The relevance of tricuspid regurgitation in patients undergoing percutaneous treatment of mitral regurgitation.

OBJECTIVES: Investigate the impact of concomitant tricuspid regurgitation (TR) on clinical outcomes during long-term follow-up in patients undergoing percutaneous treatment of mitral regurgitation (MR) with the MitraClip system. BACKGROUND: Patients undergoing mitral repair using the MitraClip frequently present with concomitant TR. It is uncertain how the presence of TR impacts the long-term outcomes of such patients. METHODS: We analyzed consecutive patients with MitraClip implantation from the prospective MitraSwiss registry. Endpoints were all-cause mortality, hospitalization for heart failure, and the composite endpoint of the two. RESULTS: We enrolled 177 patients (mean age 76 ± 9 years, 37% female). Acute procedural success was achieved in 149 (84%). Concomitant moderate or severe TR was present in 31% at baseline and 32% before discharge. After a median follow-up of 1103 days (IQR: 555-1766 days), 70 (40%) of patients had died, and 34 (19%) were hospitalized for heart failure. In multivariable analysis, TR at baseline was associated with an increase in all-cause mortality (HR: 2.34, 95% CI: 1.36-4.03, p < 0.01), hospitalization for heart failure (HR: 3.19, 95% CI: 1.37-7.41, p = 0.01), and the composite endpoint (HR: 2.00, 95% CI: 1.19-3.36, p = 0.01). CONCLUSION: Despite treatment of MR, TR did not improve in most patients. The presence of relevant TR at baseline was associated with reduced survival and higher rates of hospitalization for heart failure. More research is needed to understand the causal role of TR in such patients and to investigate if simultaneous treatment of concomitant TR may improve prognosis in patients undergoing percutaneous treatment of MR.

Obstructive sleep apnoea and the progression of thoracic aortic aneurysm: a prospective cohort study.

BACKGROUND: Obstructive sleep apnoea (OSA) is associated with an increased prevalence of aortic aneurysms and it has also been suggested that severe OSA furthers aneurysm expansion in the abdomen. We evaluated whether OSA is a risk factor for the progression of ascending thoracic aortic aneurysm (TAA). METHODS: Patients with TAA underwent yearly standardised echocardiographic measurements of the ascending aorta over 3 years and two level III sleep studies. The primary outcome was the expansion rate of TAA in relation to the apnoea-hypopnoea index (AHI). Secondary outcomes included surveillance for aortic events (composite end-points of rupture/dissection, elective surgery or death). RESULTS: Between July 2014 and March 2020, 230 patients (median age 70 years, 83.5% male) participated in the cohort. At baseline, 34.8% of patients had AHI ≥15 events·h-1. There was no association between TAA diameter and AHI at baseline. After 3 years, mean±sd expansion rates were 0.55±1.25 mm at the aortic sinus and 0.60±1.12 mm at the ascending aorta. In the regression analysis, after controlling for baseline diameter and cardiovascular risk factors, there was strong evidence for a positive association of TAA expansion with AHI (aortic sinus estimate 0.025 mm, 95% CI 0.009-0.040 mm; p<0.001 and ascending aorta estimate 0.026 mm, 95% CI 0.011-0.041 mm; p=0.001). 20 participants (8%) experienced an aortic event; however, there was no association with OSA severity. CONCLUSION: OSA may be a modest but independent risk factor for faster TAA expansion and thus potentially contributes to life-threatening complications in aortic disease.

Murine tissue factor disulfide mutation causes a bleeding phenotype with sex specific organ pathology and lethality.

Tissue factor is highly expressed in sub-endothelial tissue. The extracellular allosteric disulfide bond Cys186-Cys209 of human tissue factor shows high evolutionary conservation and in vitro evidence suggests that it significantly contributes to tissue factor procoagulant activity. To investigate the role of this allosteric disulfide bond in vivo, we generated a C213G mutant tissue factor mouse by replacing Cys213 of the corresponding disulfide Cys190-Cys213 in murine tissue factor. A bleeding phenotype was prominent in homozygous C213G tissue factor mice. Pre-natal lethality of 1/3rd of homozygous offspring was observed between E9.5 and E14.5 associated with placental hemorrhages. After birth, homozygous mice suffered from bleedings in different organs and reduced survival. Homozygous C213G tissue factor male mice showed higher incidence of lung bleedings and lower survival rates than females. In both sexes, C213G mutation evoked a reduced protein expression (about 10-fold) and severely reduced pro-coagulant activity (about 1000-fold). Protein glycosylation was impaired and cell membrane exposure decreased in macrophages in vivo. Single housing of homozygous C213G tissue factor males reduced the occurrence of severe bleeding and significantly improved survival, suggesting that inter-male aggressiveness might significantly account for the sex differences. These experiments show that the tissue factor allosteric disulfide bond is of crucial importance for normal in vivo expression, post-translational processing and activity of murine tissue factor. Although C213G tissue factor mice do not display the severe embryonic lethality of tissue factor knock-out mice, their postnatal bleeding phenotype emphasizes the importance of fully functional tissue factor for hemostasis.

Prevalence of Obstructive Sleep Apnea in Patients with Thoracic Aortic Aneurysm: A Prospective, Parallel Cohort Study.

BACKGROUND: The pathogenesis and etiology of thoracic aortic aneurysms (TAA) are largely unknown. Preliminary data from patients with aortic dissection and abdominal aneurysms suggest a causal link of obstructive sleep apnea (OSA) on aortic disease. OBJECTIVES: The aim of the study was to assess the prevalence of OSA in patients with TAA compared to a matched control group. METHOD: In this prospective parallel-cohort study, we 2-to-1 matched 208 patients with verified TAA (at the aortic sinus and/or ascending aorta) to 104 controls without TAA according to sex, age, height, weight, and left ventricular ejection fraction. All participants underwent an ultrasound of the thoracic aorta and a level III respiratory polygraphy. OSA was defined as apnea-hypopnea index ≥5/h. The prevalence of OSA was compared with conditional logistic regression and controlling for the matching variables. RESULTS: A total of 312 patients (mean age 65 ± 11 years, 82% male, mean body mass index 27 ± 4 kg/m2) were successfully 2-to-1 matched in the final model. Prevalence of OSA was significantly higher in the TAA-group when compared to the matched control group (63 vs. 47%; odds ratio 1.87 [95% CI 1.05-3.34]; p = 0.03). When applying a higher apnea-hypopnea index threshold (≥15/h), the odds ratio increased to 3.25 (95% CI 1.65-6.42; p < 0.001). The median apnea-hypopnea index was higher in patients with TAA (9.2/h [3.3-20.0] vs. 4.5/h [2.2-11.1], p < 0.001). CONCLUSIONS: Patients with TAA have a higher prevalence of OSA when compared to the general population. Since OSA is effectively treatable and might contribute to the pathogenesis of TAA, further longitudinal trials are needed to assess the association between OSA and TAA.

Ticagrelor, but not clopidogrel active metabolite, displays antithrombotic properties in the left atrial endocardium.

AIMS: Oral anticoagulation is considered standard therapy for stroke prevention in atrial fibrillation (AF). Endocardial activation triggers expression of pro-thrombotic mediators including tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1), and contributes to thrombus formation in the left atrial appendage (LAA) of AF patients. Recently, pleiotropic effects of specific P2Y12 receptor antagonists were demonstrated; however, whether these drugs possess antithrombotic effects on LAA endocardial cells currently remains unknown. METHODS AND RESULTS: LAA were obtained from 14 patients with known AF undergoing elective cardiac surgery including LAA removal at the University Hospital Zurich. LAA endocardial cells were isolated and pre-incubated with ticagrelor (10-7, 10-6, 10-5M) or clopidogrel active metabolite (CAM) (1.5 × 10-8, 1.5 × 10-7, 1.5 × 10-6 M) before stimulation with tumour necrosis factor-alpha (TNF-α) (10 ng/mL). Finally, TF and PAI-1 expression and activity were analysed. Ticagrelor, unlike CAM, concentration dependently decreased TNF-α-induced TF expression and TF activity in LAA endocardial cells. Further, ticagrelor, but not CAM reduced PAI-1 expression and enzyme activity in TNF-α-stimulated LAA endocardial cells. In contrast, TF pathway inhibitor (TFPI) remained unaffected by both dugs. CONCLUSION: Ticagrelor, but not CAM, reduces expression and activity of TF and PAI-1 in LAA endocardial cells isolated from patients with AF, indicating possible local antithrombotic effects. Such pleiotropic properties of ticagrelor may contribute to a reduction in thromboembolic complications in patients with AF.

Restraint stress enhances arterial thrombosis in vivo--role of the sympathetic nervous system.

Stress is known to correlate with the incidence of acute myocardial infarction. However, the molecular mechanisms underlying this correlation are not known. This study was designed to assess the effect of experimental stress on arterial thrombus formation, the key event in acute myocardial infarction. Mice exposed to 20 h of restraint stress displayed an increased arterial prothrombotic potential as assessed by photochemical injury-induced time to thrombotic occlusion. This increase was prevented by chemical sympathectomy performed through 6-hydroxydopamine (6-OHDA). Blood-born tissue factor (TF) activity was enhanced by stress and this increase could be prevented by 6-OHDA treatment. Vessel wall TF, platelet count, platelet aggregation, coagulation times (PT, aPTT), fibrinolytic system (t-PA and PAI-1) and tail bleeding time remained unaltered. Telemetric analysis revealed only minor hemodynamic changes throughout the stress protocol. Plasma catecholamines remained unaffected after restraint stress. Tumor necrosis factor alpha (TNF-α) plasma levels were unchanged and inhibition of TNF-α had no effect on stress-enhanced thrombosis. These results indicate that restraint stress enhances arterial thrombosis via the sympathetic nervous system. Blood-borne TF contributes, at least in part, to the observed effect whereas vessel wall TF, platelets, circulating coagulation factors, fibrinolysis and inflammation do not appear to play a role. These findings shed new light on the understanding of stress-induced cardiovascular events.

Fluoroscopy-only guided transcatheter patent foramen ovale closure: the importance of pre-procedural echocardiography.

Objectives: Percutaneous closure of a patent foramen ovale (PFO) to prevent recurrent paradoxical thromboembolic events has become the standard of care. However, it remains uncertain if transesophageal echocardiography (TOE) guidance improves procedural success with an existing comprehensive pre-procedural TOE. The aim of the study was to compare the effectiveness of percutaneous PFO closure guided by fluoroscopy (FS) only vs TOE plus FS. Methods: Consecutive patients undergoing percutaneous PFO closure between February 2017 and April 2023 were analyzed. Based on pre-procedural echocardiography, patients were scheduled either for an FS-only or TOE/FS-guided procedure. The primary-endpoint was effective PFO-closure (residual-shunt grade 0/1 at 6-month follow-up). The secondary-endpoints included procedural safety/efficacy and major adverse cardiovascular events during hospital stay and at the 6-month follow-up. Results: Two hundred-three patients (mean age 51.8 ± 12.5 years, 39.4% women, Risk of Paradoxical Embolism score = 7 [IQR = 6-7]) underwent PFO closure with FS-only guidance (88 patients, 43.3%) or TOE/FS guidance (115 patients, 56.7%). The main indications for PFO closure were cryptogenic stroke (179 patients, 88.2%) and peripheral embolism (13 patients, 6.4%). At baseline, a right-to-left shunt of grade 2 or higher was present in 199 patients (98%). The procedure time in the FS group was shorter (13 minutes in the FS group vs 16.5 minutes in the TOE/FS group, P = .002). The immediate procedural success was 99.5%. At 6 months, effective closure was achieved in 195 patients (96.1% [FS group: 97.7% vs TOE/FS group 97.8%, P = .29]). The rates of atrial fibrillation and recurrent thromboembolic events were not different among the procedural strategies (3.9% [P = .47] and 0.5% [P = .43]). Conclusions: After comprehensive pre-procedural echocardiography workup, PFO closure with FS guidance only seems equally safe and effective as TOE/FS guidance. A standardized pre-procedural echocardiography protocol facilitates procedural planning with excellent echocardiographic and clinical outcomes.

Antithrombotic properties of Tafamidis: An additional protective effect for transthyretin amyloid cardiomyopathy patients.

INTRODUCTION: Tafamidis is a molecular chaperone that stabilizes the transthyretin (TTR) homo-tetramer, preventing its dissociation and consequent deposition as amyloid fibrils in organ tissues. Tafamidis reduces mortality and the incidence of hospitalization for cardiovascular causes in patients with TTR amyloid (ATTR) cardiomyopathy. As ATTR cardiomyopathy is associated with a high risk of thromboembolic complications, we hypothesized that tafamidis may have a direct ancillary anti-thrombotic effect. METHODS: Primary human aortic endothelial cells (HAECs) were treated with tafamidis at clinically relevant concentrations and with plasma of patients, before and after the initiation of treatment with tafamidis. The expression of TF was induced by incubation with Tumor Necrosis Factor α (TNFα). Intracellular expression of tissue factor (TF) was measured by western blot. TF activity was measured by a colorimetric assay. Gene expressions of TF were measured by quantitative polymerase chain reaction. RESULTS: Treatment with tafamidis dose-dependently reduced the expression and activity of TNFα-induced TF. This effect was confirmed in cells treated with patients' plasma. Signal Transducer and Activator of Transcription 3 (STAT3) phosphorylation was significantly inhibited by tafamidis. Incubation of HAECs with tafamidis and the STAT3 activator colivelin partially rescued the expression of TF. CONCLUSIONS: Treatment with tafamidis lowers the thrombotic potential in human primary endothelial cells by reducing TF expression and activity. This previously unknown off-target effect may provide a novel mechanistic explanation for the lower number of thromboembolic complications in ATTR cardiomyopathy patients treated with tafamidis.

Current and Evolving Multimodality Cardiac Imaging in Managing Transthyretin Amyloid Cardiomyopathy.

Amyloid transthyretin (ATTR) amyloidosis is a protein-misfolding disease characterized by fibril accumulation in the extracellular space that can result in local tissue disruption and organ dysfunction. Cardiac involvement drives morbidity and mortality, and the heart is the major organ affected by ATTR amyloidosis. Multimodality cardiac imaging (ie, echocardiography, scintigraphy, and cardiac magnetic resonance) allows accurate diagnosis of ATTR cardiomyopathy (ATTR-CM), and this is of particular importance because ATTR-targeting therapies have become available and probably exert their greatest benefit at earlier disease stages. Apart from establishing the diagnosis, multimodality cardiac imaging may help to better understand pathogenesis, predict prognosis, and monitor treatment response. The aim of this review is to give an update on contemporary and evolving cardiac imaging methods and their role in diagnosing and managing ATTR-CM. Further, an outlook is presented on how artificial intelligence in cardiac imaging may improve future clinical decision making and patient management in the setting of ATTR-CM.

Red Flags Suggesting Cardiac Transthyretin Amyloidosis (ATTR) in Clinical Practice.

Cardiac wtATTR is caused by extracellular deposition of misfolded proteins in the heart. It mostly affects elderly men and is still clearly underdiagnosed. Recognizing red flags suggesting wtATTR is key for a timely diagnosis, enabling the patient to profit from effective therapies. If general practitioners suspect cardiac amyloidosis, it is crucial to rapidly exclude AL-amyloidosis by immunoelectrophoresis, immunofixation as well as light-chain assay, because AL-amyloidosis needs urgent hematologic therapy. After that, the patient should be referred to the cardiologist for further assessment.

[A Transient Hypertrophic Cardiomyopathy?] / Eine transiente hypertrophe Kardiomyopathie?

A Transient Hypertrophic Cardiomyopathy? Abstract. We report on a 79-year-old female patient after blunt chest trauma. Based on T-negative findings on 12-lead ECG and apical left ventricular hypertrophy on echocardiography and cardiac MRI examination, apical hypertrophic cardiopathy was postulated. Subsequently, it was shown that these findings were present only transiently and completely normalized in the course. The apical changes were not due to hypertrophy of cardiomyocytes but to myocardial edema. Both Takotsubo syndrome and contusio cordis were considered as causes.

Renal dysfunction and outcome in left ventricular non-compaction.

BACKGROUND: While renal function has been observed to inversely correlate with clinical outcome in other cardiomyopathies, its prognostic significance in patients with left ventricular non-compaction cardiomyopathy (LVNC) has not been investigated. The aim of this study was to determine the prognostic value of renal function in LVNC patients. METHODS: Patients with isolated LVNC as diagnosed by echocardiography and/or magnetic resonance imaging in 4 Swiss centers were retrospectively analyzed for this study. Values for creatinine, urea, and estimated glomerular filtration rate (eGFR) as assessed by the CKD-EPI 2009 formula were collected and analyzed by a Cox regression model for the occurrence of a composite endpoint (death or heart transplantation). RESULTS: During the median observation period of 7.4 years 23 patients reached the endpoint. The ageand gender-corrected hazard ratios (HR) for death or heart transplantation were: 1.9 (95% confidence interval [CI] 1.4-2.6) for each increase over baseline creatinine level of 30 µmol/L (p < 0.001), 1.6 (95% CI 1.2-2.2) for each increase over baseline urea level of 5 mmol/L (p = 0.004), and 3.6 (95% CI 1.9-6.9) for each decrease below baseline eGFR level of 30 mL/min (p ≤ 0.001). The HR (log2) for every doubling of creatinine was 7.7 (95% CI 3-19.8; p < 0.001), for every doubling of urea 2.5 (95% CI 1.5-4.3; p < 0.001), and for every bisection of eGFR 5.3 (95% CI 2.4-11.6; p < 0.001). CONCLUSIONS: This study provides evidence that in patients with LVNC impairment in renal function is associated with an increased risk of death and heart transplantation suggesting that kidney function assessment should be standard in risk assessment of LVNC patients.

Hypoattenuated Leaflet Thickening After Implantation of the ACURATE neo or the ACURATE neo2 Transcatheter Heart Valve.

Subclinical leaflet thrombosis, identified as hypoattenuated leaflet thickening (HALT) on cardiac computed tomography scan, has been observed after transcatheter aortic valve replacement (TAVR). However, data on HALT after the implant of the supra-annular ACURATE neo/neo2 prosthesis are limited. This study aimed to determine the prevalence and risk factors for the development of HALT after TAVR with the ACURATE neo/neo2. A total of 50 patients who received the ACURATE neo/neo2 prosthesis were prospectively enrolled. Patients underwent a contrast-enhanced multidetector row cardiac computed tomography scan at before, after, and 6 months after TAVR. At the 6-month follow-up, HALT was detected in 16% (8 of 50 patients). These patients had a lower implant depth of the transcatheter heart valve (8 ± 2 mm vs 5 ± 2 mm, p = 0.001), less calcified native valve leaflets, a better expansion of the frame at the level of the left ventricular outflow tract, and were less often hypertensive. Thrombosis of the sinus of Valsalva occurred in 18% (9/50). There was no difference in the anticoagulation regimen between patients with and without thrombotic findings. In conclusion, HALT was present in 16% of patients at 6 months follow-up, patients presenting with HALT had a lower implant depth of the transcatheter heart valve, and HALT was detected in patients on oral anticoagulation therapy.

Direct Oral Anticoagulants Versus Vitamin K Antagonists for the Treatment of Left Ventricular Thrombi-Insights from a Swiss Multicenter Registry.

Current guidelines recommend vitamin K antagonists (VKAs) for the treatment of a left ventricular thrombus (LVT). However, direct oral anticoagulants (DOACs) show superior safety and efficacy compared with VKAs in most thromboembolic disorders. Nevertheless, DOACs remain poorly investigated for the treatment of LVT. To describe the thrombus resolution rate and clinical efficacy of DOACs versus VKAs in patients with LVT, we analyzed consecutive patients with confirmed LVT from a multicenter echocardiography database. Echocardiograms and clinical end points were evaluated independently. The thrombus resolution rate and clinical outcomes were compared according to the underlying anticoagulation regimen. In total, 101 patients were included (17.8% women, mean age 63.3 ± 13.2 years), 50.5% had recently experienced a myocardial infarction. The mean left ventricular ejection fraction was 36.6 ± 12.2%. DOACs versus VKAs were used in 48 and 53 patients, respectively. The median follow-up was 26.6 (interquartile range 11.8;41.2) months. Among patients receiving VKAs compared with DOACs, the thrombus resolved more rapidly within the first month in those taking VKAs (p = 0.049). No differences were seen between the 2 groups with respect to major bleedings, strokes, and other thromboembolic events. In each group, LVT recurred in 3 of the subjects (a total of 6) after discontinuation of anticoagulation. In conclusion, DOACs appear to be a safe and effective alternative to VKAs for the treatment of LVTs, but the rate of thrombus dissolution within 1 month after initiation of anticoagulation appears to be higher with VKAs. A sufficiently powered randomized trial is required to definitively define the role of DOACs in the treatment of LVT.

Acute ST-Elevation Myocardial Infarction During Labor Due to Amniotic Fluid Embolism.

BACKGROUND Amniotic fluid embolism (AFE) is an extremely rare, life-threatening complication of labor that leads to hyper-acute induction of inflammation and disseminated intravascular coagulation (DIC). Usually, acute pulmonary hypertension results in acute right ventricular failure, while DIC manifests by hemorrhagic and ischemic complications, ultimately leading to multi-organ failure and death. CASE REPORT A 30-year-old primigravida and primipara woman with no prior medical history was admitted for labor after intrauterine fetal death at 37 weeks of gestation. After medical birth induction, she had a convulsive seizure and cardiorespiratory arrest. Short mechanical resuscitation was performed before spontaneous circulation returned. Simultaneously occurring severe vaginal hemorrhage and an ST-elevation myocardial infarction (STEMI) triggered the diagnosis of AFE. Laboratory results fulfilled the criteria for DIC, and hemostatic resuscitation and mechanical hemostasis were performed. Transesophageal echocardiography revealed hypokinesia to akinesia of the inferior wall. Owing to the ongoing DIC, coronary angiography could not be performed. After the patient's transfer to the Intensive Care Unit, ST-segment elevations resolved and the myocardial infarct was managed medically. Cardiac magnetic resonance imaging performed 3 months later demonstrated myocardial scarring in 2 different areas. Referring to the coronary artery anatomy in a computed tomography scan of the chest, the infarcted areas correlated with 2 different coronary supply territories. CONCLUSIONS AFE should be considered in women with acute cardiorespiratory failure during labor. This is the first report of a STEMI triggered by an AFE. The 2 separate areas of infarction, corresponding to the 2 different coronary territories, suggest an AFE-related thrombotic/thromboembolic etiology.

An Extremely Rare Congenital Muscle Bundle Crossing the Right Atrial Cavity.

Muscle bundles in the right atrium are an extremely rare congenital anomaly. We report the case of a patient with 2 atrial septal defects and a large muscle bundle crossing the right atrium. Only 3 comparable cases have previously been published. (Level of Difficulty: Intermediate.).

Young adults after arterial switch operation for transposition of the great arteries in Switzerland: a growing population.

BACKGROUND: Adults with transposition of the great arteries (d-TGA) after the arterial switch operation (ASO) are an evolving cohort in adult cardiology. We aimed to analyze cardiac function and cardiac events after transition to the adult clinic in Switzerland. MATERIALS AND METHODS: Adults with prior ASO enrolled in the Swiss Adult Congenital HEart disease Registry (SACHER) were included. We analyzed initial cardiac anatomy, surgical history, residual lesions and cardiac function at the time of inclusion, as well as cardiac events during follow-up. Patients were classified as complex (with ventricular septal defect) or simple (with intact interventricular septum) d-TGA. RESULTS: The cohort included 149 patients (99 simple d-TGA, 50 complex d-TGA; age 21±3 years; 71% male, follow-up 27 [15-46] months). Prior to inclusion, patients with complex d-TGA had undergone more interventions related to the left ventricular outflow tract (16% vs. 3%, p = 0.01). Functional and cardiovascular status were similar between the groups. Eleven patients (7%) had a total of 19 cardiac events (5 complications and 14 re-interventions) during follow-up. Patients with complex d-TGA had more cardiac-related complications compared to those with simple d-TGA (8% vs. 1%, p = 0.03). The frequency of re-interventions was not statistically different between the two groups (12% vs. 4%, p = 0.07). During follow-up, an increase in QRS duration was observed. Other parameters of cardiac function remained unchanged. CONCLUSION: The majority of adult ASO patients have normal functional class and cardiac function. Complex anatomy and residual lesions play a key role when regarding the occurrence of cardiac-related complications during follow-up. The role of QRS prolongation over time needs to be investigated further.

Right ventricular involvement in left ventricular non-compaction cardiomyopathy.

BACKGROUND: Left ventricular non-compaction cardiomyopathy (LVNC) features extensive trabeculations. Involvement of the right ventricle (RV) has been reported; however, distinction from normal RV trabeculation is difficult. This study aimed at assessing RV morphology and function in LVNC by cardiac magnetic resonance (CMR) and transthoracic echocardiography (TTE). METHODS: Dimensional and functional parameters were assessed according to guidelines. Novel CMR parameters were RV end-diastolic (ED) trabeculated area, RV ED trabeculated volume, and RV ED non-compacted to compacted (NC/N) ratio in short axis (SAX) as well as in four-chamber view (4CH). RESULTS: Twenty patients with LVNC and 20 controls were included. RV size and function were comparable in LVNC and controls and exhibited a good correlation between TTE and CMR. Although RV trabeculated area, RV trabeculated volume, and RV ED NC/C ratio in SAX as well as in 4CH were larger in LVNC, there was a major overlap with values in controls. RV ED NC/C ratio in SAX correlated with LV ED NC/C ratio (not in 4CH). Quantitative assessment of RV non-compaction was not feasible in TTE. CONCLUSIONS: Right ventricle size and function in LVNC can be measured by CMR and TTE, while RV trabeculation can only be quantified by CMR. RV myocardium displays more trabeculations in LVNC; however, overlap with normal individuals is extensive, not allowing separation of patients with LVNC from controls.

Tricuspid Regurgitation and Right Ventricular Function in Patients Undergoing Percutaneous Treatment of Mitral Regurgitation.

OBJECTIVES: Patients with severe mitral regurgitation (MR) frequently present with concomitant right ventricular (RV) dysfunction and tricuspid regurgitation (TR). We aimed to investigate the prognostic relevance of RV function, RV dimension, and TR in patients undergoing percutaneous intervention for MR. METHODS: Consecutive patients undergoing percutaneous mitral valve intervention were enrolled in the prospective MitraSwiss registry. Tricuspid annular plane systolic excursion (TAPSE), pulmonary artery systolic pressure (PASP), right ventricular pulmonary arterial coupling (RVC, defined as TAPSE/ PASP ratio), indexed tricuspid annulus (TA) dimension, and TR severity grade were analyzed at baseline, post procedure, and at 6-month follow-up. The endpoints of all-cause mortality, hospitalization for heart failure, and the combined endpoint of the 2 were observed during long-term follow-up (up to 4 years). RESULTS: We analyzed 218 patients (mean age, 76 ± 9 years; 36% female). Edge-to-edge mitral valve repair resulted in an increase in TAPSE and RVC ratio and a decrease in indexed TA and PASP, but concomitant TR did not change significantly. In multivariable analysis, RV dysfunction and moderate/severe TR were independently associated with increased all-cause mortality (hazard ratio, 1.61; 95% confidence interval, 1.05-2.46; P=.03 and hazard ratio, 2.10; 95% confidence interval, 1.34-3.29; P<.01, respectively) and moderate/severe TR was further an independent predictor for hospitalization for heart failure and for the combined endpoint. CONCLUSION: Treatment of MR resulted in favorable changes of RV function and dimension but did not reduce TR in the majority of patients. TR at baseline remained the strongest predictor for outcomes, outperforming parameters of RV function and dimension.

Augmentation Index in Patients with Thoracic Aortic Aneurysm: A Matched Case-Control Study.

Thoracic aortic aneurysms (TAA) may be associated with complications such as rupture and dissection, which can lead to a fatal outcome. Increased central arterial stiffness has been proposed to be present in patients with TAA compared to unmatched controls. We aimed to assess whether wall properties in patients with TAA are also altered when compared to a matched control group. Applanation tonometry was performed in 74 adults with TAA and 74 sex, age, weight, height, and left ventricular ejection fraction matched controls. Subsequently analysis of the pulse wave was done using the SphygmoCor System. For comparing the two groups, AIx was adjusted to a heart rate of 75/min (AIx@75). 148 1-to-1 matched participants were included in the final model. There was no significant difference in the Alx@75 between the TAA group and the matched control group [mean (SD) of 24.7 (11.2) % and 22.8 (11.2) %, p = 0.240]. Adjusted for known cardiovascular risk factors, there was no association between TAA and AIx@75. Patients with TAA showed comparable arterial wall properties to cardiovascular risk factor matched controls. Since higher arterial stiffness is associated with TAA progression, it remains to be investigated if increased central arterial stiffness is a relevant factor of TAA emergence.