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Mitral valve regurgitation (MR) is common in the context of heart failure and is one of the most frequent indications for invasive treatment, either cardiac surgery or percutaneous intervention. Since then, 2-dimensional (2D) Doppler imaging and 3D echocardiography have both gained in relevance as they provide detailed imaging of the functional anatomy of the mitral valve (MV) and its dynamic structure. In patients with severe MR and impaired systolic function, the terms "proportionate" and "disproportionate" help to identify which patients will benefit from medical treatments that target the LV or from transcatheter interventions that target the MV [[14]]. [Extracted from the article]

Background Obesity has been associated with subclinical diastolic dysfunction and increased risk of heart failure. Our aims were to evaluate the age- and sex-specific role of total and abdominal adiposity on diastolic function and to assess the direct and indirect pathophysiological mechanisms involved in this association. Methods and results Within a population-based study (EPIPorto), a total of 1063 individuals aged ≥ 45 years (62% female; 62.4 ± 10.6 years) were evaluated using echocardiography, anthropometrics, electrical bioimpedance and blood tests. Diastolic function was assessed with using EAE/ASE consensus criteria. Worse diastolic function grades were associated with increased BMI, fat mass % and waist-to-height ratio (p for trend < 0.001). The inverse association between adiposity and diastolic function was stronger in men and in the younger population. In multivariate analysis, waist-to-height ratio (per cm/cm) was associated with reduced E' velocity (adjusted ß: - 14.4; 95% CI: - 21.1 to - 7.6; p < 0.001) and increased E/E' ratio (adjusted ß: 9.7, 95% CI: 5.4-10.0; p < 0.001), among men < 65 years. Both direct and indirect mechanisms were involved in the E' velocity decrease by waist-to-height ratio in participants < 65 years. The effect was mainly direct in men (81.3%), while it was mostly indirect in women, through systolic blood pressure (50.8%) and inflammation (15.1%). Conclusions Adiposity, especially abdominal, was associated with worse diastolic function. This association was more important in men and in the younger population. The causal mechanisms involved were sex-specific, with mostly direct effects among men and blood-pressure-mediated among women. [ABSTRACT FROM AUTHOR]

Background: Exercise training is effective in improving functional capacity and quality of life in patients with coronary artery disease, but its effects on left ventricular systolic and diastolic function are controversial. Diastolic dysfunction is a major determinant of adverse outcome after myocardial infarction and, contrary to systolic function, no therapy or intervention has proved to significantly improve diastolic function. Data from animal studies and from patients with diastolic heart failure has suggested that exercise training can have a positive effect on diastolic function parameters. This trial aims to evaluate if a structured exercise training program can improve resting left ventricular diastolic and systolic function in patients who have had an acute myocardial infarction. Methods/Design: This is a phase II, prospective, randomized, open-label, blinded-endpoint trial that will include at least 96 consecutive patients who have had an acute myocardial infarction one month previously. Patients will be randomized (1:1) to an exercise training program or a control group, receiving standard of care. At enrolment, and at the end of the follow-up period, patients will be submitted to an echocardiography (with detailed assessment of diastolic and systolic function using recent consensus guidelines), cardiopulmonary exercise testing, an anthropometric assessment, blood testing, and clinical evaluation. Patients randomized to the intervention group will be submitted to an eight-week outpatient exercise program, combining endurance and resistance training, for three sessions per week. The primary endpoint will be the change in lateral E' velocity immediately after the eight-week exercise training program. Secondary endpoints will include other echocardiographic parameters of left ventricular diastolic and systolic function, cardiac structure, metabolic and inflammation biomarkers (high-sensitivity C-reactive protein and pro-BNP), functional capacity (peak oxygen consumption and anaerobic threshold) and anthropometric measurements. Discussion: New strategies that can improve left ventricular diastolic function are clinically needed. This will be the first trial to evaluate, in patients who have had an acute myocardial infarction, the effects of a structured program of exercise training on diastolic and systolic function, assessed by novel echocardiographic parameters. [ABSTRACT FROM AUTHOR]

Background Diabetes increases the risk of heart failure but the underlying mechanisms leading to diabetic cardiomyopathy are poorly understood. Left ventricle diastolic dysfunction (LVDD) is one of the earliest cardiac changes in these patients. We aimed to evaluate the association between LVDD with insulin resistance, metabolic syndrome (MS) and diabetes, across the diabetic continuum. Methods Within a population-based study (EPIPorto), a total of 1063 individuals aged ⩾45 years (38% male, 61.2 ± 9.6 years) were evaluated. Diastolic function was assessed by echocardiography, using tissue Doppler analysis (E' velocity and E/E' ratio) according to the latest consensus guidelines. Insulin resistance was assessed using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) score. Results The HOMA-IR score correlated to E' velocity (ρ = -0.20;p < 0.0001) and E/E' ratio (ρ = 0.20; p < 0.0001). There was a progressive worsening in E' velocity (p for trend < 0.001) and in E/E' ratio across HOMA-IR quartiles (p for trend <0.001). Individuals in the highest HOMA-IR quartile were more likely to have LVDD, even after adjustment for age, sex, blood pressure and body mass index (adjusted OR: 1.82; 95%CI: 1.09-3.03). From individuals with no MS, to patients with MS and no diabetes, to patients with diabetes, there was a progressive decrease in E' velocity (11.2 ± 3.3 vs 9.7 ± 3.1 vs 9.2 ± 2.8 cm/s; p < 0.0001), higher E/E' (6.9 ± 2.3 vs 7.8 ± 2.7 vs 9.0 ± 3.6; p < 0.0001) and more diastolic dysfunction (adjusted OR: 1.62; 95%CI: 1.12-2.36 and 1.78; 95%CI: 1.09-2.91, respectively). Conclusions HOMA-IR score and metabolic syndrome were independently associated with LVDD. Changes in diastolic function are already present before the onset of diabetes, being mainly associated with the state of insulin resistance. [ABSTRACT FROM AUTHOR]

Obesity has been associated with subclinical left ventricular (LV) diastolic dysfunction and increased risk of heart failure. Few data are available on the relative contribution of adiposity distribution and changes in myocardial structure and function. We evaluated the influence of visceral versus subcutaneous abdominal adipose tissue and epicardial fat on LV diastolic function after acute myocardial infarction. One month after acute myocardial infarction, 225 consecutive patients were prospectively enrolled and underwent anthropometric evaluation, bioimpedance analysis, detailed echocardiography, and multidetector 64-slice computed tomography scan for quantification of epicardial fat volume (EFV) and of total, subcutaneous and visceral abdominal fat areas. We found a significant association between LV diastolic dysfunction parameters and body mass index, fat-mass percentage, and waist-to-height ratio. E' velocity and E/E' ratio were correlated with total and visceral abdominal fat (r = --0.27, p <0.001 and r = 0.21, p <0.01, respectively), but not with subcutaneous fat. After multivariate analysis, increasing EFV was associated with decreased E' velocity (adjusted ß --0.11,95% confidence interval --0.19 to --0.03; p <0.01) and increased E/E' ratio (adjusted ß 0.19, 95% confidence interval 0.07 to 0.31, p <0.01). Patients with diastolic dysfunction showed higher EFV (116.7 ± 67.9 ml vs 93.0 ± 52.3 ml, p = 0.01), and there was a progressive increase in EFV according to diastolic dysfunction grades (p = 0.001). None of the adiposity parameters correlated with ejection fraction or S' velocities. In conclusion, in patients after myocardial infarction, impaired LV diastolic function was associated with increased adiposity, especially with visceral and central fat parameters. Increasing EFV was independently associated with worse LV diastolic function. [ABSTRACT FROM AUTHOR]

As recently demonstrated, angiotensin II (Ang II) induces an increase in myocardial distensibility. Although endothelin-1 and the endocardial endothelium (EE) also modulate myocardial diastolic properties, their interaction with Ang II at this level has not yet been investigated. Increasing concentrations of Ang II (from 10−8 to 10−5m) were studied in rabbit right papillary muscles in the following conditions: (1) baseline; (2) after selective removal of EE with Triton X-100; and (3) with intact EE in presence of a non-selective endothelin receptor antagonist (PD-145065), a selective endothelin type A receptor antagonist (BQ-123), an inhibitor of nitric oxide synthesis ( NG-nitro-l-arginine (l-NA) or an inhibitor of the NAD(P)H oxidase (apocynin). At baseline, Ang II induced a concentration-dependent positive inotropic effect and an increase in passive muscle length ( L) up to 1.020 ± 0.004 L/ Lmax. After restoring muscle length to maximal physiological length ( Lmax), passive tension decreased by 46.1 ± 4.0%. When the EE was removed, the effect on myocardial distensibility was abolished. With intact EE in presence of PD-145065, BQ-123 orl-NA, the effects of Ang II on myocardial distensibility were attenuated, with a maximal increase in passive muscle length of 1.0087 ± 0.0012, 1.0068 ± 0.0022 and 1.0066 ± 0.0020 L/ Lmax and a decrease in resting tension of 22.6 ± 3.6, 16.1 ± 6.0 and 20.4 ± 5.6%, respectively. In the presence of apocynin, the effect on myocardial distensibility was abolished. In conclusion, the Ang II-dependent acute increase in myocardial distensibility is abolished by the selective removal of the EE and attenuated in the presence of endothelin-1 receptor antagonists, an inhibitor of nitric oxide synthesis or an inhibitor of NAD(P)H oxidase. [ABSTRACT FROM AUTHOR]

B This article refers to 'Global longitudinal strain predicts clinical outcomes in patients with heart failure with preserved ejection fraction' by A. Brann I et al i ., published in this issue on pages 1755-1765. b Recent trials in patients with heart failure with preserved ejection fraction (HFpEF) suggest that heart failure, independently of left ventricular ejection fraction (LVEF), may take advantage of the same therapies.[1] These trials, together with new information coming from imaging studies, provide support to further discuss the initial concept that HF could be a single syndrome with different phenotypes.[2] These phenotypes must be characterized properly. The time has also come to incorporate GLS in the design of large-scale randomized clinical trials to test the role of current and future therapies for patients with the HF syndrome. The question is how can we push cardiac imaging, and especially echocardiography, to improve the phenotypic characterization of HF patients. [Extracted from the article]

Chronic heart failure (HF) is the 21st-century cardiovascular epidemic, marked by recurrent hospitalizations and high mortality rates, and represents a considerable burden on Western societies. The complex care demands of HF patients require multidisciplinary approaches, aligning with contemporary guidelines. Accordingly, the Excellence in Heart Failure Program, implemented in Portuguese tertiary hospitals, aims to establish multidisciplinary HF outpatient clinics in Portugal, improving patients' clinical outcomes. Herein, the results of its pilot project are presented, showing that the implementation of the multidisciplinary clinic resulted in a minimal number of hospitalizations and emergency visits, with only one rehospitalization reported. In addition, patients in the Program experienced significant improvements in ejection fraction (EF) and NT-proBNP levels. Despite the limited power of the sample, these findings underscore the effectiveness of the Program in the management of Portuguese HF patients, particularly in the early discharge period after heart failure, when patients are most vulnerable. [ABSTRACT FROM AUTHOR]

Introduction: There is a well-established association between atrial fibrillation (AF) and coronary artery disease. Coronary artery calcium score (CACS) is a helpful tool to refine cardiovascular (CV) risk stratification and inform on the best strategies for primary CV prevention. This study aims to evaluate the impact of opportunistic screening with CACS on risk stratification and decision of preventive therapies, in patients with AF. Methods: Cross-sectional study including patients with AF or atrial flutter undergoing cardiac computed tomography for ablation procedure planning, from 2017 to 2019. Baseline clinical and demographical data were collected. CACS was assessed in patients without coronary artery disease using the Agatston method. Results: A total of 474 patients were included (93% with AF, mean age of 58 ± 10 years, 62% male). CACS >0 was present in 254 (54%) patients. According to CACS and the Society of Cardiovascular Computed Tomography recommendations, 25% of the patients would be candidates for statin therapy and 17% would be candidates for changes in the current statin intensity; in 11 patients (8%), acetylsalicylic acid would be recommended. Conclusion: In our study, more than half of the patients undergoing cardiac computed tomography before AF catheter ablation had CACS above zero. Our findings suggest that an opportunistic evaluation of CACS at the time of ablation can be an important tool to improve CV risk stratification, with important clinical and therapeutic implications. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM) and heart failure (HF) have a tremendous impact worldwide, markedly reducing life-expectancy and quality of life. It is now known that each disease represents a risk factor for the other. Moreover, when they are combined, the prognosis is significantly worse. Until recently, these pathologies have been managed independently. However, their treatment paradigm is rapidly changing, with recent cardiovascular outcome trials showing that sodium-glucose cotransporter-2 inhibitors (SGLT-2i) are effective in the management of both diseases. This article explores the interactions between T2DM and HF and the concept of diabetic cardiomyopathy and summarizes recent data regarding the effects of SGLT-2i on HF hospitalization and the proposed pathophysiological mechanisms involved. [ABSTRACT FROM AUTHOR]

Background: Exercise training is effective in improving functional capacity and quality of life in patients with coronary artery disease, but its effects on left ventricular systolic and diastolic function are controversial. Diastolic dysfunction is a major determinant of adverse outcome after myocardial infarction and, contrary to systolic function, no therapy or intervention has proved to significantly improve diastolic function. Data from animal studies and from patients with diastolic heart failure has suggested that exercise training can have a positive effect on diastolic function parameters. This trial aims to evaluate if a structured exercise training program can improve resting left ventricular diastolic and systolic function in patients who have had an acute myocardial infarction.Methods/design: This is a phase II, prospective, randomized, open-label, blinded-endpoint trial that will include at least 96 consecutive patients who have had an acute myocardial infarction one month previously. Patients will be randomized (1:1) to an exercise training program or a control group, receiving standard of care. At enrolment, and at the end of the follow-up period, patients will be submitted to an echocardiography (with detailed assessment of diastolic and systolic function using recent consensus guidelines), cardiopulmonary exercise testing, an anthropometric assessment, blood testing, and clinical evaluation. Patients randomized to the intervention group will be submitted to an eight-week outpatient exercise program, combining endurance and resistance training, for three sessions per week. The primary endpoint will be the change in lateral E' velocity immediately after the eight-week exercise training program. Secondary endpoints will include other echocardiographic parameters of left ventricular diastolic and systolic function, cardiac structure, metabolic and inflammation biomarkers (high-sensitivity C-reactive protein and pro-BNP), functional capacity (peak oxygen consumption and anaerobic threshold) and anthropometric measurements.Discussion: New strategies that can improve left ventricular diastolic function are clinically needed. This will be the first trial to evaluate, in patients who have had an acute myocardial infarction, the effects of a structured program of exercise training on diastolic and systolic function, assessed by novel echocardiographic parameters.Trial Registration: Registered with ClinicalTrials.gov (reference: NCT02224495 ) on 21 August 2014. [ABSTRACT FROM AUTHOR]

Introduction: Recurrence of atrial fibrillation (AF) within the blanking period after catheter ablation (CA) is traditionally classified as a transient and benign event. However, recent findings suggest that early recurrence (ER) is associated with late recurrence (LR), challenging the predefined "blanking period". We aimed to determine the clinical and procedural predictors of ER and LR after CA and establish the risk of LR in patients who experience ER. Methods and Results: Retrospective single‐centre study including all patients who underwent a first procedure of AF CA between 2017 and 2019. ER was defined as any recurrence of AF, atrial flutter or atrial tachycardia >30 s within 90 days after CA and LR as any recurrence after 90 days of CA. A total of 399 patients were included, 37% women, median age of 58 years [49‐66] and 77% had paroxysmal AF. Median follow‐up was 33 months (from 13 to 61). ER after CA was present in 14% of the patients, and LR was reported in 32%. Among patients who experienced ER, 84% also had LR (p <.001). Patients with ER had a higher prevalence of moderate/severe valvular heart disease, persistent AF, previous electrical cardioversion, a larger left atrium, higher coronary artery calcium score, and higher rates of intraprocedural electrical cardioversion and cardiac fibrosis on eletroanatomical mapping compared with patients without ER. After covariate adjustment, ER and female sex were defined as independent predictors of LR (hazard ratio [HR] 4.69; 95% confidence interval [CI], 2.99–7.35; p <.001 and HR 2.73; 95% CI, 1.47–5.10; p =.002, respectively). Conclusion: The risk of LR after an index procedure of CA was significantly higher in patients with ER (five‐fold increased risk). These results support the imperative need to clarify the clinical role of the blanking period. [ABSTRACT FROM AUTHOR]

Circulating biomarkers and imaging techniques provide independent and complementary information to guide management of heart failure (HF). This consensus document by the Heart Failure Association (HFA) of the European Society of Cardiology (ESC) presents current evidence‐based indications relevant to integration of imaging techniques and biomarkers in HF. The document first focuses on application of circulating biomarkers together with imaging findings, in the broad domains of screening, diagnosis, risk stratification, guidance of treatment and monitoring, and then discusses specific challenging settings. In each section we crystallize clinically relevant recommendations and identify directions for future research. The target readership of this document includes cardiologists, internal medicine specialists and other clinicians dealing with HF patients. [ABSTRACT FROM AUTHOR]

Abstract: Angiotensin 1–7 is a bioactive heptapeptide of the renin–angiotensin system. Its cardiovascular actions have recently acquired growing relevance, mainly due to its counter-regulatory actions in the angiotensin cascade. The aim of the present study was to evaluate the actions of angiotensin 1–7 on myocardial function. Increasing concentrations of angiotensin 1–7 (10−9 to 10−5 M) were added to rabbit right papillary muscles: (1) in baseline conditions with intact endocardial endothelium (EE); (2) after selective removal of the EE with Triton X-100 (1s, 0.01%); (3) with intact EE in the presence of the Mas receptor antagonist A-779, the AT1 receptor antagonist ZD-7155, the AT2 receptor antagonist PD-123,319 or the nitric oxide synthesis inhibitor NG-nitro-l-arginine (l-NA). Concerning the effects on contractility, we observed a significant decrease on active tension, dT/dt max, peak shortening and dL/dt max of −10.5±3.6%, −8.0±3.0%, −5.3±2.6% and −5.7±2.3%, respectively. There was no change on relaxation parameters, namely dT/dt min or dL/dt min. Time to half relaxation was significantly decreased. The presence of ZD-7155 or PD-123,319 did not change these effects. However, angiotensin 1–7 effects on myocardial properties were abolished after selective EE removal and in the presence of A-779 or l-NA. In conclusion, in this animal species, angiotensin 1–7 through its binding to Mas receptor induces a negative inotropic effect modulated by the EE and nitric oxide and independent of AT1 or AT2 receptors activation. As the effects described in the present work were influenced by the endocardial endothelium, they may be disrupted in situations associated to endothelial dysfunction, as in heart failure or myocardial ischemia. [Copyright &y& Elsevier]

Abstract: Angiotensin II is an octapeptide whose effects are mediated by two types of receptors. AT1 receptors are responsible for the vasoconstrictor, positive inotropic and growth promoting properties, while AT2 receptors have been linked to vasodilator and anti-mitogenic properties. In this study we investigated the effects of selective AT2 receptor stimulation on myocardial contractility and lusitropy. Effects of selective AT2 receptor activation were evaluated in rabbit right papillary muscles (n =96) by adding increasing concentrations of H-9395, an AT2 receptor agonist, alone or in presence of a selective AT1 receptor antagonist (ZD-7155), or alternatively, by adding increasing concentrations of angiotensin II in presence of ZD-7155. In the latter conditions, selective AT2 receptor activation was also performed in presence of NG-nitro-l-Arginine, indomethacin, proadifen, hydroxocobalamin, apamin plus charybdotoxin, Hoe-140 or PD-123,319, as well as, after endocardial endothelium removal. Selective AT2 stimulation induced a negative inotropic and lusitropic effect in the first three protocols. This effect was completely abolished after selective removal of the endocardial endothelium and blunted in presence of Hoe-140, hydroxocobalamin, apamin plus charybdotoxin and PD-123,319, but maintained in presence of NG-nitro-l-Arginine, indomethacin or proadifen. Selective AT2 receptor stimulation induces a negative inotropic and lusitropic effect, which is modulated by endocardial endothelium and mediated by bradykinin B2 receptors through NO release and calcium dependent potassium channels activation. Such findings may help to better understand the therapeutic effects of selective AT1 antagonists, which are increasingly used for treating cardiovascular diseases. [Copyright &y& Elsevier]

Background: Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome for which clear evidence of effective therapies is lacking. Understanding which factors determine this heterogeneity may be helped by better phenotyping. An unsupervised statistical approach applied to a large set of biomarkers may identify distinct HFpEF phenotypes. Methods: Relevant proteomic biomarkers were analyzed in 392 HFpEF patients included in Metabolic Road to Diastolic HF (MEDIA-DHF). We performed an unsupervised cluster analysis to define distinct phenotypes. Cluster characteristics were explored with logistic regression. The association between clusters and 1-year cardiovascular (CV) death and/or CV hospitalization was studied using Cox regression. Results: Based on 415 biomarkers, we identified 2 distinct clusters. Clinical variables associated with cluster 2 were diabetes, impaired renal function, loop diuretics and/or betablockers. In addition, 17 biomarkers were higher expressed in cluster 2 vs. 1. Patients in cluster 2 vs. those in 1 experienced higher rates of CV death/CV hospitalization (adj. HR 1.93, 95% CI 1.12–3.32, p = 0.017). Complex-network analyses linked these biomarkers to immune system activation, signal transduction cascades, cell interactions and metabolism. Conclusion: Unsupervised machine-learning algorithms applied to a wide range of biomarkers identified 2 HFpEF clusters with different CV phenotypes and outcomes. The identified pathways may provide a basis for future research. More insight is obtained in the mechanisms related to poor outcome in HFpEF patients since it was demonstrated that biomarkers associated with the high-risk cluster were related to the immune system, signal transduction cascades, cell interactions and metabolism Biomarkers (and pathways) identified in this study may help select high-risk HFpEF patients which could be helpful for the inclusion/exclusion of patients in future trials. Our findings may be the basis of investigating therapies specifically targeting these pathways and the potential use of corresponding markers potentially identifying patients with distinct mechanistic bioprofiles most likely to respond to the selected mechanistically targeted therapies. [ABSTRACT FROM AUTHOR]

Background: Exercise-based cardiac rehabilitation (EBCR) plays a pivotal role in the management of acute myocardial infarction (AMI). Studies have shown that older individuals have a worse prognosis after an AMI, attesting to the importance of risk reduction strategies. We aimed at assessing the impact of age (patients dichotomized as ≥65 years old or <65 years old) on the functional benefits of an EBCR program among AMI survivors. Design: Observational, retrospective cohort study. Participants: All patients admitted due to an AMI who completed a phase II EBCR program after discharge, between November 2012 and April 2017. Intervention: EBCR program. Measurements: Functional parameters were assessed by a symptom-limited cardiopulmonary exercise test. Results: A total of 379 patients were included (30% aged ≥65 years). After the EBCR program, peak oxygen uptake (pVO2) and exercise duration increased significantly. Patients aged ≥65 years presented with more comorbidities and a lower functional capacity. Those aged ≥65 years presented significantly smaller improvements in pVO2 (0.79 ± 2.61 vs. 1.60 ± 3.11 mL/kg/min, p = 0.016) and exercise duration [75 (59–120) vs. 120 s (60–180), p = 0.002]. This was maintained after adjusting for several potential confounders. Conclusion: Older patients have a worse functional capacity than their younger counterparts. Still, a contemporary EBCR program was associated with significant functional improvements among those aged ≥65 years. The smaller improvements even after adjustments for potential confounders suggest that physiological differences may contribute to this finding. These results highlight the relevance of EBCR among this higher-risk subgroup. [ABSTRACT FROM AUTHOR]

Mitral valve cleft is a rare entity. However, it must be recognized as a differential mechanism for mitral valve regurgitation. 3D transesophageal echocardiography plays an essential role in the evaluation of single and multiple mitral valve clefts, improving morphological and functional assessment of the valve, with potential implications on surgical planning. The authors present four rare cases of mitral valve cleft presenting during adulthood, followed by a mini‐review about the role of 3D echocardiography, as well as its pitfalls, in the assessment of this complex congenital mitral valve disease. [ABSTRACT FROM AUTHOR]

The relationship of metabolic syndrome (MetS) and insulin resistance (one of its key pathophysiological mediators) with diastolic dysfunction and myocardial fibrosis is not well understood. This study aimed to evaluate the association of MetS with diastolic function and myocardial extracellular matrix (ECM) using cardiac MRI (CMRI) in a large community-based population. This cross-sectional analysis included 1,582 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) with left ventricular ejection fraction ≥50% and no history of cardiac events. Diastolic function was assessed using tagged CMRI parameters including end-diastolic strain rate (EDSR) and strain relaxation index (SRI). ECM was evaluated using extracellular volume (ECV) quantification. Participants' mean age was 67.4 ± 8.6 years, and 48.1% were males. MetS was present in 533 individuals (33.7%), and type 2 diabetes in 250 (15.8%). In the multivariable analyses, MetS (irrespective of the presence of type 2 diabetes) and higher insulin resistance were associated with impaired diastolic function (higher SRI and lower EDSR), independent of ECV. In conclusion, MetS, irrespective of the presence of type 2 diabetes, was independently associated with impaired diastole. These functional myocardial changes seem to result from intrinsic cardiomyocyte alterations, irrespective of the myocardial interstitium (including fibrosis). [ABSTRACT FROM AUTHOR]

As heart failure with preserved ejection fraction (HFpEF) rises to epidemic proportions, major steps in patient management and therapeutic development are badly needed. With the current position paper we seek to update our view on HFpEF as a highly complex systemic syndrome, from risk factors and mechanisms to long-term clinical manifestations. We will revise recent advances in animal model development, experimental set-ups and basic and translational science approaches to HFpEF research, highlighting their drawbacks and advantages. Directions are provided for proper model selection as well as for integrative functional evaluation from the in vivo setting to in vitro cell function testing. Additionally, we address new research challenges that require integration of higher-order inter-organ and inter-cell communication to achieve a full systems biology perspective of HFpEF. [ABSTRACT FROM AUTHOR]

As heart failure with preserved ejection fraction (HFpEF) rises to epidemic proportions, major steps in patient management and therapeutic development are badly needed. With the current position paper we seek to update our view on HFpEF as a highly complex systemic syndrome, from risk factors and mechanisms to long-term clinical manifestations. We will revise recent advances in animal model development, experimental set-ups and basic and translational science approaches to HFpEF research, highlighting their drawbacks and advantages. Directions are provided for proper model selection as well as for integrative functional evaluation from the in vivo setting to in vitro cell function testing. Additionally, we address new research challenges that require integration of higher-order inter-organ and inter-cell communication to achieve a full systems biology perspective of HFpEF. [ABSTRACT FROM AUTHOR]

Purpose Management of patients with mitral stenosis ( MS) depends heavily on the accurate quantification of mitral valve area ( MVA) using echocardiography. All currently used two-dimensional (2D) methods have limitations. Estimation of MVA using the proximal isovelocity surface area ( PISA) method with real time three-dimensional (3D) echocardiography may circumvent those limitations. We aimed to evaluate the accuracy of 3D direct measurement of PISA in the estimation of MVA. Methods Twenty-seven consecutive patients (median age of 63 years; 77.8% females) with rheumatic MS were prospectively studied. Transthoracic and transesophageal echocardiography with 2D and 3D acquisitions were performed on the same day. The reference method for MVA quantification was valve planimetry after 3D-volume multiplanar reconstruction. A semi-automated software was used to calculate the 3D flow convergence volume. Results Compared to MVA estimation using 3D planimetry, 3D PISA showed the best correlation (rho=0.78, P<.0001), followed by pressure half-time ( PHT: rho=0.66, P<.001), continuity equation ( CE: rho=0.61, P=.003), and 2D PISA (rho=0.26, P=.203). Bland-Altman analysis revealed a good agreement for MVA estimation with 3D PISA (mean difference −0.03 cm2; limits of agreement ( LOA) −0.40-0.35), in contrast to wider LOA for 2D methods: CE (mean difference 0.02 cm2, LOA −0.56-0.60); PHT (mean difference 0.31 cm2, LOA −0.32-0.95); 2D PISA (mean difference −0.03 cm2, LOA −0.92-0.86). Conclusions MVA estimation using 3D PISA was feasible and more accurate than 2D methods. Its introduction in daily clinical practice seems possible and may overcome technical limitations of 2D methods. [ABSTRACT FROM AUTHOR]

Aims: Despite the promising results of serelaxin as a new potential acute heart failure (HF) therapy, its clinical use preceded the understanding of the endogenous relaxin system in HF. We aimed to evaluate relaxin circulating levels in a population of acute HF and their association with clinical and echocardiographic parameters.Methods and Results: We included 117 patients from a registry of acute HF. Admission serum relaxin was measured using an enzyme-linked immunosorbent assay (ELISA) kit. Clinical, analytical, and echocardiographic parameters were compared between patients with relaxin levels above and below the median. Median age was 82 years [interquartile range (IQR) 72-87], 41% of the patients were male, and 63% had systolic dysfunction. Median serum relaxin was 31.4 pg/mL (IQR 0.6-89.8). Patients with relaxin levels above the median had more peripheral oedema (89.8% vs. 68.4%, P = 0.004) and a significantly higher sodium retention score (mean 4.8 ± 1.5 vs. 3.6 ± 2.0, P < 0.001). These patients also had significantly higher systolic pulmonary arterial pressure [median 47.0 (IQR 36.0-61.0) vs. 34.5 (IQR 25.0-51.0) mmHg, P = 0.002], higher prevalence of right ventricular (RV) systolic dysfunction (28.1% vs. 10.3%, P = 0.02), RV dilation (31.0% vs. 5.3%, P < 0.001), and right atrial dilation (66.1% vs. 36.5%, P = 0.002), and less inferior vena cava diameter variability (40% vs. 60%, P = 0.009). No differences were noted regarding admission blood pressure, left chamber dimensions, or LV function.Conclusion: In our population of acute HF patients, admission relaxin serum levels were associated with clinical and echocardiographic markers of pulmonary hypertension, RV dysfunction, and overload, suggesting a role for circulating relaxin as a biomarker in this setting. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Myocardial dysfunction has been described in patients with cirrhosis and may contribute to haemodynamic disturbances in advanced disease states. However, the prognostic impact of cardiac systolic and diastolic dysfunction in cirrhosis is controversial. We aimed to evaluate the performance of echocardiographic parameters of cardiac function as medium-term prognostic markers, in a cohort of cirrhotic patients. Methods: Ninety-eight patients (52 discharged after hospitalization for decompensated cirrhosis and 46 ambulatory) were prospectively evaluated. A comprehensive echocardiographic study, including tissue-Doppler and speckle tracking analysis, was performed at baseline. Patients were followed-up for 6months for the occurrence of death. Results: Twenty patients died during the follow-up. None of the echocardiographic parameters were associated with the occurrence of death. A Child score>10 points (HR 13.1, 95% CI 3.79–45.0, p<0.001) and a mean arterial pressure below the median (HR 3.2, 95% CI 1.14–8.80, p=0.028) were the only independent predictors of mortality in Cox regression multivariate analysis. In previously hospitalized patients, cardiac output, C-reactive protein and albumin levels were associated with 6-month mortality in univariate analysis; this association was lost after adjusting for Child score. Conclusions: Medium-term mortality in cirrhosis seems to be mainly determined by liver disease severity rather than by myocardial dysfunction. Modern echocardiographic indices of systolic and diastolic function do not seem to be useful in identifying patients at increased risk of dying. [Copyright &y& Elsevier]

Highlights: [•] Under normal conditions slow force response is dependent on AT1 receptor activity. [•] Ischemia blunts the Frank–Starling mechanism. [•] Ischemia abolishes the slow force response and induces a progressive force decline. [•] AT1 receptor antagonism rescues the contractility deterioration during ischemia. [•] AT2 receptor antagonism blunts the effects of AT1 antagonism during ischemia. [ABSTRACT FROM AUTHOR]

Background & Aims Cardiac dysfunction has been described in patients with cirrhosis. Conventional echocardiographic methods are frequently unable to detect abnormalities at rest and have limitations. We aimed to evaluate cardiac function in cirrhosis patients assessing: (i) left ventricular systolic function using speckle-tracking imaging; (ii) diastolic function using a tissue-Doppler based algorithm and comparing it with previously proposed definition of diastolic dysfunction ( DD). Methods We included 109 hospitalized and ambulatory patients with cirrhosis and 18 healthy controls. Detailed echocardiographic evaluation was performed including tissue-Doppler and speckle-tracking analysis. Results Peak systolic longitudinal strain ( PLS) was lower in patients [−19.99% (−21.88 to −18.71) vs −22.02% (−23.10 to −21.18), P = 0.003]. Ejection fraction was similar in patients and controls [64% (59-67) vs 61% (60-65), P = 0.42)]. Based on mitral-flow pattern, DD was present in 44 patients (40.4%). Patients without DD had higher cardiac output compared with those with DD [6.4 L/min (5.4-7.2) vs 5.6 L/min (4.6-6.8), P = 0.02]. Using a tissue-Doppler based definition, the prevalence of DD was 16.5%. No differences in haemodynamic variables were found in patients with and without this definition of DD. The agreement between the two definitions of DD was weak (kappa = 0.24, P = 0.003). Echocardiographic abnormalities in systolic and diastolic function were not different in compensated vs decompensated patients in different Child-Pugh classes or cirrhosis aetiologies. Conclusions Patients with cirrhosis have systolic and diastolic cardiac dysfunction at rest. Newer echocardiographic techniques may identify patients with functional impairment more accurately than conventional methods, which are more influenced by flow conditions. [ABSTRACT FROM AUTHOR]

Background: Many patients with heart failure with preserved ejection fraction (HFpEF) are women. Exploring mechanisms underlying the sex differences may improve our understanding of the pathophysiology of HFpEF. Studies focusing on sex differences in circulating proteins in HFpEF patients are scarce. Methods: A total of 415 proteins were analyzed in 392 HFpEF patients included in The Metabolic Road to Diastolic Heart Failure: Diastolic Heart Failure study (MEDIA-DHF). Sex differences in these proteins were assessed using adjusted logistic regression analyses. The associations between candidate proteins and cardiovascular (CV) death or CV hospitalization (with sex interaction) were assessed using Cox regression models. Results: We found 9 proteins to be differentially expressed between female and male patients. Women expressed more LPL and PLIN1, which are markers of lipid metabolism; more LHB, IGFBP3, and IL1RL2 as markers of transcriptional regulation; and more Ep-CAM as marker of hemostasis. Women expressed less MMP-3, which is a marker associated with extracellular matrix organization; less NRP1, which is associated with developmental processes; and less ACE2, which is related to metabolism. Sex was not associated with the study outcomes (adj. HR 1.48, 95% CI 0.83–2.63), p = 0.18. Conclusion: In chronic HFpEF, assessing sex differences in a wide range of circulating proteins led to the identification of 9 proteins that were differentially expressed between female and male patients. These findings may help further investigations into potential pathophysiological processes contributing to HFpEF. [ABSTRACT FROM AUTHOR]

We report a case of a 65‐year‐old woman with chronic primary mitral regurgitation diagnosed 10 years prior to our evaluation. We performed a 3D transesophageal echocardiography that showed an isolated cleft within the P2 segment of the posterior leaflet associated with severe mitral regurgitation. This is a rare congenital cause of mitral regurgitation, and it may occur in isolation or with associated congenital heart defects. The slitlike appearance of the leaflet can be difficult to assess by 2DTTE or even TEE. Real time 3DTEE provides superior diagnostic accuracy in the identification of scallop‐specific anatomy. [ABSTRACT FROM AUTHOR]