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Patient Questions

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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 .

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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 … Continue reading "Can you explain a little about how Calcium channel blockers and Ranolazine work in the body and why they work please?"

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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

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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.

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I’m not sure that I have seen an increase in patients presenting with CAS/CMVD but we are in rather unusual times! Certainly before lockdown I had queried the diagnosis in several of my patients and sent them off to cardiology for investigation. I think it is more my increased awareness that has changed rather than … Continue reading "Have you seen an increase in patients presenting with CAS/CMVD as a result of increased awareness?"

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Angina associated with severe coronary stenosis is triggered by exercise and relieved by rest. Angina associated with CAS or CMVD is not precipitated by excess cardiac work but by transient impairment of myocardial perfusion. But the common background is always cellular ischaemia and therefore it is difficult to imagine that pushing through might be irrelevant.

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Angina by definition is a transient Ischaemic  episodes not leading to  cellular death. As  such it should not cause chronic fatigue. However, during an anginal episode, if the ischaemic territory is large enough or if critical component of the heart are involved (e.g. Papillary muscles and mitral valve), then it may be associated with fatigue … Continue reading "Why does angina cause fatigue? "

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Myocardial ischaemia has been traditionally perceived as the consequence of atherosclerotic obstructions of the coronary vessels. More recently an overwhelming body of evidence has proven that atherosclerotic obstructions are just one of several mechanisms that can precipitate myocardial ischaemia. CAS, CMVD and Endothelial Dysfunction are included among the mechanisms that, in isolated fashion or in … Continue reading "Can you describe the relationship between CAS, CMVD and Endothelial Dysfunction?"

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The wall of the blood vessel (coronary artery) supplying the heart muscle has got three layers: the innermost layer contains endothelial cells, the middle layer contains the smooth muscle cells and the outermost layer contains collagen fibres for support. The endothelial cells naturally release a substance called nitric oxide (NO), that then diffuses along into the neighbouring smooth muscle … Continue reading "What is the difference between Endothelium Dependent CMD and non Endothelium Dependent CMD?"

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The wall of the blood vessel (coronary artery) supplying the heart muscle has got three layers: the innermost layer contains endothelial cells, the middle layer contains the smooth muscle cells and the outermost layer contains collagen fibres for support. The endothelial cells naturally release a substance called nitric oxide (NO), that then diffuses along into the neighbouring smooth muscle … Continue reading "What is the difference between Endothelium Dependent CMD and non Endothelium Dependent CMD?"

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