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Cardiac fibrosis commonly refers to the excess deposition of extracellular matrix in the cardiac muscle, but the term may also refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts. [1] Fibrotic cardiac muscle is stiffer and less compliant and is seen in the progression to heart failure.
The majority of treatment is aimed at preserving heart function and treating heart failure symptoms. [3] Light chain (AL-CM) Treatment: Since the cause of this subtype of cardiac amyloidosis is the excessive production of free light chains, the major goal of treatment is the reduction in concentration of light chains. [5]
Treatment depends on the type of cardiomyopathy and condition of disease, but may include medication (conservative treatment) or iatrogenic/implanted pacemakers for slow heart rates, defibrillators for those prone to fatal heart rhythms, ventricular assist devices (VADs) for severe heart failure, or catheter ablation for recurring dysrhythmias ...
Often, symptoms mimic those of congestive heart failure (esp. activity intolerance and dyspnea), but treatment of each is different. Beta-blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and ...
A myocardial infarction, also known as a heart attack, often result in the formation of fibrosis. [2] A myocardial infarction is an ischemic event, or a restriction of blood flow to body tissue, such as by atherothrombosis. [4] Without blood flow to the myocardium, it is deprived of oxygen, causing tissue death and irreversible damage. [5]
Histopathology of (a) normal myocardium and (b) myocardial hypertrophy. Scale bar indicates 50 μm. Rectangular "Boxcar" nuclei is a microscopic sign indicating myocardial hypertrophy. The ventricles are the chambers in the heart responsible for pumping blood either to the lungs (right ventricle) or to the rest of the body (left ventricle).
The area of dysfunction should also maintain normal perfusion, detected via Positron Emission Tomography, echocardiography with contrast, and/or thallium scintigraphy in order for a diagnosis of myocardial stunning to be considered. [1] However, there are many practical challenges to diagnosing myocardial stunning using these methods.
Primary disease of the muscle of the heart that cause LVH are known as hypertrophic cardiomyopathies, which can lead into heart failure. [citation needed] Long-standing mitral insufficiency also leads to LVH as a compensatory mechanism. [citation needed] LV mass increases with ageing. [4] Associated genes include OGN, osteoglycin. [5]
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