In a groundbreaking study conducted by Japanese scientists at the Riken research institute, a dire warning has been issued about the potential for a global crisis of heart failure following the COVID-19 pandemic. The study focuses on the prevalence of ACE2 receptors, which are targeted by the coronavirus, within the human heart. The alarming findings indicate that individuals exposed to SARS-CoV-2 may experience reduced cardiac function, raising concerns about a looming “heart failure pandemic” on a global scale.
Contrary to previous assumptions that heart failure caused by SARS-CoV-2 infection is rare or only occurs in severe cases, many studies have shown that anyone exposed to the virus is at high risk. Heart failure is currently the leading cause of elevated mortality rates worldwide, yet most health authorities are unwilling to acknowledge the link between SARS-CoV-2 infections and these cases.
The study highlights the critical role of ACE2 receptors in the heart, which the coronavirus exploits for cellular entry. These receptors are not only present but prevalent in cardiac tissues, making the heart highly susceptible to SARS-CoV-2 infection. The researchers emphasize the urgent need to establish testing systems and treatment methods in preparation for a potential “heart failure pandemic.”
As the world transitions from the acute phase of the COVID-19 pandemic, the focus shifts to the chronic health implications. The expression of ACE2 receptors in the heart raises concerns about the heart’s vulnerability to SARS-CoV-2 infection, particularly in individuals with pre-existing heart conditions.
To validate the potential risk of a heart failure pandemic, the scientists at Riken have developed a three-dimensional human cardiac tissue model using induced pluripotent stem cell-derived cardiac microtissues (CMTs). This model allows researchers to study the impact of SARS-CoV-2 on cardiac health in detail.
The experimental findings of the study reveal the dynamics of persistent SARS-CoV-2 infection in cardiac tissues. Mild infections can sustain viral presence without significant dysfunction for a month, indicating the potential for long-term, persistent infection. However, exposure to hypoxic conditions, simulating ischemic heart diseases, leads to cardiac dysfunction, intracellular viral reactivation, and disrupted vascular network formation.
The study demonstrates the persistence of viral infection within cardiac tissues, even in individuals with seemingly mild infections. Hypoxic stress exacerbates the risk of heart failure by disrupting vascular network formation and contributing to functional deterioration in infected cardiac tissues.
Contrary to expectations, the study finds that hypoxic stress does not upregulate inflammatory cytokines in the context of persistent infection. This suggests that cardiac dysfunction in persistent infection is not solely dependent on the expression level of cytokines associated with inflammatory responses.
While the study provides valuable insights into the potential cardiac consequences of persistent SARS-CoV-2 infection, further research is needed to fully understand the impact of cytokine storms and immune responses observed in vivo.
To unravel the route of SARS-CoV-2 infection to the heart and understand the complex interaction between multiple organs, researchers propose the development of multi-organ models. These advancements could aid in the development of therapeutic options and contribute to a comprehensive understanding of the virus’s impact on the body.
The revelation of a potential heart failure pandemic adds a new layer of complexity to the ongoing COVID-19 crisis. The study from Riken serves as a stark warning, urging the global healthcare community to establish testing systems, treatment methods, and a comprehensive understanding of the mechanisms underlying SARS-CoV-2 cardiomyopathy. It is a call to action for scientists worldwide to decipher the intricacies of SARS-CoV-2’s impact on the heart and develop strategies to safeguard global cardiovascular health.