Diastolic Function Research Articles

Features of early remodeling of the left heart in patients with acute myocardial infarction and concomitant hypothyroidism

Objective: to evaluate the features of structural and functional remodeling of the left heart during hospitalization in patients with ST-segment elevation myocardial infarction (STEMI) and concomitant newly diagnosed hypothyroidism. Materials and methods: the study included 133 patients with STEMI aged 40 to 88 years admitted to the Rostov Regional Clinical Hospital. All patients were divided into 3 groups depending on the newly diagnosed hypothyroidism: Group 1 (control) included patients with STEMI without hypothyroidism syndrome (n=57), Group 2A — patients with STEMI and subclinical hypothyroidism (n=42) and Group 2B — patients with STEMI and manifest hypothyroidism (n=34). Patient data, clinical symptoms, information on complications in the acute period of myocardial infarction, echocardiographic examination results were entered into a specially developed questionnaire. Results: patients with STEMI of all groups were found to have increased values of indexed LV ESV and LVM, decreased values ​​of indicators characterizing myocardial contractility, as well as the presence of stage I LVDD. Patients with subclinical hypothyroidism were found to have statistically significantly higher values ​​of the indexed LA volume than patients without hypothyroidism. The peculiarities of structural and functional remodeling of the heart in the presence of overt hypothyroidism include significantly higher linear and volumetric parameters of the LA (ILP and IOLP), a greater decrease in the contractility of the LV myocardium (lower values of SV, SI and IOC), a more pronounced impairment of diastolic properties of the myocardium (lower DT value) compared to the control group. Conclusion: in patients with STEMI and concomitant overt hypothyroidism, more pronounced remodeling of the left heart in conditions of acute myocardial injury (larger size and volume of the LA, more pronounced impairment of systolic and diastolic function of the LV).

Genetic excision of the regulatory cardiac troponin I extension in high-heart rate mammal clades.

Mammalian cardiac troponin I (cTnI) contains a highly conserved amino-terminal extension harboring protein kinase A targets [serine-23 and -24 (Ser23/24)] that are phosphorylated during β-adrenergic stimulation to defend diastolic filling by means of an increased cardiomyocyte relaxation rate. In this work, we show that the Ser23/24-encoding exon 3 of TNNI3 was pseudoexonized multiple times in shrews and moles to mimic Ser23/24 phosphorylation without adrenergic stimulation, facilitating the evolution of exceptionally high resting heart rates (~1000 beats per minute). We further reveal alternative exon 3 splicing in distantly related bat families and confirm that both cTnI splice variants are incorporated into cardiac myofibrils. Because exon 3 of human TNNI3 exhibits a relatively low splice strength score, our findings offer an evolutionarily informed strategy to excise this exon to improve diastolic function during heart failure.

PDE9A Inhibition Improves Coronary Microvascular Rarefaction and Left Ventricular Diastolic Dysfunction in the ZSF1 Rat Model of HFpEF.

Heart failure with preserved ejection fraction (HFpEF) commonly arises from comorbid diseases, such as hypertension, obesity, and diabetes mellitus. Selective inhibition of phosphodiesterase 9A (PDE9A) has emerged as a potential therapeutic approach for treating cardiometabolic diseases. Coronary microvascular disease (CMD) is one of the key mechanisms contributing to the development of left ventricular (LV) diastolic dysfunction in HFpEF. Our study aimed to investigate the mechanisms by which PDE9A inhibition could ameliorate CMD and improve LV diastolic function in HFpEF. The obese diabetic Zucker fatty/spontaneously hypertensive heart failure F1 hybrid (ZSF1) rat model of HFpEF was employed in which it was found that a progressively developing coronary microvascular rarefaction is associated with LV diastolic dysfunction when compared to lean, nondiabetic hypertensive controls. Obese ZSF1 rats had an increased cardiac expression of PDE9A. Treatment of obese ZSF1 rats with the selective PDE9A inhibitor, PF04447943 (3 mg/kg/day, oral gavage for 2 weeks), improved coronary microvascular rarefaction and LV diastolic dysfunction, which was accompanied by reduced levels of oxidative and nitrosative stress markers, hydrogen peroxide, and 3-nitrotyrosine. Liquid chromatography-mass spectrometry (LC-MS) proteomic analysis identified peroxiredoxins (PRDX) as downregulated antioxidants in the heart of obese ZSF1 rats, whereas Western immunoblots showed that the protein level of PRDX5 was significantly increased by the PF04447943 treatment. Thus, in the ZSF1 rat model of human HFpEF, PDE9A inhibition improves coronary vascular rarefaction and LV diastolic dysfunction, demonstrating the usefulness of PDE9A inhibitors in ameliorating CMD and LV diastolic dysfunction through augmenting PRDX-dependent antioxidant mechanisms.

SUMOylation of cardiac myosin binding protein-C reduces its phosphorylation and results in impaired relaxation following treatment with isoprenaline

Systolic and diastolic functions are coordinated in the heart by myofilament proteins that influence force of contraction and calcium sensitivity. Fine control of these processes is afforded by a variety of post-translation modifications that occur on specific proteins at different times during each heartbeat. Cardiac myosin binding protein-C is a sarcomeric accessory protein whose function is to interact transiently with actin, tropomyosin and myosin. Previously many different types of post-translational modification have been shown to influence the action of myosin binding protein-C and we present the first report that the protein can be modified covalently by the small ubiquitin like modifier protein tag. Analysis by mass spectrometry suggests that there are multiple modification sites on myosin binding protein-C for this tag and single point mutations did not serve to abolish the covalent addition of the small ubiquitin like modifier protein. Functionally, our data from both model human embryonic kidney cells and transfected neonatal cardiac myocytes suggests that the modification reduces phosphorylation of the filament protein on serine 282. In cardiac myocytes, the hypo-phosphorylation coincided with a significantly slower relaxation response following isoprenaline induced contraction. We hypothesise that this novel modification of myosin binding protein-C represents a new level of control that acts to alter the relaxation kinetics of cardiac myocytes.

NT-proBNP and Cardiac Troponin I, but Not Cardiac Troponin T, Are Associated With 7-Year Changes in Cardiac Structure and Function in Older Adults: The ARIC Study.

Higher circulating concentrations of NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity cardiac troponin T (hs-cTnT) and I (hs-cTnI) are associated with left ventricular remodeling and with incident heart failure. The associations of these cardiac biomarkers with changes in cardiac structure and function over time are uncharacterized. Among 2006 participants in the ARIC prospective cohort study (Atherosclerosis Risk in Communities) who were free of overt cardiovascular disease and underwent echocardiography at study visits 5 (2011- 2013) and 7 (2018-2019), we assessed the associations of NT-proBNP, hs-cTnT, and hs-cTnI concentrations at visit 5 with changes in left ventricular structure and function between visits 5 and 7 (≈7-year change) using multivariable linear regression with the biomarkers modeled as restricted cubic splines. Models were adjusted for age, sex, race, body mass index, smoking, diabetes, hypertension, and renal function at visit 5; blood pressure and heart rate at both visits; and the baseline value of the echocardiographic parameter of interest. Mean±SD age was 74±4 years at visit 5; 61% were women; and 23% were Black adults. Median (25th-75th percentile) concentrations at visit 5 of NT-proBNP, hs-cTnT, and hs-cTnI were 87 ng/L (50-157 ng/L), 9 ng/L (6-12 ng/L), and 2.6 ng/L (1.9-3.9 ng/L). In adjusted models, elevated baseline concentrations of NT-proBNP and hs-cTnI were significantly associated with 7-year decline in left ventricular systolic function (ejection fraction, longitudinal and circumferential strain) and worsening diastolic indices. In contrast, elevated baseline concentrations of hs-cTnT were not significantly associated with 7-year changes in cardiac structure, systolic function, or diastolic function (all P>0.05). Higher concentrations of NT-proBNP and hs-cTnI, but not hs-cTnT, were associated with greater declines in left ventricular function over ≈7 years in late life independently of traditional cardiovascular risk factors.AQ.

Role of Circulating Biomarkers in Diabetic Cardiomyopathy.

Type 2 diabetes mellitus (T2DM) is a metabolic disorder that has alarmingly increased in incidence in recent decades. One of the most serious complications of T2DM is diabetic cardiomyopathy (DCM), an often underrecognized yet severe condition that is a leading cause of mortality among diabetic patients. In the early stages of DCM, patients typically show no symptoms and maintain normal systolic and diastolic left ventricle function, making early detection challenging. Currently available clinical markers are often not specific enough to detect the early stage of DCM. Conventional biomarkers of cardiac mechanical stress and injury, such as natriuretic peptides (NPs) and cardiac troponin I (cTnI), have shown limited predictive value for patients with T2DM. NPs have proven efficacy in detecting diastolic dysfunction in diabetic patients when used alongside 2D echocardiography, but their utility as biomarkers is limited to symptomatic individuals. While cTnI is a reliable indicator of general cardiac damage, it is not specific to cardiac injury caused by high glucose levels or T2DM. This underscores the need for research into biomarkers that can enable early diagnosis and management of DCM to reduce mortality rates. Promising novel biomarkers that showed good performance in detecting diastolic dysfunction or heart failure in diabetic patients include galectin-3, ST2, FGF-21, IGFBP-7, GDF-15, and TGF-β. This review summarizes the current understanding of DCM biomarkers, aiming to generate new ideas for the early recognition and treatment of DCM by exploring related pathophysiological mechanisms.

Multimodality imaging and functional assessment in patients with systemic right ventricle and biventricular physiology: a retrospective single-center study.

Systemic right ventricle (sRV) dysfunction is frequent in patients with congenitally corrected transposition of great arteries (cc-TGA) and those with dextro-transposition of great arteries (D-TGA) after Mustard/Senning operations. This condition should be identified promptly. We aimed to compare echocardiographic parameters with cardiac magnetic resonance (CMR)-derived parameters in patients with sRV and to evaluate their correlation with clinical variables and exercise capacity. Patients with cc-TGA and D-TGA after Mustard/Senning who underwent standard and advanced (speckle tracking and 3D) echocardiography and CMR (including feature-speckle tracking) were included. Clinical and imaging parameters were collected. Echocardiographic-derived right ventricle end-diastolic area and end-systolic area correlated with 3D echocardiographic-derived right ventricle end-diastolic and end-systolic volume (r=0.6, p=0.006 and r=0.8, p=0.002). 3D ejection fraction (EF) correlated with fractional area change and tricuspid annular plane systolic excursion (TAPSE) (r=0.8, p=0.001 and r=0.7, p=0.03). sRV global longitudinal strain (GLS) correlated with systemic atrial strain (sAS) (r=-0.6, p=0.01). CMR-derived EF correlated with CMR-derived GLS both endocardial and myocardial (r=-0.7, p=0.007 and r=-0.6, p=0.005). sRV areas as assessed by echo correlated with CMR-derived volumes (r=0.9, p=0.0001 for diastole and r=0.8, p=0.0001 for systole). Similarly, a correlation was found between sRV echo-derived GLS and CMR-derived GLS, both endocardial and myocardial (r=0.8, p=0.001 and r=0.7, p=0.01). The only imaging parameter that correlated with peak oxygen consumption was sAS (r=0.55, p=0.04). When comparing cc-TGA and D-TGA, the former showed better GLS-derived values as assessed by CMR (CMR-derived right ventricle endocardial longitudinal strain -23.2% versus -17.2%, p=0.002; CMR-derived right ventricle myocardial longitudinal strain -21.2% versus -16.7%; p=0.05), bigger systemic atrial area (20.2 cm2/m2 versus 8.4 cm2/m2, p=0.005) and higher TAPSE values (16.2 mm versus 12.2 mm, p=0.04). Echocardiography is valid to screen for sRV dilatation and function and to guide the timing for CMR. The investigation of atrial deformation imaging may help to better understand diastolic function. Patients with cc-TGA show better cardiac function compared to patients after atrial switch. Further investigations are needed to identify imaging parameters linked to exercise capacity.

Clinical impact of diastolic dysfunction and atrial fibrillation before and after initiating hemodialysis in patients with end-stage kidney disease

Background Diastolic dysfunction with left ventricular hypertrophy and myocardial fibrosis is an important characteristic of uremic cardiomyopathy in end-stage kidney disease (ESKD). Few studies explored the relationship between changes in diastolic dysfunction and the risk of mortality or cardiovascular outcome in patients with ESKD. We investigated the clinical impact of diastolic dysfunction and atrial fibrillation (AF) on patients starting hemodialysis (HD). Methods A total of 718 patients who started HD between 2010 and 2020 were included. We classified patients according to the pre- and post-HD diastolic dysfunction grades (DDG) evaluated by echocardiography. Patients with AF were classified separately. The primary outcome was a composite outcome of all-cause mortality and cardiac complication. Results The median age was 63 years, and 61.4% were male. Patients were divided into four groups based on pre-HD echocardiography findings. After initiating HD, the patients were classified according to changes in DDG and AF. Composite outcomes were significantly higher in the pre-HD AF groups. However, after adjusting for age and history of ischemic heart disease, pre-HD AF did not affect the composite outcomes. Patients with normal post-HD diastolic function had better outcomes than those with diastolic dysfunction or AF. Furthermore, the deterioration of diastolic dysfunction after HD was associated with an increased risk of composite outcomes. Conclusions The deterioration of diastolic dysfunction and newly development of AF after initiating HD were identified as risk factors for mortality and cardiac complications, supporting the clinical importance of the appropriate management of diastolic dysfunction and AF in patients with ESKD.

Clinical utility of electrocardiographic voltage parameters for the diagnosis of hypertrophic cardiomyopathy.

While electrocardiographic parameters of hypertensive left ventricular hypertrophy (H-LVH) are well known, limited data are available regarding hypertrophic cardiomyopathy (HCM). This study was to assess the diagnostic value of electrocardiographic voltage parameters in HCM. Included patients with HCM treated between March 2015 and May 2023. Voltage parameters (S-L, Cornell, Cornell product, Lewis, Peguero, and modified Cornell voltages) and echocardiography were evaluated. Receiver operating characteristic (ROC) curves were used to assess the diagnostic value of electrocardiogram in HCM. The multiple linear regression was conducted to analyze the correlation between electrocardiogram indicators and cardiac diastolic function. The highest sensitivity for HCM was Peguero voltage (70.4%; 88.6% specificity). The Peguero voltage had high sensitivity in male (63.8%) and female patients (84.9%), those aged <65 years (71.6%) and ≥65 years (68.3%), with non-apical HCM (AHCM) (76.7%), obstructive HCM (82.1%), and non-obstructive HCM (66.9%). The sensitivity of the S-L voltage was high in AHCM (72.2%). The sensitivity for HCM reached 88.7% when the S-L and Peguero voltages were combined. The modified Cornell index had the highest area under the curve (0.88, 95% CI: 0.84-0.91), and its optimal cutoff value was 2.05 mV in males (77.6% sensitivity and 74% specificity) and 1.935 mV in females (90.6% sensitivity and 91.4% specificity). Peguero voltage (beta = 0.154, P = 0.034) and SD (beta = 0.223 P = 0.004) were independently correlated with E/e', an index of left ventricular diastolic function. The Peguero voltage had high sensitivity and specificity for detecting the presence of HCM. It was positively correlated with E/e' in patients with HCM. For AHCM, the S-L voltage was more advantageous. Combining the S-L voltage with the Peguero voltage further improves the sensitivity for HCM and thus could be used to improve the screening of HCM in clinical practice. The SD and modified Cornell voltage also had good diagnostic performance, especially in females.

Impact of empagliflozin on cardiac structure and function assessed by echocardiography after myocardial infarction: a post-hoc sub-analysis of the emmy trial

Abstract Background Empagliflozin administered after acute myocardial infarction proofed to improve cardiometabolic parameters and biomarkers, but the impact on cardiac function is still largely unknown. The aim of this post-hoc echocardiographic sub-analysis of the EMMY trial was to provide in-depth echocardiographic analysis on the effects of empagliflozin versus placebo on standard and novel echocardiographic structural and functional parameters after acute myocardial infarction. Methods In this post-hoc analysis of the EMMY trial a subset of 313 patients (157 empagliflozin vs. 156 placebo) was enrolled for post-processing analysis of echocardiographic structural and functional parameters. On top of two-dimensional and Doppler parameters, myocardial deformation analyses were performed to assess ventricular and atrial strain values. Results Left ventricular volumes showed significant differences in favor of empagliflozin over the course of the trial (change in left ventricular end-diastolic volume median [interquartile range] 8 [−3;19]% versus 13 [0;29]%, p = 0.048; left ventricular end-systolic volume −3 [−15;12]% versus 4 [−12;18]%, p = 0.044). This effect persisted after adjusting for baseline values, age, and sex. Left ventricular systolic and diastolic function overall improved over the course of the trial and parameters for diastolic function showed a distinct trend between groups but did not meet statistical significance in this cohort. Conclusion In this post-hoc analysis among patients with acute myocardial infarction, treatment with empagliflozin resulted in a significant beneficial effect on left ventricular end-diastolic and end-systolic volume, without significantly improving left ventricular or right ventricular functional parameters compared to placebo after 26 weeks. ClinicalTrials.gov registration NCT03087773. Graphical abstract

Cardiovascular Adaptation in Fetal Growth Restriction: A Longitudinal Study From Fetuses at Term to the First Year of Life.

To investigate longitudinal trends in fetal and offspring cardiovascular adaptation in fetal growth restriction (FGR). Prospective longitudinal study. Fetal Medicine Unit. Thirty-five FGR pregnancies and 37 healthy controls assessed as term fetuses (mean age 37 ± 1 weeks) and again in infancy (mean age 8 ± 2 months). Conventional echocardiographic techniques, tissue Doppler imaging and speckle tracking echocardiography. Left ventricular (LV) and right ventricular (RV) geometry and function. Echocardiographic parameters were normalised by ventricular size adjusting for differences in body weight between groups. Compared to healthy controls, late FGR fetuses showed significant alterations in cardiac geometry with more globular LV chamber (LV sphericity index, 0.56 vs. 0.52), increase in biventricular global longitudinal systolic contractility (MAPSE, 0.29 vs. 0.25 mm; TAPSE, 0.42 vs. 0.37 mm) and elevated cardiac output (combined CO: 592 vs. 497 mL/min/kg, p < 0.01 for all). Indices of LV diastolic function in FGR fetuses were significantly impaired with myocardial diastolic velocities (LV A', 0.30 vs. 0.26 cm/s; IVS E', 0.19 vs. 0.16 cm/s) and LV torsion (1.2 vs. 3.5 deg./cm, p < 0.01 for all). At postnatal assessment, FGR offspring revealed persistently increased SAPSE (0.27 vs. 0.24 mm), LV longitudinal strain (-19.0 vs. -16.0%), reduced LV torsion (1.6 vs. 2.1 deg./cm) and elevated CO (791 vs. 574 mL/min/kg, p < 0.01 for all). Perinatal cardiac remodelling and myocardial dysfunction in late FGR fetuses is most likely due to chronic placental hypoxaemia. Persistent changes in cardiac geometry and function in FGR offspring may reflect fetal cardiovascular maladaptation that could predispose to long-term cardiovascular complications in later life.

The Interplay between Severe Cirrhosis and Heart: A Focus on Diastolic Dysfunction.

Background/Objectives: Cardiovascular involvement in severe cirrhosis presents diagnostic challenges and carries significant prognostic implications. This study aims to evaluate the relationship between liver disease severity and portal hypertension with the burden of diastolic dysfunction. Methods: We prospectively enrolled patients with hepatic cirrhosis, classified according to the Child-Pugh criteria. Of the 102 patients included, 65 were classified as Group A (non-severe cirrhosis: Child-Pugh Classes A and B) and 37 as Group B (severe cirrhosis: Child-Pugh Class C). Portal vein and spleen diameters were assessed using abdominal ultrasound. All patients underwent echocardiographic evaluation. LV systolic function was assessed by measuring ejection fraction, while diastolic function was evaluated using three parameters: E/Em ratio, E/Vp ratio, and indexed left atrial volume. Results: We observed a significantly greater burden of diastolic dysfunction in Group B compared to Group A. Specifically, the E/Vp ratio was 2.2 ± 0.4 in Group B versus 1.9 ± 0.3 in Group A (p < 0.001); the indexed LA volume was 34.5 ± 3.2 mL/m2 in Group B versus 30.1 ± 2.9 mL/m2 in Group A (p < 0.001); and the E/Em ratio was 17.0 ± 3.0 in Group B versus 11.5 ± 2.8 in Group A (p < 0.001). Additionally, the mean diameters of the portal vein and spleen were larger in Group B, with measurements of 14.3 ± 2.1 mm versus 11.5 ± 1.6 mm for the portal vein and 15.0 ± 1.2 mm versus 11.7 ± 1.5 mm for the spleen (p < 0.001), which correlated with the extent of diastolic dysfunction. Conclusions: Diastolic dysfunction was prevalent in 55% of patients with liver cirrhosis. The burden of diastolic dysfunction was higher in patients with severe hepatic cirrhosis compared to those with milder forms, and it correlated with the severity of portal hypertension, as assessed by measuring portal vein diameter and spleen diameter.

Interpreting Diastolic Dynamics and Evaluation through Echocardiography.

In patients with heart failure, evaluating left ventricular (LV) diastolic function is vital, offering crucial insights into hemodynamic impact and prognostic accuracy. Echocardiography remains the primary imaging modality for diastolic function assessment, and using it effectively requires a profound understanding of the underlying pathology. This review covers four main topics: first, the fundamental driving forces behind each phase of normal diastolic dynamics, along with the physiological basis of two widely used echocardiographic assessment parameters, E/e' and mitral annulus early diastolic velocity (e'); second, the intricate functional relationship between the left atrium and LV in patients with varying degrees of LV diastolic dysfunction (LVDD); third, the role of stress echocardiography in diagnosing LVDD and the significance of echocardiographic parameter changes; and fourth, the clinical utility of evaluating diastolic function from echocardiography images across diverse cardiovascular care areas.

Comprehensive evaluation of right ventricular function in patients with acute pulmonary embolism

Objective. To study indices of right ventricular (RV) longitudinal deformation at transthoracic echocardiography (TTE) in patients with acute pulmonary embolism (APE), to determine their threshold values; to study indices of right ventricular-arterial coupling (RVAC) in patients with APE, to determine their threshold values.Methods. We examined 34 patients with acute massive and submassive pulmonary embolism. The diagnosis was made on the basis of computed-tomography pulmonary angiogram. The mean age was 61 ±13 years. Of these, 16 were women (47,1%) and 18 were men (52,9%). As a control group, 30 healthy individuals were examined: 14 males and 16 females. The mean age of the healthy individuals was 39±9,8 years. Echocardiography was performed on Vivid E95 (GE HealthCare, USA) with data postprocessing on EchoPak workstation. The indices of right ventricular (RV) systolic and diastolic function, the magnitude of global longitudinal deformation of the right ventricle (GLS RV) and longitudinal deformation of the right ventricular free wall (RVFWLS) were studied using two-dimensional speckle-tracking echocardiography. We studied indices of right ventricular-arterial coupling (RVAC). We determined the relationship of longitudinal deformation of RV and RVAC with other indices of its systolic function. Results. Mean values of traditional parameters of RV contractile function were within normal limits, whereas mean values of longitudinal strain in APE were significantly lower than normal. There was also a significant decrease ( P &lt; 0,0001) of all measured parameters of right ventricular-arterial coupling in patients with APE in comparison with the control group.Conclusions. When longitudinal deformation parameters are included in the criteria of RV dysfunction in APE, its detectability increases from 26,47% to 61,77%. The revealed decrease of right ventricular-arterial coupling parameters in APE indicates a more frequent disturbance of the connection between RV and the small circle of blood circulation

Smaller Left Ventricular Size But Preserved Function in Adolescents and Adults Born Preterm.

Prematurely born adults have increased risk for cardiovascular disease. There are limited cardiac data on US-born preterm individuals. We aimed to determine whether adolescents and adults born prematurely have altered left ventricular (LV) structure and function, and to interrogate diastolic function using isometric handgrip exercise. Adolescents and adults born moderately to extremely preterm (≤32 weeks gestation or <1500 g birth weight) were recruited from the Parkland Health Neonatal Intensive Care Unit Registry. Full-term participants were recruited from the local area. Study procedures included anthropometrics and vitals, handgrip testing, and echocardiography performed at rest and during isometric handgrip exercise. Data were reported as mean±SD. The study enrolled 107 preterm and 48 term participants. Preterm participants (gestational age: 29.5±2.5 weeks) were shorter with higher body mass index (P<0.001) compared with term participants. Preterm participants exhibited smaller LV end-diastolic volume index (50.8±10.1 versus 56.9±10.0 mL/m2, P<0.001), LV stroke volume index (29.6±6.0 versus 34.1±6.5 mL/m2, P<0.001), and LV mass index (67.2±13.1 versus 73.3±14.2 g/m2, P=0.002) compared with term individuals. Preterm participants also had subclinical reductions in LV peak systolic tissue velocity and peak early diastolic tissue velocity lateral at rest. Isometric handgrip exercise promoted a reduction in diastolic function and an increase in hemodynamic measures, but changes during isometric handgrip exercise were similar between groups. Adolescents and adults born preterm exhibit overall normal cardiac function despite smaller cardiac volumes and mass compared with individuals born full term. Effects are most pronounced at the lowest gestational ages.

Subclinical Left Ventricular Dysfunction over Seven-Year Follow-Up in Type 2 Diabetes Patients without Cardiovascular Diseases.

Subclinical left ventricular dysfunction (LVD) is common in asymptomatic patients with type 2 diabetes (T2D). This study aimed to define long-term structural and functional disorders of the left ventricle (LV) myocardium over a 7-year follow-up in patients with T2D without cardiovascular diseases (CVD). Of the 120 patients with and without T2D of both sexes aged from 45 to 75 years (57.11 ± 7.9 years), included in the study in 2012-2013, 57 responded to the follow-up study. They were divided into two groups: one with T2D (n = 29), the other without it, the control (n = 28). All patients underwent transthoracic two-dimensional echocardiography with an assessment of standard indicators of systolic and diastolic cardiac function, global longitudinal strain (GLS), laboratory diagnostics of carbohydrate metabolism disorders markers, NT-proBNP, and CRP. The median follow-up duration was 7.2 [7.0-7.8] years. During the follow-up, a statistically significant increase in the incidence of diastolic dysfunction (DD) from 53% to 61% (p = 0.004) was found in the T2D group; no significant dynamics were noted in the control group (p = 0.48). The proportion of patients with reduced GLS (<-18%) increased in the T2D group (p = 0.036). A significant difference in the frequency of decreased GLS depending on presence of T2D was demonstrated. In conclusion, T2D is an independent risk factor for the worsening of subclinical left ventricular dysfunction in asymptomatic patients with T2D without CVD over 7-year follow-up.

Pediatric cirrhotic cardiomyopathy: literature review and effect size estimations of selected parameters

Liver cirrhosis is a significant global health concern, and cirrhotic cardiomyopathy (CCM) is a notable complication affecting both adults and children. While CCM is well-studied in adults, understanding its manifestation and diagnostic criteria in pediatric patients remains a challenge. This review explores the evidence for structural and functional cardiac alterations in children with liver cirrhosis. Structural abnormalities, including increased left ventricular mass index (LVMI) and altered left ventricular wall thickness ratios, are prevalent in pediatric CCM. These abnormalities persist even after liver transplantation, highlighting the systemic impact of liver disease. Evidence suggests that altered systolic and diastolic function, as well as electrocardiographic abnormalities such as prolonged QT intervals, are common in pediatric CCM. Blood biomarkers, including brain natriuretic peptide (BNP) and troponin levels, offer insights into cardiac function in pediatric cirrhotic patients. Elevated BNP levels correlate with adverse outcomes, indicating its potential as a prognostic marker. However, further research is needed to elucidate the diagnostic utility of these biomarkers in pediatric CCM. Conclusion: This review provides estimates of the standardized mean difference among selected cardiac parameters in children with and without cirrhosis. Tailored diagnostic criteria and comprehensive assessment methods will be essential for accurate diagnosis and effective management of pediatric CCM. What is Known:• CCM adds to the burden of care of patients with cirrhosis.• Diagnostic criteria for adults are evolving, but there are no specific criteria for pediatric CCM.What is New:• Cardiac function in children with cirrhosis indicates some parameters not considered in adults are altered.• Effect size estimations for certain parameters provide a guideline for future research into pediatric CCM.

Potential Mechanisms of Epicardial Adipose Tissue Influencing Heart Failure with Preserved Ejection Fraction.

Heart failure (HF) is the predominant terminal stage and the leading cause of mortality in cardiac disease. Heart failure with preserved ejection fraction (HFpEF) affects roughly 50% of HF patients globally. Due to the global aging population, the prevalence, morbidity, and mortality of HFpEF have gradually increased. Epicardial adipose tissue (EAT), as a key visceral adipose tissue around the heart, affects cardiac diastolic function and exercise reserve capacity. EAT closely adheres to the myocardium and can produce inflammatory factors, neurotransmitters, and other factors through autocrine or paracrine mechanisms, affecting the heart function by inflammatory response, cardiac metabolism and energy supply, cardiomyocyte structure and electrical activity, and pericardial vascular function. Currently, research on the mechanism and treatment methods of HFpEF is constantly improving. EAT may play a multi-level impact on the occurrence and development of HFpEF. This review also summarizes the potential impact of EAT on the heart in HFpEF combined with other metabolism-related diseases such as obesity or diabetes over other obesity-related measures, such as body mass index (BMI) or other adipose tissue. Above all, this review comprehensively summarizes the potential mechanisms by which EAT may affect HFpEF. The objective is to enhance our comprehension and management of HFpEF. Future research should delve into the mechanistic relationship between EAT and HFpEF, and investigate interventions aimed at EAT to improve the prognosis of patients with HFpEF.

Cardiac Diastolic Function by Echocardiography in Normotensive Pregnancies vs Pregnancies Complicated by Hypertensive Disorders

Cardiac Diastolic Function by Echocardiography in Normotensive Pregnancies vs Pregnancies Complicated by Hypertensive Disorders

Effect of Sevoflurane Anesthesia on Diastolic Function: A Prospective Observational Study.

The effect of sevoflurane on left ventricular diastolic function is not well understood. We hypothesized that parameters of diastolic function may improve under sevoflurane anesthesia in patients with preexisting diastolic dysfunction compared to patients with normal diastolic function. This observational study included 60 patients undergoing breast surgery or laparoscopic cholecystectomy. Patients were assigned to diastolic dysfunction (n = 34) or normal (n = 26) groups of septal e' < 8 or ≥ 8.0 cm/s on the first thoracic echocardiography (TTE) performed before anesthesia. During anesthesia, sevoflurane was maintained at 1 to 2 minimum alveolar concentration (MAC) to maintain the bispectral index at 40 to 50. At the end of surgery, the second TTE was performed under 0.8 to 1 MAC of sevoflurane with the patient breathing spontaneously without ventilator support. Primary end point was the percentage change (Δ) of e' on 2 TTEs (Δe'). Secondary end points were ΔE/e', Δleft atrial volume index (ΔLAVI), and Δtricuspid regurgitation maximum velocity (ΔTR Vmax). These percentage changes (Δ) were compared between diastolic dysfunction and normal groups. e' (Δe': 30 [6, 64] vs 0 [-18, 11]%; P < .001), mitral inflow E wave velocity (E), mitral inflow E/A ratio (E/A), and mitral E velocity deceleration time (DT) improved significantly in diastolic dysfunction group compared to normal group. LAVI decreased in diastolic dysfunction group but did not reach statistical significance between the 2 groups (ΔLAVI:-15 [-31, -3] vs -4 [-20, 10]%, P = .091). ΔE/e' was not different between the 2 groups (11 [-16, 26] vs 12 [-9, 22]%, P = .853) (all: median [interquartile range, IQR]). TR was minimal in both groups. In this study, echocardiographic parameters of diastolic function, including septal e', E, E/A, and DT, improved with sevoflurane anesthesia in patients with preexisting diastolic dysfunction, but remained unchanged in patients with normal diastolic function.