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Ventricular arrhythmias originating from the papillary muscle of the ventricles are complex clinical problems. Catheter ablation has the potential to cure these arrhythmias. However, the procedure is usually challenging due to the specific anatomy, catheter instability and difficulty in localization of the origin of the arrhythmias. Intracardiac echocardiography (ICE) has been reported to be the suitable imaging method for assessing the location of focus in papillary muscles. We used transthoracic echocardiography (TTE), as a noninvasive cost-effective imaging supporting modality, in combination with 3D mapping to guide the exact localization and successful ablation of papillary muscle-originating premature ventricular contractions (PVCs). [ABSTRACT FROM AUTHOR]

Copyright of Medizinische Klinik: Intensivmedizin & Notfallmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The chordae tendineae, described as fibro-collagenous structures, support the leaflets of the atrioventricular valves of the heart in various ways. The chordae tendineae are composed of collagen and elastic fibers. They connect to the ventricular side of the valve leaflets' free border and hinder the leaflets from swinging back into the atrial cavity during systole. Mitral valve chordae tendineae have been classified using a variety of classification systems. To our knowledge, we report a variant chordae tendinea that has yet to be described in the literature. The variant, present only on the mitral anterior papillary muscle, did not show the characteristic appearance of the chorda tendineae. Muscular fibers were observed extending from a larger than usual mitral anterior papillary muscle, inserting into the rough zone of the anterior leaflet. Several tendinous primary and secondary true leaflet chordae emerge from the apical portion of the anterior papillary muscle, inserting into the anterior leaflet's free edge and rough zone. Contraction of this muscular chorda during systole could disrupt the mechanics of valvular closure and result in possible regurgitation across the mitral valve. Additionally, this structure may be subject to rupture during myocardial infarction, leading to valvular dysfunction. The developmental connection between the chordae and papillary muscles could explain the anomalous muscularization of the chordae tendineae observed in this case. [ABSTRACT FROM AUTHOR]

Ischemic mitral regurgitation (IMR) occurs from incomplete coaptation of the mitral valve (MV) after myocardial infarction (MI), typically worsened by continued remodeling of the left ventricular (LV). The importance of LV remodeling is clear as IMR is induced by the post-MI dual mechanisms of mitral annular dilation and leaflet tethering from papillary muscle (PM) distension via the MV chordae tendineae (MVCT). However, the detailed etiology of IMR remains poorly understood, in large part due to the complex interactions of the MV and the post-MI LV remodeling processes. Given the patient-specific anatomical complexities of the IMR disease processes, simulation-based approaches represent an ideal approach to improve our understanding of this deadly disease. However, development of patient-specific models of left ventricle–mitral valve (LV–MV) interactions in IMR are complicated by the substantial variability and complexity of the MR etiology itself, making it difficult to extract underlying mechanisms from clinical data alone. To address these shortcomings, we developed a detailed ovine LV-MV finite element (FE) model based on extant comprehensive ovine experimental data. First, an extant ovine LV FE model (Sci. Rep. 2021 Jun 29;11(1):13466) was extended to incorporate the MV using a high fidelity ovine in vivo derived MV leaflet geometry. As it is not currently possible to image the MVCT in vivo, a functionally equivalent MVCT network was developed to create the final LV-MV model. Interestingly, in pilot studies, the MV leaflet strains did not agree well with known in vivo MV leaflet strain fields. We then incorporated previously reported MV leaflet prestrains (J. Biomech. Eng. 2023 Nov 1;145(11):111002) in the simulations. The resulting LV-MV model produced excellent agreement with the known in vivo ovine MV leaflet strains and deformed shapes in the normal state. We then simulated the effects of regional acute infarctions of varying sizes and anatomical locations by shutting down the local myocardial contractility. The remaining healthy (noninfarcted) myocardium mechanical behaviors were maintained, but allowed to adjust their active contractile patterns to maintain the prescribed pressure–volume loop behaviors in the acute post-MI state. For all cases studied, the LV-MV simulation demonstrated excellent agreement with known LV and MV in vivo strains and MV regurgitation orifice areas. Infarct location was shown to play a critical role in resultant MV leaflet strain fields. Specifically, extensional deformations of the posterior leaflets occurred in the posterobasal and laterobasal infarcts, while compressive deformations of the anterior leaflet were observed in the anterobasal infarct. Moreover, the simulated posterobasal infarct induced the largest MV regurgitation orifice area, consistent with experimental observations. The present study is the first detailed LV-MV simulation that reveals the important role of MV leaflet prestrain and functionally equivalent MVCT for accurate predictions of LV–MV interactions. Importantly, the current study further underscored simulation-based methods in understanding MV function as an integral part of the LV. [ABSTRACT FROM AUTHOR]

Background Acute mitral regurgitation due to papillary muscle rupture is a severe complication of acute myocardial infarction. Transcatheter edge-to-edge repair is emerging as an effective alternative to surgical treatment, with encouraging outcomes. Leaflet adverse events are rare and are associated with relapse of significant mitral regurgitation. Case summary A 54-year-old man arrived at our hospital with a late presentation of ST-elevation myocardial infarction. During primary percutaneous coronary intervention of the circumflex coronary artery, a partial papillary muscle rupture occurred with acute severe mitral regurgitation and cardiogenic shock. Due to the severe haemodynamic instability, the patient underwent an emergent transcatheter edge-to-edge repair with MitraClip device during Impella support with mitral regurgitation resolution and haemodynamic stabilization. At 2-month follow-up, an interclip leaflet tear occurred with relapse of severe mitral regurgitation, requiring a mitral valve replacement surgery. Discussion Acute mitral regurgitation due to papillary muscle rupture is a serious complication of acute myocardial infarction. Management is based on haemodynamic stabilization and surgery. The transcatheter edge-to-edge repair is emerging as a therapeutic alternative in high-risk cases. Leaflet adverse events rarely occur during the transcatheter edge-to-edge repair procedure or before patient discharge. Our case is the first to report a late leaflet adverse event, occurring two months after the procedure and, interestingly, after an acute myocardial infarction conditioning an ischaemic mitral regurgitation. This event may be the result of the progressive adverse remodelling of left ventricular inferolateral akinetic wall, with consequent increase of tethering forces on the posterior leaflet, tensioned in the opposite direction by the clip. [ABSTRACT FROM AUTHOR]

Papillary muscles, as components of the subvalvular apparatus, play a crucial role in the proper functioning of the heart valves. Although the most commonly encountered variants can be classified traditionally, it is essential to remember that there is significant variability in their number, structure, and shape. This variability is not without clinical significance – specific papillary muscle variants translate into different prognoses, therapeutic approaches, and surgical procedures. Therefore, in our study, we conducted an analysis of available literature to determine which papillary muscle variants are most common, what their vascular supply is, and what the significance of individual variants is in daily clinical practice. To achieve this, we searched popular scientific databases such as PubMed, Google Scholar, and Scopus, using keywords such as papillary muscles, clinical aspects of papillary muscles, anatomical variability of papillary muscles, and papillary muscle rupture – as one of the most common clinical situations related to papillary muscles. This paper presents the results of our review – organised and accompanied by a table.

Mechanical load is a potent regulator of cardiac structure and function. Although high workload during heart failure is associated with disruption of cardiomyocyte t‐tubules and Ca2+ homeostasis, it remains unclear whether changes in preload and afterload may promote adaptive t‐tubule remodelling. We examined this issue by first investigating isolated effects of stepwise increases in load in cultured rat papillary muscles. Both preload and afterload increases produced a biphasic response, with the highest t‐tubule densities observed at moderate loads, whereas excessively low and high loads resulted in low t‐tubule levels. To determine the baseline position of the heart on this bell‐shaped curve, mice were subjected to mildly elevated preload or afterload (1 week of aortic shunt or banding). Both interventions resulted in compensated cardiac function linked to increased t‐tubule density, consistent with ascension up the rising limb of the curve. Similar t‐tubule proliferation was observed in human patients with moderately increased preload or afterload (mitral valve regurgitation, aortic stenosis). T‐tubule growth was associated with larger Ca2+ transients, linked to upregulation of L‐type Ca2+ channels, Na+–Ca2+ exchanger, mechanosensors and regulators of t‐tubule structure. By contrast, marked elevation of cardiac load in rodents and patients advanced the heart down the declining limb of the t‐tubule–load relationship. This bell‐shaped relationship was lost in the absence of electrical stimulation, indicating a key role of systolic stress in controlling t‐tubule plasticity. In conclusion, modest augmentation of workload promotes compensatory increases in t‐tubule density and Ca2+ cycling, whereas this adaptation is reversed in overloaded hearts during heart failure progression. Key points: Excised papillary muscle experiments demonstrated a bell‐shaped relationship between cardiomyocyte t‐tubule density and workload (preload or afterload), which was only present when muscles were electrically stimulated.The in vivo heart at baseline is positioned on the rising phase of this curve because moderate increases in preload (mice with brief aortic shunt surgery, patients with mitral valve regurgitation) resulted in t‐tubule growth. Moderate increases in afterload (mice and patients with mild aortic banding/stenosis) similarly increased t‐tubule density.T‐tubule proliferation was associated with larger Ca2+ transients, with upregulation of the L‐type Ca2+ channel, Na+–Ca2+ exchanger, mechanosensors and regulators of t‐tubule structure.By contrast, marked elevation of cardiac load in rodents and patients placed the heart on the declining phase of the t‐tubule–load relationship, promoting heart failure progression.The dependence of t‐tubule structure on preload and afterload thus enables both compensatory and maladaptive remodelling, in rodents and humans. [ABSTRACT FROM AUTHOR]

Background: Ventricular volumetry using a short-axis stack of two-dimensional (D) cine balanced steady-state free precession (bSSFP) sequences is crucial in any cardiac magnetic resonance imaging (MRI) examination. This task becomes particularly challenging in children due to multiple breath-holds. Objective: To assess the diagnostic performance of accelerated 3-RR cine MRI sequences using deep learning reconstruction compared with standard 2-D cine bSSFP sequences. Material and methods: Twenty-nine consecutive patients (mean age 11 ± 5, median 12, range 1–17 years) undergoing cardiac MRI were scanned with a conventional segmented 2-D cine and a deep learning accelerated cine (three heartbeats) acquisition on a 1.5-tesla scanner. Short-axis volumetrics were performed (semi-)automatically in both datasets retrospectively by two experienced readers who visually assessed image quality employing a 4-point grading scale. Scan times and image quality were compared using the Wilcoxon rank-sum test. Volumetrics were assessed with linear regression and Bland–Altman analyses, and measurement agreement with intraclass correlation coefficient (ICC). Results: Mean acquisition time was significantly reduced with the 3-RR deep learning cine compared to the standard cine sequence (45.5 ± 13.8 s vs. 218.3 ± 44.8 s; P < 0.001). No significant differences in biventricular volumetrics were found. Left ventricular (LV) mass was increased in the deep learning cine compared with the standard cine sequence (71.4 ± 33.1 g vs. 69.9 ± 32.5 g; P < 0.05). All volumetric measurements had an excellent agreement with ICC > 0.9 except for ejection fraction (EF) (LVEF 0.81, RVEF 0.73). The image quality of deep learning cine images was decreased for end-diastolic and end-systolic contours, papillary muscles, and valve depiction (2.9 ± 0.5 vs. 3.5 ± 0.4; P < 0.05). Conclusion: Deep learning cine volumetrics did not differ significantly from standard cine results except for LV mass, which was slightly overestimated with deep learning cine. Deep learning cine sequences result in a significant reduction in scan time with only slightly lower image quality. [ABSTRACT FROM AUTHOR]

The bicuspid valve in sheep and goat showed similar anatomical features. The left atrio ventricular opening was circular and possessed valves. Both these species contained an anterior and a posterior leaflet. The anterior leaflet was large and semicircular with two zones while the posterior leaflet had three zones. The latter was divided into 2-3 scallops by clefts. The free edges of the cusps were attached to the papillary muscles by 6-9 chordae tendinae. Morphometric observations of these leaflets didn't show any significant variations in both species. The free-edge mean length, mean depth of these valves and the mean height of the aterio-posterior commissure and the posterior-anterior commissure were with insignificant differences. Histological features also revealed a similarity in both species. The leaflets were found attached to the annulus made of densely arranged collagen bundles. Lamina radialis formed the core of the leaflet and was composed of dense collagen fibers, few elastic and reticular fibers with fibrocytes and histiocytes. The atrial and ventricular surfaces were lined by a layer of endothelium. Beneath the endothelial lining was lamina spongiosa towards the atrial side and lamina fibrosa towards the ventricular side. The mean thickness of both these valves was with insignificant differences between these two species. These valves showed a mild to weak reaction to PAS in the lamina spongiosa, whereas a moderate activity for Alcian blue was observed in the endothelial linings that confirmed the presence of neutral and acid mucopolysaccharides. The reaction to acid and alkaline phosphatase activity was strong in fibrosa, moderate in spongiosa and weak in lamina radialis. The valves were negative for Oil red O and cholesterol activity. Moderately positive succinic dehydrogenase activity was observed at the endothelial surfaces of the leaflet in both species. [ABSTRACT FROM AUTHOR]

Simple Summary: Understanding the precise anatomy of the left and right subvalvular apparatus in the domestic horse can contribute to the development of normal and comparative animal anatomy, as well as surgery, internal medicine, and biology. This study conducts such an analysis, taking into account the thickness of the left ventricular wall, the right ventricular wall, the interventricular septum, the ventricle's length, and the entire heart's width. Additionally, it examines the number of muscle bellies of the papillary muscles, the type of connection between the muscle and the heart wall, the height of muscle origin, and the length of the papillary muscle. This study calculates various proportions and compares them with descriptions of subvalvular apparatuses in other animal species, including humans, available in the literature. Due to the growing interest among veterinarians and the increasing market demands, the development of equine cardiology is necessary. Currently, veterinary medicine for companion animals needs to catch up to human medicine—equine medicine included. A common condition in older horses is aortic valve regurgitation resulting from fibrosis, while its more severe form occurs in younger horses or develops due to a bacterial infection. Mitral valve regurgitation, especially dangerous due to the possibility of sudden death, has a better prognosis if the horse has valve prolapse. Tricuspid valve regurgitation usually does not pose a clinical problem, although its severe cases may lead to heart failure. Some pathologies can be treated surgically, which requires excellent knowledge of anatomy. The object of this study consisted of twenty domestic horse hearts. The focus was on the normal and comparative anatomy of the left and right subvalvular apparatus. The number of muscular bellies of the papillary muscles and the type of connection of the muscles were analysed. Moreover, the height of muscle originating from the ventricle wall was determined, the morphological regularity of the papillary muscle was assessed, and the chordae tendineae originating from the papillary muscles were examined. The conducted research allowed for comparing domestic horses with different species through other studies, the authors of which described this particular aspect. Interspecies similarities which may be correlated with the evolutionary relatedness, as well as differences that could reflect adaptation to different lifestyles, environmental conditions, or metabolic requirements of the animals, have been found. This study expands the knowledge of animals' normal and comparative anatomy, and contributes to the development of veterinary surgery, internal medicine, and biology. [ABSTRACT FROM AUTHOR]

Catecholamine-induced cardiomyopathy (CCM) is an entity associated with increased levels of catecholamines causing subendocardial and papillary muscle cardiomyocyte degeneration and necrosis. In 2020, 49 autopsies from early rabbit deaths in a colony used for medical device biocompatibility studies were submitted for microscopic examination. Of the 49 rabbits, 26 had histologic changes consistent with CCM. No common stressor for CCM was determined in affected rabbits. Animals were generally male, were 12–16-wk-old, and were found dead or had bloating, lethargy, and/or diarrhea. Those observed with clinical signs were euthanized and autopsied per the organization's standard operating procedures. Heart lesions consisted of various degrees of apical subendocardial myocardial degeneration and necrosis. Common non-cardiac lesions included pulmonary congestion and edema, hepatic congestion and centrilobular hepatocellular degeneration, and/or variable intestinal submucosal edema. [ABSTRACT FROM AUTHOR]

Background: The electrophysiological mechanism connecting mitral valve prolapse (MVP), premature ventricular complexes and life-threatening ventricular arrhythmia is unknown. A common hypothesis is that stretch activated channels (SACs) play a significant role. SACs can trigger depolarizations or shorten repolarization times in response to myocardial stretch. Through these mechanisms, pathological traction of the papillary muscle (PM), as has been observed in patients with MVP, may induce irregular electrical activity and result in reentrant arrhythmia. Methods: Based on a patient with MVP and mitral annulus disjunction, we modeled the effect of excessive PM traction in a detailed medical imagederived ventricular model by activating SACs in the PM insertion region. By systematically varying the onset of SAC activation following sinus pacing, we identified vulnerability windows for reentry with 1 ms resolution. We explored how reentry was affected by the SAC reversal potential (ESAC) and the size of the region with simulated stretch (SAC region). Finally, the effect of global or focal fibrosis, modeled as reduction in tissue conductivity or mesh splitting (fibrotic microstructure), was investigated. Results: In models with healthy tissue or fibrosis modeled solely as CV slowing, we observed two vulnerable periods of reentry: For ESAC of −10 and −30 mV, SAC activated during the T-wave could cause depolarization of the SAC region which lead to reentry. For ESAC of −40 and −70 mV, SAC activated during the QRS complex could result in early repolarization of the SAC region and subsequent reentry. In models with fibrotic microstructure in the SAC region, we observed micro-reentries and a larger variability in which times of SAC activation triggered reentry. In these models, 86% of reentries were triggered during the QRS complex or T-wave. We only observed reentry for sufficiently large SAC regions ( > = 8 mm radius in models with healthy tissue). Conclusion: Stretch of the PM insertion region following sinus activation may initiate ventricular reentry in patients with MVP, with or without fibrosis. Depending on the SAC reversal potential and timing of stretch, reentry may be triggered by ectopy due to SAC-induced depolarizations or by early repolarization within the SAC region. [ABSTRACT FROM AUTHOR]

Cardiac myxomas in the right ventricle are a very rare condition. In this case report, we describe an exceptionally uncommon case involving a right ventricular cardiac myxoma, originating from a papillary muscle, extending to both the tricuspid valve and the right atrium. The valve was able to be repaired via artificial chorda implantation. [ABSTRACT FROM AUTHOR]

Aging is associated with cardiac contractile abnormalities, but the etiology of these contractile deficits is unclear. We hypothesized that cardiac contractile and regulatory protein expression is altered during aging. To investigate this possibility, left ventricular (LV) lysates were prepared from young (6 months) and old (24 months) Fischer344 rats. There are no age‐related changes in SERCA2 expression or phospholamban phosphorylation. Additionally, neither titin isoform expression nor phosphorylation differed. However, there is a significant increase in β‐isoform of the myosin heavy chain (MyHC) expression and phosphorylation of TnI and MyBP‐C during aging. In permeabilized strips of papillary muscle, force and Ca2+ sensitivity are reduced during aging, consistent with the increase in β‐MyHC expression and TnI phosphorylation. However, the increase in MyBP‐C phosphorylation during aging may represent a mechanism to compensate for age‐related contractile deficits. In isolated cardiomyocytes loaded with Fura‐2, the peak of the Ca2+ transient is reduced, but the kinetics of the Ca2+ transient are not altered. Furthermore, the extent of shortening and the rates of both sarcomere shortening and re‐lengthening are reduced. These results demonstrate that aging is associated with changes in contractile and regulatory protein expression and phosphorylation, which affect the mechanical properties of cardiac muscle. [ABSTRACT FROM AUTHOR]

Segmenting the left ventricle from the transgastric short-axis views (TSVs) on transesophageal echocardiography (TEE) is the cornerstone for cardiovascular assessment during perioperative management. Even for seasoned professionals, the procedure remains time-consuming and experience-dependent. The current study aims to evaluate the feasibility of deep learning for automatic segmentation by assessing the validity of different U-Net algorithms. A large dataset containing 1388 TSV acquisitions was retrospectively collected from 451 patients (32% women, average age 53.42 years) who underwent perioperative TEE between July 2015 and October 2023. With image preprocessing and data augmentation, 3336 images were included in the training set, 138 images in the validation set, and 138 images in the test set. Four deep neural networks (U-Net, Attention U-Net, UNet++, and UNeXt) were employed for left ventricle segmentation and compared in terms of the Jaccard similarity coefficient (JSC) and Dice similarity coefficient (DSC) on the test set, as well as the number of network parameters, training time, and inference time. The Attention U-Net and U-Net++ models performed better in terms of JSC (the highest average JSC: 86.02%) and DSC (the highest average DSC: 92.00%), the UNeXt model had the smallest network parameters (1.47 million), and the U-Net model had the least training time (6428.65 s) and inference time for a single image (101.75 ms). The Attention U-Net model outperformed the other three models in challenging cases, including the impaired boundary of left ventricle and the artifact of the papillary muscle. This pioneering exploration demonstrated the feasibility of deep learning for the segmentation of the left ventricle from TSV on TEE, which will facilitate an accelerated and objective alternative of cardiovascular assessment for perioperative management. [ABSTRACT FROM AUTHOR]

Objective: We aimed to evaluate the mitral valve calcification and mitral structure detected by cardiac computed tomography (cardiac CT) and establish a scoring model based on cardiac CT and clinical factors to predict early good mitral valve repair (EGMR) and guide surgical strategy in rheumatic mitral disease (RMD). Materials and methods: This is a retrospective bi-center cohort study. Based on cardiac CT, mitral valve calcification and mitral structure in RMD were quantified and evaluated. The primary outcome was EGMR. A logical regression algorithm was applied to the scoring model. Results: A total of 579 patients were enrolled in our study from January 1, 2019, to August 31, 2022. Of these, 443 had baseline cardiac CT scans of adequate quality. The calcification quality score, calcification and thinnest part of the anterior leaflet clean zone, and papillary muscle symmetry were the independent CT factors of EGMR. Coronary artery disease and pulmonary artery pressure were the independent clinical factors of EGMR. Based on the above six factors, a scoring model was established. Sensitivity = 95% and specificity = 95% were presented with a cutoff value of 0.85 and 0.30 respectively. The area under the receiver operating characteristic of external validation set was 0.84 (95% confidence interval [CI] 0.73–0.93). Conclusions: Mitral valve repair is recommended when the scoring model value > 0.85 and mitral valve replacement is prior when the scoring model value < 0.30. This model could assist in guiding surgical strategies for RMD. Clinical relevance statement: The model established in this study can serve as a reference indicator for surgical repair in rheumatic mitral valve disease. Key Points: • Cardiac CT can reflect the mitral structure in detail, especially for valve calcification. • A model based on cardiac CT and clinical factors for predicting early good mitral valve repair was established. • The developed model can help cardiac surgeons formulate appropriate surgical strategies. [ABSTRACT FROM AUTHOR]

Despite centuries of investigation, certain aspects of left ventricular anatomy remain either controversial or uncertain. We make no claims to have resolved these issues, but our review, based on our current knowledge of development, hopefully identifies the issues requiring further investigation. When first formed, the left ventricle had only inlet and apical components. With the expansion of the atrioventricular canal, the developing ventricle cedes part of its inlet to the right ventricle whilst retaining the larger parts of the cushions dividing the atrioventricular canal. Further remodelling of the interventricular communication provides the ventricle with its outlet, with the aortic root being transferred to the left ventricle along with the newly formed myocardium supporting its leaflets. The definitive ventricle possesses inlet, apical and outlet parts. The inlet component is guarded by the mitral valve, with its leaflets, in the normal heart, supported by papillary muscles located infero‐septally and supero‐laterally. There is but a solitary zone of apposition between the leaflets, which we suggest are best described as being aortic and mural. The trabeculated component extends beyond the inlet to the apex and is confluent with the outlet part, which supports the aortic root. The leaflets of the aortic valve are supported in semilunar fashion within the root, with the ventricular cavity extending to the sinutubular junction. The myocardial‐arterial junction, however, stops well short of the sinutubular junction, with myocardium found only at the bases of the sinuses, giving rise to the coronary arteries. We argue that the relationships between the various components should now be described using attitudinally appropriate terms rather than describing them as if the heart is removed from the body and positioned on its apex. [ABSTRACT FROM AUTHOR]

Approximately 1–2 per 100,000 young athletes die from sudden cardiac death (SCD) and extreme exercise may be associated with myocardial scar and arrhythmias. Racehorses have a high prevalence of atrial fibrillation (AF) and SCD but the presence of myocardial scar and inflammation has not been evaluated. Cardiac tissues from the left (LAA) and right (RAA) atrial appendages, left ventricular anterior (LVAPM) and posterior (LVPPM) papillary muscles, and right side of the interventricular septum (IVS-R) were harvested from racehorses with sudden cardiac death (SCD, n = 16) or other fatal injuries (OFI, n = 17), constituting the athletic group (ATH, n = 33), and compared to sedentary horses (SED, n = 10). Horses in the ATH group had myocyte hypertrophy at all sites; increased fibrosis at all sites other than the LAA; increased fibroblast infiltration but a reduction in the overall extracellular matrix (ECM) volume in the RAA, LVAPM, and IVS-R compared to SED horses. In this horse model, athletic conditioning was associated with myocyte hypertrophy and a reduction in ECM. There was an excess of fibrocyte infiltration and focal fibrosis that was not present in non-athletic horses, raising the possibility of an exercise-induced pro-fibrotic substrate. [ABSTRACT FROM AUTHOR]

Objective: Unknown etiology. Background: Papillary muscle rupture (PMR) is a rare complication of myocardial infarction (MI); experiencing PMR without MI makes it even more uncommon, thereby complicating its diagnosis. Therefore, we report a case of spontaneous PMR to raise awareness of this entity. Case Report: A 48-year-old man with type 2 diabetes presented to the Emergency Department (ED) after experiencing sudden shortness of breath that began the day before. He had no history of chest trauma, fever, chills, or ischemic chest pain. His vital signs showed stable blood pressure and mild tachycardia. The patient had hypoxemia that did not respond to use of a non-rebreather mask (oxygen saturation 70%). Upon examination, he had increased respiratory rate, altered sensorium, no lower-limb edema, and his chest auscultation revealed bilateral crackles. Chest radiography showed pulmonary edema. Two electrocardiograms (ECG) showed no signs of ST elevation myocardial infarction (STEMI) or RV strain. The patient was intubated but remained hypoxic despite maximum ventilation settings. Transthoracic echocardiography (TTE) performed immediately thereafter revealed acute severe mitral regurgitation with evidence of PMR. A multidisciplinary team approach was adopted early in this case, which resulted in a positive outcome. Eventually, mitral valve replacement was performed, and the patient was discharged home after 17 days, with a favorable neurological outcome. Conclusions: We report a very rare case of spontaneous PMR in a middle-aged man with no evidence of MI, infective endocarditis, or preceding chest trauma. It shows the importance of adopting an early multidisciplinary team approach and showcases the abilities of emergency medicine physicians in early recognition. [ABSTRACT FROM AUTHOR]

Purpose: For novice learners, converting two-dimensional (2D) images of echocardiography to three-dimensional (3D) cardiac structures is deemed challenging. This study aimed to develop an accurate dissection method of the heart to reproduce the transthoracic echocardiographic views on cadavers and elucidate new educational methods in human anatomy dissection courses. Methods: A total of 18 hearts were used in this study. After reflecting the anterior thoracic wall inferiorly, the hearts were excised from embalmed cadavers. Thereafter, three landmarks were set on the heart for each plane of the incision, and the hearts were incised to observe the three different echocardiographic views, which include the apical four-chamber view (A4C), parasternal long axis (PLAX) view, and parasternal short axis (PSAX) view at the papillary muscle level. If all structures for observation during routine echocardiography are clearly observed in each view, a successful incision is considered. All procedures and incisions were performed by the medical students. After a successful incision, hearts were returned to the original position in the pericardial sac for further observation. Results: The success rates of incision for each view were 83.3% (5/6 success cases), 83.3% (5/6 success cases), and 66.7% (4/6 success cases) in the A4C view, PLAX view, and PSAX view at the papillary muscle level, respectively. Conclusion: This dissection method could probably be employed to reproduce transthoracic echocardiographic views on cadaveric hearts, which is beneficial for novice learners for a deeper understanding of the anatomy. [ABSTRACT FROM AUTHOR]

Objectives: To compare cardiac computed tomography (CCT) and cardiac magnetic resonance (CMR) for the quantitative assessment of the left ventricular (LV) trabeculated layer in patients with suspected noncompaction cardiomyopathy (NCCM). Materials and methods: Subjects with LV excessive trabeculation who underwent both CMR and CCT imaging as part of the prospective international multicenter NONCOMPACT clinical study were included. For each subject, short-axis CCT and CMR slices were matched. Four quantitative metrics were estimated: 1D noncompacted-to-compacted ratio (NCC), trabecular-to-myocardial area ratio (TMA), trabecular-to-endocardial cavity area ratio (TCA), and trabecular-to-myocardial volume ratio (TMV). In 20 subjects, end-diastolic and mid-diastolic CCT images were compared for the quantification of the trabeculated layer. Relationships between the metrics were investigated using linear regression models and Bland-Altman analyses. Results: Forty-eight subjects (49.9 ± 12.8 years; 28 female) were included in this study. NCC was moderately correlated (r = 0.62), TMA and TMV were strongly correlated (r = 0.78 and 0.78), and TCA had excellent correlation (r = 0.92) between CMR and CCT, with an underestimation bias from CCT of 0.3 units, and 5.1, 4.8, and 5.4 percent-points for the 4 metrics, respectively. TMA, TCA, and TMV had excellent correlations (r = 0.93, 0.96, 0.94) and low biases (− 3.8, 0.8, − 3.8 percent-points) between the end-diastolic and mid-diastolic CCT images. Conclusions: TMA, TCA, and TMV metrics of the LV trabeculated layer in patients with suspected NCCM demonstrated high concordance between CCT and CMR images. TMA and TCA were highly reproducible and demonstrated minimal differences between mid-diastolic and end-diastolic CCT images. Clinical relevance statement: The results indicate similarity of CCT to CMR for quantifying the LV trabeculated layer, and the small differences in quantification between end-diastole and mid-diastole demonstrate the potential for quantifying the LV trabeculated layer from clinically performed coronary CT angiograms. Key Points: • Data on cardiac CT for quantifying the left ventricular trabeculated layer are limited. • Cardiac CT yielded highly reproducible metrics of the left ventricular trabeculated layer that correlated well with metrics defined by cardiac MR. • Cardiac CT appears to be equivalent to cardiac MR for the quantification of the left ventricular trabeculated layer. [ABSTRACT FROM AUTHOR]

Background Some patients affected by mitral valve (MV) prolapse (MVP) are at higher risk of ventricular arrhythmias (VAs), but the underlying pathogenesis, as well as the effects of surgery on VA, remain not fully understood. Mitral valve repair, however, represents a privileged point of view to deepen the understanding of arrhythmogenesis in this context. Hence, we report an interesting case of MV re-repair. Case summary A 52-year-old man was referred to our institution for severe mitral regurgitation (MR) due to P2 prolapse in the context of myxomatous MV degeneration. Pre-operative imaging showed systolic mitral annular disjunction, left ventricular (LV) wall curling, Pickelhaube's sign, and a prolapsing tricuspid valve (TV) with only mild regurgitation. Twenty-four-hour electrocardiogram (ECG) Holter revealed a significant burden of premature ventricular contractions (PVCs), most of them originating from anterior papillary muscle (APM), posterior papillary muscle (PPM), and mitral annulus (MA). Quadrangular resection of P2 and mitral annuloplasty were performed. One year later, relapse of severe MR due to a residual P2M1 prolapse occurred. Twenty-four-hour ECG Holter showed no PVCs from PPM and MA, while those from APM persisted. A central edge-to-edge repair was effectively used to fix the residual prolapse. After 1 year from REDO surgery, a third ECG Holter confirmed the absence of any remaining LV PVCs, but still few ectopic beats originating from TV were recorded. Discussion Here, we report a case of VA resolution after specific, anatomical triggers addressing surgical gestures. Our experience confirms that MV surgery may have a role in MVP patients' arrhythmias correction. [ABSTRACT FROM AUTHOR]

Background: Papillary muscle (PM) infarction (PMI) detected by cardiac magnetic resonance imaging (CMR) is associated with poor outcomes. Whether PM parameters provide more value for mitral regurgitation (MR) management currently remains unclear. Therefore, we examined the prognostic value of PMI using CMR in patients with MR. Methods: Between March 2018 and July 2023, we retrospectively enrolled 397 patients with MR undergoing CMR. CMR was used to detect PMI qualitatively and quantitively. We also collected baseline clinical, echocardiography, and follow‐up data. Results: Of the 397 patients with MR (52.4 ± 13.9 years), 117 (29.5%) were assigned to the PMI group, with 280 (70.5%) in the non‐PMI group. PMI was demonstrated more in the posteromedial PM (PM‐PM, 98/117) than in the anterolateral PM (AL‐PM, 45/117). Compared with patients without PMI, patients with PMI had a decreased AL‐PM (41.5 ± 5.4 vs. 45.6 ± 5.3)/PM‐PM diastolic length (35.0 ± 5.2 vs. 37.9 ± 4.0), PM‐longitudinal strain (LS, 20.4 ± 6.1 vs. 24.9 ± 4.6), AL‐PM‐LS (19.7 ± 6.8 vs. 24.7 ± 5.6)/PM‐PM‐LS (21.2 ± 7.9 vs. 25.2 ± 6.0), and increased inter‐PM distance (25.7 ± 8.0 vs. 22.7 ± 6.2, all p < 0.001). Multiple logistic regression analyses identified male sex (odds ratio [OR] = 3.65, 95% confidence interval = 1.881−7.081, p < 0.001) diabetes mellitus (OR/95% CI/p = 2.534/1.13–5.68/0.024), AL‐PM diastolic length (OR/95% CI/p = 0.841/0.77–0.92/< 0.001), PM‐PM diastolic length (OR/95% CI/p = 0.873/0.79–0.964/0.007), inter‐PM distance (OR/95% CI/p = 1.087/1.028–1.15/0.003), AL‐PM‐LS (OR/95% CI/p = 0.892/0.843–0.94/< 0.001), and PM‐PM‐LS (OR/95% CI/p = 0.95/0.9–0.992/0.021) as independently associated with PMI. Over a 769 ± 367‐day follow‐up, 100 (25.2%) patients had arrhythmia. Cox regression analyses indicated that PMI (hazard ratio [HR]/95% CI/p = 1.644/1.062–2.547/0.026), AL‐PM‐LS (HR/95% CI/p = 0.937/0.903–0.973/0.001), and PM‐PM‐LS (HR/95% CI/p = 0.933/0.902–0.965/< 0.001) remained independently associated with MR. Conclusions: The CMR‐derived PMI and LS parameters improve the evaluation of PM dysfunction, indicating a high risk for arrhythmia, and provide additive risk stratification for patients with MR. [ABSTRACT FROM AUTHOR]

This article discusses a case of papillary muscle rupture (PMR) in a 61-year-old man who was admitted with acute inferior ST-segment elevation myocardial infarction. The patient underwent coronary angiography, which revealed occlusion of multiple coronary arteries. After a stent was deployed, the patient experienced acute shortness of breath, prompting further testing with transthoracic echocardiogram (TTE) and transesophageal echocardiogram (TEE). The TEE confirmed the diagnosis of PMR, and emergency surgical intervention was performed. Unfortunately, the patient died after surgery. The article emphasizes the importance of TEE in diagnosing PMR when TTE is inadequate. [Extracted from the article]

AimsCardiac arrhythmia originating from the papillary muscle (PM) can trigger ventricular fibrillation (VF) and cause sudden cardiac death even in the absence of structural heart disease. Most premature ventricular contractions, however, are benign and hitherto difficult to distinguish from a potentially fatal arrhythmia. Altered repolarization characteristics are associated with electrical instability, but electrophysiological changes which precede degeneration into VF are still not fully understood.Methods and resultsVentricular arrhythmia (VA) was induced by aconitine injection into PMs of healthy sheep. To investigate mechanisms of degeneration of stable VA into VF in structurally healthy hearts, endocardial high-density and epicardial mapping was performed during sinus rhythm (SR) and VA. The electrical restitution curve, modelling the relation of diastolic interval and activation recovery interval (a surrogate parameter for action potential duration), is steeper in VA than in non-arrhythmia (ventricular pacing and SR). Steeper restitution curves reflect electrical instability and propensity to degenerate into VF. Importantly, we find the parameter repolarization time in relation to cycle length (RT/CL) to differentiate self-limiting from degenerating arrhythmia with high specificity and sensitivity.ConclusionRT/CL may serve as a simple index to aid differentiation between self-limiting and electrically instable arrhythmia with the propensity to degenerate to VF. RT/CL is independent of cycle length and could easily be measured to identify electrical instability in patients.

As an integral part of the mitral valve apparatus, the left ventricle papillary muscle (PM) controls mitral valve closure during systole and participates in the ejection process during left ventricular systole. Mitral regurgitation (MR) is the most immediate and predominant result when the PM is structurally or functionally abnormal. However, dysfunction of the PM is easily underestimated or overlooked in clinical interventions for MR-related diseases. Therefore, adequate recognition of PM dysfunction and PM-derived MR is critical. In this review, we systematically describe the normal anatomical variations in the PM and the pathophysiology of PM dysfunction-related diseases and summarize the commonly used parameters and the advantages and disadvantages of various noninvasive imaging modalities for the structural and functional assessment of the PM. [ABSTRACT FROM AUTHOR]

BACKGROUND: Endocardial catheter-based pulsed field ablation (PFA) of the ventricular myocardium is promising. However, little is known about PFA's ability to target intracavitary structures, epicardium, and ways to achieve transmural lesions across thick ventricular tissue. METHODS: A lattice-tip catheter was used to deliver biphasic monopolar PFA to swine ventricles under general anesthesia, with electroanatomical mapping, fluoroscopy and intracardiac echocardiography guidance. We conducted experiments to assess the feasibility and safety of repetitive monopolar PFA applications to ablate (1) intracavitary papillary muscles and moderator bands, (2) epicardial targets, and (3) bipolar PFA for midmyocardial targets in the interventricular septum and left ventricular free wall. RESULTS: (1) Papillary muscles (n=13) were successfully ablated and then evaluated at 2, 7, and 21 days. Nine lesions with stable contact measured 18.3±2.4 mm long, 15.3±1.5 mm wide, and 5.8±1.0 mm deep at 2 days. Chronic lesions demonstrated preserved chordae without mitral regurgitation. Two targeted moderator bands were transmurally ablated without structural disruption. (2) Transatrial saline/carbon dioxide assisted epicardial access was obtained successfully and epicardial monopolar lesions had a mean length, width, and depth of 30.4±4.2, 23.5±4.1, and 9.1±1.9 mm, respectively. (3) Bipolar PFA lesions were delivered across the septum (n=11) and the left ventricular free wall (n=7). Twelve completed bipolar lesions had a mean length, width, and depth of 29.6±5.5, 21.0±7.3, and 14.3±4.7 mm, respectively. Chronically, these lesions demonstrated uniform fibrotic changes without tissue disruption. Bipolar lesions were significantly deeper than the monopolar epicardial lesions. CONCLUSIONS: This in vivo evaluation demonstrates that PFA can successfully ablate intracavitary structures and create deep epicardial lesions and transmural left ventricular lesions. [ABSTRACT FROM AUTHOR]

Aims: Polyglucosan body myopathy 1 (PGBM1) is a type of glycogen storage disease where polyglucosan accumulation leads to cardiomyopathy and skeletal muscle myopathy. Variants of RBCK1 is related with PGBM1. We present a newly discovered pathogenic RBCK1 variant resulting in dilated cardiomyopathy (DCM) and a comprehensive literature review. Methods and results: Whole‐exome sequencing (WES) was utilized to detect genetic variations in a 7‐year‐old girl considered the proband. Sanger sequencing was performed to validate the variant in the patient and all the available family members, whether affected or unaffected. The variant's pathogenicity was assessed by conducting a cosegregation analysis within the family with in silico predictive software. WES showed that the proband's RBCK1 gene contained a missense likely pathogenic homozygous nucleotide variant, c.598_599insT: p.His200LeufsTer14 (NM_001323956.1), in exon 8. The computational analysis supported the variant's pathogenicity. The variant was identified in a heterozygous form among all the healthy members of the family. Variants with changes in N‐terminal part of the protein were more likely to manifest immunodeficiency and auto‐inflammation than those with C‐terminal protein modifications according to prior variations of RBCK1 reported in the literature. Conclusions: Our study offers novel findings indicating an RBCK1 variant in individuals of Iranian ancestry presenting with DCM leading to heart transplantation and myopathy without immunodeficiency or auto‐inflammation. [ABSTRACT FROM AUTHOR]

Severe acute mitral regurgitation after myocardial infarction includes partial and complete papillary muscle rupture or functional mitral regurgitation. Although its incidence is <1%, mitral regurgitation after acute myocardial infarction frequently causes hemodynamic instability, pulmonary edema, and cardiogenic shock. Medical management has the worst prognosis, and mortality has not changed in decades. Surgery represents the gold standard, but it is associated with high rates of morbidity and mortality. Recently, transcatheter interventions have opened a new door for management that may improve survival. Mechanical circulatory support restores vital organ perfusion and offers the opportunity for a steadier surgical repair. This review focuses on the diagnosis and the interventional management, both surgical and transcatheter, with a glance on future perspectives to enhance patient management and eventually decrease mortality. [Display omitted] • Severe MR developing early after MI is associated with increased risks of heart failure and mortality. • Although surgical treatment can improve survival, the incidence of adverse events and mortality remain high. • Early mechanical cardiac support and transcatheter repair techniques can expand treatment options to a broader population and potentially improve outcomes. [ABSTRACT FROM AUTHOR]

Incomplete differentiation of the mitral valve structures during fetal life results in the papillary muscles and tendon cords becoming hypoplastic, a condition termed undifferentiated papillary muscles (UDPM). This fetal abnormality causes a group of diseases that cause mitral valve dysfunction in adult life. Here, we report a case of UDPM centered on the medial posterior apex in which detailed morphological abnormalities were diagnosed preoperatively using echocardiography and three-dimensional computed tomography (3DCT) analysis, contributing to plastic surgery. The patient was a 64-year-old man who was followed up for several years for atrial functional mitral regurgitation (MR), ultimately developing heart failure. His MR was severe, and he was referred for surgery. Echocardiography revealed restrictive tendon cords primarily in the posterior apex, abnormal muscle bundles in the lower part of the valve, and findings indicative of UDPM; this was considered the main cause of MR. The patient had surgery findings similar to the preoperative diagnosis, which greatly aided the surgery. Postoperatively, the MR was well-controlled and mild. UDPM may present as various morphologic and functional abnormalities, including partial club-shaped tendinous MR and rheumatoid mitral stenosis, which are rarely accurately diagnosed preoperatively. Detailed analysis of morphological abnormalities using 3DCT or other methods may be beneficial for a successful plasty. [ABSTRACT FROM AUTHOR]

Background: Glucocorticoid (GR) and mineralocorticoid (MR) receptors are highly expressed in cardiac tissue, and both can be activated by corticosteroids. MR activation, in acute myocardial infarction (AMI), worsens cardiac function, and increase NHE activity contributing to the deleterious process. In contrast, effects of GR activation are not fully understood, probably because of the controversial scenario generated by using different doses or potencies of corticosteroids. Aims: We tested the hypothesis that an acute dose of hydrocortisone (HC), a low‐potency glucocorticoid, in a murine model of AMI could be cardioprotective by regulating NHE1 activity, leading to a decrease in oxidative stress. Materials and Methods: Isolated hearts from Wistar rats were subjected to regional ischemic protocol. HC (10 nmol/L) was added to the perfusate during early reperfusion. Infarct size and oxidative stress were determined. Isolated papillary muscles from non‐infarcted hearts were used to evaluate HC effect on sodium‐proton exchanger 1 (NHE1) by analysing intracellular pH recovery from acute transient acidosis. Results: HC treatment decreased infarct size, improved cardiac mechanics, reduced oxidative stress after AMI, while restoring the decreased level of the pro‐fusion mitochondrial protein MFN‐2. Co‐treatment with the GR‐blocker Mifepristone avoided these effects. HC reduced NHE1 activity by increasing the NHE1 pro‐inhibiting Ser648 phosphorylation site and its upstream kinase AKT. HC restored the decreased AKT phosphorylation and anti‐apoptotic BCL‐2 protein expression detected after AMI. Conclusions: Our results provide the first evidence that acute HC treatment during early reperfusion induces cardioprotection against AMI, associated with a non‐genomic HC‐triggered NHE1 inhibition by AKT and antioxidant action that might involves mitochondrial dynamics improvement. [ABSTRACT FROM AUTHOR]

Background: Mitral valve prolapse (MVP) and mitral annular disjunction (MAD) are common valvular abnormalities that have been associated with ventricular arrhythmias (VA). Cardiac magnetic resonance imaging (CMR) has a key role in risk stratification of VA, including assessment of late gadolinium enhancement (LGE). Methods: Single-center retrospective analysis of patients with MVP or MAD who had >1 CMR and >1 24 h Holter registration available. Data are presented in detail, including evolution of VA and presence of LGE over time. Results: A total of twelve patients had repeated CMR and Holter registrations available, of which in four (33%) patients, it was conducted before and after minimal invasive mitral valve repair (MVR). After a median of 4.7 years, four out of eight (50%) patients without surgical intervention had new areas of LGE. New LGE was observed in the papillary muscles and the mid to basal inferolateral wall. In four patients, presenting with syncope or high-risk non-sustained ventricular tachycardia (VT), programmed ventricular stimulation was performed and in two (50%), sustained monomorphic VT was easily inducible. In two patients who underwent MVR, new LGE was observed in the basal inferolateral wall of which one presented with an increased burden of VA. Conclusions: In patients with MVP and MAD, repeat CMR may show new LGE in a small subset of patients, even shortly after MVR. A subgroup of patients who presented with an increase in VA burden showed new LGE upon repeat CMR. VA in patients with MVP and MAD are part of a heterogeneous spectrum that requires further investigation to establish risk stratification strategies. [ABSTRACT FROM AUTHOR]

Aims: Mitral valve prolapse (MVP) is an accepted cause of sudden cardiac death (SCD) in most autopsy series. Diagnosis at autopsy relies upon subjective assessment with no established objective pathological criteria. This study set out to establish objective measurements to help pathologists dealing with SCD. Methods: We diagnosed 120 (1.5%) cases of MVP in 8108 cases of SCD. We measured the mitral annulus, anterior and posterior leaflets, rough zone and mitral annular disjunction (MAD) in 27 MVP cases and compared them to 54 age‐ and sex‐matched normal mitral valves. Results: Age of death was 39 ± 16 years, with 59 females and 61 males. History of mild MV disease was present in 19 (16%). Eleven (9%) died associated with exertion. Left ventricular hypertrophy was present in nine (15%) females and 10 (16%) males. Both MV leaflets showed thickening and ballooning in all individuals. MVP showed highly significantly increased annular circumference, elongation and thickening of both leaflets as well as increased MAD (all P < 0.001). Left ventricular fibrosis was present in 108 (90%), with interstitial fibrosis in the posterolateral wall and papillary muscle in 88 (81%) and coexisting replacement fibrosis in 40 (37%). Conclusion: This is the largest MVP associated with SCD series highlighting a young cohort with equal representation of males and females. There is involvement of both leaflets with significant annular dilatation, elongation and thickening of both leaflets with MAD. Left ventricular fibrosis explains arrhythmia. Our quantitative measurements should serve as a reference for pathologists assessing post‐mortem hearts for MVP. [ABSTRACT FROM AUTHOR]

Nerium oleander, also known as "espirradeira" in Brazil, is a shrub or small tree widely used as an ornamental plant in temperate and subtropical regions of the world. Ingestion of N. oleander can cause intoxication due to the presence of cardioactive glycosides, in both humans and animals. This study aims to report the epidemiological, clinical, postmortem, and immunohistochemical features of an outbreak of natural intoxication by N. oleander in cattle and the use of immunohistochemistry (IHC) for troponin C, for the first time, in this intoxication in the species. Twenty-eight cattle had access to pruned branches of N. oleander and 20 animals started presenting clinical signs of apathy, anorexia, ataxia, tachypnea, tremors, and recumbency ten hours after the consumption. Eight cattle progressed to death 48 hours after the clinical progression and one was submitted for necropsy. Macroscopic findings included petechiae and ecchymosis on the epicardium and endocardium. Histologically, there were multifocal areas of necrosis of individual or multiple cardiomyocytes, mainly in the left ventricular papillary muscle. Immunohistochemistry for troponin C revealed decrease or absence of cytoplasmic immunolabeling in necrotic cardiomyocytes. Although intoxication by N. oleander is uncommon in cattle, it should be considered as a differential diagnosis for other conditions that cause sudden or acute death in livestock and IHC for troponin C is an auxiliary tool in the identification of peracute and acute cardiac lesions. [ABSTRACT FROM AUTHOR]

BACKGROUND: The extent of myocardial bone tracer uptake with technetium pyrophosphate, hydroxymethylene diphosphonate, and 3,3-diphosphono-1,2-propanodicarboxylate in transthyretin amyloid cardiomyopathy (ATTR-CM) might reflect cardiac amyloid burden and be associated with outcome. METHODS: Consecutive patients with ATTR-CM who underwent diagnostic bone tracer scintigraphy with acquisition of whole-body planar and cardiac single-photon emission computed tomography (SPECT) images from the National Amyloidosis Centre and 4 Italian centers were included. Cardiac uptake was defined according to the Perugini classification: 0=absent cardiac uptake; 1=mild uptake less than bone; 2=moderate uptake equal to bone; and 3=high uptake greater than bone. Extent of right ventricular (RV) uptake was defined as focal (basal segment of the RV free wall only) or diffuse (extending beyond basal segment) on the basis of SPECT imaging. The primary outcome was allcause mortality. RESULTS: Among 1422 patients with ATTR-CM, RV uptake accompanying left ventricular uptake was identified by SPECT imaging in 100% of cases at diagnosis. Median follow-up in the whole cohort was 34 months (interquartile range, 21 to 50 months), and 494 patients died. By Kaplan-Meier analysis, diffuse RV uptake on SPECT imaging (n=936) was associated with higher all-cause mortality compared with focal (n=486) RV uptake (77.9% versus 22.1%; P<0.001), whereas Perugini grade was not associated with survival (P=0.27 in grade 2 versus grade 3). On multivariable analysis, after adjustment for age at diagnosis (hazard ratio [HR], 1.03 [95% CI, 1.02-1.04]; P<0.001), presence of the p.(V142I) TTR variant (HR, 1.42 [95% CI, 1.20-1.81]; P=0.004), National Amyloidosis Centre stage (each category, P<0.001), stroke volume index (HR, 0.99 [95% CI, 0.97-0.99]; P=0.043), E/e' (HR, 1.02 [95% CI, 1.007-1.03]; P=0.004), right atrial area index (HR, 1.05 [95% CI, 1.02-1.08]; P=0.001), and left ventricular global longitudinal strain (HR, 1.06 [95% CI, 1.03-1.09]; P<0.001), diffuse RV uptake on SPECT imaging (HR, 1.60 [95% CI, 1.26-2.04]; P<0.001) remained an independent predictor of all-cause mortality. The prognostic value of diffuse RV uptake was maintained across each National Amyloidosis Centre stage and in both wild-type and hereditary ATTR-CM (P<0.001 and P=0.02, respectively). CONCLUSIONS: Diffuse RV uptake of bone tracer on SPECT imaging is associated with poor outcomes in patients with ATTRCM and is an independent prognostic marker at diagnosis. [ABSTRACT FROM AUTHOR]

Background: Left ventricular (LV) decompression is an essential strategy for improving early survival in patients with refractory cardiogenic shock. Low pump flow in patients on extracorporeal life support (ECLS) with LV apex decompression is a life-threatening issue. However, identifying the underlying causes of low flow can be challenging. Case presentation: A 38-year-old woman with COVID-19-related fulminant myocarditis was treated with central ECLS with LV apex decompression. The pump flow in the intensive care unit (ICU) was intermittently low, and low flow alerts were frequent. The initial evaluation based on pressure monitor waveforms and transthoracic echocardiography failed to identify the underlying cause. Prompt bedside transesophageal echocardiography (TEE) revealed that the anterolateral papillary muscle was suctioned into the vent cannula of the LV apex during systole. The patient underwent a repeat sternal midline incision in the operating room, and the cannula at the LV apex was repositioned. There were no further suction events after the repositioning, and the patient was weaned from ECLS 12 days after admission to the ICU. The patient was discharged in a stable condition and without neurological deficits. Conclusions: TEE is an important diagnostic tool to identify the underlying cause of low flow flow in patients undergoing ECLS with LV apex decompression. [ABSTRACT FROM AUTHOR]

Cardiovascular toxicity is one of the more common causes of attrition in preclinical and clinical drug development. Preclinical cardiovascular safety assessment involves numerous in vitro and in vivo endpoints which are being continually reviewed and improved to lower the incidence of cardiovascular toxicity that manifests only after the initiation of clinical trials. An example of notable preclinical toxicity is necrosis in the papillary muscle of the left ventricle in dogs that is induced by exaggerated pharmacological effects of vasodilators or positive inotropic/vasodilating off-target drug effects. Two distinct, small-molecule inhibitors that target an intracellular kinase, Compound A and Compound B, were profiled in 2-week dose-range finding and 4-week toxicity studies. Serum cardiac troponin (cTnI) was evaluated after a single dose and after 2-week and 4-week repeat dose studies with each kinase inhibitor. Acute effects on hemodynamic (heart rate, blood pressures, left ventricular contractility) and electrocardiographic (QTcV, PR, QRS intervals) endpoints by each inhibitor were assessed in an anesthetized dog cardiovascular model. Cardiovascular degeneration/necrosis with and without fibrosis was observed in dogs and correlated to increases in serum cTnI in repeat-dose toxicity studies. At the same doses used in toxicologic assessments, both kinase inhibitors produced sustained increases in heart rate, left ventricular contractility, and cardiac output, and decreases in mean arterial pressure. Cardiac pathology findings associated with these 2 kinase inhibitors were accompanied not only by cardiac troponin elevations but also associated with hemodynamic changes, highlighting the importance of the link of the physiologic—toxicologic interplay in cardiovascular safety assessment. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide OBJECTIVES Recurrence of tricuspid regurgitation (TR) after tricuspid annuloplasty can occur in cases where a dilated right ventricle exists and subsequent leaflet tethering follows. We previously reported a new technique of the right ventricular papillary muscle approximation (RV-PMA) for functional TR associated with leaflet tethering. The objective of this study is to elucidate the mid-term outcomes and evaluate the durability of RV-PMA. METHODS Between January 2014 and March 2023, we applied RV-PMA in 20 patients of advanced functional TR with severe leaflet tethering. The indication of the technique was severe TR with leaflet tethering height >8 mm, and/or a right ventricular end-diastolic diameter >45 mm. The patients were followed up with echocardiography before discharge and at annual interval thereafter. RESULTS There was no perioperative mortality. In the echocardiography performed before discharge, TR was decreased to mild or less in 85%, and a significant improvement in right ventricular end-diastolic diameter and tethering height were achieved (53–45 mm and 11.1–4.4 mm, respectively). Furthermore, during the median 3-year follow-up period, TR was kept controlled mild or less in 80% of the cases. CONCLUSIONS RV-PMA is considered to be a safe, effective and durable technique as an additional approach for tricuspid annuloplasty. [ABSTRACT FROM AUTHOR]

Introduction: The anatomically correct chordae tendineae originate from the apical part of the papillary muscles of the ventricles and attach to the corresponding free margins of the atrioventricular valves. Together with the papillary muscles, they contribute to the effective contraction of the ventricles, creating the so-called "annular-ventricular continuity". Aim of the research: This publication aimed to evaluate and analyse the impact of chordae tendineae pathology of the atrioventricular valves on the clinical presentation of a patient. Material and methods: A systematic review of the literature was performed in the PubMed, Web of Science, and Scopus databases and according to the PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Results and conclusions: This review allowed us to distinguish 6 groups of characteristic pathological lesions of chordae tendineae such as thickening, elongation, shortening, fibrosis, complete absence, or histopathological changes of the chordae tendineae. Most of the cases resulted from congenital underlying diseases, and treatment mainly consisted of surgical correction.. [ABSTRACT FROM AUTHOR]

Aims: Acute mitral regurgitation (MR) in the setting of myocardial infarction (MI) may be the result of papillary muscle rupture (PMR). This condition is associated with high morbidity and mortality. We aim to evaluate the feasibility of transcatheter edge‐to‐edge mitral valve repair (TEER) in this acute setting. Methods and results: We analysed data from the International Registry of MitraClip in Acute Mitral Regurgitation following acute Myocardial Infarction (IREMMI) of 30 centres in Europe, North America, and the middle east. We included patients with post‐MI PMR treated with TEER as a salvage procedure, and we evaluated immediate and 30‐day outcomes. Twenty‐three patients were included in this analysis (9 patients suffered complete papillary muscle rupture, 9 partial and 5 chordal rupture). The patients' mean age was 68 ± 14 years. Patients were at high surgical risk with median EuroSCORE II 27% (IQR 16, 28) and 20 out of 23 (87% were in cardiogenic shock). All patients were treated with vasopressors, and 17 out of 23 patients required mechanical support. TEER procedure was performed on the median 6 days after the index MI date IQR (3, 11). Procedural success was achieved in 87% of patients. The grade of MR was significantly decreased after the procedure. MR reduction to 0 or 1 + was achieved in 13 patients (57%), to 2 + in 7 patients (30%), P < 0.01. V‐Wave was reduced from 49 ± 8 mmHg to 26 ± 10 mmHg post‐procedure, P < 0.01. Sixteen out of 23 patients (70%) were discharged from hospital and 5 of them required reintervention with surgical mitral valve replacement. No additional death at 1 year was documented. Conclusions: TEER is a feasible therapy in critically ill patients with PMR due to a recent MI. TEER may have a role as salvage treatment or bridge to surgery in this population. [ABSTRACT FROM AUTHOR]

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Background and aimsDespite different etiopathogenesis, Fabry Disease cardiomyopathy (FDc) and sarcomeric hypertrophic cardiomyopathy (HCM) share a similar hypertrophic phenotype, including anomalies of the mitral valve apparatus (AMVA). Some of these anomalies have also been described in the pre-hypertrophic stage of both diseases. This cardiovascular magnetic resonance (CMR) study aimed to: (i) compare AMVA between FDc and HCM with a similar degree of left ventricular hypertrophy (LVH), to add new insights into differential diagnosis; (ii) assess whether AMVA represent an early and progressive alteration in FDc; (iii) propose simple and potentially reproducible measurements of AMVA.MethodsThis observational, retrospective study enrolled: (i) 80 Fabry patients, divided into three groups with increasing severity of cardiac phenotype (20 patients LVH-/normal T1, 20 patients LVH-/low T1 and 40 patients LVH+), and (ii) 40 patients with HCM. All patients underwent CMR. The LVH + FDc and the HCM groups were matched for age, sex, body surface area and left ventricular (LV) mass. The following AMVA were measured on cine images: papillary muscles (PMs) hypertrophy (maximal diameter (Dmax) of anterolateral (Al) and posteromedial (Pm) PM), apical displacement, anteriorization of Al PM and anterior mitral valve leaflet (AMVL) elongation. Reference values for defining AMVA were derived from a matched healthy control group (n = 40).ResultsBoth HCM and FDc LVH + patients showed PMs hypertrophy, with a greater degree in the FDc LVH + group [Dmax Al PM 16 ± 3.4 vs. 15 ± 3.1 mm, p 0.017; Dmax Pm PM 14 ± 4.0 vs.12 mm (10.0–14.0), p 0.039] As compared to controls, both HCM and FDc LVH + patients showed PMs apical displacement (HCM 83% vs. healthy volunteers 8%, p

Transthoracic echocardiography and cardiac magnetic resonance imaging revealed a well-defined globular mass attached to the anterolateral papillary muscle. The mass was hyperintense on T1 and T2 weighted images with suppression of signal on fat saturated and short tau inversion recovery (STIR) images. This imaging established the diagnosis of cardiac lipoma attached to the anterolateral papillary muscle, Papillary muscle is a very rare location of lipoma, which is rarely reported in the literature. [ABSTRACT FROM AUTHOR]

Mitral valve repair techniques in ventricular functional mitral regurgitation are controversial due to ongoing debates about long-term repair durability in the setting of left ventricular remodelling. To address the limitations of conventional annuloplasty, subannular techniques, such as papillary muscle relocation, have been developed. However, the limited reproducibility of these techniques has hindered their widespread adoption. In this context, we introduce a simplified and reproducible method for papillary muscle relocation. This method utilizes transoesophageal echocardiographic guidance and premeasured polytetrafluoroethylene loops to streamline the procedure. [ABSTRACT FROM AUTHOR]

The remodeling of the heart that occurs as a result of chronic disease progression is a difficult process to detect and monitor without the use of clinical and paraclinical investigations. In this context, echocardiography is the main diagnostic method. In degenerative cardiomyopathies, changes such as hypertrophy or dilatation of part of the left ventricle (LV), significant thickening of the interventricular septum, ventricular hypokinesis, abnormal anterior mitral valve motion during systole, and thickening of the papillary muscles are commonly observed. Cardiac remodeling can also be assessed by sinus rhythm disturbances such as atrial fibrillation or sinus tachycardia. Atrial fibrillation (AF), often associated with atrial fibrosis, is the most common chronic arrhythmia in medical practice, with heart failure being one of its causes. Biochemical indicators of cardiac remodeling include lactate dehydrogenase and creatine phosphokinase. [ABSTRACT FROM AUTHOR]

Objective : Ischaemic secondary mitral regurgitation (ISMR) after surgery is due to the displacement of papillary muscles resulting from progressive enlargement of the left ventricle end-diastolic diameter (LVEDD). Our aim was to prove that if the interpapillary muscle distance (IPMD) is surgically stabilized, an increase in LVEDD will not lead to a recurrence of ischaemic mitral regurgitation (MR). Methods: Ninety-six patients with ISMR, who underwent surgical revascularisation and annuloplasty, were randomly assigned in a 1:1 ratio to undergo papillary muscle approximation (PMA). At the 5-year follow-up, we assessed the correlation between PMA and echocardiographic improvements, the effect size of PMA on echocardiographic improvements, and a prediction model for recurrent MR using inferential tree analysis. Results : There was a significant correlation between PMA and enhancements in both the α and β angles (Spearman's rho > 0.7, p < 0.01). The α angle represents the angle between the annular plane and either the A2 annular-coaptation line or the P2 annular-coaptation line. The β angle indicates the angle between the annular plane and either the A2 annular-leaflet tip line or the P2 annular-leaflet tip line. PMA led to substantial improvements in LVEDD, tenting area, α and β angles, with a large effect size (Hedge's g ≥ 8, 95% CI ORs ≠ 1). The most reliable predictor of recurrent MR grade was the interpapillary distance, as only patients with an interpapillary distance greater than 40 mm developed ≥ 3 + grade MR. For patients with an IPMD of 40 mm or less, the best predictor of recurrent MR grade was LVEDD. Among the patients, only those with LVEDD greater than 62 mm showed moderate (2+) MR, while only those with LVEDD less than or equal to 62 mm had absent to mild (1+) MR. Conclusion: Prediction of recurrent ischaemic MR is not independent of progressive LVEDD increase. PMA-based surgical procedure stabilises IPMD. [ABSTRACT FROM AUTHOR]