Factors associated with physician decision making on withholding cardiopulmonary resuscitation in prehospital medicine.

This study seeks to identify factors that are associated with decisions of prehospital physicians to start (continue, if ongoing) or withhold (terminate, if ongoing) CPR in patients with OHCA. We conducted a retrospective study using anonymised data from a prehospital physician response system. Data on patients attended for cardiac arrest between January 1st, 2010 and December 31st, 2018 except babies at birth were included. Logistic regression analysis with start of CPR by physicians as the dependent variable and possible associated factors as independent variables adjusted for anonymised physician identifiers was conducted. 1525 patient data sets were analysed. Obvious signs of death were present in 278 cases; in the remaining 1247, resuscitation was attempted in 920 (74%) and were withheld in 327 (26%). Factors significantly associated with higher likelihood of CPR by physicians (OR 95% CI) were resuscitation efforts by EMS before physician arrival (60.45, 19.89-184.29), first monitored heart rhythm (3.07, 1.21-7.79 for PEA; 29.25, 1.93-442. 51 for VF / pVT compared to asystole); advanced patient age (modelled using cubic splines), physician response time (0.92, 0.87-0.97 per minute) and malignancy (0.22, 0.05-0.92) were significantly associated with lower odds of CPR. We thus conclude that prehospital physicians make decisions to start or withhold resuscitation routinely and base those mostly on situational information and immediately available patient information known to impact outcomes.

Outcomes of emergency or urgent mitral valve repair in patients with papillary muscle rupture and active infective endocarditis.

BACKGROUND: Emergency or urgent surgery is often required in patients with papillary muscle rupture and active mitral valve infective endocarditis. The aim of this study was to analyze the outcomes of patients with active endocarditis who underwent emergency or urgent mitral valve repair. METHODS: From 2005 to 2014, 154 ischemic mitral regurgitation patients and 41 infective endocarditis patients underwent mitral valve repair in our institution; 23 had emergency operations due to papillary muscle rupture, and 18 with active infective endocarditis underwent urgent surgery. RESULTS: Cardiopulmonary bypass time (141.4 ± 43.3 versus 145.3 ± 46.5 min) and crossclamp time (77.7 ± 34.1 versus 79.2 ± 33.0 min) were similar in the papillary muscle rupture and elective ischemic mitral regurgitation subgroups, and major postoperative complications were comparable. Hospital mortality was 17.4% in the papillary muscle rupture subgroup and 8.4% in the elective ischemic mitral regurgitation subgroup. Cardiopulmonary bypass time (103.6 ± 37.0 versus 75.5 ± 20.8 min) and crossclamp time (61.7 ± 21.2 versus 45.3 ± 18.0 min) were significantly longer in infective endocarditis patients. There were no major complications or hospital deaths. Eight years postoperatively, overall survival was 94.4% and 86.5% in the papillary muscle rupture and elective ischemic mitral regurgitation subgroups, respectively (p = 0.730). Overall survival was 100% in both infective endocarditis subgroups. CONCLUSION: The feasibility and effectiveness of emergency or urgent mitral valve repair in patients with papillary muscle rupture and active infective endocarditis are satisfactory. Early and mid-term outcomes are comparable to those of elective operations.

IRAK3 gene silencing prevents cardiac rupture and ventricular remodeling through negative regulation of the NF-κB signaling pathway in a mouse model of acute myocardial infarction.

Cardiac rupture and ventricular remodeling are recognized as the severe complications and major risk factors of acute myocardial infarction (AMI). This study aims to evaluate the regulatory roles of interleukin-1 receptor-associated kinase 3 (IRAK3) and nuclear factor-κB (NF-κB) signaling pathway in cardiac rupture and ventricular remodeling. Microarray analysis was performed to screen AMI-related differentially expressed genes and IRAK3 was identified. The models of AMI were established in male C57BL/6 mice to investigate the functional role of IRAK3. Afterwards, lentivirus recombinant plasmid si-IRAK3 was constructed for IRAK3 silencing. Next, cardiac function parameters were measured in response to IRAK3 silencing. The regulatory effects that IRAK3 had on myocardial infarct size and the content of myocardial interstitial collagen were analyzed. The regulation of IRAK3 silencing on the NF-κB signaling pathway was further assayed. The obtained results indicated that highly expressed IRAK3 and activated NF-κB signaling pathway were observed in myocardial tissues of mouse models of AMI, accompanied by increased expression of matrix metalloproteinase (MMP)-2/9 and tissue inhibitor of metalloproteinase 2 (TIMP-2). Notably, IRAK3 gene silencing inhibited the activation of NF-κB signaling pathway. Furthermore, IRAK3 gene silencing led to the decreased thickness of infarct area and collagen content of myocardial interstitium, alleviated diastolic, and systolic dysfunctions, as well as, facilitated cardiac functions in mice with AMI, corresponding to decreased expression of MMP-2/9 expression and increased expression of TIMP-2. Taken together, silencing of IRAK3 inactivates the NF-κB signaling pathway, and thereby impeding the cardiac rupture and ventricular remodeling, which eventually prevents AMI progression.

Mitral Chordae Rupture as a Possible First-Time Presentation for Graves’ Disease.

Graves' disease is a common cause of hyperthyroidism that can lead to multiple cardiovascular complications. Herein is described the case of a 44-year-old male who presented with new-onset atrial fibrillation and mitral regurgitation secondary to flail anterior mitral leaflet with chordae tendineae rupture. This is a rare complication for Graves' disease, and has been reported only twice previously. It was hypothesized that this complication is secondary to Graves'-associated myxomatous degeneration of the mitral valve in the presence of a hyperdynamic circulation.

Post-Coital Acute Rupture of a Fenestrated Aortic Valve.

Fenestrated aortic valve is a frequent condition which is, for most of the time, asymptomatic and generally has no influence on aortic valve competence. However, aortic valve regurgitation could occur, especially in the case of fibrous strand rupture. In this situation, acute aortic regurgitation is poorly tolerated and requires urgent surgical correction. Herein is presented the case of a 70-year-old patient who was admitted as an emergency for acute heart failure after coital exertion. Echocardiography revealed severe acute aortic regurgitation due to leaflet prolapse. Intraoperative inspection of the valve showed a strand rupture of the isolated fenestration.

[Papillary Muscle Rupture after Repair of Ischemic Left Ventricular Free Wall Rupture; Report of a Case].

A 67-year-old man experienced acute inferior myocardial infarction. Echocardiography and computed tomography showed massive pericardial effusion. He underwent emergency operation for ischemic ventricular free wall rupture. During the operation, an oozing type rupture was found on the inferior wall and the bleeding was completely controlled by applying fibrin glue sheets. On the 5th day after the operation, ventricular tachycardia appeared with hemodynamic deterioration. Echocardiography showed a ruptured posteromedial papillary muscle with massive mitral regurgitation. Intra-aortic balloon pumping was introduced and emergency repair operation was performed. The mitral valve was replaced with a bioprosthetic valve. The postoperative course was uneventful.

Use of a sandwich technique to repair a left ventricular rupture after mitral valve replacement.

One difficulty with external repair of left ventricular rupture after mitral valve replacement is collateral bleeding in friable myocardium adjacent to the rupture. The bleeding is caused by tension on the closing sutures, whether or not pledgets have been used. We report the case of a 69-year-old woman who underwent an uneventful mitral valve replacement. After cardiopulmonary bypass was terminated, brisk bleeding started from high in the posterior left ventricular wall, typical of a type III defect. We undertook external repair, placing a plug of Teflon felt into the cavity of the rupture and sandwiching it into place with pledgeted mattress and figure-of-8 sutures. The space occupied by the plug decreased the distance needed to obliterate the defect and thereby reduced the tension on the sutures necessary to achieve hemostasis. This simple technique enabled closure of the defect and avoided collateral tears that would have compromised an otherwise successful repair. Two years postoperatively, the patient had normal mitral valve function and no left ventricular aneurysm. In addition to reporting the patient's case, we review the types of left ventricular rupture that can occur during mitral valve replacement and discuss the various repair options.

Curious case of calciphylaxis leading to acute mitral regurgitation.

Calciphylaxis is uncommon and typically seen in patients with end-stage renal disease. It has been defined as a vasculopathic disorder characterised by cutaneous ischaemia and necrosis due to calcification, intimal fibroplasia and thrombosis of pannicular arterioles. We present the case of a 74-year-old woman with chronic kidney disease stage III who developed calciphylaxis leading to mitral valve calcification, chordae tendineae rupture and acute mitral regurgitation. Although an alternative explanation can typically be found for non-uraemic calciphylaxis, her evaluation did not reveal any usual non-uraemic causes including elevated calcium-phosphorus product, hyperparathyroidism, or evidence of connective tissue disease. Her wounds improved with sodium thiosulfate, pamidronate, penicillin and hyperbaric oxygen therapies but she ultimately decompensated with the onset of acute mitral regurgitation attributed to rupture of a previously calcified chordae tendineae. This case highlights an unusual case of calciphylaxis without clear precipitant as well as a novel manifestation of the disease.

Dynamic evaluation of the loop technique using the U-Clip.

BACKGROUND: We set out to evaluate mitral valve repair with the loop technique under dynamic conditions, using a U-Clip to anchor the loop unit to a papillary muscle. METHODS: Mitral valve prolapse was artificially developed by resecting 4 chordae tendineae of a resected porcine heart. The loop unit was anchored to the papillary muscle using U-Clips. Each chordal loop was fixed on the prolapsed leaflet. A roller pump perfused the left ventricle. The left ventricular pressure was maintained at 250 mm Hg. Morphological assessment of the loop reconstruction was performed using an endoscope. RESULTS: 10 independent chordal reconstructions were performed. In all cases, the loop unit remained anchored against pressures exceeding 250 mm Hg. Upon increasing the water filling volume, rupture of a chorda tendinea occurred in 7 cases, rupture of the papillary muscle occurred in 2 cases, and left ventricle rupture occurred in 1 case. In all rupture cases, the loop unit remained anchored to the papillary muscle. CONCLUSION: This dynamic evaluation of the loop technique using U-Clips to anchor the loop unit to a papillary muscle showed that the loop technique using U-Clips is a safe method.

Mitral valve plasty for idiopathic rupture of mitral valve posterior chordae in infants.

INTRODUCTION: Idiopathic mitral valve chordal rupture is rare among infants. Once it has occurred, acute heart failure progresses, and emergency surgical repair is necessary in most cases. Our surgical experience with idiopathic mitral valve chordal rupture is reported. PATIENTS AND METHODS: From September 2008 to May 2012, four infants (3 males, 1 female; median age 5.5 months) underwent mitral valve plasty for severe mitral valve regurgitation due to prolapse of posterior mitral valve leaflet. Patient history, surgical procedure, operation time, mortality, postoperative echocardiography data (mitral valve regurgitation grade: 0-trivial, mild, moderate, severe, transmitral flow: TMF) and pathology were examined. RESULTS: Three cases required emergency surgery; 1 case, elective surgery. Intraoperative findings showed chordal rupture of the P2 segment in 3 cases and P1 + P3 segments in 1 case. Quadrangular resection with annular plication was performed for 1 case. Quadrangular resection with annular plication and the Kay procedure were performed for 3 cases. Mitral valve regurgitation improved from severe to trivial-mild in all cases. Pathological examination showed a myxomatous degenerative change in the mitral valve. CONCLUSION: Mitral valve plasty was performed for idiopathic mitral valve chordal rupture in infants. The surgical procedures were the same as for adult cases and achieved satisfactory results.

Left main occlusion secondary to aortic root rupture following transcatheter aortic valve replacement managed by left main stenting.

Acute left main coronary occlusion secondary to a periaortic root hematoma secondary to annular rupture during transcatheter heart valve deployment is reported.

Lack of haptoglobin results in unbalanced VEGFα/angiopoietin-1 expression, intramural hemorrhage and impaired wound healing after myocardial infarction.

Decreased haptoglobin (Hp) functionality due to allelic variations is associated with worsened outcome in patients after myocardial infarction (MI). However, mechanisms through which haptoglobin deficiency impairs cardiac repair remain to be elucidated. In the present study, we identified novel molecular alterations mediated by Hp involved in early and late cardiac repair responses after left coronary artery ligation in Hp(-/-) and wild-type (WT) mice. We observed a higher mortality rate in Hp(-/-) mice despite similar infarct size between groups. Deaths were commonly caused by cardiac rupture in Hp(-/-) animals. Histological analysis of 3 and 7days old non-ruptured infarcted hearts revealed more frequent and more severe intramural hemorrhage and increased leukocyte infiltration in Hp(-/-) mice. Analyses of non-ruptured hearts revealed increased oxidative stress, reduced PAI-1 activity and enhanced VEGFα transcription in Hp(-/-) mice. In line with these observations, we found increased microvascular permeability in Hp(-/-) hearts 3days after infarction. In vitro, haptoglobin prevented hemoglobin-induced oxidative stress and restored VEGF/Ang-1 balance in endothelial cell cultures. During long-term follow-up of the surviving animals, we observed altered matrix turnover, impaired scar formation and worsened cardiac function and geometry in Hp(-/-)mice. In conclusion, haptoglobin deficiency severely deteriorates tissue repair and cardiac performance after experimental MI. Haptoglobin plays a crucial role in both short- and long-term cardiac repair responses by reducing oxidative stress, maintaining microvascular integrity, myocardial architecture and proper scar formation.