Early IHSS and Central Sleep Apnea

Can early IHSS or mild valve insufficiency be a possible cause for severe Central Sleep apnea?  If so, what is the best means of diagnosis and intervention?  I have had a pacemaker placed for bradycardia, and have been using an Adapto-Servo ventilator (4 sleep studies this past year), but have had minimal relief of fatigue and progressive general neuropathy.

My ejection fraction is 54%.  E/A ration is 0.9.  Trace mitral and pulmonic and mild tricuspid insufficiency.  The pulmonic and tricuspid changes are new.  I have an occasional murmur, only once very marked one day after exercise.

I do 4 miles 4 times a week on the treadmill (in an hour).  I have been doing this for 3 years without any increase in exercise tolerance or improvement of endurance.  My Dad had IHSS.

[CCFCardio MD1]

It would rare for hypertrophic cardiomyopathy (or IHSS as it is sometimes known) to cause central sleep apnea.  Trace and mild changes in valvular function are very common and do not cause abnormal pathologies such as central sleep apnea.  Neuropathy is often times seen in patients with diabetes.  Perhaps further testing for it would be helpful.

[DSA]

Thank you for your input in regards to IHSS/valve dysfunction and Central Sleep apnea.
It seems more likely perhaps that the Central Sleep apnea may be causing the cardiac changes we have seen (bradycardia, etc).  We have been told that these effects can be bi-directional.

Fasting blood sugars have always been normal.  GTT testing has shown mild elevations (up to 180 post prandial), but home testing has yielded no indication of blood sugar etiology for the extreme fatigue.  Other neuropathy etiologies have been ruled out and we suspect that perhaps the neuropathy may be related to hypoxemic episodes.
  
Given the hypoxic stress of severe Cental Sleep apnea that has not responded to the most advanced CPAP device, and the history of elevated tri-glycerides and cholesterol (now well controlled with medication and diet), would you say a cardiac cath. would be advisable to determine blockage risk, or is this too invasive without any current symptoms of angina or chest pain?