Transient myocardial ischemia is reversible with no residual damage, unless severe and prolonged enough to cause cell death. Inducible ischemia may get worse if the responsible mechanism changes.
What is Subendocardial perfusion defect – is that Microvascular dysfunction?
The subendocardial layers of the left ventricular wall are more sensitive to ischemia. Infarcts start in the subendocardium and progressively extend to the mid and subepicardial layers if ischemia is severe and prolonged enough. It is not exclusive of microvascular dysfunction, but of any mechanism that may precipitate myocardial infarction .
Can you explain a little about how Calcium channel blockers and Ranolazine work in the body and why they work please?
Calcium transients are an essential mechanism in muscle cell contractile function. Calcium channel blockers reduce the tone of vascular smooth muscle cells, resulting in vasodilation and reduced resistance to flow and in the prevention of hypercontraction in response to stimuli.
Ranolazine is a metabolic modulator that favours cell utilisation of glucose instead of free fatty acids in ATP synthesis.
What is the cause/mechanism of the delayed angina reported, where patients perform an activity but angina is felt hours later?
Angina reported hours after activity simply is not triggered by that activity but by other mechanisms. The heart does not “remember” what has he been doing hours before.
How is it that the oximeter can show acceptable levels of oxygen when we are struggling with Ischaemia? Does microvascular ischaemia not show on an Oximeter?
Ischemia is a condition of the cardiac muscle precipitated by local mechanisms. It is not directly related to hypoxia in the systemic circulation, with the possible exception of rare and dramatic conditions of systemic severe hypoxia.
What is the difference between reading oxygen levels on an Oximeter and via an ABG blood test? Which is the best test or the best indication for INOCA patients?
The Oximeter reads the Oxygen saturation of circulating haemoglobin, that is the percentage of Hb bound to oxygen. ABG blood test provides much more detailed information on circulation arterial blood gases, including oxygen and Carbon dioxide concentrations, pH, Hb etc etc
Is Cadasil a known cause for INOCA?
CADASIL (Cerebral Autosomal Dominat Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a dominant autonomic disease associated with migraine, cognitive impairment, cerebral infarcts and eventually dementia. I am not aware of an association with INOCA
8.2% increased MACE over 5.4 years was recently reported by the WISE study – what does/could this mean for the significance of INOCA diagnosis/treatment for the future?
This observation further supports the notion that outcome of ischemic patients is dictated by extension and severity of myocardial ischemia more than by the mechanisms responsible for ischemia.
Is CMVD systemic or is it just in the coronary vessels?
This is a very important question with limited scientific evidence to support any answer. However, the physiology of the coronary circulation is so peculiar that systemic microvascular dysfunction (if it does exist) would have unique consequences in the coronary circulation.
Can Coronary Microvascular Dysfunction get better or will it just get worse?
Coronary Microvascular Dysfunction is a dynamic condition that can be stable or get better or worse in time, either spontaneously or in association with treatment. It has been reported that MD can resolve after a few months after an acute coronary syndrome.
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