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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.

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.

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., (© 2018 Wiley Periodicals, Inc.)

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.

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.

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.

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.

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.

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.

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.

Acute left main coronary occlusion secondary to a periaortic root hematoma secondary to annular rupture during transcatheter heart valve deployment is reported., (Copyright © 2013 Wiley Periodicals, Inc.)

Although annulus rupture is one of the most severe complications of transcatheter aortic valve implantation (TAVI), the incidence and mechanism of this complication remain unclear. Out of 387 consecutive TAVI cases in our institution, the incidence of annulus rupture was 1.0% (4/387). The first two patients died because of hemodynamic collapse due to tamponade on day 0. Both surviving patients had undergone preprocedural multidetector computed tomography which revealed large calcifications in the epicardial fat part of the aortic annulus. In both cases, annulus rupture occurred after deployment of a balloon expandable valve suggesting that mechanical compression of this "vulnerable area" by calcification may cause annulus rupture., (Copyright © 2012 Wiley Periodicals, Inc.)

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., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Background and Aim of the Study: Mitral regurgitation (MR) is a common valvular disease throughout the world. Various diagnostic techniques have been developed to assess the causes and severity of MR, and the therapeutic approaches to this disease have been widely documented. However, treatments for chronic MR remain controversial, and various animal models of chronic MR (including chordae tendineae rupture, rapid pacing and ischemia) have been developed to study the pathophysiology and therapeutic approaches to this condition. The study aim was to review the animal MR models that have been developed using a mitral valve chordae tendineae rupture technique., Methods and Results: Among the animals used for these investigations, dogs and sheep have been most commonly used as models of MR induced by mitral valve chordae tendineae rupture, mainly due to considerations of cardiac size. Chordae tendineae cutting is performed using either closed- or open-chest techniques. In the closed-chest model, long flexible grasping forceps are positioned percutaneously in order to tear the mitral valve chordae. In the open-chest model, cardiopulmonary bypass is performed, and either selected chordae are cut under direct visualization or a non-specified number of chordae are cut, using a metal device inserted through the left ventricular apex. Whichever model is used, MR has been found to become chronic at three to six months after the induction of MR by chordae rupture. The reported mortality and complication rates of these models are high., Conclusion: In the long term, the experimental evolution of chronic MR is similar to the evolution occurring naturally in patients suffering from the condition. Hence, these models could be useful in understanding the disease better, and in testing new therapeutic modalities. The present review summarizes the physiological effects of each of these techniques, and compares the advantages and disadvantages of each procedure.

Background: Takotsubo cardiomyopathy (TSC) and its complications, such as cardiac rupture (CR), are increasingly being reported in the literature. CR is associated with rapid clinical decline and is uniformly fatal if not surgically repaired. To identify patients who developed CR we performed an analysis of all available indexed cases in the literature and compared them with a control group of patients with TSC without rupture., Hypothesis: Takotsubo cardiomyopathy patients with cardiac rupture do not differ significantly from those without rupture., Methods: MEDLINE (2009) was searched for all TSC case reports with CR. Eleven case reports were identified. Using a random sampling method, we selected 12 case reports of TSC without rupture (control). We included our patient with TSC with rupture as the 12th case of TSC cohort with CR (CR group). Demographic and clinical characteristics were compared between CR group and control., Results: All patients in the TSC group with rupture were female and were significantly older than controls. TSC group with rupture had significantly higher frequency of ST elevation in lead II and absence of T-wave inversion in lead V5 on hospital admission than controls. Mean ejection fraction, systolic blood pressure, and double product, a measure of oxygen demand, was significantly higher in the rupture group compared to controls. The CR group was associated with less frequent use of β-blocker as compared to controls., Conclusions: CR as a complication of TSC could be more common than recognized. Higher double product and ejection fraction suggest higher fluctuation of intracardiac pressure and may cause CR in TSC. Use of β blockers in TSC may provide protection against CR., (© 2011 Wiley Periodicals, Inc.)

Right ventricular heart rupture is a devastating complication associated with negative pressure wound therapy (NPWT) in cardiac surgery. The use of a rigid barrier has been suggested to offer protection against this lethal complication by preventing the heart from being drawn up and damaged by the sharp sternum bone edges. The aim of this study was to investigate the haemodynamic effects of placing a rigid barrier over the heart to protect it from rupture during NPWT. Eight pigs underwent median sternotomy followed by NPWT at --70 and --120 mmHg, using foam, with or without a rigid plastic disc between the heart and the sternal edges. The heart frequency, cardiac output, mean systemic arterial pressure, mean pulmonary artery pressure, central venous pressure and left atrial pressure were recorded. Cardiac output was not affected by NPWT, regardless of whether a rigid barrier was used. Heart frequency decreased during NPWT without a disc, and showed a tendency towards a decrease when using a rigid disc. The blood pressure decreased during NPWT without a disc, and showed only a tendency towards a decrease when a disc was inserted between the heart and the sternum. In conclusion, the results of this haemodynamic study show that a rigid disc can safely be placed over the heart during NPWT, to prevent heart rupture. The haemodynamic effects of NPWT in sternotomy wounds are slightly reduced by the presence of the rigid disc., (© 2011 The Authors. © 2011 Blackwell Publishing Ltd and Medicalhelplines.com Inc.)

Cardiac tamponade (CT) is a pathophysiologic continuum where hemodynamic embarrassment occurs as a result of progressive, decreased venous return that impairs diastolic ventricular filling, which in turn, when uncorrected, severely compromises cardiac output. While CT is classically associated with high intrapericardial pressures due to rapidly accumulating large pericardial effusions, low-pressure CT is a recognized entity in which a comparatively low intrapericardial pressure could result in cardiac chamber compression and subsequent cardiovascular collapse. In this article, we highlight a previously unreported scenario of rapidly re-accumulating, acute CT in the setting of left ventricular rupture in a patient who had presumably presented with low-pressure CT due to hemoperiardium.

Background: Possible changes in the incidence and outcome of cardiac rupture in patients with ST-elevation myocardial infarction over a long period of time have not been investigated., Methods and Results: The incidence of cardiac rupture in ST-elevation myocardial infarction patients and its mortality rate were investigated during a 30-year period divided into 5 intervals (1977 to 1982, 1983 to 1988, 1989 to 1994, 1995 to 2000, and 2001 to 2006). Of a total of 6678 consecutive patients, 425 experienced a free wall rupture (280 with cardiac tamponade: 227 with electromechanical dissociation and 53 with hypotension) or a septal rupture (145). After the exclusion of referrals from other centers (n=44), the incidence of definite cardiac rupture (septal rupture, anatomic evidence of free wall rupture, or electromechanical dissociation) declined progressively (6.2% in 1977 to 1982 to 3.2% in 2001 to 2006; P<0.001) in parallel with a progressive use of reperfusion therapy (0% to 75.1%; P<0.001). In addition, among patients with cardiac rupture, there was a progressive fall in the rate of death (94% to 75%; P<0.001) despite a trend toward increasing age (66+/-8 to 75+/-8 years; P<0.054) in conjunction with better control of systolic blood pressure at 24 hours (130+/-24 versus 110+/-18 mm Hg; P<0.001); an increased use of reperfusion therapy (0% to 59%; P<0.001), beta-blockers (0% to 45%; P<0.001), angiotensin-converting enzyme inhibitors (0% to 38%; P<0.001), and aspirin (0% to 96%; P<0.001); and a lower use of heparin (99% to 67%; P<0.001)., Conclusions: The decline in the incidence in cardiac rupture and its rate of death over the last 30 years appears to be associated with the increasing use of reperfusion strategies and adjunct medical therapy.

Left ventricular (LV) false aneurysm is an uncommon complication of myocardial infarction. Conventional treatment mandates surgical repair but is associated with significant perioperative risk. We present a case of successful percutaneous closure of a LV false aneurysm in a patient at high operative risk who suffered cardioembolic stroke related to thrombus within the aneurysm. The primary aim of treatment was to prevent recurrent embolic event.

Mitral regurgitation (MR) is a serious complication of coronary heart disease. The functional form is the most frequent, often presenting with a dynamic character. The presence, and in particular the severity of MR and its dynamic character have a major impact on the medium and long term prognosis. The mechanisms responsible for MR are complex and occur in a state of disequilibrium between traction forces and closing forces, for which the significance is partly affected by the presence of asynchrony in left ventricular contraction. The therapeutic management of these patients is difficult. In cases of proven asynchrony, implantation of a biventricular pacemaker is justified. A mitral surgical procedure may be envisaged in cases of severe MR where bypass surgery is planned. In cases of moderate MR at rest, an evaluation of its dynamic character on effort can assist with the decision to undertake combined surgery. Mitral regurgitation (MR) is a common and serious complication of ischemic heart disease. Three general forms are distinguished: MR related to acute rupture of the mitral pillar, ischemic MR and functional MR.

Cardiac rupture remains a fatal complication of acute myocardial infarction (MI) with its mechanism partially understood. We hypothesized that damage to the collagen matrix of infarcted myocardium is the central mechanism of rupture and therefore responsible for the difference in the incidence of rupture between genders. We examined left ventricular (LV) remodeling during the acute phase post-MI in 129sv mice. Following induction of MI, we monitored rupture events and assessed the extent of LV remodeling by echocardiography. Muscle tensile strength, content of insoluble and soluble collagen, expression and activity of matrix metalloproteinases (MMPs) and density of inflammatory cells were determined in the infarcted and non-infarcted myocardium. We then tested the effects of MMP inhibition on rupture. Compared to female mice, males with MI displayed greater extent of LV remodeling, reduced muscle tensile strength, loss of insoluble collagen, local inflammatory response and MMP-9 activation, changes associated with a 3 times higher incidence of rupture than in females. MMP-9 expression by circulating blood mononuclear cells was also increased in male mice with acute MI. Treatment of male mice with an MMP inhibitor reduced MMP activity and halved rupture incidence. Our findings demonstrate that the differences in the severity of inflammation, MMP activation and damage to collagen matrix account for gender difference in cardiac rupture. Our study illustrates the breakdown of fibril collagen as a central mechanism of cardiac rupture.

Background: Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A-deficient (SR-A(-/-)) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction., Methods and Results: Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A(-/-) and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A(-/-) mice than in WT mice (P=0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A(-/-) mice and 12% (6 of 51 mice) in WT mice (P=0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Real-time reverse transcription-polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Furthermore, SR-A(-/-) mice showed augmented expression of tumor necrosis factor-alpha and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-alpha and decreased interleukin-10 expression in activated SR-A(-/-) macrophages., Conclusions: The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-alpha and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

Objective: The objective of this study was to evaluate, using echocardiography, the functioning of the mitral valve apparatus in patients submitted to standardized bovine pericardium chordae implantation to substitute ruptured chordae tendineae or elongated chordae with a significant degree of thinning., Method: Standardized bovine pericardium chordae were implanted in 23 patients with mitral valve insufficiency due to ruptured or elongated chordae with significant thinning. The ages of the patients varied from 23 to 84 years old (mean 62 years old). The most common cause was fibroelastic degeneration affecting 20 (87.0%) patients. The standardized bovine pericardium chordae were manufactured in sets connected at both ends by two polyester-reinforced rods thereby forming a single block. The bovine pericardium chordae measure 2 mm wide with 3 mm between the chordae. The sets of bovine pericardium chordae are produced in lengths varying from 20 to 35 mm. In 17 (73.9%) patients bovine pericardium chordae were implanted in the posterior cusp and in 6 (26.1%) in the anterior cusp. All the patients were evaluated in the postoperative period by echocardiography after a mean follow-up of six months., Results: The echocardiography in the postoperative period demonstrated an absence of reflux in 11 (47.8%) patients, slight reflux in 8 (34.8%) and slight to moderate reflux in 3 (13.0%). The opening and mobility of the mitral valve was normal in the 22 surviving patients., Conclusion: The echocardiography demonstrated good functioning of the mitral valve apparatus in patients submitted to the implantation of standardized bovine pericardium chordae to substitute ruptured chordae tendineae or elongated chordae with a significant degree of thinning.

Background: Concurrent atrial ischemia is usually overlooked in acute myocardial infarction (MI) due to its subtle electrocardiographic (ECG) changes, lack of clear-cut clinical picture, and prognostic significance. PR-segment depression in the inferior leads is a simplified ECG sign for detecting possible underlying atrial ischemia., Hypothesis: The purpose of this study was to document the incidence, clinical characteristics, and prognostic implications of this ECG sign in the setting of acute inferior MI., Methods: Demographics, clinical characteristics, and outcomes of 463 consecutive patients presenting with acute inferior MI were reviewed. The in-hospital ECG was examined by two independent reviewers. The results were then compared between those with and without ECG sign., Results: Profound PR-segment depression > or = 1.2 mm in inferior leads was found in 9 of 463 (1.9%) patients. Patients with atrial ischemia tended to present earlier (2.4 +/- 2.6 vs. 7.0 +/- 8.2 h, p = 0.000) and had a higher frequency of first-degree atrioventricular block (77.8 vs. 30.6%, p = 0.028) and supraventricular arrhythmias (55.5 vs. 20.2%, p = 0.022). Of greater importance, it was significantly associated with an increased rate of cardiac free-wall rupture (33.3 vs. 2.0%, p = 0.001) and in-hospital mortality (44.4 vs. 11.7%, p = 0.015)., Conclusion: Profound PR-segment depression > or = 1.2 mm in inferior leads was associated with a complicated hospital course and poor short-term outcome in acute inferior MI. These patients were at high risk for the development of atrioventricular block, supraventricular arrhythmias, and cardiac free-wall rupture.

Atrial dissection is an uncommon entity, defined as a gap from the mitral or tricuspid annular area to the interatrial septum or atrial wall, creating a new chamber with or without communication into the true left or right atrium. We present the interesting images of an atrial dissection-like appearance in the right atrium, which was actually caused by an ileus due to metastatic renal cell carcinoma in a 82-year-old man. The causes of true atrial dissection were also briefly discussed.

Plaque rupture plays a role in the majority of acute coronary syndromes. Rupture has been associated with stress concentrations, which are affected by tissue properties and anatomy. In this study rupture was not approached as an acute syndrome, but rather as the culmination of a chronic injury or fatigue process. The aim of our study was to investigate the impact of anatomy, tissue properties, and blood pressure on a fatigue mechanism. Incremental crack propagation was dynamically simulated based on evolving stress distributions. Stresses were resolved by a finite element solver, using vessel stiffness properties derived from in vivo data. Plaque fatigue crack growth per pressure pulse was estimated using an adapted Paris-relation. It was demonstrated that cracks begin at the lumen wall at areas of stress concentration, depending on the shape of the lumen, thickness of the fibrous cap and stiffness of the plaque components. Mean or pulse pressure did not affect initiation location. Cracks extended radially and grew at a rate that was highly dependent on both mean and pulse pressure and on lipid stiffness. Rupture rate depended on blood pressure and lipid stiffness. It was concluded that a fatigue mechanism in a pulsatile cardiovascular pressure environment reconciles clinical evidence of acute plaque rupture at seemingly low stress levels, and it could provide a framework for developing strategies to create a biomechanically benign environment which is least conducive to plaque rupture.

Background: Mitral regurgitation from chordae tendinae rupture (CTR) may cause severe clinical symptoms and is a progressive disease that eventually results in the need for mitral valve surgery. Early recognition of CTR and identification of risk factors are important because early intervention increases the chances of survival. Hypertension may increase mitral valve complex mechanical strain and cause the chordae tendinae to rupture., Method: Using a cross-sectional study of medical files in one medical center in Taiwan, we enrolled 98 patients with mitral CTR and classified them into two groups, comprising 68 subjects (69%) without obvious predisposing factors (primary group) and 30 subjects (31%) with known predisposing causes (secondary group)., Result: Of the subjects, 63 (64%) were men with a mean age of 57.5 +/- 1.5 years. The posterior mitral leaflet was most commonly involved (64%). The known predisposing factors in secondary group include mitral valve prolapse, infective endocarditis, and rheumatic heart disease. The patients who had primary CTR were older (59.9 +/- 1.6 v 52.1 +/- 3.1 years, P = .029), had a higher prevalence of hypertension (56% v 30%, P = .018) and complained more often of dyspnea (82% v 53%, P = .003) than the patients in the secondary group. Using binary logistic regression analyses, the variation in primary group was found to be independently explained by age (P = .039, odds ratio = 1.039, 95% confidence interval = 1.002 to 1.077) and hypertension (P = .048, odds ratio = 2.717, 95% confidence interval = 1.008 to 7.326)., Conclusion: We conclude that hypertension was an independent predictor for primary CTR in this study.

Background: We investigated the potential contributions of tumor necrosis factor-alpha (TNF-alpha) on the incidence of acute myocardial rupture and subsequent chronic cardiac dysfunction after myocardial infarction (MI) in TNF knockout (TNF-/-) mice compared with C57/BL wild-type (WT) mice., Methods and Results: Animals were randomized to left anterior descending ligation or sham operation and killed on days 3, 7, 14, and 28. We monitored cardiac rupture rate, cardiac function, inflammatory response, collagen degradation, and net collagen formation. We found the following: (1) within 1 week after MI, 53.3% (n=120) of WT mice died of cardiac rupture, in contrast to 2.5% (n=80) of TNF-/- mice; (2) inflammatory cell infiltration and cytokine expression were significantly higher in the infarct zone in WT than TNF-/- mice on day 3; (3) matrix metalloproteinase-9 and -2 activity in the infarcted myocardium was significantly higher in WT than in TNF-/- mice on day 3; (4) on day 28 after MI compared with sham, there was a significant decrease in LV developed pressure (74%) and +/-dP/dt(max) (68.3%/65.3%) in WT mice but a less significant decrease in +/-dP/dt(max) (25.8%/28.8%) in TNF-/- mice; (5) cardiac collagen volume fraction was lower in WT than in TNF-/- mice on days 3 and 7 but higher on day 28 compared with TNF-/- mice; and (6) a reduction in myocyte apoptosis in TNF-/- mice occurred on day 28 compared with WT mice., Conclusions: Elevated local TNF-alpha in the infarcted myocardium contributes to acute myocardial rupture and chronic left ventricle dysfunction by inducing exuberant local inflammatory response, matrix and collagen degradation, increased matrix metalloproteinase activity, and apoptosis.

Given their low incidence, mechanical complications of AMI represent a diagnostic and therapeutic challenge for the EP. When the panoply of medical interventions has reached its limitation, surgical treatment plays a role in the management of the patient who has AMI. For patients who have CS and severe compromise of myocardial reserve, surgical intervention might represent the only means of restoring blood flow to the myocardium. For patients who have mechanical complications, correction of the defect before the onset of terminal organ failure might provide long-term survival.

Premenopausal women are much less prone to develop cardiovascular disease than men of similar age, but this advantage no longer applies after menopause. We previously found that male mice have a significantly higher rate of cardiac rupture than females during the acute phase of myocardial infarction (MI); however, the effects of sexual hormones on chronic remodeling are unknown. We hypothesized that estrogen (E) may protect the heart from chronic remodeling and deterioration of function post-MI, whereas testosterone (T) may have adverse effects. Mice (4 wk old) of both genders were divided into four groups: female groups consisted of 1) sham ovariectomy (S-Ovx) + placebo (P) (S-Ovx + P), 2) S-Ovx + T, 3) Ovx + P, and 4) Ovx + T; and male groups consisted of 1) sham castration (S-Cas)+ P (S-Cas + P), 2) S-Cas + 17beta-estradiol (E), 3) Cas + P, and 4) Cas + E. MI was induced 6 wk later. Echocardiography was performed to assess cardiac function and left ventricular dimensions (LVD). Myocyte cross-sectional area (MCSA) was measured at the end of the study. In females, both testosterone and ovariectomy decreased ejection fraction (EF) and increased LVD, and when combined they aggravated cardiac function and remodeling further. Testosterone significantly increased MCSA. In males, castration or estrogen increased EF and reduced LVD, whereas castration significantly reduced MCSA. Our data suggest that estrogen prevents deterioration of cardiac function and remodeling after MI, but testosterone worsens cardiac dysfunction and remodeling and has a pronounced effect when estrogen levels are reduced.

Background and Aim of the Study: Rupture of chordae tendineae is the main cause of mitral valve insufficiency, and often requires corrective surgery. The precise mechanisms of chordal rupture, however, are unknown., Methods: Failure mechanics were measured in porcine mitral valve chordae (37 anterior marginal, 40 anterior basal, 35 posterior marginal, and 38 posterior basal). Full-length chordae were weighed, measured, and stretched to failure in an Instron tensile testing machine. The ruptured ends were characterized under a dissecting microscope., Results: Marginal chordae had 68% thinner cross-sectional areas and failed at 68% less load and 28% less strain than basal chordae. Chordae from the posterior leaflet were 35% thinner and failed at 43% less load and 22% less strain than anterior leaflet chordae. Failure strength was lowest for posterior marginal chordae. Chordae most frequently tore just below the leaflet insertion, in what was often their narrowest section., Conclusion: Overall, the marginal chordae and posterior leaflet chordae were thinner and required less strain and load to fail than basal chordae and anterior leaflet chordae, respectively. These results support previous reports of decreased extensibility in marginal chordae. The high incidence of ruptures in the posterior marginal chordae of diseased mitral valves may be due to an inherent weakness in these chordae.

Left atrial dissection is an uncommon entity. It is generally associated with mitral valve replacement, but other predisposing factors should be considered in pathogenesis. We discuss a series of 11 patients with pathologically confirmed left atrial dissection who had been diagnosed previously by transesophageal echocardiography. Predisposing factors and surgical or pathologic findings were reviewed to identify the pathogenic mechanism and to explain the clinical course, hemodynamic disorder, and echocardiographic features. Dissection of the coronary sinus secondary to retrograde cardioplegia, endocarditis, cardiac rupture after myocardial infarction, and blunt chest trauma also could be related to its development. Transesophageal echocardiography identified a mobile intimal flap of the atrial wall that was creating a false chamber and allowed accurate diagnosis of prosthetic mitral valve function, endocarditis complications, and a left ventricular pseudoaneurysm after acute myocardial infarction. Color flow Doppler was particularly useful in identifying complications: communication between the false chamber and true left atria, permitting mitral regurgitation through the periannular route; development of atrial shunts; and severe tricuspid regurgitation caused by disruption of the anterior papillary muscle.

Two patients, a 56-year-old man and an 81-year-old woman who were admitted to hospital because of anteroseptal acute myocardial infarction, were initially treated successfully with direct percutaneous transluminal coronary angioplasty. However, both patients later developed sudden cardiogenic shock due to cardiac tamponade caused by left ventricular free wall rupture (LVFWR). Prompt, life-saving pericardiocentesis was performed, then fibrin-glue was percutaneously injected into the pericardial space. After the procedure, there was no detectable pericardial effusion on echocardiography and the hemodynamic state became stable. The surgical treatment was the standard procedure for LVFWR, but percutaneous fibrin-glue therapy can also be considered for oozing type LVFWR.

Unlabelled: In our experience electromechanical dissociation (EMD) is the most common mechanism of fatal cardiac arrest in patients with acute myocardial infarction (AMI)., Methods: We reviewed retrospectively 82 autopsy cases of AMI in whom the medical record documented EMD as terminal cardiac arrest in order to outline the clinical and pathologic features of different subgroups: 26 cases with external cardiac rupture (CR) were compared with 56 cases without CR. In turn, inside the latter series, 16 cases of sudden EMD were compared with 40 cases of EMD occurring in the terminal phase of cardiac shock., Results: In comparison with those without CR, patients with CR showed at multiple regression analysis less evidence of left ventricular failure (p < 0.05); less extended infarct areas (p < 0.01); more frequent sudden EMD (p < 0.05). Most patients with CR had massive pericardial effusion; cardiac rhythm at the onset of EMD was seldom slow in those cases. In the group without CR no discriminant characteristics were found in cases of sudden EMD vs cases preceded by cardiac shock., Conclusions: In case of CR EMD occurs in less extensively damaged hearts and is generally sudden; in AMI without CR EMD may affect patients with severe depression of pump performance, but not necessarily in shock. EMD after an AMI may result from several factors: cardiac tamponade is prevalent in the presence of CR; in cases without CR our data don't permit to conjecture a distinct pathogenesis for sudden EMD in comparison with cases preceded by shock.