[H] gouty heart

[andyh]

Jpgregorich@aol.com wrote:
Hi,
I'll give you some thoughts, *not* definitive, but maybe a starting place for
discussion (have had the same question, and regarding the heart, will have to
conclude with another question to the List).

In working the EYE section of the Complete Rep, by way of example, there are
references such as:
EYES; INFLAMMATION; arthritic, gouty, rheumatic (K242, G203): achy., acon.,
ant-c., Ant-t., apis, arn., ars., arum-m., bell., bor., bry., cact., Calc.,
caust., cham., chin., clem., cocc., colch., coloc., dig., dulc., euphr.,
Form., graph., hep., ilx-a., kali-bi., kali-i., kalm., led., lith-c., Lyc.,
med., merc., merc-c., mez., mim-h., nux-v., Phyt., psor., puls., Rhus-t.,
Sep., sil., spig., staph., sulph., syph., ter., thuj.

I have been taking this to indicate an inflammation with concomitant
arthritic, gouty, or rheumatic symptoms, which can all present about the same
in their diminutive form, prior to extensive diagnosis. This helps
differentiate the inflammation using one sure concomitant.

However, in the eye section, there is also the following:
EYES; GOUT: bell., berb., bry., caust., coloc., euph., lith-c., lyc., merc.,
nux-v., rhus-t., staph.

This I assume refers to symptoms of the eye itself referrable to high uric
acid concentration and crystal deposition. GOUT is traditionally defined as
an inflammation of the joints, which are absent in the eye (or the heart),
since a joint requires bone. However, a broader definition includes any
consequence of disturbed uric acid metabolism (liver=production,
kidneys=excretion, so overproduction or under excretion leads to high blood
levels (Hyperuricemia). How that is determined in the eye (or the heart)
gets to the heart (pun intended) of your question.

In fact, the following symptoms relate to gout of the EYE, from

http://www.emedicine.com/oph/topic506.htm

__________________________________________________________________
The folklore surrounding gout also has involved the eye, and, prior to the
20th century, a myriad of common and unusual ocular symptoms
falsely were ascribed to the gout. All manifestations of gout in the eye are
secondary to deposition of urate crystals within ocular tissue.

Conjunctival nodules containing needlelike crystals have been
described within the interpalpebral areas, sometimes associated with a
mild marginal keratitis.

Band keratopathy with refractile, yellow crystals in the deep corneal
epithelial cells and at the level of Bowman membrane are not
uncommon.

Symptoms of visual blurring from the corneal haze or foreign body
sensation due to epithelial breakdown can be treated with scraping
of the epithelium and removal of the crystals.

Gout rarely can be associated with anterior uveitis and has been
mentioned by Duke-Elder as a cause of hemorrhagic iritis.

Scleritis and tenonitis also have been described.

In addition to the cornea, urate crystals have been described
clinically in the lens and sclera and on postmortem examination in the
tarsal cartilage and in the tendons of extraocular muscles.

also, FROM:
http://www.ucdmc.ucdavis.edu/health/a-z ... erity.html

Cataracts.

Dry eye syndrome (sensation of sand, foreign object may be included)
---------------------------------------------------------------------

Regarding the gouty symptoms of the HEART, I have found a couple of links, but
it seems that the modern understanding of the effect of uric acid on the heart
is not profound (or I just havent found the right source). What is known is
that Gout and heart disease do often go together, so it in fact could be a not
insignificant factor in heart disease, or it could just be a concomitant. One
reference theorized that gout is an idiosyncratic response and actually
protects the heart!

----------------------------------------------------------------------------------------

from:http://www.ucdmc.ucdavis.edu/health/a-z ... erity.html

Gout and Heart Disease

Gout often accompanies heart problems, including high blood pressure,
coronary artery disease, and congestive heart failure. Hyperuricemia, in
fact, has been associated with a higher risk of death from these
conditions. One 2001 study reported that disease activity in gout may
contribute to unhealthy cholesterol and lipid levels. Some interesting
evidence, however, suggests that hyperuricemia may occur as a
response to inflammatory damage that occurs with heart disease and may
even be protective.

-----------------------------------------------------------------------------------------

So, thus far I have not found any SYMPTOMS of the heart referrable to uric
acid crystals there. So practitioners in the past either knew how to
recognize it (seems quite possible, since the rubrics refer directly to the
chest and heart, respectively), OR just recognized it via concomitants.

The rubrics(COMPLETE):

CHEST; GOUT: abrot., adon., ars., aspar., aur., bell., benz-ac., cact., calc.,
calc-i., carb-v., caust., colch., conv., cupr., ferr-p., hep., iod., kalm.,
lach., led., lyc., lycps., nat-m., phos., puls., spong., stroph., thyr.

CHEST; GOUT; heart (K833, G704): abrot., adon., ars., aspar., aur., bell.,
benz-ac., cact., calc., calc-i., carb-v., caust., colch., conv., cupr.,
ferr-p., hep., iod., kalm., lach., led., Lyc., lycps., nat-m., phos., puls.,
spong., stroph., thyr.
A primary gouty rubric, referenced to joints:

EXTREMITY PAIN; GOUTY; joints: abrot., acon., aesc., agar., Agn., alum.,
am-be., am-c., am-m., am-p., ambr., anac., anag., ant-c., ant-t., apis,
apoc-a., arbu., Arg., arist-cl., Arn., ars., ars-h., ars-i., asaf., asar.,
astac., aur., aur-ar., aur-i., aur-m-n., ba-sv., bac., bapt., bar-c., bar-i.,
Bell., bell-p., benz-ac., berb., bism., bor., bov., Bry., bufo, cact., caj.,
Calc., calc-f., calc-i., Calc-p., Calc-s., canth., caps., carb-an., carb-v.,
carbn-s., carl., Caust., cham., chel., chin., chin-ar., chin-s., cinnb.,
cocc., Colch., colchin., coloc., con., cupr., cypr., daph., dros., dulc.,
elmen, eup-per., eup-pur., ferr., ferr-ar., ferr-i., ferr-p., ferr-pic.,
form., form-ac., franz., gast., get., graph., guai., hell., hep., hyos.,
iber., ign., iod., irid., jab., kali-ar., kali-bi., Kali-c., kali-i., kali-m.,
kali-n., kali-p., kali-sil., kalm., laur., Led., lith-br., lith-c., Lyc.,
m-arct., m-aust., m-p-a., Mag-c., mag-m., mag-p., mang., mang-acet., med.,
menis., meny., Merc., merc-d., mez., nat-ar., nat-c., nat-l., nat-m., nat-p.,
nat-s., nat-sal., nit-ac., nux-m., Nux-v., ol-j., ox-ac., pancreat., petr.,
ph-ac., phase., phos., phyt., piloc., plb., podo., Psor., puls., querc.,
rad-br., ran-b., ran-s., rhod., Rhus-t., ruta, Sabin., sac-alb., sal-ac.,
samb., sang., sars., sec., Sep., sil., spig., Spong., squil., stann., Staph.,
stel., stram., stront-c., sul-ac., sul-i., Sulph., tab., tarax., tax.,
thlaspi, thuj., til-c., urea, urt-u., valer., verat., verat-v., verb.,
viol-o., viol-t., zinc.

common to all these rubrics are:
abrot., ars., aur., Bell., benz-ac., cact., Calc., calc-i., carb-v., Caust.,
Colch., cupr., ferr-p., hep., iod., kalm., Led., Lyc., nat-m., phos., puls.,
Spong.

This means that adonis, asparagus, convallaria, lachesis, lycps, strophanthus,
thyroidinum are NOT known for joint gout, but ARE known for heart gout.
Perhaps study of the heart symptoms of these remedies might be fruitful? Will
list some sx here, so list members can comment if desired:

vermuelen concordant : (Heart symptoms)

Adonis, - Pains: Precordial pain, palpitation and dyspnoea.
Observed: Mitral and aortic regurgitation. Chronic aortitis. Fatty heart
pericarditis. Rheumatic endocarditis [Kalm.]. Marked venous engorgement.
Cardiac asthma [Queb.]. Myocarditis, irregular cardiac action, constriction
with vertigo. Pulse rapid, irregular.
Asparagus, - Pains: [11] Rheumatic constrictive, in cardiac region,
forcing him to cry out; turns blue in face, when urinating, esp. when voiding
last drops, dropsy of chest.
Observed: Palpitation, with oppression of chest. Pulse intermittent,
weak; pain about left shoulder and heart, with bladder disturbances. [6] Heart
throbs strongly, and it extends over a large area. [7] Irregular heart's
action. Pulse slightly accelerated; feeble; [11] accelerated when sitting.
[11] Visible palpitation at night; throbbing of carotids. Heart beat twofold.
Palpitation: while sitting leaves of book in his hand tremble; with anxious
restlessness, worse motion or ascending; after eating.
Convallaria, - Sensations: As if heart beat throughout chest.
Pains: Discomfort in precordial region in afternoon.
Observed: Endocarditis, with extreme orthopnoea. Palpitation from least
exertion. Angina pectoris. Extremely rapid and irregular pulse. [5] Sounds
feeble, with anaemic murmur over jugular veins. Fluttering during exertion,
then redness of face and sensation as if heart stopped beating and started up
again suddenly, causing faint, sick feeling. Valvular disease of heart, with
scanty urine and dropsy. In several cases it relieved oedema, so that the
patient could lie down.
Lachesis, - Sensations: [11] Palpitation with pain as if heart was
hanging by a thread, and every beat would tear it off; after menses. Fulness
at heart, as if pressing against side or had not free play. As if heart turned
over and ceased beating for a moment, then commenced again with increased
force. Heart seems to stand still and then starts with a tremendous bound,
followed by rapid tremor. Anxiety about heart. As if heart were too large for
containing cavity. As if heart intermits a single beat, producing slight cough
which seems to re-establish circulation.
Pains: Cramplike, in precordial region. [11] Now and then a sudden stitch
in region of heart, which makes her weak.
Observed: Palpitation, with fainting spells, esp. during climacteric.
Palpitation from constricted feeling, with anxiety. Cyanosis; [2] neonatorum.
Irregular beats. [2] Carditis; metastatic. Senile arteriosclerosis. Pulse
weak, intermittent; slow; irregular. [5] Intolerance of pressure over heart [&
pain and numbness of left arm]. [7] Feels beating of heart, with great
weakness. [8] PALPITATION WORSE WARM ROOM; MORNING ON WAKING. [11] Heartbeat
accelerated by quick motion. Palpitation better sitting down or lying on right
side; with fainting and anxiety. Chronic palpitation of young girls. Tremulous
irritability of heart after scarlatina or fevers. Palpitation after sudden
excitement; with paleness of face. Visible palpitation of heart. Favours
resorption of exudate in pericarditis. Induration of veins and surrounding
cellular substance.
Lycopus, --- Sensations: [11] Of pressing outward in cardiac region.
Pains: In precordium; constriction, tenderness. [11] Rheumatoid aching in
precordial region and at apex, followed by pains in left wrist, inner side of
right calf, and in subclavicular region, and again in left wrist and region of
apex. Acute darting, with intermissions of pulse and heartbeat. Throbbing, in
heart. Sharp, shooting, c left scapula.
Observed: Pulse weak, irregular, intermittent, tremulous, rapid.
Cyanosis. Heart's action tumultuous and forcible. Palpitation from nervous
irritation, with oppression around heart. Heart disease with rheumatoid,
flying pains. [2] Action tumultuous, violent; excessively rapid, stormy; [7]
could be heard several feet from bed. Laboured heart at night. Palpitation and
cardiac distress worse when thinking of it. Pulse doesn't synchronise with
heart. [5] Feeble, irritable heart, with cold limbs and general nervousness.
Cardiac disease following rheumatic fever. [7] Beats of heart more distinct on
right side of sternum; [11] first sound replaced by blowing sound of mitral
regurgitation heard upwards in clavicular region, and particularly between
scapulae; second sound pointed, short, sharp. Cardiac pulsation scarcely
perceptible to touch. Cardiac depression, with intermittent pulse and
faintness; also on quickly ascending. On waking, laboured cardiac action, with
frequent intermissions. Pulse quickened at each inspiration; scarcely
perceptible; extremely variable; extremely compressible. [11] Heartbeat slow
and weak. Heart disease with pain and oedema of left arm, hand, leg and foot.
Aneurysm of large vessels near heart.
Strophanthus, --- Sensations: [3] Sense of lively action.
Pains: In heart. [2] Stitches and twitches at apex beat.
Observed: Pulse quickened. Heart's action weak, rapid, irregular, due to
muscular debility; and insufficiency. [2] Chronic, nervous palpitation and
arrest of breathing. Pulse; rapid alternating with slow. [9] Intense
palpitation from comparatively slight exertion.
Thyroidinum --- Sensations: [2] Jumping sensation at heart. [3] As if
blood were rushing downwards through body.
Pains: Severe, in heart. [2] Heart pain c axilla; clutching,
constricting, worse lying down; causes short breath.
Observed: Weak, frequent pulse, with inability to lie down. Tachycardia
[Naja.]. Palpitation from least exertion; [2] hammering; beats felt in ears.
Ready excitability of heart. Heart's action weak, with numbness of fingers.
[2] Valvular diseases of heart. [3] Hypertrophy after hard labour.
Is there a cardiologist on the List who can determine a common thread that
runs through the symptoms of the above remedies, or has an idea about symptoms
of heart gout?
===========================================================
RESOURCES on GOUT IN GENERAL:

Via the UCDavis website:

The Processes in the Body Leading to Hyperuricemia and Gout

Gout is an arthritic condition (inflammation of the joints) that mostly
affects men age 40 and older. It is nearly always associated with chronic
hyperuricemia, a long-lasting abnormally high concentration of uric acid
in the blood.

Metabolism of Purines. The process leading to hyperuricemia and gout
begins with the metabolism of purines, which are nitrogen-containing
compounds that are important for energy. Purines can be divided into
two types:

Endogenous. Endogenous purines are manufactured within
human cells.

Exogenous. Endogenous purines are obtained from foods.

All mammals except humans possess an enzyme called uricase that
breaks purines down into a very soluble product called allantoin. Without
uricase, purine ultimately breaks down into uric acid , which can build up
in body tissues if it is not adequately eliminated in urine.

Uric Acid and Hyperuricemia. Uric acid is produced in the liver and enters
the bloodstream. The path leading to high concentrations of uric acid
and gout is the following:

Most uric acid eventually passes through the kidneys and is
excreted in the urine. The rest is disposed of in the intestines,
where it is processed and broken down by bacteria.

Normally these processes keep the concentration of uric acid in
the blood plasma (the liquid part of the blood) at a healthy level,
which is below 6.8 milligrams per deciliter (6.8 mg/dL).

Under certain circumstances, however, the body produces too
much uric acid or excretes too little. [ See What Causes Gout?]
In either case, concentrations of uric acid increase in the blood.
This condition is known as hyperuricemia.

If concentrations of uric acid reach 7 mg/dL and above, the
blood becomes supersaturated and needlelike crystals of a salt
called monosodium urate (MSU) form.

In time, as MSU crystals accumulate, they cause inflammation
and pain, characteristic symptoms of gout.

Gout and Other Conditions Associated with Hyperuricemia

High levels of uric acid are associated not only with gout but also with a
number of other conditions. They can occur independently but may also
develop one after the other if gout is untreated.

Acute Gouty Arthritis. Acute gouty arthritis is the stage at which the first
symptoms of gout appear. It most often occurs in men.

Chronic Tophaceous Gout and Tophi. After several years, persistent
gout develops called chronic tophaceous gout. This long-term condition
often produces tophi, which are solid deposits of MSU crystals that form
in the joints, cartilage, bones, and elsewhere in the body. In some
cases, tophi break through the skin and appear as white or
yellowish-white, chalky nodules that have been described as looking like
crab eyes.

Without treatment, tophi develop on average about 10 years after the
onset of the disease, although their first appearance can range from
three to 42 years. They are more apt to appear early in the course of the
disease in older people. In the elderly population, women appear to be
at higher risk for tophi than men.

Today, drug therapy has reduced the prevalence of chronic tophaceous
gout to as little as 3% of patients. Certain groups, such as transplant
patients receiving cyclosporine, however, still face a high risk of
developing tophi.

Uric Acid Nephrolithiasis (Kidney Stones). Uric acid nephrolithiasis occurs
when kidney stones form from uric acid. In one study, however, patients
with these stones were more likely to have elevated levels of uric acid in
their blood than in their urine, suggesting that gout is responsible for
these stones. Uric acid and other kidney stones are present in 10% to
25% of patients with primary gout, a prevalence more than 1,000 times
that of the general population. In gout caused by other conditions
(called secondary gout), the reported incidence reaches 42%.

It should be noted that uric acid stones can also form in the absence of
gout or hyperuricemia. Also, not all of the kidney stones in patients with
gout are composed of uric acid; some are composed of calcium oxalate,
calcium phosphate, or those substances combined with uric acid. [ See
Well-Connected Report Kidney Stones.]

Chronic Uric Acid Interstitial Nephropathy. Chronic uric acid interstitial
nephropathy occurs when crystals slowly form in the structures and tubes
that carry fluid from the kidney. It is reversible and not likely to injure
the
kidneys.

Kidney Failure. Sudden overproduction of uric acid can occasionally
block the kidneys and cause them to fail. This occurrence is very
uncommon but can occur with the following conditions:

After chemotherapy for leukemia or lymphoma.

After severe heat stress from vigorous exercise.

Following epileptic seizures.

After corticosteroid therapy for severe allergic reactions.
______________________________________________
http://www.emedicine.com/oph/topic506.htm

story: With joint involvement, patients experience pain in the distal
extremities. With kidney stones, patients experience acute flank pain.

Physical: The classic attack of acute primary gouty arthritis occurs in a
portly middle-aged man and produces fairly sudden inflammation of a
single joint, most commonly the metatarsal-phalangeal joint of the great
toe, resulting in intense pain, tenderness, and swelling.

The folklore surrounding gout also has involved the eye, and, prior to the
20th century, a myriad of common and unusual ocular symptoms
falsely were ascribed to the gout. All manifestations of gout in the eye are
secondary to deposition of urate crystals within ocular tissue.

Conjunctival nodules containing needlelike crystals have been
described within the interpalpebral areas, sometimes associated with a
mild marginal keratitis.

Band keratopathy with refractile, yellow crystals in the deep corneal
epithelial cells and at the level of Bowman membrane are not
uncommon.

Symptoms of visual blurring from the corneal haze or foreign body
sensation due to epithelial breakdown can be treated with scraping
of the epithelium and removal of the crystals.

Gout rarely can be associated with anterior uveitis and has been
mentioned by Duke-Elder as a cause of hemorrhagic iritis.

Scleritis and tenonitis also have been described.

In addition to the cornea, urate crystals have been described
clinically in the lens and sclera and on postmortem examination in the
tarsal cartilage and in the tendons of extraocular muscles.

Causes: Attacks are caused by the deposition of monosodium urate monohydrate
within the joint space. Precipitating factors can include
emotional stress, dehydration, surgery, and thiazide diuretics. Attacks tend
to be recurrent and usually are self-limited. Recurrent attacks of
acute gouty arthritis can result in chronic arthritis with limitation of
joint mobility.

Uric acid levels may be elevated as a result of primary gout. It is an
autosomal dominant error of metabolism. It can occur secondarily from
increased production of uric acid or decreased excretion of uric acid. The
latter is seen in chronic renal disease. Excessive uric acid production
primarily occurs in patients on chemotherapy for malignancies, especially
those of the hematopoietic or lymphatic systems. This can be
expected because uric acid is the metabolic end product of purines, which
are present in high concentration in cell nuclei. Other causes of
secondary gout include chronic lead poisoning; polycystic kidney disease,
systemic cyclosporine therapy; sarcoidosis; psoriasis; and
hyperparathyroidism.
Also:http://www.ucdmc.ucdavis.edu/health/a-z ... erity.html

HOW SERIOUS IS GOUT?

Gout rarely poses a long-term health threat if properly treated. It does,
however, remain a source of short-term pain and incapacity for
thousands of Americans.

Pain and Disability

Left untreated, gout can develop into a painful and disabling chronic
disorder. Persistent gout can destroy cartilage and bone, causing
irreversible joint deformities and loss of motion. Tophi can grow to the
size of handballs and can destroy bone and cartilage in the joints, similar
to the process in rheumatoid arthritis. If they lodge in the spine, tophi
can cause serious damage including compression, although this is very
rare. In extreme cases, joint destruction results in complete disability.

Kidney Conditions

Kidney Stones. Kidney stones occur in between 10% and 40% of gout
patients, and can occur at any time after the development of
hyperuricemia. Although the stones are usually composed of uric acid,
they may also be mixed with other materials.

Kidney Disease. About 25% of patients with chronic hyperuricemia
develop progressive kidney disease, which sometimes ends in kidney
failure. It should be noted, however, that many experts believe that
chronic hyperuricemia is unlikely to be a common cause of kidney
disease. In most cases, the kidney disease comes first and causes high
concentrations of uric acid.

Gout and Heart Disease

Gout often accompanies heart problems, including high blood pressure,
coronary artery disease, and congestive heart failure. Hyperuricemia, in
fact, has been associated with a higher risk of death from these
conditions. One 2001 study reported that disease activity in gout may
contribute to unhealthy cholesterol and lipid levels. Some interesting
evidence, however, suggests that hyperuricemia may occur as a
response to inflammatory damage that occur with heart disease and may
even be protective.
Other Medical Conditions Associated with Gout

The following are some conditions that are associated with long-term
gout:

Cataracts.

Dry eye syndrome.

Complications in the lungs (in rare cases, uric acid crystals occur
in the lungs).
Sites discussing relation of gout to heart disease (but not that great or to
the point about actual symptoms:

http://healingwelluro.subportal.com/hea ... 04772.html

http://www.jr2.ox.ac.uk/bandolier/booth ... chear.html

[Robyn]

Hi
This exerpt is from Hale - Diseases of the Heart, p. 45-46 (B.Jain
Publishers)
"The gouty diathesis gives a liability to functional derangement of the
heart's action. Attacks of palpitation occur in such persons before the
joints are affected, and cease when tumefaction is present. The presence of
an undue quantity of lithic acid in the blood is supposed to be a cause -
acting as an irritant to the nerves which control cardiac action."

also
Diaphragmatic Gout ( from a 100 year old dictionary) refers to angina
pectoris

Regards

Robyn

sensations