Aspects of transthoracic echocardiography protocol in obese patients

Aim. To study the diagnostic value of the left atrial stiffness index (LASI) of heart failure with preserved ejection fraction (HFpEF) depending assessed by transthoracic echocardiography (TTE) in the diagnosis on diastolic stress test (DST) results.Material and methods. DST was performed in cases of insufficient criteria for increased left ventricular filling pressure assessed by TTE. One hundred patients were examined (52,0% men, 66,1±5,4 years). Patients with a ratio of early transmitral flow velocity to early diastolic mitral annulus velocity (E/e') ratio >15 in DST were included in group I (n=45), patients with E/e' <15 — group II (n=55). The speckle tracking echocardiography was used to assess left atrial reservoir strain (LASr).Results. Significant differences were identified between the groups in sex (40,0% of men in group I and 61,8% in group II, respectively; p=0,044), body mass index (32,9 [29,5;36,0] and 29,6 [27,3;31,8] kg/m2; p=0,001), hypertension stage (2,9±0,3 and 2,5±0,8, p=0,037), the presence of coronary artery disease (88,9 and 67,3%; p=0,016), NYHA heart failure class (2,0±0,4 and 1,5±0,7; p=0,003). TTE revealed significant differences in the left atrium volume index (31,9 [28,5;36,0] and 27,8 [24,1;34,6] ml/m2; p=0,039), E/e' ratio (10,9 [9,7;12,5] and 9,3 [7,4;10,8]; p<0,001), LASr (23,5 [19,3;28,3] and 28,9 [25,6;32,2]%, p<0,001) and LASI (0,46 [0,38;0,56] and 0,30 [0,25;0,39]; p<0,001). According to ROC analysis, the largest area under the curve (AUC), optimal sensitivity and specificity in HFpEF diagnosis were observed in LASI (AUC=0,829, p<0,001; 77,8 and 74,5%, respectively). Lower classification quality was shown by the H2FPEF score (AUC=0,701, p=0,001; 66,7 and 69,1%), while the HFA-PEFF score was not significant in the pretest detection of HFpEF (AUC=0,608, p=0,065; 53,3 and 61,8%).Conclusion. LASI with a cut-off point >0,38 has the greatest ability to detect HFpEF among the possible pretest diagnostic methods.

Section: Relationships Andunclassified

Left atrial stiffness index in the identification of heart failure with preserved ejection fraction

Shirokov,

Yaroslavskaya,

Kosterin

et al. 2024

“…Гипертрофию ЛЖ диагностировали с учетом индекса массы тела (ИМТ): если ИМТ соответствовал нормальной или избыточной массе тела, массу миокарда (ММ) ЛЖ индексировали к площади поверхности тела, и критериями для гипертрофии ЛЖ считали значение индекса ММ ЛЖ (ИММЛЖ) >115 г/м 2 для мужчин и >95 г/м 2 для женщин [10,14]. Если ИМТ соответствовал Ож, ММ ЛЖ индексировали к росту в степени 2,7; в этом случае гипертрофию ЛЖ диагностировали при ИММЛЖ >50 г/м 2,7 для мужчин и >47 г/м 2,7 для женщин [15,16]. Отсутствие данных о весе пациентов во время госпитализации не позволило проиндексировать абсолютные значения параметров ЭхоКГ на госпитальном этапе исследования.…”

Section: Introductionunclassified

Changes of clinical and echocardiographic parameters within a year after COVID-19 pneumonia in patients without cardiovascular diseases, depending on the obesity presence

Yaroslavskaya,

Shirokov,

Krinochkin

et al. 2023

Aim. To study the changes of clinical and echocardiographic parameters in people without cardiovascular diseases (CVDs) within a year after coronavirus disease 2019 (COVID-19) depending on the obesity presence.Material and methods. During the year after COVID-19 pneumonia, the clinical and echocardiographic parameters of 21 patients with obesity and without CVD were compared. The group both without CVDs and obesity consisted of 52 patients comparable by sex and age.Results. Newly developed CVDs were registered in 55% and 17% of the group with and without obesity, respectively. Left ventricular (LV) global longitudinal strain 3 months (-18,4±2,3 vs -20,6±2,2%, p=0,010) and one year after COVID-19 pneumonia (-18,8±1,8 vs -20,8±2,5%, p=0,021) was lower in the group with obesity. Lateral (e' later) (10,8±3,3 vs 13,1±2,9 cm/s (p=0,007)) and septal (e' sept) (8,5±2,7 vs 10,1±2,0 cm/s (p=0,011)) early diastolic mitral annulus velocity, as well as the ratio of early and late diastolic LV filling (E/A) (1,1±0,3 vs 1,2±0,3 (p=0,019)) at the end of the follow-up were lower in the group with obesity.Conclusion. In people without CVDs during a year after COVID-19 pneumonia, a high prevalence of newly developed CVD was noted in 55% and in 17% of people with and without obesity, which was accompanied by worse LV systolic and diastolic function in the group with obesity.

Role of epicardial adipose tissue in the pathogenesis of chronic inflammation in heart failure with preserved ejection fraction

Dzhioeva,

Timofeev,

Metelskaya

et al. 2024

Self Cite

According to the recent World Health Organization statistics, cardiovascular disease (CVD) is one of the leading causes of high mortality worldwide. While obesity is a major and persistent risk factor for CVD, the cause of this condition, the pathological molecular connection between peripheral fat depots and the heart, remains poorly understood. The aim of this review is to introduce the reader to the metabolic activity of epicardial adipose tissue (EAT), the consequences of excessive epicardial fat accumulation and the development of heart failure (HF).EAT is visceral adipose tissue that is in direct contact with the myocardium and coronary vessels and can influence cardiac function through both mechanical effects and more subtle paracrine molecular mechanisms. HF with preserved ejection fraction (HFpEF) is closely associated with obesity and patterns in fat distribution. Excessive amounts of EAT are associated with abnormal hemodynamics in HFpEF, with the potential for direct mechanical effects on the heart causing a constriction-like effect and local myocardial remodeling effects resulting from the secretion of inflammatory mediators. However, patients with excess EAT tend to have more subcutaneous adipose tissue, making it difficult to determine a cause-and-effect relationship between epicardial fat and HFpEF. This review provides evidence that excess EAT is an important part of HFpEF pathogenesis.