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In the northern hemisphere, the winter months are approaching, and colds and respiratory illnesses will become commonplace. In fact, data from Oceania indicate that the influenza wave could be particularly aggressive in 2022-23.
To this we must add that it will most likely come along with the next wave of covid-19 with the current, more effective options. That is why the WHO has already warned that Europe needs to take action and strengthen primary health care. We’ll need it.
In addition to the usual respiratory symptoms (which can range from the common cold to deadly pneumonia), another worrying fact is worth paying attention to: SARS-CoV-2 and other respiratory viruses can cause cardiovascular symptoms.
In fact, our knowledge of the effects of other pandemics indicates that these symptoms can affect life expectancy, causing premature death months or years later.
Lessons from Past Pandemics
After the 1918 flu, the scientific literature of the time described rare cases of brain fog and chronic fatigue, two symptoms associated today with COVID-19. But in addition to the usual flu symptoms, the 1918 flu left a very disturbing long-term sequel: the wave of heart attacks that rocked the world between 1940 and 1959. This wave was strange, obviously inexplicable, but today we already know it was due to the previous influenza pandemic. In some survivors, the virus left a time bomb.
This wave of cardiovascular disease has particularly affected men, as has the influenza pandemic itself, and now covid-19. As a possible explanation, it has been suggested that an unusual immune response in men between the ages of 20 and 40 in 1918 could account for the higher adult mortality of survivors.
But more than that, intrauterine exposure to the 1918 flu virus was associated with a greater likelihood of heart disease after age 60.
Subsequent studies have shown that infection with the influenza virus increases the development of atherosclerotic plaques and therefore the possibility of heart attacks. Damage to the vascular endothelium accelerates plaque formation and therefore the risk of heart attacks.
SARS-CoV-2 infection and cardiovascular disease
After the first months of the pandemic, data began to be collected showing an increase in cardiovascular damage after infection with SARS-CoV-2. The most common complications were heart failure, myocardial damage, arrhythmias, and acute coronary syndrome.
To explain these symptoms, two possibilities are considered, both based on consistent evidence:
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BUT unbalanced immune response against the background of a viral infection causes an inflammatory process that causes vascular damage. Inflammation, culminating in a cytokine storm, can cause vasculitis or vascular inflammation. So in people who already have the onset of cardiovascular disease, this inflammation will speed up the process.
This explains why people with cardiovascular disease and risk factors such as diabetes, hypertension and hypercholesterolemia are most affected by Covid-19.
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SARS-CoV-2 enters cells using the ACE2 protein, which is abundant in endothelial cells that line blood vessels. This protein is essential for cardiovascular function, blood pressure regulation, electrolyte control, vascular repair, and inflammation.
Thus, if the virus enters the bloodstream, it will enter these cells, causing endothelial damage accompanied by inflammation leading to vasculitis and thrombosis, two symptoms of infection. In addition, the S protein itself generates inflammatory signals in endothelial cells, further exacerbating the situation.
An increase in the number of abortions in women with covid-19
Because SARS-Cov-2 attacks the endothelium, it is possible that it causes irreparable damage to highly vascularized tissues, including the placenta.
This explains the increase in the number of abortions in women who have had COVID-19. In fact, the profiles of vascular damage in pregnant women with COVID-19 are similar to those found in cases of preeclampsia, an imbalance in blood pressure that causes vascular damage and miscarriages.
In addition, other studies have shown that in early pregnancy, the virus can cause fetal organ damage associated with a generalized inflammatory process.
Vaccines and myocarditis? no evidence
The effect of protein S on the endothelium has been associated with possible vascular damage caused by mRNA-based vaccines. In these vaccines, the mRNA they contain generates this protein in the tissues so that the immune system recognizes it and activates against it. But this damage cannot be proven.
Although attempts are being made to raise the alarm about vaccine-associated myocarditis, scientific evidence does not support these concerns. Recent post on JAMA showed that of the approximately 192.5 million vaccinated in the US, only 8.4 per million had symptoms of myocarditis, of which only 92 needed more specific treatment than conventional anti-inflammatory drugs, and none of them died.
There is no reason for such panic. Myocarditis symptoms reported a few days after vaccination are mild and likely indicate a somewhat more aggressive inflammatory response in these individuals, but not direct damage to the S protein. In fact, blood S protein levels after vaccination are very low. and its effect on the endothelium is transient, disappearing after a few days.
Prevention of vascular damage, another reason to get vaccinated
Taking into account all the data accumulated to date and the precedents of previous pandemics, it can be concluded that covid-19, like other acute respiratory infections, can exacerbate the course of cardiovascular diseases and reduce life expectancy, either by accelerating vascular damage or by generating new damage. . This damage can lead to death even months or years after infection.
Fortunately, vaccination has been shown to be effective against these effects as well as against covid-19. The rationale is simple: if the virus cannot enter the bloodstream, it cannot affect the cardiovascular system.
Another reason not to let the coronavirus infect us without being prepared. Vaccination saves lives even years later.
Guillermo López Lluch, Professor of Cell Biology. Junior Research Fellow at the Andalusian Center for Developmental Biology. Researcher of metabolism, aging, immune system and antioxidants, Pablo de Olavide University
This article was originally published on The Conversation. Read the original.
Source: RPP

I’m Liza Grey, an experienced news writer and author at the Buna Times. I specialize in writing about economic issues, with a focus on uncovering stories that have a positive impact on society. With over seven years of experience in the news industry, I am highly knowledgeable about current events and the ways in which they affect our daily lives.