My belief is that most of the time, people get catastrophic endocarditis when they have a naturally weakened immune system, or when their immune system is battling something else, or just when rotten luck allows an entrepreneurial bacterium to colonize on some serendipitous backwater by the valve.
However, I think that people get valve-adjacent endocarditis, or at least the start of it, much more often than we think.
We are all often subjected to bacteremia (bacteria loose in the bloodstream), probably much more often from eating mishaps than from dental procedures. And there are bacteria from various cuts, scrapes and other everyday physical damages. While the blood is a relatively sterile environment at best, the body generally handles these incursions quite well, when we are healthy and active. After all, we're adapted to many of life's vicissitudes. But should we have a slight abnormality in the flow around a valve, or an infected gumline, throat, or other area that becomes a constant source of bacterial flow, we raise our chances of infections at internal sites, particularly in the heart or the bones.
I believe that most "senile" valve calcification (and maybe much of the other types) is caused by prior infection sites, where the body has successfully battled the infecting bacterium or virus, but has left scarred epithelium (skin) in its wake that attracts calcium, phosphorus, and the other building blocks of apatite (cardiolytic apatite, as the phrase was coined). Secondarily, consistently irritated spots, especially associated with damaged or bicuspid valves, can serve as the host site, as the epithelium is damaged there, as well.
This explanation makes so much sense to me, that I am at a loss to determine why I've never read it stated that way elsewhere. The closest I've seen is the theory that the damaged valve leaflets themselves attract the chemicals. Yet the bulk of the apatitic growth is at the base of the valve, and only later does it coat the damaged leaflets. Perhaps doctors are reluctant to believe that we can recover from any form of endocarditis without actual hospitalization, or they underestimate the value that effective antibiotics can bring in allowing us to recover unknowingly from these deep, internal infections.
Most of us won't ever face catastrophic endocarditis, where the valve needs to be replaced immediately from the infection. Some few of us on the site have truly faced it, and live with its aftermath (I have not). However, I believe many of us have had a close cousin to it, or a start to it that the body managed to snuff out early. Then we recovered, with collateral damage being the slow accumulation of protective calcific sheathing on the wound site.
One attempt to prove this would be to see if the number of calcified valves has increased since the advent of antibiotics. If these drugs are letting us live after these infections, then the later effects (calcification) would appear more often, as the hosts would not have died from the original disease state.
I haven't had time to pursue a proof for this yet, but I will eventually give it a try.
Best wishes,
However, I think that people get valve-adjacent endocarditis, or at least the start of it, much more often than we think.
We are all often subjected to bacteremia (bacteria loose in the bloodstream), probably much more often from eating mishaps than from dental procedures. And there are bacteria from various cuts, scrapes and other everyday physical damages. While the blood is a relatively sterile environment at best, the body generally handles these incursions quite well, when we are healthy and active. After all, we're adapted to many of life's vicissitudes. But should we have a slight abnormality in the flow around a valve, or an infected gumline, throat, or other area that becomes a constant source of bacterial flow, we raise our chances of infections at internal sites, particularly in the heart or the bones.
I believe that most "senile" valve calcification (and maybe much of the other types) is caused by prior infection sites, where the body has successfully battled the infecting bacterium or virus, but has left scarred epithelium (skin) in its wake that attracts calcium, phosphorus, and the other building blocks of apatite (cardiolytic apatite, as the phrase was coined). Secondarily, consistently irritated spots, especially associated with damaged or bicuspid valves, can serve as the host site, as the epithelium is damaged there, as well.
This explanation makes so much sense to me, that I am at a loss to determine why I've never read it stated that way elsewhere. The closest I've seen is the theory that the damaged valve leaflets themselves attract the chemicals. Yet the bulk of the apatitic growth is at the base of the valve, and only later does it coat the damaged leaflets. Perhaps doctors are reluctant to believe that we can recover from any form of endocarditis without actual hospitalization, or they underestimate the value that effective antibiotics can bring in allowing us to recover unknowingly from these deep, internal infections.
Most of us won't ever face catastrophic endocarditis, where the valve needs to be replaced immediately from the infection. Some few of us on the site have truly faced it, and live with its aftermath (I have not). However, I believe many of us have had a close cousin to it, or a start to it that the body managed to snuff out early. Then we recovered, with collateral damage being the slow accumulation of protective calcific sheathing on the wound site.
One attempt to prove this would be to see if the number of calcified valves has increased since the advent of antibiotics. If these drugs are letting us live after these infections, then the later effects (calcification) would appear more often, as the hosts would not have died from the original disease state.
I haven't had time to pursue a proof for this yet, but I will eventually give it a try.
Best wishes,
