The age is one of the main non-modified factors which reduces the elasticity of vessels and increases the appearance of atherosclerotic plaques. A number of studies have revealed that in some people, vascular changes occur at a younger age, while the presence of only classical risk factors does not explain the development of cardiovascular events in young people. This phenomenon is described as a syndrome of early, or accelerated, vascular aging (EVA). Aspects of this premature process include endothelial dysfunction, increased arterial stiffness, thickening of the intima-media complex and impaired dilatation of the central arteries, an increase of the reflected wave, hypertrophy of small vessels with a decrease in their lumen. Accelerated aging of the vascular wall increases the frequency of complications, therefore, recently "vascular age” is considered as an important predictor of individual risk of cardiovascular events. The review describes factors and mechanisms that trigger the process of EVA, genetic aspects of vascular damage and the biology of telomeres. Changes in hemodynamics and structural and functional properties of arteries during physiological and accelerated aging are presented. Currently, several indicators have been proposed that indicate arterial wall damaging and progression of vascular aging. The carotid-femoral pulse wave velocity is included in the list of indicators of subclinical target organs damage in ESH-ESC Guidelines for the management of arterial hypertension. The results of studies on the developing the new diagnostic markers for identifying individuals with "normal" or "early" ("accelerated") vascular aging are presented. Therapeutic strategies are aimed at decreasing the influence of factors that provoke EVA and include a non-pharmacological approach and medical intervention. The paper describes methods of therapeutic correction of the EVA syndrome.
The speckle tracking method allows one to quantify the temporal and spatial characteristics of myocardial contraction. Importantly, it does not depend on a scanning angle and allows one to record the movement of speckles in 2D mode in any direction, unlike tissue Doppler imaging. This examination is non-invasive, safe for patients, and economically more beneficial in comparison with other modern methods of assessing heart contractility: MRI and scintigraphy. Diagnostic thresholds are suggested for obtaining peak values of all types of global strains and strain rates by sampling a healthy group, which can reveal early signs of left ventricle contractility failure. Correlation relationships of deformation parameters between themselves and with left ventricular hemodynamic indices, as well as anthropometric parameters in healthy subjects highlight the features of heart contraction biomechanics. However, currently this method is scarcely studied because no generally accepted normal range of strain values exists. •It is necessary to have sufficient qualification and skills in dealing with the XStrain™ Esaote software to obtain optimal values of myocardial deformation.•The study results expand the database of this software for users and determine the normal range of the left ventricular contractility parameters.•The revealed interrelationships of strain values in healthy individuals are relevant for understanding how the contractility mechanisms are altered in patients, and open up the prospect of studying the heart's compensatory possibilities.
Background. In order to provide personalized medicine and improve cardiovascular outcomes, a method for predicting adverse left ventricular remodeling (ALVR) after ST-segment elevation myocardial infarction (STEMI) is needed. Methods. A total of 125 STEMI patients, mean age 51.2 (95% CI 49.6; 52.7) years were prospectively enrolled. The clinical, laboratory, and instrumental examinations were performed between the 7th and 9th day, and after 24 and 48 weeks, including plasma analysis of brain natriuretic peptide (BNP), transthoracic echocardiography, analysis of left ventricular-arterial coupling, applanation tonometry, ultrasound examination of the common carotid arteries with RF signal amplification. Results. Patients were divided into 2 groups according to echocardiography: “ALVR” (n = 63)—end-diastolic volume index (EDVI) >20% and/or end-systolic volume index (ESVI) >15% after 24 weeks compared with initial values; “non-ALVR” (n = 62)—EDVI <20% and ESVI <15%. In the ALVR group, hard endpoints (recurrent myocardial infarction, unstable angina, hospitalization for decompensated heart failure, ventricular arrhythmias, cardiac surgery, cardiovascular death) were detected in 19 people (30%). In the non-ALVR group, hard endpoints were noted in 3 patients (5%). The odds ratio of developing an adverse outcome in ALVR vs. non-ALVR group was 8.5 (95% CI 2.4–30.5) (p = 0.0004). According to the multivariate analysis, the contribution of each of the indicators to the relative risk (RR) of adverse cardiac remodeling: waist circumference, RR = 1.02 (95% CI 1.001–1.05) (p = 0.042), plasma BNP—RR = 1.81 (95% CI 1.05–3.13) (p = 0.033), arterial elastance to left ventricular end-systolic elastance (Ea/Ees)—RR = 1.96 (95% CI 1.11–3.46) (p = 0.020). Conclusion. Determining ALVR status in early stages of the disease can accurately predict and stratify the risk of adverse outcomes in STEMI patients.
29 June 2016 in Rational Pharmacotherapy in Cardiology
This work reviews the reasons why the characteristics of left ventricular (LV) contractility, in particular, and 2D speckle echocardiography-based peak rates of global longitudinal strain (GLS), are not widely used in clinical practice. Authors present the analysis of new indicators proposed for the assessment ofLVcontractile function based on longitudinal strain taking into account the involvement of individual segments. The authors show that the assessment of myocardial work indicators characterizing the relationships between contractile and pump functions is a promising approach for the study ofLVcontractile function. The analysis of postsystolic strain index (PSI) is presented to illustrate its clinical implementation in the studies of viable myocardium in ischemic conditions and evaluating the effectiveness of cardiac resynchronization therapy (CRT).