Background: According to the ventricular myocardial band model, the diastolic isovolumetric period is a contraction phenomenon. Our objective was to employ speckle-tracking echocardiography (STE) to analyze myocardial deformation of the left ventricle (LV) and to confirm if it supports the myocardial band model. Methods: This was a prospective observational study in which 90 healthy volunteers were recruited. We evaluated different types of postsystolic shortening (PSS) from an LV longitudinal strain study. Duration of latest deformation (LD) was calculated as the time from the start of the QRS complex of the ECG to the latest longitudinal deformation peak in the 18 segments of the LV. Results: The mean age of our subjects was 50.3 ± 11.1 years. PSS was observed in 48.4% of the 1620 LV segments studied (19.8%, 13.5%, and 15.1% in the basal, medial, and apical regions, respectively). PSS was more frequent in the basal, medial septal, and apical anteroseptal segments (>50%). LD peaked in the interventricular septum and in the basal segments of the LV. Conclusions: The pattern of PSS and LD revealed by STE suggests there is contraction in the postsystolic phase of the cardiac cycle. The anatomical location of the segments in which this contraction is most frequently observed corresponds to the main path of the ascending component of the myocardial band. This contraction can be attributed to the protodiastolic untwisting of the LV.

Left ventricular ejection fraction (LVEF) results from the combined action of longitudinal and circumferential contraction, radial thickening, and basal and apical rotation. The study of these parameters together may lead to an accurate assessment of the cardiac function. Ninety healthy volunteers, categorized by gender and age (≤ 55 and > 55 years), were evaluated using two-dimensional speckle tracking echocardiography. Transversal views of the left ventricle (LV) were obtained to calculate circumferential strain and left ventricular twist, while three apical views were obtained to determine longitudinal strain (LS) and mitral annular plane systolic excursion (MAPSE). We established the integral myocardial function of the LV according to: 1. The Combined Deformation Parameter (CDP), which includes Deformation Product (DP) - Twist x LS (° x %) - and Deformation Index (DefI) -Twist / LS (° / %)-; and 2. the Torsion Index (TorI): Twist / MAPSE (° / cm). The mean age of our patients was 50.3 ± 11.1 years. CDP did not vary with gender or age. The average DP was − 432 ± 172 ° x %, and the average DefI was − 0.96 ± 0.36 ° / %. DP provides information about myocardial function (normal, pseudonormal, depressed), and the DefI quotient indicates which component (s) is/are affected in cases of abnormality. TorI was higher in volunteers over 55 years (16.5 ± 15.2 vs 13.1 ± 5.0 °/cm, p = 0.003), but did not vary with gender. The proposed parameters integrate values of twisting and longitudinal shortening. They allow a complete physiological assessment of cardiac systolic function, and could be used for the early detection and characterization of its alteration.

Adherence to treatment in the secondary prevention of ST-elevation myocardial infarction (STEMI) improves survival and quality of life. To measure treatment adherence and its association with the frequency of achievement of cardiometabolic targets in patients with STEMI. A total of 157 adults with STEMI < 12 hours, with successful reperfusion, and in phase 3 of cardiac rehabilitation were included. Demographic variables were collected, and adherence as well as achievement of cardiometabolic targets were measured. Univariate, bivariate (chi-square, Student's t test, or Mann-Whitney U test, depending on distribution), and multivariate logistic regression analyses were performed (p < 0.05). Adherence was 75%, with a higher percentage of patients meeting LDL cholesterol (54% vs. 21%, p < 0.001), triglyceride (79% vs. 46%, p < 0.001), and glycated hemoglobin (63% vs. 23%, p < 0.001) targets compared to the non-adherent group. Adherence was an independent factor for achieving cardiometabolic targets, with an odds ratio (OR) of 9.8 (95% confidence interval [95% CI]: 3.6-16.3; p < 0.001). Treatment adherence was associated with a higher frequency of achievement of cardiometabolic targets.

Misfolded proteins, including islet amyloid polypeptide (hIAPP), serum amyloid A (SAA), and amyloid-betas (Aβs) such as Aβ1-40 and Aβ1-42 oligomers, collectively referred to in our work as amyloid oligomers, have been implicated in the development of both metabolic and cardiovascular diseases. However, their potential role as early biomarkers of myocardial damage remains insufficiently explored. We conducted a systematic review following PRISMA guidelines and epistemic meta-analysis to investigate the association between misfolded protein oligomers and early myocardial injury. All English- and Spanish-language articles with titles, abstracts, or keywords relevant to the research topic and indexed in at least one of the following databases—PubMed, BIREME, or Web of Science—were included. A comprehensive search across major databases identified 30 eligible studies. Thirty studies met inclusion criteria, in humans and animals, and in vitro. Amyloid oligomers were consistently elevated in patients with acute myocardial infarction, type 2 diabetes, or coronary artery disease compared with controls. In specific individual cohorts, a higher SAA concentration correlated with major adverse cardiovascular events, where it acted as an independent predictor of mortality in reperfused AMI (RR 5.8; 95% CI: 1.3–27.7) and cardiac rupture (OR 8.8; 95% CI: 1.7–25.6). Our findings support the hypothesis that protein misfolding contributes to early myocardial injury and highlight its potential as a novel source of cardiometabolic biomarkers.

Desde el conocimiento del infarto del ventrículo derecho, el interés por las características del ventrículo derecho ha sido cada vez mayor. Ahora se sabe que la función ventricular derecha es un predictor de mortalidad en diferentes contextos. El ventrículo derecho es una cavidad de baja presión, alta compliancia y alto volumen. Para llevar a cabo su función normal se encuentra acoplado a la circulación pulmonar y al ventrículo izquierdo. Ante alteraciones agudas de sobrecarga de presión, volumen e isquemia, se dilata para adaptarse a su nueva carga. Su manifestación puede ser disfunción o falla ventricular que progresará a choque cardiogénico por involucro del ventrículo derecho. Diversas entidades pueden ser la causa de la disfunción aguda: el infarto del ventrículo derecho (alteraciones de la contractilidad por isquemia) y la tromboembolia pulmonar de alto riesgo (aumento de la poscarga). Ambas comparten una fisiopatología ventricular similar y alta mortalidad sin tratamiento. Entender la anatomía fisiológica, la disfunción y la falla ventricular aguda es importante para definir un diagnóstico oportuno y un tratamiento orientado a la fisiopatología. En esta primera parte se toma en consideración la anatomía fisiológica y la disfunción/falla aguda ventricular derecha y su desenlace en el choque cardiogénico, desde la perspectiva de estas dos entidades. En otro trabajo se revisará el tratamiento orientado al choque cardiogénico por involucro ventricular derecho.