• I grew up in Los Angelese but have lived in Seattle, WA since 1991. (USA)
• Diagnosed with cardiac sarcoidosis December 2020 at the age of 53.
• Diagnosis through heart block, cardiac MRI, and PET scan.
• First PET scan showed extensive inflammation, but not a lot of scarring.
• Sarcoidosis mainly localized to heart.
• ICD implanted December 2020.
• 40 mg prednisone started late January 2021.
• Second PET scan in late April 2021 showed reduced inflammation, but still present.
• Changed to 20 mg prednisone.
• Third PET scan in October 2021 showed inflammation milder but still present. Lowering prednisone and adding methotrexate.
• Fourth PET scan March 18, 2022 showed methotrexate didn't help much
• No shocks from ICD so far (never experienced racing heart).

My first symptom was sudden heart block on September 27, 2020. I had driven to a park where I was going for a walk. When I parked and got out of the car, everything suddenly looked overexposed, so much so that I was having a hard time seeing the ground or where I was walking. It felt when you stand up too quickly, but a much more extreme version. After a while my vision got a bit better and I started walking. I noticed that even the slightest incline was making me short of breath. I was hoping it was a temporary condition, due to dehydration or having slept badly, or perhaps due to the fact that I had been doing jump rope in my apartment during the pandemic. But I noticed over the next few days that no matter what I was doing -- walking up stairs, walking up a hill -- my heart rate never went over 50 beats per minute. This is called bradycardia, the heart beating too slowly.

I called my doctor and about a week later and did an EKG, which showed heart block. (Heart block is when the electric signal from the sinus node -- the heart's natural pacemaker -- gets blocked on its way to the AV node where the ventricle pumping action of the heart reacts to the signal by squeezing/pumping. Sarcoidosis can cause heart block because the inflamation/scarring can interfere with that pathway.) In my case I was fortunate that my heart fell back to an "escape rhythm," which is when ventricle pumping is triggered by a backup mechanism that is unrelated to the signal from the sinus node, and which typically beats anywhere from 30 to 50 beats per minute. (There are different types/degrees of heart block and here I'm only describing my particular situation.)

The heart block was a blessing in disguise. It alerted me to having CS relatively early. I was also lucky to be saved by my escape rhythm.

I was referred to a cardiologist. He told me I had heart block, and that there were a few possible causes: that I had been bitten by a tick, that a medication I was taking was affecting my heart, that I needed a pacemaker due to aging, or that I had an infiltrative condition such as sarcoidosis. Well, I had not been bitten by a tick. I went off a medication (imipramine) that can have heart effects, but that didn't change the heart block. And we figured sarcoidosis was improbable so it was likely just an age-related need for a pacemaker.

Still, they did want me to do a cardiac MRI just to make sure it wasn't sarcoidosis. I believe it's only recently that this hospital screens for cardiac sarcoidosis as a matter of course, so I'm very lucky for that.

There was a scheduling error with the cardiac MRI, so it was actually about eight weeks between the initial conversation with the cardiologist and when the cardiac MRI happened. In the interim I told the cardiologist that I was waking sometimes with a panting sort of feeling. He asked me to do an echocardiogram, which didn't show anything unusual. I also did a 48-hour Holter monitor test which didn't show anything unusual. The panting feeling seemed to resolve itself.

I had the cardiac MRI on December 15, 2020, and the cardiologist called me the next day to tell me it was likely cardiac sarcoidosis and he was referring me to a heart failure / cardiac sarcoidosis specialist at another hospital. That was a very hard night for me because I immediately Googled everything and it sounded likely that I had two to five years to live. I had already joined the forum pacemakerclub.com (when I thought I just needed a pacemaker) so I went there to ask some questions. Some of the people were supportive, but I didn't come away with much reassurance.

I was able to talk to the specialist on the phone a couple days later, and it gave me a lot of relief. I asked him directly if I was going to die from this, and he told me I would eventually die from something, but probably not from this. He told me that the good part of the MRI was that it showed I had a left ventricular ejection fraction (LVEF, or just EF) of 66%, which was a sign that my heart was still relatively strong. He told me that in about a third of cases the sarcoidosis goes away on its own, in a third of cases the inflammation can be treated and doesn't come back so medication can be stopped, and in a third of cases it's necessary to take medication on an ongoing basis.

The specialist recommended (actually insisted on) an ICD and on December 22 I had a dual-chamber Abbott Gallant implanted. The surgery went well and the recovery was easy. I had basically zero pain and was able to walk around the next day. The wound has healed very well and at this point (September 2021) it's hardly noticeable. I was worried about the bump from the ICD but that has been a non-issue. When I met with the electrophysiologist he set my pacemaker to a minimum of 60 beats per minute and a maximum of 130 beats per minute. I was concerned that 130 would be too low when I wanted to exercise but it's been fine. They told me I was being paced most of the time, meaning that my heart by itself (i.e., my escape rhythm) was beating slower than 60 beats per minute and the pacemaker part of the ICD had to trigger the beats to keep me at 60 beats per minute. I was also lucky in the choice of ICD model because it sends data to the electrophysiologist using a phone app that communicates through cellular data or WIFI, so you don't need a special transmitter box to keep next to your bed, as with earlier ICD models. (ICDs send a nightly update to the electrophysiologist when anything unsual has been recorded that day.)

I had my first PET scan in early January 2021 at the University of Washington (UW). UW is more strict with the pre-scan diet than other test sites I've heard about. UW only lets you eat meat cooked in oil, fish, and eggs for the whole day before the scan. I'm vegan so in my case I only ate tofu cooked in oil. I at two pounds of fried tofu the day before the test, which sounds like a lot but it's actually just 800 calories of tofu, plus the calories from the oil. I mention this because the number of calories eaten might affect the the validity of the test for me, as I discuss below.

(For more information about the UW pre-scan diet and how PET scans work in general, see this UW PDF file.)

The results from the PET scan were worse than I was imagining. The summary said I had "extensive inflammation throughout the heart," and went on to enumerate the various places that were inflamed. The words "extensive" and "extreme" appeared multiple times.

The PET also showed a LVEF of about 50%, significantly lower than the 66% from the cardiac MRI. The specialist told me that the cardiac MRI is the most accurate measure of LVEF (better than echocardiogram, which is better than PET scan). So it was a bit unclear whether the 50% meant much.

In addition to the inflammation, in January of 2020 I experienced a number of episodes of what felt like angina -- my heart aching, with a tight, heavy feeling. It would last for several minutes or even an hour. One thing I noticed was that the pain would often go away when I walked quickly or exercised in any way. The cardiologist couldn't explain it but suggested that I either had coronary artery disease, or perhaps it was just an esophageal spasm. I did eventually do a cardiac stress test, which showed that my aerobic fitness was typical for my age, and that I didn't have more than 70% artery blockage. (That is, the stress test can only tell if you have 70% or greater blockage, and I did not.) Also, the aching went away around March 2021 and I rarely felt it after that. So my best guess is that it was/is a muscle spasm, perhaps from anxiety.

A blood test in late 2020 showed a high level of creatinine, which indicates that the kidneys are not working well. I met with a nephrologist, who did some tests, which didn't show anything conclusive. A couple months later my creatinine was down within the normal range. The theory is that the stress on my system from the heart block temporarily interfered with kidney function.

I spent a lot of time in the first months of 2021 reading websites and scientific papers about cardiac sarcoidosis. Doctors and scientists have been aware of sarcoidosis for over 100 years, but there has been little progress in understanding the cause. In addition to understanding the state of knowledge about the disease, I wanted to figure out why I in particular got it. I couldn't help but believe that something in my environment must have triggered it. And indeed the current scientific understanding is that getting sarcoidosis is usually a combination of being genetically predisposed to it, and a triggering event that makes it start expressing itself. My research was a long and winding road but, in summary, I first believed my triggering event was inhaling small feather particles from a cheap feather comforter, and then believed that it was nanoparticles of metal escaping from a broken wall heater that was arcing. There is a particular infamous paper that claims metallic nanoparticles are the only possible cause since whatever causes sarcoidosis must be too small to see or we would have seen it by now. That same author, along with some Japanese researchers, also proposed that, based on DNA from destroyed cells that are found in sarcoid granulomas (DNA suggesting the attacking bacterial cells are related to the bacteria that causes acne), the disease can be treated with antibiotics. At various times, each of these ideas/theories preoccupied my attention, but in the end I read enough that I didn't believe any of them. I have another guess, that the triggering event might have been exposure to bacteria from rotting food, but I am resigned to never knowing. Knowing is especially hard because it's hard to know how long after the triggering event(s) the disease takes to manifest clinically, so it's not like you can just review all of the possible events in the last year, or whatever.

The heart failure / sarcoidosis specialist started me on 40 mg prednisone at the end of January 2021. He called this a "fairly high dose," but having heard others' stories I know that many people take a higher dose, up to 60 mg, 80 mg, or even higher. My specialist says it's dangerous to keep people on 20 mg or higher for more than a year, so his usual approach is to use 40 mg for a three-month "blast," then do a PET scan, and then, if things are moving in the right direction, switch to 20 mg of prednisone for another three months or perhaps more.

Along with prednisone I started other medications, mostly to protect from the effects of the steroid. These include vitamin D, vitamin B12, calcium, famotidine (to protect the stomach from ulcers), plus a medication to protect from pneumocystis, which is a dangerous fungal infection that can affect people with compromised immunity. For pneumocystis I originally took a yellow liquid called Atovaquone which costs something like $1000 for a three-week supply (covered by insurance, thank heavens). Later I switched to Bactrim, an antibiotic, which is very cheap and actually more effective. I didn't start on Bactrim initially because it has a very small chance of causing serious liver damage, so it is necessary to do some blood tests every few months. I was already so overwhelmed by all of the medication and doctors that I didn't want to deal with yet another worry at that time. With the Bactrim I take a probiotic to protect my healthy bacteria.

For me, the side effects of prednisone have been mild. I have not had anything like mood swings, which many people say is the hardest part. I actually lost 25 pounds on my first month of prednisone, but that was due to my extreme anxiety, as described below. Now that I am over the anxiety, I feel that prednisone makes me want to eat more, but I am going on lots of long walks (often up to 12 miles, with lots of hills) and swimming, so I feel it's more or less under control. I did get the puffy "moon face" side effect, but did not get the common "buffalo hump" on the back of my neck. Recently (August/September 2021) I've noticed that scratches and small cuts take longer to heal than normal; they go through the same process of scabbing and healing, but slower, like maybe one-third as fast as normal.

I managed to get the Pfizer covid vaccine (two shots) in March 2021. I didn't feel any side effects from the immunization aside from a sore arm, and I was told that it was unknown whether it benefits people with a compromised immune system (because the point of the vaccine is to create a strong enough immune response that the body can later apply the same response to the actual virus). However, a few months later I did a "spike" antibody test and it came back positive, meaning that I had at least some antibodies. My infectious disease specialist seemed to think it was likely that I was protected as much as normal vaccine recipients, but it's still unclear. It could also be that I had covid without symptoms before I even knew I had CS, and got the antibodies from that. I also got a covid booster shot in August 2021, and again I had no reaction aside from a mildly sore arm.

I did a second PET scan in April 2021. There were some bureaucratic mistakes and the scan got scheduled two weeks earlier than was planned (after only two and half months on prednisone instead of three months), but the specialist said that was fine (which surprised me, but later he told me that "prednisone is not an exact science"). For this second PET scan, UW asked me to do the special diet for two days before the scan, instead of one day. So I ate fried tofu for two days, and each day I ate about twice as much as I did during the one day before the first PET scan. A couple days after the scan, UW called me to say that the results of the scan were "invalid" and I needed to repeat the scan, at their expense. I still don't know what was wrong with the scan, but I repeated it again 10 days later, this time eating exactly as did before the first scan (one day, with two pounds of fried tofu). This time the result was valid and showed I had significant reduction of inflammation, but still some inflammation. The words "mild" and "residual" appeared a few times in the report and of course those were music to my ears.

Based on the result, the specialist reduced the prednisone to 20 mg per day, but extended the original timeline so that I would take 20 mg for six months instead of three.

The PET scan also showed a LVEF that was a bit lower than the 50% in the previous scan. Again, it was not clear how to interpret this because of the poor accuracy of PET scan measure of ejection fraction.

As I alluded to above, the hardest part of this whole experience for me was the anxiety, and not the heart issues or medication regimen. I've had an anxiety disorder since my teenage years, but this was the most severe and extended period of anxiety in my life. At first I thought maybe it was the prednisone that was causing the anxiety (prednisone causes agitation and insomnia for some), but actually the anxiety was already pretty high before I even started taking prednisone, and I now believe the anxiety was 100% internally generated. I got in touch with a good psychiatrist and he initially gave me benzodiazepines, but I was worried about becoming tolerant or addicted to them. Luckily I was allowed to go back on imipramine, the antidepressant/antianxiety medication that has always helped me, and at 250 mg, a higher dose than I'd taken before. It was not clear that I would be able to take such a high dose because imipramine can affect heart rate, but I did an EKG after I had ramped up and the electrophysiologist allowed me to continue. This has been a huge, huge relief and I am now able to go through this experience with reasonable concern but not utter terror.

Before all of this, I was planning a trip to Romania, which was on hold due to the pandemic. Nevertheless I asked the specialist if it would be okay to do the trip while I was being treated, and he said yes. He gave me a prescription of Amiodarone (a medication that can prevent arrythmias like ventricular tachycardia) just in case, but I didn't have to use it. I went during the second half of July 2021. I found the flight and the whole trip very easy. (Romania has a lower covid rate than Seattle.)

One of the common side effects of long-term prednisone is cataracts. I learned that all humans develop cataracts eventually, but steroids can make them develop faster. An eye exam did show some cataract warning signs, but I actually had those signs before the CS and the steroids. The opthamologist said we could wait a while before doing anything. I learned that cataract surgery is very routine, so we'll see if I need that at some point.

Another possible side effect of long-term steroid use is osteoporosis. I requested a bone density scan, and the result was that I have moderate osteoporosis. The endocrinologist said that osteoporosis could not have developed so quickly, just by taking 40 mg of steroids for five months. So the thought is that it was a coincidental pre-existing condition, for I don't know how many years. I have never broken a bone. Perhaps I've had it for a long time and I've just been lucky. In any event, the endocrinologist started me on Fosamax. I have read that Fosamax can be effective within a few months. I'll have another bone scan at the end of 2021.

My third PET scan is scheduled for October 18, 2021. Physically I'm feeling good at present, and I'm very grateful for that. I'm actually feeling like I'm in the best aerobic shape that I've been in for years. I can walk up many flights of stairs quickly, I can walk 12 miles with lots of hills. I can swim 25 meters under water without coming up for air. I am calm, eating well, sleeping well, and excited about many projects I'm working on. I'm very grateful to all the people who have been so supportive, including people in the Cardiac Sarcoidosis Facebook group.

In terms of current symptoms, something I've noticed in recent weeks is what I think are mild episodes of PVCs (premature ventricular contractions). I feel these especially right after I lay down and especially about 10 PM. I will talk with the specialist about this. I did have (what I believe were) occasional PVCs previously in my life going back to childhood. What I experience now actually feels more mild than those PVCs. What I feel now is less of a pounding and more of a mild flutter. I take my pulse and feel that the beat is irregular (it feels like one beat out of every four is skipped, even though I know a PCV is actually an early contraction that starts in the ventricle), but overall the episodes are mild and brief.

I should mention one other thing I've experienced from time to time during the treatment. It is a very mild burning sensation, which feels like it's coming more from my lungs than my heart. As my specialist told me, 90% of people with cardiac sarcoidosis also have some lung involvement. I need to talk to the specialist about these rare and very mild sensations of burning, but for now I like to imagine that it's the feeling of tiny amounts of sarcoidosis in my lungs burning off. :)

I am praying that the October PET scan will show enough improvement that I can start decreasing the prednisone down to zero, or at least down to a 10 mg or less. Actually, even if the inflammation is not gone I think the prednisone will be reduced to 10 mg, but with methotrexate added. Methotrexate works well for many of the people in the Facebook group. If that doesn't work my guess is that the specialist will suggest Remicade, also called infliximab, a mono-clonal antibody which interferes with the body's immune reaction in a different way, and which I've heard is effective for many for whom prednisone and methotrexate didn't work.

Basically, I still have inflammation. Dr. M. was glad it was milder, but it seemed the most important thing is that it's still there at all, and he wasn't focused on the words "increased uptake" vs. "decreased uptake" in the PET report, which I had found confusing. He says for most people the inflammation would be gone now ("we would have knocked it out," as he says).

As I predicted, he wants to lower the prednisone dose and start methotrexate. He said I can go immediately down to 10 mg prednisone (from 20 mg currently). That was a bit surprising to me because I thought people normally tapered down slower than that. He said if I feel super wiped out I could go back up to 15 for a while. So I'll take 10 starting tomorrow morning. Because of the lower prednisone amount I should be able to stop taking the Bactrim (which I was taking to guard against pneumocystis, which is a risk with a suppressed immune system), but I'll check with the infectious disease doctor on that. (He also asked if I had the covid vaccine while on 40 mg and seemed a bit concerned when I said yes. But when I told him I tested positive for antibodies on the "spike" test he was relieved.) For methotrexate he's starting me at a 2.5 mg pill and adding 2.5 mg each week until I'm at 10 mg (four pills). You just take it once a week. I was surprised by the dose since it seems like many people in the Facebook group take 25 mg per week. You also take folic acid with the methotrexate to limit its side effects. You also monitor your liver, which I was already doing for the Bactrim. I have generally heard good things about the effectiveness of methotrexate in the Facebook group. He wants me to do this regimen for three months and then do another PET scan. If the inflammation is still there he will refer me to a rheumatologist to try one of the "biologics" like Remicade or Humira, which I've also heard good things about on the Facebook group. (Those are expensive so you have to show the insurance company that you've tried the older medications first.) When talking about the rheumatologist he actually referred to himself as "just a lowly cardiologist." That changed my whole mental model of the cosmos. 🤯

Other things that were discussed:

• He's still only 90% sure this is sarcoidosis. He said biopsy is still not recommended since it has an 80% chance of false negative (i.e., only 20% chance that it will detect sarcoidosis if you have it). Instead, he's having me do an ANA test, which is a blood test that checks for other possible candidates.
• He was mildly concerned that my resting pulse is about 100 beats per minute these days. It's been creeping up slowly over these months. He says it's possibly/likely due to the prednisone. I will keep him posted on how it changes as I start the lower dose. There are medications you can take to normalize heart rate, such as metoprolol (a beta blocker), but he feels I've got enough medication going on so we'll monitor the heart rate for now.
• He was mildly concerned about the PVCs that I'm experiencing. They are still only about 1% of my heart beats. He says they are not super close together, which would be more worrisome. Again, these could be caused by prednisone and I will keep him up to date on how this changes with the medication adjustments.
• Although the endocrinologist thought it was too quick for my osteoporosis to be caused by the prednisone, Dr. M said that he's definitely seen it happen to people like in six months. He says with the lower prednisone and the Fosamax it should improve quickly.
• I recently uploaded all the data from my device so they could look at the PVCs. That data also showed that I am still being paced 99% of the time, meaning that the normal electrical conduction from my sinus node to my AV node is still not working, or at least not working quickly enough. He said if it looks like I will need pacing long term, he will recommend switching to another device that triggers both the left and right sides, because having it triggered only from one side can tire the heart out. I didn't really understand all of that, but I'll learn about it as needed. I guess I was both lucky and unlucky to get the heart block, lucky in that it alerted me to the problem early, but unlucky in that it may be a permanent condition even after the inflammation is gone. But I guess it's possible that when the remaining inflammation is cleared my electrical conductivity will return.
• This latest PET scan showed 49% ejection fraction (EF is a fundamental measure of heart health and normal EF is generally 50% to 75%). Dr. M is skeptical about EF readings from PET scans, and prefers to consider my earlier cardiac MRI and echocardiogram, which both show me well into the normal range. He said if I start feeling badly they would do another echocardiogram (which is a fairly good measure of EF), but otherwise he's not worried about it.
• I asked him in many ways about the overall health of my heart, how concerned to be about the remaining inflammation etc. He said the reduced inflammation is good, and it's good that subjectively I feel good, and it's good I haven't had any shocks or racing heart beat. He said things should only get safer from here on out, but that is no guarantee of no shocks. I asked him about the scarring. My understanding is that they check for scarring both directly and indirectly. I believe the cardiac MRI is the only way to check directly. I was under the impression that the cardiac MRI didn't work well if you already have a device in place. He said not always, but in my case it's probably not an option because the placement of the lead electrodes are right in the spot where it seems I would have scarring, so they'll mess up what they would need to see. The indirect method, I believe, is to look at the patterns of blood flow. The worry is that scar tissue builds up and the left ventricle loses elasticity and the ability to pump effectively. In my case there is some reduced perfusion (blood flow) in a particular area in the left ventricle, in the lower-right corner. This latest PET scan showed the same perfusion as in the April PET scan, so that seems to indicate it hasn't gotten worse. I asked if the reduced inflammation I have is less likely to cause additional scarring. He said it's a bit hard to predict. He said he's certainly seen people with raging inflammation end up with virtually no scarring. So basically neither panic or comfort on that question. He did refer to my heart strength as healthy/normal several times, so that was nice. He also told me about a patient with 20% EF who was out running marathons. So you can make up for low EF by strengthening the heart in general.
• He said there were no restrictions on my activities, exercise, travel, etc.

PET SCAN SUMMARY

1. The left ventricular cavity size is normal.
2. Global left ventricular function is mildly to moderately reduced, EF 42%.
3. PET evidence of an overall large area of mildly to moderately reduced perfusion in the mid to apical inferoseptum, apical anteroseptum, mid to apical anterior wall, apical lateral wall, apical inferior wall and true apex.
4. PET evidence of an overall large area of moderate to intense inflammation in the entire inferoseptum, basal to mid anteroseptum and anterior wall as well as patchy uptake in the RV free wall.
5. Compared to the prior study on 10/18/21, perfusion abnormalities are similar on direct comparison of the images. The severity of inflammation has increased significantly on today's study and patchy inflammation in the RV free wall is more apparent on today's study.

I just had my first Remicade infusion. It was briefly harrowing, but not for the expected reason. There was a severe nurse there who told me (20 minutes before the infusion was to start) they might not be able to give me Remicade. She asked me if I had heart failure and I said I didn't know. I said I had an echocardiogram two days ago that showed a 46% ejection fraction. She made a so-so gesture with her hand. Two lucky things: one is that Dr. P was available to talk to her. I don't know exactly what Dr. P said to her. The other is that I got the echocardiogram result at 1 am last night. If it hadn't arrived I would have had to choose between telling her that my latest PET scan showed an EF of 42%, or of saying that the cardiologist has been going with my cardiac MRI reading of 65% from a year and a half ago. And I wouldn't have known which to choose because at that moment I didn't know if I was more likely to get the infusion if she thought it was justified by having heart failure, or if it's contraindicated for heart failure (which I subsequently learned it is). All of this was really surprising because of course the whole thing was approved well in advance by Dr. M and Dr. P, and by the insurance plan, and on this Facebook group there are all sorts of stories of people getting Remicade with low EFs. And nowhere did I hear about a heart failure contraindication, including reading I had done on the web.

The actual procedure was very easy. It was just two hours (they had told me three, with the possibility of going to 1.5 for later infusions, so that was another disconnect). I was worried that the needle would start aching after a while but that didn't happen. When I was done I walked back home quickly uphill and felt good as usual. They said there might be some flu-like muscle soreness today or tomorrow and I can take ibuprofen. They gave me a printout to read that listed the possible side effects. The main one is increased risk of infection, including colds, etc. But Dr. P said in practice she hasn't seen much of that.

The other thing I learned is that you do what they call a "loading dose," meaning they actually give you the same amount in the first three infusions at 0, 2, and 6 weeks that they give you once you get to the ongoing six-week schedule. So it's not a slow start as I was thinking but a fast start, which I guess gets your body used to the concept quickly, or something.

So I'm now full of a live monoclonal antibody derived from human and murine proteins. For karma's sake I should probably leave out some cheese for the mouse that visits me late at night in the condo...

I had an appointment with Dr. M today. I wasn't expecting much from it, but I did get a better idea of his thinking on the situation.

He is definitely a bit scattered. He started by breaking the news to me that I'd probably have to start on Remicade, and I reminded him that I'm already on it, and that he and Dr. P had a conversation about me starting it.

He says my case is definitely trickier than expected. By contrast he met with three other cardiac sarcoidosis cases today and they all cleared up with the first round of prednisone (although they are all in worse shape because they caught the issue later). He is glad my inflammation is not worsening, but frustrated that it hadn't improved much.

He is not worried about the ejection fraction number. He thinks the lowering EF is most likely due to the type of pacemaker I have, which is dual chamber: it senses a signal in the right atrium and passes it to the right ventricle to cause the contraction. But the left ventricle doesn't get the signal in time (because I have a "left bundle branch block"), so it's beating a bit out of sync with the right and therefore has less squeeze power. He thinks I should probably be upgraded to a three-lead ICD, called a CTRD. I think the plan is not to worry about that until the six-month trial of Remicade is over. I asked if it made sense that the EF would lower over time, as opposed to just immediately being lower after they put in the ICD. He said yes it is common to see it lower over time. But he said it wasn't due to any permanent damage, so he seemed to be saying that my "true" EF is probably still quite high, but it is masked by this problem. It's not a sign of my heart fundamentally getting weaker.

So the plan is to take the Remicade for six months. If it doesn't work, he would send me to his mentor, Dr. R at University of Washington.

My resting heart rate has been between 90 and 100 for a number of months. It was 60 after getting the ICD and I don't remember exactly when it started to get quite high. He thinks it's likely due to one or more of my medications. I thought he had said it wasn't concerning. But he is in fact concerned it, and my understanding is that's because we want the heart to be calm in my situation, not in a revved-up state. So he is putting me on a beta blocker called metoprolol. He says it is a very safe drug but can cause tiredness. I don't really need anything to make me more tired at this point. He said the tiredness is usually not so severe. If I try it and I'm not tolerating it well I can cut back or stop it and discuss it with him. He said I should start monitoring my blood pressure daily to make sure it doesn't go too low. (I already have low blood pressure, usually about 110/70.)

He is glad that I don't really have any symptoms. He said I am not in heart failure, and if I was there would be big symptoms like significant swelling in the legs, significant changes in feeling of well-being as I moved from one position to another, and some others. At the same time, he's not saying "wow, since you have no symptoms you have a very minor case." He says we don't want to wait until symptoms before getting rid of the inflammation.

I had an appointment with Dr. M today. I wasn't expecting much from it, but I did get a better idea of his thinking on the situation.

He is definitely a bit scattered. He started by breaking the news to me that I'd probably have to start on Remicade, and I reminded him that I'm already on it, and that he and Dr. P had a conversation about me starting it.

He says my case is definitely trickier than expected. By contrast he met with three other cardiac sarcoidosis cases today and they all cleared up with the first round of prednisone (although they are all in worse shape because they caught the issue later). He is glad my inflammation is not worsening, but frustrated that it hadn't improved much.

He is not worried about the ejection fraction number. He thinks the lowering EF is most likely due to the type of pacemaker I have, which is dual chamber: it senses a signal in the right atrium and passes it to the right ventricle to cause the contraction. But the left ventricle doesn't get the signal in time (because I have a "left bundle branch block"), so it's beating a bit out of sync with the right and therefore has less squeeze power. He thinks I should probably be upgraded to a three-lead ICD, called a CTRD. I think the plan is not to worry about that until the six-month trial of Remicade is over. I asked if it made sense that the EF would lower over time, as opposed to just immediately being lower after they put in the ICD. He said yes it is common to see it lower over time. But he said it wasn't due to any permanent damage, so he seemed to be saying that my "true" EF is probably still quite high, but it is masked by this problem. It's not a sign of my heart fundamentally getting weaker.

So the plan is to take the Remicade for six months. If it doesn't work, he would send me to his mentor at University of Washington.

I had thought he wasn't concerned about my heart rate. My resting heart rate has been between 90 and 100 for a number of months. It was 60 after getting the ICD and I don't remember exactly when it started to get quite high. He thinks it's likely due to one or more of my medications. I thought he had said it wasn't concerning. But he is in fact concerned it, and my understanding is that's because we want the heart to be calm in my situation, not in a revved-up state. So he is putting me on a beta blocker called metoprolol. He says it is a very safe drug but can cause tiredness. I don't really need anything to make me more tired at this point. He said the tiredness is usually not so severe. If I try it and I'm not tolerating it well I can cut back or stop it and discuss it with him. He said I should start monitoring my blood pressure daily to make sure it doesn't go too low. (I already have low blood pressure, usually about 110/70.)

He is glad that I don't really have any symptoms. He said I am not in heart failure, and if I was there would be big symptoms like significant swelling in the legs, significant changes in feeling of well-being as I moved from one position to another, and some others. At the same time, he's not saying "wow, since you have no symptoms you have a very minor case." He says we don't want to wait until symptoms before getting rid of the inflammation.