In a somewhat narrow diagnostic lens, Alzheimer’s Disease (AD) has been considered a brain specific disease characterized by the presence of β-Amyloid plaques and tau neural fibrillary tangles and neural inflammation; these pathologies lead to neuronal death and consequently clinical symptoms such as memory loss, confusion, and impaired cognitive function. However, for decades researchers have noticed a link between various cardiovascular abnormalities and AD - such as heart failure (HF), coronary artery disease (CAD), atrial fibrillation (AF), and vasculopathy. A considerable volume of work has pointed at this head to heart connection, focusing mainly on associations between cerebral hypoperfusion and neuronal degradation. However, new evidence of a possible systemic or metastatic profile to AD calls for further analysis of this connection. β amyloid aggregations - biochemically and structurally akin to those found in the typical AD pathology - are now known to be present in the hearts of individuals with idiopathic dilated cardiomyopathy (iDCM) as well as the hearts of patients with AD. These findings suggest a potential systemic profile of proteinopathies, and a new hypothesis for the link between peripheral and central symptoms of HF and AD. Herein, we provide an overview of the cardiovascular links to Alzheimer’s disease.

Background Particulate matter (particles < 2.5 μm [ PM 2.5 ]) exposure during the in utero and postnatal developmental periods causes cardiac dysfunction during adulthood. Here, we investigated the potential priming effects of preconception exposure of PM 2.5 on cardiac function in adult offspring. Methods and Results Male and female friend leukemia virus b (FVB) mice were exposed to either filtered air ( FA ) or PM 2.5 at an average concentration of 38.58 μg/m 3 for 6 hours/day, 5 days/week for 3 months. Mice were then crossbred into 2 groups: (1) FA male × FA female (both parents were exposed to FA preconception) and, (2) PM 2.5male × PM 2.5female (both parents were exposed to PM 2.5 preconception). Male offspring were divided: (1) preconception FA (offspring born to FA exposed parents) and, (2) preconception PM 2.5 (offspring born to PM 2.5 exposed parents) and analyzed at 3 months of age. Echocardiography identified increased left ventricular end systolic volume and reduced posterior wall thickness, reduced %fractional shortening and %ejection fraction in preconception PM 2.5 offspring. Cardiomyocytes isolated from preconception PM 2.5 offspring showed reduced %peak shortening, −dL/dT, TPS 90 and slower calcium reuptake (tau). Gene and protein expression revealed modifications in markers of inflammation ( IL ‐6, IL ‐15, TNF α, NF қB, CRP , CD 26E, CD 26P, intercellular adhesion molecule 1, and monocyte chemoattractant protein‐1) profibrosis (collagen type III alpha 1 chain), oxidative stress ( NOS 2), antioxidants (Nrf2, SOD , catalase), Ca 2+ regulatory proteins ( SERCA 2a, p‐ PLN , NCX ), and epigenetic regulators (Dnmt1, Dnmt3a, Dnmt3b, Sirt1, and Sirt2) in preconception PM 2.5 offspring. Conclusions Preconception exposure to PM 2.5 results in global cardiac dysfunction in adult offspring, suggesting that abnormalities during development are not limit...

The coronavirus disease-2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly grown into a pandemic. According to initial reports, the lungs were thought to be the primary target, but recent case studies have shown its reach can extend to other organs including the heart and blood vessels. The severity of cardiac complications of COVID-19 depends on multiple underlying factors, with air pollutant exposure being one of them as reported by several recent studies. Airborne particulate matter attracts heightened attention due to its implication in various diseases, especially respiratory and cardiovascular diseases. Inhaled particulate matter not only carries microorganisms inside the body but also elicits local and systemic inflammatory responses resulting in altering host’s immunity and increasing susceptibility to infection. Previous as well as recent studies have documented that particulate matter acts as a “carrier” for the virus and aids in spreading viral infections. This review presents the mechanisms and effects of viral entry and how pollution can potentially modulate pathophysiological processes in the heart. We aimed to concisely summarize studies examining cardiovascular (CV) outcomes in COVID-19 patients and postulate on how particulate matter can influence these outcomes. We have also reviewed evidence on the use of rennin-angiotensin system (RAS) inhibitors, namely, ACE inhibitors and angiotensin receptor blockers, in patients with COVID-19. The interplay of pollution and SARS-CoV-2 is essential to understanding the effects of accentuated cardiovascular effects of COVID-19 and deserves in depth experimental investigations.

Objective Exposure of fine particulate matter (PM2.5) to pregnant dams has been shown to be strongly associated with adverse cardiovascular outcomes in offspring at adulthood, however, effects evident during neonatal periods are unclear. We designed this study to examine cardiac function of neonatal mice (14 days old) exposed to in utero PM2.5. Methods Pregnant FVB female mice were exposed either to filtered air (FA) or PM2.5 at an average concentration of 91.78 μg/m3 for 6h/day, 5 days/wk (similar to exposure in a large industrial area) throughout the gestation period (20 days). After birth, animals were analyzed at day 14 of life. Results Fourteen day old mice exposed to PM2.5 during in utero period demonstrated decreased fractional shortening (%FS, 41.1±1.2% FA, 33.7±1.2% PM2.5, p<0.01) and LVEDd (2.87±0.08 mm FA, 2.58±0.07 mm PM2.5, p<0.05) compared to FA exposed mice. Contractile kinetics and calcium transients in isolated cardiomyocytes from PM2.5 exposed mice illustrated reduced peak shortening (%PS, 16.7±0.5% FA, 14.7±0.4% PM2.5, p<0.01), negative contractile velocity (- dL/dT, -6.91±0.3 μm/s FA, -5.46±0.2 μm/s PM2.5, p<0.001), increased time to relaxation 90% (TR90, 0.07±0.003 s FA, 0.08±0.004 s PM2.5, p<0.05), decreased calcium transient amplitude (Δ340/380, 33.8±3.4 FA, 29.5±2.8 PM2.5) and slower fluorescence decay rate (τ, 0.72±0.1 s FA, 1.16±0.15 s PM2.5, p<0.05). Immunoblotting studies demonstrated alterations in expression of Ca2+ handling proteins- SERCA-2A, p-PLN, NCX and CaV1.2 in hearts of 14 day old in utero PM2.5 exposed mice compared to FA exposed hearts. Conclusion PM2.5 exposure during the critical in utero period adversely affects the developing mouse fetus leading to functional cardiac changes that were evident during the very early (14 days) stages of adolescence. These data demonstrated that exposure to PM2.5 during the gestation period significantly impacts cardiovascular outcomes early in life.