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Types Of Rheumatic Heart Fever

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Rheumatic fever is a disease, a preventable disease that usually has its onset in childhood following a

hemolytic streptococcus infection. Whereas the most prominent symptom of rheumatic fever is polyarthritis, the most serious damage occurs in the heart, where every structural component is likely to be the site of an inflammatory reaction. This is known as different types of rheumatic heart fever. The heart damage and the joint lesions as well, are not infectious in origin, in the sense that these tissues are invaded and directly damaged by destructive organisms; rather, they represent a sensitivity phenomenon, occurring in response to prior contact with a bacterium: specifically, the beta hemolytic streptococcus.

Blood leukocytes accumulate in the affected tissues to form nodules, which eventually are replaced by scars. The myocardium is certain to be involved in this inflammatory process, i.e., rheumatic myocarditis develops, which temporarily weakens the contractile power of the heart. The pericardium likewise is affected, i.e., rheumatic pericarditis also occurs during the acute illness. These myocardial and pericardial complications usually are without serious consequences; on the other hand, the effects of rheumatic endocarditis are permanent and often crippling.

Rheumatic endocarditis anatomically manifests itself first by tiny translucent vegetations, which resemble beads about the size of the head of a pin, arranged in a row along the free margins of the valve flaps. These tiny beads look harmless enough and may disappear without injuring the valve flaps, but more often their results are serious. They are the starting point of a process that gradually thickens the flaps after years, rendering them just a little shorter, just a little thicker than normal, just a little shriveled along their edges— not much, but enough to prevent them from closing the orifice of the valve perfectly. Hence a leak develops; the valve is said to be “regurgitant.” In other patients the inflamed margins of the valve flaps become adherent, with the result that the valve orifice is narrowed, or “stenotic.” This is one of the more dangerous types of rheumatic heart fever.

A very small percentage of patients die as the immediate result of acute rheumatic fever; when death does occur at this stage, usually it is due to acute myocarditis. Most patients recover with gratifying speed and their recovery ostensibly is complete. However, although free of symptoms, the patient is left with certain permanent residuals that often gradually lead to progressive valvular deformities. The extent of cardiac damage, or even its existence, may not have been apparent on clinical examinations during the acute phase of the disease.

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Eventually, however, the heart murmurs that are characteristic of valvular stenosis, regurgitation, or both,

become audible on auscultation and, in some patients, even detectable as “thrills” on palpation. The myocardium usually can compensate for these valvular defects very well for a time, despite its increased burden. As long as it can do so, the patient remains in apparent good health. However, sooner or later it fails to compensate—and de-compensation, when it occurs, is signaled by the manifestations of congestive heart failure.

The patient with rheumatic endocarditis should be confined to bed as long as he is febrile and remain quiet thereafter until the erythrocyte sedimentation rate (a fair though nonspecific index of rheumatic activity) returns to normal. Salicylates customarily are prescribed in large doses, and invariably to good effect, so far as the elimination of fever and arthritis are concerned. However, neither these nor any other drugs appear to affect the development or the progress of rheumatic endocarditis.

The patient with rheumatic endocarditis, whose valve function is faulty but whose disease is quiescent, does not require therapy as long as his heart pumps effectively. Nevertheless, he faces the threat of recurrent attacks’ of acute rheumatic fever, of bacterial endocarditis, of embolism from vegetations or mural thrombi in the heart, and of eventual cardiac failure. The relation between valvular disease and congestive heart failure and the treatment of heart failure.

Unfortunately, rheumatic fever is prone to recur unless forestalled by prophylactic antimicrobial therapy, and each attack renders the patient more susceptible to a subsequent recurrence. Furthermore, each attack adds to the valvular damage already present, further impairing cardiac function and hastening the. advent of eventual de-compensation, Obviously, it is in the area of prevention that the medical team can make its most significant contribution to the welfare of the patient with rheumatic endocarditis. It is important to learn about the various types of rheumatic heart fever.

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A patient with heart disease should learn to regulate his activity according to his individual response. The goal is always to prevent progression of disease and the development of congestive heart failure.

 

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