Tuesday, April 2, 2013


Formed in the middle trimester of pregnancy  under influence  of harmful factors                                                                                                                             
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

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
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.

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)

              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.

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.


              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.


              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 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.



                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
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 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.

*    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.

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
             Calcium channel blockers

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
                                   See full size image
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.