, using single cell RNA-seq, that fibulin-3 was highly expressed in quiescent murine cardiac fibroblasts, with expression highest prior to injury and late post-infarct (from ~ day-28 to week-8). In humans, fibulin-3 was upregulated in left ventricular tissue and plasma of heart failure patients. Fibulin-3 knockout (Efemp1-/-) and wildtype mice were subjected to experimental myocardial infarction. Fibulin-3 deletion resulted in significantly higher rate of cardiac rupture days 3-6 post-infarct, indicating a weak and poorly formed scar, with severe ventricular remodelling in surviving mice at day-28 post-infarct. Fibulin-3 knockout mice demonstrated less collagen deposition at day-3 post-infarct, with abnormal collagen fibre-alignment. RNA-seq on day-3 infarct tissue revealed upregulation of ECM degradation and inflammatory genes, but downregulation of ECM assembly/structure/organisation genes in fibulin-3 knockout mice. GSEA pathway analysis showed enrichment of inflammatory pathways and a depletion of ECM organisation pathways. Fibulin-3 originates from cardiac fibroblasts, is upregulated in human heart failure, and is necessary for correct ECM organisation/structural integrity of fibrotic tissue to prevent cardiac rupture post-infarct.

Porphyromonas gingivalis, a periodontal pathogen, impairs post-infarcted myocardium by inhibiting autophagosome-lysosome fusion.

While several previous studies have indicated the link between periodontal disease (PD) and myocardial infarction (MI), the underlying mechanisms remain unclear. Autophagy, a cellular quality control process that is activated in several diseases, including heart failure, can be suppressed by Porphyromonas gingivalis (P.g.). However, it is uncertain whether autophagy impairment by periodontal pathogens stimulates the development of cardiac dysfunction after MI. Thus, this study aimed to investigate the relationship between PD and the development of MI while focusing on the role of autophagy. Neonatal rat cardiomyocytes (NRCMs) and MI model mice were inoculated with wild-type P.g. or gingipain-deficient P.g. to assess the effect of autophagy inhibition by P.g. Wild-type P.g.-inoculated NRCMs had lower cell viability than those inoculated with gingipain-deficient P.g. This study also revealed that gingipains can cleave vesicle-associated membrane protein 8 (VAMP8), a protein involved in lysosomal sensitive factor attachment protein receptors (SNAREs), at the 47th lysine residue, thereby inhibiting autophagy. Wild-type P.g.-inoculated MI model mice were more susceptible to cardiac rupture, with lower survival rates and autophagy activity than gingipain-deficient P.g.-inoculated MI model mice. After inoculating genetically modified MI model mice (VAMP8-K47A) with wild-type P.g., they exhibited significantly increased autophagy activation compared with the MI model mice inoculated with wild-type P.g., which suppressed cardiac rupture and enhanced overall survival rates. These findings suggest that gingipains, which are virulence factors of P.g., impair the infarcted myocardium by cleaving VAMP8 and disrupting autophagy. This study confirms the strong association between PD and MI and provides new insights into the potential role of autophagy in this relationship.

Papillary muscle rupture after transcatheter aortic valve implantation: A case report and literature review.

We present a case of posterior papillary muscle rupture associated with severe eccentric mitral regurgitation following transcatheter aortic valve implantation, that was successfully treated with transcatheter edge to edge mitral repair and review similar cases in literature.

Endogenous interleukin-22 prevents cardiac rupture after myocardial infarction in mice.

Myocardial infarction (MI) can result in fatal myocardial rupture or heart failure due to adverse remodeling and dysfunction of the left ventricle. Although recent studies have shown that exogenous interleukin (IL)-22 shows cardioprotective effect after MI, the pathophysiological significance of endogenous IL-22 is unknown. In this study, we investigated the role of endogenous IL-22 in a mouse model of MI. We produced MI model by permanent ligation of the left coronary artery in wild-type (WT) and IL-22 knock-out (KO) mice. The post-MI survival rate was significantly worse in IL-22KO mice than in WT mice due to a higher rate of cardiac rupture. Although IL-22KO mice exhibited a significantly greater infarct size than WT mice, there was no significant difference in left ventricular geometry or function between WT and IL-22KO mice. IL-22KO mice showed increase in infiltrating macrophages and myofibroblasts, and altered expression pattern of inflammation- and extracellular matrix (ECM)-related genes after MI. While IL-22KO mice showed no obvious changes in cardiac morphology or function before MI, expressions of matrix metalloproteinase (MMP)-2 and MMP-9 were increased, whereas that of tissue inhibitor of MMPs (TIMP)-3 was decreased in cardiac tissue. Protein expression of IL-22 receptor complex, IL-22 receptor alpha 1 (IL-22R1) and IL-10 receptor beta (IL-10RB), were increased in cardiac tissue 3 days after MI, regardless of the genotype. We propose that endogenous IL-22 plays an important role in preventing cardiac rupture after MI, possibly by regulating inflammation and ECM metabolism.

Cardiac rupture in acute myocardial infarction: a cardiac magnetic resonance study.

AIMS: We assessed the feasibility of cardiac magnetic resonance (CMR) and the role of myocardial strain in the diagnostic work-up of patients with acute myocardial infarction (AMI) and a clinical suspicion of cardiac rupture (CR). METHODS AND RESULTS: Consecutive patients with AMI complicated by CR who underwent CMR were enrolled. Traditional and strain CMR findings were evaluated; new parameters indicating the relative wall stress between AMI and adjacent segments, named wall stress index (WSI) and WSI ratio, were analysed. A group of patients admitted for AMI without CR served as control. 19 patients (63% male, median age 73 years) met the inclusion criteria. Microvascular obstruction (MVO, P = 0.001) and pericardial enhancement (P < 0.001) were strongly associated with CR. Patients with clinical CR confirmed by CMR exhibited more frequently an intramyocardial haemorrhage than controls (P = 0.003). Patients with CR had lower 2D and 3D global radial strain (GRS) and global circumferential strain (in 2D mode P < 0.001; in 3D mode P = 0.001), as well as 3D global longitudinal strain (P < 0.001), than controls. The 2D circumferential WSI (P = 0.010), as well as the 2D and 3D circumferential (respectively, P < 0.001 and P = 0.042) and radial WSI ratio (respectively, P < 0.001 and P: 0.007), were higher in CR patients than controls. CONCLUSION: CMR is a safe and useful imaging tool to achieve the definite diagnosis of CR and an accurate visualization of tissue abnormalities associated with CR. Strain analysis parameters can give insights into the pathophysiology of CR and may help to identify those patients with sub-acute CR.

Cardiac rupture during acute myocardial infarction : Autopsy study (2004-2020).

INTRODUCTION: Cardiac rupture is a rare but critical complication of myocardial infarction with an incidence of 1 to 3% of cases. We aimed in this autopsy study to analyze the anatomical, epidemiological, cardiac, and coronary profiles of cardiac rupture in the Monastir region. METHODS: We conducted a descriptive study with retrospective data collection of all cases of myocardial infarction complicated by a cardiac rupture over seventeen years (2004-2020). RESULTS: Thirty-one cases were included in this study. The mean age of the cases was 67 years with a male predominance. Sixteen cases (57%) had cardiovascular risk factors. The most common symptomatology reported before death was acute chest pain in 57% of cases. Fourteen cases (45%) corresponded to the definition of sudden cardiac death. At autopsy, the heart had a mean weight of 452.78 grams. A large hemopericardium was associated in 90% of cases. Myocardial rupture involved the posterior wall of the left ventricle in 50% of cases. The myocardial rupture occurred at a site of acute myocardial infarction in 86% of cases and on a myocardial scar in 14% of cases. The coronary study showed double or triple vessel atherosclerotic coronary artery disease in 57% of cases with fresh thrombi at the infarct-related coronary in 11% of cases. CONCLUSIONS: Our analysis found that cardiac rupture mostly involved elderly subjects with underlying cardiovascular risk factors. Our findings sustain that age is a determining prognostic factor after acute coronary syndrome with the need for further education and awareness-raising efforts to speed up access to care for these patients.