> We went into it thinking that [the risk] was going to be most pronounced and evident in people who smoked a lot or had diabetes, heart disease, kidney disease, or some [other] risk factors. What we found is that even in people who did not have any heart problems start with, were athletic, did not have a high BMI, were not obese, did not smoke, did not have kidney disease or diabetes—even in people who were previously healthy and had no risk factors or problems with the heart—COVID-19 affected them in such a way that manifested the higher risk of heart problems than people who did not get COVID-19.
They found that even mild COVID damaged otherwise healthy people's hearts so badly that their risk for heart problems are now comparable to those of obese people.
In other words, it does damage your heart. That damage might result in a heart attack, reflected in the increased hazard ratio.
> They found that even mild COVID damaged otherwise healthy people's hearts so badly that their risk for heart problems are now comparable to those of obese people.
> In other words, it does damage your heart. That damage might result in a heart attack, reflected in the increased hazard ratio.
This seems an inaccurate reading of what's in the study. They did not find that all people who had COVID had heart damage, which would be the case if "it does damage your heart" were true. Instead it found that some previously healthy people now had some heart damage.
Just one person but i was an early case (family member went to Wuhan 1-2 times each month. During the firsr year of COVID, as early as march of 2020, i had serious issues with gut and hearth inflamation - repeated bouts that started as back pain, became chest pain, elevated heart-rate to 150 for ~3 days at a time, 24 hours a day. Gradyally the episodes became less frequent leading up to a stroke type event co current with a presumed second bout of covid. Was forced back to work about a week after the issue, and the only other coworker who was near me contracted covid about 10 days later.
Following the Stroke type event I lost virtually all of my talent at writing, And ultimately my job, which was very humbling. Ive spent the past year working gig jobs when i can, and fortunately all long covid symptoms have gone away. I feel like my brain is close to 100% but i lack the confidence in myself, my memory, and my writing and am constantly second guessing myself and assume im wrong if in a contested discussion.
It really sucks, yet im probably one of the lucky ones
Finding this out would require doing mass exploratory surgery on asymptomatic people, which is obviously unethical, because it would kill a substantial number of them and damage all of their hearts.
First, the study does not even use the term "mild". They did look at three levels of severity: non-hospitalized, hospitalized, and admitted to ICU. The "non-hospitalized" group surely includes people who would describe their case as "worse than any flu", as well as those would describe theirs as "mild" (e.g. a few sniffles for a few days, like a number of my friends recently.)
Second, the hazard ratios differ widely between the three levels of severity. For example, for MACE (major adverse cardiac events) versus the contemporary control group, hazard ratios are:
Non-hospitalized 1.26
Hospitalized 2.41
ICU 4.36
One would expect a similar gradation of risk by severity among the "non-hospitalized" group.
>They found that even mild COVID damaged otherwise healthy people's hearts so badly that their risk for heart problems are now comparable to those of obese people.
False.
The study did NOT look for heart damage in the study population as a proximal cause for other cardiac events, it simply looked at incidence of cardiac events. Your interpretation is one possible explanation as to why this might be, but the study neither supports nor disproves this explanation.
Increased incidence is evidence as is the known link between viral infections and heart problems.
Suppose your car doesn’t start. That supports the possibility of a dead battery, it also supports broken wire or anything else that’s a possible cause. What it doesn’t support is your car being in proper working order.
If your car doesn’t start and you haven’t used it in 2 months, well it could be something else but …
>Suppose your car doesn’t start. That supports the possibility of a dead battery, it also supports broken wire or anything else that’s a possible cause. What it doesn’t support is your car being in proper working order.
Yes, these are hypotheses. But they are not meaningful in a scientific sense until you design a study and set about to try to disprove them. OP's claim was in relation to precisely what a scientific paper did or did not prove. Therefore, the appropriate level of rigour we need to apply here is a scientific one.
It is the study’s author referring to damage, he wasn’t willing to say what kind.
“even in people who were previously healthy and had no risk factors or problems with the heart—COVID-19 affected them in such a way that manifested the higher risk of heart problems than people who did not get COVID-19.
It was really eye-opening that the risk was also evident in people who did not have severe COVID-19 that necessitated hospitalization or ICU care. People who got COVID-19 and were asymptomatic
…
Why would SARS-CoV-2, the virus that causes COVID 19, which we all thought about as a respiratory virus, attack the heart up to a year down the road?”
I am sure the author would love to preform a more detailed study, but calling his conclusions unscientific seems to be overreaching.
I'm not calling the author's conclusions unscientific. At. All. He does not refer to damage, he does not draw conclusions about the mechanism which leads the cohort to have a higher risk of heart problems, and he certainly doesn't draw conclusions about individuals within the cohort, only the cohort as a whole.
Other people reading into the study things that aren't there is what I am calling out.
He's asking the same question I'm asking: "Why"? The scientist who conducted the study is saying his findings raises more questions, as any good study is likely to do. - I'm not sure why so many people want to read between the lines versus picking up the line of inquiry and doing further studies. There are any number of reasons why we could see heart issues from covid. Simply saying 'well, it must be direct damage to the heart, case closed' is completely reductive.
I agree he doesn’t know what specific method of action(s) or type of damage(s) is involved.
I suspect multiple different things result from getting COVID that directly or indirectly cause harm. The study only looks at the effects without digging into the proximate causes.
He did say: What we found is that even in people who did not have any heart problems start with, … —COVID-19 affected them in such a way that manifested the higher risk of heart problems than people who did not get COVID-19.
That doesn’t imply that COVID caused damage directly, it could have done something else and that something else caused damage. But that still means COVID started a chain of events resulting in heart damage.
Why would SARS-CoV-2, the virus that causes COVID 19, which we all thought about as a respiratory virus, attack the heart up to a year down the road?
> In other words, it does damage your heart. That damage might result in a heart attack, reflected in the increased hazard ratio.
Or it only damages the heart in a small number of patients, and that damage always results in heart conditions. It is not possible to tell the difference between these two possibilities without actually taking a sample and looking for asymptomatic heart damage in the affected patients, which this study did not do.
No, there's not enough data to be sure either way, but given that some/most people experience absolutely no lingering symptoms the simplest explanation is that even mild disease cases damage in some people.
EDIT: to be clear. We have no idea if the outcome-generating process is continuous or discontinuous. You seem to think it's continuous, analogous to risks from smoking or obesity, but others would assume not.
Lingering symptoms isn’t a useful diagnostic tool in this case. Hart damage is generally invisible up until people have a significant problem. This is why young marathon runners occasionally die of undiagnosed heart problems and the elderly get in depth testing before voluntary medical procedures.
Hypothetically, if 3/4 of population has the baseline risk and 1/4 the population has 8x the risk then you could say most people are at identical risks. But unless you can determine which population someone was in that’s irrelevant.
> We went into it thinking that [the risk] was going to be most pronounced and evident in people who smoked a lot or had diabetes, heart disease, kidney disease, or some [other] risk factors. What we found is that even in people who did not have any heart problems start with, were athletic, did not have a high BMI, were not obese, did not smoke, did not have kidney disease or diabetes—even in people who were previously healthy and had no risk factors or problems with the heart—COVID-19 affected them in such a way that manifested the higher risk of heart problems than people who did not get COVID-19.
They found that even mild COVID damaged otherwise healthy people's hearts so badly that their risk for heart problems are now comparable to those of obese people.
In other words, it does damage your heart. That damage might result in a heart attack, reflected in the increased hazard ratio.