Left Ventricular Diastolic Dysfunction Research Articles

Age- and sex-dependent cardiovascular impact of maternal perinatal stress and altered dopaminergic metabolism in the medulla oblongata of the offspring.

M Maternal Major Depressive Disorder with Peripartum Onset presents health risks to the mother and the developing fetus. Using a rat model of chronic mild stress, we previously reported on the neurodevelopmental impact of maternal perinatal stress on their offspring; the present study examined the cardiovascular impact of maternal perinatal stress on their offspring. The cardiovascular impact was assessed in terms of blood pressure and echocardiographic parameters. The results examined by a three-way ANOVA showed a significant association of cardiovascular parameters with maternal perinatal stress, and offspring sex and age. Increased blood pressure was observed in adolescent female and adult male offspring of stress-exposed dams. Echocardiography showed an increase in left atrial dimension and a reduction in left ventricular systolic function in adolescent stress-exposed female offspring. Increased interventricular septum thickness at end-diastole and left ventricular diastolic dysfunction were observed in adult stress-exposed male offspring. The underlying mechanisms of cardiovascular impact were examined in stress-exposed adult offspring by assessing the levels of neurotransmitters and their metabolites in the medulla oblongata using high-performance liquid chromatography. A significant decrease in homovanillic acid, a dopamine metabolite and indicator of dopaminergic activity, was observed in adult stress-exposed female offspring. These results suggest a significant sex- and age-dependent impact of maternal stress during the peripartum period on the cardiovascular system in the offspring that extends to adulthood and suggests a multigenerational effect. The presented data urgently need a follow-up to confirm its potential clinical and public health relevance.

Diastolic Dysfunction in Hypertension: A Comprehensive Review of Pathophysiology, Diagnosis, and Treatment.

Diastolic dysfunction refers to impaired relaxation or filling of the ventricles during the diastolic phase of the cardiac cycle. Left ventricular diastolic dysfunction (LVDD) is common in hypertensive individuals and is associated with increased morbidity and mortality. LVDD serves as a critical precursor to heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF). The pathophysiology of LVDD in hypertension is complex, involving alterations in cardiac structure and function, neurohormonal activation, and vascular stiffness. While the diagnosis of LVDD relies primarily on echocardiography, management remains challenging due to a lack of specific treatment guidelines for LVDD. This review offers an overview of the pathophysiological mechanisms underlying LVDD in hypertension, diagnostic methods, clinical manifestations, strategies for managing LVDD, and prospects for future research.

Left atrial stiffness index – an early marker of left ventricular diastolic dysfunction in patients with coronary heart disease

AimsTo evaluate the correlation between left atrial stiffness index (LASI) and left ventricular diastolic function in patients with coronary heart disease (CHD) by Autostrain LA technique.MethodsThis was a retrospective analysis that included a total of 82 CHD patients who had suitable image quality for left atrial strain measurement. According to the 2016 ASE/EACVI guidelines for the echocardiographic assessment of diastolic dysfunction, the patients were divided into three groups: normal left ventricular diastolic function group (n = 26), indeterminate left ventricular diastolic function (n = 36), and left ventricular diastolic dysfunction (LVDD) (n = 20). The left atrial conduit strain (LAScd), Left atrial contractile strain (LASct), left atrial reservoir strain (LASr) and its derived parameters, including LASI and left atrial filling index (LAFI), were compared among the three groups. Furthermore, we conduct a correlation analysis between LASI and left ventricular diastolic function in patients with CHD.ResultsLASr and LAScd in normal group were higher than those in indeterminate group, LASr and LAScd in indeterminate group were higher than those in LVDD group, LASI in normal group was lower than that in indeterminate group, and LASI in indeterminate group was lower than that in LVDD group (P < 0.001). LASct in both normal and indeterminate groups was higher than that in LVDD group (P < 0.05). The LAFI of normal group was lower than that of indeterminate group and LVDD group (P < 0.001). LASI was positively correlated with E/e’(r = 0.822) (P < 0.001). LASr and E/e’ were negatively correlated (r = -0.637) (P < 0.001).ConclusionLASI is closely related to the changes of left ventricular diastolic function in CHD patients.

Factors associated with left ventricular diastolic dysfunction in adults from a region of the Andes in Peru

To determine the factors associated with left ventricular diastolic dysfunction (LVDD) in adults residing in a region of the Andes in Peru. A case-control study was conducted on adults living at an altitude of more than 3000 meters in Peru. Cases consisted of patients diagnosed with LVDD through echocardiography, whereas controls were adults without LVDD, as confirmed by echocardiography. A total of 50 cases and 100 controls were included in the study. Among them, 38.7% had high blood pressure, and 41.3% were overweight. Upon adjusted analysis, age 60 or older (aOR: 4.06; 95%CI: 1.29-12.8), female sex (aOR: 2.24; 95%CI: 1.01-4.96) and left ventricular hypertrophy (aOR: 3.17; 95%CI: 1.41-7.17) were identified as statistically significant factors associated with LVDD. The risk of LVDD is associated with older adults, female gender, and left ventricular hypertrophy among individuals residing above 3000 meters altitude in a region of the Andes, in Peru.

MRI Assessment of Diastolic Dysfunction in People Living With the Human Immunodeficiency Virus: Correlation With Markers of Disease Activity.

Despite the advent of combination antiretroviral therapy, people living with human immunodeficiency virus (PLWH) are at an increased risk for cardiac disease. To explore the presence and extent of diastolic atrial and left ventricular dysfunction in PLWH using cardiac MRI in correlation with clinical markers of disease activity. Prospective. A total of 163 participants comprising 101 HIV-infected individuals (age: 52 years [42-62 years]; 92% male) and 62 age- and sex-matched healthy volunteers (age: 51 years [30-72 years]; 85% male). 3.0 T, cardiac MRI including balanced steady-state free precession (SSFP) for the short-axis, two-, three-, and four-chamber views were performed. Assessment of cardiac function and strain analysis were accomplished by CVI42 software. Blood samples for CD4+ T cells and cardiac risk factors were also collected before MRI. Independent t tests, Mann-Whitney U test, Pearson's correlation analysis, and multivariate linear analyses (significance level: P < 0.05). PLWH had a significantly larger left atrial volume maximum index (LAVImax: 32.6 ± 8.7 vs. 28.7 ± 8.1 mL/m2), minimum (LAVImin: 14.8 ± 5.5 vs. 11.5 ± 5.4 mL/m2,), and prior to atrial contraction (LAVIpre-a: 23.4 ± 6.7 vs. 19.7 ± 7.2 mL/m2) as compared to healthy volunteers. The LA reservoir (LAtEF: 55.0 ± 10.2 vs. 61.4 ± 10.4; Sls: 29.0 ± 8.1 vs. 33.8 ± 11.8), conduit (LApEF: 28.4 ± 8.2 vs. 32.3 ± 11.3, P = 0.01; Sle: 16.3 ± 6.5 vs. 18.9 ± 8.2), and booster pump function (LAaEF: 37.4 ± 12.4 vs. 42.7 ± 13.1, P = 0.01, Sla: 12.7 ± 5.1 vs. 14.9 ± 5.7) were all significant impaired in PLWH. Global circumferential left ventricular diastolic strain rate (LVGCS-d) was significantly lower in the HIV patients. Multivariate analysis results showed that Nadir CD4+ T cells had a significant adverse association with LVGCS-d (β = 0.51). LA structure abnormalities and LV diastolic dysfunction were manifested in PLWH, with Nadir CD4+ T cell counts potentially serving as a risk factor for early cardiac diastolic dysfunction. 2 TECHNICAL EFFICACY: Stage 3.

Phosphodiesterase 9A inhibition improves aging-related increase in pulmonary vascular resistance in mice.

As individuals age, there is a gradual decline in cardiopulmonary function, often accompanied by cardiac pump dysfunction leading to increased pulmonary vascular resistance (PVR). Our study aims to investigate the changes in cardiac and pulmonary vascular function associated with aging. Additionally, we aim to explore the impact of phosphodiesterase 9A (PDE9A) inhibition, which has shown promise in treating cardiometabolic diseases, on addressing left ventricle (LV) dysfunction and elevated PVR in aging individuals. Young (3 months old) and aged (32 months old) male C57BL/6 mice were used. Aged mice were treated with the selective PDE9A inhibitor PF04447943 (1 mg/kg/day) through intraperitoneal injections for 10 days. LV function was evaluated using cardiac ultrasound, and PVR was assessed in isolated, ventilated lungs perfused under a constant flow condition. Additionally, changes in PVR were measured in response to perfusion of the endothelium-dependent agonist bradykinin or to nitric oxide (NO) donor sodium nitroprusside (SNP). PDE9A protein expression was measured by Western blots. Our results demonstrate the development of LV diastolic dysfunction and increased PVR in aged mice. The aged mice exhibited diminished decreases in PVR in response to both bradykinin and SNP compared to the young mice. Moreover, the lungs of aged mice showed an increase in PDE9A protein expression. Treatment of aged mice with PF04447943 had no significant effect on LV systolic or diastolic function. However, PF04447943 treatment normalized PVR and SNP-induced responses, though it did not affect the bradykinin response. These data demonstrate a development of LV diastolic dysfunction and increase in PVR in aged mice. We propose that inhibitors of PDE9A could represent a novel therapeutic approach to specifically prevent aging-related pulmonary dysfunction.

Relationship of High Sensitive C-Reactive Protein and Lipid Profile with Left Ventricular Diastolic Dysfunction in Patients with Subclinical Hypothyroidism

Relationship of High Sensitive C-Reactive Protein and Lipid Profile with Left Ventricular Diastolic Dysfunction in Patients with Subclinical Hypothyroidism

Metabolic remodeling and calcium handling abnormality in induced pluripotent stem cell-derived cardiomyocytes in dilated phase of hypertrophic cardiomyopathy with MYBPC3 frameshift mutation

Hypertrophic cardiomyopathy (HCM) is an inherited disorder characterized by left ventricular hypertrophy and diastolic dysfunction, and increases the risk of arrhythmias and heart failure. Some patients with HCM develop a dilated phase of hypertrophic cardiomyopathy (D-HCM) and have poor prognosis; however, its pathogenesis is unclear and few pathological models exist. This study established disease-specific human induced pluripotent stem cells (iPSCs) from a patient with D-HCM harboring a mutation in MYBPC3 (c.1377delC), a common causative gene of HCM, and investigated the associated pathophysiological mechanisms using disease-specific iPSC-derived cardiomyocytes (iPSC-CMs). We confirmed the expression of pluripotent markers and the ability to differentiate into three germ layers in D-HCM patient-derived iPSCs (D-HCM iPSCs). D-HCM iPSC-CMs exhibited disrupted myocardial sarcomere structures and an increased number of damaged mitochondria. Ca2+ imaging showed increased abnormal Ca2+ signaling and prolonged decay time in D-HCM iPSC-CMs. Cell metabolic analysis revealed increased basal respiration, maximal respiration, and spare-respiratory capacity in D-HCM iPSC-CMs. RNA sequencing also showed an increased expression of mitochondrial electron transport system-related genes. D-HCM iPSC-CMs showed abnormal Ca2+ handling and hypermetabolic state, similar to that previously reported for HCM patient-derived iPSC-CMs. Although further studies are required, this is expected to be a useful pathological model for D-HCM.

The association between TSH and thyroid hormones in the normal or subclinical dysfunction range with left ventricular diastolic dysfunction

Thyroid hormones modulate the cardiovascular system. However, the effects of subclinical thyroid dysfunction and euthyroidism on cardiac function remain unclear. We investigated the association between left ventricular (LV) diastolic dysfunction and subclinical thyroid dysfunction or thyroid hormones within the reference range. This cross-sectional study included 26,289 participants (22,197 euthyroid, 3,671 with subclinical hypothyroidism, and 421 with subclinical thyrotoxicosis) who underwent regular health check-ups in the Republic of Korea. Individuals with thyroid stimulating hormone (TSH) levels > 4.2 µIU/mL and normal free thyroxine (FT4, 0.78–1.85 ng/dL) and triiodothyronine (T3, 76–190 ng/dL) levels were defined as having subclinical hypothyroidism. Individuals with serum TSH levels < 0.4 µIU/mL and normal FT4 and T3 levels were defined as having subclinical thyrotoxicosis. The cardiac structure and function were evaluated using echocardiography. LV diastolic dysfunction with normal ejection fraction (EF) was defined as follows: EF of > 50% and (a) E/e’ ratio > 15, or (b) E/e’ ratio of 8–15 and left atrial volume index ≥ 34 mL/m2. Subclinical hypothyroidism was significantly associated with cardiac indices regarding LV diastolic dysfunction. The odds of having LV diastolic dysfunction was also increased in participants with subclinical hypothyroidism (adjusted odds ratio [AOR] 1.36, 95% confidence interval [CI], 1.01–1.89) compared to euthyroid participants. Subclinical thyrotoxicosis was not associated with LV diastolic dysfunction. Among the thyroid hormones, only serum T3 was significantly and inversely associated with LV diastolic dysfunction even within the normal range. Subclinical hypothyroidism was significantly associated with LV diastolic dysfunction, whereas subclinical thyrotoxicosis was not. Serum T3 is a relatively important contributor to LV diastolic dysfunction compared to TSH or FT4.

Left atrial strain assessment unveils left ventricular diastolic dysfunction in neonates with transient tachypnea of the newborn: A prospective observational study.

An inadequate clearance of lung fluid plays a key role in the pathogenesis of transient tachypnea of the newborn (TTN). To evaluate if left ventricular diastolic dysfunction contributes to reduced clearance of lung fluid in TTN. This was a prospective, observational study. Echocardiography and lung ultrasound were performed at 2, 24 and 48 h of life (HoL) to assess biventricular function and calculate lung ultrasound score (LUS). Left atrial strain reservoir (LASr) provided surrogate measurement of left ventricular diastolic function. Twenty-seven neonates with TTN were compared with 27 controls with no difference in gestation (36.1 ± 2 vs. 36.9 ± 2 weeks) or birthweight (2508 ± 667 vs. 2718 ± 590 g). Biventricular systolic function was normal in both groups. LASr was significantly lower in cases at 2 (21.0 ± 2.7 vs. 38.1 ± 4.4; p < 0.01), 24 (25.2 ± 4.5 vs. 40.6 ± 4.0; p < 0.01) and 48 HoL (36.5 ± 5.8 and 41.6 ± 5.2; p < 0.01), resulting in a significant group by time interaction (p < 0.001), after adjusting for LUS and gestational diabetes. A logistic regression model including LUS, birth weight and gestational diabetes as covariates, showed that LASr at 2 HoL was a predictor of respiratory support at 24 HoL, with an adjusted odds ratio of 0.60 (CI 0.36-0.99). LASr was reduced in neonates with TTN, suggesting diastolic dysfunction, that may contribute to the delay in lung fluid clearance.

Energy wavelet signal processed ECG and standard 12 lead ECG: Diagnosis of early diastolic dysfunction.

Left ventricular (LV) diastolic dysfunction (LVDD) is the result of impaired LV relaxation and identifies those at risk of developing heart failure. Echocardiography has been used as the gold standard to identify early LVDD. The signal processed electrocardiogram (hsECG) has demonstrated effectiveness to detect early LVDD. Whether or not the standard 12‑lead electrocardiogram (ECG) can accurately predict early LVDD is not known. A standard 12‑lead ECG including signal processing (hsECG) was performed in 569 patients. Patients with atrial fibrillation, bundle branch block, pre-excitation, left ventricular hypertrophy or known cardiovascular disease were excluded, leaving 464 examinations for analysis. Early LVDD was diagnosed by established methods using echocardiography. Repolarization abnormalities (T wave discordance) in V1, V6, I and aVL and the hsECG were compared to the echocardiographic findings to establish diagnostic accuracy. A total of 84 (18.1%) patients were diagnosed with early LVDD. A combination of a borderline or abnormal finding on the hsECG produced the best diagnostic model (sensitivity 84.5%, specificity 47.9%). The best performing ECG lead was V1 with a sensitivity of 38.1% and specificity of 92.1%. Regression analysis demonstrated increasing age and V1 to be predictive of LVDD. The hsECG displayed reasonable ability to detect early LVDD. Other than V1, repolarization abnormalities on the standard 12‑lead ECG did not. While lead V1 showed promise in detecting LVDD, whether this or any other simple ECG variable can predict future LVDD would be of further interest.

Measurement of left atrial size as a predictor of severity of illness in sickle cell disease

BackgroundSickle cell disease (SCD) is characterized by microvascular occlusion which leads to multiorgan damage, including left ventricular diastolic dysfunction. Left ventricular diastolic dysfunction has been shown to be an independent risk factor for death in SCD patients. Left atrial dilation (LAD) has been used as a surrogate marker for identification of left ventricular diastolic dysfunction. ObjectiveInvestigate the association of LAD, as determined by echocardiography, with increased disease burden in SCD as reflected by increased emergency department (ED) utilization, increased hemolysis markers, and worsening anemia. MethodsA retrospective cohort study of patients from a single university hospital were selected from a national registry. Age, sickle cell phenotype, echocardiogram findings, ED utilization, baseline hemoglobin, and lab values needed for calculation of hemolytic index were recorded for each patient. Patients were then stratified into two distinct groups based on the presence or absence of LAD to compare ED utilization, baseline hemoglobin and hemolytic index between the two groups. Results129 patients met the criteria for inclusion with 88 having normal left atrial volume and 41 with LAD. There was a higher percentage of high ED utilizers in the LAD group compared to the normal left atrial volume group [34% vs. 17%, p = 0.03]. Average hemoglobin was lower in the LAD group compared with the normal left atrial volume group [mean 8.57 g/dL vs. 9.47 g/dL, p = 0.011]. The mean hemolytic index was higher in the LAD group when compared with the normal left atrial volume group [0.44 vs. −0.21, p < 0.001]. ConclusionsLAD was associated with higher ED utilization, lower hemoglobin level, and more hemolysis in patients with SCD.

Left Atrial Roof Enlargement Is a Distinct Feature of Heart Failure With Preserved Ejection Fraction.

It remains unknown to what extent intrinsic atrial cardiomyopathy or left ventricular diastolic dysfunction drive atrial remodeling and functional failure in heart failure with preserved ejection fraction (HFpEF). Computational 3-dimensional (3D) models fitted to cardiovascular magnetic resonance allow state-of-the-art anatomic and functional assessment, and we hypothesized to identify a phenotype linked to HFpEF. Patients with exertional dyspnea and diastolic dysfunction on echocardiography (E/e', >8) were prospectively recruited and classified as HFpEF or noncardiac dyspnea based on right heart catheterization. All patients underwent rest and exercise-stress right heart catheterization and cardiovascular magnetic resonance. Computational 3D anatomic left atrial (LA) models were generated based on short-axis cine sequences. A fully automated pipeline was developed to segment cardiovascular magnetic resonance images and build 3D statistical models of LA shape and find the 3D patterns discriminant between HFpEF and noncardiac dyspnea. In addition, atrial morphology and function were quantified by conventional volumetric analyses and deformation imaging. A clinical follow-up was conducted after 24 months for the evaluation of cardiovascular hospitalization. Beyond atrial size, the 3D LA models revealed roof dilation as the main feature found in masked HFpEF (diagnosed during exercise-stress only) preceding a pattern shift to overall atrial size in overt HFpEF (diagnosed at rest). Characteristics of the 3D model were integrated into the LA HFpEF shape score, a biomarker to characterize the gradual remodeling between noncardiac dyspnea and HFpEF. The LA HFpEF shape score was able to discriminate HFpEF (n=34) to noncardiac dyspnea (n=34; area under the curve, 0.81) and was associated with a risk for atrial fibrillation occurrence (hazard ratio, 1.02 [95% CI, 1.01-1.04]; P=0.003), as well as cardiovascular hospitalization (hazard ratio, 1.02 [95% CI, 1.00-1.04]; P=0.043). LA roof dilation is an early remodeling pattern in masked HFpEF advancing to overall LA enlargement in overt HFpEF. These distinct features predict the occurrence of atrial fibrillation and cardiovascular hospitalization. URL: https://www.clinicaltrials.gov; Unique identifier: NCT03260621.

Left Atrial Strain for assessment of left ventricle diastolic dysfunction in acute coronary syndrome patients.

Patients with acute coronary syndrome (ACS) have a high incidence of Left ventricle diastolic dysfunction (DD). Latest algorithms for the assessment of DD lay on 2D parameters and describe a grading to quantify its severity. However, there persists a "gray zone" of values in which DD remains indeterminate. to analyze the diagnostic value of Left atrium strain (LAS) for categorization of LV DD and assessment of LV filling pressures in ACS patients. Cross-sectional study that prospectively evaluated 105 patients presenting ACS with preserved LV ejection fraction (LVEF). Patients were divided in 4 groups according to the DD grade. Mean values of LAS, corresponding to three phases of atrial function: reservoir (LASr), conduit (LAScd) and contraction (LASct), were obtained by speckle-tracking echocardiography. Mean age was 60±10 years, with a gender ratio of 6.14. LASr and LASct were significantly lower according to DD severity (p combined=0.021, p combined=0.034; respectively). E/e' ratio was negatively correlated to LASr (r= - 0.251; p= 0.022) and LASct (r= -0.197; p=0.077). Left atrial volume index (LAVI) was also negatively correlated to LASr (r= -0.294, p= 0.006) and LASct (r= -0.3049, p=0.005). Peak tricuspid regurgitation was negatively correlated to LASr (r=-0.323, p=0.017) and LASct (r=-0.319, p=0.020). Patients presenting elevated LV filling pressures had lower LASr and LASct (p=0.049, p=0.022, respectively) compared to patients witn normal LV filling pressures. ROC curve analysis showed that a LASr < 22% (Se= 75%, Sp= 73%) and a LASct < 13% (Se= 71%, Sp=58%) can increase the likelihood of DD grade II or III by 4.6 (OR= 4.6; 95% CI: 1.31-16.2; p=0.016) and 3.7 (OR= 3.7; 95% CI: 1.06-13.1; p= 0.047), respectively. LAS is a valuable tool, which can be used to categorize DD in ACS patients.

Impact of Pre-Transplant Left Ventricular Diastolic Pressure on Primary Graft Dysfunction after Lung Transplantation: A Narrative Review.

Lung transplantation (LT) constitutes the last therapeutic option for selected patients with end-stage respiratory disease. Primary graft dysfunction (PGD) is a form of severe lung injury, occurring in the first 72 h following LT and constitutes the most common cause of early death after LT. The presence of pulmonary hypertension (PH) has been reported to favor PGD development, with a negative impact on patients' outcomes while complicating medical management. Although several studies have suggested a potential association between pre-LT left ventricular diastolic dysfunction (LVDD) and PGD occurrence, the underlying mechanisms of such an association remain elusive. Importantly, the heterogeneity of the study protocols and the various inclusion criteria used to define the diastolic dysfunction in those patients prevents solid conclusions from being drawn. In this review, we aim at summarizing PGD mechanisms, risk factors, and diagnostic criteria, with a further focus on the interplay between LVDD and PGD development. Finally, we explore the predictive value of several diastolic dysfunction diagnostic parameters to predict PGD occurrence and severity.

Myocardial performance imaging for the early identification of cardiac dysfunction in neonates with sepsis

PurposeThe assessment of cardiac performance in septic new-borns is crucial for detecting hemodynamic instability and predicting outcome. The aim of the study is to assess myocardial performance in neonates with sepsis for the early identification of cardiac dysfunction.Patients and methodsA case control study was carried out from September 2022 to May 2023 at the Neonatal Intensive care unit, Kasturba Medical College, Manipal. A total of 68 neonates were included in the study, with 33 females and 35 males. The study population was further subdivided into 3 groups namely preterm septic neonates (n = 21), term septic neonates (n = 10) and non-septic healthy controls (n = 37). The cardiac structure and function were assessed using conventional method, Tissue Doppler imaging (Sm) and speckle tracking echocardiography (GLS). The study was approved by the Institutional Ethics Committee at Kasturba Medical College, Manipal (approval number IEC: 90/2022). The CTRI registration number for the study is CTRI/2022/09/045437 and was approved on September 12, 2022. Prior to the neonate’s enrolment, informed consent was obtained from their mothers or legal guardians.ResultsOut of the total 68 neonates, 31 were cases and 37 were controls which included 33 females and 35 males. LV systolic function was not statistically significant between cases and controls. E/A ratio of the mitral valve was significantly lower in septic newborns than in healthy neonates. (1.01 ± 0.35 vs 1.18 ± 0.31, p < 0.05) preterm neonates showed significantly lower Lateral E’ and RV E’ velocities than term neonates. TAPSE was significantly lower in septic preterm neonates. (8.61 ± 1.28 vs. 10.7 ± 2.11, p < 0.05) No significant difference was noted in the Myocardial Performance Index between septic neonates and healthy neonates. LV Global Longitudinal Strain was slightly lower in preterm septic neonates than in term neonates with sepsis.ConclusionSeptic newborns are associated with LV diastolic dysfunction, RV systolic dysfunction and substantially higher pulmonary systolic pressures.

Structural and functional changes of the heart in patients with coronary heart disease who have had coronavirus disease COVID-19

The aim of the study: to investigate the effect of the previous COVID-19 coronavirus disease on the features of cardiac remodeling in patients with coronary heart disease (CHD). Materials and methods. 71 patients with CHD were involved in the study: stable angina pectoris II–III FC (age 69.0 (64.0; 76.0) years): 1 group (main) – 31 patients with CHD in long COVID-19 period; group 2 (comparison) – 40 patients with CHD without a history of COVID-19. Features of cardiac remodeling and energy work of the left ventricular (LV) myocardium were assessed using the echocardiography method. Results. CHD patients with a history of COVID-19 had greater changes in linear and volumetric parameters of the heart, an increase in the degree of hypertrophy of the LV myocardium, frequency of registration of LV diastolic dysfunction against the background of an increase in the mean pressure in the pulmonary artery, end-systolic pressure, decrease in global LV contractile function (LVF) compared to patients without COVID-19 history (p &lt; 0.05). In CHD patients who suffered from COVID-19, there was an increase in the estimated energy expenditure of the LV myocardium: shock work by 14.77 % (U = 461.5; p &lt; 0.05), potential energy by 34.68 % (U = 316.5; p &lt; 0.05) and the pressure-volume zone by 17.78 % (U = 373.0; p &lt; 0.05), which indicates a decrease in the speed of myocardial recovery in long COVID period. It was established that the presence of COVID-19 in the history of patients with CHD is associated with an increased risk of LV dilatation by 5.6 times (95 % CI 1.71–18.29; p &lt; 0.05), LV myocardial hypertrophy by 3.05 times (95 % CI 1.79–5.91; p &lt; 0.05), LV diastolic dysfunction by 1.44 times (95 % CI 0.91–2.29; p &lt; 0.05), an increase in energy expenditure during heart work by 1.66 times (95 % CI 0.68–4.02; p &lt; 0.05). Conclusions. Patients with coronary heart disease have more significant structural and functional changes and energy expenditure during the work of the heart, which proves the negative impact of SARS-CoV-2 on the state of cardiac remodeling in patients with CHD in long COVID-19 period.

Development and validation of a nomogram to predict risk of septic cardiomyopathy in the intensive care unit

The aim of this study was to develop a simple but effective nomogram to predict risk of septic cardiomyopathy (SCM) in the intensive care unit (ICU). We analyzed data from patients who were first admitted to the ICU for sepsis between 2008 and 2019 in the MIMIC-IV database, with no history of heart disease, and divided them into a training cohort and an internal validation cohort at a 7:3 ratio. SCM is defined as sepsis diagnosed in the absence of other cardiac diseases, with echocardiographic evidence of left (or right) ventricular systolic or diastolic dysfunction and a left ventricular ejection fraction (LVEF) of less than 50%. Variables were selected from the training cohort using the Least Absolute Shrinkage and Selection Operator (LASSO) regression to develop an early predictive model for septic cardiomyopathy. A nomogram was constructed using logistic regression analysis and its receiver operating characteristic (ROC) and calibration were evaluated in two cohorts. A total of 1562 patients participated in this study, with 1094 in the training cohort and 468 in the internal validation cohort. SCM occurred in 13.4% (147 individuals) in the training cohort, 16.0% (75 individuals) in the internal validation cohort. After adjusting for various confounding factors, we constructed a nomogram that includes SAPS II, Troponin T, CK-MB index, white blood cell count, and presence of atrial fibrillation. The area under the curve (AUC) for the training cohort was 0.804 (95% CI 0.764–0.844), and the Hosmer–Lemeshow test showed good calibration of the nomogram (P = 0.288). Our nomogram also exhibited good discriminative ability and calibration in the internal validation cohort. Our nomogram demonstrated good potential in identifying patients at increased risk of SCM in the ICU.

Nonsteroidal Mineralocorticoid Receptor Antagonist Finerenone Improves Diastolic Dysfunction in Preclinical Nondiabetic Chronic Kidney Disease.

The mineralocorticoid receptor plays a significant role in the development of chronic kidney disease (CKD) and associated cardiovascular complications. Classic steroidal mineralocorticoid receptor antagonists are a therapeutic option, but their use in the clinic is limited due to the associated risk of hyperkalemia in patients with CKD. Finerenone is a nonsteroidal mineralocorticoid receptor antagonist that has been recently investigated in 2 large phase III clinical trials (FIDELIO-DKD [Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease] and FIGARO-DKD [Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease]), showing reductions in kidney and cardiovascular outcomes. We tested whether finerenone improves renal and cardiac function in a preclinical nondiabetic CKD model. Twelve weeks after 5/6 nephrectomy, the rats showed classic signs of CKD characterized by a reduced glomerular filtration rate and increased kidney weight, associated with left ventricular (LV) diastolic dysfunction and decreased LV perfusion. These changes were associated with increased cardiac fibrosis and reduced endothelial nitric oxide synthase activating phosphorylation (ser 1177). Treatment with finerenone prevented LV diastolic dysfunction and increased LV tissue perfusion associated with a reduction in cardiac fibrosis and increased endothelial nitric oxide synthase phosphorylation. Curative treatment with finerenone improves nondiabetic CKD-related LV diastolic function associated with a reduction in cardiac fibrosis and increased cardiac phosphorylated endothelial nitric oxide synthase independently from changes in kidney function. Short-term finerenone treatment decreased LV end-diastolic pressure volume relationship and increased phosphorylated endothelial nitric oxide synthase and nitric oxide synthase activity. We showed that the nonsteroidal mineralocorticoid receptor antagonist finerenone reduces renal hypertrophy and albuminuria, attenuates cardiac diastolic dysfunction and cardiac fibrosis, and improves cardiac perfusion in a preclinical nondiabetic CKD model.

Diastolic Dysfunction of the Left and Right Ventricles in Patients with Calcium Pyrophosphate Crystal Storage Disease and Osteoarthritis.

The frequency and risk factors for the development of diastolic dysfunction (DD) in patients with CPPD and OA have not been studied. The objective of this study was to determine the frequency and identify risk factors (RF) for the development of DD of the left and right ventricles (LV and RV) in patients with calcium pyrophosphate crystal deposition disease (CPPD) and osteoarthritis (OA). The study included 26 patients with CPPD and with knee OA 18-65 years old, matched in age and gender, without cardiovascular disease (CVD), type 2 diabetes mellitus (DM2), and rheumatic diseases. Conventional risk factors (TRF) of CVD were assessed, and echocardiography was performed. The frequency of DD in patients with CPPD and OA was quite high and almost did not differ in both groups: it was detected in 19 patients, of which 11 (42%) had CPPD and 8 (31%) had OA (p = 0.39). Type 1 LV DD was detected in 10 (39%) patients with CPPD and in 8 (31%) with OA (p = 0.11); type 1RV DD was detected in 8 (31%) patients with CPPD and in 7 (27%) patients with OA (p = 0.17); and type 1 LV DD and RV DD was detected in 7 (27%) patients with both CPPD and with OA. DD types 2 and 3 were not detected in both groups. There were no differences in both groups in CV risk factors, except for the level of CRP (it was higher in CPPD) (p = 0.03). In the CPPD group, mean values of LV E/E' (p = 0.02), LVDT (p = 0.03), LVMI (p = 0.04) were significantly higher than in patients with OA. On the contrary, in patients with OA, indices EDV (p = 0.004) and TVC (p = 0.02) were higher. There were direct correlations between diastolic function indices and the following factors in CPPD: LVL, PWLV and PTH level (r = 0.7, p <0.005), LV E' and PTH level (r = 0.7, p < 0.005). Inverse correlations were found between the level of PTH and IS (r = -0.5, p < 0.005), LVMI (r = -0.5, p < 0.005), and the level of vitamin D and VDDT (r = -0.6, p < 0.005). Direct correlations in OA were found between the level of CRP and PVAdiast (r = 0.6, p < 0.005), and the level of sUA (r = 0.7, p < 0.005), and the level of vitamin D and E/E'LV (r = 0.6, p < 0.005). A high prevalence of LV and RV DD was found in patients with CPPD and OA. The presence of DD in CPPD was associated with lower vitamin D levels, and in OA with a higher level of sUA and a lower level of PTH.