u Cardiomegaly at birth, its
rapid progress
u Early formation of cardiac hump
u Progressive
left-heart
cardiac insufficiency, refraction to the therapy
u
Physical and psychomotor
retardation
u
ECG: high R waves, shortening of QRS complex, proof tachycardia with a tendency to increase
u
EchoCS: hypertrophy of the left ventricle with further its
expansion and increase of the
left auricle, areas of akinesia in the left ventricle, declines of FО of the
left ventricle
u
Prognosis is unfavorable
Form of heart at early congenital carditis
Form of heart at early congenital carditis
Fibroelastosis as a result of
early congenital carditis
LATE
CONGENITAL CARDITIS
u
Formed in the 3-rd trimester of pregnancy under the action
of harmful factors
u Often prematurity, perinatal
progressive hypotrophy
u Proof arrhythmias from birth
u Mild
cardiomegaly
u
Possible right and left heart insufficiency
u
ECG: the voltage of waves is dicreased, different arrhythmias and
conduction impairments which are
interrupted by medicines
u
EchoCG – moderate dilatation of the left ventricle, hypokinesia
of its walls, without the morphological
changes
Form of heart at late congenital carditis
ACUTE CARDITIS
u
beginning is
related directly to the action of etiologic factor, to the viral
infection, after introduction
of vaccine, medicines, allergic reactions,
intensifying of chronic infection
Clinics:
u
Pale skin, weakness, decline
of appetite, shortness of breath, for elder children cardialgia, heartbeating
u
Enlarged heart
u
Weakness of apex beat
u
Weakness of heart tones,
arrhythmias, soft systolic
murmur
on the apex
u
Decreased arterial pressure
u Signs
of left heart insufficiency
u
ECG: decrease of waves voltage, conduction
impairments, arrhythmias
u
EchoCS: myocardium is diffuse or local thick, dilatation of pericardium, possible presence of liquid in
pericardium
u
Acute phase indexes, usually,
within the limits of norm
u
Increased
levels of LDG1, LDG2, creatininphosphokinase
u
Dependency
upon predominance of cardialgia, arrhythmia or sings of cardiac insufficiency,
clinical variants are marked out, more frequently
there are their combinations
SUBACUTE CARDITIS
Occurs through 3 - 4 mths after acute carditis or is diagnosed occasionally.
Clinics
u
unpleasant feelings, interruptions of the heart , palpitation
u
periodic
cardialgias
u moderate cardiomegaly, mainly
due to the left ventricle
u
weakness of heart tones
u
arrhythmias, functional systolic murmur
u moderate
signs of cardiac insufficiency
v
ECG: arrhythmias, conduction impairments, signs of hypoxia of myocardium
v EchoCS: signs of CF, hypokinesia of the left ventricle
CHRONIC CARDITIS
u More
frequently is diagnosed as
primary-chronic with the sings of
chronic left heart failure
u Possibly
occurs after acute or subacute carditis lasting
more than 12 – 18 months
u Increasing cardiac insufficiency on a
background of cardiomegaly of
different degree
u Tachy-, bradycardia, weakeness of cardiac tones
u Physical retardation
u Cardiac hump
uEncephalopathy, anaemia, immunological deficite
u ECG: arrhythmias, violations of rhythm, dysmetabolic and hypoxic changes
in myocardium, hypertrophy of
the left ventricle
uEchoCS: dilatation of the left ventricle cavity, decreased retractive function of myocardium (dilatation form);
rarely the hypertrophic
variant of carditis develops due to the
hypertrophy of the left
ventricle walls
and decreasing of rejection fraction
TREATMENT OF CARDITIS
u
REGIME: duration
of the bed regime is determined according to the
degree of cardiomegaly and cardiac
insufficiency, on the average 2 –
6 weeks with gradual expansion
u DIET: Table № 10, uses of
salt and
liquid according to the degree of cardiac insufficiency:excluding
of
extractive and piquant products, replacing them on products
with potassium and vitamines
PATOGENETIC THERAPY
At acute carditis: glucocorticoids (prednisolon 0,5 - 1,5 mg/kg)
2 - 4 weeks at a middle
and severe
forms with gradual
decreasing of dose, nonsteroid
anti-inflammatory drugs (Aspirin 100 mg/kg,
Ibuprophen 10-15 mg/kg, Voltaren 2 - 3 mg/kg,
Indometacin 2,5 - 3 mg/kg,
Misulid 5-10 mg/kg, Mephenamin acid of 50 mg/kg,
Amizon 50 mg/kg) -
4 weeks with gradual
decreasing of dose during 2-3 weeks
At subacute and chronic: chinoline derivatives
(Delagil 5 mg/kg, Planquenil 8 mg/kg) 4-6 mths, then decrease to 1/2 dose and give
by years
Nonsteroid
anti-inflammatory drugs (scheme like for acute)
Antibiotic therapy is used only at bacterial carditis with high activity
SYMPTOMATIC THERAPY
u
Cardiotropic medicines which improve the function of myocardium: (ATP, Phosphaden, Potassium
orotatis, Panangin, Asparcam, Riboxin, Mildronat, Cardonat, Carniton) 1 -1,5 month
u
Cardiac glycosides (Strophanthin of 0,012
mg/kg, Digoxin in the supporting dose of 0,01 - 0,02 mg/kg)
at cardiac insufficiency
u
Diuretics ( Lasix 1- 3 mg/kg,
Veroshpiron 1-3 mg/kg,
Hypothiazid 2-5 mg/kg)
u Peripheral vasodilatators (Phentolaminum 2 mg/kg,
Captopryl 0,5-1 mg/kg,
anticoagulants (Heparin of 100 U/kg), antiaggregants ( Curantil 2,5 - 3 mg/kg),
antiarhythmical (Anaprillin, Obzidan - 1,0 - 2,0 mg/kg)
Prophylaxis
A primary
prophylaxis foresees prevention of infecting of feotus during pregnancy, hardiness of child, treatment of acute and chronic
infections, clinical observation of the children of the group of risk on cardio-vascular diseases.
The secondary
prophylaxis is directed on prevention of complications and relapse of process,
arrived at the clear observance of principles of clinical supervision of
patients.
The prognosis of nonrheumatic carditis depends on
its variant
u
Early congenital carditises are, as a rule, severe and quite often result in a fatal outcome in
the first years and even months of life.
u
At a late congenital carditis at
adequate and in good time appointed therapy a process can be
chronic without progress of cardiac changes; possibly and convalescence.
Kawasaki disease
Kawasaki disease
usually, but not always, affects children aged five years and under. It may
damage the heart muscle or coronary arteries. It is named after the Japanese
paediatrician who identified the disease. The cause is unknown but the disease
is probably caused by an abnormal reaction to a common germ. Kawasaki disease is not contagious, although
it can occur in clusters.
Symptoms
The main symptom of Kawasaki disease is
persistent fever (over 38.5°C) for five days or longer. There is usually no
obvious explanation for the fever and it generally does not respond to
paracetamol. Other symptoms, usually caused by inflammation of small blood
vessels known as vasculitis, may include:
Ø
A rash, sometimes in the groin region
Ø
Red, swollen and cracked lips
Ø
Red eyes
Ø
Bright red, swollen tongue
Ø
Swollen hands and feet
Ø
Red rash on palms of hands and soles of feet
Ø
Swollen lymph nodes.
From an 8 year old child with Kawasaki
disease, this aneurysmally dilated epicardial coronary artery is occluded by
thrombus.
Diagnosis
There is no test to diagnose Kawasaki disease.
Diagnosis is made by excluding other possible causes of symptoms. Diagnosis may
require blood tests and an echocardiogram to examine the heart for any changes
in the coronary arteries.
Most children who have Kawasaki disease and
receive proper treatment will make a full recovery. A few children will develop
heart problems, including damage to the coronary arteries. If no treatment is
given, about 25 per cent of patients experience inflammation of the coronary
arteries, which supply blood to the heart muscle. This can cause irregularities
with these blood vessels which may disturb the flow of blood.
Treatment
The treatment for Kawasaki disease is
intravenous gammaglobulin (immunoglobulin), made from donated blood
transfusions. Large doses of intravenous gammaglobulin will usually stop the
fever and other symptoms of Kawasaki
disease. Treatment should be administered within 10 days of the onset of fever
to minimise heart problems.
Children may also be prescribed
aspirin for some weeks following the onset of Kawasaki disease, to prevent problems with
coronary arteries. However, aspirin should only be given to children on the
advice of a doctor, paediatrician or cardiologist. Aspirin is not usually
recommended for children because of the risk of Reye’s syndrome, a rare but
potentially fatal disease.
Cardiomyopathy
Cardiomyopathy is a chronic and progressive disease in which the heart
muscle is abnormally enlarged, thickened and stiffened. The condition typically
begins in the walls of the heart's lower chambers and in more severe cases also
affects the walls of the upper chambers. The actual muscle cells as well as the
surrounding tissues of the heart become damaged. Eventually, the weakened heart
loses the ability to pump blood effectively and heart failure or irregular
heartbeats may occur.
Cardiomyopathy is
nondiscriminatory in that it can affect any adult or child at any stage of
their life. It is not gender, geographic, race or age specific. It is a rare
disease when diagnosed in infants and young children. Cardiomyopathy continues
to be the leading reason for heart transplants in children.
First term "cardiomyopathy" was offered by W.Bridgen in 1957. In obedience to his determination cardiomyopathy is a group of myocardium illnesses of
unknown etiology and uncoronarogenic origin. During prolonged time this conception was changed repeatedly, generating a mess in
terminology. In a consequence, due to introduction of modern methods of
diagnostics, both invasive and uninvasive,
it was succeeded to derive many cardiomyopathies, and World
Organization of Health offers many classifications,
last from which was presented in 1995.
“Cardiomyopathy” is
a term that refers to the inability of the heart muscle to contract
appropriately to meet the demands of the body. There are several types of
cardiomyopathies defined by the World Health Organization on the basis of their
pathologic or pathophysiologic features:
“Dilated cardiomyopathy” or DCM,
“Hypertrophic cardiomyopathy” or HCM,
“Restrictive cardiomyopathy” or RCM,
“Ischemic cardiomyopathy” or ICM (cardiomyopathies
are due to or associated with specific systemic diseases).
One particular type
of cardiomyopathy which primarily affects the right ventricle is called
Arrhythmogenic Right Ventricular Dysplasia / Cardiomyopathy or ARVD / C.
The morphologic features of the cardiomyopathies are shows in this
illustration. For comparison the normal architecture of the left ventrilce is
shown in the top right illustration. In
DCM the left ventricle shows increase in size and volume. In HCM the ventricular walls are thick and
the ventricular chamber is consequently reduced in volume. In RCM the ventricular wall may or may not
be thicker. The restriction to the wall movement may be due to disease(s) that
affect the endocardium of the heart or that actually infiltrate the myocardium.
Actuality
With
the pediatric population, cardiomyopathy occurs in approximately 12 children
out of every million with about 1,000-5,000 new cases diagnosed each year
worldwide. The majority of diagnosed children are infants under the age of 12
months with fewer cases between the ages of 1 to 12 years. When cardiomyopathy
is diagnosed in children before puberty, it is considered extremely unusual and
it may not have the same causes, manifestations or disease progression as
cardiomyopathy in adults.
CLINICS OF CMP
Symptoms:
u Many patients with cardiomyopathy may experience arrhythmia (abnormal
heart beats) which can be life threatening. Other symptoms may include
palpitations, fatigue, difficulty breathing (especially during exercise), poor
appetite, shaking, sweating, chest pain, syncope, upset stomach, failure to
grow and others.
Cardiovascular Tests
u
Electrocardiogram
u
Echocardiogram
u
24-hour Holter monitor
u
Memory event recorders (for
certain symptoms)
u
Some patients may need
genetic testing, cardiac catheterization, MRI, heart biopsy and EP testing
u
Blood and urine testing is performed in all
patients
Step-by-step
diagnostic approach
Initial diagnosis of
cardiomyopathy rests on historical factors and physical exam findings.
Laboratory findings vary depending on specific aetiology. ECG, chest
radiography, echocardiogram, cardiac MRI, cardiac catheterisation and
endomyocardial biopsy are the diagnostic tests of choice. These tests are often
non-specific, pointing only to the pathophysiological consequences of
cardiomyopathy rather than its specific aetiology. Ultimately the aetiological
diagnosis of these conditions requires a combination of all these modalities,
as no one available test is specific enough to lead to an individual cause.
History
History is a critical
component in diagnosis of cardiomyopathies. Emphasis should be placed on risk
factors for specific causes. Medical illnesses, family history, and alcohol and
drug exposure may predispose to the development of primary and secondary
cardiomyopathies.
History
of present illness
The most common symptoms
associated with cardiomyopathy are often non-specific, such as fatigue and
weight loss. Evaluation for symptoms of congestive heart failure (CHF) such as
orthopnoea, paroxysmal nocturnal dyspnoea and oedema is important.
Medical history
History of coronary artery
disease (CAD) and subsequent cardiac ischaemia should be excluded, since
specific therapy targeted at lesion revascularisation may improve symptoms.
History of any of causes of
secondary cardiomyopathies including infiltrative, storage, toxicity,
endomyocardial, inflammatory, endocrine, cardiofacial and
neuromuscular/neurologic causes, nutritional deficiencies, autoimmune or
collagen diseases, electrolyte imbalance and cancer therapy as listed in
American Heart Association (AHA) scientific statement should be addressed.
Family history
Family history of
premature cardiac death or arrhythmia may indicate risk of primary
cardiomyopathy. Specific questions may elucidate hereditary causes of secondary
cardiomyopathy including infiltrative diseases (familial autosomal dominant
amyloidosis, Gaucher's, Hunter, Hurler's), storage diseases (Fabry, glycogen
storage, Niemann-Pick), diabetes mellitus, Noonan's syndrome, lentiginosis,
Friedreich ataxia, Duchenne/Becker muscular dystrophy, Emery-Dreifuss muscular
dystrophy, myotonic dystrophy, neurofibromatosis and tuberous sclerosis as
listed in AHA aetiological classification.
Physical examination
No specific physical examination findings are consistent
with a particular cause but examination is directed towards looking for signs
of cardiac failure. A sustained prominent apical beat on palpation is
consistent with LVH. A diffusely palpable cardiac beat with apical displacement
may be seen with ventricular dilatation. Auscultation of the heart may reveal
murmurs, an S4 gallop (heard in types of cardiomyopathy that involve increased
left ventricular pressure) or an S3 gallop (heard when there is increased left
ventricular volume).
Auscultation of the lungs typically demonstrates
crackles, indicating pulmonary congestion. Pedal and leg oedema and jugular
venous distension may also be present.
Initial tests
An ECG, although
commonly non-specific, may show specific abnormalities that point to an
individual aetiology. A normal ECG has approximately a 98% negative predictive
value when systolic dysfunction is suspected. Immediate laboratory tests should
include a FBC, a comprehensive metabolic profile and B-type natriuretic
peptide. Patients with chest pain require cardiac markers including troponins
and CK-MB. In addition a CXR (lateral and PA) is recommended.
Echocardiogram and
further investigation.
24-hour Holter monitor
Echo СG
Paroxismal
tachycardia
Echocardiography cannot
usually diagnose specific causes of cardiomyopathy alone. However, in
combination with history, physical examination and laboratory findings, it is
an extremely useful and noninvasive diagnostic tool. An echocardiogram helps to
distinguish the cardiomyopathies with respect to pathophysiology. It can
differentiate between hypertrophic, restrictive or dilated in most cases. It
may suggest a diagnosis of arrhythmogenic right ventricular dysplasia or
athlete's heart.
Newer available modalities
include cardiac MRI and cardiac CT. Cardiac MRI is a useful method for
uncovering the aetiology of cardiomyopathy because it provides excellent
contrast and spatial resolution of the heart. It is also noninvasive, readily
available and not operator dependent. It has the ability to assess ventricular
end-diastolic volumes, presence of intracardiac thrombi, stroke volume,
ejection fraction and valvular pathology.
Cardiac catheterisation may
be performed if echocardiography results are ambiguous. Ventricular and atrial
pressures are measured, which allow for the calculation of pressure gradients
across cardiac valves and the left ventricular outflow tract. Catheterisation
of the heart allows for ventriculography to be performed. Ejection fraction,
ventricular size and wall motion, and left ventricular outflow tract size can
be estimated, and the presence of valvular regurgitation can be evaluated.
Additionally, coronary angiography can be performed to evaluate for coronary
arterial disease as a cause of ischaemia.
Endomyocardial
biopsy
When a small piece of heart muscle tissue is
needed for examination, a heart biopsy can be performed. A catheter is
carefully threaded into an artery or vein to gain access into the heart. A
bioptome (catheter with jaws in its tip) is then introduced. Once the bioptome
is in place, three to five small pieces of tissue from the heart muscle are
removed. The test is performed routinely after heart transplantation to detect
potential rejection. It may also be performed when cardiomyopathy, myocarditis,
cardiac amyloidosis, or other disorders are suspected.
Electron
micrographs of cardiac biopsy specimens. A. Normal heart. B. Vacuole
formation. C. Myofibrillar dropout. D. Necrosis (magnification 5, ×100).
In very rare circumstances, an endomyocardial
biopsy is needed to help differentiate disease processes and guide therapy. It
is useful in the diagnosis of the following causes of cardiomyopathy:
§
Inflammatory/immune cardiomyopathy: Lymphocytic
myocarditis, rheumatic carditis, sarcoidosis, giant cell myocarditis, cardiac
allograft rejection, Chagas cardiomyopathy, hypersensitivity myocarditis.
§
Infectious cardiomyopathy: Toxoplasmosis, Lyme
carditis, cytomegalovirus (CMV).
§
Infiltrative cardiomyopathy: glycogen storage,
haemochromatosis, right ventricular lipomatosis, amyloidosis.
§
Cardiac tumours: cardiac or non-cardiac origin.
§
Miscellaneous specific cardiomyopathies: Anthracycline
cardiotoxicity, endocardial fibrosis, endocardial fibroelastosis, Fabry
disease, carcinoid disease, irradiation injury, Kearns-Sayre syndrome,
Henoch-Schonlein purpura, chloroquine cardiomyopathy, carnitine deficiency,
hypereosinophilic syndrome
§
Non-specific abnormalities.
Dilated
cardiomyopathy
The most common form is dilated
cardiomyopathy. In most cases the cause of dilated CM remains unknown. It may
be caused by viruses, metabolic diseases, infectious
diseases, AIDS, obesity, nutritional deficiency, alcohol, radiation,
chemotherapy, adverse drug reactions, carnitine-deficiency, severe anemia or it
may be genetic (familial type). Unknown reason is idiopathic form.
PEDIGREE of
family form of CMP
1 - death is in intrauterine period, 2 -
death to 1 year, 3 - death in 29
years, 4 - proband, 6 years, presence
of clinical displays
Symptoms of dilatation
cardiomyopathy
u Catching
one's breath
u Apathy,
rapid fatigueability
u Edema of lower extremities
u Rapid set of weight
u Fainting fits, dizziness
u
Strong palpitation, pulsation
u
Stethalgia and
high pressure
a, Heart from an
individual with dilated cardiomyopathy. Note the dilated left ventricle and
thin ventricular walls. In life this ventricle pumped poorly. b, Illustration of dilated cardiomyopathy (left), showing a
dilated left atrium and left ventricle, bulging interventricular septum from
left to right, and thin ventricular walls. For comparison, a normal heart is
shown on the right. IVC, inferior vena cava; IVS, interventricular septum; LA,
left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; SVC,
superior vena cava.
Prognosis
Mortality for DCM is highest in the first year after
diagnosis with a reported survival at 1 and 5 years after first presentation of
79% and 61% respectively. Early deaths are principally caused by severe heart
failure. Some late deaths are sudden, presumably due to arrhythmia, in children
who fail to recover to normal ventricular function. While it is accepted that
the risk of mortality is high there is less agreement as to predictors of poor
outcome. Failure of improvement or deterioration in shortening fraction,
ventricular arrhythmias, detection of mural thrombus, presentation at age
>2years, endocardial fibroelastosis and left ventricular and diastolic
pressure > 20mmHg have all been put forward as adverse prognostic factors.
HYPERTROPHIC CARDIOMYOPATHY
It is the form of
cardiomyopathy characterized by progressive cardiac dilation and
contractile/systolic dysfunction, usually with concomitant hypertrophy. It is the second most common type of
cardiomyopathy.
In this condition
the heart walls (mainly the middle wall) become excessively thickened.
Blood flow through
the heart is restricted. Most cases of this type of cardiomyopathy are genetic
in nature.
RESTRICTIVE
CARDIOMYOPATHY
u
Restrictive
cardiomyopathy is a disease of the heart muscle that causes the walls of your
heart to get stiff. This restricts (holds back) some of the blood and oxygen that
is pumped out of your heart to your body.
u With restrictive cardiomyopathy, the muscle
wall of the left ventricle in your heart gets stiff and is not very flexible.
It is difficult for blood to get inside the ventricle because the muscle is so
stiff. This means less blood gets pumped out to your body.
Signs and Symptoms:
n
Abnormal or distant heart sounds
n
Cough
n
Crackles heard when caregivers listen to your chest
n
Fatigue (tiredness)
n
Nausea, bloating, and poor appetite because fluid
collects around the stomach, liver, and intestines
n
Shortness of breath, especially:
ü
With activity
ü
At night
ü
When lying flat
n
Swollen legs and feet caused by retaining fluid
n
Veins in your neck are distended (stick out)
n Weakness
Arrhythmogenic
Right Ventricular Dysplasia
This is a very rare cardiomyopathy that usually manifests later in
adults. It is a progressive condition where the heart muscle is replaced with
fatty tissue. Patients may present with palpitations, syncope and ventricular
tachycardia. Most cases are genetic in nature.
Treatment of
cardiomyopathy
A physician may recommend
that the patient first make lifestyle changes, including:
•
Rest adequately
•
Control weight
•
Exercise moderately
•
Limit sodium in the diet
•
Many patients will require
treatment with multiple heart medications. Some patients may require
implantation of a pacemaker and/or defibrillator. Cardiomyopathy is one of the
two leading reasons for heart transplantation in children.
•
The goal of treatment is to control or
prevent heart failure and complications such as blood clots, arrhythmias and
sudden death.
•
Growth failure is present in over one-third
of patients. A diet rich in fruits, vegetables, whole grains, and fish with
omega-3 fatty acids (tuna, salmon, trout) is
beneficial in most patients. Nutritional supplements to consider include
co-enzyme Q10, L-carnitine, and taurine (an amino acid).
•
Restrictions: Most of the patients are
restricted from any strenuous exercise and competitive sports.
Medications to control the
symptoms of heart failure that can accompany dilated cardiomyopathy:
•
Angiotensin converting enzyme (ACE) inhibitors
•
Anticoagulants
•
Beta-blockers
•
Calcium channel blockers
•
Digitalis
•
Diuretics
•
Nitrates
•
Vasodilators
Patients with
severe congestive heart failure that is associated with dilated cardiomyopathy
may require a heart transplant.
Treatment of HCMP
Treatment is indicated only at
presence of clinic or risk factors of the
sudden death.
u General measures are limitation of the high physical loadings and sport. The everyday loadings are not limited.
u Antibiotics
are used for the
prophylaxis of infection endocarditis.
u Basis of therapy of HCMP is the preparations with a negative ionotropic action. There are
β-adrenoblockers
or calcium antagonists of Verapamilum group. Preparations are appointed in maximally doses for all the life.
u Antiunrhythmical preparations are
indicated at severe
disorders of rhythm. The best
are Cordaron or Dizopiramid.
u At development in patients the dilatation of cavities and systole
disfunction treatment of cardiac insufficiency on general principles is conducted. There are used the inhibitors of ACE
(angiotensin converting enzyme), antagonists of receptors of angiotensin, diuretics, cardiac glycozides, β-adrenoblockers, spirolacton.
Implantation of
cardioverter-defibrillator at HCMP
Surgical treatment of HCMP
Surgical treatment of HCMP
is indicated at: Absence of clinical effect
from active medicinal therapy
for the patients with CMP hypertrophy. A
classic operation is intraortal septal
myoectonomy by A.Morrow.
By an alternative there is the successive
double-chamber electro-cardio-stimulation (ECS)
with the shortened atrioventricular delay. This method of ECS
changes the order of excitation and reduction of ventricles: in the beginning
excitation of an apex, then intraventricular
septum.
The gradient of obstruction goes down due to the decline of regional
contractility of intraventricular septum.
Cellular
cardioplastic by the bone marrow cells
A
method of directed neoangiogenesis is
a cellular transplantation, most suitable for patients with cardiomyopathy.
n An angiogenesis is a process at which new vessels are formed from the
elements of already existing and until now this way was considered the unique mechanism
of vessels formation in
postnatal period.
n Vesical genesis is the formation of primary vessels from
cells-predecessors during embryonic development.
Recommendations of American cardiologists
Ten easy steps in the treatment of
cardiomyopathy (heart failure)
u Step 1: MSM and chromium, more energy
and improved oxygen transport MSM and chromium can be used to supply the body
with more energy. MSM improves the oxygen transport in the body, not an
unnecessary luxury for patients suffering from heart failure. Chromium improves
the metabolising of carbohydrates which increases the amount of bio-energy
(ATP)
u
Step 2: Q-10, L-Carnitine
and Taurine, the basis of the cardiomyopathy protocol.After introducing MSM and
chromium (4 to 6 weeks) the basic protocol can begin: CoQ10, L-carnitine and
taurine Q-10 is one of the three basic supplements from the protocol.Q-10 plays
an important part in the mitochondria (power plants) of the heart cells. Q-10
improves the generation of energy in the heart so the heart can function better
and the EJF is elevated.
L-Carnitine improves the burning of fatty
acids (fat) Heart cells depend for their energy supply mostly on the burning of
fat. Disruption of the process of fat burning can cause cardiomyopathy. The
underlying cause of this disruption could be hereditary (genetic) so the body
is not able to produce sufficient carnitine. Other Scientific Studies support
the use of L-carnitine in the treatment of cardiomyopathy. Q-10 and L-Carnitine
act synergicly (they augment each other). Thus it is sensible to use both
supplements simultaneously.
Taurine also belongs to the group of three
basic supplements for the treatment of cardiomyopathy (heart failure). Other
Scientific Studies support the use of Taurine in the treatment of
cardiomyopathy.
u Step 3: Alpha Lipoic Acid and Vitamins C and E, prevention of
arteriosclerosis. After another 4 to 6 weeks the third phase of the protocol
can be introduced: Alpha lipoic acid, vitamin E and vitamin C. This phase has
special significance for patients that suspect their cardiomyopathy was caused
by a heart infarct. Alpha lipoic acid and vitamins E and C supply the body with
sufficient water- and fat-soluble antioxydants. This provides an increased protection
against the progression of cardiovascular disease.
u
Step 4: Magnesium and
Potassium, treatment cardiac arrhythmia and high blood pressure
If cardiac arrhythmia persists after
the introduction of the third phase magnesium can be employed to try and
alleviate the arrhythmia. Magnesium also plays an important part in the
treatment of cardiomyopathy, lowering blood pressure and prevention of other
cardiovascular disease. Supplementation of Potassium can alleviate cardiac
arrhythmia. Bananas and fruit juice are sources of potassium. Try eating 4 to 5
bananas a day and see if this brings about an improvement. Potassium
supplementation is also a possibility. The smallest effective dose is the best
dose. Have your bloodserum values checked on a regular basis when using a
potassium supplement. Give this information to your doctor.
u
Step 5: More exercise
If you start feeling better after circa
six months consult your cardiologist whether he approves more exercise. It is
often sufficient to take a walk for half an hour every day (seven days a week).
Take care not to get out of breath during your walking.”Walk and talk”.
u
Step 6: Nutrition
Sunflower oil Alert In the late nineteen
fifties the promotion began: saturated fats are bad. Eat more essential fatty
acids. Eat less carbohydrates. Eat more fiber. Eat food with a low glycemic
index.
u
Step 7: Selenium. A
deficiency of selenium can cause cardiomyopathy. Unfortunately the cardiologist
does not measure the level of selenium in the blood. That is why this cause is
overlooked
u Step 8: DHEA. Blood screening of cardiomyopathy patients
indicates that these patients generally have lower DHEA levels. The level of
DHEA in the blood is in direct proportion to the severity of the cardiomyopathy.
DHEA is probably able to protect the heart against changing shape. DHEA is a
hormone.
u
Step 9: Growth hormone
releasers. Research indicates that patients diagnosed with cardiomyopathy
without a known cause often have blood levels of growth hormone that are too
low.
u Step
10: Maintenance protocol.
