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.

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.

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.

Managing blunt cardiac injury.

Blunt cardiac injury (BCI) encompasses a spectrum of pathologies ranging from clinically silent, transient arrhythmias to deadly cardiac wall rupture. Of diagnosed BCIs, cardiac contusion is most common. Suggestive symptoms may be unrelated to BCI, while some injuries may be clinically asymptomatic. Cardiac rupture is the most devastating complication of BCI. Most patients who sustain rupture of a heart chamber do not reach the emergency department alive. The incidence of BCI following blunt thoracic trauma remains variable and no gold standard exists to either diagnose cardiac injury or provide management. Diagnostic tests should be limited to identifying those patients who are at risk of developing cardiac complications as a result of cardiac in jury. Therapeutic interventions should be directed to treat the complications of cardiac injury. Prompt, appropriate and well-orchestrated surgical treatment is invaluable in the management of the unstable patients.

Cardiac Myocyte-Specific Overexpression of FASTKD1 Prevents Ventricular Rupture After Myocardial Infarction.

Background The mitochondrial mRNA-binding protein FASTKD1 (Fas-activated serine/threonine [FAST] kinase domain-containing protein 1) protects myocytes from oxidative stress in vitro. However, the role of FASTKD1 in the myocardium in vivo is unknown. Therefore, we developed cardiac-specific FASTKD1 transgenic mice to test the effects of this protein on experimental myocardial infarction (MI). Methods and Results Transgenic mouse lines with cardiac myocyte-specific overexpression of FASTKD1 to varying degrees were generated. These mice displayed normal cardiac morphological features and function at the gross and microscopic levels. Isolated cardiac mitochondria from all transgenic mouse lines showed normal mitochondrial function, ATP levels, and permeability transition pore activity. Male nontransgenic and transgenic mice from the highest-expressing line were subjected to 8 weeks of permanent coronary ligation. Of nontransgenic mice, 40% underwent left ventricular free wall rupture within 7 days of MI compared with 0% of FASTKD1-overexpressing mice. At 3 days after MI, FASTKD1 overexpression did not alter infarct size. However, increased FASTKD1 resulted in decreased neutrophil and increased macrophage infiltration, elevated levels of the extracellular matrix component periostin, and enhanced antioxidant capacity compared with control mice. In contrast, markers of mitochondrial fusion/fission and apoptosis remained unaltered. Instead, transcriptomic analyses indicated activation of the integrated stress response in the FASTKD1 transgenic hearts. Conclusions Cardiac-specific overexpression of FASTKD1 results in viable mice displaying normal cardiac morphological features and function. However, these mice are resistant to MI-induced cardiac rupture and display altered inflammatory, extracellular matrix, and antioxidant responses following MI. Moreover, these protective effects were associated with enhanced activation of the integrated stress response.

Cardiac Rupture Due to a Fall from Height: The 'Water Hammer' Effect.

BACKGROUND: Cardiac injury in trauma patients can be secondary to either blunt or penetrating trauma and is a significant cause of death. The commonest etiological factors for blunt cardiac injury include motor vehicle collisions, falls, and crush or blast injuries. The incidence of blunt cardiac injury following falls is reported to be between 5 and 50%.CASE REPORT: A combat pilot lost his life in an aircraft accident. Although he had ejected successfully just before the aircraft caught fire and his parachute had deployed fully, it was engulfed in the ball of fire rising up from the burning aircraft wreckage, causing the parachute to burn up. As a result, the pilot had a free fall from an estimated height of 70-80 ft (21-24 m). Autopsy revealed a ruptured right atrium and endocardial tears at the right atrioventricular junction. The left side of the heart and the coronary arteries were unscathed. The histopathological finding showed evidence that the cardiac injuries sustained were antemortem. The cause of death was ascertained to be due to cardiac rupture, leading to hemorrhagic shock.DISCUSSION: Cardiac rupture in this case appears to be a case of the 'water hammer' effect, the right atrium being the commonest site of blunt cardiac rupture. It is possible that the individual landed on his feet after his parachute got burnt in the ball of fire and the violent compression of the lower limb and abdominal veins, caused by the sudden hyperflexion of the lower limbs over the abdomen, caused the cardiac rupture in this case.CONCLUSION: The possibility of blunt cardiac trauma should always be kept in mind while dealing with survivors of ejection at low levels.Sharma MD, Gupta N, Rajkumar T, Sharma A. Cardiac rupture due to a fall from height: the 'water hammer' effect. Aerosp Med Hum Perform. 2022; 93(10):755-757.

Acute Mitral Regurgitation Due to Chordae Tendineae Rupture: A Rare Presentation of Cardiac Amyloidosis.

BACKGROUND In cardiac amyloidosis (CA), misfolded proteins deposit in the extracellular space of cardiac tissue. These deposits classically cause restrictive cardiomyopathy with diastolic dysfunction. Although there are at least 30 proteins known to cause amyloid aggregates, 2 main types make up most diagnosed cases: light chain amyloidosis (AL) and transthyretin amyloidosis (ATTR). Since CA is considered a rare condition, it is often underdiagnosed or recognized in the advanced stages. Once amyloid deposits involve the heart tissue, they are associated with a worse outcome and higher mortality rates, especially in patients presenting symptoms of heart failure. CASE REPORT We report a case of a 22-year-old man presenting with acute severe mitral regurgitation, secondary to posterior mitral leaflet chordae tendineae rupture (CTR). Surgical mitral valve replacement with a mechanical prosthesis was performed, and cardiac tissue biopsy samples were obtained. After surgery, the patient improved significantly but suddenly presented with hemodynamic deterioration, until he died due to severe hemodynamic compromise and multiorgan failure. Although the etiology of the CTR was not established before surgical intervention, the histopathological analysis suggested CA. CONCLUSIONS CA diagnosis can be complex, especially in a 22-year-old-man with atypical clinical and imaging manifestations. In this patient, other differential diagnoses were considered, since CA presenting in a young patient is a rare phenomenon and acute mitral regurgitation secondary to CTR presents more frequently in other heart conditions. Furthermore, rapid postoperative deterioration resulted in the patient's death before biopsy samples were available because suspicion of amyloidosis had not been raised until that point.

Acute mitral valve regurgitation secondary to papillary muscle rupture due to infective endocarditis.

BACKGROUND: Papillary muscle rupture due to infective endocarditis is a rare event and proper management of this condition has not been described in the literature. Our case aims to shed light on treatment strategies for these patients using the current guidelines. CASE PRESENTATION: This case presents a 58-year-old male with acute heart failure secondary to papillary muscle rupture. He underwent an en bloc resection of his mitral valve with a bioprosthetic valve replacement. Specimen pathology later showed necrotic papillary muscle due to infective endocarditis. The patient was further treated with antibiotic therapy. He recovered well post-operatively and continued to do well after discharge. CONCLUSION: In patients who present with papillary muscle rupture secondary to infective endocarditis, clinical symptoms should drive the treatment strategy. Despite the etiology, early mitral valve surgery remains treatment of choice for patients who have papillary muscle rupture leading to acute heart failure. Culture-guided prolonged antibiotic treatment is vital in this category of patients, especially those who have a prosthetic valve implanted.

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.

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.

Conservative treatment of left ventricular pseudoaneurysm after mitral valve replacement due to early left ventricular rupture: a case report.

BACKGROUND: Left ventricular pseudoaneurysm due to early left ventricle rupture is a serious complication after cardiac surgery. Urgent surgery is recommended in most cases with a high mortality rate. Conservative treatment of a left ventricular pseudoaneurysm due to early left ventricle rupture is very rare. CASE PRESENTATION: We present a 61-year-old woman with left ventricular pseudoaneurysm after mitral valve replacement due to early left ventricle rupture. This patient was treated in a conservative approach. This patient had an uneventful recovery. She was in good condition and remained asymptomatic 3.5 years after mitral valve surgery. CONCLUSION: This case suggests that medical treatment left ventricular pseudoaneurysm patients has a limited but acceptable role in selected and unusual circumstances.

Perioperative Extracorporeal Membrane Oxygenation for Refractory Cardiopulmonary Failure Complicating Papillary Muscle Rupture.

The prognosis of papillary muscle rupture (PMR) leading to acute mitral regurgitation, pulmonary oedema, and cardiogenic shock remains dismal, with survival dependent on prompt recognition and surgical intervention. The use of extracorporeal membrane oxygenation (ECMO) for circulatory and/or respiratory support in critically ill patients failing conventional treatment has significantly increased in the past few years, mainly owing to technology improvements that have rendered the provision of this technique simpler and safer. In this report, four cases of refractory cardiopulmonary collapse complicating ischaemic and traumatic PMR successfully managed perioperatively with ECMO are presented. In this context, a review of the potential role of perioperative ECMO support for cardiogenic shock secondary to cardiac mechanical complications is also provided.

[A woman with an abnormality in the pericardial cavity]. / Een vrouw met een afwijking rondom het hart.

An 84-year-old woman was found dead at home. There were no suspicious circumstances. Non-contrast enhanced post mortem CT was performed to establish the cause of death. CT showed hyperdense fluid in the pericardial cavity consistent with hemopericardium secondary to left ventricular rupture caused by acute myocardial infarction.

Mid-Term Follow-Up of Neonatal Neochordal Reconstruction of Tricuspid Valve for Perinatal Chordal Rupture Causing Severe Tricuspid Valve Regurgitation.

BACKGROUND: Papillary muscle rupture in the perinatal period is a rare event that leads to severe mitral or tricuspid insufficiency due to a flail leaflet. Neonatal tricuspid chordal reconstruction for this condition is rarely reported. Early recognition and treatment have the potential to be lifesaving. We present our surgical experience with five such patients, along with their midterm follow-up. METHODS: Between August 2010 and November 2012, five neonates (aged 1-30 days) underwent surgery for severe atrioventricular valve regurgitation. All neonates had severe tricuspid regurgitation due to ruptured chordae. In addition, two had moderate mitral regurgitation; one due to ruptured chordae of the posterior mitral leaflet and the other due to prolapse of the anterior mitral leaflet. All underwent emergent surgery where the ruptured chordae to the anterior tricuspid leaflet were replaced with neochordae made with expanded polytetrafluoroethylene (ePTFE) suture. The mitral valve was repaired in two patients. RESULTS: All patients survived surgery without the need for postoperative mechanical circulatory assist. Predischarge echocardiograms showed good coaptation of tricuspid and mitral leaflets with minimal regurgitation in all. At follow-up between 75 months to 102 months, four patients had excellent outcomes with less than mild tricuspid regurgitation. One child with flail tricuspid and mitral leaflets developed progressive tricuspid and mitral regurgitation requiring surgical re-repair at 20 months following the initial surgery. CONCLUSION: Repair of chordal rupture of the tricuspid valve in neonates using ePTFE neo-chordae can provide acute salvage and gratifying midterm results in the management of this potentially fatal condition.

Clinical characteristics and protective factors in patients with acute myocardial infarction undergoing in-hospital myocardial free wall rupture: a single-center, retrospective analysis.

Myocardial free wall rupture (MFWR) refers to laceration of the heart ventricle or atria, which is a rare but fatal complication of acute myocardial infarction (AMI). In this study, we aim to identify the clinical characteristics and protective factors of free wall rupture after myocardial infarction. This is a single-center, retrospective observational analysis. The study screened all patients admitted to the cardiology department of the First Affiliated Hospital of Xi'an Jiaotong University between January 2013 and April 2018. The biochemical, clinical, angiographic and echocardiographic features of these patients were then collected and analyzed. Among the 5946 screened patients with AMI, 23 patients with a diagnosis of MFWR after AMI were enrolled in the present study. 18 (78.3%) patients were diagnosed with acute ST segment elevated myocardial infarction and the remaining 5 (21.7%) have acute non-ST segment elevated myocardial infarction. Early-phase MFWR happened in 12 (52.2%) and late-phase accounted for 8 (34.8%) in total. Late-phase MFWR had lower left ventricle ejection fraction value (45.8%±5.6% vs 63.0±3.8%, p<0.001) as compared with early-phase. Patients who survived from MFWR has higher ACE inhibitor/angiotensin II receptor blocker (ACEI/ARB) and ß-blocker coverage in the in-hospital treatment of AMI (ACEI/ARB: 100.0% vs 35.3%, p=0.014; ß-blocker: 100.0% vs 47.1%, p=0.048). The present study provides evidence for better understanding of the clinical characteristics and protective functions in MFWR after AMI. Reduced cardiac function is correlated with higher incidence of later phase free wall rupture. Higher ACEI/ARB and ß-blocker coverage in the AMI treatment strategy is associated with lower MFWR incidence.

Aortic valve perforation in the setting of Cogan's syndrome.

Cogan's syndrome is a rare disorder characterized by the coexistence of ocular and audio-vestibular manifestations. Systemic manifestations are quite unusual with pan-vasculitis and cardiac involvement reported in the form of aortitis with aortic aneurysm, dissection, or extremely rare aortic valve perforation. Hereby, we report a case of a 56-year-old woman presented with ocular, audio-vestibular, and systemic manifestations with medium-sized vasculitis in the form of multiple splenic artery aneurysms, superior mesenteric artery thrombosis, and cardiovascular involvement in the form of aortic regurgitation due to noncoronary cusp perforation. To the best of our knowledge, this is the second case to report aortic perforation in the setting of Cogan's syndrome.

A Coronary Conundrum: Papillary Muscle Rupture and Ischemic Mitral Regurgitation Secondary to Coronary Thromboembolism in Antiphospholipid Syndrome.

Antiphospholipid syndrome (APS) is an autoimmune disorder that has a strong propensity for a hypercoagulable state and is known to be associated with venous and arterial thromboembolism. We describe an uncommon case of APS in the setting of non-Hodgkin's lymphoma, with thromboembolism, and a rare complication after an uncommon etiology of myocardial infarction. This case highlights the importance of early and appropriate type of anticoagulation to reduce the morbidity and mortality in patients with APS.