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.

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.

[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 Staged Repair of Double Rupture after Acute Myocardial Infarction:Report of a Case].

Double rupture is a very rare, and life-threatening complication after acute myocardial infection (AMI), which defined as the coexistence of any two of the three types of rupture include left ventricular free wall repture (LVFWR), ventricular septal perforation (VSP) and papillary muscule repture (PMR). We report here a case of successful staged repair of double rupture combined LVFWR and VSP. A 77-year-old woman with diagnosis of AMI in the anteroseptal area fell into cardiogenic shock suddenly just before starting coronary angiography. Echocardiography showed left ventricular free wall rupture, then an emergent operation was performed under intraaortic balloon pumping (IABP) and percutaneous cardiopulmonary support (PCPS) assistance using bovine pericardial patch and felt sandwich technique. Intraoperative transesophageal echocardiography revealed ventricular septal perforation on the apical anterior wall. Her hemodynamic condition was stable, therefore we selected a staged VSP repair to avoid surgery on freshly infarcted myocardium. Twenty-eight days after the initial operation, VSP repair was performed using the extended sandwich patch technique via right ventricle incision. Postoperative echocardiography revealed no residual shunt.

[Ventricular Pseudoaneurysm after Sutureless Repair of Postinfarction Free Wall Rupture of the Left Ventricle:Report of a Case].

We herein report a case of a left ventricular pseudoaneurysm following sutureless repair for left ventricular free wall rupture. A 78-year-old woman underwent emergency sutureless repair for left ventricular free wall rupture following acute myocardial infarction. Three months later, echocardiography revealed an aneurysm in the postero-lateral wall of the left ventricle. The ventricular aneurysm was incised during reoperation, and defect in the left ventricular wall was closed with a bovine pericardial patch. Histopathologically, the aneurysm wall did not contain any myocardium, confirming the diagnosis of pseudoaneurysm. Although sutureless repair is a simple and highly effective method for oozing-type left ventricular free wall rupture, post-procedural pseudoaneurysm can develop both in acute and chronic phases. Consequently, long-term follow-up is mandatory.

Heart Rate Reduction with Ivabradine Prevents Cardiac Rupture after Myocardial Infarction in Mice.

PURPOSE: Cardiac rupture is a fatal complication following myocardial infarction (MI). An increase in heart rate (HR) is reportedly an independent risk factor for cardiac rupture during acute MI. However, the role of HR reduction in cardiac rupture after MI remains to be fully elucidated. We aimed to evaluate the therapeutic efficacy of HR reduction with ivabradine (IVA) on post-MI cardiac rupture in mice. METHODS: We induced MI in mice by ligating the left anterior descending coronary artery. Subsequently, we subcutaneously implanted osmotic pumps filled with IVA solution or vehicle (Veh) in the surviving MI mice at 24 h postoperatively. We biochemically analyzed the myocardium on day 5, additionally observed the mice for 10 days, and analyzed the rates of cardiac rupture and non-cardiac rupture death, and survival after MI. RESULTS: HR was significantly lower in the IVA-treated mice, whereas blood pressure was comparable between the two groups. Compared to the Veh-treated mice, apoptosis was significantly reduced in the MI border zone in the IVA-treated mice. Although there were no differences in the infarct size of the surviving MI mice between the two groups, HR reduction with IVA significantly reduced cardiac rupture (rupture rate 26 and 8% in the Veh-treated and IVA-treated groups, respectively) and improved survival after MI. CONCLUSION: Our findings suggest that HR reduction with IVA prevents cardiac rupture after MI. This may be particularly effective in MI patients with a high HR who are either unable to adequately tolerate ß-blockers or whose HR remains high despite receiving ß-blockers.

Idiopathic posterior papillary muscle rupture; a case report.

BACKGROUND: Papillary muscle rupture is a rare condition. Its clinical presentation, diagnosis and management can be very challenging for the clinician. CASE PRESENTATION: A 73-year-old woman with hypertension presented with chest pain, ST-segment changes, and elevated serum troponin levels. Coronary angiography was normal. Echocardiography revealed normal ventricular function, flail posterior mitral leaflet, and severe mitral regurgitation. She underwent emergent mitral valve replacement. CONCLUSION: The diagnostic and management strategies of this uncommon presentation are discussed.

Functional uni-ventricular heart due to post-myocardial infarction ventricular septum rupture.

Ventricular septum defect (VSD) is an often lethal complication caused by myocardial infarction. We report a rare case of post-myocardial infarction ventricular septum rupture in a patient after extracorporeal cardiopulmonary resuscitation (eCPR). In the bedside echocardiography after VA ECMO cannulation, we noticed the circular, hypertrophied left ventricle with the disintegrated inter-ventricular septum (maximum dehiscence 3.3 cm), accompanied by decreased left-ventricular ejection fraction and the right ventricle being compressed by the left ventricle's free septal wall. There was no pressure-relevant inter-ventricular separation resulting in left-to-right-shunting and therefore resulting in a fully functional uni-ventricular heart.

Acute aortic regurgitation due to fibrous strand rupture.

A 60-year-old male presented with sudden onset chest pain and pulmonary edema. The investigation confirmed torrential aortic regurgitation of a bicuspid valve. At surgery, a ruptured fibrous strand was identified which had been supporting the left-right cusp commissure with loss of attachment to the aortic wall. This case demonstrates that fibrous strands may be present as a supporting structure of the aortic valve, and rupture can be a rare cause of torrential aortic regurgitation, similar in pathogenesis to how it may be associated with acute severe mitral regurgitation and chordae tendineae rupture.

Treatment of severe acute mitral regurgitation following thoracoabdominal aortic aneurysm repair.

An asymptomatic 63-year-old male with chronic type B aortic dissection underwent repair of an expanding 6.1 cm extent I thoracoabdominal aortic aneurysm. His postoperative course was complicated by respiratory failure from severe acute mitral regurgitation likely due to papillary muscle rupture, which was corrected with transcatheter MitraClip edge-to-edge repair.

VA-ECMO With Pericardiocentesis and Autologous Blood Transfusion - Stabilisation Strategy in Acute Cardiac Free Wall Rupture.

A 68-year old lady present with left ventricular free wall rupture and cardiac arrest post-myocardial infarction. This article illustrates a strategy combining pericardiocentesis with autologous transfusion together with VA-ECMO as a bridge to definitive surgical repair.

[Ventricular Free Wall Rupture].

Left ventricular free wall rupture( LVFWR) is a potentially fatal complication after acute myocardial infarction (AMI). Its onset is often unpredictable and circulatory collapse develops abruptly. When cardiac tamponade is detected after AMI, pericardial drainage should be performed promptly. If percutaneous drainage is ineffective, surgical drainage should be performed without hesitation. Veno-arterial extracorporeal oxygenation (VA-ECMO) cannot necessarily provide effective brain protection because of elevated venous pressure. Although suture-less repair often results in sufficient hemostasis, recurrent rupture sometimes develops. If any type of LVFWR is suspected, immediate surgical intervention can save lives.

[Left Ventricular Rupture after Mitral Valve Replacement].

Ventricular rupture after mitral valve surgery is rare but a serious complication associated with high mortality rate. Of the 2,338 patients who underwent mitral valve surgery, 8 patients (0.7%) suffered from left ventricular rupture in our institution. All developed left ventricular rupture after mitral valve replacement and 3 patients( 37.5%) died within 30 days. To prevent left ventricular rupture, preservation of the mitral loop, appropriate valve sizing, and perioperative hemodynamic management to unload ventricular pressure are needed. Surgical repair for left ventricular rupture should be performed under cardiac arrest. Combination of external approach and endoventricular repair is recommended but epicardial tissue sealing may be an only option for patients with friable ventricular muscles and undetermined location of ruptured site. Use of intraaortic balloon pumping (IABP), percutaneous cardiopulmonary support (PCPS) and Impella are also important technique to unload left ventricular pressure and to maintain systemic hemodynamics.

Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction.

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.

In utero fetal left ventricular rupture and pseudoaneurysm formation: a case report.

BACKGROUND: Cardiac ventricular aneurysms affect 1 in 200,000 live births. To the best of our knowledge, no reported cases of a left ventricular pseudoaneurym and in utero rupture exist to guide optimal management. CASE PRESENTATION: We present a case of fetal left ventricular rupture with a large pericardial effusion, cardiac tamponade and subsequent pseudoaneurysm formation with concerns for a poor prognosis. Interventional drainage of the pericardial effusion led to resolution of tamponade and significant improvement in fetal condition. A multidisciplinary team was utilised to plan birth to minimise risk of pseudoaneurysmal rupture and a catastrophic bleed at birth. CONCLUSION: For similar cases we recommend consideration of birth by caesarean section, delayed cord clamping and a prostaglandin E1 infusion, to reduce the systemic pressures on the left ventricle during transition from fetal to neonatal circulations, until definitive surgical repair. In this case, this resulted in a successful outcome.

An unusual case of mitral valve chordal rupture.

In this report, we present a rare case of severe mitral regurgitation due to isolated mitral valve chordal rupture without valve leaflet prolapse in a patient with Fabry cardiomyopathy. This finding could be due to subvalvular apparatus storage of glycosphingolipids rather than fibro-elastic deficiency, underlying how close cardiological follow-up of Fabry patients must be comprehensive and not only focused on left ventricular hypertrophy and arrhythmias.

Left ventricular free wall rupture: A real nightmare.

Left ventricular free wall rupture (LVFWR) is a rarest but often lethal mechanical complication of acute myocardial infarction (AMI). The mortality rate for LVFWR is described from 75% to 90% and it is the cause for 20% of in-hospital deaths after AMI. Death results essentially from the limited time available for emergent intervention after onset of symptoms. Emergency surgery is indicated and normally the rupture site is easily identified, but it may not be apparent macroscopically, corresponding to transmyocardial or subepicardial dissection with an external rupture far from the infarction site, or already thrombosed and contained. Repair of the ventricular wall is usually achieved either by suturing the edges of the tear or closing it with patches of artificial material or biological tissues, usually using some kind of biological glue. However, several cases of successful conservative management have been described. In this Editorial, I comment on the metanalysis conducted by Matteucci et al, published in this issue of the Journal, including 11 nonrandomized studies and enrolling a total of 363 patients, which brings a great deal of new knowledge that can help not only in the prevention but also in the management of this dreadful complication of AMI.

Edge-to-edge mitral repair for iatrogenic chordal rupture related to Impella 5.0.

Iatrogenic chordal rupture with severe mitral regurgitation is a rare but serious complication associated with the use of Impella device. We present a case of a 47-year-old man with ischemic cardiomyopathy who required insertion of an Impella 5.0 device. During Impella support, he developed acute pulmonary edema secondary to newly diagnosed posterior mitral valve chordal rupture and subsequent severe mitral regurgitation. He underwent implantation of a durable left ventricular assist device with concomitant edge-to-edge mitral valve repair through the apex.

Meta-analysis of surgical treatment for postinfarction left ventricular free-wall rupture.

BACKGROUND: Left ventricular free-wall rupture (LVFWR) is one of the most lethal complications after acute myocardial infarction (AMI). The optimal therapeutic strategy is controversial. The current meta-analysis sought to examine the outcome of patients surgically treated for post-AMI LVFWR. METHODS: A comprehensive literature review was performed to identify articles reporting outcomes of subjects who underwent LVFWR surgical repair. The primary endpoint was operative mortality. A meta-analysis was performed to assess the associations of predefined variables of interest and clinical prognosis. RESULTS: Of the 3132 retrieved articles, 11 nonrandomized studies, enrolling a total of 363 patients, fulfilled the inclusion criteria and were included in this analysis. The mean age of patients was 68 years. The operative mortality rate was 32% (n = 115). Meta-analysis revealed reduced operative risk in patients with oozing type rupture, as compared to blowout type (risk ratios [RR]: 0.47; 95% confidence interval [CI]: 0.33-0.67; p < .0001); RR was also significantly reduced in subjects in whom LVFWR was treated with sutureless technique, as compared to those undergoing sutured repair (RR: 0.59; 95% CI: 0.41-0.83; p = .002). Increased risk of operative mortality was demonstrated in patients who required postoperative extracorporeal membrane oxygenation (ECMO) support (RR: 2.39; 95% CI: 1.59-3.60; p < .0001). CONCLUSIONS: Surgical treatment of postinfarction LVFWR has a high operative mortality rate. Blowout rupture, sutured repair and postoperative ECMO support are factors associated with increased risk of operative mortality.

Nuclear Receptor Nur77 Controls Cardiac Fibrosis through Distinct Actions on Fibroblasts and Cardiomyocytes.

Fibrosis is a hallmark of adverse cardiac remodeling, which promotes heart failure, but it is also an essential repair mechanism to prevent cardiac rupture, signifying the importance of appropriate regulation of this process. In the remodeling heart, cardiac fibroblasts (CFs) differentiate into myofibroblasts (MyoFB), which are the key mediators of the fibrotic response. Additionally, cardiomyocytes are involved by providing pro-fibrotic cues. Nuclear receptor Nur77 is known to reduce cardiac hypertrophy and associated fibrosis; however, the exact function of Nur77 in the fibrotic response is yet unknown. Here, we show that Nur77-deficient mice exhibit severe myocardial wall thinning, rupture and reduced collagen fiber density after myocardial infarction and chronic isoproterenol (ISO) infusion. Upon Nur77 knockdown in cultured rat CFs, expression of MyoFB markers and extracellular matrix proteins is reduced after stimulation with ISO or transforming growth factor-ß (TGF-ß). Accordingly, Nur77-depleted CFs produce less collagen and exhibit diminished proliferation and wound closure capacity. Interestingly, Nur77 knockdown in neonatal rat cardiomyocytes results in increased paracrine induction of MyoFB differentiation, which was blocked by TGF-ß receptor antagonism. Taken together, Nur77-mediated regulation involves CF-intrinsic promotion of CF-to-MyoFB transition and inhibition of cardiomyocyte-driven paracrine TGF-ß-mediated MyoFB differentiation. As such, Nur77 provides distinct, cell-specific regulation of cardiac fibrosis.