Heart & Cardiology/RVSP pressure and PH
QUESTION: I have written to you in the past and have had echos every 3-6 mos for 2 1/2 years. For the past 4 echos (2 yr span) the RVSP via echo has been 60 and remained the same. It had been 48 on the first echo 2 1/2 years ago. I had sleep apnea and started cpap therapy and the pressure has remained at 60 which I know is high moderate. If the pressure remains at this, what damage will it do to my heart? Is it typical to see a stalling for this long? My cardio wants to wait a year to do the next echo. Do you agree this is a wise course?
ANSWER: Hello Cathy.
Probably no damage. Right heart failure is an unlikely possibility.
Yes, typical to remain the same as years go by.
Yes, a year is reasonable.
---------- FOLLOW-UP ----------
QUESTION: I just received my last 2 echo copies and am confused. My cardio never mentined anything to me except the RVSP being 60. I will post the results and would appreciate your thoughts. Does the increase of the measured value mean my heart is starting to be damaged?
3/10 RVSP was 46
Left Atrium 3.1
aortic root 2.82
RV diastole 2.43
LV diastole 4.81
LV systole 3.36
interventricular septal thickness 1.07
LV posterior wall thickness 0.992
4/13 RVSP 60
Left Atrium 4.1
aortic root 3.1
RV diastole 2.8
LV diastole 5.6
LV systole 3.6
interventricular septal thickness 1.1
LV posterior wall thickness 1.1
There is currently no cure for PAH. However, the past two decades have seen significant advances with the development and clinical implementation of a number of medications that specifically target the aberrant regulatory and structural changes in the pulmonary arterial bed [McLaughlin et al. 2009; Farber and Loscalzo, 2004]. In addition to chronic adjunctive therapy, three classes of drugs have been developed and approved for the treatment of PAH: endothelin-1 (ET-1) receptor antagonists (ERAs), prostanoids, and phosphodiesterase type 5 (PDE-5) inhibitors. All three classes of medication have been shown to favorably affect hemodynamic parameters and to improve functional capacity and exercise tolerance [McLaughlin et al. 2009]. Furthermore, a variety of other substances that play roles as mediators through a final common pathway of pulmonary angiogenesis have emerged as appealing therapeutic targets and are currently the subject of intensive laboratory and clinical research. This review article provides an overview of these current therapeutic options and future potential targets. The whole article can be found at medscape.com/viewarticle/755890
I think you need treatment now to prevent heart failure.
Please write back if this note doesn’t answer all your questions.