BACKGROUND: Behavior change support systems (BCSSs) have the potential to help people maintain healthy lifestyles and aid in the self-management of coronary heart disease (CHD). The Persuasive Systems Design (PSD) model is a framework for designing and evaluating systems designed to support lifestyle modifications and health behavior change using information and communication technology. However, evidence for the underlying design principles behind BCSSs for CHD has not been extensively reported in the literature.
OBJECTIVE: This scoping review aims to identify existing health BCSSs for CHD, report the characteristics of these systems, and describe the persuasion context and persuasive design principles of these systems based on the PSD framework.
METHODS: Using the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews) guidelines, 3 digital databases (Scopus, Web of Science, and MEDLINE) were searched between 2010 to 2022. The major inclusion criteria for studies were in accordance with the PICO (Population, Intervention, Comparison, and Outcome) approach.
RESULTS: Searches conducted in the databases identified 1195 papers, among which 30 were identified as eligible for the review. The most interesting characteristics of the BCSSs were the predominant use of primary task support principles, followed by dialogue support and credibility support and the sparing use of social support principles. Theories of behavior change such as the Social Cognitive Theory and Self-Efficacy Theory were used often to underpin these systems. However, significant trends in the use of persuasive system features on par with behavior change theories could not be established from the reviewed studies. This points to the fact that there is still no theoretical consensus on how best to design interventions to promote behavior change in patients with CHD.
CONCLUSIONS: Our results highlight key software features for designing BCSSs for the prevention and management of CHD. We encourage designers of behavior change interventions to evaluate the techniques that contributed to the success of the intervention. Future research should focus on evaluating the effectiveness of the interventions, persuasive design principles, and behavior change theories using research methodologies such as meta-analysis.

Human cystic echinococcosis (CE) is a parasitic infection caused by the larval stage of the tapeworm Echinococcus granulosus sensu lato, primarily affecting the liver and lungs. Although the heart is affected in only 0.02-2% of all CE cases, a considerable number of cases have been, and continue to be, published. However, due to the rare occurrence of cardiac CE and the resulting lack of clinical trials, knowledge about various aspects of the disease remains limited. To obtain a clearer picture of anatomical, clinical, diagnostic as well as therapeutic aspects of cardiac CE, we systematically reviewed the literature published between 1965 and 2022. The anatomical pattern of the affected cardiac structures follows the extension of the supplying capillary bed. The majority of patients (82.7%) are symptomatic and present with prolonged non-specific symptoms such as dyspnoea, chest pain and palpitations. Acute complications generally derive from cyst rupture, occur in 18.3% of cases and manifest as embolism, pericardial tamponade, or anaphylactic reaction in 83.2%, 17.8% and 10.9% of these cases, respectively. As for CE cysts localized in other organs, the diagnosis of cardiac CE is made by imaging. Serology plays a minor role due to its limited sensitivity. Unlike abdominal CE cysts, cardiac CE cysts are usually resected independent of their stage (active/inactive), because their presence impairs cardiac performance and carries the risk of long-term sequelae. More than 80% of patients are treated with a single surgical intervention. We found a disease-related case fatality rate of 11.1%. Since local recurrence was reported up to 108 months and secondary CE up to 72 months after surgery, patients should be followed up for a minimum of 10 years.

BACKGROUND: Ultramarathon running poses physiological challenges, impacting cardiac function. This systematic review and meta-analysis explore the acute effects of single-stage ultramarathon running on cardiac function.
METHODS: Preferred Reporting Items for Systematic Reviews and Meta-Analyses recommendations were followed. Searches covered Medline, Embase, CINAHL, SPORTDiscus, Web of Science, Central Cochrane, and Scopus. Random effects meta-analyses assessed left ventricular (LV) and right ventricular (RV) variables, expressed as mean differences (MD) with 95% confidence intervals (CI).
RESULTS: Among 6972 studies, 17 were included. Post-ultramarathon reductions were found in LV end-diastolic diameter (LVEDD) (-1.24; 95% CI = -1.77, -0.71 mm), LV end-diastolic volume (LVEDV) (-9.92; 95% CI = -15.25, -4.60 ml), LV stroke volume (LVSV) (-8.96 ml, 95% CI -13.20, -4.72 ml), LV ejection fraction (LVEF) (-3.71; 95% CI = -5.21, -2.22%), LV global longitudinal strain (LVGLS) (-1.48; 95% CI = -2.21, -0.76%), E/A (-0.30; 95% CI = -0.38, -0.22 cm/s), .E\' (-1.35 cm/s, 95% CI -1.91, -0.79 cm/s), RV fractional area change (RVFAC) (-3.34, 95% CI = -5.84, -0.84%), tricuspid annular plane systolic excursion (TAPSE) (-0.12, 95% CI = -0.22, -0.02 cm), RV global longitudinal strain (RVGLS) (-1.73, 95% CI = -2.87, -0.59%), with increases in RV end-diastolic area (RVEDA) (1.89, 95% CI = 0.63, 3.14 cm2), RV Peak A\' (1.32 cm/s, 95% CI 0.20, 2.44), and heart rate (18.24, 95% CI = 15.16, 21.32). No significant differences were observed in LV end-systolic diameter (LVESD), LV end-systolic volume (LVESV), RV end-diastolic diameter (RVEDD), RV Peak E\', and RV Peak S\'.
CONCLUSIONS: Evidence suggests immediate impairment of systolic and diastolic cardiac function post-ultramarathon running.

Fetal growth restriction (FGR) increases cardiovascular risk by cardiac remodeling and programming. This systematic review and meta-analysis across species examines the use of echocardiography in FGR offspring at different ages. PubMed and Embase.com were searched for animal and human studies reporting on echocardiographic parameters in placental insufficiency-induced FGR offspring. We included six animal and 49 human studies. Although unable to perform a meta-analysis of animal studies because of insufficient number of studies per individual outcome, all studies showed left ventricular dysfunction. Our meta-analyses of human studies revealed a reduced left ventricular mass, interventricular septum thickness, mitral annular peak velocity, and mitral lateral early diastolic velocity at neonatal age. No echocardiographic differences during childhood were observed, although the small age range and number of studies limited these analyses. Only two studies at adult age were performed. Meta-regression on other influential factors was not possible due to underreporting. The few studies on myocardial strain analysis showed small changes in global longitudinal strain in FGR offspring. The quality of the human studies was considered low and the risk of bias in animal studies was mostly unclear. Echocardiography may offer a noninvasive tool to detect early signs of cardiovascular predisposition following FGR. Clinical implementation yet faces multiple challenges including identification of the most optimal timing and the exact relation to long-term cardiovascular function in which echocardiography alone might be limited to reflect a child\'s vascular status. Future research should focus on myocardial strain analysis and the combination of other (non)imaging techniques for an improved risk estimation.NEW & NOTEWORTHY Our meta-analysis revealed echocardiographic differences between fetal growth-restricted and control offspring in humans during the neonatal period: a reduced left ventricular mass and interventricular septum thickness, reduced mitral annular peak velocity, and mitral lateral early diastolic velocity. We were unable to pool echocardiographic parameters in animal studies and human adults because of an insufficient number of studies per individual outcome. The few studies on myocardial strain analysis showed small preclinical changes in FGR offspring.

BACKGROUND: Cryostimulation and cold-water immersion (CWI) have recently gained widespread attention due to their association with changes in cardiovascular and cardiac autonomic control responses. Therefore, the aim of the present systematic review and meta-analysis was to identify the global impact of such cold exposures on cardiovascular and cardiac autonomic activity.
METHODS: Three databases (PubMed, Embase, Web-of-Science) were used. Studies were eligible for inclusion if they were conducted on healthy participants using cryostimulation and/or CWI. The outcomes included measurements of blood pressure (BP), heart rate (HR), and heart rate variability (HRV) indices: RR interval (RR), Root mean square of successive RR interval differences (RMSSD), low frequency band (LF), high frequency band (HF), and LF/HF ratio.
RESULTS: Among the 27 articles included in our systematic literature review, only 24 were incorporated into the meta-analysis. Our results reveal a significant increase in HRV indices: RMSSD (Standardized mean difference (SMD) = 0.61, p < 0.001), RR (SMD = 0.77, p < 0.001), and HF (SMD = 0.46, p < 0.001), as well as significantly reduced LF (SMD = -0.41, p < 0.001) and LF/HF ratio (SMD = -0.25, p < 0.01), which persisted up to 15 min following cold exposure. Significantly decreased heart rate (SMD = -0.16, p < 0.05), accompanied by slightly increased mean BP (SMD = 0.28, p < 0.001), was also observed. These results seem to depend on individual characteristics and the cooling techniques.
CONCLUSIONS: Our meta-analysis suggests that cryostimulation and/or CWI exposure enhance parasympathetic nervous activity. There is scarce scientific literature regarding the effect of individual characteristics on cold-induced physiological responses.

OBJECTIVE: This systematic review explores cardiac adaptation in monochorionic (MC) twins with twin-twin transfusion syndrome (TTTS) or selective fetal growth restriction (sFGR) and assesses the risk of congenital heart defects (CHDs).
METHODS: Adhering to PRISMA guidelines, 63 studies were reviewed (49 on cardiac adaptation, 13 on CHD, one on both). A narrative synthesis of cardiac adaptation patterns was performed. Additionally, a meta-analysis compared the livebirth prevalence of CHD in TTTS and sFGR against uncomplicated MC twins.
RESULTS: In TTTS recipients, cardiac function may be impaired for diastolic, systolic, as well as global functions, while in donors, cardiac function is generally preserved. In sFGR, large twins may show hypertrophic cardiomyopathy, and small twins may show impaired systolic function. Co-occurrence of TTTS and sFGR magnifies cardiac impact but is often underreported. Meta-analysis for CHD prevalence revealed a relative risk ratio of 3.5 (95% CI: 2.5-4.9) for TTTS and 2.2 (95%CI: 1.3-3.5) for sFGR compared with uncomplicated MC twins.
CONCLUSIONS: This study highlights the well-documented cardiac adaptation in TTTS, contrasting with limited understanding in sFGR. Elevated CHD risks were observed in both conditions. Enhanced cardiovascular surveillance is warranted in complicated MC twin pregnancies. Future research should explore cardiac adaptation in sFGR and its long-term consequences.

BACKGROUND: Hypertrophic Cardiomyopathy (HCM) is a complex cardiac condition characterized by hypercontractility of cardiac muscle leading to a dynamic obstruction of left ventricular outlet tract (LVOT). Mavacamten, a first-in-class cardiac myosin inhibitor, is increasingly being studied in randomized controlled trials. In this meta-analysis, we aimed to analyse the efficacy and safety profile of Mavacamten compared to placebo in patients of HCM.
METHODS: We carried out a comprehensive search in PubMed, Cochrane, and clinicaltrials.gov to analyze the efficacy and safety of mavacamten compared to placebo from 2010 to 2023. To calculate pooled odds ratio (OR) or risk ratio (RR) at 95% confidence interval (CI), the Mantel-Haenszel formula with random effect was used and Generic Inverse Variance method assessed pooled mean difference value at a 95% CI. RevMan was used for analysis. P<0.05 was considered significant.
RESULTS: We analyzed five phase 3 RCTs including 609 patients to compare mavacamten with a placebo. New York Heart Association (NYHA) grade improvement and KCCQ score showed the odds ratio as 4.94 and 7.93 with p<0.00001 at random effect, respectively. Cardiac imaging which included LAVI, LVOT at rest, LVOT post valsalva, LVOT post-exercise, and reduction in LVEF showed the pooled mean differences for change as -5.29, -49.72, -57.45, -36.11, and -3.00 respectively. Changes in LVEDV and LVMI were not statistically significant. The pooled mean difference for change in NT-proBNP and Cardiac troponin-I showed 0.20 and 0.57 with p<0.00001. The efficacy was evaluated in 1) A composite score, which was defined as either 1·5 mL/kg per min or greater increase in peak oxygen consumption (pVO2) and at least one NYHA class reduction, or a 3·0 mL/kg per min or greater pVO2 increase without NYHA class worsening and 2) changes in pVO2, which was not statistically significant. Similarly, any treatment-associated emergent adverse effects (TEAE), treatment-associated serious adverse effects (TSAE), and cardiac-related adverse effects were not statistically significant.
CONCLUSIONS: Mavacamten influences diverse facets of HCM comprehensively. Notably, our study delved into the drug\'s impact on the heart\'s structural and functional aspects, providing insights that complement prior findings. Further large-scale trials are needed to evaluate the safety profile of Mavacamten.

Coronary artery calcium (CAC) scoring is a powerful tool for atherosclerotic cardiovascular disease risk stratification. The nongated, noncontrast chest computed tomography scan (NCCT) has emerged as a source of CAC characterization with tremendous potential due to the high volume of NCCT scans. Application of incidental CAC characterization from NCCT has raised questions around score accuracy, standardization of methodology including the possibility of deep learning to automate the process, and the risk stratification potential of an NCCT-derived score. In this review, the authors aim to summarize the role of NCCT-derived CAC in preventive cardiovascular health today as well as explore future avenues for eventual clinical applicability in specific patient populations and broader health systems.

BACKGROUND: Fabry disease is a multisystemic disorder characterized by deposition of globotriaosylceramide (Gb3) and its deacylated form in multiple organs, sometimes localized in specific systems such as the nervous or cardiovascular system. As disease-modifying therapies are now available, early diagnosis is paramount to improving life quality and clinical outcomes. Despite the widespread use of non-invasive techniques for assessing organ damage, such as cardiac magnetic resonance imaging (MRI) for patients with cardiac disease, organ biopsy remains the gold standard to assess organ involvement.
METHODS: The cases of two patients, father and daughter with a W162C mutation, are described. The father presented with late-onset, cardiac Fabry disease, subsequently developing systolic dysfunction and heart failure. His daughter, while asymptomatic and with normal cardiac assessment (except for slightly reduced native T1 values by cardiac MRI), had already initial myocyte Gb3 deposits on the endomyocardial biopsy, allowing her to start therapy precociously and potentially modifying the course of her disease. A review of the literature concerning the W162C mutation is then provided, showing that it is usually associated to classic, multisystemic Fabry disease rather than the cardiac-restricted form as in these two cases.
CONCLUSIONS: Three main points can be concluded from this report. First, the W162C mutation can present with a more variegate phenotype than that predicted on a molecular basis. Second, endomyocardial biopsy was shown in this case to precede non-invasive investigation in determining organ involvement, justifying further studies on this potentially reliable technique, Third, difficulties can arise in the management of asymptomatic female carriers.

Congenital heart disease (CHD) is the most frequently occurring birth defect. Majority of the earlier reviews focussed on the association of genetic factors with CHD. A few epidemiological studies provide convincing evidence for environmental factors in the causation of CHD. Although the multifactorial theory of gene-environment interaction is the prevailing explanation, explicit understanding of the biological mechanism(s) involved, remains obscure. Nonetheless, integration of all the information into one platform would enable us to better understand the collective risk implicated in CHD development.
Great strides in novel genomic technologies namely, massive parallel sequencing, whole exome sequencing, multiomics studies supported by system-biology have greatly improved our understanding of the aetiology of CHD. Molecular genetic studies reveal that cardiac specific gene variants in transcription factors or signalling molecules, or structural proteins could cause CHD. Additionally, non-hereditary contributors such as exposure to teratogens, maternal nutrition, parental age and lifestyle factors also contribute to induce CHD. Moreover, DNA methylation and non-coding RNA are also correlated with CHD. Here, we inform that a complex combination of genetic, environmental and epigenetic factors interact to interfere with morphogenetic processes of cardiac development leading to CHD. It is important, not only to identify individual genetic and non-inherited risk factors but also to recognize which factors interact mutually, causing cardiac defects.