Myocardial diseases are due to a specific heart muscle disorder or a known infiltrative metabolic or toxic or neuromuscular disorder. But may be caused by;
• An acute or chronic inflammatory disease (Myocarditis)
• Idiopathic myocardial disease ( Cardiomyopathy)
Cardiomyopathy is a series of disorders causing primary heart muscle dysfunction that is often leading to heart failure or sudden death. There are three main types of cardiomyopathy;
• Dilated Cardiomyopathy
• Hypertropic Cardiomyopathy
• Restrictive Cardiomyopathy
Roles of gene in cardiomyopathy
There are some genes which synthesis some certain proteins which form structure and do some certain function of heart muscle. But some defects of genes caused for the dysfunctions of the heart scientist. The following Table 1.1 gene proteins have been linked to Cardiomyopathy.
Gene proteins Function Defects
Actin Basic structure of muscle function. Hypertropic Cardiomyopathy
Desmin Intermediate filament between cardiac and skeletal muscle. Inherited Cardiomyopathy
Dystrophin Regenerating muscle fibers. Cardiomyopathy, Muscular dystrophy & other disorders
Tafazzin Musculoskeletal function Inherited Cardiomyopathy
β-myosin Family of creating myosin, involve in contraction & relaxation. Inherited Cardiomyopathy
Table 1.1 – Link between gene protein & cardiomyopathy
Other causes for primary dysfunction of cardiomyopathies are results from hypertension, valvular disease, congenital heart disease, obvious myocardities, systemic metabolic disturbances, nutritional disorders (e.g., wet beriberi),and hypersensitivity diseases (e.g., acute rheumatic fever). Deficiency of frataxin, which is an essential mitochondrial protein, leads to progressive neurodegeneration and cardiomyopathy. Progressive heart failure is due to diastolic resection and / or valvular dysfunction is caused by eosinophilic endomyocardial disease2. CoQ10 (Coenzyme Q (ubiquinone) 10) depletion during statin therapy which is used to treatment of hypercholesterolemia might be associated with subclinical cardiomyopathy and this situation can be reversed by treating CoQ103. Ion channels, such as those encoded by the potassium channel genes KCNQ and HERG which are contribute to normal heart function in humans and when they are malfunctioning, cardiomyopathies or arrhythmias is caused in humens12.

Clinical features of Cardiomyopathies
Some people who develop cardiomyopathy which may have no signs and symptoms in the early stages of the disease. But with the advancing the disease, signs and symptoms usually appear. These signs and symptoms which are most commonly associated with the syndrome called as congestive heart failure. They may include: 18

• Shortness of breathing
• dyspnoea
• Cardiac arrhythmias
• Dizziness & fainting
• Syncope due to the cardiac arrhythmias.
• Ejection fraction is les than 25 %( normal- 50%-65%) due to the ineffective ventricular contraction.
• Swelling in the lower limbs
• Chest pain is due to the reduced blood supply to the myocardium; Angina pectoris.
• tachycardia
• Elevated jugular venous pulse.
• Cardiomegaly
• Emboli formation
• Weakness and reduced activities are due to the low energy.
• Sudden death is due to the severe heart failure. Most of time this may be first symptom.
Investigation of cardiomyopathy
The investigations are use to differential diagnosed of cardiomyopathy. These investigations include a diligent clinical history and examination, blood tests, and ophthalmologic, otologic, dermatological, gastroenterological, nephrological, hematological, and neurological examinations7. The transthoracic, transesophageal and stress echocardiography, contrast echocardiography (CE) are used to improve the diagnostic accuracy of technically when used in combination with harmonic imaging13. Demonstrated benefits of CE include improvement in the accuracy of left ventricular (LV) measurements which are endocardial border marking out and LV opacifiication, regional wall motion assessment, and assessment of noncompaction cardiomyopathy, thrombus detection, Doppler signal enhancement and conjunctive use with stress echocardiography13.

Electrocardiography is used to differential diagnoses and that demonstrate the characteristic features of different types of cardiomyopathy. Changes in ST segment, T wave and Q wave can be shown.
As well as there should be analyzed the whole blood, coagulation, electrolyte parameters, and inflammatory and enzyme values will be within the normal range7, 16.
Regular pulmonary function tests should be done in addition to the routine biopsy controls and the laboratory tests as well as electrocardiography, echocardiography and radiography.
Chest X ray is used to demonstrate the generalized cardiac enlargement.
Blood flow per unit of myocardial volume is calculated using 3D surface-based registration between the imaging of heart wall thickness from cardiac magnetic resonance imaging (MRI) and from myocardial perfusion from single –photon emission computed tomography (SPECT) 8.
Transesophageal echocardiogram (TEE).

Cardiac catheterization
24 hours Holter monitor (heart monitor)
Physical examinations- Listen to the heart and lungs with stethoscope, abnormal heart sounds or murmurs and abnormal heart beats.
Pedigree analysis which generally shows the autosomal dominant inheritance and that may provide prognostic information, (e.g. – history of sudden death). Genetic analysis where available confirms the diagnosis, may provide prognostic information and facilitates assessment of relatives21.
Exercise test and ECG ambulatory recordings provide prognostic information21.
Treatments of cardiomyopathy
The treating management involves the conventional treatment of heart failure and arrhythmias. The goals of management are to reduce symptoms, retard disease progression and prevent complications.
Sevoflurane postconditioning is as effective as preconditioning in protecting myocardial function after global ischemia11. The combination of sevoflurane preconditioning and postconditioning therapy is accessible no additional benefit over either intervention alone11.
Carvedilol and metropolis succinate treatments are efficient in chronic heart failure ;( CHF) 9, 15. The improvement is more significant in patients with non-ischemic CHF, but as well as this treatment therapy improve subjective and submaximum parameters of the functional status of patients with CHF without changing maximal physical ability9. Therapy with beta-adrenoblockers may be resulted in a significant decrease in CHF9, 15.
Anticoagulant treatment is used to a history of embolization, a severe ventricular dilation and dysfunction, or documented atrial fibrillation21.
Diuretics agents are highly effective for the relief of congestive symptoms but should not be used in isolation because of they aggravate activation of neurohormones that may be contribute to progression of disease21.
Angiotensin converting enzyme (ACE) inhibitors are antagonizing activation of the renin-angiotensin- aldosterone, (RAAS) 17, 21. That is useful in relief of patient with hypertension.
Beta blockers which are antagonizing activation of sympathetic nervous system that helps to prevent arrhythmias21.
Permanent pacing, anti-arrhythmic therapy or implantable cardioverter-defibrillators may be obtainable21.
Corticosteroid therapy
Prolong bed rest.
Avoidance of alcohol.
Nutritional supplement
Cardiac transplantation is done in severe congestive cardiomyopathy in relatively young adult.

Dilated Cardiomyopathy (DCM)
Definition: – A condition in which the heart’s ability to pump blood is reduced because of the left ventricle; (one of two pumping chambers of heart) is enlarged or dilated.
This is the most common form of the Cardiomyopathy. Responding for 10,000 deaths of each year in the United State is dilated cardiomyopathy. The dilated cardiomyopathy may represent a late stage of myocardities. DCM is characterized by dilatation and systolic dysfunction of the left ventricle or right ventricle, in the absence of loading conditions, (hypertension, and valve disease) 2, 21.
One of the causes of degenerative heart disease is idiopathic dilated cardiomyopathy that is 7.6% of the patients1. The myocardial infraction (MI) in 36.6%, ischemic heart disease in 25.4%, and Barlow’s disease in 17.8% are the other major causes of patients with degenerative heart disease1.

Causes for dilated Cardiomyopathy
• Autoimmune response- An autoimmune response occurs immune system of own body mistakes body cells as foreign materials and attacks them. Therefore own body cells can cause severe damage to the attached tissue.
• A large number of different myocardial insults; viral nucleic acids from coxsackievirus B and other enteroviruses.
• Alcohol abuse- Due to the raising of ethanol toxicity and coronary artery disease or hypertention19.
• Myocardial injury caused by cobalt and certain chemotherapeutic agents, including doxorubicin, cyclophosphamide and other anthracyclines.
• Late in pregnancy or several weeks to months post partum. That is known as peripartum cardiomyopathy, which is a special form of dilated cardiomyopathy19.
• Defects in sarcomere protein genes- e.g. – β myosin, cardiac troponin T. Sarcomere forms the basic functional structure of the muscle. Therefore defects of gene causes for heart failure with inherited dilated Cardiomyopathy due to the poor contraction of muscle fibers19.
• Abnormal cytoskeleton proteins – e.g. – desmin, Dystrophin associated protein. This is associated with muscular dystrophies and inherited cardiomyopathy19.
• Primary heart muscle disease- e.g. – amyloidosis.
• Cardiovascular disease- e.g. – ischemia, rheumatic, systemic hypertension.
• Connective tissue disorders- e.g. –systemic lupus erythematosus, systemic sclerosis.
• Glycogen storage disease- e.g. – pompé’s disease.
• Presence of hepatitis C virus causes the chronic infections and idiopathic dilated cardiomyopathy as well.

Clinical features
Symptoms depend on the relative degree of heart failure (right or left heart failure) and occurrence of cardiac arrhythmias and emboli.
• Syncope is due to the ventricular arrhythmias or conduction disease or with pulmonary or systemic embolism21.
• Appearing third or fourth heart sound and basal crackles.
• Mitral or tricuspid valvular regurgitation.
• Death results from severe heart failure conditions.
Investigation
• The echocardiogram reveals dilation of the left ventricle or right ventricle with poor global contraction.
• ECG changes- diffuse non-specific ST segment and T wave changes in conduction disturbances, sinus tachycardia, conduction abnormalities and sinus arrhythmias, (atrial fibrillation, ventricular premature conduction or ventricular tachycardia)21.
• Cardiac biopsy which shows variable fibrosis and nonspecific leucocytes infiltration. –e.g. – amyloid. Generally there is not indicated outside specialist career21.
• Angiography is performed to eliminate coronary artery disease in all individual at risk21.

Treatment
In treating management, the causes of cardiomyopathy should be treated.
• The dilated left ventricular (LV) base can be reshaped by undersized mitral annuloplasty (MAP) in patients with dilated cardiomyopathy and MAP is used in functional mitral regurgitation (MR) as well14.

Hypertropic Cardiomyopathy (HMC)
Alternative names20
• IHSS- Idiopathic Hypertropic Subaortic Stenosis.
• ASH- Asymmetric Septal Hypertrophy.
• HOCM- Hypertropic Obstructive Cardiomyopathy
Definition
HMC is a cardiac disorder in which heart muscles become markedly thick. That is most prominent in the left ventricle and interventricular septum.
Because of this thick –walled ventricle, diastolic filling is impaired and it is also characterized by myocardial hypertrophy, intermittent ventricular outflow obstruction, and by a powerful, hyperkinetic contraction that rapidly eject blood from the ventricular cavities19, 20. The most of HMCs cases are inherited; (50%) 20. HMC is associated with Noonan’s syndrome, Friedreich’s ataxia, glycogen storage disease and mitochondrial myopathies21.
Hypertrophic cardiomyopathy can develop at any age, but the condition tends to be more severe among those diagnosed during childhood
Causes for hypertropic cardiomyopathy
• Abnormalities in cytoskeletal proteins19.
• Mutation involving the heavy chains of β-myosin, α-tropomyosin, and troponins I and T19.
• As a result of an alcohol septal ablation, there is an improvement of symptoms and a reduction in dynamic obstruction in most patients with hypertrophic obstructive cardiomyopathy.4
Clinical features
• Some patients have no symptoms and may not recognize that they have the hypertropic cardiomyopathy until it is found during a regular medical exam. A double apical pulsation- Forceful contraction produces a palpable forth heart sound.
• A jerky carotid pulse- Because of sudden obstruction to the left ventricular outflow and rapid ejection during diastole.
• An ejection systolic murmur- Due to the left ventricular outflow obstruction late in systole that can be increased by physical manoeuvres that decrease after load, e.g. – valsalva, or standing, can be decreased by manoeuvres that increase after load and venous return, e.g.- squatting21.
• A pan systolic murmur due to the mitral regurgitation (secondary to systolic anterior motion; (SAM)) 21.
• Appearing the fourth heart sound21.
• Dyspnoea is due to impaired relaxation of the cardiac muscle. Therefore left ventricular filling and empting are impaired. Systolic ventricular function remains good until the very late stages of disease when progressive dilation may occur.
• Light –headedness – especially after activity or exercise.
• Shortness of breathing occurs when lying down position. Sometimes the first symptom of hypertropic cardiomyopathy is sudden death, caused by severe cardiac arrhythmias among the young patients21. As well as hypertropic cardiomyopathy is major caused for death of young athletes who seem completely healthy, but die during serious exercise.
Investigation
• The ECG is can be used to demonstrates the left ventricular hypertrophy by changing ST segment and T wave, abnormal Q waves, most commonly in the inferolateral leads occur in 25-50% of patients21.
• The echocardiogram with Doppler ultrasound- This is the most common test for diagnose. It shows septal hypertrophy than the posterior wall hypertrophy, abnormal mitral valve movement and very strongly contracting ventricle.
• The calculated blood flow per unit of myocardial volume of HMC group is 1/7 times that of normal in the apex8.

Treatment
Firstly, sudden death must be avoided by anti-arrhythmic treatment.
• Beta blockers and versapamil, either along or in combination to use as treatment of chest pain and dyspnoea21.
• Disopyramide which is second line therapy for patient with obstructive hypertrophic cardiomyopathy21.
• Dual chamber pacing used with significant left ventricular obstruction and refractory symptoms.
• Occasionally resection of septal myocardium may be indicated.
• Surgical myectomy can be performed as a treatment of alcohol ablation with hypertropic obstructive cardiomyopathy and that was successful in researching4.

Restrictive cardiomyopathy (RCMP)
This is least common form of cardiomyopathy. The heart muscle becomes rigid and less elasticity, interfering with the expansion and filling of chambers of the heart with blood between heartbeats or contractions20, 21. This prevents the heart from enough blood. But filling of ventricles is rapid but ends abruptly when the stiff heart stops expanding. Because of the “inflow” of blood in to the heart is compromised, symptoms of heart failure can result. This restrictive cardiomyopathy usually affects older people.
The conditions associated with the restrictive cardiomyopathy are amyloidosis ;( commonest), sarcoidosis, Loeffler’s endocardities and endomyocardial fibrosis, there is myocardial and endocardial fibrosis associated with eosinophilia. In the restrictive cardiomyopathy thrombus formation is common condition.
• Idiopathic restrictive cardiomyopathy is familial that is associated with mutation in sarcomeric protein, troponin I. left ventricular thrombectomy in a patient with acute hypereosinophilia and congestive heart failure associated with severe mitral regurgitation and restrictive cardiomyopathy21.
• It may occur idiopathically or as a cardiac manifestation of systemic diseases such as scleroderma, amyloidosis, Churg-Strauss syndrome, cystinosis, sarcoidosis, lymphoma, Gaucher’s disease, hemochromatosis, Fabry’s disease, pseudoxanthoma elasticum, hypereosinophilic syndrome, carcinoid, Noonan’s syndrome, reactive arthritis, or Werner’s syndrome and various neuromuscular disorderses7, 20, 21.
• The patient with amyloidosis has a worse prognosis than those with other forms of deseases often recur after transplantation.
Clinical features
• Dyspnoea, fatigue and embolic symptoms.
• Restrictive to ventricular filling (e.g. Right ventricle) cause in persistently increased venous pressures and consequent hepatic enlargement, ascites and dependent edema.
• Physical sings are similar to those of constrictive pericardities21.
• An elevated JVP with diastolic collapse (Friedreich’s sing) 21.
• An elevation of venous pressure with inspiration ;( kussmual’s sing) 21.
• Fourth heart sound is common in early disease21.
• A cardiac enlargement. But in idiopathic condition, cardiac size may remain normal.
• Third heart sound may be present in advanced disease as well.
Investigation
Investigations of RCMP include a helpful clinical history, physical examination and as well as other common clinical an extracardiac tests
• Chest X-ray which demonstrates the pulmonary venous congestion, cardiac shape can be normal or cardiomegaly, and arterial enlargement21.
• ECG which usually has low- voltage and ST segment and T wave abnormalities.
• The echocardiogram which shows symmetrical myocardial thinking and an often a normal systolic ejection fraction, but impaired ventricular filling21.
• Cardiac catheterization which heamodynamic studies help dysfunction from constrictive pericardities.
• Endomyocardial biopsy in contact with other cardiomyopathies is often useful in this condition and may permit a specific diagnosis such as amyloidosis to be made. When there is no revealed possible caused of extracardiac examinations for RCMP, endomyocardial biopsy is indicated as well7, 21.

Treatment
• There is no special treatment for restrictive cardiomyopathy but in idiopathic RCMP effective, therapeutic option are only treatments of cardiac congestion and a causal therapy can be obtainable21.
• Cardiac failure and embolic manifestation treatment should be prescribed.
• Cardiac transplantation occurs in some severe cases.
• Treating causes for the restrictive cardiomyopathy; e.g.-in primary amyloidosis uses combination therapy with melphalan plus prednisolone with or without colchicines that improves survival of patient.
• Liver transplantation may be effective in familial amyloidosis due to the production of mutant prealbumin can lead to reversal of the cardiac abnormalities21.
Other types of cardiomyopathies
Arrhythmogenic right ventricular cardiomyopathy (ARVCM)
This is characteristic by progressive fibro fatty replacement of myocardium of right ventricle21. This is lead to ventricular arrhythmias and risk of sudden death of early stages and right ventricular or biventricular failure in its later stages.
At least 50% of cases are familial that is most commonly with an autosomal dominant pattern of inheritance21.
A rare form of arrhythmogenic right ventricular cardiomyopathy is associated with dermatological abnormalities such as Naxos disease is caused by a mutation in a gene encoding a myocyte structural protein (plakoglobin) found in desmosomes and gap junction21.

Clinical features
• Severe symptomatic ventricular arrhythmias or syncope.
• Present with right heart failure, later stage of disease in which left ventricular dilation and severity of arrhythmias may paradoxically diminish.
• This is often asymptomatic but first symptom may be sudden death.
Investigation
• ECG which most commonly demonstrates the T wave inversion in precordial related to the right ventricle (V1-V3 leads). A small amplitude potentials occurring at the end of the QRS complex (epsilon waves) may be present. Incomplete or complete right bundle branch block (RBBB) is seen21.
• Signal averaged ECG which indicates the presence of late potentials, delayed depolarization of individual muscle cell.
• Echocardiogram is in low normal and in more advanced cases may demonstrate right ventricular dilatation and aneurysm formation associated in some case with related left ventricular dilation.
• MRT scan in which demonstrate the morphological abnormalities of right ventricle and capable of demonstrating fatty infiltration21.
• Right ventricular angiography which demonstrates enlargement and abnormal motion of myocardium of R ventricle.
• Right ventricular biopsy demonstrates the fibro fatty replacement.
• Holter monitoring in which demonstrates regular extra systole of right ventricular origin and runs of none continuous or continuous ventricular tachycardia21.
• Genetic testing.
Treatment
• β- Blockers use in first line treatment for patient with non-life threatening arrhythmias21.
• Amiodarone or sotalol for symptomatic arrhythmias, refractor or life threatening arrhythmias and ICD may be required.
• Cardiac transplantation occurs in intractable arrhythmias or cardiac failure.

Ischemic cardiomyopathy
Ischemia is the localized blood deficiency caused by constriction or destruction of blood vessels that supply to that area. Myocardial ischemia happens when a coronary artery supply to the part of the heart becomes narrowed or blocked for a short time and leads to hypoxia by unable to reach oxygen-rich blood that part of the heart. In most cases of ischemia, this temporary blood shortage to the heart causes the accumulation of “P factor” and pain in the chest called angina pectoris. In certain other cases, there is no pain. These cases are called silent ischemia. If the myocardial ischemia is severe and prolonged, there can irreversible changes occur in the heart muscle and result is the MI.
Ischemic cardiomyopathy is the loss or weakening of heart muscle tissue caused by ischemia or silent ischemia. The ischemia usually results from coronary artery disease and heart attacks.
Treatment for ischemic cardiomyopathy is similar to that for other forms of cardiomyopathy, with special concentration given to treating coronary artery disease. For patients whose hearts have been seriously damaged by ischemic cardiomyopathy, there may be recommend that a heart transplant.
Ampulla (takotsubo) cardiomyopathy
This type of cardiomyopathy is caused by secondary adrenal insufficiency resulting mainly deficiency of ACTH and cortisol in the blood10. Activation of the sympathetic nervous system, adrenocortical failure, and hypoglycemic attack are also trigged with the takotsubo cardiomyopathy10. The development of some of the case of tokotsubo cardiomyopathy is associated with septal ventricular hypertrophy and intraventricular obstruction6.
Electrocardiography showed ST segment elevation; prolong QT interval and T wave inversion in leads V (1-6)6,10.Other investigations are included the insulin tolerance tests, ventriculogram and ultra sound studies of the heart.
Cardiac dysfunction due to both cardiomyopathy and adrenal cortical failure can be recovered by careful monitoring of cardiac function and appropriate treatments10. Taxonomic confusion occurs as well5.
Stress- induced cardiomyopathy (SICMP)
Stress induced cardiomyopathy is an imitated acute coronary syndromes (ACS) that is often associated with sings of cardiac failure5. There is significance correlation among the female gender with a short height (<158cm), a small body surface area (<1.9m2) and a hypoplastic branching coronary arteries mainly in the apical region of the heart.5 By researching there is found out that more tendency to get this SICMP for Mediterranean and Indo-Asian women, who represent 85% of cases5.
In the most of cases, the symptoms become chronic and medical treatments of SICMP rarely improve dyspnea and chest pain. Because of that the quality of life is reduced5.

List of references
References
1) Gatti G, Pugliese P, Preliminary experience in mitral valve repair using the Cosgrove-Edwards annuloplasty ring Department of Cardiac Surgery, Villa Torri Hospital, viale Filopanti, 12-40126 Bologna, Italy,2003 Sep. giusep.gatti@tiscali.it
2) Reis FJ, Viana M, oliveira M, Sousa TA Parana R ,Prevalence of hepatitis C and B virus infection in patients with idiopathic dilated cardiomyopathy in Brazil: a pilot study, 2007 Jun, Bahiana School of Medicine and Public Health
3) Littarru GP, Langsjoen,Coenzyme Q10 and statins: biochemical and clinical implication, Institute of Biochemistry, Polytechnic University of the Marche, Via Ranieri, 60131 Ancona, Italy, 2007 Jun. G.littarru@univpm.it
4) Nagueh SF,Buergler JM, Quinones MA, Spencer WH 3rd, Lawrie GM,Outcome of surgical myectomy after unsuccessful alcohol septal ablation for the treatment of patients with hypertrophic obstructive cardiomyopathy, 2007 Aug, Methodist DeBakey Heart Center and Department of Cardiology, Methodist Hospital, Houston, Texas, USA. snagueh@tmh.tmc.edu
5) Cocco G, Chu D, Stress-induced cardiomyopathy: A review, 2007 Jul, Marktgasse 10a, Postfach 119, CH-4310 Rheinfelden 1, Switzerland.
6) Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Fiscella A, Intraventricular obstruction in a patient with tako-tsubo cardiomyopathy, 2007 Aug, Division of Cardiology, “Cannizzaro” Hospital, Catania, Italy.
7) Stöllberger C, Finsterer J, Extracardiac medical and neuromuscular implications in restrictive cardiomyopathy, 2007 Aug, Medizinische Abteilung, Krankenanstalt Rudolfstiftung. Fukami T, Sato H, Wu J, Lwin TT, Yuasa T, Kawano S, Iida K, Akatsuka T, Hontani H, Takeda T, Tamura M, Yokota H, Quantitative evaluation of myocardial function by a volume-normalized map generated from relative blood flow, Department of Bio-system Engineering, Faculty of Engineering, Yamagata University, Yonezawa, Yamagata 992-8510, Japan,2007 Jul. fukami@yz-yamagata-u.ac.jp.
9) Poltavskaia MG, Syrkin AL, Andreev DA, Svet AV, Sarkisova EA, Kalashnikov VIu, The effects of beta-adrenoblocker therapy on the physical working capacity of patients with chronic heart failure of various origin, [Article in Russian], 2007.
10) Sakihara S, Kageyama K, Nigawara T, Kidani Y, Suda T, Ampulla (Takotsubo) Cardiomyopathy Caused by Secondary Adrenal Insufficiency in ACTH Isolated Deficiency, 2007 Jul Department of Endocrinology and Metabolism, Hirosaki University School of Medicine.
11) Deyhimy DI, Fleming NW, Brodkin IG, Liu H Anesthetic preconditioning combined with postconditioning offers no additional benefit over preconditioning or postconditioning alone, 2007Aug, Department of Anesthesiology and Pain Medicine, University of California, Davis, CA, USA.
12) Ocorr K, Perrin L, Lim HY, Qian L, Wu X, Bodmer R,Genetic control of heart function and aging in Drosophila,2007 Jul, Burnham Institute for Medical Research, Program for Systems and Developmental Biology, Center for Neurosciences and Aging, La Jolla, CA 92037, USA
13) Honos G, Amyot R, Choy J, Leong-Poi H, Schnell G, Yu E, Contrast echocardiography in Canada: Canadian Cardiovascular Society/Canadian Society of Echocardiography position paper, 2007 Apr, Sir Mortimer B Davis Jewish General Hospital, Montreal, Quebec, Canada. ghonos@cardio.jgh.mcgill.ca
14) Koyama T, Soga Y, Unimonh O, Nishimura K, Komeda M, Mitral annuloplasty as a ventricular restoration method for the failing left ventricle: a pilot study, 2007 Mar, Department of Cardiovascular Surgery, Kyoto University, Graduate School of Medicine, Kyoto, Japan.
15) Brixius K, Lu R, Boelck B, Grafweg S, Hoyer F, Pott C, Mehlhorn U, Bloch W, Schwinger RH, Chronic treatment with carvedilol improves Ca2+-dependent ATP consumption in triton X-skinned fiber preparations of human myocardium, 2007 Jul, Department of Molecular and Cellular Sport Medicine, German Sport University, Cologne, Germany .
16) Strecker T, Zimmermann I, Wiest GH, Pulmonary and cardiac recurrence of sarcoidosis in a heart transplant recipient, [Article in German], 2007 May, Zentrum für Herzchirurgie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. thomas.strecker@herz.imed.uni-erlangen.de
17) Lefebvre HP, Brown SA, Chetboul V, King JN, Pouchelon JL, Toutain PL, Angiotensin-converting enzyme inhibitors in veterinary medicine, 2007, UMR 181 INRA-ENVT Physiopathologie et Toxicologie Expérimentales, National Veterinary School, Toulouse cedex 03, France. h.lefebvre@envt.fr
18) Diseases and Conditions, cardimyopathy, 2006 march, MayoClinic.com.
19) J.C.F Underwood, General and systemic pathology, 319-21, 322b, 4th edition.
20) Parakrama Chandrasoma, Clive. R.Taylor, Concise pathology, 175-6, 248, 355, 360, 374, 2nd edition.
21) Fraveen .J. Kumar & Michal Clark, Clinical medicine, 848-53, 6th edition.

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