#17,840
In the opening weeks and months of the COVID pandemic we saw reports of a steep rise in sudden heart attacks around the country, which prompted JAMA to publish an original investigation which found a substantial increase in out-of-hospital cardiac arrests in New York City during the peak of their first COVID-19 wave, finding:
From March 1 to April 25, 2020, New York City, New York (NYC), reported 17 118 COVID-19–related deaths. On April 6, 2020, out-of-hospital cardiac arrests peaked at 305 cases, nearly a 10-fold increase from the prior year.
Also in the summer of 2020 (see JAMA: Two Studies Linking SARS-CoV-2 Infection To Cardiac Injury), we examined the results of 39 autopsies on COVID cases, that showed even when pneumonia is the presumed cause of death - and even without overt histopathic evidence of acute myocarditis - the heart often shows a high viral load of SARS-COV-2.
A second, and arguably even more worrisome study, found a remarkable incidence of cardiac injury and myocardial inflammation among a relatively young cohort (avg. age 49 & without pre-existing cardiac hx) of COVID patients who mainly recovered at home but continued to experience a variety of symptoms following their illness.
An accompanying editorial (see Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter? by Clyde W. Yancy, MD, MSc1,2; Gregg C. Fonarow, MD3,4) raised serious concerns over the long-term impact of COVID on public health.
Despite attempts to paint COVID as a relatively mild `flu-like' illness for most people, we continue to see evidence that it can cause significant extrapulmonary impacts, including :
AHA: COVID-19 May Trigger New-Onset High Blood Pressure
JAMA: Additional Evidence Of A Post-COVID/Diabetes Link
The Lancet: Neurological and Psychiatric Risk Trajectories After SARS-CoV-2 Infection
MMWR: Post–COVID-19 Symptoms and Conditions Among Children and Adolescents
Repeated COVID infections have been linked to worse outcomes (see Nature: Acute and Postacute Sequelae Associated with SARS-CoV-2 Reinfection), leaving many researchers concerned that our increasingly laissez faire towards the virus may be steering us towards a future with increased early deaths and disability from these infections.Nature: Long-term Effects of SARS-CoV-2 Infection on Human Brain and Memory
Although the question was first seriously asked in the summer of 2020 (see Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter?), this week we have new research into the potential for COVID to spark a `Heart Failure Pandemic' in the years ahead.
Prior research has shown that the SARS-CoV-2 virus can infect the heart (see Cardiovascular Tropism and Sequelae of SARS-CoV-2 Infection), and infection has been linked to myocarditis, pericarditis, blood clots, and arrhythmia.
Researchers from Kyoto University (Japan) created a SARS-CoV-2 persistent infection model using human iPS cell-derived cardiac microtissues (CMTs) and found that mild infections could persist without serious impact for a month or more.
However, when stressed by hypoxia (mimicking ischemic heart disease), cardiac function deteriorated and the virus showed reactivation in cardiomyocytes (heart muscle cells).
While it is worth repeating that their findings are based on an in vitro model, but their findings align with others we've seen over the past 4 years, giving their conclusions additional weight. Due to its length, I've only posted the Abstract and some excerpts, so follow the link to read it in its entirety.
I'll return with a postscript after the break.
Predicted risk of heart failure pandemic due to persistent SARS-CoV-2 infection using a three-dimensional cardiac model
Kozue Murata 1 3, Akiko Makino 2, Keizo Tomonaga 2, Hidetoshi Masumoto 1 3 4Show more
https://doi.org/10.1016/j.isci.2023.108641 Get rights and content
Highlights
• Persistent SARS-CoV-2 infection model of human cardiac tissue was established
• Hypoxic stress to the persistent infection model led to cardiac dysfunction• ACE2 and SARS-CoV-2 S protein expression were elevated after the hypoxic stress• This research may predict a “heart failure pandemic” in the post COVID-19 era
Summary
Patients with chronic cardiomyopathy may have persistent viral infections in their hearts, particularly with SARS-CoV-2, which targets the ACE2 receptor highly expressed in human hearts. This raises concerns about a potential global heart failure pandemic stemming from COVID-19, an SARS-CoV-2 pandemic in near future. Although faced with this healthcare caveat, there is limited research on persistent viral heart infections, and no models have been established.
In this study, we created an SARS-CoV-2 persistent infection model using human iPS cell-derived cardiac microtissues (CMTs). Mild infections sustained viral presence without significant dysfunction for a month, indicating persistent infection.
However, when exposed to hypoxic conditions mimicking ischemic heart diseases, cardiac function deteriorated alongside intracellular SARS-CoV-2 reactivation in cardiomyocytes and disrupted vascular network formation. This study demonstrates that SARS-CoV-2 persistently infects the heart opportunistically causing cardiac dysfunction triggered by detrimental stimuli such as ischemia, potentially predicting a post COVID-19 era heart failure pandemic.
(SNIP)
DiscussionThe human iPS cell-based cardiac tissue model established in the present study is the first report to experimentally demonstrate SARS-CoV-2 persistent infection of the human heart exhibiting functional deterioration caused by the opportunistic intracellular reactivation of viral infection.
We experimentally demonstrated that cardiac tissues under persistent infections with SARS-CoV-2 are at high risk of cardiac dysfunction with additional hypoxic stress (Figure 2B). In other words, the explosive increase in the number of virus-infected patients due to the COVID-19 pandemic may have led to an enormous increase in the number of patients at potential risk for future heart failure.
These patients would be predicted to maintain cardiac function superficially despite being at marginal risk. In clinical practices, such high-risk patients should be identified by detecting the virus itself or the viral genome in endocardial biopsy tissue or by monitoring blood troponin levels. According to our study, cardiac dysfunction associated with persistent infection was the result of increased ACE2 expression in cardiomyocytes in response to additional stress (Figure 2D), reactivation of SARS-CoV-2 in cardiomyocyte (Figure 2C), and disruption of the vascular network-like structure (Figure 2E). Hence, apart from viral clearance from the heart, strategies that can inhibit these processes are being considered as potential therapeutic approaches.
(SNIP)
In conclusion, this report may serve as a warning for the possibility of a heart failure pandemic in the post COVID-19 era. As a countermeasure against this global healthcare risk, this model would serve as a useful tool to investigate the mechanism of the onset and the progression of SARS-CoV-2 cardiomyopathy and to develop therapeutic options.
Despite the preponderance of evidence suggesting that repeated COVID infections increase the risk for developing a wide range of chronic health problems, as a society we seem to be assuming the best case scenario.
Vaccination Trends Update:
Reported on Friday, December 22nd, 2023.
- The percent of the population reporting receipt of the updated 2023-24 COVID-19 vaccine is 7.6% (95% confidence interval: 6.7-8.4) for children and 18.5% (17.8-19.2) for adults 18+, including 37.3% (35.2-39.5) among adults 65+.
