ChookityPop
Senior Member
- Messages
- 607
I developed angina, shortness of breath, fatigue last summer but my ECG and ultrasound was fine. I now learned about microvascular dysfunction thanks to @pattismith which apparently stands for 20-30% of Angina cases. What annoys me is that none of the cardiologists didnt mention this at all. I will now get a PET or Cardiac MRI.
This reminds me of small fiber neuropathy. As there you can have length dependant and NON length dependant SFN. Where I live they only to skin biopsies looking for length dependant SFN which obviously wont diagnose a huge percentage of NLD SFN. What is going on with the medical system and medical professionals. There is incompetance everywhere I see and it blows me away.
"Microvascular angina or ‘Cardiac syndrome X’ are diagnostic terms used to describe angina in patients with non-obstructive epicardial coronary artery disease and hint at underlying coronary microvascular dysfunction (CMD). It is becoming increasingly recognised that a significant proportion of patients (20-30%) with angina fall into this category,(1) necessitating a change in our understanding of ischaemic heart disease - it is no longer synonymous purely with obstructive epicardial coronary artery disease (CAD)."
* Coronary microvascular dysfunction (CMD) is common, especially in women. Most patients with CMD also have some epicardial CAD.
* CMD can be due to different structural and functional abnormalities affecting the coronary microvasculature.
* A diagnosis of ‘microvascular angina’ i.e. caused by CMD relies on the exclusion of obstructive epicardial CAD.
* Functional tests are not sensitive or specific for CMD and therefore are not diagnostic.
* CMD can be diagnosed by measuring physiological surrogates of microvascular function such as coronary flow reserve (CFR) using Invasive and non-invasive (PET, CMR, Echo) techniques.
* A CFR value of <2 is highly suggestive of CMD.
* There is no proven and validated treatment for CMD. Current strategies involve optimising management of risk factors such as diabetes, hypertension and hyperlipidaemia and trialling anti-anginal therapies for symptom control.
I have TSHDS and Plexin D1 antibodies I bet this is relevant.
Small Vessel Vasculitis in Small Fiber Neuropathy with TS-HDS, FGFR-3, or Plexin D1 antibodies (P14-8.007)
Conclusions: Inflammation was seen in a small portion of seropositive biopsies, but suggests an immune mechanism at the ganglion level, and provides further proof of autoimmunity in seropositive-SFN. These patients often have moderate to severe SFN symptoms and pain, exam findings, and disability. Further studies may be indicated to assess whether biopsy-inflammation is a marker for immunomodulatory treatment responsiveness. https://n.neurology.org/content/100/17_Supplement_2/4882
This reminds me of small fiber neuropathy. As there you can have length dependant and NON length dependant SFN. Where I live they only to skin biopsies looking for length dependant SFN which obviously wont diagnose a huge percentage of NLD SFN. What is going on with the medical system and medical professionals. There is incompetance everywhere I see and it blows me away.
"Microvascular angina or ‘Cardiac syndrome X’ are diagnostic terms used to describe angina in patients with non-obstructive epicardial coronary artery disease and hint at underlying coronary microvascular dysfunction (CMD). It is becoming increasingly recognised that a significant proportion of patients (20-30%) with angina fall into this category,(1) necessitating a change in our understanding of ischaemic heart disease - it is no longer synonymous purely with obstructive epicardial coronary artery disease (CAD)."
* Coronary microvascular dysfunction (CMD) is common, especially in women. Most patients with CMD also have some epicardial CAD.
* CMD can be due to different structural and functional abnormalities affecting the coronary microvasculature.
* A diagnosis of ‘microvascular angina’ i.e. caused by CMD relies on the exclusion of obstructive epicardial CAD.
* Functional tests are not sensitive or specific for CMD and therefore are not diagnostic.
* CMD can be diagnosed by measuring physiological surrogates of microvascular function such as coronary flow reserve (CFR) using Invasive and non-invasive (PET, CMR, Echo) techniques.
* A CFR value of <2 is highly suggestive of CMD.
* There is no proven and validated treatment for CMD. Current strategies involve optimising management of risk factors such as diabetes, hypertension and hyperlipidaemia and trialling anti-anginal therapies for symptom control.
I have TSHDS and Plexin D1 antibodies I bet this is relevant.
Small Vessel Vasculitis in Small Fiber Neuropathy with TS-HDS, FGFR-3, or Plexin D1 antibodies (P14-8.007)
Conclusions: Inflammation was seen in a small portion of seropositive biopsies, but suggests an immune mechanism at the ganglion level, and provides further proof of autoimmunity in seropositive-SFN. These patients often have moderate to severe SFN symptoms and pain, exam findings, and disability. Further studies may be indicated to assess whether biopsy-inflammation is a marker for immunomodulatory treatment responsiveness. https://n.neurology.org/content/100/17_Supplement_2/4882
