Comorbid conditions commonly affect people with multiple sclerosis (MS). Population-based studies indicate that people with MS have an increased incidence of ischemic heart disease, cerebrovascular disease, peripheral vascular disease, and psychiatric disorders as compared to people without MS. People with MS from underrepresented minority and immigrant groups have higher comorbidity burdens. Comorbidities exert effects throughout the disease course, from symptom onset through diagnosis to the end of life. At the individual level, comorbidity is associated with higher relapse rates, greater physical and cognitive impairments, lower health-related quality of life, and increased mortality. At the level of the health system and society, comorbidity is associated with increased health care utilization, costs and work impairment. A nascent literature suggests that MS affects outcomes from comorbidities. Comorbidity management needs to be integrated into MS care, and this would be facilitated by determining optimal models of care.

https://www.frontiersin.org/articles/10.3389/fimmu.2023.1197195/pdf

Etiology, effects and management of comorbidities in multiple sclerosis: recent advances

The blood platelet plays an important role but often remains under-recognized in several vascular complications and associated diseases. Surprisingly, platelet hyperactivity and hyperaggregability have often been considered the critical risk factors for developing vascular dysfunctions in several neurodegenerative diseases (NDDs) like Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. In addition, platelet structural and functional impairments promote prothrombotic and proinflammatory environment that can aggravate the progression of several NDDs. These findings provide the rationale for using antiplatelet agents not only to prevent morbidity but also to reduce mortality caused by NDDs. Therefore, we thoroughly review the evidence supporting the potential pleiotropic effects of several novel classes of synthetic antiplatelet drugs, that is, cyclooxygenase inhibitors, adenosine diphosphate receptor antagonists, protease-activated receptor blockers, and glycoprotein IIb/IIIa receptor inhibitors in NDDs. Apart from this, the review also emphasizes the recent developments of selected natural antiplatelet phytochemicals belonging to key classes of plant-based bioactive compounds, including polyphenols, alkaloids, terpenoids, and flavonoids as potential therapeutic candidates in NDDs. We believe that the broad analysis of contemporary strategies and specific approaches for plausible therapeutic treatment for NDDs presented in this review could be helpful for further successful research in this area.

Antiplatelet drugs: Potential therapeutic options for the management of neurodegenerative diseases.

Multiple sclerosis (MS), traditionally perceived as a neurodegenerative disease, exhibits significant vascular alternations, including blood–brain barrier (BBB) disruption, which may predispose patients to increased cardiovascular risks. This vascular dysfunction is intricately linked with the infiltration of immune cells into the central nervous system (CNS), which plays a significant role in perpetuating neuroinflammation. Additionally, oxidative stress serves not only as a byproduct of inflammatory processes but also as an active contributor to neural damage. The synthesis of these multifaceted aspects highlights the importance of understanding their cumulative impact on MS progression. This review reveals that the triad of vascular damage, chronic inflammation, and oxidative imbalance may be considered interdependent processes that exacerbate each other, underscoring the need for holistic and multi-targeted therapeutic approaches in MS management. There is a necessity for reevaluating MS treatment strategies to encompass these overlapping pathologies, offering insights for future research and potential therapeutic interventions. Whole-body cryotherapy (WBCT) emerges as one of the potential avenues for holistic MS management approaches which may alleviate the triad of MS progression factors in multiple ways.

Targeting Vascular Impairment, Neuroinflammation, and Oxidative Stress Dynamics with Whole-Body Cryotherapy in Multiple Sclerosis Treatment

Elevated blood pressure (BP) was associated with higher risk of heart failure, but the relationship between BP-lowering via antihypertensive drugs and diminution of heart failure was inconclusive. This study aimed to estimate the causal association of BP with heart failure, and explore the effects of BP-lowering through different antihypertensive drug classes on heart failure risk using Mendelian randomization analysis with genetic variants as instrument variables.Genetic variants associated with BP were derived from UK Biobank ( n = 317 754) and the genome-wide association study (GWAS) meta-analysis of UK Biobank and International Consortium of Blood Pressure ( n = 757 601). Heart failure summary association data were contributed by HERMES Consortium (47 309 heart failure cases and 930 014 controls). Inverse variance weighted (IVW) was performed to estimate causality between exposure and outcome, and weighted median was utilized as sensitivity analysis, and Mendelian randomization-Egger regression was used to identify pleiotropy of instrument variables. Multivariable Mendelian randomization (MVMR) was applied to control for the confounders.Genetically predicted SBP and DBP were associated with heart failure [SBP: odds ratio (OR) = 1.355, 95% confidence interval (CI) 1.201-1.529; DBP: OR = 1.348, 95% CI 1.213-1.498] in UK Biobank. Likewise, in the GWAS meta-analysis of UK Biobank and International Consortium of Blood Pressure, the causal associations were observed between SBP, DBP and heart failure (SBP: OR = 1.237, 95% CI 1.188-1.289; DBP: OR = 1.337, 95% CI 1.245-1.437). Genetically determined β-blockers and calcium channel blockers (CCBs) were associated with lower risk of heart failure (β-blockers: OR = 0.617, 95% CI 0.453-0.839; CCBs: OR = 0.730, 95% CI 0.625-0.851). No association was found between angiotensin receptor blockers (ARBs) and heart failure (OR = 1.593, 95% CI 0.647-3.924). When adjusted for smoking, alcohol, physical activity, fruit and vegetable intake, the results were stable.Our study indicates causal associations between SBP, DBP, and heart failure, and suggests the preventive effects of heart failure by BP-lowering using β-blockers and CCBs. 

Genetically predicted blood pressure, antihypertensive drugs and risk of heart failure: a Mendelian randomization study

Novel biomarkers are required to improve cardiovascular disease prediction in patients with type 2 diabetes (T2D) as a high-risk population. This study was conducted to examine whether coronary artery disease (CAD) risk assessment can be improved by substituting high-density lipoprotein (HDL)-bound paraoxonase 1 (PON1) activity for HDL cholesterol (HDL-C) concentration in patients with T2D.In this study, we studied 139 patients with T2D (mean age 64.12 ± 8.17 years) who underwent coronary angiographic examination. The initial rate of substrate hydrolysis was spectrophotometrically assayed in kinetic mode for measuring PON1 activity. Receiver operating characteristic (ROC) graphs are created by plotting true positivity versus false positivity. In patients with HbA1c ≥ 7%, PON1 (AUC = 0.7, p = 0.029) and nonHDL-C/PON1 (AUC = 0.75, p = 0.013) were significantly more capable of differentiating patients with CAD from those without CAD compared to HDL-C and nonHDL-C/HDL-C. Also, the predictive power of PON1 (AUC = 0.64, p = 0.029) and nonHDL-C/PON1 (AUC = 0.71, p = 0.004) were significantly higher in comparison with HDL-C and nonHDL-C/HDL-C for CAD characterization in patients aged ≥50 years. Moreover, PON1 and nonHDL-C/PON1 are associated with the incidence of CAD with an AUC of 0.7 (p = 0.026) and AUC of 0.64 (p = 0.087), respectively, among subjects with low HDL-C.PON1 and the ratio of nonHDL-C/PON1 significantly improve the prediction of severe CAD in T2D patients and in patients with HbA1c ≥ 7%, age ≥50 years, or low HDL-C. PON1 activity and lipid ratios using this enzyme may be valuable as substitutes of HDL-C for increasing clinical efficacies in cardiovascular risk assessment. 

Can HDL cholesterol be replaced by paraoxonase 1 activity in the prediction of severe coronary artery disease in patients with type 2 diabetes?

Background Observational studies suggested that multiple sclerosis (MS) is associated with cardiovascular diseases (CVDs). However, the causal association has not been fully elucidated. Thus, we aim to assess the causality of the associations of MS with risk of CVDs. Methods A two-sample Mendelian randomization (MR) study was performed to explore the causality. Genetic instruments were identified for MS from a genome-wide association study (GWAS) involving 115,803 individuals. Summary-level data for CVDs were obtained from different GWAS meta-analysis studies. MR analysis was conducted mainly using the inverse-variance weighted (IVW) method. Sensitivity analyses were further performed to ensure the robustness of the results. Results This MR study found suggestive evidence that genetic liability to MS was associated with an increased risk of coronary artery disease (CAD) [odds ratio (OR), 1.02; 95% confidence interval (CI), 1.00–1.04; p = 0.03], myocardial infarction (MI) (OR, 1.03; 95% CI, 1.00–1.06; p = 0.01), heart failure (HF) (OR, 1.02; 95% CI, 1.00–1.04; p = 0.02), all-cause stroke (AS) (OR, 1.02; 95% CI, 1.00–1.05; p = 0.02), and any ischemic stroke (AIS) (OR, 1.02; 95% CI, 1.00–1.05; p = 0.04). The null-association was observed between MS and the other CVDs. Further analyses found little evidence of pleiotropy. Conclusions We provided suggestive genetic evidence for the causal associations of MS with increased risk of CAD, MI, HF, AS, and AIS, which highlighted the significance of active monitoring and prevention of cardiovascular risk to combat cardiovascular comorbidities in MS patients.

/pdf/multiple-sclerosis-and-the-risk-of-cardiovascular-diseases-a-2kvybzwf.pdf

Multiple Sclerosis and the Risk of Cardiovascular Diseases: A Mendelian Randomization Study

Observational studies have shown an association between mental health and coronary artery disease (CAD) in patients with diabetes. Nevertheless, whether these associations are causal is still unknown. In this two-sample Mendelian randomization (MR) study, we aimed to assess the causality between mental health and CAD in patients with diabetes.Single-nucleotide polymorphisms (SNPs) associated with: depression (807,553 individuals), anxiety (83,556 individuals) and neuroticism (329,821 individuals) were identified from the largest genome-wide association studies (GWAS). Summary-level data for CAD were extracted from the recently published GWAS of 15,666 diabetic patients (3968 CAD cases and 11,696 controls). The inverse-variance weighted (IVW) method was used for the main analysis. Sensitivity analyses included weighted median, maximum likelihood, and the MR-Egger method. Genetic liability to depression was significantly associated with a higher risk of CAD in patients with diabetes (odds ratio [OR], 1.286; 95%CI，1.018-1.621；p = 0.035). For anxiety and neuroticism, no causal association with CAD in patients with diabetes was observed. Consistent results were obtained in most sensitivity analyses.This MR study provides genetic evidence that depression is a potential risk factor for CAD in patients with diabetes. However, anxiety and neuroticism were not causally associated with CAD in patients with diabetes. Mental health treatments should be enhanced to prevent CAD in patients with diabetes. 

http://www.nmcd-journal.com/article/S0939475322000187/pdf

Association of mental health with the risk of coronary artery disease in patients with diabetes: A mendelian randomization study.

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Multiple Sclerosis and the Risk of Cardiovascular Diseases: A Mendelian Randomization Study

Association of mental health with the risk of coronary artery disease in patients with diabetes: A mendelian randomization study.