Myocardial Mechanics Research Articles

Early cardiovascular involvement in dengue fever: A prospective study with two-dimensional speckle tracking echocardiography

Cardiac abnormalities in dengue infection have been conventionally identified by clinical manifestations. The primary objective of our prospective observational study was to assess true cardiovascular involvement and early myocarditis in 150 hospitalised, confirmed cases of dengue fever, through myocardial strain detection using two-dimensional speckle tracking echocardiography. Myocarditis was defined on the basis of European Society of Cardiology (ESC) 2013 criteria. Cardiac biomarkers, namely, creatine phosphokinase myocardial band was elevated in 28.6% and Troponin-T in 23.3% patients. Electrocardiography was abnormal in 64.6% while 6% patients had two-dimensional structural echocardiographic abnormalities. Myocardial dysfunction was suspected in 27.3% based on ESC criteria and strain analysis. The severe dengue group had lower longitudinal strain [-16.4 (6.3)] and circumferential strain [-15.7 (6.7)]. Two-dimensional speckle tracking echocardiography was found to be useful in improving the understanding of early myocardial mechanics in dengue fever.

Galectin-3 and sST2: associations to the echocardiographic markers of the myocardial mechanics in systemic sclerosis – a pilot study

BackgroundProgressive cardiac fibrosis is the central aspect of the myocardial involvement in systemic sclerosis (SSc). We hypothesized that circulating biomarkers of the cardiac fibrosis may be useful in the early diagnosis of the cardiac manifestation in this disease. Thus, we investigated the potential correlations between the levels of galectin-3, soluble suppression of tumorigenicity-2 (sST2) and the echocardiographic markers of the myocardial mechanics in SSc patients.MethodsForty patients (57.3 ± 13.7 years, 36 female) were investigated. In addition to the conventional echocardiography, tissue Doppler and speckle tracking-derived strain techniques were used to assess the function of both ventricles and atria. To estimate the correlations between galectin-3 and sST2 levels and the echocardiographic variables, partial correlation method was used with age as correcting factor.ResultsIn age adjusted analysis galectin-3 level showed significant correlation with left ventricular global longitudinal strain (r = 0.460, p = 0.005); grade of left ventricular diastolic dysfunction (r = 0.394, p = 0.013); septal e’ (r = − 0.369, p = 0.021); septal E/e’ (r = 0.380, p = 0.017) and with the grade of mitral regurgitation (r = 0.323, p = 0.048). No significant correlation was found between sST2 levels and the echocardiographic variables.ConclusionsGalectin-3 levels, but not sST2 levels show significant correlation with the parameters of the left ventricular systolic and diastolic function. Galectin-3 may be a useful biomarker for the screening and early diagnosis of SSc patients with cardiac involvement.

Left Ventricular Mechanics Differ in Subtypes of Aortic Stenosis Following Transcatheter Aortic Valve Replacement.

BackgroundLeft ventricular (LV) mechanics are impaired in patients with severe aortic stenosis (AS). We hypothesized that there would be differences in myocardial mechanics, measured by global longitudinal strain (GLS) recovery in patients with four subtypes of severe AS after transcatheter aortic valve replacement (TAVR), stratified based upon flow and gradient.MethodsWe retrospectively evaluated 204 patients with severe AS who underwent TAVR and were followed post-TAVR at our institution for clinical outcomes. Speckle-tracking transthoracic echocardiography was performed pre- and post-TAVR. Patients were classified as: (1) normal-flow and high-gradient, (2) normal-flow and high-gradient with reduced LV ejection fraction (LVEF), (3) classical low-flow and low-gradient, or (4) paradoxical low-flow and low-gradient.ResultsBoth GLS (−13.9 ± 4.3 to −14.8 ± 4.3, P < 0.0001) and LVEF (55 ± 15 to 57 ± 14%, P = 0.0001) improved immediately post-TAVR. Patients with low-flow AS had similar improvements in LVEF (+2.6 ± 9%) and aortic valve mean gradient (−23.95 ± 8.34 mmHg) as patients with normal-flow AS. GLS was significantly improved in patients with normal-flow (−0.93 ± 3.10, P = 0.0004) compared to low-flow AS. Across all types of AS, improvement in GLS was associated with a survival benefit, with GLS recovery in alive patients (mean GLS improvement of −1.07 ± 3.10, P < 0.0001).ConclusionsLV mechanics are abnormal in all patients with subtypes of severe AS and improve immediately post-TAVR. Recovery of GLS was associated with a survival benefit. Patients with both types of low-flow AS showed significantly improved, but still impaired, GLS post-TAVR, suggesting underlying myopathy that does not correct post-TAVR.

Left atrial phasic echocardiographic functional analysis in relation to diastolic left ventricular hemodynamic parameters acquired during right heart catheterization

IntroductionDoppler echocardiography has become the leading non-invasive tool for hemodynamic screening and follow-up in various clinical situations. Our objective was to assess whether left atrium (LA) functional echocardiographic parameters correlate with hemodynamic left ventricle (LV) filling parameters measured during right heart catheterization (RHC) in various disease states.MethodsEchocardiographic examinations of 71 consecutive patients that had RHC within 24 h were studied retrospectively using LA/LV feature tracking analysis. Echocardiographic and myocardial mechanics characteristics were then correlated with the RHC findings.ResultsThe best correlation were demonstrated between the trans-tricuspid gradient in the echocardiogram and the right ventricle (RV) systolic pressure in the RHC (R2 = 0.41, p < 0.0001). Mitral E/E’ annular velocity ratio did not correlate with capillary wedge pressure (CWP) while E velocity correlated significantly with CWP (R2 = 0.29, p = 0.0007). Among 38 patients in sinus rhythm, echocardiographic diastolic dysfunction strongly correlated with elevated LA pressure in RHC (CWP ≥ 12 mmHg, p = 0.001), with 96% sensitivity and 80% specificity. LA minimal volume index (LAVmin-i) as measured by echocardiogram was significantly correlated with elevated LA pressure in RHC (p = 0.04, criterion ≥ 27 ml) regardless of rhythm.ConclusionsIn patients with sinus rhythm, diastolic dysfunction was found to be sensitive and specific for elevated CWP ≥ 12 mmHg at RHC. In all patients regardless of rhythm, LAVmin-i was found to correlate best with elevated LA pressure at RHC. This may suggest a new tool for assessment of diastolic dysfunction in all subjects.

Effects of dispersed fibres in myocardial mechanics, Part II: active response.

This work accompanies the first part of our study "effects of dispersed fibres in myocardial mechanics: Part I passive response" with a focus on myocardial active contraction. Existing studies have suggested that myofibre architecture plays an important role in myocardial active contraction. Following the first part of our study, we firstly study how the general fibre architecture affects ventricular pump function by varying the mean myofibre rotation angles, and then the impact of fibre dispersion along the myofibre direction on myocardial contraction in a left ventricle model. Dispersed active stress is described by a generalised structure tensor method for its computational efficiency. Our results show that both the myofibre rotation angle and its dispersion can significantly affect cardiac pump function by redistributing active tension circumferentially and longitudinally. For example, larger myofibre rotation angle and higher active tension along the sheet-normal direction can lead to much reduced end-systolic volume and higher longitudinal shortening, and thus a larger ejection fraction. In summary, these two studies together have demonstrated that it is necessary and essential to include realistic fibre structures (both fibre rotation angle and fibre dispersion) in personalised cardiac modelling for accurate myocardial dynamics prediction.

Multiphysics Computational Modelling of the Cardiac Ventricles.

Development of cardiac multiphysics models has progressed significantly over the decades and simulations combining multiple physics interactions have become increasingly common. In this review, we summarise the progress in this field focusing on various approaches of integrating ventricular structures. electrophysiological properties, myocardial mechanics, as well as incorporating blood hemodynamics and the circulatory system. Common coupling approaches are discussed and compared, including the advantages and shortcomings of each. Currently used strategies for patient-specific implementations are highlighted and potential future improvements considered.

Effects of dispersed fibres in myocardial mechanics, Part I: passive response.

It is widely acknowledged that an imbalanced biomechanical environment can have significant effects on myocardial pathology, leading to adverse remodelling of cardiac function if it persists. Accurate stress prediction essentially depends on the strain energy function which should have competent descriptive and predictive capabilities. Previous studies have focused on myofibre dispersion, but not on fibres along other directions. In this study, we will investigate how fibre dispersion affects myocardial biomechanical behaviours by taking into account both the myofibre dispersion and the sheet fibre dispersion, with a focus on the sheet fibre dispersion. Fibre dispersion is incorporated into a widely-used myocardial strain energy function using the discrete fibre bundle approach. We first study how different dispersion affects the descriptive capability of the strain energy function when fitting to ex vivo experimental data, and then the predictive capability in a human left ventricle during diastole. Our results show that the chosen strain energy function can achieve the best goodness-of-fit to the experimental data by including both fibre dispersion. Furthermore, noticeable differences in stress can be found in the LV model. Our results may suggest that it is necessary to include both dispersion for myofibres and the sheet fibres for the improved descriptive capability to the ex vivo experimental data and potentially more accurate stress prediction in cardiac mechanics.

Left atrial volumetric and functional properties in hemophilia – insights from a three-dimensional speckle-tracking echocardiographic MAGYAR-Path study

Hemophilia is an inherited disorder due to deficiencies in factor VIII (type A) and factor IX (type B). Abnormalities in myocardial mechanics could be theorized due to hemophilia-associated hypocoagubility and related quantitative and qualitative changes of the blood. The present study aimed a detailed assessment of left atrial (LA) volumetric and functional properties in patients with hemophilia using three-dimensional speckle-tracking echocardiography (3DSTE). The study consisted of 12 subjects with hemophilia type A and 2 cases with hemophilia type B (mean age: 40.8 ± 19.1 years, all males). Results of hemophilia patients were compared to that of 23 age-, gender- and risk factor-matched controls (42.4 ± 9.0 years, all males). Routine two-dimensional Doppler echocardiography and 3DSTE were performed in all subjects. LA volumes respecting cardiac cycle did not differ between controls and hemophilia patients. From LA volume-based functional properties, LA stroke volumes were similar between the groups examined in all phases of LA function. While total atrial emptying fraction featuring LA reservoir function was reduced in patients with hemophilia compared to that of controls, passive and active atrial emptying fraction characterizing LA conduit and booster pump functions were similar between the groups. From LA strains, peak mean segmental circumferential and longitudinal LA strains were impaired in patients with hemophilia, other peak LA strains were similar between the groups. LA strains at atrial contraction did not differ between groups of hemophilia patients and controls. Hemophilia is not associated with LA volumetric changes, but mild LA functional abnormalities are present.

Liposomal nanoparticle-based miR-155 antagonist regulates Th17/Treg signaling pathway and its inhibitory effect against myocarditis

Abnormal expression of miR-155 is related to degree of myocardial fibrosis in myocarditis. This study mainly explored the role of miR-155 in myocardial fibrosis and possible mechanisms. Forty Balb/c mice were randomly separated into blank group, model group, miR-155 group, and DMSO group (n = 10). Fibrosis area and expression of TGF-β and α-SMA in each group were observed. Fibroblasts were then isolated and miR-155mRNA expression, expression of Collagen I, α-SMA, Th17 cell number, Treg cell number, and expressions of IL-6, IL-10, IL-17, STAT3, RORγt, and Foxp3 were also investigated. The model group and DMSO group had the highest fibrosis area, while the blank group and miR-155 group had the lowest fibrosis area. However, the fibrosis area for miR-155 group was higher than the blank group (P &gt;0.05). No significant difference was found between model group and DMSO group (P &gt;0.05). Compared to blank and miR-155 groups, expressions of TGF-β and α-SMA in the model and DMSO group were significantly up-regulated (P &lt;0.05). No significant difference was found between the model and DMSO groups, or between blank and miR-155 groups P &lt; 0.05). Compared to blank and miR-155 groups, the levels of Collagen I, α-SMA, IL-6, IL-10, IL-17, STAT3, RORγt, and Foxp3 in the model and DMSO groups were significantly up-regulated (P &gt; 0.05). No significant difference was found between model and DMSO groups, or between blank and miR-155 groups (P &lt; 0.05). The number of Th17 cells was significantly increased, while Treg cells were significantly decreased in the model and DMSO groups (P &lt; 0.05). In contrast, Th17 cells were significantly decreased, while Treg cells were significantly increased in the blank and miR-155 groups (P &lt; 0.05). No significant difference was found between the model and DMSO groups, or between blank and miR-155 groups (P &lt; 0.05). Moreover, miR-155 inhibited myocarditis and myocardial fibrosis. The mechanism is mainly related to Th17/Treg signaling pathway, where miR-155 decreased Th17 cells, increased Treg cells, inhibited the secretion of Collagen I and α-SMA, and reduced the levels of fibroblast molecules. The miR-155 also interacted with STAT3 pathway to stimulate the activity of inflammatory cells, inhibit the secretion of inflammatory factors, further improving the inflammatory response of myocarditis, and ultimately improving the degree of myocarditis myocardial fibrosis.

Диспластическое сердце. Деформация миокарда левого желудочка при недифференцированной дисплазии соединительной ткани

Cardiac syndromes occupy a special place among the manifestations of undifferentiated connective tissue dysplasia (UCTD), since it is the severity of dysplastic stigmatization of the cardiovascular system (CVS) that determines the individual life and work prognosis in people with UCTD. Predicting adverse cardiovascular events is relevant, in particular, for young women with UCTD, since protecting the health of such patients in a critical demographic situation in the country (low birth rate and high mortality) is one of the most important tasks of modern medicine. Ultrasound estimation of myocardial deformation indicators in clinical practice provides accurate information about the early stages of cardiovascular diseases (CVD) with a preserved ventricular ejection fraction (EF), which makes it possible to detect early violations of myocardial mechanics and subclinical signs of heart failure (HF).

Acute myocardial damage in new coronavirus infection (COVID-19)

Introduction. Acute respiratory distress syndrome (ARDS) and cardiovascular events, acute myocardial injury being the most frequent of the latter, are among the leading causes of death in COVID-19 patients. The lack of consensus on acute myocardial injury pathogenesis mechanisms, the patients management, treatment an rehabilitation logistics, the anticoagulant treatment in identified SARS-CoV-2 or suspected COVID-19 patients setting indicates the need to assess, analyze and summarize the available data on the issue.Materials and methods. Scientific publications search was carried out in PubMed, Google Scholar databases for the period from December 2019 to September 2021.Results and Discussion. Cardiospecific troponin I increase beyond reference limits is reported to occur in at least every tenth patient with identified SARS-CoV-2, the elevated troponin detection rate increasing among persons with moderate to severe course of the infection. The mechanisms of acute myocardial injury in patients with COVID-19 are poorly understood. By September 2021, there are several pathogenesis theories. A high frequency viral myocarditis direct cardiomyocytes damage is explained by the high SARS-CoV-2 affinity to ACE2 expressed in the myocardium. The cytokine storm related myocardial damage is reported a multiple organ failure consequence. Coagulopathy may also trigger myocardial microvessels damage. Up to every third death of SARS-CoV-2 infected persons is related to the acute myocardial injury. At the same time, due to the high incidence of the acute myocardial injury, it is rather difficult to assess the true incidence of acute myocardial infarction in patients with COVID-19. In the pandemic setting, the waiting time for medical care increases, the population, trying to reduce social contacts, is less likely to seek medical help. In this regard, in order to provide effective medical care to patients with acute myocardial infarction, it is necessary to develop algorithms for providing care adapted to the current epidemiological situation.Conclusion. The treatment of patients with probable development of acute myocardial damage against the background of new coronavirus infection should be performed in accordance with the current clinical guidelines. Anticoagulant therapy should be administered in a prophylactic dose under control of hemostasis parameters and a wide range of biochemical parameters.

Plasma Exosomes at the Late Phase of Remote Ischemic Pre-conditioning Attenuate Myocardial Ischemia-Reperfusion Injury Through Transferring miR-126a-3p.

Background: Remote ischemic pre-conditioning (RIPC) alleviated the myocardial ischemia-reperfusion injury, yet the underlying mechanisms remain to be fully elucidated, especially at the late phase. Searching a key component as a transfer carrier may provide a novel insight into RIPC-mediated cardioprotection in the condition of myocardial ischemia-reperfusion.Objective: To investigate the cardioprotective effect of plasma exosomes at the late phase of RIPC and its potential signaling pathways involved.Methods and Results: Exosomes were isolated from the plasma of rats 48 h after the RIPC or control protocol. Although the total plasma exosomes level had no significant change at the late phase of RIPC (RIPC-exosome) compared with the control exosomes (Control-exosome), the RIPC-exosome afforded remarkable protection against myocardial ischemia-reperfusion (MI/R) injury in rats and hypoxia-reoxygenation (H/R) injury in cells. The miRNA array revealed significant enrichment of miR-126a-3p in RIPC-exosome. Importantly, both miR-126a-3p inhibitor and antagonist significantly blunted the cardioprotection of RIPC-exosome in H/R cells and MI/R rats, respectively, while miR-126a-3p mimic and agomir showed significant cardioprotection against H/R injury in cells and MI/R injury in rats. Mechanistically, RIPC-exosome, especially exosomal miR-126a-3p, activated the reperfusion injury salvage kinase (RISK) pathway by enhancing the phosphorylation of Akt and Erk1/2, and simultaneously inhibited Caspase-3 mediated apoptotic signaling.Conclusions: Our findings reveal a novel myocardial protective mechanism that plasma exosomes at the late phase of RIPC attenuate myocardial ischemia-reperfusion injury via exosomal miR-126a-3p.

CMR-derived myocardial strain analysis differentiates ischemic and dilated cardiomyopathy\u2014a propensity score-matched study

Left ventricular (LV) longitudinal, circumferential, and radial motion can be measured using feature tracking of cardiac magnetic resonance (CMR) images. The aim of our study was to detect differences in LV mechanics between patients with dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) who were matched using a propensity score-based model. Between April 2017 and October 2019, 1224 patients were included in our CMR registry, among them 141 with ICM and 77 with DCM. Propensity score matching was used to pair patients based on their indexed end-diastolic volume (EDVi), ejection fraction (EF), and septal T1 relaxation time (psmatch2 module L Feature tracking provided six parameters for global longitudinal, circumferential, and radial strain with corresponding strain rates in each group. Strain parameters were compared between matched pairs of ICM and DCM patients using paired t tests. Propensity score matching yielded 72 patients in each group (DCM mean age 58.6 ± 11.6 years, 15 females; ICM mean age 62.6 ± 13.2 years, 11 females, p = 0.084 and 0.44 respectively; LV-EF 32.2 ± 13.5% vs. 33.8 ± 12.1%, p = 0.356; EDVi 127.2 ± 30.7 ml/m2 vs. 121.1 ± 41.8 ml/m2, p = 0.251; native T1 values 1165 ± 58 ms vs. 1167 ± 70 ms, p = 0.862). There was no difference in global longitudinal strain between DCM and ICM patients (− 10.9 ± 5.5% vs. − 11.2 ± 4.7%, p = 0.72), whereas in DCM patients there was a significant reduction in global circumferential strain (− 10.0 ± 4.5% vs. − 12.2 ± 4.7%, p = 0.002) and radial strain (17.1 ± 8.51 vs. 21.2 ± 9.7%, p = 0.039). Our data suggest that ICM and DCM patients have inherently different myocardial mechanics, even if phenotypes are similar. Our data show that GCS is significantly more impaired in DCM patients. This feature may help in more thoroughly characterizing cardiomyopathy patients.

Myocardial Mechanics in Hypertensive Disorders of Pregnancy: a Systematic Review and Meta-Analysis.

Global longitudinal strain (GLS) is becoming routinely used to direct the medical management of various cardiac diseases, but its application in pregnancy is unclear. Our objective was to perform a meta-analysis and pool multiple study data to consolidate the evidence base for the role of GLS in the assessment of women with hypertensive disorders of pregnancy (HDP). Electronic database searches were performed in PubMed/Medline and EMBASE for research articles reporting GLS in pregnancies complicated by HDP and normotensive pregnancies that have been published up to September 2021. The meta-analysis included 17 studies with a pooled sample size of 1723 participants, which included 951 women with HDP, of which 680 were preeclamptic, and 772 controls. The primary random-effects pooled analysis demonstrated a statistically significant weighted mean difference in GLS between the HDP and control group (mean difference: 3.08% [CI, 2.33-3.82], P<0.001). When analyzed including only preeclamptic studies, there was also a statistically significant mean difference (mean difference: 2.98% [95% CI, 1.97-3.99], P<0.001). This meta-analysis demonstrates that HDP is associated with greater cardiac maladaptation, evidenced by a significantly reduced GLS compared with normal pregnancy. Echocardiography should be considered as a screening tool in women with HDP to enable early cardiovascular risk prevention through national initiatives.

Abstract 13167: Multiscale Mechanisms of Right Ventricular Injury in Bronchopulmonary Dysplasia

Introduction: Bronchopulmonary dysplasia (BPD) is the most common complication of premature birth. Whether right ventricular (RV) injury or chronically increased afterload are more responsible for long-term RV dysfunction in BPD is unknown. We aim to determine key drivers of RV dysfunction in BPD using both experimental data and a computational model. We hypothesize that decreased mitochondrial energetics and active force generation are critical contributors. Methods: Male and female Sprague-Dawley rats were delivered at term to timed-pregnant dams and exposed to either room air (Nx) or 85% fraction inspired O 2 (Hx) for 4, 8, or 14 days. Multiscale experimental data was obtained at postnatal day 21 and used to parameterize the previously published computational model of the heart and circulation, which integrates myocardial mechanics and mitochondrial energetics. Results: Despite increased RV afterload in the 8-and 14-day exposure groups (Fig. 1A) and significant RV hypertrophy in the 14-day group (Fig. 1B), there was no change in ejection fraction (EF) due to high variability (Fig. 1C). We used the computational model to explore how multiscale features of RV injury impact RV EF (Fig. 1D). Whereas decreased mitochondrial function, decreased cross-bridge maximum force, and increased RV afterload further reduce predicted RV EF in the 14-day Hx rat with the lowest EF (red symbol) and RV EF in the 14-day Nx rat with the highest EF (blue symbol), EF can be restored in a simulated reversal of these injuries in the Hx rat. Conclusions: Our approach provides valuable insight into key features of RV injury in BPD. Different degrees and combination of injuries at multiple scales can explain functional heterogeneity and may enable more accurate predictions of long-term RV dysfunction. Figure 1: Measurements of (A) RV afterload, (B) RV Fulton index and (C) RV EF as well as computational model predictions of (D) RV EF for one 14D Hx (red) and one 14D Nx rat (blue).

Abstract 14008: Three Dimensional Surface Strain Computation From Three Dimensional Echocardiographic Images of the Right Ventricle in Idiopathic Pediatric Pulmonary Hypertension

Introduction: Right Ventricular (RV) dysfunction is the primary aspect of acute right ventricular failure, commonly realized in pulmonary arterial hypertensive (PAH) patients. As a standard clinical assessment for PAH, echocardiographic strain provides a mechanical measure of ventricular deformation during RV contraction. Current strain computation via 2D echo is limited in that imaging and strain are confined to a 2D plane, and thus the technique is unable to fully visualize the asymmetrical deformation of the RV. We believe 3D surface (3DS) strain, obtained from 3D echo (3DE) will overcome this limitation and more thoroughly evaluate myocardial mechanics. In this initial work, we hypothesize that end-systolic 3DS longitudinal and shear freewall strain group means computed from 3DE-cardiac data of the RV will differ between healthy and PAH patient groups. Methods: 3DS strain (longitudinal, circumferential, shear; principal strains, principal angle, and max shear) was computed on the RV freewall at end-systole with finite element analysis post-processing techniques from RV surface meshes obtained from 3DE from 10 normal children and 43 children with idiopathic PAH. Results: 3DS longitudinal and circumferential strain group means were significantly different (p&lt;0.0001, p=0.0002, respectively), and the 3DS shear strain mean difference approached significance (p=0.0532). Further, the 3DS max and min principal strain group means were also different (p=0.0001, p&lt;0.001, respectively), as were the max shear strain group means (p=0.0275), while the group mean difference of the principal strain angle approached significance (p=0.1055). Conclusions: These results suggest that 3DS strain is a promising approach to strain computation with potential to yield more mechanical knowledge of different segments of RV dysfunction. Future work should be directed in the evaluation of focused regional strain specific towards RV dysfunction and evaluate for prognosis.

Abstract 11382: Left and Right Ventricular Strain Mechanics in Fetal Arrhythmia

Introduction: Assessment of ventricular mechanics in fetuses with tachyarrhythmia poses significant challenges. Strain analysis measures myocardial deformation and has been shown to be a very sensitive marker of ventricular systolic dysfunction compared to traditional measurements. Global and regional myocardial deformation has not been well described in fetuses with arrhythmias. Hypothesis: We hypothesize that left and right ventricular myocardial mechanics are impaired in fetuses with tachyarrhythmias compared to normal fetuses in sinus rhythm. Methods: Retrospective review of fetuses with tachyarrhythmia (groups 1 and 2) and gestational age (GA) matched normal fetuses with normal cardiac anatomy (group 3) from 2000 to 2018 at a single institution, with IRB approval. Fetuses with isolated ectopy and congenital heart disease were excluded from all groups. Strain analysis was performed using VVI software. Arrhythmia type, medications, cardiovascular profile score and postnatal outcome were collected. Results: 18 fetuses with tachyarrhythmia with GA between 21 to 36.5 weeks were analyzed; 18 fetuses of similar GA with normal cardiac anatomy in sinus rhythm served as controls. 3 fetuses were delivered close to term and did not have strain assessment in sinus rhythm. Both LV global longitudinal strain (-4.44 ± 2.82%) and strain rate (-1.24 ± 0.85%) and RV global longitudinal strain (-6.76 ± 2.09%) and strain rate (-1.41 ± 0.55%) were reduced in tachyarrhythmia (Group 1) and recovered when in sinus rhythm (Group 2) but still reduced compared to controls (Group 3). Global longitudinal velocity was not different between patients in Group 2 and 3 (Table &amp; Fig 1). Conclusions: Strain parameters remain abnormal in fetuses with tachyarrhythmia despite conversion to sinus rhythm when compared to GA matched controls. Serial evaluation of strain will help guide therapy and monitor ventricular function in this patient population.

Physical exercise attenuates stress-induced hypertension in rats but not the impairments on the myocardial mechanics.

Acute and chronic stresses have become a health problem in the contemporary society, and prolonged exposure to stressful events are related to the pathogenesis of cardiovascular diseases. Physical exercise is a well-recognized effective nonpharmacological therapy for cardiovascular diseases and stress-induced injuries. Thus, this study evaluated the effect of exercise on the cardiac remodelling of chronically stressed rats. Wistar adult rats were used (n = 10 each group) and chronic stress protocol consisted of restricting movement in individual rodent restrainers (60 min, 5 days/week, 12 weeks); and exercise consisted of swimming sessions in a pool (60 min, 5 days/week, 12 weeks). During protocol, blood pressure was measured in conscious rats, and at the end cardiac morphology/function was assessed. Animals exposed to stress exhibited continuous rise in blood pressure from the sixth week, but exercise attenuated it. Similarly, restrained rats increased serum corticosterone compared with nonstressed rats, but exercise also prevented it. No changes were found in cardiac mass, but chronic stress not only impaired the steady state contractions of the cardiac muscle, but also reduced inotropic responses to stretching, increasing calcium and beta-adrenergic receptor stimulation. Despite this, exercise was unable to prevent these functional impairments induced by stress, and instead, the association of stress and physical exercise worsened myocardial compliance. Despite the known benefits to the cardiovascular system, our results indicate that aerobic swimming exercise for 12 weeks reduced blood pressure but did not impede the chronic stress-induced myocardial damages in rats.

Left ventricular mechanical, cardiac autonomic and metabolic responses to a single session of high intensity interval training.

High-intensity interval training (HIIT) produces significant health benefits. However, the acute physiological responses to HIIT are poorly understood. Therefore, we aimed to measure the acute cardiac autonomic, haemodynamic, metabolic and left ventricular mechanical responses to a single HIIT session. Fifty young, healthy participants completed a single HIIT session, comprising of three 30-s maximal exercise intervals on a cycle ergometer, interspersed with 2-min active recovery. Cardiac autonomics, haemodynamics and metabolic variables were measured pre-, during and post-HIIT. Conventional and speckle tracking echocardiography was used to record standard and tissue Doppler measures of left ventricular (LV) structure, function and mechanics pre- and post-HIIT. Following a single HIIT session, there was significant post-exercise systolic hypotension (126 ± 13 to 111 ± 10mmHg, p < 0.05), parallel to a significant reduction in total peripheral resistance (1640 ± 365 to 639 ± 177dyne⋅s⋅cm5, p < 0.001) and significant increases in baroreceptor reflex sensitivity and baroreceptor effectiveness index (9.2 ± 11 to 24.8 ± 16.7ms⋅mmHg-1 and 41.8 ± 28 to 68.8 ± 16.2, respectively) during recovery compared to baseline. There was also a significant increase in the low- to high-frequency heart rate variability ratio in recovery (0.7 ± 0.48 to 1.7 ± 1, p < 0.001) and significant improvements in left ventricular global longitudinal strain (- 18.3 ± 1.2% to - 29.2 ± 2.3%, p < 0.001), and myocardial twist mechanics (1.27 ± 0.72 to 1.98 ± 0.72°·cm-1, p = 0.028) post-HIIT compared to baseline. A single HIIT session is associated with acute improvements in autonomic modulation, haemodynamic cardiovascular control and left ventricular function, structure and mechanics. The acute responses to HIIT provide crucial mechanistic information, which may have significant acute and chronic clinical implications.

Myocardial adaptation and exercise performance in patients with pulmonary arterial hypertension assessed with patient-specific computer simulations.

Myocardial function and exercise reserve are important determinants of outcome in pulmonary arterial hypertension (PAH) but are incompletely understood. For this study, we performed subject-specific computer simulations, based on invasive measurements and cardiac magnetic resonance imaging (CMR), to investigate whole circulation properties in PAH at rest and exercise and determinants of exercise reserve. CMR and right heart catheterization were performed in nine patients with idiopathic PAH, and CMR in 10 healthy controls. CMR during exercise was performed in seven patients with PAH. A full-circulation computer model was developed, and model parameters were optimized at the individual level. Patient-specific simulations were used to analyze the effect of right ventricular (RV) inotropic reserve on exercise performance. Simulations achieved a high consistency with observed data. RV contractile force was increased in patients with PAH (127.1 ± 28.7 kPa vs. 70.5 ± 14.5 kPa, P < 0.001), whereas left ventricular contractile force was reduced (107.5 ± 17.5 kPa vs. 133.9 ± 10.3 kPa, P = 0.002). During exercise, RV contractile force increased by 1.56 ± 0.17, P = 0.001. In silico experiments confirmed RV inotropic reserve as the important limiting factor for cardiac output. Subject-specific computer simulation of myocardial mechanics in PAH is feasible and can be used to evaluate myocardial performance. With this method, we demonstrate marked functional myocardial adaptation to PAH in the resting state, primarily composed of increased contractile force development by RV myofibers, and we show the negative impact of reduced RV inotropic reserve on cardiac output during exercise.NEW & NOTEWORTHY Computer simulations of the myocardial mechanics and hemodynamics of rest and exercise were performed in nine patients with pulmonary arterial hypertension and 10 control subjects, with the use of data from invasive catheterization and from cardiac magnetic resonance. This approach allowed a detailed analysis of myocardial adaptation to pulmonary arterial hypertension and showed how reduction in right ventricular inotropic reserve is the important limiting factor for an increase in cardiac output during exercise.