I am old (80 yr) but not frail (lifetime athlete) with no comorbidities or prescription medications so far. An excellent but overactive immune system has given me many allergies and sensitivities to chemicals, including most antibiotics, so it has been necessary to live a nontoxic, drug-free life.
I asked my Dr. why a second TAVR instead of SAVR, because I may need a new valve within 10 years. He said after age 90 they will probably not replace the valve. I asked him was he just planning to let me die then, and he said that comorbidities would probably cause death near that age anyway. Not a very promising prognosis.
Since his conference of doctors recommended the second TAVR, and he has a good reputation for TAVR surgery, with no better alternative I felt obliged to acquiesce. Hopefully the next ten years will produce better valve surgery choices and/or this TAVR-in-TAVR will last longer than ten years.
Thank you for your comment about LP(a).
I have a history of high LDL cholesterol over many years and wonder if it is hereditary LP(a), so I called my siblings and found the following:
Obese brother age 76 has high LDL cholesterol, had 2 heart attacks with stents installed.
Brother age 71 has high LDL cholesterol and progressing aortic stenosis.
Sister age 73 has high LDL cholesterol.
Dad died at 73 of heart attack and Mom at 92 of “natural causes”.
Perhaps our heart problems are hereditary.
Thank you for your detailed information. These type of details are very helpful to other members. At age 80, I understad better why your cardiologist is having you get a TAVR in TAVR.
I have a history of high LDL cholesterol over many years and wonder if it is hereditary LP(a),
Elevated Lp(a) is hereditary. In fact, our genes are about 95% in control of our Lp(a) levels and it runs strongly in families. Lifestyle changes, such as diet and exercise, have close to zero impact on Lp(a) levels, which makes it different than LDL.
Given that your TAVR valve, which is a tissue valve, calcified so soon, I would definitely suggest getting your Lp(a) tested. Per your question, high Lp(a) does often come with high genetic LDL, but often LDL is normal and Lp(a) is elevated. My brother and I have very high Lp(a) levels and relatively normal LDL levels. This seems to be the pattern in our family, normal LDL, but very high Lp(a).
Lp(a) is causal for heart disease and valve disease. In that your family has a history of heart disease and aortic stenosis, all should probably get checked. It is important to know, not just for your generation, but the younger folks in your family as well. It is often completely overlooked by GPs and cardiologists, even though worldwide guidelines are now calling for all individuals to be tested at least once in their lifetime.
Although it has been known to be highly correlated with aortic stenosis for years, earlier this year the first study was published showing a strong correlation with early calcification of bioprosthetic tissue valves. If an individual is shown to have very high Lp(a), they should probably take this into account in their valve choice. It could have been several things which caused your TAVR to calcify after only 4 years, but you should do the simple blood test to determine if the likely culprit is elevated Lp(a).
One reason why its good to know is that there is now a treatment for high Lp(a)- PCSK9-I, such as Repatha. Repatha is used to lower LDL, but one big side benefit is that it also lowers Lp(a). For me, Repatha lowered my Lp(a) 40%. So now my level is only 2x what it should be, instead of 3.5x as high as it should be. Also, there are several more effective treatments in the pipeline, with one which lowers Lp(a) by 80% expected to get FDA approval next year. Also, statins, which are used to treat high LDL, do not lower Lp(a). In fact, they usually raise it for most individuals. Not a problem if your Lp(a) is normal, but can increase one's risk if your Lp(a) is elevated. This is why when individuals present with both elevated LDL and Lp(a), they are often treated with both statin and PCSK9-I, and sometimes just PCSK9-I.
On my mom's side of the family, there is a history of men dying at young ages of heart disease. We now know that very high Lp(a) runs in the family and have taken steps to mitigate. To be clear, elevated Lp(a) is not a death sentence. It correlates strongly with early onset heart disease and valve disease, but many people who are elevated go through life without these issues. Also, as mentioned, there is a moderately effective treatment, with more promising treatments in the pipeline with FDA approval expected soon.
Here is some additional info on Lp(a) from the American Heart Association
https://www.heart.org/en/health-topics/cholesterol/genetic-conditions/lipoprotein-a
