Endothelial-Dysfunction/MVD Anginal Treatment in Females?
Joan, I posted but somewhere it disappeared, so here goes again:
Mild to moderate Endothelial-Dysfunction and presumed MVD with chronic angina - clear cath 3 years ago, etc. The source of my angina is 95% emotion stimulated. I believe this unfortunately titled article explains why - it's the missing link!
My cocktail is currently Coreg 3.125 - 2x am/pm, Nitro SR 2.5, .81 Aspirin, Pravastatin, Niacin, Fish Oil, Vit D, Nitro-Quick. Soon to try Diltiazem addition, but the caution against benzo use has held me back - as Xanax really helps - AT THE SOURCE. I use Xanax at will, thanks to my understanding internist, and this has increased over time to appx 1x per day - 0.25, which at present seems a little inadequate. I am having increasing breakthrough CP and SOB through experiencing day to day emotions - ANY emotions in the course of daily living: happy, excited, sad, pressured, etc., so I suspect it's time to change up meds and UP my my Coreg or my nitro from 1 x p/d to 24/7, sadly.
I've considered trying clonazepam with longer duration, but the reason I've preferred the shorter acting, is because I have hypopnea and use Bi-PAP. I am further compromised by some congenital nasal obstruction that should be surgically fixed. Night time respiratory depression is not beneficial so I like the benzo to wear off by bedtime.
I'd like to address the gap between the "pure" cardiac and the psychoactive meds. My cardiologist refers me to psychiatry dept if we go in that direction, which is not only time consuming and expensive, and creates a prejudicial attitude of "it's emotional", (i.e. female) and creates an additionally predjudicial insurance burden (dual diagnosis). It tackles the issue from a Descartian perspective - "separate body systems". Cardiac vs Psych med utilization (and I'm not just talking about anti-depressants). Historically, the "Type A" explanation in males, i.e. anger, pressure has done a vast disservice to female cardiology and diagnostic subtleties, but of course, the mechanisms for understanding these differences have radically improved via cardiac MRI, etc. The article attached illuminates a reasonable (and to me spot on) explanation of this difference in male vs female symptom expression.
The gap in meds needs to change in two ways. It would be helpful if drug development were to tackle angina from the amygdala perspective...hopefully, without respiratory depression. If there were newer antidepressants that didn't have risk of ischemic side effects, as do SSRIs, SNRIs, it would be great. Older line meds (Tri-cylics), Buspar and Gabapentin are non-ischemic, however, the side effect (weight gain depending on the person or the dose) or the med itself may not be advantageous per the individual's response.
Barring frontal lobotomy or meds that reduce one to a career of full time nap-taking, it would be helpful to have a non-addictive med that has two primary targets: vasodialation and dampening of the sympathetic/parasympathetic response to emotional stimulation (while functional on a daily requirements basis - ie driving, working, thinking, etc). Long acting would be nice, but that's frosting on the cake. Maybe it could be a medication pairing that could be adjusted proportionally, with ratios according to individual symptom expression. As long as I'm wishing, I should include that the vasodialation could be reversible or modified. I always wonder if I had an auto accident or something, will I bleed out from nitro.
I'd love your feedback; I'm all eyes and ears. Best, Mary
See..I am catching up. Just got a note from MedHelp that I have 964 questions to answer. I'll get right on that! Don't worry about bleeding out from nitro....just hope they give you more to catch up with that kind of trauma. That's why I don't drive much or on fast roads....I don't think I'd survive a big crash. Two episodes of being rear bumped set me off .Love Joan.
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