9th October 2017
In this blog I would like to highlight some of the evidence that is not there. The missing link, the lost chord. The thief that steals in, in the night. The thing that is not there when you look for it.
“As I was going up the stair
I met a man who wasn’t there!
He wasn’t there again today,
Oh how I wish he’d go away!”
When I came home last night at three,
The man was waiting there for me
But when I looked around the hall,
I couldn’t see him there at all!
Go away, go away, don’t you come back any more!
Go away, go away, and please don’t slam the door…”
There was a theory, indeed there still is, that a myocardial infarction starts with damage to the heart muscle (myocardium), and the blood clot forms afterwards. Carlos Monteiro, a Brazilian researcher with whom I often communicate, promotes and supports this, the ‘myogenic theory of heart disease’. He is not alone.
Now, superficially this idea may sound completely daft. However, there is a great deal of evidence that can be gathered to support it. First, in a significant number of myocardial infarctions, no blood clot can be found. Here, from a paper entitled ‘Myocardial infarction without obstructive coronary artery disease.’
‘A substantial minority of myocardial infarction (MI) patients have no obstructive coronary artery disease (CAD) at angiography. Women more commonly have this type of MI, but both sexes are affected.1’
So, how can you have an MI, if there is no blood clot, and no blockage of a coronary artery? A very good question M’lud.
There is also an increasingly recognised form of ‘heart attack’ called Takotsubo cardiomyopathy, named after the Japanese octopus pot. This is where you have all the signs and symptoms of a myocardial infarction, but it is not a myocardial infarction. It is due to extreme levels of stress – both positive or negative. Here I quote from the British Heart Foundation:
This condition is also called acute stress-induced cardiomyopathy, broken heart syndrome and apical ballooning syndrome.
Takotsubo cardiomyopathy was first reported in Japan in 1990. The word ’Takotsubo’ means ‘octopus pot’ in Japanese, as the left ventricle of the heart changes into a similar shape as the pot – developing a narrow neck and a round bottom.
The condition can develop at any age, but typically affects more women than men. The good news is that often the condition is temporary and reversible.
What are the symptoms of Takotsubo cardiomyopathy? The main symptoms of Takotsubo cardiomyopathy are chest pain, breathlessness or collapsing, similar to a heart attack. In some cases, people may also suffer palpitations, nausea and vomiting.’2
You can, in fact, die from Takotsubo cardiomyopathy. Another myocardial infarction that is not a myocardial infarction.
Equally, you can find that people can suffer from a myocardial infarction days, or even weeks, after a blood clot blocked the artery. Here is a paper entitled ‘Plaque Instability Frequently Occurs Days or Weeks Before Occlusive Coronary Thrombosis.’
‘In at least 50% of patients with acute STEMI, coronary thrombi were days or weeks old. This indicates that sudden coronary occlusion is often preceded by a variable period of plaque instability and thrombus formation, initiate days or weeks before onset of symptoms.’3
So, there you go. You can have four types of myocardial infarction:
- A myocardial infarction with no obstructive arterial disease
- A myocardial infarction cause by stress, with no obstructive arterial disease
- A myocardial infarction that happens weeks after the thrombus forms
- The ‘classic’ myocardial infarction with thrombus formation followed rapidly by infarction.
What are we to make of this gentle reader? Three forms of ‘myocardial infarction’ that cannot be linked in time, or in any other way, to thrombus formation. Or, to put it another way the infarction a.k.a. the bit where the heart muscle becomes seriously damaged, is not related to a blockage in the artery either immediately, or at all.
In addition to this, there is the observation of ‘the completely blocked coronary artery, without myocardial infarction’. Here is a case history from the British Medical Journal:
‘A 75 year old man was admitted because of stable angina pectoris without any history of myocardial infarction. His risk profile consisted of arterial hypertension and hypercholesterolaemia. At the time he was being treated with 100 mg aspirin, 100 mg metoprolol, 20 mg pravastatin, and 40 mg isosorbide mononitrate daily. ECG showed sinus rhythm, no Q waves, and slight T wave inversions at lead aVL and I. A bicycle stress test resulted in horizontal ST segment depression of 2 mm at 75 W. Coronary angiography was performed and revealed coronary artery disease with complete occlusion of the proximal part of the left coronary artery.’ 4
At this point you could very reasonably argue that there truly is no consistent association between blood clots, arterial obstruction, and myocardial infarction. Or, to put it another way, the widely held view that the blood clot, and subsequent arterial occlusion, immediately precedes the infarction, is contradicted by evidence.
Which leads to the inevitable conclusion that something else must be going on. Perhaps it is true that the infarction, due to extreme stress and build of lactic acid does come first. Then, as a consequence, the clot forms in the artery.
Hmmmm. I don’t think so. However, in order to understand what is actually going on it is necessary, unfortunately, to dig even deeper, to find the man that isn’t there. Banksy, a man who paints on walls, is never seen, but we know he was there because, otherwise, you can’t explain the painting.