High Left Ventricular Diastolic End Pressure (LVEDP) - Heart Disorders Message Board

huckfinn · 07-28-2007, 01:05 PM

I was hoping that someone could help me understand possible causes of this measurement being abnormally high, from self experience or otherwise

I was reading over my cath results and found this listed under "diagnosis and principal findings", among other things:

Mildly elevated left ventricular end-diastolic pressure = 24 mmhg

I looked up the normal values and was extremely shocked to find that normal LVEDP values are either 5-12 mmhg or 8-13 mmhg, depending on which reference is most correct. I cannot believe the error in the description of this measurement in the report!

I also read that an LVEDP of >20 mmhg was considered diastolic heart failure. I am fairly sure that it is not due to stenosis of my aorta or my aortic valve since the cath stated "no pressure gradient across the aorta or aortic valve". I assume that means no pressure drop across my aorta/aortic valve as compared to my LV output pressure.

I have looked up the causes of high LVEDP, and the only one that seems possible for me is MVP, but in this case it seems the mitral valve regurgitation would have to be extreme. I have been told my MVR was very mild.

I need to find the normal pulmonary vein pressure. It would have to be at least 24 mmhg, if MVR is my problem. Don't you think?

I plan to request a call from my cardiologist's nurse, Monday morning. My EF is fine at 50. I do have coronary artery disease of the LAD, with 4 overlapping stents, with an existing re-stenosis of 30% to 40% in this series of end to end, connected stents.

Thanks kindly for any thoughts you may have on my problem

Lenin · 07-29-2007, 07:45 AM

I'm thinking it MIGHT be mitral valve stenosis...that's what the literature suggests. .

But in truth the mitral valve stenosis doesn't sound straightforward to me because in MVS one would THINK that the amount of blood passing from left atrium to left ventricle would be DECREASED and thus the BP in the left ventricle would always be low. MAybe it's too early in the morning.

I'm also seeing the same references to congestive heart failure with high LVDEP that you are...stretched venrticle overfilling and emptying poorly...

<I'm scratching my head.>

This may sound silly: Is it reasonable to asssume that with MVS, the atrial pressure must get quite high to provide the LV with enough blood and that this high atrial pressure is transmitted to the resting LV at end diastole?

I'm just brainstorming here, huck. I'll think about it more today.

Normal Pulmonary Venous pressure is around 12 mm. Hg

(Sometimes a GOOD TEXTBOOK is worth a hundred internet searches...and I don't have a good cardiac text.)

At least you have thought through many ramifications and should be completely ready for a meeting with you cardiolofgist...don't let him out of your sights until he answers all the questions you have.

KenKeith is sharp on heart-failure issues and he'll probably weigh in.

started04 · 07-29-2007, 10:52 AM

Lenin has it correct. Some perspective with a visual description.

LVEDP is in direct relationship to heart stroke/volume. Graphically with a stroke/volume on the vertical axis and LVEDP on the horizontal there will be a half bell curve and when it peaks there will be a sharp decline. The sudden drop occurs to an EF greater than 75%, and then there is decompensation to heart failure ...EF below 29%.

Some insight the intracardiac pressure enlarges chambers and more volume, and the enlargement increases stroke contractions (increase in cardiac output) to meet blood/oxygen demand. Sttonger stroke contractions are due to Frank-Startling mechanism. For an analogy of the phenomonon would be to take a hand spring and when stretched it has a stronger recoil, but over stretched it loses its elasticity. An over stretched heart chamber will decompensate.

LVEDP may be elevated without an increase in LV end diastolic volume because of diminished ventricular compliance due to ischemia, hypertrophy, fibrosis (heart muscle impairment), etc And increasing afterload not only reduces stroke/volume, but it increases LVEDP.

huckfinn · 07-29-2007, 02:28 PM

Thanks so much to both of you guys

You keep hitting the nail on the head...

In the mail yesterday, I received all of my past cardiology records dating back to 1993. Whew, I had forgot how long I have been seeing these doctors. The Cleveland Clinic, back a couple of months ago, lost all of my personal medical records. This is why I ordered all of my records from my cardiology group.

In addition to all of the records, I received the actual results and the doctor's interpretation of an echocardiogram I had performed about 3 weeks ago. Shocked and amazed I wasn't, due to knowing my LVEDP pressure. My Left Atrium is enlarged. 5 of the 6 other echo measurements are very close to the abnormal range.

I have went through these records and am amazed at the abnormalities that were never reported to me, but of course they were sent to my PCP.

Overall, I think that I have had poor revascularization of blood flow to my heart muscle, due to my anatomy and less than a proactive approach (too conservative) to my treatment of CAD.

Time and time again I see where a report has mentioned hypokinesis of my inferior and mid-anterior wall. I discovered another coronary anomaly that I had no idea of; a tiny subtotal high OM1. I need to look this up, but my cardio told my PCP that this is why I was having chest pain and nothing could be done because this artery could not be stented. Gee, I wish someone had of told me....

I also got the "raw" results of my 64 slice CT coronary artery scan that I had in September of 2006. Wow, for those of you that do not already know this, they check all of the major organs, lungs and chest for any abnormalities, in addition to the coronary arteries and chamber functions of the heart.

I have a few lung nodules noted and "evidence of past granulomatous infection". I also have "scattered calcified hilar nodes and mediastinal nodes". No clue here...Should another doctor have been told?

Sorry for the OT stuff and sour attitude. Sometimes I don't understand why things work like they do, in the world of medicine.

Lately I have been busy writing to a cardiologist and surgeon at the Cleveland Clinic. I have been desperately listing reasons why my MID-CAB surgery should be expedited.

I have to go for an evaluation (cath) before I can find out if I am sick enough to have it. I have all kinds of reports stating how diseased (also still blocked 35%-40% and un-stentable) my LAD is, and how it can never be stented again. (4 stents already)

How long can you wait to have a massive heart attack, when you have extremely high cholesterol, cannot tolerate statins and are just plain chicken?

Thanks for the vent. I feel better already

Lenin and Keith, thanks so much for the research and reply. Maybe I can return the favor.

Y'all keep smiling

flowergirl2day · 07-29-2007, 03:20 PM

Huck,

Quote:

Gee, I wish someone had of told me....

I, too have a problem with doctors not being very forthcoming with information. They tend to dwell on the positive too much. I wonder if they do it to spare themselves being questioned by us..time is precious... $$$ ...

, or if they think we''ll be happier not knowing. My feeling is that unless it is something we must be made aware of because it requires a treatment, we just don't hear about it.

Good luck with your cath/angio. Hope all goes well.

Flowergirl