Ventricle Diastolic Dysfunction Research Articles

Right Ventricle Diastolic Dysfunction in Tetralogy of Fallot Patients Affecting Surgical Outcome

Right Ventricle Diastolic Dysfunction in Tetralogy of Fallot Patients Affecting Surgical Outcome

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.

Left Atrial Peak Systolic Strain as an Indicator Pathway of Diastolic Dysfunction of the Left Ventricle.

Left atrial peak systolic strain (LA-PSS) imaging is an emerging index of left atrial function, and it was shown to be decreased in heart failure with preserved ejection fraction (EF). We aimed to determine whether LA-PSS could be used as an additional diagnostic parameter to current existing guidelines for the presence of left ventricle diastolic dysfunction (LVDD). A total of 190 consecutive adult patients with cardiovascular risk factors and normal left ventricle EF with no prior history of heart failure were included in the study. Speckle tracking software was used to study ventricular parietal deformity, left ventricle global longitudinal systolic strain, and LA-PSS. The median left ventricle global longitudinal systolic strain was -19%, with a significant difference ( P < 0.001) between patients with normal diastolic function versus those with LVDD. The median LA-PSS was 33% (30% to 38%) ( P < 0.001). Most patients (61%) had grade 1 atrial dysfunction based on PSS (range 24%-35%). The analysis of the area under the receiver operating characteristic curve of the LA-PSS as a potential indicator pathway of LVDD was 67% [95% confidence interval (CI), 62-72], and 75% (95% CI, 70-80), when the indeterminate pattern was included. The decreased LA-PSS made it possible to reclassify patients with an indeterminate pattern of diastolic function in 96% of cases. These results support the potential role of LA-PSS as an additional parameter for the diagnosis of LVDD in patients with normal EF, and may be integrated into the guidelines for routine evaluation of patients.

Dynamics of Right Ventricle Pressure During Stress Echocardiography in Patients with Heart Failure with Preserved Ejection Fraction

Shortness of breath during physical exertion is a non-specific symptom that can hide such potentially dangerous diseases as structural or functional bronchopulmonary, coronary heart disease, structural cardiac disease, but the frequent cause is left ventricle diastolic dysfunction due to its significant hypertrophy. Pathogenetic mechanisms leading to this symptom require detailed study for the possibility of a comprehensive approach in the treatment of such patients with the aim of maximally improving their prognosis and quality of life. Objective — evaluate changes in right ventricle systolic pressure during stress echocardiography in patients with LV myocardial hypertrophy and clinical manifestations of heart failure, search for other mechanisms leading to clinical symptoms. Materials and methods. The study included 49 patients with shortness of breath during physical exertion, who underwent further diagnostic examination after exclusion of coronary stenotic lesions by invasive coronary and ventricular angiography. Patients were excluded from bronchopulmonary pathology using spirometry and chest radiography, structural heart pathology using echocardiography, microvascular angina using echocardiography with intravenous dipyridamole infusion, and the change in systolic pressure in the right ventricle was investigated using echocardiography during a physical exercise test. Results and discussion. There were no cases of infiltrative lung changes, signs of emphysema, or other manifestations of significant pathology according to X-ray data. Spirometry also showed the absence of significant functional abnormalities. Echocardiography revealed significant hypertrophy of LV myocar­dium (thickness of IVS — on average (14.1 ± 0.5) mm, posterior wall thickness — on average (13.5 ± 0.3) mm) with the presence of LV diastolic dysfunction and echocardiographic signs of increased end-diastolic pressure in the LV, which was confirmed invasively during coronary and ventricular angiography. In 9 (18.4 %) cases, heart wall thickening was due to hypertrophic cardiomyopathy according to cardiac MRI, these patients had LV outflow tract obstruction and mild pulmonary hypertension at rest. Conducting strain imaging showed the presence of signs of myocardial ischemia (segmental contractility disorder) with varying degrees of severity (from 1 to 5 segments), which spread to the IVS, the apex of the heart and, less often, to the anterior wall of the LV. All patients experienced an increase in pulmonary artery systolic pressure during exercise, on average, from (37.4 ± 2.1) to (47.1 ± 1.6) mm Hg. Conclusions. The pathogenic mechanism underlying shortness of breath in patients with LV myocardial hypertrophy involves transient pulmonary hypertension occurring during exercise due to left ventricular diastolic dysfunction. Another contributing factor is the development of myocardial ischemia during physical exertion, which, in the absence of coronary stenosis and microvascular angina, is attributed to inadequate supply of coronary blood flow volume velocity relative to the significant left ventricular hypertrophy.

ВЛИЯНИЕ ПЕРЕНЕСЕННОЙ НОВОЙ КОРОНАВИРУСНОЙ ИНФЕКЦИИ НА СТРУКТУРНО-ФУНКЦИОНАЛЬНЫЕ ПАРАМЕТРЫ ПРАВЫХ ОТДЕЛОВ СЕРДЦА И ЛЕГОЧНУЮ ГЕМОДИНАМИКУ У БОЛЬНЫХ ХРОНИЧЕСКОЙ ОБСТРУКТИВНОЙ БОЛЕЗНЬЮ ЛЕГКИХ

Abstract. Introduction. This paper presents the interim results of a prospective clinical study, in which we studied the long-term influence of 2019 novel coronavirus infection (2019-nCoV) on pulmonary-cardiac relationships in patients with chronic obstructive pulmonary disease. Aim: Studying the effect provided by the previous 2019-nCoV on the structural and functional parameters of the right ventricle of the heart and on pulmonary hemodynamics in patients with chronic obstructive pulmonary disease. Materials and Methods. Over the years 2021-2023, we examined 43 patients with stable chronic obstructive pulmonary disease, having a history of 2019-nCoV by transthoracic echocardiography. The study consisted of two control points: on day 8-12 in the hospital and the follow-up visit to the clinic 12 months after 2019-nCoV. The study included a control group of 30 stable chronic obstructive pulmonary disease patients having no 2019-nCoV history. Results and Discussion. We found that the structural and functional strains of the right heart are aggravated in the acute period of 2019-nCoV in patients with chronic obstructive pulmonary disease. Thus, as compared to the control group, the maximum right atrium width (p&lt;0.05), right ventricle anterior wall thickness (p&lt;0.05), and basal right ventricle diameter values were significantly higher. Echocardiographic signs of right ventricle diastolic dysfunction Type 1 were found in 36,3% of cases and Type 2 in 23.3%. Pulmonary artery diameter and mean pulmonary artery pressure were higher than in those of the control group, as well. In 44% of patients, the value of pulmonary artery acceleration time was less than 105 ms (χ2 = 4.59; p&lt;0.05). Persistently high linear and volumetric right atrium and right ventricle indicators were registered in patients after 12 months of follow-up. Signs of the Type 1 diastolic dysfunction were found in 62.7% of patients. There was a tendency to decrease the mean pulmonary artery pressure and pulmonary artery acceleration time values. Conclusions. Thus, according to echocardiography, the combination of chronic obstructive pulmonary disease and 2019-nCoV leads to the aggravation of right ventricle diastolic dysfunction and the progression of pulmonary hypertension. These signs persisted for a long time (12 months).

Septic Cardiomyopathy.

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-induced myocardial dysfunction represents reversible myocardial dysfunction which ultimately results in left ventricular dilatation or both, with consequent loss of contractility. Studies on septic cardiomyopathy report a wide range of prevalence ranging from 10% to 70%. Myocardial damage occurs as a result of weakened myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Mitochondrial dysfunction is the leading problem in the development of septic cardiomyopathy and includes oxidative phosphorylation, production of reactive oxygen radicals, reprogramming of energy metabolism, and mitophagy. Echocardiography provides several possibilities for the diagnosis of septic cardiomyopathy. Systolic and diastolic dysfunction of left ventricular is present in 50-60% of patients with sepsis. Right ventricular dysfunction is present in 50-55% of cases, while isolated right ventricular dysfunction is present in 47% of cases. Left ventricle (LV) diastolic dysfunction is very common in septic shock, and it represents an early biomarker, it has prognostic significance. Right ventricular dysfunction associated with sepsis patients with worse early prognosis. Global longitudinal stress and magnetic resonance imaging (MRI) of the heart are sufficiently sensitive methods, but at the same time MRI of the heart is difficult to access in intensive care units, especially when dealing with critically ill patients. Previous research has identified two biomarkers as a result of the integrated mitochondrial response to stress, and these are fibroblast growth factor-21 (FGF-21) and growth differentiation factor-15 (GDF-15). Both of the mentioned biomarkers can be easily quantified in serum or plasma, but they are difficult to be specific in patients with multiple comorbidities. Mitochondrial dysfunction is also associated with reduced levels of miRNA (microRNA), some research showed significance of miRNA in sepsis-induced myocardial dysfunction, but further research is needed to determine the clinical significance of these molecules in septic cardiomyopathy. Therapeutic options in the treatment of septic cardiomyopathy are not specific, and include the optimization of hemodynamic parameters and the use of antibiotic thera-pies with targeted action. Future research aims to find mechanisms of targeted action on the initial mechanisms of the development of septic cardiomyopathy.

Sleep quality and cardiovascular risk in the watch setting in the Far North

Background. The study shows gender differences in sleep quality and also association of sleep disturbances (SD) with cardiovascular diseases (CVD). The watch work contributes to the biorhythms of the body disorders, including SD. Autonomous nervous system is the key regulator of circadian rhythms.Aim: To study sleep quality (SQ) in the gender aspect and cardiovascular risk in the workers of the Far North watch.Material and methods. In Yamburg, the settlement in the Far North (68° 21’ 40” north latitude), 99 males (M) and 81 females (F) with SD and normal sleep, comparable in age, northern experience, level of office blood pressure (BP) were examined. SQ analysis was conducted according to the questionnaire (Pittsburg Sleep Quality Index – PSQI). 24-hour BP monitoring, biochemical blood analysis, ultrasound examination of the carotid arteries, echocardiography, and assessment of autonomic changes was performed.Results. M significantly more often than F assessed their sleep subjectively better (p = 0.046); M and F with SD had elevated variability of systolic BP at night (p = 0.036; p = 0.039), BP 24-hour profile disorder did not depend on SQ (p = 0.2607), SD in both genders was accompanied by the increase of volumes and indices of left atrium (p = 0.0285; p = 0.0445), enhanced probability of left ventricle diastolic dysfunction for 1.9 times. SD in F enhanced the level of insulin (p = 0.0267), С-peptide (p = 0.0424), NTpro-BNP (p = 0.042) and was accompanied by autonomic dysfunction.Conclusion. In the conditions of the Arctic watch, SD is often revealed in F, is accompanied by the signs of autonomic dysfunction, more evident in F. 24-hour BP profile disorder typical for the watch work is not connected with SQ and more evident in M. SD in both genders is associated with atrial remodeling, the formation of diastolic dysfunction, but an increase in the frequency of atherosclerotic lesions of the carotid arteries, an increase in vascular inflammation factors, metabolic disorders, and neurohumoral activation, more pronounced in F, which may determine an increased risk of CVD in F in Arctic watch work conditions.

The Correlation between Elevated HDL-Cholesterol, Body Mass Index, and Presence of Thyroid Nodules: A Retrospective Analysis

Background: Elevated high-density lipoprotein-cholesterol (HDL-cholesterol) levels have been linked to unfavorable outcomes in various clinical settings, but the association with thyroid nodules remains unclear. We aimed to analyze the correlation between elevated HDL-cholesterol and the presence of thyroid nodules along with certain demographic and clinical findings. Methods: In this retrospective study, the patients were divided into three groups based on their body mass index (BMI): &lt;25, 25–29, and &gt;30 and evaluated. Data of 677 patients aged between 15 and 95 years (52.6 ± 15.6) were evaluated. The entire study population comprised 516 females (76.2%). Results: Thyroid nodules (67.1%) and left ventricle diastolic dysfunction (LVDD) (58.1%) were the two most frequent findings in the overall cohort. In the multivariate regression model, BMI, heart rate, and HDL-cholesterol values were significant and independent predictors (p = 0.000 for all) of the presence of thyroid nodules. The presence of thyroid nodules is higher in females, particularly within the higher BMI groups [odds ratio (OR) = 1.048 (CI = 1.02–1.08) for BMI &lt; 25, p = 0.003; OR = 1.094 (CI = 1.05–1.14) for BMI 25–29, p = 0.000; OR = 1.115 (CI = 1.05–1.19) for BMI ≥ 30]. This higher incidence is not observed in males. Conclusion: While the precise mechanisms underlying this association are yet to be fully elucidated, elevated HDL-cholesterol may serve as an indicator of thyroid nodules rather than a marker of cardiovascular protection.

Predictors of coronary tortuosity in patients with chronic coronary syndrome.

Aim Coronary artery tortuosity is a common coronary angiographic finding. This tortuosity can cause myocardial ischemia even in the absence of significant coronary artery stenosis. Our aim was to compare the demographic, clinical and echocardiographic features of patients with chronic coronary syndrome (CCS) and with and without coronary artery tortuosity.Material and methods 361 patients who underwent elective coronary angiography (CAG) due to CCS were included in the study. These patients divided into two groups, those with coronary tortuosity (Group 1) and those without (Group 2). Univariable and multivariable logistic regression analysis was performed to identify predictors associated with coronary artery tortuosity.Results The mean age of the 361 CCS patients (44 % female; 56 % male) was 56.7±11.5 years. In the univariable regression analysis, age, female sex, hypertension (HT), PR interval, QTc interval, ST / T segment changes, left ventricle diastolic dysfunction (LVDD), left ventricle hypertrophia (LVH) were identified as predictors of coronary tortuosity. In the multivariable regression analysis, age (OR: 1.059; 95 %CI: 1.032-1.087, p&lt;0.001) and hypertension (OR: 0.484; 95 %CI: 0.278-0.843, p=0.01) were identified as independent predictors of coronary tortuosity.Conclusion Coronary artery tortuosity is an angiographic finding that develops as a result of adaptive mechanisms in the heart and can cause myocardial ischemia. Predictors of coronary artery tortuosity in patients with CCS were long PR and QTc intervals, ST / T segment changes, LVH, LVDD, advanced age, and female gender. Evaluation of these demographic, electrocardiographic, and echocardiographic data may help clinicans to anticipate coronary artery tortuosity in patients with CCS and to be precautious for PCI.

Evaluation of Left Ventricular Diastolic Function Using a Tissue-Doppler Imaging Based Algorithm According to 2016 Ase/Eacvi Guidelines in Patients with Decompensated Liver Cirrhosis: A Prospective Observational Study

Abstract Background Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism. The prevalence of cirrhosis has nearly doubled over the last decade, and the number of hospitalizations has similarly increased. Aim of the Work We aimed to correlate between the severity of liver cirrhosis using new MELD score and left ventricle diastolic dysfunction using tissue doppler imaging. Patients and Methods A prospective observational study in ICU of Theodor Bilharz Research Institute Hospital and Ain Shams University Hospitals for 6 months from June 2021 till end of November 2021 on hepatic patients who were admitted to ICU of Theodor Bilharz Research Institute Hospital and Ain Shams University Hospitals. Results In the studied group, the mean age was 53.13±9.44 years with males constituting more than half of them (57.8%). The mean MELD score was 24.08±6.01, and the mean left ventricular ejection fraction (LVEF %) was 60.43±5.49%. There were 5 patients (5.6%) with normal LV diastolic function and 85 patients (94.4%) with abnormal LV diastolic dysfunction. Out of the 90 patients, 5 patients were normal, 44 patients (48.9%) had a grade I LVDD, 28 patients (31.1%) had a grade II LVDD and 13 patients (14.4%) had a grade III LVDD. There was a highly statistically significant positive association between the grades of left ventricular diastolic dysfunction according to ALT, AST, T.Bilirubin, D.Bilirubin, INR and Creatinine. Additionally, there was a highly statistically significant negative association between grading of left ventricular diastolic dysfunction according to platelet count and sodium levels. Conclusion There was a statistically significant correlation found between the severity of liver cirrhosis represented by the new MELD score and the grade of left ventricular diastolic dysfunction. Therefore, in order to prepare the best post-procedural management of cirrhotic patients, echocardiography is required for all patients before any interventional procedure or liver transplantation regardless of the stage of cirrhosis. The mechanism of cardiac involvement in patients with cirrhosis seems to be complex and multifactorial.

Cardiac Tamponade as the Cause of Pulmonary Edema: Case Report

Introduction: Cardiac tamponade is an emergency syndrome that requires fast diagnosis and treatment; otherwise patient follows obstructive shock and cardiac arrest. Case report: A 70-year-old female was brought to the emergency department with hypoxemia. She had a history of progressive dyspnea over the past three weeks. Past medical history includes smoking. On physical examination: tachypnea, hypoxemia (SaO2 89%), jugular venous distention, arterial pressure 220/100 mmHg, heart rate rhythmic of 82 bpm. On pulmonary auscultation: diffuse and bilateral crackles. Lung ultrasound showed a bilateral B line and the echocardiogram demonstrated a pericardial effusion with signs of tamponade. A pericardiocentesis evacuated 620 ml of hemorrhagic fluid and the patient was transferred to the intensive care unit, hemodynamically stable, with SaO2 95%. At the ICU the echocardiogram, showed resolution of the cardiac tamponade and a tumor adhered to the lateral wall of the left ventricle. Chest CT demonstrated: a left lung tumor, infiltrating the pericardial sac. A pericardium biopsy demonstrated undifferentiated carcinoma. Discussion: Cardiac tamponade diagnosis requires a high level of suspicion. Respiratory failure, chest pain, and shock, observed in cardiac tamponade, are also present in different diseases. The most common finding of cardiac tamponade is dyspnea (78% of cases). Our patient had dyspnea due to pulmonary edema, secondary to left ventricle diastolic dysfunction caused by the tamponade. A bedside echocardiogram made the diagnosis of cardiac tamponade and guided the effective pericardiocentesis. Conclusion: Cardiac tamponade must be suspected in all cases of acute dyspnea. Echocardiogram is the method of choice for the diagnosis and for guiding the pericardiocentesis.

Kharakter i chastota komorbidnykh urazhen sertsia u khvorykh na systemnyi chervonyi vovchak, shcho yikh diahnostovano za dopomohoiu ekhokardiohrafii, vyiavlennia i kharakterystyka yikhnikh syntropichnykh variantiv

Introduction. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by damage of different organs and systems. It has been proven that cardiovascular events are proportionally more frequent in SLE affected persons in comparison with general population of corresponding age and sex. Echocardiography is most oftenly used due to its wide availability, ease of implementation, non-invasiveness, safety for visualization of anatomical features, assessment of structure and function of the heart and main vessels. Syntropic comorbid lesions are the non-random combination of two or more syndromes or nosological units with common genetic and/or etiological and pathogenetic mechanisms in a person, which may under certain circumstances influence each other's course. The aim of the study. To investigate nature and frequency of comorbid heart lesions in patients with systemic lupus erythematosus, diagnosed by echocardiography, to identify and characterize their syntropic variants. Materials and methods. 125 patients were included in the study after signing the voluntary Consent to participate, in accordance with the requirements of the Helsinki Declaration of Human Rights, the Council of Europe Convention on Human Rights and Biomedicine, in a randomized manner with preliminary stratification based on the presence of SLE, as well as heart lesions detected by echocardiography. The study included 110 women (88.00 %) and 15 men (12.00 %) aged 18 to 74 years (mean age 42.48 ±1.12 years). All patients with SLE were stratified into five groups based on the evaluation of SLE activity (Systemic Lupus Erythematosus Disease Activity Index scale - SLEDAI). All participants were patients of the Rheumatology Department of Lviv Regional Clinical Hospital. The study included two phases, during which the nature and frequency of comorbid heart lesions, detected by echocardiography, followed by elimination and characterization of syntropic lesions were determined. Results. About half of SLE patients with comorbid heart lesions have mitral valve (MV) insufficiency, and about 1/3 of patients have mitral valve stenosis with left ventricle (LV) diastolic dysfunction. With decreasing frequency we recorded thickening of the aortic valve (AV) leaflets, increased thickness of the interventricular septum (IS), pericardial effusion, enlargement of the left atrial (LA) cavity, enlargement of the right ventricle (RV), increased thickness of the posterior wall of LV in diastole, prolapse of MV, pulmonary hypertension, insufficiency of the tricuspid valve (TV), increase in the diameter of the ascending aorta, AV insufficiency, systolic dysfunction of the LV, enlargement of the LV cavity in diastole. Mitral stenosis and aortic stenosis were found in one case only. Having studied comorbid heart lesions in SLE affected patients, we found that some of them depend statistically reliable on the activity of disease. Therefore, we consider heart valve thickening, pulmonary hypertension, pericardial effusion, and heart failure to be syntropic heart lesions in patients with SLE. Other lesions, the frequency of detection of which does not depend on the activity of SLE, was related to its accompanying diseases. Conclusions. In patients with SLE, mitral valve insufficiency, thickening of the mitral valve leaflets, diastolic dysfunction of the left ventricle, thickening of the aortic valve leaflets, increased thickness of the interventricular septum, and pericardial effusion dominate among the comorbid heart lesions diagnosed by echocardiography. Syntropic heart lesions in patients with SLE included thickening of the mitral valve leaflets, pulmonary hypertension, pericardial effusion, and mitral valve insufficiency. Keywords: systemic lupus erythematosus, comorbid lesions of the circulatory system, syntropic lesions, heart valve lesions, diagnosis, echocardiography.

Evaluation of diastolic dysfunction in children with hypertrophic cardiomyopathy and its relationship with development of myocardial fibrosis

BackgroundPatients with hypertrophic cardiomyopathy may develop symptoms of shortness of breathing due to diastolic dysfunction which is not related to the severity of left ventricular outflow tract obstruction. As these patients usually develop a non-ischemic pattern of myocardial fibrosis, this may represent a mechanism for increased myocardial stiffness leading to impaired diastolic filling. The study aimed to determine the prevalence of myocardial fibrosis assessed by magnetic resonance imaging in children with hypertrophic cardiomyopathy and to evaluate its relationship with echocardiographic parameters including left ventricle diastolic dysfunction and to find echocardiographic indices which correlates with myocardial fibrosis as detected by cardiac magnetic resonance. A cross-sectional study was done for data of 50 children with hypertrophic cardiomyopathy from July 2018 to July 2021, patients were divided into (group 1) having myocardial fibrosis and (group 2) with no myocardial fibrosis, and results of echocardiographic parameters were compared between the two groups.ResultsResults showed strong relationship between presence of myocardial fibrosis and each of the following: Interventricular septum thickness, lower lateral and septal early diastolic tissue velocities (E′), E/E′ ratio, presence of left ventricular out flow tract obstruction and the grade of diastolic dysfunction.ConclusionsThe trans-mitral lateral and septal E/E′ (early mitral inflow to early diastolic mitral annular velocity ratio) allows early detection of left ventricular diastolic dysfunction in children with hypertrophic cardiomyopathy. The prevalence of diastolic dysfunction is higher in obstructive hypertrophic cardiomyopathy. The diastolic dysfunction severity is higher in patients with myocardial fibrosis.

Abstract 635: ESAM Deficiency-related Coronary Microvascular Dysfunction Contributes To Left Ventricle Diastolic Dysfunction In HFpEF

Coronary microvascular dysfunction and vascular inflammation have been linked to heart failure with preserved ejection fraction (HFpEF), but the underlying molecular mechanisms remain incompletely understood. Endothelial cell-selective adhesion molecule (ESAM) has been recently implicated as one of the biomarkers for heart failure. The biological function of ESAM is to regulate inflammatory cell adhesion, permeability and angiogenesis. Here, we examined the mechanistic role of ESAM in contributing left ventricle (LV) diastolic dysfunction in a mouse model of human HFpEF. We employed wild type (WT) mice and mice with homozygous genetic deficiency of ESAM (ESAM -/- ), with or without uninephrectomy and aldosterone infusion (UNX-Aldo, for 4-week). Using echocardiography, we found that WT mice with UNX-Aldo develop LV diastolic dysfunction, as indicated by a significantly reduced E/A ratio (E=early, A=late mitral inflow peak velocities), increased E/e’ ratio, isovolumic relaxation time (IVRT) and E wave deceleration time. UNX-Aldo significantly increased the serum soluble ESAM levels, along with elevated MMP2/9 levels, as potential mediators of ESAM ectodomain shedding. When compared to WT, ESAM -/- mice with UNX-Aldo displayed significant worsening of LV diastolic dysfunction, as indicated by increased IVRT, and the development of pulmonary edema and fibrosis. An unbiased automated tracing and 3D reconstruction of coronary microvasculature revealed that ESAM -/- mice had a significantly reduced coronary microvascular density. Arteries of ESAM -/- mice exhibited impaired endothelial sprouting and in cultured endothelial cells siRNA-mediated ESAM knockdown reduced tube formation. Thus, we propose that ESAM plays a role in the proper myocardial vascularization, hence the maintenance of myocardial perfusion. Deficiency, or augmented ectodomain shedding of ESAM impairs myocardial vascularization, whereby it contributes to the development of LV diastolic dysfunction, and could have mechanistic and diagnostic implications in human HFpEF.

Microvascular impairment in heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) is a cardiovascular disease characterized by diastolic dysfunction. Main risk factors include advanced age, sex (women being more susceptible), and comorbidities like obesity, type 2 diabetes, and renal dysfunction. The etiology of the disease is poorly known. Our pathophysiological hypothesis is that metabolic disorders and renal dysfunction induced by the risk factors generate a systemic pro-inflammatory state and hemodynamical changes that, accumulating with age, are responsible for endothelial dysfunction and pathological reorganization of the microvascular morphology, leading to diastolic dysfunction. The objective of the study was, using an HFpEF mouse model, to (1) identify the metabolic disorders and the renal dysfunction, (2) evaluate the pro-inflammatory state, (3) quantify the cardiac microvascular morphology, and (4) characterize the cardiac diastolic function. Experiments were done on 14-week-old female C57BL/Ks mice, predisposed to renal dysfunction, deficient for leptin receptors, and hence developing obesity and type 2 diabetes. 8-week-old male C57BL/6J mice, lacking HFpEF risk factors, were used as healthy control. Glycemia, triglyceridemia, cholesterolemia, and % pro-inflammatory cells were analyzed on blood samples. 3D imaging of glomeruli was done by light-sheet microscopy (LSM) on optically cleared kidneys. 3D imaging of the coronary capillary network was done by LSM on optically cleared hearts. Diastolic pressure, developed pressure, and relaxation rate was measured on Langendorff's isolated perfused hearts. Compared to controls, HFpEF mice showed increased plasmatic glucose, triglyceride, and cholesterol concentration, and increased monocyte and granulocyte %. Their kidneys had decreased glomerular volume, and compactness. The coronary capillary network was altered in the left and right ventricles. Isolated hearts showed left ventricle diastolic dysfunction. Our study suggests that risk factors induce diastolic dysfunction related to coronary microvascularisation morphological alteration via a systemic pro-inflammatory state. Further studies are needed to investigate hemodynamic alteration and endothelial dysfunction.

Mice with endothelial cell-selective adhesion molecule deficiency develop coronary microvascular rarefaction and left ventricle diastolic dysfunction.

Endothelial cell-selective adhesion molecule (ESAM) regulates inflammatory cell adhesion and transmigration and promotes angiogenesis. Here, we examined the role of ESAM in cardiac vascularization, inflammatory cell infiltration, and left ventricle (LV) diastolic function under basal and hemodynamic stress conditions. We employed mice with homozygous genetic deletion of ESAM (ESAM-/- ) and also performed uninephrectomy and aldosterone infusion (UNX-Aldo) to induce volume and pressure overload. Using echocardiography, we found that ESAM-/- mice display no change in systolic function. However, they develop LV diastolic dysfunction, as indicated by a significantly reduced E/A ratio (E=early, A=late mitral inflow peak velocities), increased E/e' ratio, isovolumic relaxation time (IVRT), and E wave deceleration time. An unbiased automated tracing and 3D reconstruction of coronary vasculature revealed that ESAM-/- mice had reduced coronary vascular density. Arteries of ESAM-/- mice exhibited impaired endothelial sprouting and in cultured endothelial cells siRNA-mediated ESAM knockdown reduced tube formation. Changes in ESAM-/- mice were accompanied by elevated myocardial inflammatory cytokine and myeloperoxidase-positive neutrophil levels. Furthermore, UNX-Aldo procedure in wild type mice induced LV diastolic dysfunction, which was accompanied by significantly increased serum ESAM levels. When compared to wild types, ESAM-/- mice with UNX-Aldo displayed worsening of LV diastolic function, as indicated by increased IVRT and pulmonary edema. Thus, we propose that ESAM plays a mechanistic role in proper myocardial vascularization and the maintenance of LV diastolic function under basal and hemodynamic stress conditions.

Left atrial strain evaluation to assess left ventricle diastolic dysfunction and heart failure with preserved ejection fraction: a guide to clinical practice : Left atrial strain and diastolic function.

Although frequently unrecognized, left atrium (LA) function plays a key role in global cardiac performance as it modulates left ventricle (LV) filling through three main functions: the LA reservoir, conduit and booster pump. Given the interdependence between the LA and the LV, it is known that LA dimension and/or LA function can be used as a surrogate for LV diastolic function.Recently, LA deformation analysis using 2-dimensional (2D) speckle tracking echocardiography (STE) strain emerged as a promising non-invasive technique that can help to estimate LV filling pressures (LVFP) and diagnose heart failure with preserved ejection fraction (HFpEF), as recently proposed in the recent 2022 European Association of Cardiovascular Imaging (EACVI) consensus which included LA reservoir strain as an additive parameter to estimate LVFP.This article aims to review the latest evidence regarding the role of LA strain in the assessment and management of LV diastolic dysfunction (LVDD) and HFpEF, providing a clinical guide with tips and tricks to use LA strain as a new technique to help to estimate LVFP.

The Outcomes of Coronary Artery Bypass Surgery after 18 Months-Is There an Influence of the Initial Right Ventricle Diastolic Dysfunction?

This study aimed to investigate the association of preoperative right heart filling indicators with outcomes after coronary artery bypass grafting (CABG) at an 18 month follow up. Patients who underwent CABG at a single center were included in this study. In addition to the baseline preoperative indicators and perioperative data, initial parameters of the right ventricle (RV) systolic and diastolic function were assessed. Among the 189 patients, a total of 19 (10.0%) MACE (cardiovascular death, nonfatal myocardial infarction and stroke) were recorded during an 18 month follow up. In patients with the development of MACE during the initial examination, the following changes in RV function were revealed compared with the group without MACE: a decrease in the e't index (8.2 versus 9.6 cm/s, p = 0.029), an increase in the Et/e't ratio (5.25 vs. 4.42, p = 0.049) and more frequent presence of RV pseudonormal filling (p = 0.03). In the binary logistic regression analysis, the development of MACE 18 months after CABG was associated with the nonconduction of PCI before surgery, the presence of peripheral atherosclerosis, an increase in IVST and Et/e't and a decrease in LVEF. RV diastolic dysfunction in the preoperative period was associated with the development of MACE within 18 months after CABG, and the ratio Et/e't was one of the independent predictors of MACE in a multiple regression analysis. This makes it expedient to include an assessment of not only systolic but also diastolic RV function in the preoperative examination. The inclusion of an assessment of RV diastolic function in the pre-CABG evaluation of patients deserves further study.

Right ventricular myocardial performance index (Tei) in premature infants

The objective of this study was to evaluate the right ventricular myocardial performance index) based on echocardiography in very low birth weight premature neonates, close to hospital discharge. This was a prospective cross-sectional study that included premature neonates with birth weight <1,500 g and gestational age <37 weeks at the Intermediate Neonatal Unit of Bonsucesso Federal Hospital from July 2005 to July 2006. The infants underwent two-dimensional color Doppler echocardiography, being the right ventricular myocardial performance index evaluated close to hospital discharge. We compared the neonatal and echocardiographic variables in neonates with and without bronchopulmonary dysplasia. A total of 81 exams were analyzed. The mean birth (standard deviation) weight and gestational age were 1,140 (235) g and 30 (2.2) weeks, respectively. The incidence of bronchopulmonary dysplasia was 32%. The mean right ventricle myocardial performance index (standard deviation) of the sample was 0.13 (0.06). We found a significant difference in aortic diameter [non-bronchopulmonary dysplasia 0.79 (0.07) vs. bronchopulmonary dysplasia 0.87 (0.11) cm, p=0.003], left ventricle in diastole [non-bronchopulmonary dysplasia 1.4 (0.19) vs. bronchopulmonary dysplasia 1.59 (0.21) cm, p=0.0006], ventricular septal thickness [non-bronchopulmonary dysplasia 0.23 (0.03) vs. bronchopulmonary dysplasia 0.26 (0.05) cm, p=0.032], and "a" measurement [(= sum of the isovolumetric contraction time, ejection time, and isovolumetric relaxation time) when calculating the myocardial performance index (p=0.01)]. Higher "a" interval in neonates with bronchopulmonary dysplasia suggests right ventricle diastolic dysfunction. We conclude that the right ventricle myocardial performance index is an important indicator both of ventricular function and for serial follow-up testing of very low birth weight premature neonates, especially those with bronchopulmonary dysplasia.

Does Premature Ventricular Complex Impair Left Ventricular Diastolic Functions?

A higher frequency of premature ventricular complexes is associated with a higher risk of premature ventricular complex-induced cardiomyopathy. Although there are several studies on the systolic functions of the left ventricle in this patient group, it is clearly not known how the diastolic functions of the left ventricle are affected. This study examined the effect of premature ventricular complex on left ventricle diastolic functions using diastolic strain rate. The trial included 57 patients with frequent premature ventricular complexes and 54 healthy volunteers. The patient was evaluated using echocardiography in its entirety. The vendor-independent software system determined systolic and diastolic strain parameters via 2-dimensional speckle tracking analysis. Using the auto strain 3P semi-automated endocardial boundary tracking instrument, the global longitudinal strain was measured from the apical 4-chamber, 2-chamber, and long axis. The diastolic strain rate was determined by averaging the strain rates of 17 cardiac segments at 2 distinct periods of diastole. In the patient group, early diastolic strain rate was significantly lower than that in the control group (1.62 ± 0.58 vs. 1.25 ± 0.38, P <.001). There were found to be significant negative connections between PVC's electrocardiographic QRS wave length and early diastolic strain rate and coupling interval and early diastolic strain rate. Significant positive associations between coupling interval and early diastolic strain rate were discovered (P <.001 and P <.001, respectively). Patients with premature ventricular complex exhibited a lower early diastolic strain rate than healthy individuals. The early diastolic strain rate can be used to predict left ventricle diastolic dysfunction, and persons with premature ventricular complex may have a higher risk of left ventricle diastolic dysfunction than the general population.