I have a few questions about
hypertrophicHypertrophic cardiomyopathy cardiomyopathy, having been diagnosed about 5 years ago at the age of 45. For the
firstFirst progesterone mc10
First progesterone mc5
First-progesterone vgs 100
First-progesterone vgs 200
First-progesterone vgs 25
First-progesterone vgs 400
First-progesterone vgs 50
First-testosterone
First-testosterone mc time on a recent echo, I read in the report moderate pulmonary hypertension with a
systolicBlood pressure
Mitral valve prolapse right
ventricularParoxysmal supraventricular tachycardia (psvt)
Ultrasound, ventricular septal defect - heartbeat
Ventricular assist device
Ventricular fibrillation
Ventricular septal defect
Ventricular tachycardia pressurePressure ulcer of 48. Never any mention of PH before. Is this a natural progression of my HCM?
Could pacing have caused this? ( I have had a pacer for the last 4 years which did cause my gradient to fall from 60 at rest to 15 but has not improved my symptoms of chest pain and SOB.)
Is the PH diagnosis
reliableReliable gentle laxative just by echo?
Is this an indicator of a poorer prognosis?
Should my treatment change if I do have PH? I am currently on a beta blocker, calcium channel blocker, and Norpace plus the pacer which was inserted for bradycardia from all the meds and also in an effort to reduce the obstruction, if I understand correctly.
My provocable gradient with Dobutrex is 160, with exercise is only in the 40's although when I have a stress echo, I am always fasting which I do not believe is a true indicator of how I feel every day when I have eaten. (Symptoms are so much worse after eating even a small meal, that I feel my gradient has to be higher when not fasting.) Why are stress echoes done while fasting and do you think that is an accurate way of measuring gradient (obstuction)in an HCM [patient?
Thank you for your insight.