Instrumentos de avaliação multidimensional de fragilidade para uso no cuidado de idosos com doença cardiovascular / Multidimensional frailty assessment tools for use in the care of older adults with cardiovascular disease / Instrumentos de evaluación multidimensional de la fragilidad en la atención de adultos mayores con enfermedad cardiovascular

Objetivo: identificar quais os instrumentos disponíveis para avaliação multidimensional da fragilidade em idosos com doença cardiovascular, potencialmente aplicáveis durante a realização do Processo de Enfermagem. Método: revisão sistemática conduzida em oito bases de dados/portais, para identificação de estudos que apresentassem instrumentos multidimensionais de avaliação de fragilidade em idosos com doença cardiovascular e que fossem aplicáveis ao processo de enfermagem. Resultados: foram incluídos 19 instrumentos multidimensionais. O Brief Frailty Index for Coronary Artery Disease foi desenvolvido para uso no cuidado cardiovascular de idosos. O Frailty Index for Adults e o Maastricht Frailty Screening Tool for Hospitalized Patients foram desenvolvidos para uso no Processo de Enfermagem. Conclusão: apesar de apenas um instrumento ter sido desenvolvido para o idosos com doença cardiovascular e apenas dois serem aplicáveis ao processo de enfermagem, a maioria deles tem potencial de adaptação e validação para uso nesta população durante a avaliação de enfermagem.

Objective: to identify which tools are available for multidimensional frailty assessment of older adult with cardiovascular disease and which are potentially applicable during the Nursing Process. Method: a systematic review conducted in eight databases/portals to identify studies that presented multidimensional frailty assessment tools for older adult with cardiovascular disease and that were applicable to the nursing process. Results: a total of 19 multidimensional tools were included. The Brief Frailty Index for Coronary Artery Disease was developed for use in the cardiovascular care of older adult. The Frailty Index for Adults and the Maastricht Frailty Screening Tool for Hospitalized Patients were developed for use in the Nursing Process. Conclusion: although only one tool was developed for older adults with cardiovascular disease and only two are applicable to the nursing process, most of them have the potential to be adapted and validated for use in this population during nursing assessment.

Objetivo: identificar qué instrumentos están disponibles para la evaluación multidimensional de la fragilidad en personas mayores con enfermedad cardiovascular, que se puedan aplicar en el Proceso de Enfermería. Método: revisión sistemática realizada en ocho bases de datos/portales, para identificar estudios que presentaran instrumentos multidimensionales para la evaluación de la fragilidad en adultos mayores con enfermedad cardiovascular y que fueran aplicables al proceso de enfermería. Resultados: se incluyeron 19 instrumentos multidimensionales. El Brief Frailty Index for Coronary Artery Disease se desarrolló para usarlo en el cuidado cardiovascular de las personas mayores. El Frailty Index for Adults y la Maastricht Frailty Screening Tool for Hospitalized Patients se elaboraron para ser usados en el Proceso de Enfermería. Conclusión: aunque sólo se elaboró un instrumento para adultos mayores con enfermedad cardiovascular y sólo dos son aplicables al proceso de enfermería, la mayoría de ellos tienen el potencial para ser adaptados y validados para ser usados en esa población en la evaluación de enfermería.

Association of retinal age gap with chronic kidney disease and subsequent cardiovascular disease sequelae: a cross-sectional and longitudinal study from the UK Biobank.

Background: Chronic kidney disease (CKD) increases the risk of cardiovascular disease (CVD) and is more prevalent in older adults. Retinal age gap, a biomarker of aging based on fundus images, has been previously developed and validated. This study aimed to investigate the association of retinal age gap with CKD and subsequent CVD complications. Methods: A deep learning model was trained to predict the retinal age using 19 200 fundus images of 11 052 participants without any medical history at baseline. Retinal age gap, calculated as retinal age predicted minus chronological age, was calculated for the remaining 35 906 participants. Logistic regression models and Cox proportional hazards regression models were used for the association analysis. Results: A total of 35 906 participants (56.75 ± 8.04 years, 55.68% female) were included in this study. In the cross-sectional analysis, each 1-year increase in retinal age gap was associated with a 2% increase in the risk of CKD prevalence [odds ratio 1.02, 95% confidence interval (CI) 1.01-1.04, P = .012]. A longitudinal analysis of 35 039 participants demonstrated that 2.87% of them developed CKD in follow-up, and each 1-year increase in retinal age gap was associated with a 3% increase in the risk of CKD incidence (hazard ratio 1.03, 95% CI 1.01-1.05, P = .004). In addition, a total of 111 CKD patients (15.81%) developed CVD in follow-up, and each 1-year increase in retinal age gap was associated with a 10% increase in the risk of incident CVD (hazard ratio 1.10, 95% CI 1.03-1.17, P = .005). Conclusions: We found that retinal age gap was independently associated with the prevalence and incidence of CKD, and also associated with CVD complications in CKD patients. This supports the use of this novel biomarker in identifying individuals at high risk of CKD and CKD patients with increased risk of CVD.

Synergy Between NK Cells and Monocytes in Potentiating Cardiovascular Disease Risk in Severe COVID-19.

BACKGROUND: Evidence suggests that COVID-19 predisposes to cardiovascular diseases (CVDs). While monocytes/macrophages play a central role in the immunopathogenesis of atherosclerosis, less is known about their immunopathogenic mechanisms that lead to CVDs during COVID-19. Natural killer (NK) cells, which play an intermediary role during pathologies like atherosclerosis, are dysregulated during COVID-19. Here, we sought to investigate altered immune cells and their associations with CVD risk during severe COVID-19. METHODS: We measured plasma biomarkers of CVDs and determined phenotypes of circulating immune subsets using spectral flow cytometry. We compared these between patients with severe COVID-19 (severe, n=31), those who recovered from severe COVID-19 (recovered, n=29), and SARS-CoV-2-uninfected controls (controls, n=17). In vivo observations were supported using in vitro assays to highlight possible mechanistic links between dysregulated immune subsets and biomarkers during and after COVID-19. We performed multidimensional analyses of published single-cell transcriptome data of monocytes and NK cells during severe COVID-19 to substantiate in vivo findings. RESULTS: During severe COVID-19, we observed alterations in cardiometabolic biomarkers including oxidized-low-density lipoprotein, which showed decreased levels in severe and recovered groups. Severe patients exhibited dysregulated monocyte subsets, including increased frequencies of proinflammatory intermediate monocytes (also observed in the recovered) and decreased nonclassical monocytes. All identified NK-cell subsets in the severe COVID-19 group displayed increased expression of activation and tissue-resident markers, such as CD69. We observed significant correlations between altered immune subsets and plasma oxidized-low-density lipoprotein levels. In vitro assays revealed increased uptake of oxidized-low-density lipoprotein into monocyte-derived macrophages in the presence of NK cells activated by plasma of patients with severe COVID-19. Transcriptome analyses confirmed enriched proinflammatory responses and lipid dysregulation associated with epigenetic modifications in monocytes and NK cells during severe COVID-19. CONCLUSIONS: Our study provides new insights into the involvement of monocytes and NK cells in the increased CVD risk observed during and after COVID-19.

RNF149 Destabilizes IFNGR1 in Macrophages to Favor Post-Infarction Cardiac Repair.

BACKGROUND: Macrophage-driven inflammation critically involves in cardiac injury and repair following myocardial infarction (MI). However, the intrinsic mechanisms that halt the immune response of macrophages, which is critical to preserve homeostasis and effective infarct repair, remain to be fully defined. Here, we aimed to determine the ubiquitination-mediated regulatory effects on averting exaggerated inflammatory responses in cardiac macrophages. METHODS: We used transcriptome analysis of mouse cardiac macrophages and bone marrow-derived macrophages to identify the E3 ubiquitin ligase RNF149 (RING finger protein 149) as a modulator of macrophage response to MI. Employing loss-of-function methodologies, bone marrow transplantation approaches, and adenovirus-mediated RNF149 overexpression in macrophages, we elucidated the functional role of RNF149 in MI. We explored the underlying mechanisms through flow cytometry, transcriptome analysis, immunoprecipitation/mass spectrometry analysis, and functional experiments. RNF149 expression was measured in the cardiac tissues of patients with acute MI and healthy controls. RESULTS: RNF149 was highly expressed in murine and human cardiac macrophages at the early phase of MI. Knockout of RNF149, transplantation of Rnf149-/- bone marrow, and bone marrow macrophage-specific RNF149-knockdown markedly exacerbated cardiac dysfunction in murine MI models. Conversely, overexpression of RNF149 in macrophages attenuated the ischemia-induced decline in cardiac contractile function. RNF149 deletion increased infiltration of proinflammatory monocytes/macrophages, accompanied by a hastened decline in reparative subsets, leading to aggravation of myocardial apoptosis and impairment of infarct healing. Our data revealed that RNF149 in infiltrated macrophages restricted inflammation by promoting ubiquitylation-dependent proteasomal degradation of IFNGR1 (interferon gamma receptor 1). Loss of IFNGR1 rescued deleterious effects of RNF149 deficiency on MI. We further demonstrated that STAT1 activation induced Rnf149 transcription, which, in turn, destabilized the IFNGR1 protein to counteract type-II IFN (interferon) signaling, creating a feedback control mechanism to fine-tune macrophage-driven inflammation. CONCLUSIONS: These findings highlight the significance of RNF149 as a molecular brake on macrophage response to MI and uncover a macrophage-intrinsic posttranslational mechanism essential for maintaining immune homeostasis and facilitating cardiac repair following MI.

Exploring the Function of Epicardial Cells Beyond the Surface.

The epicardium, previously viewed as a passive outer layer around the heart, is now recognized as an essential component in development, regeneration, and repair. In this review, we explore the cellular and molecular makeup of the epicardium, highlighting its roles in heart regeneration and repair in zebrafish and salamanders, as well as its activation in young and adult postnatal mammals. We also examine the latest technologies used to study the function of epicardial cells for therapeutic interventions. Analysis of highly regenerative animal models shows that the epicardium is essential in regulating cardiomyocyte proliferation, transient fibrosis, and neovascularization. However, despite the epicardium's unique cellular programs to resolve cardiac damage, it remains unclear how to replicate these processes in nonregenerative mammalian organisms. During myocardial infarction, epicardial cells secrete signaling factors that modulate fibrotic, vascular, and inflammatory remodeling, which differentially enhance or inhibit cardiac repair. Recent transcriptomic studies have validated the cellular and molecular heterogeneity of the epicardium across various species and developmental stages, shedding further light on its function under pathological conditions. These studies have also provided insights into the function of regulatory epicardial-derived signaling molecules in various diseases, which could lead to new therapies and advances in reparative cardiovascular medicine. Moreover, insights gained from investigating epicardial cell function have initiated the development of novel techniques, including using human pluripotent stem cells and cardiac organoids to model reparative processes within the cardiovascular system. This growing understanding of epicardial function holds the potential for developing innovative therapeutic strategies aimed at addressing developmental heart disorders, enhancing regenerative therapies, and mitigating cardiovascular disease progression.

Efficacy and Safety of Bempedoic Acid in Patients With Hyperlipidemia and Non-alcoholic Fatty Liver Disease.

Hyperlipidemia and its association with cardiovascular diseases have been significant public health concerns for many decades. Statins have long been the primary therapeutic option for lowering cholesterol levels and reducing cardiovascular mortality. However, a substantial number of patients either do not achieve optimal lipid goals with maximally tolerated statin doses or experience statin intolerance. In recent years, there have been remarkable developments in the field of hyperlipidemia management, leading to the approval of novel hypolipidemic drugs in North America and Europe. This article reviews the clinical development of bempedoic acid, a promising new drug, alone and in combination with ezetimibe, as an alternative approach to managing hyperlipidemia. The Phase I trials established the safety and tolerability of bempedoic acid, paving the way for further investigation in Phase II and Phase III trials. Multiple phase II studies evaluated the lipid-lowering efficacy of bempedoic acid as monotherapy or in combination with other hypolipidemic agents, showing significant improvements in lipid levels and inflammatory markers. The recently approved fixed drug combination of bempedoic acid and ezetimibe presents a viable option for patients who need additional LDL-C lowering alongside dietary modifications and maximally tolerated statin therapy.

Practical weight management to minimize pregnancy complications and promote women's health: the possibility of interpregnancy care.

Pregnancy is an excellent opportunity to provide medical interventions to women. It is also a stress test used to predict health. Numerous studies have demonstrated that the pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) are critical factors for pregnancy complications such as hypertensive disorders of pregnancy (HDP), gestational diabetes mellitus (GDM), large or small gestational age infants, and spontaneous preterm birth (sPTB). These complications are associated with an increased risk of cardiovascular disease (CVD), which is a leading cause of mortality in women. In addition, complications adversely affect the short- and long-term prognoses of children. Optimal GWG to reduce complications is recommended based on pre-pregnancy BMI; however, racial differences should also be noted. The values in the Japanese guidelines are lower than those in the American Institute of Medicine guidelines. The Asian BMI thresholds for CVD risk are also lower than those in Europe. Therefore, weight management should be based on racial/genetic background. Interpregnancy weight gain or loss has also been reported to be associated with the risk of pregnancy complications; however, few studies have been conducted in Asian populations. Our previous reports suggested that avoiding an excess of 0.6 kg/m2/year of annual BMI gain may reduce the risk of HDP or GDM, and insufficient gain of < 0.25 kg/m2/year may increase sPTB recurrence. Annual BMI is useful for practical weight control during interpregnancy. Based on these findings, effective approaches should be established to improve the health of women and their offspring.

Overview of Panax ginseng and its active ingredients protective mechanism on cardiovascular diseases.

ETHNIC PHARMACOLOGICAL RELEVANCE: Panax ginseng is a traditional Chinese herbal medicine used to treat cardiovascular diseases (CVDs), and it is still widely used to improve the clinical symptoms of various CVDs. However, there is currently a lack of summary and analysis on the mechanism of Panax ginseng exerts its cardiovascular protective effects. This article provides a review of in vivo and in vitro pharmacological studies on Panax ginseng and its active ingredients in reducing CVDs damage. AIM OF THIS REVIEW: This review summarized the latest literature on Panax ginseng and its active ingredients in CVDs research, aiming to have a comprehensive and in-depth understanding of the cardiovascular protection mechanism of Panax ginseng, and to provide new ideas for the treatment of CVDs, as well as to optimize the clinical application of Panax ginseng. METHODS: Enrichment of pathways and biological terms using the traditional Chinese medicine molecular mechanism bioinformatics analysis tool (BATMAN-TCM). The literature search is based on electronic databases such as PubMed, ScienceDirect, Scopus, CNKI, with a search period of 2002-2023. The search terms include Panax ginseng, Panax ginseng ingredients, ginsenosides, ginseng polysaccharides, ginseng glycoproteins, ginseng volatile oil, CVDs, heart, and cardiac. RESULTS: 132 articles were ultimately included in the review. The ingredients in Panax ginseng that manifested cardiovascular protective effects are mainly ginsenosides (especially ginsenoside Rb1). Ginsenosides protected against CVDs such as ischemic reperfusion injury, atherosclerosis and heart failure mainly through improving energy metabolism, inhibiting hyper-autophagy, antioxidant, anti-inflammatory and promoting secretion of exosomes. CONCLUSION: Panax ginseng and its active ingredients have a particularly prominent effect on improving myocardial energy metabolism remodeling in protecting against CVDs. The AMPK and PPAR signaling pathways are the key targets through which Panax ginseng produces multiple mechanisms of cardiovascular protection. Extracellular vesicles and nanoparticles as carriers are potential delivery ways for optimizing the bioavailability of Panax ginseng and its active ingredients.

Socioeconomic status and cardiovascular mortality in over 170,000 cancer survivors.

AIMS: Cardiovascular health is acknowledged as a crucial concern among cancer survivors. Socioeconomic status (SES) is an essential but often neglected risk factor for cardiovascular disease (CVD). We conducted this study to identify the relationship between SES and CVD mortality in cancer survivors. METHODS AND RESULTS: Using the National Health Insurance Service-National Health Examinee database, we identified cancer survivors diagnosed and surviving beyond 5 years post-diagnosis. SES was assessed based on insurance premiums and classified into 5 groups. The primary outcome was overall CVD mortality. This study analyzed 170 555 individuals (mean age 60.7 ± 11.9 years, 57.8% female). A gradual increase in risk was observed across SES groups: adjusted hazard ratios (95% confidence intervals) for overall CVD mortality were 1.15 (1.04-1.26), 1.28 (1.15-1.44), 1.31 (1.18-1.46), and 2.13 (1.30-3.49) for the second, third, and fourth quartile, and medical aid group (the lowest SES group) compared to the highest SES group, respectively (p for trend < 0.001). The lowest SES group with hypertension exhibited a 3.4-fold higher risk of CVD mortality compared to the highest SES group without hypertension. Interaction analyses revealed that low SES synergistically interacts with hypertension, heightening the risk of CVD mortality (synergy index 1.62). CONCLUSION: This study demonstrates a significant correlation between low SES and increased CVD mortality among cancer survivors. Particularly, the lowest SES group, when combined with hypertension, significantly escalates CVD mortality. Our findings underscore the critical importance of recognizing SES as a significant risk factor for CVD mortality in this population of cancer survivors.

Our population-based cohort study, involving over 170 000 cancer survivors, demonstrates a significant association between socioeconomic status (SES) and cardiovascular disease (CVD) mortality.

Mitochondrial unfolded protein response mechanism and its cardiovascular protective effects.

The mitochondrial unfolded protein response (UPRmt) is a cytoprotective response in response to cellular stress that is activated in response to mitochondrial stress to maintain intra-protein homeostasis, thereby protecting the cell from a variety of stimuli. The activation of this response has been linked to cardiovascular diseases. Here, we reviewed the current understanding of UPRmt and discussed its specific molecular mechanism, mainly in mammals, as well as addressing its protective role against cardiovascular diseases, so as to provide direction for further research on UPRmt and therapies targeting cardiovascular diseases in the future.

Arterial aneurysm and dissection: toward the evolving phenotype of Tatton-Brown-Rahman syndrome.

BACKGROUND: Tatton-Brown-Rahman syndrome (TBRS) is a rare disorder, caused by DNMT3A heterozygous pathogenic variants, and first described in 2014. TBRS is characterised by overgrowth, intellectual disability, facial dysmorphism, hypotonia and musculoskeletal features, as well as neurological and psychiatric features. Cardiac manifestations have also been reported, mainly congenital malformations such as atrial septal defect, ventricular septal defect and cardiac valvular disease. Aortic dilatation has rarely been described. METHODS: Here we have undertaken a detailed clinical and molecular description of eight previously unreported individuals, who had TBRS and arterial dilatation and/or dissection, mainly thoracic aortic aneurysm (TAA). We have also reviewed the seven previously published cases of TAA in individuals with TBRS to try to better delineate the vascular phenotype and to determine specific follow-up for this condition. RESULTS: We include eight new patients with TBRS who presented with arterial aneurysms mainly involving aorta. Three of these patients presented with dissection that required critical surgery. CONCLUSIONS: Arterial aneurysms and dissections are a potentially lethal, age-dependent manifestation. The prevalence of aortic disease in individuals with TBRS is far in excess of that expected in the general population. This cohort, together with individuals previously published, illustrates the importance to consider dilatation/dissection, mainly in aorta but also in other arteries. Arterial vascular weakness may therefore also be a cardinal feature of TBRS and vascular surveillance is recommended.

Treatment drop-in in a contemporary cohort used to derive cardiovascular risk prediction equations.

BACKGROUND: No routinely recommended cardiovascular disease (CVD) risk prediction equations have adjusted for CVD preventive medications initiated during follow-up (treatment drop-in) in their derivation cohorts. This will lead to underestimation of risk when equations are applied in clinical practice if treatment drop-in is common. We aimed to quantify the treatment drop-in in a large contemporary national cohort to determine whether equations are likely to require adjustment. METHODS: Eight de-identified individual-level national health administrative datasets in Aotearoa New Zealand were linked to establish a cohort of almost all New Zealanders without CVD and aged 30-74 years in 2006. Individuals dispensing blood-pressure-lowering and/or lipid-lowering medications between 1 July 2006 and 31 December 2006 (baseline dispensing), and in each 6-month period during 12 years' follow-up to 31 December 2018 (follow-up dispensing), were identified. Person-years of treatment drop-in were determined. RESULTS: A total of 1 399 348 (80%) out of the 1 746 695 individuals in the cohort were not dispensed CVD medications at baseline. Blood-pressure-lowering and/or lipid-lowering treatment drop-in accounted for 14% of follow-up time in the group untreated at baseline and increased significantly with increasing predicted baseline 5-year CVD risk (12%, 31%, 34% and 37% in <5%, 5-9%, 10-14% and ≥15% risk groups, respectively) and with increasing age (8% in 30-44 year-olds to 30% in 60-74 year-olds). CONCLUSIONS: CVD preventive treatment drop-in accounted for approximately one-third of follow-up time among participants typically eligible for preventive treatment (≥5% 5-year predicted risk). Equations derived from cohorts with long-term follow-up that do not adjust for treatment drop-in effect will underestimate CVD risk in higher risk individuals and lead to undertreatment. Future CVD risk prediction studies need to address this potential flaw.

PANoptosis: Novel insight into regulated cell death and its potential role in cardiovascular diseases (Review).

PANoptosis, a complex form of proinflammatory programmed cell death, including apoptosis, pyroptosis and necroptosis, has been an emerging concept in recent years that has been widely reported in cancer, infectious diseases and neurological disorders. Cardiovascular diseases (CVDs) are an important global health problem, posing a serious threat to individuals' lives. An increasing body of research shows that inflammation has a pivotal role in CVDs, which provides an important theoretical basis for PANoptosis to promote the progression of CVDs. To date, only sporadic studies on PANoptosis in CVDs have been reported and its role in the field of CVDs has not been fully explored. Elucidating the various modes of cardiomyocyte death, the specific molecular mechanisms and the links among the various modes of death under various stressful stimuli is of notable clinical significance for a deeper understanding of the pathophysiology of CVDs. The present review summarizes the molecular mechanisms of apoptosis, pyroptosis, necroptosis and PANoptosis and their prospects in the field of CVDs.

Marital Quality-A Neglected Player in the Prevention of Cardiovascular Diseases: A Systematic Review of Longitudinal Studies.

PURPOSE OF REVIEW: Marital quality (MQ) is a psychosocial factor that has been neglected in cardiovascular prevention guidelines, although its association with cardiovascular diseases has been identified in several studies. Therefore, we aim to investigate how MQ either in positive or negative dimensions affect different cardiovascular risk factors and diseases. RECENT FINDINGS: We systematically searched different databases in September 2023 for longitudinal studies conducted to assess the contribution of MQ to well-established cardiovascular risk factors and diseases. Two independent researchers screened studies and carried out data extraction and quality assessment of included ones. From 12,175 potential studies screened, 40 were included. The presence of significant heterogeneity in methodology, follow-up, and subsequent effect estimates made it unfeasible to do a meta-analysis. Despite the variation, most studies found a significant association of negative MQ measures with physical inactivity (2/2), high levels of smoking (4/5) and alcohol (3/3) use, increased metabolic syndrome risk (3/3), elevated type 2 diabetes mellitus (T2DM) risk and poor T2DM management (3/6), elevated cardiovascular disease risk and progression (9/11), increased body weight and obesity risk (2/3), elevated blood pressure and hypertension risk (7/8). Positive MQ measures were mainly associated with improvement in blood pressure control (2/2), reduced T2DM risk and its good management (1/1), reduced body weight and obesity risk (2/2), and increased survival in cardiovascular diseases (4/4). Based on current evidence, MQ seems to play a crucial role in developing established cardiovascular risk factors and diseases and is worth considering in preventive strategies.

Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis.

In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. However, it has been long recognized that diffuse intimal thickening (DIM), which precedes the formation of early fatty streaks in humans, primarily consists of lipid-loaded smooth muscle cells (SMCs) and their secreted proteoglycans. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques. Given that SMCs are a major component of the vascular wall, they serve as a significant source of microvesicles and exosomes, which have the potential to regulate the physiology of other vascular cells. Notably, more than half of the foam cells present in atherosclerotic lesions are of SMC origin. In this review, we describe several mechanisms underlying the formation of intimal foam-like cells in atherosclerotic plaques. Based on these mechanisms, we discuss novel therapeutic approaches that have been developed to regulate the generation of intimal foam-like cells. These innovative strategies hold promise for improving the management of atherosclerosis in the near future.

Impact of cardiac rehabilitation on erectile dysfunction in cardiovascular patients: a systematic review and meta-analysis.

Background: Cardiovascular diseases (CVDs) and erectile dysfunction (ED) frequently co-occur, significantly affecting the quality of life of individuals. Aim: To assess the impact of cardiac rehabilitation (CR) on ED in patients with CVD through a systematic review and meta-analysis. Methods: This study analyzed randomized controlled trials and other studies comparing CR with usual care for adult males (≥18 years) with any cardiac disease. Literature searches were extensive, and the risk of bias was evaluated by the Cochrane Collaboration tool. Data from 6 studies involving 668 participants were included in the meta-analysis. Outcomes: The primary outcome was the improvement in ED, as measured with the International Index of Erectile Function. Results: A statistically significant improvement in erectile function was observed across 6 studies, with a Morris dppc2 effect size of 0.38 (95% CI, 0.17-0.59). Despite initial high heterogeneity (I 2 = 95.7%), identification and correction for selective outcome reporting bias mitigated this issue. Clinical Translation: CR has a modest but statistically significant impact on improving ED in patients with CVD, indicating its potential positive contribution to the quality of life of this group. Strengths and Limitations: The study's strengths include a comprehensive literature search and a rigorous methodological approach. Limitations involve high heterogeneity among studies and a low level of evidence due to small sample sizes and study quality; however, the source of heterogeneity was identified and mitigated following risk-of-bias assessment. Conclusion: The results suggest that CR has a statistically significant but modest impact on improving ED in patients with CVD. Clinicians should consider the integration of CR into the clinical management of these individuals. This study underscores the potential for CR to contribute positively to the quality of life for patients with CVD by addressing associated ED (PROSPERO: CRD42022374625).

Triglyceride-Glucose Index as Predictor for Hypertension, CHD and STROKE Risk among Non-Diabetic Patients: A NHANES Cross-Sectional Study 2001-2020.

BACKGROUND: Cardiovascular disease (CVD) is a leading cause of global mortality. Early intervention and prevention of CVD depend on accurately predicting the risk of CVD. This study aimed to investigate the association between the TyG index and the risk of coronary heart disease (CHD), congestive heart failure (CHF), heart attack (HA), stroke, and hypertension (HTN) among patients without diabetes in the United States. METHODS: In this retrospective, cross-sectional study, we used data from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2020. We conducted several regression analysis models and calculated the sensitivity and specificity of (TyG) index for predicting the onset of CHD, CHF, HA, stroke, and HTN. RESULTS: A total of 10,937 individuals without diabetes participated in our study. Individuals with a TyG index greater than 8.96 displayed significant increasing in various parameters, including BMI, systolic/diastolic blood pressure, total cholesterol, LDL, and Apo-B levels (p < 0.001). Almost all regression models ensured that a higher TyGI value was associated with higher odds of having CHD, CHF, HA, stroke, and HTN, which patients with a TyGI value higher than 8.96 have odds ratios of 2.24-5.58 for CHD, 1.68-4.42 for stroke, 2.45-3.77 for HA and 1.75-3.93 for HTN comparing than patients with a TyGI value lower than 8.11 (p-value < 0.05).We evaluated the predictive value of the TyG index for each endpoint, obtaining the following area under the curve (AUC) values: 54.75% for CHF (95% CI: 0.542-0.614), 52.32% for stroke (95% CI: 0.529-0.584), 55.67% for HA (95% CI: 0.595-0.646), 55.59% for HTN (95% CI: 0.574-0.597), and 50.31% for CHD (95% CI: 0.592-0.646). CONCLUSION: The TyG index showed a strong correlation with cardiovascular risk factors in individuals without diabetes, however it was a poor predictor of almost studied cardiovascular diseases.

Occupational health and safety portrait of lobster fishers from a St. Lawrence Gulf community.

Lobstering industry workers are known to have poor overall health and low safety records, but there is still a gap in information concerning Canadian lobster fishers. This study aimed to report occupational health and safety characteristics of an Atlantic Canada community of lobster fishers and to assess differences between captains and deckhands. Twenty-eight participants (10 captains, 18 deckhands) were questioned and self-reported on lifestyle, general health status, work-related musculoskeletal disorders and traumatic injuries. The data collected reveal both groups' high prevalence of cardiometabolic and musculoskeletal health issues. Captains reported more occupational exposition and health issues, and showed poorer lifestyle habits than deckhands. Fishers reported potential solutions to reduce occupational risks, presented as three types: lifestyle, working behaviours and leadership. This study evaluated a community of Canadian lobster fishers regarding their occupational health and safety. Potential avenues for mitigating occupational risk specific to this community will nurture future implementation.

Cholesterol Lowering in Older Adults: Should We Wait for Further Evidence?

PURPOSE OF REVIEW: Current guidelines for primary and secondary prevention of cardiovascular events in adults up to age 75 years are well-established. However, recommendations for lipid-lowering therapies (LLT), particularly for primary prevention, are inconclusive after age 75. In this review, we focus on adults ≥ 75 years to assess low-density lipoprotein-cholesterol (LDL-C) as a marker for predicting atherosclerotic cardiovascular disease (ASCVD) risk, review risk assessment tools, highlight guidelines for LLT, and discuss benefits, risks, and deprescribing strategies. RECENT FINDINGS: The relationship between LDL-C and all-cause mortality and cardiovascular outcomes in older adults is complex and confounded. Current ASCVD risk estimators heavily depend on age and lack geriatric-specific variables. Emerging tools may reclassify individuals based on biologic rather than chronologic age, with coronary artery calcium scores gaining popularity. After initiating LLT for primary or secondary prevention, target LDL-C levels for older adults are lacking, and non-statin therapy thresholds remain unknown, relying on evidence from younger populations. Shared decision-making is crucial, considering therapy's time to benefit, life expectancy, adverse events, and geriatric syndromes. Deprescribing is recommended in end-of-life care but remains unclear in fit or frail older adults. After an ASCVD event, LLT is appropriate for most older adults, and deprescribing can be considered for those approaching the last months of life. Ongoing trials will guide statin prescription and deprescribing among older adults free of ASCVD. In the interim, for adults ≥ 75 years without a limited life expectancy who are free of ASCVD, an LLT approach that includes both lifestyle and medications, specifically statins, may be considered after shared decision-making.

Palliative Pharmacotherapy for Cardiovascular Disease: A Scientific Statement From the American Heart Association.

Cardiovascular disease exacts a heavy toll on health and quality of life and is the leading cause of death among people ≥65 years of age. Although medical, surgical, and device therapies can certainly prolong a life span, disease progression from chronic to advanced to end stage is temporally unpredictable, uncertain, and marked by worsening symptoms that result in recurrent hospitalizations and excessive health care use. Compared with other serious illnesses, medication management that incorporates a palliative approach is underused among individuals with cardiovascular disease. This scientific statement describes palliative pharmacotherapy inclusive of cardiovascular drugs and essential palliative medicines that work synergistically to control symptoms and enhance quality of life. We also summarize and clarify available evidence on the utility of guideline-directed and evidence-based medical therapies in individuals with end-stage heart failure, pulmonary arterial hypertension, coronary heart disease, and other cardiomyopathies while providing clinical considerations for de-escalating or deprescribing. Shared decision-making and goal-oriented care are emphasized and considered quintessential to the iterative process of patient-centered medication management across the spectrum of cardiovascular disease.