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Nikhil Prasad  Fact checked by:Thailand Medical News Team Feb 03, 2024  2 weeks, 4 days, 6 hours, 30 minutes ago

BREAKING! Japanese Scientists Warn Of Imminent Heart Failure Pandemic! Millions Predicted To Die Due To Rampant SARS-CoV-2 Viral Persistence In Heart!

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BREAKING! Japanese Scientists Warn Of Imminent Heart Failure Pandemic! Millions Predicted To Die Due To Rampant SARS-CoV-2 Viral Persistence In Heart!
Nikhil Prasad  Fact checked by:Thailand Medical News Team Feb 03, 2024  2 weeks, 4 days, 6 hours, 30 minutes ago
Medical News: As the world navigates the shifting landscape of the COVID-19 pandemic, a team of Japanese scientists from the prestigious RIKEN Center for Biosystems Dynamics Research in Kobe and Kyoto University have sounded an urgent alarm. Their groundbreaking research, conducted using a sophisticated three-dimensional cardiac model, has unearthed disturbing evidence pointing towards an imminent heart failure pandemic. The crux of their findings lies in the revelation of persistent SARS-CoV-2 infections lurking within human hearts, potentially triggering widespread cardiac dysfunction on a global scale.

Imminent Heart Failure Pandemic! Millions Predicted To Die
Due To Rampant SARS-CoV-2 Viral Persistence In Heart!

Thailand Medical News would like to add that with the current mRNA vaccines also causing not only myocarditis but also a variety other cardiovascular related issues along with many drugs that are cardiotoxic being used in COVID-19 treatments and also other diseases along with the fact  that SARS-CoV-2 is already targeting the heart tissues and cells coupled with the fact that constant vaccinations and constant infections are making humans even more vulnerable and susceptible…the cumulative effects of all these are simply life threatening and alarming even to people who seem and look healthy.

With billions around the world already exposed to the SARS-CoV-2 virus and bilions of mRNA vaccine doses adminstered and with millions getting reinfected constantly, the future is indeed grim an d millions are expected to eventually succumb!
The ACE2 Receptor and Vulnerability of the Heart
At the forefront of this burgeoning concern are patients grappling with chronic cardiomyopathy. The research illuminates the perilous vulnerability of their hearts to persistent viral invasions, particularly by SARS-CoV-2. This insidious virus targets the ACE2 receptor, a protein abundantly expressed in human cardiac tissue. The implications of this heightened susceptibility cast a foreboding shadow, raising fears of an impending global crisis in cardiovascular health as a consequence of the COVID-19 pandemic.
Historical Context and Evolution of Research
Even prior to the dawn of the COVID-19 era, scientific inquiries hinted at the presence of viral genetic material within endocardial biopsies sourced from individuals afflicted with idiopathic chronic cardiomyopathy. These early revelations suggested a profound intertwining of viral infections with cardiac pathogenesis. However, the exploration of persistent viral infections within cardiac tissues remained relatively scant before the advent of 2019. The seismic impact of the COVID-19 pandemic has since thrust this issue into the spotlight, exponentially expanding the cohort of individuals vulnerable to future heart failure owing to lingering SARS-CoV-2 infections.
Establishing the SARS-CoV-2 Persistent Infection Model
In a groundbreaking endeavor, the research team devised a novel model to simulate persistent SARS-CoV-2 inf ections employing human-induced pluripotent stem cell-derived cardiac microtissues (CMTs). These intricately crafted CMTs, comprising a mosaic of cardiomyocytes and other essential cardiac cell components, faithfully mirror the structural and functional intricacies of the human heart.
Intriguingly, the experiments unveiled that mild infections were capable of sustaining viral presence within the cardiac microenvironment for an extended duration, up to a month, without precipitating significant functional impairment, indicative of persistent infection.
Impact of Hypoxic Stress on Cardiac Dysfunction
However, the precarious balance was disrupted when the persistently infected CMTs were subjected to hypoxic conditions mimicking ischemic heart diseases. In a distressing turn of events, the infected CMTs exhibited pronounced cardiac dysfunction concomitant with intracellular reactivation of SARS-CoV-2 within cardiomyocytes and perturbation of vascular network formation. This revelation underscores the heart's vulnerability to opportunistic assaults, whereby detrimental stimuli such as ischemia can act as catalysts precipitating cardiac dysfunction in the presence of persistent viral infections.
Detailed Results and Insights
The evaluation of cardiac function through a meticulous video-based analysis unveiled a spectrum of responses to SARS-CoV-2 infection. Notably, mild, moderate, and high titers of viral infection elicited varying degrees of functional deterioration, with high titers manifesting sustained impairment reminiscent of clinical cases necessitating heart transplantation. Histological and immunofluorescent analyses provided further insights, confirming the expression of SARS-CoV-2-derived spike protein within cardiomyocytes without inducing significant apoptosis or disrupting the structural integrity of cardiomyocytes.

Hypoxic Stress Experimentation
To corroborate the hypothesis positing the predisposition of individuals with mild SARS-CoV-2 infections towards developing cardiac dysfunction under additional stressors, the researchers subjected both infected and non-infected CMTs to hypoxic stress. This experimental maneuver unveiled a stark contrast in outcomes, with persistently infected CMTs showcasing a notable absence of functional recovery in response to hypoxic insult, in stark juxtaposition to their non-infected counterparts. Intriguingly, the hypoxic stress served as a trigger for the upregulation of intracellular ACE2 expression within cardiomyocytes, facilitating the reactivation of SARS-CoV-2 and exacerbating vascular network disruption, thereby exacerbating functional deterioration.
Role of Inflammatory Cytokines
Intrigued by the intricate interplay between inflammatory cytokines and cardiac dysfunction under hypoxic stress in the context of persistent infection, the research team embarked on an exploratory quest to unravel this enigma. Surprisingly, the analysis revealed a conspicuous absence of upregulation in the expression levels of representative inflammatory cytokines such as IL-6, TNF-α, IL-1β, and IFN-γ under hypoxic stress, irrespective of the presence of persistent SARS-CoV-2 infection. This unexpected finding suggests that the observed decline in cardiac function is not contingent upon the expression levels of cytokines implicated in inflammatory responses.
Discussion and Implications
The establishment of a human iPS cell-based cardiac tissue model represents a watershed moment in elucidating the enigmatic realm of persistent SARS-CoV-2 infections and their deleterious impact on cardiac health. The findings underscore the profound implications for individuals harboring mild SARS-CoV-2 infections, who may unwittingly teeter on the precipice of cardiac dysfunction, particularly under the duress of additional stressors.
The Limitations and Future Directions
While the study yields invaluable insights, it is imperative to acknowledge inherent limitations that may temper the interpretation of findings. The in vitro nature of the model and the absence of immune-related cells underscore the need for caution in extrapolating the results to complex physiological scenarios. Future research endeavors should endeavor to validate and extend these findings by exploring multi-organ models that can better capture the intricate interplay between different tissues and organs, thereby fostering a more comprehensive understanding of SARS-CoV-2-induced cardiac dysfunction.
In conclusion, the seminal research conducted by Japanese scientists offers a sobering glimpse into the ominous specter of a heart failure pandemic looming on the horizon. As the world grapples with the aftershocks of the COVID-19 pandemic, it is imperative to heed these findings and mobilize concerted efforts to mitigate the burgeoning threat posed by persistent SARS-CoV-2 infections in the heart. The establishment of therapeutic strategies hinges upon a nuanced comprehension of the intricate mechanisms underpinning SARS-CoV-2-induced cardiac dysfunction, underscoring the imperative for sustained research endeavors aimed at safeguarding global cardiovascular health in the post-COVID-19 landscape.
The study findings were published in the peer reviewed journal: iScience.
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