CardioSomatics

BACKGROUND: Until recently, takotsubo syndrome (TS) was considered a fairly benign disease in both early and late periods. However, in recent years, in-hospital complications in the acute period of TS are common and can be life-threatening.

AIM: Based on clinical and laboratory-instrumental data, this study aimed to build models for predicting the risk of developing in-hospital complications in patients with TS during the acute period.

MATERIALS AND METHODS: This prospective cohort study included 60 patients with TS, with an average age of 65.5±13.4 years. In the acute period (7–14 days), standard clinical and laboratory examination, peripheral arterial tonometry using the «EndoPAT 2000» apparatus, and psychological testing using validated questionnaires (hospital anxiety and depression scale and Beck depression scale) were performed.

RESULTS: The integrated model for predicting the risk of acute heart failure (AHF) development (pulmonary edema and cardiogenic shock) identified admission LVEF as the leading prognostic parameter. With LVEF ≤40.5%, the probability of AHF in patients with TS in the acute period was 62.5%, and in patients with TS and QTc interval >487 ms, the risk reached 100%. The sensitivity and specificity of the developed model were 72.7% and 97.4%, respectively. The integrated model for predicting the development of cardiovascular complications (CVCs) revealed that the number of leukocytes in the peripheral blood was the leading risk factor for adverse events in patients with TS in the acute period. With a leukocyte count >11.1×10⁹/L, the risk of CVCs in patients with TS increased to 89.9%, and if the erythrocyte count was >4.69×10¹²/L or ≤4.29×10¹²/L, it could reach 100%. The sensitivity and specificity of the resulting model were 92.6 and 97.0%, respectively.

CONCLUSION: The models proposed in this study for predicting the likelihood of developing severe AHF and the overall risk of CVCs in the acute period of TS are personalized and easy to use, allowing for the selection of optimized treatment techniques.

BACKGROUND: This study focuses on the development of new approaches to the management of patients with acute decompensation of heart failure (ADHF) using sodium-glucose cotransporter type 2 (iHLT-2) inhibitors, particularly dapagliflozin, and its role in early treatment initiation.

AIM: Our aim was to determine the predictors of severe ADHF outcomes in patients with low left ventricular ejection fraction (LVEF) and the role of early initiation of iGLT-2 therapy (within the first 24 h).

MATERIALS AND METHODS: This prospective randomized study included a total of 140 patients hospitalized with ADHF between January 1 to September 1, 2023. The patients were randomized into two groups: in group 1, iGLT-2 therapy was started within 24 h from the moment of admission (n=70), and in group 2, standard therapy was implemented (n=70). Hospital data were analyzed. The endpoint was the persistence of congestion in one or both circulatory circuits with New York Heart Association Functional Classes III–IV, indicating severe ADHF.

RESULTS: The initial demographic and clinical characteristics of both groups were comparable. In both groups <47% patients did not receive optimal drug therapy (excluding iGLT-2) for chronic heart failure, and no differences were found in this indicator (p=0.081). iGLT-2 therapy did not demonstrate a significant effect on the likelihood of an adverse ADHF outcome (odds ratio [OR]=0.88; 95% confidence interval [CI] 0.43–1.78, p=0.719). Multivariate analysis showed an increase in the probability of this outcome for every 1000 pg/mL increase in N-terminal propeptide of brain natriuretic hormone (NT-proBNP) (OR=1.72, 95% CI 1.37–2.17; p <0.001), blood urea per 1 mmol/L (OR=1.54, 95% CI 1.21–1.97; p=0.001), pulmonary hypertension (OR=7.08, 95% CI 2.15–23.34; p=0.001), and a decrease in the probability of outcome with a 1% increase in LVEF (OR=0.91, 95% CI 0.84–0.99; p=0.031). The sensitivity and specificity of the adverse outcome model were 91.3 and 85.1%, respectively.

CONCLUSION: The leading predictors of an unfavorable ADHF outcome include increased levels of NT-proBNP and blood urea, pulmonary hypertension, and decreased LVEF.

Chronic heart failure (CHF) is a global medical, social, and economic problem. It is a syndrome caused by imbalanced neurohumoral regulation of the cardiovascular system, which is accompanied by impaired systolic and/or diastolic function of the heart. Currently, the search and study of new biological markers that can help in the early diagnosis of CHF, serve as a laboratory tool for assessing treatment effectiveness, or be used as prognostic markers and risk stratification criteria are ongoing. Researchers focused on studying the role of Klotho protein, fibroblast growth factor 23 (FGF23), and sclerostin in patients with CHF. Klotho expression decreases as the body ages, and impaired production has been reported in various aging-related diseases. The FGF23 / Klotho axis plays a key regulatory role in cardiovascular pathology. Laboratory, clinical, and genetic studies have suggested that sclerostin is associated with heart disease, although available data are not entirely consistent. Clinical work conducted on the study of the Klotho protein, FGF-23, and sclerostin indicates the potentially important diagnostic and prognostic significance of their analysis in patients with CHF. Thus, more studies of the issues related to serial testing of these biological markers, including in the aspect of the multibiomarker model, are needed.

Around 64 million persons in the world have heart failure (HF). HF patients with left ventricle ejection fraction (LVEF) of ≥50% are classified as having HF with preserved ejection fraction (HFpEF). It is estimated that about fifty percent of all HF is HFpEF. Our aim was to provide evidence of contemporary data regarding diagnosis and management of HFpEF. We conducted literature search through online search such as Google Scholar and PubMed Central (PMC), focusing on diagnosis and management of HFpEF. Several criteria exist for the diagnosis of HFpEF, including EF >50%, evidence of diastolic dysfunction, elevated brain natriuretic peptide. High (≥15) or intermediate (9–14) E/eʹ index indicates the likelihood of HFpEF. SGLT2I decrease E/eʹ, indicating improvement of LV diastolic function as mentioned in several studies. Treatment duration to achieve this effect spans from 3 months to 1 year. SGLT2I have positive effect on echocardiographic parameter HFpEF patients. In the researches included in the review, E/eʹ was mainly used as primary end point.

BACKGROUND: Spontaneous coronary artery dissection (SCAD) is a disease that develops unrelated to intracoronary intervention, atherosclerosis, aortic dissection, or mechanical trauma and causes a false lumen (intramural hematoma) in the wall of the coronary artery (CA) with impaired blood flow in it and myocardial ischemia in the affected region of the CA. SCAD most often develops in young and middle-aged adults (aged ≤50 years); among women, it becomes the culprit in 24%–35% of cases of acute myocardial infarction (MI). SCAD is a risk factor for MI, and incorrect interpretation of the angiographic picture and intravascular imaging methods can lead to incorrect tactics of patient behavior.

CLINICAL CASE DESCRIPTION: This article presents a clinical case of SCAD leading to the development of MI in a young woman with concomitant connective tissue dysplasia and hereditary thrombophilia. The angiographic disease course resembled focal atherosclerosis, and in the course of invasive management, complications had arisen, confirming the probable genesis of coronary artery obstruction.

CONCLUSION: SCAD is a complex disease, with a sudden onset and an ambiguous prognosis. In most cases, SCAD develops in young women in the absence of cardiovascular factors. It is difficult to diagnose because its signs and symptoms are similar to more common diseases, mainly MI. SCAD can masquerade as focal stenosis on an angiogram, mimicking an atherosclerotic plaque. The «gold standard» for diagnosing SCAD is optical coherence tomography (OCT). OCT enables the visualization of the state of all coronary artery walls and elucidates the pathogenetic mechanisms of MI. If performing OCT is impossible after diagnostic coronary angiography in young patients in suspected cases, the likelihood of DST and SCAD risk must be assessed to avoid errors in choosing treatments. The technical accessibility of intracoronary imaging methods reduces the frequency of diagnostic and, consequently, treatment errors.