OT? Aortic valve replacement

Yep…and the cardiologist might well be relieved if that were to happen. Patients who choose to ignore advice are litigation time bombs very often…and a pot of gold for personal injury/malpractice lawyers. It’s much easier way to sever the doctor-patient relationship from the patient’s side than the other way round.

One of my professors back in Days of Yore always reminded us not to be afeard of pithing the patient off (pardon my lithp) with repeated good advice. They might eventually follow it. If not, they might well remember the advice was given when they’re looking for someone to blame when the spit hits the fan

VeeEnn,

Not every patient will listen to every doctor. Taking agency another doctor might help communicate with him.

Indeed. Hence the admonition of one of my dental school professors. A good many won’t understand what they’re being told, either. Or, come to that, relay any conversation accurately when giving an account to other parties.

Obviously, the ASCVD 10 year risk calculation missed out the obvious. That a significantly elevated LDL-C isn’t just a risk factor. It’s a state of affairs where actual harm is being done to the walls of the cardiovascular system. Every. Single. Day that the LDL-C is elevated. Just like with an elevated A1c. Additionally, the 10 yr risk from today (or whenever the last appointment where the discussion took place was) doesn’t take account of the existing pathology from the previous decades when advice was ignored

An experiment for any interested parties to make is to pull up the ASCVD risk calculator and to plug in the numbers from their most recent lipid profile and start tinkering with the age. Starting at 40 (I don’t think there’s the option to plug in a younger age). Notice how the risk increases with age, even if the other values remain the same…which most folk are aware doesn’t usually happen in real life. That’s because damage is constantly happening with the passage of time…and progressing with compound interest. The reason cardiologists take elevated LDL-C seriously. Also the reason why sudden cardiac death is still frequently the first symptom of heart disease when folk don’t address dyslipidemia appropriately.

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Just like that, I check my email and a related article by the Skeptical Cardiologist pops up…

Profiles in Prevention: Tracking How Coronary Plaque Responds to Treatment Profiles in Prevention: Tracking How Coronary Plaque Responds to Treatment

The ASVCD calculator puts me at 20% risk of an event in the next 10 years, but with self care down to about $7.5%. The calculator does not know I have reduced my sugar and A1C to prediabetic. The Weight has been reduced by 35 pounds. That I exercise, etc…I have met the goals for the 7.5% risk factor.

It’s just a reprieve for a few months. But unless the numbers improve, it is likely that come summer, I’ll begin taking a statin. The prescription is already in the system with a begin date sometime in mid-June.

Indeed it does not. The straight-up old ASCVD calculator (minus any of the more recent refinements) doesn’t factor in all the other risk multipliers that increase risk in folk whose vessels are also under assault from marinating in a rich mix of glucose and insulin in addition to the atherogenic particles measured by a standard lipid panel. Or how long these adverse conditions have been in effect, silently causing damage.

This is where individual variation needs to be applied…and where the individual themselves can exercise a bit of honest introspection, knowing as they do how long they’ve allowed these adverse conditions to scamper along unchecked.

I suspect that, for people like me, whose numbers are what they are almost entirely due to familial hypercholesterolemia alone, the standard risk calculator underestimates my risk of a cardiovascular event. Certainly that’s what bamboozled my PCPs for the past couple of decades. I find myself in the position of a lifelong spendthrift and LAMMer (living above my means) who’s suddenly having to do a Dave Ramsey to avoid penury in my senior years. A victimof The Curse of the Healthy Lifestyle!

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I just looked at my recent numbers again and it shows:

HDL Cholesterol 59 mg/dL
LDL Chol Calc (NIH) 142 mg/dL [reference range 0 to 99]
VLDL Cholesterol Cal 11 mg/dL [reference range 5 to 40]
Triglycerides 64 mg/dL

If the VLDL is low but the LDL is high, do I have less to worry about? Or it is still worrisome that the LDL is so high? (AI says still worrisome, so I’ll probably begin the statin when I get back home in a month and a half.)

Since I am on the topic, and since I have such recent bloodwork, I just now ran the PREVENT calculator with the latest numbers. These are the results:

Estimated 10-year risk of CVD 5.7%
Estimated 10-year risk of ASCVD 3.9%
Estimated 10-year risk of Heart Failure 2.5%

These chances seem low to me, but I suppose the goal is to be close to 0%.

Less to worry about than what? My LDL-C had never been that high. Additionally to that, I’ve never been fat, never been sedentary for extended periods but, once properly investigated, a CAC scan showed a score of over 700 (significant disease burden) and a CT angiogram showed 3 major coronary arteries with greater than 80% blockage. All of which had happened whilst I wasn’t taking a statin (or other lipid lowering medication) Probably would not have happened if I had been taking a statin.

What that tells you (and you’ve had the opportunity to read this multiple times…including in this very thread) very few people have good cause to imagine that they can escape biological reality. It’s the LDL-C particles…specifically Apo-b, aided and abetted by Lp(a) … that initiate the disease process.

As an afterthought, I’d suggest thinking about a “risk factor” a bit differently (and this applies equally to A1c/prediabetes) Rather than thinking these elevated test scores as a biomarker that may or may not apply to you in the disease assessment stakes, perceive them for what they really are. Disruptions to a healthy environment for your cardiovascular system that are actually causing damage.

My results (from December bloodwork, I don’t know why the doctor didn’t include it in the April bloodwork, and now I am annoyed that he didn’t) for those are:

Apolipoprotein B 103 mg/dL (reference: less than 90)
Lipoprotein (a) 8.8 nmol/L (reference: less than 75)

I did the CAC scan last October, and my score was 13.4. The report is full of medical gobbledegook but appears to say “no blockage”.

The PREVENT calculator doesn’t ask for any of these things though (as far as I recall).

Interesting; my surgeon (stent for my heart attack in 2001) is also (and has been) my cardiologist since then. I didn’t know you could have different doctors.

JimA

Most likely, your stent was placed by an intervention cardiologist and is the person also following you. Wendy…and my husband’s…valve and aorta replacement was performed by a cardiothoracic surgeon. My husband was followed jointly by the surgeon and intervention cardiologist and now solely by the intervention.

Stent placement isn’t considered “surgery” in the same way as it’s not an open heart procedure.

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Why are you annoyed with the doctor? If you’ve had the opportunity to see for yourself where the problem lies already (elevated Apo-b) and ignored it, it seems to me that your ire is misplaced.

You’ve been equipped with the levels of the relevant biomarkers plus evidence that you do, in fact, have a degree of coronary artery disease AND had the opportunity to read the significance of all these minus “medical gobbledegook” in this very thread to name but one source. There’s an excellent reason for your cardiologist to recommend statins/a more aggressive lipid lowering regimen (to the point of your annoyance) … as opposed to simply tinkering with your diet ineffectually. Waiting for the crushing chest pain, glimpse of The Grim Reaper/feeling of impending doom that announces BLOCKAGE!!! (from either an increasing burden of calcified plaque or the rupture of unstable “soft” plaque which a CAC scan doesn’t show) could possibly invite the attentions of litigation conscious relatives who don’t understand why no one said anything. Possibly wouldn’t do you a power of good should you survive the heart attack, come to that.

It sounds to me like a follow up order for apoliprotein b would have helped measure whether, and to what extent, your condition may be worsening. I would definitely contact the doctor’s office in writing, text or email, and ask why the tests weren’t ordered?

I did exactly that when my doctor failed to order d3 and tsh tests given my past history of low d3 and elevated tsh and she apologized for the oversight and ordered the tests.

Mainly because he doesn’t spend much time with me to discuss any of this stuff. He never even mentioned Apo B in our conversation, I first found out about it here in THIS discussion. Even the AI that I used didn’t mention it.

I’m also annoyed because he didn’t include Apo B in the most recent bloodwork. To be fair, the most recent one was ordered by my GP, not by my cardiologist, but they each have access to all the records, AND it was supposed to be a full lipid panel.

Like I said, if necessary, I would take the statin, but I want to know which items exactly they measure to determine success. A few years ago, I took losartin for 15 months and it seemed to me that it wasn’t doing anything. I mentioned that to the doctor and he said the only way to determine that is to stop taking it and compare BP from the month before to the month after. At the time, I took my BP 3x day and recorded it in my phone. Sure enough, the BP in the month after stopping the medication looked exactly like the month with the medication. My BP is higher in the morning, medium at midday, and lower in the evening. Now a few years later, my GP wants me to try a different BP medication. So maybe by summer I’ll be on TWO medications!

I’ve been waiting for a long time. My grandfather had a heart attack at age 45, then he finally stopped smoking. He was a character - he stopped mid-cigarette, and put the ashtray and the half box of cigarettes on the small kitchen shelf above the table where the sugar, salt, etc was placed when not in use. That half box of cigarettes sat there on the shelf for decades. I suppose it was there to remind him to never smoke again LOL.

And my father had a heart attack at age 47 and one month and 6 days. His attack happened at the gym (I had left the gym about 20 minutes earlier, and he planned on going home with a friend later). We received a call at home from the friend telling us about the attack, and my mom and I went to the hospital immediately, turns out we got to the hospital before the ambulance did. I don’t recall all the details, but apparently that MI wasn’t due to blockage but more due to “spasm” (or whatever they called it, really I don’t quite recall, but that was the gist of it). They treated him with a new revolutionary drug called TPA (one of the first genetically engineered drugs) to thin the blood, and later (after it was approved in the USA) he began taking lipitor, and still takes it today nearly 40 years later. I remember that the TPA required signing a special approval form acknowledging the risks (mainly brain issues because of how much and how rapidly it thins the blood and breaks clots). It was also godawful expensive at $20,000 a dose (in 1988 that was a heck of a lot of money, but insurance approved it or most of it).

So when I turned 47 and one month and 6 days, I happened to be at the gym at 7:20pm, I paused my workout and after a minute or two, I told my friends “3 … 2 … 1 … okay, I beat my dad, no heart attack yet” :joy:

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Over a 6 month period? Nah. For starters, Lp(a) is currently a once in a lifetime recommendation. It’s a biomarker that’s a sign of a genetic predisposition and is unaffected by lifestyle or currentmedications. You have a higher level…or you do not. Mark does not.

Apo-b, again, is probably unnecessary to keep tracks on as closely as regular LDL-C as a measure of disease progression once it’s been established as, at least partly, responsible for that elevated LDL-C. If LDL-C hasn’t dropped precipitously since the last test…and it seems to me there’s not much reason to expect it would have … then manifestly, the Apo-b hasn’t changed enough to alter the course of the disease process. “There Disease Process” being advancing ASCVD.

I’m all for folk being vigilant over their health and being their own advocate (for very obvious reasons, given my experience) but asking why tests are not being repeated within such a short space of time when nothing much was done with the information first time doesn’t seem to me to quite fall into that category.

Incidentally, I’m as interested in checking the success of my lipid lowering strategy as anyone. … statin and PCSK9 inhibitor. … and did ask if there was merit in further follow up with a CT angiogram. This was after a year with my LDL-C down in the low 30s. Apparently not. The Gold Standard seems to be a reduction in progress of symptoms or, in someone asymptomatic like myself, no progression beyond that. A bit disappointing but the predictive value of any change that might be visible isn’t good enough to balance the excess radiation incurred.

Fair enough. A doctor could offer a similar explanation as to why folllowup was unnecessary in April, and the patient would understand the process better.

I used to resolve many disputes as a lawyer and as a mediator hired to mediate disputes between lawyers by 1) opening up lines of communication and 2) giving my clients copies of a book called, “Don’t Sweat the Small Stuff.”

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It should be <70.

Mine is 86. We are doubling my rosuvastatin to 10 mg.

I have had a lot of family members die in their late 80s from strokes. No, thank you.

That 70 level on the LDL is where the risks of plaque truly drop off.

VeeEnn, your situation is different. The average Joe needs to avoid creating plaque simply.

I tolerate rosuvastatin well. Brand name Crestor. Crestor has some advantages over Lipitor… let me look…

Crestor (rosuvastatin) generally offers higher potency than Lipitor (atorvastatin), resulting in greater reductions of “bad” (LDL) cholesterol and higher increases in “good” (HDL) cholesterol at comparable or lower doses

There is actually more on Crestor versus Lipitor if you query Google.

LPA is genetically determined. It is unaffected by diet and there isn’t really a treatment for it. For those reasons, it isn’t commonly tested for. If LPA is elevated, it is an indicator you should be examining and reducing your other risk factors as much as possible however.