Editorial on the Research TopicNovel approaches in cardiac imagingOver the past decade, advancements in cardiovascular imaging –3 have cThis Special Issue delves into these significant aspects through 16 original research articles, an updated literature review, a systematic review and meta-analysis, and a case report. Here is a brief overview of these articles.Chen et al. suggested a novel pipeline for labeling and imaging myocardial and vascular structures, which could be implemented in cardiac studies for examining heart structures at the single-cell level.Guo et al. introduced a pioneering technology that combines diagnostic ultrasound with cyclic Arg-Gly-Asp-modified microbubbles targeting GP IIb/IIIa receptors. This approach can rapidly identify advanced atherosclerotic plaques and concurrently provide targeted therapy by dissolving activated and aggregated platelets.El-Saadi et al. conducted a head-to-head comparison of myocardial strain using fast-strain encoding and feature tracking imaging in acute myocardial infarction. Both techniques exhibit acceptable agreement with two-dimensional echocardiography for longitudinal strain, with fast-strain encoding demonstrating higher sensitivity and specificity for detecting infarcted segments.Zhang et al. evaluated left ventricular function in hypertrophic cardiomyopathy patients with preserved ejection fraction using left ventricular strain patterns derived by cardiac magnetic resonance feature tracking. The results suggest that left ventricular strain patterns are more sensitive than conventional ejection fraction for detecting subclinical cardiac dysfunction in hypertrophic cardiomyopathy. Also, strain patterns correlate with cardiac biomarkers, such as cardiac troponin and N-terminal prohormone of the brain natriuretic peptide.Vattay et al. investigated the relationship between quantitative plaque metrics from coronary computed tomography angiography and segmental myocardial ischemia assessed using dynamic perfusion. Their findings suggest that total plaque volume is independently associated with myocardial blood flow but not with the severity of coronary stenosis.Tang et al. explored the additional effects of mitral regurgitation on left ventricular strain impairment in patients with essential hypertension. Results showed that global peak strain was significantly more impaired in hypertensives with mitral regurgitation than in those without valvular insufficiency. Interestingly, the degree of mitral regurgitation was independently correlated with left ventricular global radial peak strain, circumferential peak strain, and global longitudinal peak strain.Yu et al. assessed the diagnostic capability of real-time four-dimensional transesophageal echocardiography in detecting implant-related thrombus in patients who have undergone transcatheter left atrial appendage closure or have a cardiac implantable electronic device. The novel technique demonstrated a superior thrombus detection rate compared to conventional two-dimensional echocardiography. Furthermore, this real-time four-dimensional transesophageal echocardiography approach revealed distinct imaging features between a thrombus on an occluder and an electronic device.Wang et al. investigated the utility of myocardial work parameters derived from pressure-strain loops in assessing cardiac function and predicting clinical prognosis in patients with pulmonary hypertension. The technique yielded two novel indices: right ventricular global constructive work and pulmonary arterial systolic pressure estimate. Both were predictive of clinical outcomes in patients with pulmonary hypertension.Dejea et al. described the customization of an isolated, perfused heart system compatible with synchrotron-based x-ray phase contrast imaging. This innovative setup enables high-spatial resolution studies of heart architecture throughout the cardiac cycle, offering insights into the structural dynamics of the heart, including the effects of pharmaceuticals and other agents on the cardiac cycle.Wang et al. compared longitudinal changes in color Tissue Doppler Imaging curves between normal controls and individuals at risk of future cardiac events. Noteworthy, they demonstrated that this technique could reveal an accelerated aging process in the hearts of individuals with cardiac risk factors. Consequently, they proposed Tissue Doppler Imaging as a valuable tool for identifying high-risk patients in a clinical setting.Zhu et al. assessed fetal cardiovascular parameters using a two-dimensional speckle tracking technique to distinguish the size and systolic function differences in the left and right ventricles during pregnancy. They discovered that fetal cardiovascular physiology is characterized by a larger right ventricular volume  and greater left ventricular outputs, as indicated by higher ejection fraction, cardiac output, and stroke volume values.Muraru et al. evaluated whether left ventricular volumes and ejection fraction measurements obtained by three-dimensional echocardiography offer any additional prognostic value over those acquired by two-dimensional echocardiography. Notably, in a total of 725 consecutive patients, left ventricular ejection fraction and end-systolic volume derived from three-dimensional echocardiography showed a stronger association with outcomes than the corresponding two-dimensional parameters.Chen et al. proposed a novel method for labeling and imaging myocardial and vascular structures by using fluorescent dyes and transgenic markers. This innovative technique elucidates the three-dimensional morphology and spatial arrangement of cardiomyocytes and highlights structural differences in endothelial cells and capillaries. Overall, this new pipeline can define the structures of the entire heart at the single-cell level.Beyls et al. investigated whether right ventricular longitudinal shortening fraction, a two-dimensional speckle tracking parameter used to assess right ventricular systolic function, yields consistent results regardless of whether it is assessed with conventional transthoracic echocardiography or transesophageal echocardiography. Crucially, the authors demonstrated that the values of the right ventricular longitudinal shortening fraction obtained with the two techniques are interchangeable.Kusunose et al. applied a previously developed artificial intelligence model to predict heart failure and calculate the probability of elevated pulmonary artery wedge pressure. The findings showed the potential for using an artificial intelligence model on chest x-ray to predict pulmonary artery wedge pressure and its capacity to supplement prognostic information from other conventional clinical prognostic factors in heart failure. According to the authors of the study, these findings could enhance the accuracy of prediction models in heart failure, potentially leading to more informed clinical decision-making.Erevik et al. aimed to determine the left ventricular response to increased exercise duration and intensity using novel echocardiographic tools to evaluate myocardial work and fatigue. They found that increased exercise intensity and duration during a cardiopulmonary exercise test and a 91-km mountain bike leisure race were associated with increased myocardial wasted work post-exercise, without changes in left ventricular ejection fraction and global longitudinal strain compared to baseline. These findings suggest that markers of myocardial inefficiency may precede a reduction in global left ventricular function, thus serving as early indicators of myocardial fatigue.Yao et al. critically reviewed the benefits and limitations of four current ultrasound imaging modalities for assessing plaque vulnerability, considering the biological characteristics of the vulnerable plaque, and their value in clinical diagnosis, prognosis, and treatment efficacy assessment.Sharma et al. conducted a systematic review and meta-analysis of the clinical application of longitudinal layer-specific strain as a diagnostic and prognostic instrument in ischemic heart disease. Their findings demonstrated that epicardial longitudinal layer-specific strain was the most significant diagnostic marker in patients with stable angina pectoris, whereas endocardial longitudinal layer-specific strain was the strongest diagnostic marker in patients with acute coronary syndrome. Furthermore, endocardial circumferential strain was a significant predictor of adverse outcomes in stable patients, while epicardial longitudinal layer-specific strain was the best predictor of outcomes in unstable patients.Lin et al. presented a case of multiple biventricular aneurysms in arrhythmogenic cardiomyopathy, emphasizing that the pathological characteristics of arrhythmogenic cardiomyopathy can be better visualized using high-frequency linear ultrasound, with provides superior resolution.In conclusion, future technological advancements, as discussed in this Special Issue, are expected to underscore the role of cardiovascular imaging in evaluating underlying pathophysiologic processes, thereby bridging the gap between pathophysiology, molecular medicine, and cardiovascular imaging , 10. Acc


Significant  Many studies suggest that increased QTd is associated with increased risk of ventricular arrhythmias3 and sudden death6. In this regard, an increased QTd has been documented in patients with arterial hypertension and left ventricular (LV) hypertrophy7. In addition to clinical environments, LV hypertrophy is observed in athletes completing regular training10. The LV hypertrophic cardiac response serves as a reactive mechanism to compensate for volume overload experienced during endurance training or pressure overload experienced during resistance training12. Although athletes develop impressive LV tissue growth, it is unknown whether this exercise-induced LV hypertrophy is associated with increased QTd like that observed in patients with hypertensive myocardial hypertrophy7.Prolonged QT dispersion (QTd) derived from electrocardiograms has been used as an indicator of abnormal ventricular repolarization for several cardiac diseases14 or combined with echocardiographic parameters20 in athletes and the general population. While the available evidence suggests that exercise may affect echocardiographic parameters  in athletes, research directly comparing between athletes and sedentary control groups has yielded equivocal findings pertaining to QTd20. Namely, similar,19 lower,17 or even higher20 corrected QTd measures have been reported in athletes compared to control groups. Inconsistent findings across studies potentially reflect disparities in QTd across sexes , age groups , and sports .Increased interest has emerged in quantifying QTd, either in isolation21, limited research has compared QTd and echocardiographic parameters across athletes competing in different sports varying in terms of the predominant type of overload imposed. In this way, sports may be classified according to the mechanical demands they elicit22 based on the peak static components  and the peak dynamic components  undertaken by athletes. To our knowledge, only three studies have compared electrocardiographic parameters in isolation14 or combined with echocardiographic parameters19 across athletes competing in sports with different mechanical demands, showing similar15 or prolonged19 QTd in athletes undertaking static training compared to athletes undertaking dynamic training as their predominant form of exercise. The equivocal findings across studies directly comparing QTd between athletes predominantly undertaking static and dynamic forms of exercise or between athletes and control groups suggest more research is needed to develop a definitive consensus regarding the sport-specific cardiac features developed in athletes23. Also, no evidence is available concerning the associations between QTd and echocardiographic parameters in athletes. In addition to indicating sport-specific cardiac features, QTd and echocardiographic data in athletes will provide insight as to whether structural cardiac remodeling in response to training produces abnormalities in cardiac function and QTd, which is vital in distinguishing an athletic heart from pathological cardiac hypertrophy. Therefore, the aims of this study were to: 1) compare QTd and echocardiographic parameters between athletes competing in different sports and sedentary controls; and 2) assess the associations between QTd and echocardiographic parameters among these athletes.Despite evidence suggesting that cardiac remodeling varies in response to pressure overload (concentric hypertrophy) or volume overload (eccentric hypertrophy)14. Inclusion criteria for participation in the study were as follows: (a) at least 3 years of training and competition experience immediately prior to participation in the study, performing ≥ 6 h·week−1 of exercise (for athletes); (b) compliance with the banned substance list; (c) free from injury/illness; (d) 18–39 years of age; and (e) sedentary participants to have never been involved in any sports training or competition and completing < 2 h·week−1 of physical exercise prior to the study. The exclusion criteria were as follows: (a) history of cardiovascular disorders; (b) history of diabetes mellitus; (c) history of arterial hypertension; (d) history of dyslipidemia; or (e) use of medications known to alter cardiac conduction. Training characteristics  for the athletes recruited in this study are described in Table A total of 130 highly trained male athletes competing at the national level in their respective sport and 43 age-matched healthy controls with a sedentary lifestyle volunteered to participate in this study. Athletes consisted of long-distance runners (n = 12), volleyball athletes (n = 14), football athletes (n = 39), powerlifters (n = 26), and bodybuilders (n = 39). Analyses using G*power software  indicated our study was sufficiently powered given n = 150 was recommended , based on research examining the influence of sex and type of sport on QTd in elite athletesA cross-sectional experimental design was adopted. All participants underwent clinical examination including a medical interview, measurement of general characteristics , as well as electrocardiographic and echocardiographic screening at the Clinic for Cardiovascular Diseases. All assessments were carried out in the morning between 08:00 and 10:00.A 12-lead electrocardiogram was recorded after a 5-min resting period in the supine position using a conventional surface electrocardiogram device  at 25 mm/s and 1 mV/cm voltage. The QT interval was measured manually from the onset of the QRS complex to the end of the T wave, defined as the point of return of the T wave to the isoelectric line or to the nadir between the T and U waves in cases where a U wave was present. If the end of the T wave could not be determined reliably, or when the T wave was isoelectric or of very low amplitude, the QT measurement was not made in that lead and was excluded from the analysis. In all participants, the QT interval was measurable in at least nine electrocardiogram leads. QTd was calculated as the difference between the longest and shortest QT interval. Corrected QTd was defined as the difference between maximum and minimum corrected QT (QTc) interval. QT interval was corrected for heart rate by using Bazett’s formula [QTc = QT/√]. R–R interval was determined as: 60/ heart rate. All electrocardiograms were read by two experienced cardiologists, with any disagreements resolved through discussion, or consulted with a third cardiologist for a consensus decision. The intra- and inter-rater reliability (coefficient of variation percentage) for QT measurements were 5% and 10% respectively.25. Intra-rater variability (coefficient of variation percentage assessed from a random sample of 10 echocardiographic measurements) was < 5%. A second cardiologist was available and consulted for opinion or re-measurement in cases where there was any uncertainty. Left atrium diameter, aortic root diameter, LV end-diastolic diameter, LV end-systolic diameter, intra-ventricular septal wall thickness (ISWT), posterior wall thickness (PWT), and LV mass were taken in the parasternal long-axis view. LV mass and aortic root diameter were indexed to body surface area. Body surface area (BSA) was determined as26: BSA = 0.007184 * height0.725 * body mass0.425. Relative wall thickness (RWT) was calculated as: (2 × PWT)/LV end-diastolic diameter. LV geometric pattern was characterized as either24: (1) concentric hypertrophy ; (2) eccentric hypertrophy ; (3) concentric LV remodeling ; or a (4) normal pattern .Two-dimensional M-mode echocardiograms were performed using commercially-available equipment . All measurements were performed by the same experienced cardiologist in accordance with the guidelines of the American Society of EchocardiographyTransmitral diastolic blood flow was registered using pulsed-wave Doppler from the apical position of the transducer using the section of the four-chamber view. The sample volume was placed at the level of the top of the mitral leaflets in the open position. Diastolic transmitral flow velocities (early [E] and late [A]), E/A ratio, and deceleration time of the LV were determined. Systolic function of the LV was determined using LV ejection fraction  and fractional shortening. The peak systolic (s′), as well as early (e′) and late (a′) diastolic mitral tissue velocities were measured at the medial and lateral side of the mitral annulus. E/e′ was also calculated.no effect (≤ 0.03), minimum effect (0.04–0.24), moderate effect (0.25–0.63), and strong effect (≥ 0.64). Associations between corrected QTd and echocardiographic parameters were determined using Pearson product-moment correlations with 95% confidence intervals (CIs). Correlation magnitudes were interpreted as27: trivial (0–0.10), small (0.11–0.30), moderate (0.31–0.50), large (0.51–0.70), very large (0.71–0.90), almost perfect (0.91–0.99), and perfect (1.00).Data were analyzed using IBM SPSS Statistics , with statistical significance accepted at p ≤ 0.05. Normality of all data was verified with quantile–quantile (Q-Q) plots, as well as skewness and kurtosis coefficients. All data are expressed as the mean ± standard deviation. Differences in general characteristics, electrocardiographic, and echocardiographic variables between long-distance runners, volleyball athletes, football athletes, powerlifters, bodybuilders, and sedentary controls were assessed using one-way analyses of variance (ANOVA) with Bonferoni post-hoc tests. The effect size of each ANOVA was determined using partial eta squared  different between groups. Post-hoc analyses revealed a significantly (p < 0.001) higher body height in volleyball athletes compared to all other groups. Also, BSA was significantly higher in volleyball athletes compared to long-distance runners (p = 0.031) and football athletes (p = 0.003). On the other hand, volleyball athletes possessed a significantly lower BMI compared to powerlifters (p = 0.005), bodybuilders (p < 0.001), and sedentary controls (p = 0.008). BMI was also significantly higher in bodybuilders (p < 0.001) and powerlifters (p = 0.022) compared to football athletes, as well as in bodybuilders compared to long-distance runners (p = 0.008). Body mass was significantly higher in bodybuilders compared to football athletes (p = 0.003).Body height, BSA, BMI, and body mass were significantly  different between groups. Post-hoc analyses revealed a significantly shorter RR-interval in sedentary controls compared to volleyball athletes (p = 0.004), football athletes (p < 0.001) and powerlifters (p = 0.001). Also, the RR-interval was significantly shorter (p < 0.001) in bodybuilders compared to football athletes. Bodybuilders and powerlifters exhibited a significantly higher QTd and corrected QTd (p < 0.001) compared to all other groups. In addition, sedentary controls exhibited a significantly higher QTd compared to long-distance runners (p < 0.001), volleyball athletes (p = 0.032), and football athletes (p < 0.001). Likewise, corrected QTd was significantly higher in sedentary controls (p < 0.001) compared to long-distance runners, volleyball athletes, and football athletes.RR-interval, QTd, and corrected QTd were significantly  different between groups. Post-hoc analyses revealed a significantly larger left atrium diameter in each athlete group  compared to sedentary controls. Sedentary controls displayed a significantly smaller aortic root diameter than volleyball athletes (p = 0.03), as well as a significantly smaller aortic root index than football athletes (p = 0.002). Further, a significantly larger LV end-diastolic diameter was observed in long-distance runners (p = 0.030), volleyball athletes (p < 0.001), and football athletes (p < 0.001) compared to sedentary controls, in volleyball athletes compared to bodybuilders (p < 0.001) and powerlifters (p < 0.001), as well as in long-distance runners (p = 0.023) and football athletes (p < 0.001) compared to bodybuilders. Likewise, volleyball athletes (p = 0.006) and football athletes (p = 0.011) had a significantly larger LV end-systolic diameter than bodybuilders. In addition, ISWT, PWT, and RWT were significantly larger in bodybuilders and powerlifters (p < 0.001) compared to long-distance runners, volleyball athletes, football athletes, and sedentary controls. ISWT and PWT were also significantly larger in volleyball athletes  and football athletes  compared to sedentary controls. LV mass was significantly heavier in each athlete group  compared to sedentary controls. Furthermore, LV mass was significantly heavier in powerlifters (p < 0.001) and bodybuilders (p = 0.009) compared to football athletes, as well as in powerlifters (p = 0.004) compared to long-distance runners. Likewise, LV mass index was significantly higher in each athlete group  compared to sedentary controls, as well as in long-distance runners (p = 0.007), volleyball athletes (p = 0.030), and football athletes (p < 0.001) compared to powerlifters.Structural parameters were significantly , football athletes , powerlifters , bodybuilders , and sedentary controls . Similarly, significant, moderate-large correlations were found between corrected QTd and PWT in long-distance runners , football athletes , powerlifters , and bodybuilders . Significant, moderate correlations were found between corrected QTd and LV index in football athletes , powerlifters , and bodybuilders . Also, corrected QTd was significantly (moderate-large) correlated with RWT in long-distance runners , LV end-diastolic diameter in volleyball athletes , LV end-systolic diameter in football athletes , and aortic root diameter in sedentary control .Significant, minimum) different between groups. A significantly higher LV ejection fraction was observed in long-distance runners (p < 0.001), volleyball athletes (p = 0.001), and football athletes (p = 0.014) compared to sedentary controls, in long-distance runners compared to powerlifters (p = 0.004) and bodybuilders (p < 0.001), as well as in volleyball athletes compared to bodybuilders (p = 0.011). Likewise, a significantly higher fractional shortening was observed in long-distance runners (p < 0.001), volleyball athletes (p < 0.001), and football athletes (p = 0.002) compared to sedentary controls, as well as in long-distance runners and volleyball athletes compared to powerlifters (p = 0.001 and p = 0.035) and bodybuilders (p < 0.001 and p = 0.007).LV ejection fraction and fractional shortening were significantly  and fractional shortening  only in football athletes.Significant inverse, minimum) different between groups. A significantly faster mitral valve inflow peak A (p = 0.006) was observed in bodybuilders compared to football athletes. Bodybuilders exhibited a significantly lower E/A ratio compared to long-distance runners (p = 0.016) and football athletes (p = 0.040). Furthermore, a significantly higher e'/a' was observed in volleyball athletes compared to football athletes (p = 0.029) and bodybuilders (p = 0.002), as well as in long-distance runners compared to sedentary controls (p < 0.001).Mitral valve inflow peak A, E/A ratio, and e'/a' were significantly . On the other hand, mild LV hypertrophy induced by volume overload in long-distance runners, volleyball athletes, and football athletes appears to be accompanied with a reduced QTd. These hypertrophic responses appear to be physiological adaptations to the exercise load stimuli experienced by each group of athletes, without impairing systolic and diastolic function.28 which found an exercise-induced bradycardia at rest resulting in a significantly (p < 0.001) longer RR-interval compared to sedentary controls. In this way, longer RR-intervals observed in long-distance runners, volleyball athletes, and football athletes were also accompanied by reduced QTd and corrected QTd compared to sedentary controls, powerlifters, and bodybuilders in our study. These findings contrast past observations reporting similar  or higher corrected QTd  in athletes from various sports compared to controls. Discrepancies in study findings may relate to several factors since exercise-induced adaptations produce varied cardiac remodeling in response to volume overload (during exercise involving isotonic muscle contractions) or pressure overload (during exercise involving isometric muscle contractions)29, as well as in male athletes compared to female athletes29, and in adults compared to adolescent or middle-aged athletes29. On the other hand, our findings agree with data reported in male athletes competing in highly dynamic sports who had a shorter corrected QTd compared to athletes predominantly undertaking static exercise  and sedentary controls . Previous evidence suggests that the nature of the stress on the heart (volume or pressure overload) predominantly determines the phenotype31. Although physiological hypertrophy is initially induced as a compensatory response to pressure overload, with concentric growth of the ventricle, this type of hypertrophy may progresses into pathological LV hypertrophy characterized by preferential cardiomyocytes thickening as opposed to lengthening, with sarcomeres aligned in parallel33. Intermittent pressure overload activates signaling pathways that lead to pathological molecular, structural, and functional changes dissimilar to changes seen following endurance-based exercise (swimming or running)33. In this regard, cardiovascular events and deaths have been reported to occur in a higher (p < 0.05) proportion of hypertensive patients with concentric hypertrophy  compared to eccentric hypertrophy 34. Collectively, our findings indicate reduced QTd in long-distance runners, volleyball athletes, and football athletes, which reflects homogeneous ventricular repolarization in dynamic-trained athletes compared to the general population and athletes predominantly undertaking static exercise35.We observed longer RR-intervals in most athlete groups  compared to sedentary controls. Our data align with meta-analytic evidence encompassing 298 participants who completed at least 4 weeks of aerobic exercise14. Together, these data parallel those observed in bodybuilders who were using large doses of androgenic anabolic steroids (range: 63–175 mg·day−1)19. In this previous research, bodybuilders exhibited longer corrected QTd  compared to sedentary controls19. While findings from our study should be interpreted cautiously due to participants self-reporting no anabolic steroid use, longer QTd in static-trained athletes compared to sedentary controls may relate to exercise-induced cardiac remodeling with increased ISWT17. In support of this assertion, existing evidence36 in hypertensive patients with LV hypertrophy suggests an increase in QTd occurs in patients with ISWT > 12 mm. Also, parallel increases in QTd and ISWT were further underpinned by correlation data for most athlete groups  and the sedentary controls we examined. Advanced LV hypertrophy, as we observed in powerlifters and bodybuilders, is associated with reduced action potential amplitude, reduced membrane potential, shortened action potential duration, or electrical quiescence in cardiac cells37, which may underpin the increased QTd in these groups. In turn, a better understanding regarding the role of cardiac mass and ISWT in mediating QTd needs to be elucidated in future research. In addition, future studies are warranted to investigate the mechanisms underlying the associations between QTd with PWT and LV mass.Both groups of predominantly static-trained athletes (powerlifiters: 60.3 ± 7.3 ms and bodybuilders: 57.4 ± 5.7 ms) possessed significantly greater corrected QTd compared to sedentary controls (48.0 ± 8.2 ms). Our findings align with previous cross-sectional data demonstrating a significantly (p < 0.01) higher corrected QTd in athletes mainly undertaking static exercise (elite gymnasts: 61.7 ± 9.3 ms) compared to non-athletes (45.6 ± 10.9 ms)2 and RWT < 0.42) or eccentric LV hypertrophy (LV mass index > 115 g/m2 and RWT < 0.42) were observed in most long-distance runners (58% and 33%), volleyball athletes (50% and 50%), and football athletes (56% and 41%) likely due to the chronic volume overload they experienced throughout their exercise history. On the other hand, concentric LV hypertrophy (LV mass index > 115 g/m2 and RWT > 0.42) was observed in most powerlifters (58%) and bodybuilders (54%) likely due to the chronic pressure overload they experienced throughout their exercise history. Further, athletes participating in dynamic sports  displayed ISWT (~ 11 mm) and LV PWT (~ 10 mm) within the normal range for the general population . In contrast, powerlifters and bodybuilders displayed ISWT (~ 12.5 mm) and LV PWT (~ 11.5 mm) exceeding the normal range for the general population. These structural parameters we observed in powerlifters and bodybuilders represent remodeling adaptations in response to training that fall within a 'grey zone' where extreme expressions of athlete’s heart and mild morphological forms of hypertrophic cardiomyopathy may overlap. Although these likely remodeling adaptations in powerlifters and bodybuilders mimic pathological hypertrophic cardiomyopathy, their LV end-diastolic diameters (~ 52–53 mm) were within clinically accepted partition values for the general population (45–55 mm), which is a useful and sensitive marker in distinguishing an athletic heart from hypertrophic cardiomyopathy diagnosis. Our results parallel to those reported in a previous meta-analysis10 including strength-trained athletes  who exhibited a significantly larger RWT  and ISWT , as well as a trend toward a larger PWT  compared to long-distance runners (n = 413). Collectively, the observed structural differences across groups may be considered as sport-specific physiological adaptations, that are largely benign and related to the exercise histories of each group.Our echocardiographic data indicative of structural parameters suggest different cardiac responses were apparent across groups, which is likely related to the stress imposed during the various forms of exercise they undertake. Given the different athlete groups predominantly completed dynamic  or static exercises (powerlifters and bodybuilders), distinct load-specific patterns in LV hypertrophy emerged among them. Namely, normal , further supporting adaptive  physiological cardiac remodeling in athlete groups predominantly undertaking dynamic  or static exercise (powerlifters and bodybuilders). Although we observed a significantly higher ejection fraction and fractional shortening at rest in long-distance runners compared to athletes mainly undertaking static exercise, as well as in athletes namely completing dynamic exercise compared to sedentary controls, effect size analyses revealed minimal10 showing comparable contractility between athletes predominantly undertaking dynamic exercise (long-distance runners: 68.8% [65.1–72.6%]), static exercise , or mixed exercise regimes (cyclists and rowers: 66.1% [62.9–69.3%]), and sedentary controls (67.2% [64.5–69.8%]). In contrast to our findings, some evidence suggests that male athletes predominantly undertaking dynamic exercise demonstrate diminished ejection fractions at rest compared to sedentary controls . An identified mechanism underlying the impaired LV contractility observed in endurance-trained athletes is LV cavity enlargement to assist in establishing adequate stroke volume to perfuse the body. In this regard, Abergel et al.41 reported a higher LV index (141 ± 21 g/m2) in world-class professional cyclists than we observed in long-distance runners (112 ± 11 g/m2), volleyball athletes (115 ± 14 g/m2), football athletes (112 ± 15 g/m2), powerlifters (128 ± 13 g/m2), and bodybuilders (120 ± 11 g/m2).In addition to LV structural parameters, LV systolic indicators were also within clinically accepted reference ranges for the general population . Compared to physiological cardiac hypertrophy, pathological hypertrophy is accompanied by disturbances in resting diastolic parameters. Specifically, in hypertensive patients increased LV mass and wall thickness is associated with diastolic filling abnormalities43. Comparable to concentric hypertrophy, it was found that eccentric LV hypertrophy produces diastolic filling pattern abnormalities in obese patients, characterized by diminished E/A ratio and prolonged deceleration time11. Nevertheless, our collective echocardiographic findings indicate cardiac variations between groups with different exercise histories occur primarily at a structural level rather than a functional level.Left ventricular diastolic function is commonly assessed with E/A ratio and eʹ-wave to help identify the nature of hypertrophy as well as deceleration time to indicate LV compliance. Given the reference limits for normal diastolic function are 0.8–2.0 for E/A ratio19. Second, our data are limited to males in selected sports. In turn, the provided results may not be indicative of female athletes and athletes competing in other sports  given cardiac remodeling and QTd have been shown to vary across sexes29 and load stimuli29. Third, although adult, national-level athletes with at least 3 years of training and competitive experience were recruited in our study, differences in the training programs undertaken across athletes may have contributed to the inter-individual variations in electrocardiographic and echocardiographic parameters. Fourth, in recruiting national-level participants across various sports, only 12 long-distance runners and 14 volleyball athlete participated in this study. Consequently, large cohort studies examining QTd and echocardiographic parameters in male and female athletes competing across a wider range of sports should be conducted in the future.Some limitations of our investigation should be acknowledged when interpreting the findings. First, use of performance-enhancing drugs was self-reported among participants with no urine or serum measurements taken. Accordingly, drug screening is warranted to ensure athletes are not using banned substances, which may affect cardiac remodeling and/or QTdOur findings suggest QTd and LV remodeling differs among athletes depending on the type of sport they compete in. Advanced LV hypertrophy, predominantly concentric in nature, was evident with an accompanying higher QTd in athletes predominantly undertaking static exercise (powerlifters and bodybuilders). On the other hand, LV hypertrophy toward the upper threshold of the normal reference range with an accompanying shorter QTd was apparent in athletes predominantly completing dynamic exercise . Our collective data indicate that athletes competing in various sports may experience alterations in structural cardiac parameters that reflect physiological hypertrophy with normal systolic and diastolic function. Despite physiological hypertrophy, significantly longer QTd in powerlifters and bodybuilders indicate that sports practitioners predominantly prescribing static exercise should regularly perform electrocardiographic and echocardiographic screening to assist in capturing impaired ventricular repolarization among their athletes.


Recently, a novel left atrioventricular coupling index (LACI) has been introduced providing prognostic value to predict cardiovascular events beyond common risk factors in patients without cardiovascular disease. Since data on cardiovascular magnetic resonance (CMR)-derived LACI in patients following acute myocardial infarction (AMI) are scarce, we aimed to assess the diagnostic and prognostic implications of LACI in a large AMI patient cohort.In total, 1046 patients following AMI were included. After primary percutaneous coronary intervention CMR imaging and subsequent functional analyses were performed. LACI was defined by the ratio of the left atrial end-diastolic volume divided by the left ventricular (LV) end-diastolic volume. Major adverse cardiac events (MACE) including death, reinfarction or heart failure within 12 months after the index event were defined as primary clinical endpoint.LACI was significantly higher in patients with MACE compared to those without MACE (p < 0.001). Youden Index identified an optimal LACI cut-off at 34.7% to classify patients at high-risk (p < 0.001 on log-rank testing). Greater LACI was associated with MACE on univariate regression modeling  and after adjusting for baseline confounders and LV ejection fraction (LVEF) on multivariate regression analyses . Furthermore, LACI assessment enabled further risk stratification in high-risk patients with impaired LV systolic function .Atrial-ventricular interaction using CMR-derived LACI is a superior measure of outcome beyond LVEF especially in high-risk patients following AMI.Trial registration ClinicalTrials.gov, NCT00712101 and NCT01612312The online version contains supplementary material available at 10.1186/s12968-023-00929-w. Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide although there have been substantial improvements in prognosis over the past decades . EffortsCurrently, little is known about the importance of left atrioventricular coupling and applicability and prognostic implications of LACI following AMI. Therefore, we aimed to assess the prognostic value of CMR-derived LACI in a large multicenter study of patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) treated by primary percutaneous coronary intervention (PCI).After undergoing primary PCI for AMI, 1168 patients underwent CMR imaging, amongst them 1046 had a complete and analyzable imaging data set and were included to this CMR substudy . To assess LV global longitudinal strain (GLS), LV epi- and endocardial borders were manually tracked in 2- and 4-chamber [Within 10 days after the index event an identical CMR protocol was applied in all patients. The protocol was performed on 1.5 or 3 T CMR scanners at the respective study sites including balanced steady-state free precession sequences (bSSFP) of long-axis 2- and 4-chamber views as well as short axis (SAx) stacks. Typical bSSFP sequence parameters were as follows: TR 3.2 ms, TE 1.2 ms, flip angle 60°, 8 mm slice thickness in SAx. More detailed information on CMR scan protocols have been published previously . Likewis-chamber . Likewis-chamber . After m-chamber . LACI was calculated as a ratio between CMR-derived LA EDV and LV EDV as previously defined . LA and LACI value is expressed as a percentage. Consequently, a higher LACI reflects a greater imbalance between the LA and LV volumes at ventricular end-diastole suggesting greater impairment of left atrioventricular coupling Fig. A. In addAll-cause mortality, reinfarction or heart failure associated with rehospitalization within the first year after AMI were counted as major adverse cardiac event (MACE), which was defined as the primary clinical endpoint of this study. In case of multiple occurrences of MACE within one patient, a prioritization was made as follows: death > reinfarction > heart failure. Furthermore, each patient could only account for one MACE.Categorical parameters are presented in absolute numbers and percentages while continuous parameters were tested for normal distribution using Shapiro–Wilk test and are reported as mean with interquartile range (IQR). For the assessment of correlations, the spearman´s rank correlation coefficient was used. Non-parametric Mann–Whitney U test was used for comparisons of continuous data sets. An optimal dichotomization cut-off value for LACI was determined using Youden’s Index. Moreover, patients with a LVEF ≤ 35% were classified as a high-risk group according to established clinical practice. To analyze occurrence of clinical endpoints the Kaplan–Meier method was applied and log-rank testing was used for assessing differences between groups. Cox proportional regression models were applied for the calculation of univariate hazard ratios (HRs) in context of MACE and mortality evaluation. Only variables with a p-value < 0.05 were included in further multivariable regression calculations. A stepwise approach with thresholds of 0.05 and 0.1 for p-values to keep or remove variables respectively was used in multivariate calculations. Due to significant correlations of LACI and LA or LV volumes only one of these parameters was included in multivariate regression models in each case. In addition, the improvement in discrimination by adding LACI to a risk prediction model containing LVEF was assessed using net reclassification improvement (NRI) and integrated discrimination improvement (IDI) measurements . ReproduA total of 1168 patients  underwent initial CMR imaging in median 3 days (IQR 2–4 days) after the acute index event. Due to incomplete scan protocol or insufficient image quality 1046 patients  entered final functional analyses for this study; 2 patients were lost to follow-up and not further included in outcome calculations . There was no difference of LACI between patients with STEMI or NSTEMI (p = 0.12). Underlying parameters of LA EDV and LV EDV significantly correlated . There was no correlation of LACI with LV functional parameters  but with LA functional parameters : r = -0.67, p < 0.001). A detailed overview of CMR parameters is displayed in Table Amongst the 1046 study patients that entered final outcome analyses, 73 MACE were documented during 1-year follow-up . In patients with MACE LACI was significantly higher compared to those patients without MACE   and remained significantly associated with MACE after adjusting for baseline confounders and LVEF on multivariate cox regression analyses   and heart failure  but not in those with reinfarction .Assessing the prognostic improvement in discrimination of different models, the addition of LACI to LVEF resulted in significant improvement using IDI p = 0.013) and continuous NRI (p = 0.02). Furthermore, Kaplan–Meier plots and using optimal cut-off values identified by Youden Index LACI assessment enabled further risk stratification in high-risk patients according to reduced LVEF ≤ 35% (p < 0.001 on log-rank testing) Fig. , while t3 and conThe aim of this work was to assess a novel CMR-derived LACI and confirm its prognostic value in a large cohort of patients with AMI.Recently, LACI was defined and proven to possess prognostic value as well as to improve risk classifications in the multi-ethnic population of the MESA study. Likewise, the results of our study demonstrated prognostic implications of this novel index in a large AMI patient cohort. Especially in patients at high-risk according to reduced LVEF LACI evaluation enabled further risk stratification and therefore could optimize clinical patient management.While commonly used volumetric analyses largely disregard the atrioventricular interplay, a combination of simultaneous LA and LV EDV measurements expressed by LACI can be suggested to allow evaluation of the holistic cardiac performance more accurately.Currently, many guideline recommendations and clinical decisions (e.g. for ICD device therapy) are mainly based on a LVEF cut-off of 35% which alone may not be sufficient for this purpose . ConsequOf note, the identified cut-off value of the current study was considerably higher than reported in previous literature . However. Furthermore, especially during end-diastole the LA is directly exposed to LV pressure making it an appropriate surrogate parameter for LV diastolic function [Since a greater LACI suggests an increased mismatch with a disproportionately enlarged LA in relation to LV, this index represents a simple approach to unmask several pathophysiological mechanisms of cardiac performance. LA size is considered as an appropriate barometer of LV filling pressure . Furtherfunction . In thisfunction  and besifunction , both LAfunction , 25. Whefunction . Howeverfunction  and to bfunction , 28. ConIt is noteworthy, that the alternatively calculated LACI ES showed no association with MACE in our study cohort, which, however, is in line with previous findings of the MESA study  and undeSimilar to the calculation of LACI, first imaging studies already applied and implemented functional deformation assessments to evaluate the atrioventricular interplay for optimized diagnostic and prognostic purposes , 32. EspHowever, although LACI assessment per se cannot replace or achieve a similar level of prognostic power like LA or LV strain parameters can provide, it is important to consider its role as an index parameter measuring atrioventricular proportions and a growing volumetric mismatch could indicate an aspect of cardiac functional failure that might not be adequately captured by (isolated) LA and/or LV strain deterioration. Consequently, not only amongst LA and LV volumetric analyses but also in addition to strain measurements LACI calculation could give clinicians additional prognostic data to identify patients at higher risk for MACE.Of note, deformation imaging relies on accurate data acquisition and compared to LACI calculation time-consuming post-processing . FurtherOur study has several limitations. CMR imaging was performed at several study sites using different CMR-vendors. However, all centers followed an identical study protocol and centralized image post-processing was performed in an experienced and blinded core laboratory. It is noteworthy, that an optimal timepoint for CMR imaging in patients following AMI is not known and, therefore, it cannot be excluded that further changes of atrioventricular coupling might occur at later stages after AMI. Due to contraindications and length of an CMR scanning procedure only stable and preselected patients were included in this study, which might lead to a selection bias with a lower event rate. Nevertheless, the study demonstrated significant associations of LACI with MACE which could be even more pronounced in the presence of more MACE.This study confirmed previous findings of calculating a CMR-derived LACI for optimizing risk stratification of cardiovascular events and demonstrated its usability and prognostic value in patients following AMI. LACI was significantly associated with MACE in AMI patients at 1-year follow-up and enabled better risk stratification than sole LA or LV volume analyses especially in high-risk patients according to reduced LVEF. Simple calculation of LACI adds a further valuable parameter for the identification of patients at higher risk for MACE and can be easily implemented in clinical routine.Additional file 1: Figure S1. Kaplan–Meier curves for survival analyses in subgroup of low-risk patients. Left atrioventricular coupling index (LACI) and survival in low-risk patients according to left ventricular ejection fraction (LVEF) after acute myocardial infarction. Incidence of MACE (major adverse cardiac events) according to high and low LACI classified according to Youden Index.


Among patients with wide QRS complexes of nonRBBB morphologies on ECG, there are those with preserved left septal Purkinje activation, i.e., intraventricular conduction delay (IVCD) . UnfortuIVCD and trueLBBB differ in the ventricular activation sequence. While during trueLBBB, LV lateral wall activation is postponed due to the trans-septal conduction delay, IVCDs have various LV activation patterns . Left veThe activation sequence of ventricular segments may be easily visualized using an ultra-high-frequency ECG (UHF-ECG). We hypothesized that by studying UHF-ECG ventricular activation sequences during the spontaneous rhythm and RVSP, we could discriminate between trueLBBB and IVCD and observe different responses to RV septal pacing.Ventricular depolarization patterns were visualized using UHF-ECG in two patients with heart failure and wide QRS complexes. Patient 1 had a history of transmural myocardial infarction of the anterior wall, left ventricular ejection fraction (LVEF) of 20%, and a spontaneous QRS complex of IVCD morphology with QRSd of 170 ms. Patient 2 had heart failure due to severe aortic regurgitation with an LVEF of 42% and developed a new-onset 1st-degree AV block with LBBB after transfemoral aortic valve insertion. RVSP was performed in both patients using a Select Secure 3830  lead. The pacing location was just below the level of the tricuspid valve, visualized using contrast or by identifying the position of the His bundle using another 3830 lead—Fig. In patient 1, the delay between V1 and V8 activation was 19 ms (Fig. Studied patients differed in their UHF-ECG ventricular activation sequence during spontaneous rhythm and RVSP. The patient with IVCD presented with minimal interventricular dyssynchrony and the latest activation under V5. On the other hand, the patient with a trueLBBB had significant dyssynchrony and the latest activation under lead V8 during spontaneous rhythm. RVSP resulted in a different set of changes in ventricular synchrony. In patient 1, the interventricular dyssynchrony increased due to the additional trans-septal delay, which was absent during spontaneous rhythm. In patient 2, UHF-ECG interventricular dyssynchrony decreased during RVSP. This happened because, during pacing of the basal interventricular septum, the trans-septal and consequent LV activation started immediately after pacing; however, RV lateral wall activation was postponed by the time interval required for the electrical wave-front to reach the right bundle branch Purkinje fibers located in the distal part of the RV septum.In patients with heart failure and wide QRS complexes on ECG, we demonstrated different ventricular activation patterns during a spontaneous rhythm and in response to RV septal pacing. Further research is needed to determine if the assessment of ventricular depolarization using UHF-ECG can discriminate between trueLBBB vs. IVCD or even those with mixed levels of block, i.e., a combination of trueLBBB and IVCD.


Noninvasive right ventricular (RV) myocardial work (RVMW) determined by echocardiography is a novel indicator used to estimate RV systolic function. To date, the feasibility of using RVMW has not been verified in assessing RV function in patients with atrial septal defect (ASD).Noninvasive RVMW was analysed in 29 ASD patients  and 29 age- and sex-matched individuals without cardiovascular disease. The ASD patients underwent echocardiography and right heart catheterization (RHC) within 24 h.The RV global work index (RVGWI), RV global constructive work (RVGCW), and RV global wasted work (RVGWW) were significantly higher in the ASD patients than in the controls, while there was no significant difference in RV global work efficiency (RVGWE). RV global longitudinal strain (RV GLS), RVGWI, RVGCW, and RVGWW demonstrated significant correlations with RHC-derived stroke volume (SV) and SV index. The RVGWI (area under receiver operating characteristic curve [AUC] = 0.895), RVGCW (AUC = 0.922), and RVGWW (AUC = 0.870) could be considered good predictors of ASD and were superior to RV GLS (AUC = 0.656).The RVGWI, RVGCW, and RVGWW could be used to assess RV systolic function and are correlated with RHC-derived SV and SV index in patients with ASD.The online version contains supplementary material available at 10.1186/s12947-023-00306-8 Atrial septal defect (ASD) is a common form of congenital heart disease with an estimated prevalence of 1 in 1000 live births . The ratEchocardiography plays a crucial role in the evaluation of RV function . TricuspRecently, noninvasive RV myocardial work (RVMW) by echocardiography was demonstrated as a novel and reliable indicator to assess RV systolic performance , 8. RVMWTo date, noninvasive RVMW has not been applied to assess RV systolic function in patients with ASD. Therefore, the present study was designed to achieve the following objectives: (i) compare the RVMW between ASD patients and healthy controls; (ii) explore the correlations between the noninvasive RVMW and RV stroke volume (SV) and SV index measured by right heart catheterization (RHC) in ASD patients; and (iii) explore the possibility of using RVMW indices to evaluate myocardial performance among patients with ASD.A total of 57 ASD patients (> 17 years of age) were prospectively recruited in Xiamen Cardiovascular Hospital between May and August of 2022. The study flow chart is shown in Fig. Transthoracic echocardiographic images were obtained by a Vivid E95 ultrasound system (GE Vingmed Ultrasound) according to the recommended protocols , 12. TwoThe LV ejection fraction, TAPSE, RV FAC, RV Sʹ, RV basal diameter, and tricuspid annular diameter were measured in line with the current guidelines , 4, 13. 2 + RA pressure (estimated by the inferior vena cava)  mmHg% vs. 22.0 [9.0-37.5] mmHg%, P < 0.001), while RVGWE showed no significant difference between ASD patients and controls.All enrolled patients had left-to-right colour Doppler shunts, and the median ASD size was 11.0 (8.0-18.5) mm. Table 2), RV cardiac output (8.9 ± 3.7 L/min), RV cardiac index (5.5 ± 2.4 L/min/m2) were increased in patients with ASD. SPAP calculated by RHC showed no significant difference from SPAP estimated by echocardiography . The mean Qp/Qs ratio was 1.9 ± 0.8 in the patients with ASD.RHC data of patients with ASD are summarized in Table r = -0.478, P = 0.009 and r = -0.488, P = 0.007, respectively), none of the standard echocardiographic parameters of RV systolic function were significantly correlated with RV SV or the RV SV index. However, RVGWI showed moderate correlations with RV SV and SV index , RVGCW showed weak correlations with RV SV and SV index , and RVGWW showed weak correlations with RV SV and SV index .The correlations between RHC-derived SV and SV index and the echocardiographic parameters of RV systolic function were calculated in the ASD group Table . Except ROC analysis was performed to determine whether standard echocardiographic parameters and RVMW indices could identify patients with ASD Table ; Fig. 3.Intra-observer and inter-observer variabilities of RVGWI, RVGCW, RVGWW, and RVGWE are presented in Table This study is a proof-of-concept study to identify the feasibility of using noninvasive RVMW in ASD patients. Assessing RVMW may enhance the understanding of the pathophysiology of RV myocardial systolic function in ASD patients.In our study, RV FAC showed no significant difference between ASD patients and controls, which was consistent with previous research . TAPSE aIn patients with ASD, there was an increased volume load on the right ventricle, which subsequently led to an enlargement of the RV cavity , 23. HowThe increased RV preload of ASD patients leads to an increase in the volume of blood in the pulmonary circulation and ultimately increases the afterload . The RVGCompared with TAPSE, RV FAC, RV Sʹ, and RV longitudinal strain, RVMW integrates myocardial systolic function, RV pressure and cardiac cycle into the RV PSL. The function of the right ventricle is more susceptible to afterload than that of the left ventricle . In addiExcept for RV GLS, none of the standard echocardiographic parameters were significantly correlated with RHC-derived SV or SV index. Conversely, the RVGWI, RVGCW, and RVGWE showed positive correlations with RHC-derived SV and SV index. According to the ROC analysis, the RVGWI, RVGCW, and RVGWE could be considered good predictors of ASD and are superior to load-dependent RV GLS. Although the correlations between the three RVMW indices and RHC-derived RV SV and SV index are weak and moderate, RVMW is the best noninvasive method to evaluate RV systolic function in ASD patients compare to standard RV systolic indices.Conventional echocardiographic RV systolic function parameters were used to examine RV myocardial contractile performance in ASD patients, but none of these parameters incorporated the effect of pre- or afterload on the right ventricle , 29–31. This study is a single-centre study, and the sample size of ASD patients included was small. Noninvasive RVMW was not validated by radionuclide ventriculography or cardiovascular magnetic resonance. Additionally, RVMW was acquired by using a single-provider platform specifically designed for measuring LVMW. The RV GLS was calculated by measuring the strains of the interventricular septum and RV free wall because of the irregular and complicated RV anatomy . TherefoRVGWI, RVGCW, and RVGWW are feasible indicators that assess RV systolic function and correlate with RHC-derived SV and SV index in patients with ASD. Noninvasive RVMW may predict RV systolic function and correlate with RHC-derived SV and SV index in patients with ASD, with possible prognostic implications. Further studies are required to verify the clinical role of noninvasive RVMW.Additional file 1: Supplementary Figure 1. Correlations of RV GLS, RVGWI, RVGCW, and RVGWWwith RHC-derived stroke volume and stroke volume index. GLS, globallongitudinal strain; RHC, right heart catheterization; RV, right ventricular;RVGCW, RV global constructive work; RVGWE, RV global work efficiency; RVGWI, RVglobal work index; RVGWW, RV global work waste. Additional file 2: Supplementary Figure 2. The Bland–Altman analysis for assessinginter-observer variability of right ventricular global work index (RVGWI),right ventricular global constructive work (RVGCW), right ventricular global wasted work (RVGWW), and right ventricular globalwork efficiency (RVGWE).


Type 2 diabetes (T2D) and obesity induce left ventricular (LV) dysfunction. The underlying pathophysiological mechanisms remain unclear, but myocardial triglyceride content (MTGC) could be involved.This study aimed to determine which clinical and biological factors are associated with increased MTGC and to establish whether MTGC is associated with early changes in LV function.A retrospective study was conducted using five previous prospective cohorts, leading to 338 subjects studied, including 208 well-phenotyped healthy volunteers and 130 subjects living with T2D and/or obesity. All the subjects underwent proton magnetic resonance spectroscopy and feature tracking cardiac magnetic resonance imaging to measure myocardial strain.via end-systolic volume index  and stroke volume index , but not with longitudinal strain . Interestingly, the associations between MTGC and strain measures did not persist in multivariate analysis. Furthermore, MTGC was independently associated with LV end-systolic volume index , LV end-diastolic volume index , and LV mass .MTGC content increased with age, body mass index (BMI), waist circumference, T2D, obesity, hypertension, and dyslipidemia, but the only independent correlate found in multivariate analysis was BMI . MTGC was correlated to LV diastolic dysfunction, notably with the global peak early diastolic circumferential strain rate , the global peak late diastolic circumferential strain rate  and global peak late diastolic longitudinal strain rate . MTGC was also correlated to systolic dysfunction Predicting MTGC remains a challenge in routine clinical practice, as only BMI independently correlates with increased MTGC. MTGC may play a role in LV dysfunction but does not appear to be involved in the development of subclinical strain abnormalities. The dramatic rise in prevalence rates of obesity and type 2 diabetes (T2D) has led to an increasing risk of cardiovascular disease and death , 2. Epid1H-MRS) techniques enabling accurate non-invasive exploration of myocardial steatosis in humans  and LV diastolic dysfunction in patients with T2D , and only used data collected before the intervention (bariatric surgery or antidiabetic medication) from patients enrolled in interventional studies   . All proth percentile) against subjects with high MTGC (MTGC >75th percentile).The subjects were categorized into two groups based on clinical status: a healthy group, or a non-healthy (i.e. living with T2D and/or obesity) group. They were also categorized based on MTGC quartiles in order to compare subjects with low MTGC  and glucose profile (fasting plasma glucose (FPG), fasting plasma insulin (FPI) and HbA1c). Insulin resistance was assessed based on the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) calculated as follows: fasting plasma glucose (mmol/L) × fasting plasma insulin (mUi/mL)/22.5 .1H-MRS to assess left ventricular structure and function and MTGC. MRI exams were performed using a 3T scanner  using a 32-element phased array coil.All subjects underwent cardiovascular MRI and Data on cardiac structure and function was obtained using a steady-state free precession (SSFP) cine sequence in short-axis view covering the left ventricle from base to apex. End-systolic volume (ESV), end-diastolic volume (EDV), and LV mass were measured using dedicated vendor-supplied post-processing software . Left ventricular stroke volume (SV), cardiac output and ejection fraction (LVEF) were then calculated. SV, ESV, EDV, LV mass and cardiac output were indexed to body surface area. To determine LV diastolic function, velocity-encoded mitral valve inflow images were used to derive early (E) and late (A) peak diastolic transmitral flow velocities using an Argus workstation for quantitative flow analysis, as previously described . MTGC was determined and expressed as a percentage of tissue water content (%TG = TG/water × 100) with the resonances of triglycerides and water integrated in the frequency domain and taking into account the saturation due to incomplete relaxation.To determine the molecular content of triglycerides and water in the myocardium, an ECG-gated, single-voxel, point-resolved spectroscopy sequence (PRESS) was used, as previously described , 23–25. LV myocardial strain was quantified on cine SSFP images using a feature tracking (FT) software developed in Matlab  and previously employed in several studies –31. To ibetareg package in R  and R statistical software (version 4.1.3). Data were expressed as mean ± standard deviation (SD) when normally distributed, and as median (interquartile range) when non-normally distributed. A Fisher test was performed to compare qualitative variables between the two groups. Quantitative variables were compared using an unpaired t-test when the data was normally distributed, or a Mann-Whitney U test otherwise. Bivariate correlations were performed using Pearson or Spearman coefficients, as appropriate. We also performed multivariate analysis using generalized linear models to assess the effect of MTGC independently of other variables. MTGC was modeled using a beta distribution (the age in R ). To takInter-rater reproducibility was evaluated for peak strain measurements by two independent readers on four subjects. Intra-rater reproducibility was evaluated by repeating strain measurements four times in four different subjects by the same observer at intervals of a few days between each measurement. Intra-observer reproducibility was excellent, with a coefficient of variation of 2.1% for GCS and 5.5% for GLS. Inter-observer reproducibility was satisfactory, with a coefficient of variation of 1.7% for GCS and 2.3% for GLS.The baseline characteristics of subjects included in this study are reported in Subjects living with T2D or obesity were significantly older and had a higher BMI and higher waist circumference than healthy subjects. Among the 101 subjects living with T2D, median duration since onset of disease was 8 years  and median HbA1c was 7.38% . In total, 91 subjects were taking biguanides, 52 were taking sulfonylureas and glinides, and 21 were taking DPP-IV inhibitors. No subjects were taking iSGLT2.As expected, insulin resistance assessed by HOMA-IR was significantly higher in subjects living with T2D and/or obesity than in healthy volunteers .Analysis of biochemical parameters showed that even when subjects living with T2D or obesity were treated by lipid-lowering drugs, they nevertheless had significantly higher plasma triglycerides  and significantly lower plasma high-density lipoprotein (HDL) cholesterol  than healthy subjects.Participants were categorized based on MTGC quartiles Figure 2As expected, subjects living with T2D had higher MTGC  than subjects with no T2D . Likewise, subjects with obesity, hypertension or dyslipidemia had higher MTGC than healthy subjects. In a subgroup analysis, comparing patients with low MTGC quartiles versus patients with high MTGC quartiles in the healthy subjects subgroup and the T2D and/or obesity patients subgroup, a higher proportion of T2D patients was found in the high MTGC quartile as expected Table 3AAs shown in the flowchart Figure 1As patients living with T2D or obesity were significantly older and had a higher BMI than the healthy subjects, all subsequent analyses were adjusted for age, gender, and BMI. Subjects living with T2D or obesity had a significantly higher concentricity index and higher LV mass (p<0.0001) and significantly lower cardiac index, ventricular volumes , mitral peak E-wave velocity and E/A ratio (p<0.0001) than healthy subjects , peak E-wave velocity and mitral E/A ratio were significantly lower in the high MTGC subgroup than in the low MTGC subgroup (p<0.0001) Table 4.In a subgroup analysis, comparing patients with low MTGC quartiles versus patients with high MTGC quartiles in the healthy subjects subgroup and the T2D and/or obesity patients subgroup, only ESV and EDV were still significantly lower in high MTGC subjects in the T2D and/or obesity patients subgroup  and to LV mass Table 5BRegarding systolic strain parameters, MTGC was not correlated with GLS . Regarding diastolic strain parameters, MTGC was negatively correlated with EDSRc  and positively correlated with LDSRc and LDSRl  Table 5AMultivariate analysis showed that the diastolic strain parameters, both EDSRc and LDSRl remained independently associated with MTGC  even after adjusting for age, gender, BMI, hypertension, and T2D Table 5CTo the best of our knowledge, this is the first study using MRI to assess the effect of MTGC on early LV function changes in such a large cohort of very well-phenotyped healthy volunteers and non-healthy subjects without heart failure.The main findings of this study were: 1) among the many clinical and biological parameters studied, BMI was the only independent correlate of MTGC; 2) MTGC was independently associated with LV volumes and LV mass; 3) MTGC was not independently associated with systolic and diastolic strain measures.As previously reported , 33, MTGth percentile), which highlights the hypothesis that BMI alone cannot predict MTGC and that it is therefore important to look further than BMI alone to phenotype ectopic fat depots in patients living with metabolic disease and unhealthy obesity.In multivariate regression analyses, only BMI was found to be an independent determinant of MTGC, but all the parameters included in the analysis together explained only 20% of the MTGC variance, suggesting that obesity per se is not sufficient to cause myocardial steatosis. In addition, 14 healthy volunteers were found to belong to the high MTGC quartile subgroup (MTGC > 75via lipolysis to the myocardium, but chronic accumulation of triglycerides in the myocardium could drive an overload of toxic lipid intermediates that could, along with other processes such as inflammation or fibrosis, contribute to LV dysfunction (Studies conducted in healthy volunteers have shown that a short-term very-low-calorie diet leads to an accumulation of myocardial triglyceride , 37 and function , 41. We function , 42. On function –45.1H-MRS human studies report similar associations (Multiple animal studies , 10 suppciations –51, but ciations , 15. Furciations  found a ciations . HoweverFor several years now, myocardial strain and strain rates have emerged as key parameters for detecting subclinical alteration in LV function, and are now displacing conventional cardiac function parameters for LV function analysis –55. MyocRegarding systolic strain, very few studies have found an association between MTGC and LV systolic dysfunction, and only a handful of them performed a strain measurement , 51, 60.MTGC was correlated to diastolic function abnormalities, and notably with the global peak early diastolic circumferential strain rate, which is one of the main parameters currently used to study diastolic function in MTGC studies , 61. In Regarding early diastolic dysfunction, myocardial steatosis was also found to be independently associated with impaired diastolic strain rate. Ng et al.  studied Nyman et al. found that MTGC was not a determinant of diastolic function, whereas it was correlated with early LV diastolic dysfunction in univariate analysis . LikewisPatients living with T2D or obesity have traditionally been characterized as having diastolic dysfunction with normal systolic function , 67. WhiThis work has some strengths. It was performed in a large cohort of subjects, whereas to our knowledge, most previous MTGC studies were performed on small cohorts with less than a hundred subjects. Moreover, we only included subjects who were free of heart failure, in order to analyze the early abnormalities of LV function. Regarding strain measurement, we used MRI-FT, which is a promising tool with good feasibility and reproducibility for global strain measurement . In addi1H-MRS is an established non-invasive method that has demonstrated high diagnostic accuracy for the assessment of myocardial steatosis (However, this study has also some limitations. First, other biomarkers could have been considered to predict MTGC, such as β-hydroxybutyrate, a ketone body that may be inversely associated with increased MTGC . Unfortuteatosis . Third, In conclusion, in a large cohort of healthy and non-healthy subjects, only BMI remained independently associated with increased MTGC in multivariate analysis, which suggests the existence of unknown factors to predict the rise of MTGC. Further prospective studies are required in order to identify these factors.Using MRI to study myocardial triglyceride content and systolic and diastolic LV function simultaneously with MRI-FT tracking for strain measurement, we found that MTGC is associated with LV dysfunction. However, this relationship is non-linear, and MTGC does not appear to be involved in early changes in LV function. The impact of myocardial steatosis on LV function therefore remains a matter of ongoing debate, and future longitudinal studies are needed in a large cohort of healthy and non-healthy age-matched subjects in order to conclusively determine whether increased MTGC is associated with LV dysfunction.The original contributions presented in the study are included in the article/The studies involving human participants were reviewed and approved by NCT01284816, NCT02042664, NCT03118336. The patients/participants provided their written informed consent to participate in this study.All authors contributed to the article and approved the submitted version.


The cardiac magnetic resonance tissue tracking (CMR-TT) technique was used to obtain left atrial strain and strain rate in patients with myocardial infarction (MI) and to evaluate the utility of this technique in the quantitative assessment of myocardial infarction for distinguishing acute from chronic myocardial infarction.We retrospectively analyzed 36 consecutive patients with acute myocardial infarction (AMI) and 29 patients with chronic myocardial infarction (CMI) who underwent CMR and 30 controls. Left atrial (LA) and ventricular functions were quantified by volumetric, and CMR-TT derived strain analysis from long and short left ventricular view cines. Receiver Operating Characteristics (ROC) analysis was used to determine the diagnostic accuracy of CMR-TT strain parameters for discriminating between acute and chronic myocardial infarction.p < 0.001) and LA functional parameters (p < 0.001), but there was no difference between AMI and normals.AMI and CMI participants had impaired LA reservoir function, conduit function and LA booster pump dysfunction compared to the controls. LA strain was more sensitive than LV global strain for the assessment of the MI stage. Peak late-negative SR yielded the best areas under the ROC curve (AUC) of 0.879, showing differentiation between acute and chronic myocardial infarction of all the LA strain parameters obtained. The highest significant differences between chronic myocardial infarction and normal myocardium were also found in the LV strain (CMR-TT-derived LA strain is a potential and robust tool in demonstrating impaired LA mechanics and quantifying LA dynamics, which have high sensitivity and specificity in the differential diagnosis of acute versus chronic myocardial infarction. Their use is thus worth popularizing in clinical application. Myocardial infarction (MI) is caused by a substantial decrease or complete cessation of blood flow to a portion of the myocardium, causing the damaged tissue to be replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. Subsequent compensatory fibrosis of the injured myocardium is prone to systolic and diastolic dysfunction . MI is aCardiovascular magnetic resonance tissue tracking (CMR-TT) technology has been widely used in clinical research and practice for a variety of heart diseases in recent years, which is an approach to assess myocardial deformation from steady-state free precession (SSFP) cine CMR by the tracking of tissue voxel motion . CMR-TT In this study, we aim to compare the impact on LA function between patients with AMI and CMI, as assessed through simultaneous LA and LV structural and functional analyses using CMR-TT, and explore the capability of LA function and strain for distinguishing AMI from CMI.Between January 2016 and December 2021, 36 consecutive patients with AMI and 29 patients with CMI who received CMR examination at our hospital were retrospectively recruited in this study, with an equal gender and age distribution. Inclusion criteria for patients with AMI were as follows: (1) the patients had to have a first-time AMI with an identified culprit coronary vessel;(2) All patients received successful reperfusion therapy by percutaneous coronary intervention. AMI was diagnosed by history, electrocardiographic changes, cardiac biomarker abnormalities, and coronary angiography following the consensus of the American College of Cardiology and the European Society of Cardiology . The incStudy participants underwent cardiac MRI with clinical 1.5T scanners. We obtained tissue characterization and function in two- and four-chamber long-axis views and short-axis images of the left ventricle with cardiac vector ECG and respiratory gating for scanning. The scan parameters of cine images of Philips Achieva were: TR/TE = 3.38/1.69 ms, FOV: 69.8 cm×32 cm; layer thickness 8 mm, layer interval 2 mm, matrix 192 × 180, and flip angle 60°. Gadopentetate glucosamine (Gd-DTPA) was used as the contrast agent at a dose of 0.2 mmol/kg and an infusion rate of 2.0 ml/s. After the contrast agent was injected, 20 ml of saline was injected at the same rate, and delayed enhancement scans of the heart were done 15 min after the contrast agent was injected intravenously. The delayed enhancement scan parameters were TR/TE = 6.12/3.00 ms, layer thickness 8 mm, layer spacing 2 mm, matrix 152 × 200.All CMR analysis was performed offline using commercially available software . The left ventricular function parameters were performed by drawing out the endo- and epicardial border on LV short-axis cine images (papillary muscles were excluded). The software automatically tracked the displacement of the endocardium and epicardium to quantify the left ventricular myocardium movement. And then, the LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), LV ejection fraction (LVEF), LV cardiac output (CO), LV cardiac index (CI), and LV mass (LVM) were well obtained. LV strain values were acquired by autonomously tracking the deformation of myocardial motion during the cardiac cycle, including left ventricle global peak strain radial (LV-GPSr), left ventricle global peak strain circumferential (LV-GPSc) and left ventricle global peak strain longitudinal (LV-GPSl). LGE was taken as the golden standard to identify infarcted segments. Infarct size was defined as the hyper-enhanced area with a signal intensity threshold ≥ 5 standard deviations (SD) above the remote myocardium’s mean signal intensity.LA volumetric indices were measured by semi-automated tracing of the LA endocardial and epicardial border in end-systole and end-diastole in long-axis two- and four-chamber views excluding pulmonary veins and the LA appendage. Maximum LA volumes were assessed in ventricular end-systole (LAVmax), at ventricular diastole before atrial contraction (LAVpac), and at late ventricular diastole after atrial contraction (LAVmin). Left atrial fractions were defined as fractional volume changes according to the following equations: LA total EF = (LAVmax − LAVmin) × 100%/LAVmax, LA passive EF = (LAVmax − LAVpre-a) × 100%/LAVmax, LA active EF = (LAVpre-a − LAVmin) × 100%/LAVpre-a. The software automatically derived the strain and strain rate values for each tissue point and was represented as a strain curve from which LA strain and strain rate for each period were recorded  in 20 randomly selected subjects . Intra-observer reproducibility was established by the same observer who re-analyzed the same 20 subjects after 1 Month. Inter-observer reproducibility was assessed by two investigators blinded to each other’s results.P value < 0.05 indicated a statistically significant difference.SPSS version 26.0  was used for statistical analyses. Normally distributed continuous variables were verified using Kolmogorov–Smirnov test. Measurement data were expressed as mean ± SD. Categorical variables were compared using Fisher’s exact test or χ2 tests. Comparisons of continuous variables among three groups were performed using one-way analysis of variance (ANOVA), followed by the Tukey or Games-Howell post hoc pairwise comparison test, respectively. Categorical variables were expressed as numbers and percentages. Independent samples t-test was used to compare the global left ventricular strain and Infarct volume in patients with AMI and CMI. The Receiver Operating characteristic Curve (ROC) was used to analyze the value of LA strain and strain rate parameters in identifying AMI and CMI. Initially, 81 patients were included; however, 11 patients were excluded due to poor image quality, and five patients were dropped because no LGE images were available. In the final study cohort, 36 patients with AMI and 29 patients with CMI were included for analysis in this study with sample size- and sex-matched controls. There were no significant differences in gender or body Mass Index among the three groups. The complete baseline characteristics were shown in Table As shown in Table p < 0.05). The CMI, however, had a lower maximal capacity than acute patients(p = 0.047). LA total EF, passive and active EF showed significantly reduced in CMI cases compared to those in AMI and controls. Left atrial reservoir, conduit functional, and booster pump parameters, including strain and strain rate, showed significantly different among these three groups  Figs.  and 4.Of all the LA strain and strain rate parameters obtained, SRa yielded the best AUC Fig.  of 0.879LA volumetric and deformation parameters were reproducible on an intra- and inter-observer level. The CV% and ICC were summarized in Table The current study investigated the diagnostic accuracy of LA function and strain parameters by CMR-TT for differentiating between AMI and CMI. Our findings demonstrate using quantitative tissue approaches in noncontrast methods can be used to detect the stage of MI. Based on the LA deformation and strain measurement, LA strain and strain rate are the predominant parameters for differentiating AMI from CMI. The results of our study provide several vital advances: (I) there were significant differences in the strain and strain rate parameters among AMI, CMI, and controls; these parameters could be utilized to track the stage of myocardial infarction in MI patients; (II) SRa of LA was the best at differentiating between AMI and CMI, with high diagnostic accuracy in all patients; (III) Patients with acute and chronic myocardial infarction can be identified by LA function parameters; however, there is no difference between the AMI and normal groups; (IV) The left global ventricular strain cannot be utilized the key difference between AMI and CMI. As a result, quantitative measurement of LA strain and strain rate could be a valuable tool for non-invasive evaluation, detection, and differentiation of acute and chronic infarction.LA function is closely related to changes in overall heart function, which has significance for clinical research. Echocardiographic imaging of myocardial deformation can reveal impairments of LA function. Still, CMR is the “gold standard” for evaluating cardiac morphology and function with high accuracy and repeatability that allows comprehensive evaluation of left atrial structure and function from multiple perspectives . In our LA modulates LV diastolic filling and cardiac performance during hemodynamic stress or exertion by reservoir, conduit, and booster pump functions . PreservLeft ventricular performance and LVEF are most often quantified to assess cardiac function in cardiovascular diseases . This stMyocardial strain analysis has been developed as a more accurate evaluation of myocardial deformation, with the potential to overcome the limitations of EF and contribute to assessing global and regional myocardial deformation during the cardiac cycle , 42. PreThis study’s major limitations might be explained by its small sample size and the individual variation between the participants. Larger samples would still be needed to determine the diagnostic threshold and promote the quantitative diagnosis between AMI and CMI afforded by this technology. Secondly, there is no classification of the duration of CMI. It’s probable that the longer it lasts, the more prominent alterations in left cardiac parameters will be. Thirdly, differences in strain measurements caused by various scan machines cannot be excluded.CMR-TT-derived LA strain is a potential and robust tool in demonstrating impaired LA mechanics and quantifying LA dynamics, which have high sensitivity and specificity in the differential diagnosis of acute versus chronic myocardial infarction, and its use is thus worth popularizing in clinical application.


Left ventricular (LV) remodeling is a dynamic process, which is characterized by changes in ventricular size, shape, and wall thickness, thus altering myocardial geometry and function, and is considered as a negative prognostic factor in patients with heart failure (HF). Hypertension, type 2 diabetes (T2D), and obesity are strongly correlated with the development and the progression of LV remodeling, LV hypertrophy, and LV systolic and/or diastolic dysfunction. Indeed, the beneficial impact of exercise training on primary and secondary prevention of cardiovascular disease (CVD) has been well-established. Recent studies have highlighted that exercise training enhances functional capacity, muscle strength and endurance, cardiac function, and cardiac-related biomarkers among patients with established coronary artery disease (CAD) or HF, thus substantially improving their cardiovascular prognosis, survival rates, and need for rehospitalization. Therefore, in this review article, we discuss the evidence of LV remodeling in patients with cardiometabolic risk factors, such as hypertension, T2D, and obesity, and also highlight the current studies evaluating the effect of exercise training on LV remodeling in these patients. It is estimated that more than 26 million adults suffer from heart failure (HF) worldwide, with the prevalence rates growing rapidly . AccordiLV remodeling is a dynamic process, which is characterized by changes in ventricular size, shape, and wall thickness, thus altering myocardial geometry and function . It is cMany complex and multifactorial mechanisms resulting in transcriptional, signaling, structural, and electrophysiological changes are involved in this process of LV remodeling. More specifically, oxidative stress and altered intracellular calcium metabolism provoke cardiomyocyte hypertrophy, thus resulting in impaired contraction and relaxation, as well as an increased risk for fatal ventricular arrythmias and sudden cardiac death . Of noteOn the one hand, LV remodeling predicts adverse clinical outcomes, and possible regression seems to limit them, thus improving patient prognosis. On the other hand, short-term improvement in LV remodeling mediated by novel pharmaceutical agents and medical devices is associated with long-term improvement of clinical outcomes among patients with LV dysfunction . More spIn this review article, we discuss the evidence of LV remodeling among patients with cardiometabolic risk factors, such as hypertension, T2D, and obesity, and we also focus on current studies evaluating the effect of exercise training on LV remodeling in these patients.Exercise training typically increases heart rate and blood pressure, leading to specific cardiac changes among healthy individuals, especially highly trained athletes . This coInterestingly, athletes may have a 15–20% increase in LV wall thickness, a 10% increase in LV cavity size, and a 24% increase in RV cavity size. LV thickness up to 15 mm is commonly apparent in most athletes, while the most thickened region is the anterior portion of the ventricular septum . NeverthChronic hemodynamic overload in hypertension provokes major structural and functional changes leading to LVH. More specifically, chronically increased blood pressure can cause LV pressure overload, thus increasing the LV workload and resulting in LVH . This clTypical echocardiographic structural findings, including concentric remodeling, concentric hypertrophy or even a combination of concentric and eccentric hypertrophy, along with increased LV wall thickness and LV diastolic and systolic dimensions, have been described. Interestingly, healthy individuals, who do not exceed blood pressure levels above 150 mmHg during exercise, do not stimulate cardiac remodeling, and as a result, they are less likely to develop LVH . So far,T2D is a systemic disease with detrimental macro- and micro-vascular complications. Patients with T2D have a 2.5-fold increased risk to develop HF independently of age or concomitant comorbidities, such as CAD and dyslipidemia, whereas these patients represent one third of the HF population in clinical trials . The terDiabetes-induced LV diastolic dysfunction caused by prolonged and delayed LV filling and relaxation is often presented in the absence of concomitant impairments in LV systolic function . MoreoveObesity is a multifactorial metabolic disorder characterized by a heterogeneous complex of biological, socioeconomic, and environmental factors leading to adverse health outcomes . AccordiObesity is associated with atherosclerosis, abnormalities in the coronary microvasculature, and as a result, an increased risk for CAD. Furthermore, excess adipose tissue accumulation leads to major hemodynamic changes, including plasma volume expansion increased blood pressure, cardiac output, as well as myocardial wall stress . EctopicAccording to the current literature, exercise training leads to a substantial reduction in resting systolic and diastolic blood pressure, as well as in LVH among hypertensive patients ,38, as pTurner et al. were among the first to report that exercise training may induce regression of LVH and LV concentric remodeling among patients with mild or moderate hypertension . SpecifiFurthermore, low-fit individuals with hypertension seem to have a higher LV mass index when compared to the moderate and high-fit individuals . In thisSo far, there is evidence that exercise training may improve both LV systolic and diastolic function in patients with diabetes, resulting in favorable changes in stroke volume, LVEF, end-systolic volumes, as well as LV filling . Both enFurthermore, Otten et al. reported that supervised exercise training (3 weeks/hour) paired with a paleolithic diet  resulted in favorable metabolic and cardiac changes with a decrease in triglycerides levels and LV mass to end-diastolic volume ratio and an increase in LVEDV and stroke volume, among overweight and obese patients with T2D . SimilarPhysical activity improves LVH among patients with obesity and hypertension. In more details, higher physical activity was associated with a reduction in the LV mass index and an improvement in LVH, as well as cardiac biomarkers, such as N-terminal pro-atrial natriuretic peptide (NT-pro BNP) and a mid-regional sequence of pro-A-type natriuretic peptide (MR pro-ANP) . SimilarMain studies evaluating the effect of exercise training on LV remodeling in patients with cardiometabolic risk factors, such as hypertension, T2D, and obesity, are summarized below in LV remodeling following acute myocardial infraction (AMI) is a complex process characterized by fibroblast proliferation, collagen deposition, scar formation, as well as ventricular expansion, resulting in LV dysfunction and HF, thus negatively affecting long-term prognosis in these patients . The benExercise training started early after STEMI reduces stress-induced hypoperfusion and improves LV function and contractility. Exercise-induced changes in myocardial perfusion and function is associated with the absence of unfavorable LV remodeling and with an improvement of cardiovascular functional capacity . The benObesity and physical inactivity are considered major lifestyle risk factors for the development and progression of HFpEF . Indeed,Physical activity and fitness substantially reduce the risk of developing HF and improve the cardiovascular prognosis among patients with established HF . InteresAccording to the current literature, exercise training has been associated with a substantial improvement in LV diastolic function . MoreoveOne possible explanation for the favorable effect of exercise training on LV remodeling is the reduction in blood pressure . AfterloMoreover, increased vasculogenesis through the activation of endothelial progenitor cells ameliorates ischemia and reperfusion injury. Exercise modifies shear stress conditions and further modulates the bioavailability of endothelial nitric oxide (NO), which limits oxidative burden, thus promoting vasodilation and improving vascular endothelial function . SpecifiMoreover, an exercise-mediated reduction in myocardial collagen has been also described. So, another possible mechanism of an exercise-mediated improvement in LV dysfunction is the upregulation of miRNA-29, which has been associated with a drop in collagen gene expression . MoreoveAccording to the 2019 American College of Cardiology (ACC) in collaboration with (AHA) Guideline on the Primary Prevention of CVD, in general, healthy individuals should undergo at least 150 min/week of accumulated moderate-intensity physical activity. Otherwise, 75 min/week of vigorous-intensity physical activity to reduce the risk of atherosclerotic CVD . In totaThe European Association of Preventive Cardiology Exercise Prescription in Everyday Practice and Rehabilitative Training (EXPERT) tool is an interactive, digital training, and support system, which aims to help sports medicine specialists, family physicians, cardiologists, and other medical specialists prescribe clinically effective and medically safe exercise training programs for patients with established CVD or cardiometabolic risk factors . In furtImproving exercise capacity and optimizing safety of cardiorespiratory programs play a pivotal role in promoting cardiovascular health. Exercise training exerts beneficial changes to LV remodeling, thus improving cardiac function and structure among patients with cardiometabolic risk factors. These favorable effects are mainly attributed to positive hemodynamic changes in vascular function, cardiac energy metabolism, and autonomic balance. This has the potential to be most impactful in primary care health facilities and countries with limited resources. Implementing basic exercise programs might be a cost-effective strategy to prevent and manage CVD among patients with cardiometabolic risk factors, especially in resource-constrained settings. Thus, it is of major importance that a guided, detailed, and personalized exercise prescription is offered by all physicians based on the individual’s behavioral habits and wishes and cardiovascular profile and needs, so as to achieve better treatment, as well as health outcomes.