Heart attack is one of the most common reasons we BigD-ers shuffle off this mortal coil.  Not because the kidneys have anything to do with managing our heart chemically, but because without kidneys we fill up with fluid and raise our blood pressure, putting stress on what is usually a pretty reliable ticker (heart failure is often the cause of death for people who decide not to go on, or give up dialysis).  Constant fluid overloads over a long period gradually wear out hearts, they get tired and emotional and without regular maintenance, become unreliable, or worse.

My 19+years off and on dialysis (mostly on) makes me a paid-up member of this group.  The main way my heart plays up is Atrial Fibrillation (AF), where it beats out of rhythm.  AF can be anything from mild (I hardly notice it) to severe (where because it is doing such a lousy job of pumping blood and the oxygen it carries that I find it hard to stay upright).  When in AF, my heart beats faster (to keep up the blood flow), but no matter how hard it tries, my blood pressure is always low.  In fact, if I’m in the early stages, a fast pulse and low BP when I am clearly above my base weight are great indicators that I’ve gone into AF.

Of course there are side effects (besides being slower than a three-legged turtle).  Because the heart is doing a lousy job of moving blood around, it can pool in inconvenient places, and even cause clots.  Not good, but only disastrous if that happens in the brain (the most common cause of a stroke), or the heart (causing a heart attack).  So if I’m in AF for more than a day or two, I take Warfarin, (Coumadin, Jantoven, Marevan, Uniwarfin) an anticoagulant, to minimise clotting.  This in itself has an effect for BigD-ers: we must ensure that clinic staff know we’re on it so they can use a smaller amount of Heparin during each run, and I wait longer for bleeding to stop after the needles come out.  This also applies to any cuts and scratches I inflict upon my body parts.

So the ideal situation is to not go into AF, or to catch it early.

Stopping it before it starts

The best way to stop it before it starts is to visit a cardiologist regularly.  The cardiologist I go to is excellent.  His stated aim is to keep people alive longer than we would be without his help – an excellent objective say I.  And he’s done a sterling job so far.  I’ve had AF for more than 10 years.

In the early days he zapped my heart back into rhythm with those electric paddles we have all seen on our favourite TV show (anyone remember Dr Ben Casey? Sadly I do… but I digress).

Since those early days, he has had me taking two heart medications:

• Metoprolol, a beta blocker (it blocks the electrical impulses that pass to the lower heart), that reduces heart rate and AF, and the force of heart muscle contractions to lower blood pressure. Since starting, I usually score a heart rate of around 55 BPM – much the same as all the athletic types in the family.  Since I choose not to share how I achieve it, most people think I am incredibly fit, which I see this as a positive side effect
• Flecainide (Tambocor), which also blocks electrical signals in the heart that cause an irregular heartbeat, is used for serious AF (I used to take Amiodarone, but it gradually became less effective, so I was weaned off it and onto it’s big shot replacement).

These two have mostly kept AF at bay.  Once in a blue moon I forget to take a dose, and AF can make a tentative appearance.  But once these little white friends are back into my system, it fades away.

Catching it early

This was a little more difficult until recently.  Apart from feeling “out of rhythm” and confirming it by checking my pulse (easy with a fistula), my main measure was the low BP/fast heart rate/above base weight I mentioned previously.

That was until I got my hands on a miracle machine.  It came about like this.  Julie went to see our No 2 son, Liam in London month or so ago.  One of the social events he arranged was to get together with Malcolm, one of his excellent friends who stayed with us when he was a student doctor on placement at the Royal Melbourne Hospital.  The world turned, as it is wont to do, and he is now Malcolm Finlay, Consulting Cardiologist (yes way!).  He was trialling a new mini ECG/heart monitor for the iPhone, called the AliveCor Heart Monitor.

He demonstrated it and to her and obviously thought it a valuable tool.  It is a small metal and plastic plate about the size of a business card.  You place two fingers at either end, on the metal pads and hold it close to the iPhone while it is running the associated App.  It immediately picks up the signal from the plate and displays a heartbeat signal comparable to readings from Lead I of a standard ECG. (Other signals are available: a left knee-right hand combination gives me a Lead II signal and placing it on the lower left side of the chest, below my enormous pecs, mimics the signal from the Anterior Precordial Lead,) One of my AliveCor ECGs on the website (click to view)

As regular readers will know, over the last few months, I became quite unwell well, with fevers, lethargy, persistently low haemoglobin level (HB) and generally feeling crappy.  Also, gradually (so gradually I didn’t realise it was happening), my muscles and joints began to stiffen and lock up.  I was walking around like a wizened old man: bent over, no flexibility, only just able to touch my toes.

I eventually spent a couple of weeks in two different hospitals.  But it seemed that no-one could find the problem, until one young and enthusiastic doctor thought he recognised it, because it was his specialty.  He sent me for a full body MRI and which confirmed his hunch.  I had something I could barely pronounce: Polymyalgia Rheumatica (PMR).

Polymyalgia means “pain in many muscles”, which is pretty accurate.  The textbook says it causes pain and stiffness in people aged 50 and over (I’m 62 – Check!), including:

• Muscle pain and stiffness, particularly in the neck, shoulders, hips and upper arms (Check!)
• Stiffness that worsens after resting – for example, when getting up in the morning (or getting out of a car after a 30 minute drive – Check!)
• Fatigue (Check!)
• Difficulty sleeping (not me!)
• Difficulty raising arms above shoulder height (Check!)
• Unexplained weight loss (I lost 5 kilos (11lb) – Check!).
• The onset is usually sudden (Check!).

The pain and stiffness came from inflammation when my white blood cells attacked my larger joints causing swelling in the shoulders and hips, and in the tissues around them.  The reason for PMR is unknown, though it may be triggered by respiratory viruses.

Apart from people over 50, women are more likely to develop it than men and interestingly, Caucasians are most susceptible especially people of Northern European (Scandinavian) origin (where my ancestors hail from!).

The good news is that it is pretty easy to treat, with my old friend from transplant days, Prednisone (/Prednisolone).  I have disliked and dreaded taking this drug since my first transplant.  It has many side effects on the bones, body and brain, but the one I dislike the most is the tissue-thin skin that bruises and tears at the lightest brush against a hard or sharp surface.

Still, after just two days of 20mg, my symptoms faded away.  It has simply eliminated the inflammation and all the nasty symptoms that came with it.  I feel ten years younger.  Toe touching is no longer a problem.

I have to take the Prednisone for at least a year, in gradually reducing doses until I find a level that just keeps the PMR at bay.  I am reducing the amount I take by 1mg a month .  (It’s a bad idea to stop or slow Prednisone suddenly: that can lead to an Addison crisis, and that’s not for me.)

One interesting reaction to being free of PMR is the rise in my HB level.  It has soared to 15+ gm/dL a dangerously high levels for people on dialysis, increasing my risk of thrombosis (blood clots).  Obviously the PMR suppressed my (or EPO’s) ability to create red blood cells.  Once removed, red blood cell production went into overdrive.

My nephrologist wanted it back down ASAP, so he has reduced my EPO and more traumatically, told staff to dump my blood at the end of three runs, rather than returning it to me.  That’s about 250mls of blood each time.   300ml of blood equates roughly to an HB level of 1 gm/dL, so the maths is right.  It just feels very wrong throwing blood-filled lines into the bin, especially after struggling to get every red cell back when my HB was so low.

Anyway, after all that time and drama, I’m back to being my sprightly self: walking, going to the gym and generally feeling exuberantly dangerous to myself and others.