11
May
cardiomyopathy Section XI of the competition network pharmaceutical mergers and acquisitions?
Ones devour the small or merged? Pharmaceutical giants face huge selection of ings more thematic . GSK acquired Reliant Pharmaceutical $ 1,650,000,000
Britain's largest pharmaceutical company GlaxoSmithKline (NYSE: GSK) completed the acquisition of Reliant Pharmaceutical companies, for the 1.65 billion purchase price moreIn recent years, clinical, and pathologists will be of unknown cause which is not secondary to systemic or other organ system diseases, primary myocardial damage to be called primary cardiomyopathy (primary cardiomyopathy). It is non-rheumatic, non-hypertensive, non-coronary cardiac structure and function of the pathological changes. The pathological process is metabolic rather than inflammatory, in the pathogenesis with other known causes of heart disease caused by unrelated. On the contrary, if the known causes of heart disease and is related to or associated with or secondary to a systemic disease, it is called secondary cardiomyopathy (secondary cardiomyopathy). Primary cardiomyopathy is less common, but the distribution around the world. The concept of this disease, the pathological changes in the definition and there are different, classification is also more confusing.
Is the driving force of myocardial systolic and diastolic cardiac structure, physical (such as hypoxia), chemical (such as drugs, toxins) and biological (such as the infectious agen

t), and other risk factors are particularly sensitive. Myocardial injury usually presents with mild hypertrophy of the nucleus and organelles, showed severe damage cell structure and cell necrosis of the remodeling, and thus lead to fibrosis. These changes not only the basic disease cardiomyopathy, but also has a compensatory adaptive significance.
First, primary cardiomyopathy
1980, WHO will be divided into three types of primary cardiomyopathy:
(A) dilated cardiomyopathy
Dilated (congestive) cardiomyopathy dilated (congestive) cardiomyopathy of unknown cause is the final outcome of various heart diseases, heart cavity expansion and a high cardiac output significantly decreased (heart failure) was characterized. Most cases can be found autoantibodies against endocardium, and its meaning is unclear pathogenesis. Age 20 to 50 years old, more men than women. Because both sides of the heart failure patients with multiple medical treatment. Most patients often sexual aggravation of heart failure death or heart rhythm often occurs due to sudden death.
Lesions
Eye of both sides of the typical changes in ventricular hypertrophy, expansion of the four cardiac chambers, thinning of the apex blunt circular (eccentric hypertro
Microscopically, cardiac muscle cell hypertrophy and often show different degrees of elongation and sarcoplasmic degeneration, loss of contraction of components. Hypertrophy of myocardial cells of the whole cell elongation, and its diameter more than in the normal range, but its nuclear large stain. Myocardial interstitial fibrosis is the most common type of cardiomyopathy changes can be seen around the perivascular and myocardial cells thin collagen fiber bundles, or instead of dense fibrosis lesions. Interstitial fibrosis and left ventricular endocardial usually, myocardial else. Endomyocardial fibrosis is usually mild, but significant fibrosis at the mural thrombus. In addition, some cases can be seen lymphocytic interstitial myocarditis, which is characterized by lymphocytic infiltration of multiple lesions associated with myocardial cell degeneration and necrosis.
(B) hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (hypertrophic cardoiomyopathy) is characterized by asymmetrical septal hypertrophy, abnormal myocardial cell hypertrophy, and systolic mitral valve orientation disorders such as sails to move forward. Hypertrophy of the muscle wall compliance decreased, resulting in increased resistance to ventricular filling. Clinical manifestations of varying degrees of ventricular filling rather than emptying delay is limited. According to the phenomenon of left ventricular outflow tract obstruction with or without obstruction can be divided into two types of non-obstructive. Or two right ventricular outflow tract ventricular outflow tract obstruction who are rare. Often leads to sudden death, infective endocarditis can be complicated.
Lesions
Eye of both sides of the ventricular hypertrophy significantly, heart weight increased, the average heart weight for the normal 1 to 2 times (with an average adult heart weight 582g, a few up to 1000g). Most cases of septal thickness greater than the left ventricular free wall (Figure 8-34, Figure 8-35), hypertrophy can be limitations, can affect the heart at the base (under the aortic valve), ventricular septal, or apical area in central . Move forward with the septal mitral valve systolic results of the s can lead to mitral valve thickening and subaortic endocardial fibrosis. Before the occurrence of heart failure, left ventricular generally not expansion.Heart cross-section of the icon (top , asymmetric ventricular septal hypertrophy (taken from Becker and Anderson)Ventricular cross-sectional (top , left ventricular cavity narrow, uniform thickening of the heart wall, the myocardial fibrosis area covered with white, ventricular septal and posterior wall thickness ratio is only slightly larger than normal (1.4)
Microscopically, cardiac muscle cell hypertrophy significantly, large and strong nuclear staining (Figure 8-36), nuclear Zhou Youliang area surrounded by staining proved to be glycogen accumulation, with a certain diagnosis. Disordered arrangement of myocardial cells than other cardiomyopathy staggering, and often has spiral-shaped or winding was arranged in clusters (Figure 8-37), cells without myofibrils arranged in parallel, but in all directions, each staggered. Interstitial fibrosis are often foci formation, but to intimal fibrosis, especially in the area under the aortic intimal fibrosis is prominent. Hypertrophy of the interventricular septum in the coronary artery wall thickening often.Cardiac hypertrophy, and a large stain 360 (taken from Edwards)Electron microscopy, mainly for the side adjacent cells appear intercalated disc connections between cells; from the bottom of a myofibrillar Z band filaments can be inserted into another different angle of the Z band of myofibrils to form a woven-like arrangement. Sometimes can be seen from the broadening of the Z filaments with radiation in all directions. However, the contralateral side of muscle cells and muscle fiber connection arrangement disorder hypertrophic cardiomyopathy is not unique to the changes.
(C) restrictive cardiomyopathy
Restrictive cardiomyopathy (restrictive cardiomyopathy) is characterized by restricted ventricular filling. Typical endometrial and endometrial lesions were ventricular myocardium progressive fibrosis, leading to reduced ventricular compliance, cardiac stenosis. Thus, also known as endomyocardial fibrosis (endomyocardial fibrosis).
Lesions
Eye of the right ventricle intimal fibrosis, especially in the apex is obvious, intimal thickening of about 2 ~ 3mm, white, the surface may have thrombosis. Intimal fibrous thickening of the apex of upward spof the papillary muscles can be, Rouzhu buried, including depression, tendons thicken and shorten, can lead to three regurgitation. Intimal fibrosis, mainly in the left ventricular inflow tract or apex, the surface may have thrombosis. When the mitral valve leaflet and left ventricular posterior wall after the adhesion, causing mitral regurgitation.
Microscope, showing thickening of the intima is mainly dense hyaline collagen fibers, may have calcification. Visible surface of the old mural thrombus. Subendocardial common atrophy, degeneration change.
In addition, eosinophilic endocarditis cardiomyopathy (eosinophilic endomyocardial disease) may be the subtype of the type of cardiomyopathy. Infiltration in endomyocardial Department eosinophils degranulation, release of cationic protein, can cause the department's focal necrosis and myocardial fibrosis. Ventricular inflow tract and apex of the mural thrombus and fibrosis can lead to ventricular restrictive filling obstacles.
Second, Keshan disease
Keshan disease (Keshan disease) is an endemic cardiomyopathy (endemic cardiomyopathy). In 1935, the first popular in Keshan County in Heilongjiang Province, was a clear understanding of the nature of the disease, then in order to name names, still in use. The disease occurs mainly in northeast China, northwest, north and southwest along the inaccessible mountainous or hilly areas. Pathology to myocardial degeneration, necrosis and scarring after the repair is characterized. Often clinically acute or chronic heart failure performance.
Cause
Since the 50s a lot of research on the etiology of this disease, but so far inconclusive. At first considered a regional epidemic of viral myocarditis, which may be related to coxsackie virus group B, but the virus isolation and serological test has not been regular positive results. Ward in recent years found that the selenium content of food was significantly lower than non-endemic area, the patient's hair and blood selenium levels were significantly lower than non-endemic area population. Taking selenium Keshan disease can be controlled as part of the attack. 1974 to 1977, areas of selenium in the prevention of disease, the results showed that selenium supplementation of children by their hair K
Lesions
The disease mainly in the cardiac lesions can be severe degeneration, necrosis and scar formation. Degeneration of skeletal muscle may also have mild or small focal necrosis.
Eye , the heart was increased to varying degrees, both sides of ventricular expansion, resulting in the heart of nearly spherical shape. Weight also increased, longer course of chronic-type cases, the heart weight increased even more, the heaviest of more than 500g. The expansion chambers of the heart is myogenic, cardiac wall thinning, papillary muscles and Rouzhu become flat. Between left ventricular Rouzhu few cases, left and right atrial mural thrombus within a formation. If the thrombus off, can cause lung, kidney, spleen, brain and other organs of the embolization
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