@stockrock thanks for your reply @DocMcstuffins you are right,...

@stockrock thanks for your reply @DocMcstuffins you are right, we
do need to keep an open mind, I have gone and done a bit more research in this area and this is what I have come up with!

so the intramyocardial injection is necessary for the immediate activation of the stem cells to start having an effect. As a result you get (from what I understand) reduction in endothelial dysfunction, formation of more collateral channels thus improving cardiac perfusion. Now Inflammation as we know plays a key role in atherosclerotic plaque formation (macrophages endocytose LDL’s and deposit themselves into the tunica intima + media etc), as well as causing hypercoagulability, so this makes sense as to how it reduces further myocardial infarction as well as the fact it seems to halt further progression of heart failure, reducing inflammation by maintaining a higher level of cardiac output and as a result meeting the bodies metabolic requirements for longer (remember that heart failure is defined as the inability for the heart to provide oxygenated blood to meet the bodies metabolic demand).

The mechanism for stroke reduction could be as a result of multiple reasons

firstly, the most obvious reason is atrial fibrillation, as mentioned earlier, haemostasis within the left atrial appendage due to afib is a common cause of ischemic stroke, I would be very interested to know if there was a reduction in the frequency or prevalence of Atrial fib in patients provided with the stem cells. Afib can be a consequence of MI, so if we reduce The recurrence of MI then we may reduce frequency of afib. Afib can also be cause by left ventricular enlargement/dysfunction which may be secondary to hypertension, dilated cardiomyopathy, valve dysfunction which are also all causes of heart failure. If we reduce the progression of heart failure secondary to these ailments by reducing inflammation, improving endothelial dysfunction and reducing the likelihood of further MI through the pathway explained above, then we should see a reduction in stroke.

secondly, as previously mentioned, heart failure is the inability for the heart to meet the bodies metabolic demand. As result there may be an element of cerebral ischemia occurring resulting in damaged and inflammed areas of the brain, thus increasing the risk of stroke. If we reduce the progression of heart failure, we reduce the amount of ischemia occurring within the brain/body.

thirdly, the body attempts to improve circulation in CHF patients by activation of the sympathetic nervous system and the renin angiotensin - aldosterone system to perfuse areas of the body that aren’t achieving adequate blood flow. As a consequence there is a hypercoagulable state, increased aggregation of thrombocytes, and reduced fibrinolysis in patients with CHF, the longer we halt progression of heart failure, the less sympathetic activation required to meet metabolic demands and as a result, less clotting.

fourthly, left ventricular hypokinesia is another cause of thrombus formation in heart failure patients due to the same mechanism as AF, if we stop progression of heart failure, this means less left ventricular hypokinesia and thus less clot formation in the atrium and again less stroke occurrence.

Lastly, there is evidence of endothelial dysfunction in CHF patients, rheological alterations consistent with increased blood velocity, and malfunctioning of cerebral autoregulation, this seems to more prevalent in CHF patients suffering hypotension which is essentially decompensated heart failure (probably class 4) so if we reduce progression, we reduce stroke.

I am sure there a many other reasons as to why stroke would have been reduced, but this seems to answer the question a bit better as to why a direct injection may be preferable to IV infusion and to some of the mechanisms responsible. I have posted a table below as to some further causes of stroke in heart failure.