Re: New Endo & The Right Questions

June 17, 2006

Hi Gordon

You have a few things going on.

As far as Endos I wish you luck on your new dr. Two many of them told me I was

fine. grrrr

I have been through 6 endos in the last year. One of which I had a almost to

yelling visit with Endo#6 last week as to the condition i am in and why?.

She didnt even have the recent CCP she ordered. Her nurse calls me A week later

it showed below range K+, low range NA+

It would have been nice to know at the time of the visit.

I also have a adrenal adenoma. I get results of labs next week on aldosterone &

renin.I hope this is my problem.

Any way do tell what your visit is with the new Endo and good luck.

Regards

ita

June 17, 2006

In a message dated 6/17/06 1:44:55 PM, syracuse46567@... writes:

Greetings

OK I have my first appt with the new Endo on Friday and I want to get

this off on the right foot. I will be submitting a rather thick med

record on Monday that has all the info on me.

My Neph who is also my primary will aslo be submitting his notes to the

new Endo prior to the appt.

And there will be fresh labs, I will post those when I get them.

The following is a mini history.

The patient has a history of hypertension for an unknown duration.

Were you born with it or what. when was it first detected and how?

He

knows of systolic pressures of 210 in the not so distant past with

diastolics in the mid 100's. He had been treated with a variety of

antihypertensive agents and has reasonable good control of his blood

pressure now with systolics in the 140 to 160 range on three

medications.

and the meds are?

What kind of problems did he have with other meds?

There has been some juggling of his medications of late to

facilitate the work up of possible hyperaldosteronism but he is

currently taking Coreg 25mg twice a day, Klonidine .1mg twice a day and

Norvasc 10mg once a day. He also takes supplemental potassium of 40 meq

daily because of spontaneous hypokalemia with levels as low as

approximately 2.5.

What other Sx were associated with the low K? What was going on that it was so low!

More recently he has gotten those up into the mid

three range with supplementation as I mentioned. An abdominal CT was

obtained and revealed focal thickening of the right distal limb of the

adrenal gland which could have represented a small functioning adenoma.

The radiology team recommended an MRI which was preformed, this showed a

1.2 by 1.3 cm lesion which did not drop out of phase and was consistent

with an adenoma. When his serum aldosterone level was checked it was 26

which is quite high in somebody who has hypertension and hypokalemia but

his plasma renin activity was 3.4 and therefore the ratio of aldo to PRA

was not greater than 20 and therefore not absolutely diagnostic for

hyperaldosteronism.

Please give the normals for this lab. It is PRA or renin direct? What was he on when these were drawn?

The elevated PRA could have been due to the ACE

inhibitor that was on at the time and so at my recommendation you

stopped that medication for several weeks and followed up with

retesting. On retesting he had an aldosterone of 52 with a PRA of .5

giving him a ratio of 104 clearly putting him in the range of

hyperaldosteronism. We then tried a high salt suppression test which he

did by taking oral salt tablets as well as salting his food. The

adequacy of this was determined by 24 hr urine collection which showed

almost 400 meq of sodium being excreted in his urine per day, clearly a

massive sodium load was obtained.

Well about what many Finns eat but good job.

In this setting his 24hr aldosterone

level only dropped to 13 micrograms which is well above the six

microgram cut off one would expect for that sort of salt load.

Other

investigators use a cut off at slightly higher up to 12 micrograms, but

by either criteria, he clearly demonstrates nonsuppressability and

therefore by definition has primary hyperaldosteronism.

Certainly has personal hyperaldosteronism and indeed I would say group hyperaldosteronism See Dr. Grim's article on the evolution of PA.

The issue at this time is whether the adenoma on the right is the source

of the problem, it seems likely that this is the case. In fact studies

have shown that in patients over the age of 40 the incidence of

non-function adrenal nodules is high enough that one can be fooled and

there have been studies which have shown that patients with

characteristics very much like the subjects who do have a lateralizing

nodule in fact have bilateral source of their excess hormone secretion

which would not be treated surgically but would in fact be treated with

spironolactone. Therefore I think in a man of his age it is reasonable

to lateralize him first. That is why I am recommending adrenal venous

sampling. If he dose show lateralization of his aldosterone levels this

would lead me to refer him for laparoscopic adrenalectomy. If in fact he

does not lateralize on the venous sampling we will treat him with

aldactone as I mentioned.

The AVS should be done during ACTH infusion.

This was dated 16APR03

Results of cortisol and aldosterone levels have returned and have

indicated a successful cannulation of both adrenal veins. The exact

values are in the OMR but the final aldosterone levels show 6031 on the

right versus 2041 on the left. This is a 3:1 ratio which is uncorrected

for the typical diluation on the left which is seen because of the

addition of the left inferior phrenic vein which adds into the left

adrenal vein. Normally this is corrected by the cortisol values. However

the cortisol values were not measured precisely but rather were recorded

just as greater than 63.

Ask the lab to dilute them and run them again. The lab must not be used to doing adrenal vein studies if they did not dilute it and run it again. I would refuse to pay.

Therefore we have borderline lateralization. If anything the

lateralization is less significant when the dilution factor is taken

into account. I have consulted on this issue. The conversation confirms

that it is impossible to tell at this point whether the right lesion

seen on CT and MRI is responsible for the hyperaldosteronism. Therefore

we will try medical therapy first, 50mf of aldactone following blood

pressure and potassium closely and adjusting other blood pressure

medications downward as necessary. If we get complete remission of

hypertension on this or slightly higher dose of aldactone, that can be

considered a diagnostic test, indicating aldosterone producing adenoma

and I would recommend right adrenalectomy. If we get partial correction

of his hypertension with aldactone, that is more consistent with

idiopathic hyperaldosteronism from a bilateral source and we will

continue with medical therapy. It was also discussed that sometimes

surgical debulking is recommended of one adrenal in order to bring the

hypertensive load down to more manageable levels, so regardless of the

outcome of medical therapy, it is possible that we will pursue surgical

therapy.

I would push Sprio up to 400 and or use Inspar is Spiro did not work. The other drugs he is on do not usually work well in PA. See my article.

Calculation

Cortisol

[R] 0- 22.1 / 5min >63 / 30min >63 [L] 0- 27.2 / 5min >63 / 30min >63

IVC 0- 3.4 / 5 min 9.6 / 30 min 18.8

Aldo

[R] 0- 79 / 5min 4575 / 30min 6031 [L] 0- 122 / 5min 1674 / 30min 2041

IVC 0- 4 / 5min 15 / 30min 31

`Borderline lateralization'

Gordon has recovered well from his bilateral adrenal vein sampling. We

spent a long time discussing what our plan will be. Currently I have him

on 50mg of aldactone. He is still on Coreg 12.5mg daily, Norvasc 10mg

and clonidine0.1 mg a day, in addition to 40 meq of potassium.

My plan today is to check potassium and I will call him with that number

tomorrow. We will adjust his potassium if necessary. Regardless we will

increase his aldactone to 100mg a day. I have given him a prescription

for that and I would like to discontinue his Coreg, which would get rid

of one of his medications and probably the most likely defender with

respect to the ED. My plan is to push the Aldactone as high as need be,

trying to wean him off first Coreg, then the Norvasc and finally the

clonidine. We will decide based on how easy this plan is whether or not

to go for a debulking operation to his adrenals. We have essentially

settled on a diagnosis of bilateral adrenal hyperplasia since he did not

lateralize at his adrenal vein sampling.

Meds

Spironolactone 150mg

Tricor 145mg

Diovan 80mg

Norvasc 10mg

[all in the AM]

I was discharged from military service in 1990 and sought no medical

attention until one night there was blood in my semen. What was your BP at discharge? Please get if from the VA or miliatry.

You did not mention family Hx of HTN or low K.

I was seen by my wife's Primary Dr. right away and she stopped the

exam after listening to my heart and BP it was well over 220/110.

A Echocardiogram was ordered and showed a ejection fraction of less than

16% and a fair amount of damage.

Enter my Cardiologist who worked with the primary, I was put on a host

of meds to bring down the BP. By this time the labs were back and I did

not fall into any of the usual situations.

Enter my Endocrinologist who is a Professor at Harvard Medical School.

He ordered a Cat scan which picked up "focal thickening of the right

distal limb of the adrenal gland. Then came the MRI which confirmed the

cat scan. The lesion measured 1.2 x 1.3 cm.

Venous sampling was next as was a salt load test.

Between the three of them I was taking nine meds. But over time I was

weaned off most of them.

I achieved stability, BP in the 110/50 range, EF had risen to 55%, on

the down side ED had become part of my life which Viagra helped.

Classical response to Spirnolactone.

Now I have relocated to Florida and it is time for my annual follow up.

My new Endocrinologist is not pleased with the new labs, seems that my

kidneys are taking a beating I have a GFR of 39 and falling, a

appointment with a kidney specialist is next week.

Do a 24 hr urine collection. Get all your old creatinine values.

In the past month, I have lost most of my sense of taste, my hands and

legs are starting to swell ever so slightly, there is a slight heaviness

in my chest, my urine has turned clear and I keep dropping things. And

the BP is on the rise 138/75 with a spike of 155/85.

I was hospitalized over 2005 Thanksgiving weekend, chest pains and

shortness of breath sent me to the ER, the suspected root cause in my

mind was the stress in my life at that point in time. I was living with

a lesbian who was "trying" to go "straight" and was unsucessful.

The following is from the hospital records for that stay

Kidney consultation report.

Assessment and Plan

1. Primary hyperaldosteronism with hypertension.

2. His blood pressure in the ER today was 153/87, and his temperature

was 100.5. The patient has been evaluated by Cardiology services. Most

likely the patient has chronic kidney disease which is worsening

secondary to hypertensive nephrosclerosis. In light of the fact that he

has suspected metabolically active right adrenal adenoma, he may benefit

from laparoscopic resection of the adenoma from several perspectives: 1]

There may be a 50% chance his blood pressure will improve; 2] if the

adenoma is left in place, he may have worsening cardiac fibrosis by the

effects of the hyperaldosteronism, which has been shown by the Rales

study; 3] there is concern that if the patient has persistent

hypertension for many more years, he will most likely have worsening

renal function which may lead to end-stage renal disease developing to

the necessity of dialysis. We will need to obtain the most recent CT

scan of the adrenal glands and I will also be checking a 24 hour urine

for aldosterone levels. This will help us to evaluate whether the

patient would benefit from right adrenal adenoma resection. Furthermore,

the patient does have mild hypercalcemia, which is 10.2. Will also check

an intact PTH level. In addition, the patient did have mildly elevated

TSH level 5.10, T3 level was normal at 30.9, his T4 level was normal at

9.6. Currently the patient does have a low blood pressure, therefor, I

will not be increasing his Diovan or his Aldactone,

I would stop the Diovan as it does not work in PA.

According to the

patient, he is considering the option of resection of an adenoma if the

work up indicates that it is required. The patient, in spite of having

mildly low blood pressure, he is asymptomatic and has no complaints at

this time. Will repeat his blood pressure. He may benefit from lowering

his blood pressure medications in terms of dosage if he persistently has

low blood pressure. The most recent blood pressure level was 87/50.

This is the most likely reason for the "worsening of renal function"

Labs 28NOV05 @ 0500 26NOV05 @ 2013

Chemistry

Glucose 111 119

Bun 37 35

Creatinine 1.9 2.3

Sodium 135 135

Potassium 4.1 3.7

Chloride 100 101

CO2 24 22

Calcium 9.5 10.8

Phosphorus 3.4

Magnesium 1.7

Alt [gpt] 35

Ast [got] 39

Alk Phos 44

Bilirubin total 0.5

Albumin 4.2

Total Protein 7.8

Hematology

Wbc 6.8 7.4

Rbc 4.41 4.79

Hgb 13.9 15.0

Hct 40.4 44.1

Mcv 91.6 92.0

Mch 31.6 31.3

Mchc 34.5 34.0

Rdw 12.6 12.4

Platelet 234 255

Mpv 9.0 8.7

Differential

Segs 50 51

Lymphocyte 34 36

Monocyte 10 9

Eosinophil 6 4

Basophils 0 0

Cardiac consult

Additional lab info

D-dimer is 0.09, troponin less than 0.04, myoglobin 156, cpk 868, cpk-mb

4.2, inr 1.1, ptt 28.7

Ekg demonstrates sinus rhythm, with frequent premature ventricular

contractions, T wave inversions in the lateral leads, possible lateral

ischemia. Chest x-ray reveals cardiomegaly.

MOst likely due to low cardiac K.

Impression

1. Exertional chest pain and shortness of breath. Symptoms are

suggestive of angina. Patient has a history of negative stress test in

March 2005 and a normal ejection fraction in March 2005.

2. History of dilated cardiomyopathy with normalization of left

ventricular function.

Classic for severe HTN and PA.

3. Frequent premature ventricular contractions.

4. Cardiac enzymes consistent with rhabdomyolysis.

Most likley due to low K.

5. History of severe hypertension.

6. Primary hyperaldosteronism with complete workup in the past.

7. Chronic renal failure.

Recommendations

1. Acute chest pain protocol, labs, and telemetry monitoring.

have you ever had an angiogram of the heart?

2. Check thyroid function tests.

3. Check brain natriuretic peptide level.

4. Will treat patient with aspirin, IV nitroglycerin, beta blocker, and

renally adjusted Lovenox.

5. Would discontinue Tricor as this is a possible etiology of

rhabdomyolysis.

6.Will check 2d echocardiogram.

7. Exercise treadmill, Myoview stress test, risk of cardiac

catheterization based on clinical course.

MRI

The liver is homogeneous as is the spleen. The left adrenal gland is

unremarkable. A 1cm nodule is noted along the medial limb of the right

adrenal gland which remains stable in size when compared with report of

the examination of 12DEC03 [CAT] and 13 JAN03 [MRI]. There is a lack of

signal drop out of phase T1 imaging being atypical for a benign lesion.

However, it is felt to be benign due to lack of interval change and is

likely the expression of a adenoma. The kidneys are unremarkable. No

pancreatic mass is seen. No abdominal aortic aneurysm or retroperitoneal

adenopathy is noted at the level scanned. No abdominal ascites is seen.

There is no dilatation of the biliary tree nor of the pancreatic duct.

Renal Untrasound

Right kidney measures 10.7cm in length. Left kidney measures 10.1cm in

length

There is a cresccentic right perinephric fluid collection of uncertian

etiology. No calculus or hydronephrosis is identified.

Have you ever been injured in the kidneys? or had hematuria?

The visualized portions of the intraabdominal aorta and intrahepatic IVC

are grossly unremarkable. The spleen measures 12.8cm in length.

Impression: Indeterminate small right perinephric fluid collection.

Hematoma?

Since the hospital stay the changes have been:

Weight gain of +40 lbs

Most likley due to Norvasc??

Edema in arms and legs

ED, 100mg Viagra uneffective

Current meds: Inspra 50mg (am/pm), Nifedical XL 30mg (am), Valsartan

160mg (am), Hydrochlorothiazide 12.5mg (am)

BP average is 130/90

After repeated requests to write scripts for lab work so I could be

monitored were ignored, I fired my Endo.

I gave my Neph the PA info as suggested by Dr. Grim and was told that it

was interesting but that he was going to continue my present treatment.

And no labs have been ordered by anyone since the hospital stay, until I

told my Neph that I have an appt with the new Endo.

So what questions do you all suggest I ask for this first appt?

Why did you gain the 40 lbs?

Is it OK if I start the DASH diet? This will markedly reduce your need for BP meds.

Review my family Hx with me to be sure I dont have GRA. Consider doing genetic test but the Harvard guy should have done that-esp if anyone in famly has had HTN or early heart disease.

Keep us postee.

You clearly have Primary Aldo. Bumps on the adrenal are seen in GRA as well.

I would not do repeat AVS unless things cant be controlled with meds and DASH. I am not sure you have had a good trial of DASHing and good medical management. You should have a 24 hr urine collected on your current diet to see how much salt you are eating-esp hidden salt.

Keep us posted.

Gordon

May your pressure be low!

C.E. Grim, B.S., M.S., M.D.

Specializing in Difficult to Control High Blood Pressure

and the Physiology and History of Survival During

Hard Times and Heart Disease today.

June 17, 2006

Do we have a complete ita's story yet?

May your pressure be low!

C.E. Grim, B.S., M.S., M.D.

Specializing in Difficult to Control High Blood Pressure

and the Physiology and History of Survival During

Hard Times and Heart Disease today.

June 17, 2006

I can barely walk when my TSH gets to 4.0. I now keep it at about 1.00. In 2002, the American Association of Clinical Endocrinologists recommended an upper cut-off TSH = 3.00 as indicative of hypothyroidism or subclinical hypothyroidism. The association that represents laboratory members recommended an even lower cut-off level (I think it was about 2.5 but can't find the article right now). There is disagreement as to what TSH level should be reached before treatment is initiated. Certainly, you should get your antibodies measured.

While you obviously have much other going on, your thyroid function should not be dismissed. See http://www.aace.com/pub/positionstatements/subclinical.php

Val

-----Original Message-----From: hyperaldosteronism [mailto:hyperaldosteronism ]On Behalf Of gnenjnj

TSH level 5.10

Weight gain of +40 lbsEdema in arms and legs

June 18, 2006

In a message dated 6/18/06 12:17:36 PM, syracuse46567@... writes:

Here are aditional notes and letters while I was being brought under

control.

Cardiologist notes:

We started him on a ACE inhibition and beta blockade. He devoled a

cough with the ACE. This was also discontinued because he is in the

process of a work up for Secondary hypertension. He comes to the

office reporting intermittent fatigue and ED while on the increased

dose of Carvedilol.

ACEs and BB dont work in Primary aldo. See my article and take it to this Cards

EKG demonstrates normal sinus rhythm with left atrial abnormality,

normal axis and intervals. There was no change when compared with

the prior other than a shower heart rate.

My inpression is that Gordon is doing relatively well albeit still

poor BP control. The optimal goal will be to eventually get him on a

ARB, for now I have taken the liberty of starting him on Norvasc

10mg qd

ARBS dont work either in PA see my article and take to this Dr.

Dated 25FEB03

EKG demonstrated normal sinus rhythm, with normal axis, prolonged PR

interval, and t-wave inversion in leads 1, and AVL. These are

unchanged from his prior. The left atrial abnormality and prominent

voltage, noted on previous EKG's are not present at this time.

With regard to his heart I believe he is doing better. Though

somewhat fatigued, I believe this to be related to the beta blockade

and/or reduction in circulating epinephrine levels. Nevertheless the

inprovement in the left atrial abnormality and voltage suggest to me

that some component of the elevated filling pressures and/or heart

dilation has inproved.

The most imperative intervention from my standpoint is to increase

his beta blockade and add ACE inhibition to further continue and

improve remodeling of his heart. My hope is that this can occur

expeditiously as soon as the issue surrounding the possible

adrenalectomy are ironed out.

Once again these drugs do not work in PA.

Dated 02MAY03

Additional letter from my orginal ENDO:

Gordon has been experiencing a bump in his creatinine levels. On

24MAR03 it was 0.9 and in APR03 it rose to 1.1 and in MAY03 it was

at 1.2 and at the end of MAY04 1.4.

On 17JUN03 he was strady at 1.4 this was accompanied by a BUN that

has ranged from 26 to 29 and a potassium level that has been steady

at 4.4. BP measurments range from 130/70 to 160/80 the 160 bump may

reflect rebound hypertension after discontinuing his Clonidine.

My impression is that we are in a little bit of a bind. If the

rising creatinine is just a temporary bump due to dehydration due to

overzealous Aldactone administration, then that is fine. We can

watch over time and hope it resolves. However if it limits us in

pushing the aldcatone up then it going to be very difficult to treat

his hypertension medically, and we are going to have to consider a

surgical debulking operation which may or may not be efficacious.

Dont know any data on debulking procedures. Ask for references to published articles.

There certainly is no literature on the subject, although this is

current pratice in certian cases performed by a Dr. at the Mayo

Clinic who is the worlds expert on this condition.

I know that the Caridologist wants to add an ACE inhibitor. However

on the face of his rising creatinine right now, I do not think that

would be wise. His Coreg is also causing problems with fatigue and

ED. However I certainly understand the Cardiologist' ED. However I ce

that medication on board.

Ultimately of course we are going to have to balance all of our

competing interests and desires as specialist to come up with the

best regimen for Gordon whatever that may be.

Dated 25JUN03

Cardiologist letter:

As we are all aware Gordon continues to be a difficult case. There

is no "correct" medical regimen that will adequately treat both his

cardiomyopathy which is likely due to hypertension and adrenal

excess, and the adrenal hyperplasia itself while at the same time

have no serious side effects.

Well yes there is. It is called mineralocorticoid blockade with Spriro or Inspar. Take him my article

Along these lines BP control is obviously of paramount importance.

He has had suboptimal control with BP ranging in the most part

between 130 occasionally 170. The aldosterone does not seem to be

sufficient and he seems to have some mild renal dysfunction which

may or may not have been related to this agent.

One may question the need for an ACE inhibitor in a patient where

renin levels are suppressed or normal (as has been demonstrated in

his case) and whether heart failure trial results are truly

applicable to him.

Good he his thinking.

However the vascular protective effects that are

independent of BP control with this class of medication are well

established and the lesser defined mechanisms to inprove mycardial

remodeling, possibly mediated through the bradykkinin axis, may be

of paramount import in long term improvement in left ventricular

systolic function for him.

Humbug. You treat heart failure by treating the cause, In your case it it aldo and salt.

In summary, if his kidneys can tolerate it with only a small

increase in creatinine, I think the beneficial effects of this

medication, as far as vascular protection, mycardial remodeling, and

possibly even BP control (if there is some component of renin-

angiotensin activation) is important.

Certainly his morbidity in the coming years will be related mainly

to complications of his mycardial dysfunction, including overt

congestive symptoms and possibly even future arrhythmic events since

it apprears as though he only has adrenal hyperplasia. I do believe

that it is possible to control his BP medically and that ACE

inhibitor should be part od this strategy.

But it wont work.

The same holds true for his beta blocker, but the benefit is even

less theoretical and there is supportive data that more substantial.

It is the only class of medication that has been shown to lead to

improvement in ejection fraction in those with myopathic ventricles.

Again, his morbidity and longevity will not be measured, in my

estmation, by adrenal hyperplasia since the conversion to malignancy

is rare and not altered by any specific medical therapy. Instead,

his low ejection fraction is a well known surrogate marker for

inpared survival and anything that we can do to improve this will

hopefully improve his long term survival.

We must, however, balance the use of this medication with his

quality of life at the Endo has pointed out, especially in light of

his ED. I also wonder if the anti-androgen effect of the sprro may

also be a contributor to the ED.

Dated 28JUL03

Endo progress note:

BP of 138/80 with a pulse of 68, This is a little higherthan I would

prefer and I suspect the Cardiologist would prefer, so I have

increased his Aldactone from 100mg to 150mg a day.

I am also going to check his testosterone given his presistant ED

even off beta blocker. Certainly the other antihypertensive drugs

could be contributing, although it is formally possible that he

could be mildly hypogonadal as well.

Dated 11FEB04

Good. It is most likely tghe BB. would not do testoterone by an Endo would.

May your pressure be low!

C.E. Grim, B.S., M.S., M.D.

Specializing in Difficult to Control High Blood Pressure

and the Physiology and History of Survival During

Hard Times and Heart Disease today.

June 18, 2006

In a message dated 6/18/06 1:02:15 PM, syracuse46567@... writes:

Orginal Echocardiogram 31DEC02

Left Atrium: the feft atrium is markedly dilated.

Right Atrium/Interatrial Septum: The right atrium is mildly dilated.

Left Ventricle: the left ventricular cavity is moderately dilated.

There is severe global left ventricular hypokinesis. Overall left

ventricular systolic function is severely depressed.

Right Ventricle: The right ventricular cavity is mildly dilated.

Right ventricular systolic function apprears depressed.

Aorta: The aortic root is normal in diameter.

Aortic Valve: The aortiv valve leaflets (3) appear structurally

normal with good leaflet excursion and no aortic regurgitation.

Mitral Valve: The mitral valve leaflets are mildly thickened.

Moderate (2+) mitral regurgitation is seen. (Due to acoustic

shadowing, the severity of mitral regurgitation may be significantly

UNDERestimated.

Tricuspid Valve: Mild tricuspid (1+) regurgitation is seen. There is

moderate pulmonary artery systolic hypertension.

Pulmonic Valve/Pulmonary Artery: The pulmonic valve leaflets appear

structurally normal with physiologic pulmonic regurgitation.

Pericardium: There is no pericardial effusion.

L Atruim long axis 6.0cm

L Atrium four chamber length 6.7cm

R Atrium four chamber length 6.2cm

L Ventricle septal wall thickness 1.1cm

L Ventricle inferolateral thickness 1.1cm

L Ventricle diastolic dimention 6.7cm

L Ventricle systolic dimension 5.6cm

L Ventricle fractional shorting 0.16

L Ventricle ejection fraction less than 20%

Aorta valve level 3.6cm

Aorta ascending 3.0cm

Mitral valve E wave 1.4 m/sec

Mitral valve A wave 0.4 m/sec

Mitral valve E/A ratio 3.50

Mitral valve E wave deceleration time 110msec

TR gradient (+RA = PASP) 54 mm Hg

Current EF is 55% as the Echo showed while in the Hosp NOV05

What was your BP at the first study? and K?

May your pressure be low!

C.E. Grim, B.S., M.S., M.D.

Specializing in Difficult to Control High Blood Pressure

and the Physiology and History of Survival During

Hard Times and Heart Disease today.

June 18, 2006

We have had at least one other person on our site with severe CHF that reversed with proper Dx. From Cincinatti as I recall.

May your pressure be low!

C.E. Grim, B.S., M.S., M.D.

Specializing in Difficult to Control High Blood Pressure

and the Physiology and History of Survival During

Hard Times and Heart Disease today.

June 18, 2006

Hi Gordon,

The first thing I would ask is, how familiar are you with PA and how

many patients have you treated with it.

Good luck,

a

>

> Greetings

>

> OK I have my first appt with the new Endo on Friday and I want to get

> this off on the right foot. I will be submitting a rather thick med

> record on Monday that has all the info on me.

>

June 18, 2006