A heart attack also known as myocardial infarction or MI , which can damage the muscles that control the opening and closing of the valve. Other: Autoimmune disease, such as lupus. Marfan syndrome , a disease of connective tissue that can affect heart valves. Exposure to high-dose radiation, which may lead to calcium deposits on the valve.
The aging process, which can cause calcium deposits to develop on the heart valves, making them stiff or thickened and less efficient with age. What are the symptoms of valvular heart disease? When it develops more suddenly, people may experience the following symptoms: Shortness of breath Chest pain Fatigue Dizziness or fainting Fever Rapid weight gain Irregular heartbeat How is valvular heart disease diagnosed?
How is valvular heart disease treated? Philadelphia, PA: Elsevier Saunders; Data are from the Multiple Cause of Death Files, , as compiled from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program. Get Email Updates. To receive email updates about this page, enter your email address: Email Address. What's this? Links with this icon indicate that you are leaving the CDC website. Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website.
You will be subject to the destination website's privacy policy when you follow the link. MMP-1 has a high affinity to fibrillar collagens and is able to initiate collagenolysis. The majorities of studies addressing the role of MMPs were performed in human plasma and myocardium tissues during acute episodes of rheumatic fever and are scarce in the chronic disease phase, particularly in valves 71 — Proinflammatory MMPs also play a role in the modulation of calcification by elastin degradation.
Exposure of elastin and matrix-bound cytokine generation after tissue injury create a milieu, which promotes the smooth muscle cell changes into osteoblastic phenotype 74 , Calcification is a very common finding in rheumatic mitral valves, however, the cellular mechanisms responsible for the calcification in RHVD are not well-understood Figure 3B. Previous study reported that mineralization occurs in areas of inflammation and neoangiogenesis, which express vascular endothelial growth factor VEGF This molecule is able to regulate bone remodeling by attracting endothelial cells and by stimulating osteoblast differentiation Another potential mechanism involved in mitral valve mineralization in RHVD is through calcification-competent extracellular vesicles derived from smooth muscle cells, VICs or macrophages 77 — Together, the immune response triggered by pharyngeal GAS infection results in a cascade of cellular and humoral events that culminate in the production of antibodies and generate self-reactive clones of lymphocytes capable of interacting with valve components leading to leaflet tissue degeneration.
Neoangiogenesis is a common feature of HVD acting as a facilitator of inflammation by allowing the entry of immune cells and soluble inflammatory factors into the valvular tissue. Besides, vascular networks promote the weakening of valve tissue by changing the normal architecture 80 , A variety of growth factors can regulate angiogenesis, including vascular endothelial growth factor VEGF -A and MMPs that degrade fibrillar collagen or proteoglycan proteins allowing endothelial cells sprouting vessels by migration Thus, angiogenesis besides contributing to tissue remodeling also can compromise mechanical stability of extracellular matrix.
For the first time, we shown that mitral valves from patients with RHVD show an abundant neovascular network characterized by accumulation of large immature vessels, which is lacking in CAVD tissue Figures 4A,B.
Figure 4. Histological comparison between neoangiogenesis in rheumatic mitral valve and calcific aortic valve. C Representative immunofluorescence image showing cell co-expressing LYVE-1 and podoplanin demonstrating presence of lymphatic vessels in rheumatic mitral valves.
Besides blood vessels, lymphatic vasculature network was also observed in heart valves from patients with end stage RHVD as detected by colocalization of lymphatic endothelial cell receptor LYVE-1 and podoplanin well-known markers of lymphatic endothelial cells 83 Figures 4C,D. These vessels play role in lymph transport, tissue interstitial fluid absorption and serve as an entrance point for immune cells, favorable for optimal tissue function.
Autopsy results of adult heart valves show that lymphatic vessels in pathologic conditions such as RHVD present in a high It is likely that neolymphogenesis is beneficial in the early phases of disease to maintain tissue homeostasis, but if become uncontrolled during the disease progression, may lead to pathological maladaptation.
Persistent local inflammation impairs lymphatic contraction causing altered fluid transport In addition, accumulation of collagen and fibrogenic molecules produced by smooth muscle cells and fibroblasts into the perilymphatic space causes capillary fibrosis and impairs vascular function Thus, although lymphatic vessels are accumulating in lesions in large numbers, they are not able to exert their function properly.
In addition to growth factors and cytokines, hormones also participate in regulating angiogenesis. Estradiol influences hyaluronic acid synthesis, a major ECM ligand for the LYVE-1, suggesting an indirect effect on lymphatic homeostasis 87 , Also, while estrogen is described to reduce cardiovascular risk in women, it has been reported as a risk factor for disorders of lymphatic vascular system.
Thus, excessive neolymphoangiogenesis observed in rheumatic mitral valves obtained predominantly from female patients, could be induced by estrogen which in turn can aggravate vessel sprouting in association with proinflammatory milieu.
No therapies are available to prevent or treat RHVD. Antibiotic prophylaxis is given to prevent repetitive episodes of ARF, and potentially limit the disease progression to severe valve dysfunction. However, there is no robust evidence of efficacy of secondary antibiotic prophylaxis in preventing recurrences of ARF 9.
Corticosteroids or intravenous immunoglobulins were tested in clinical trials to reduce the risk of heart valve lesions in patients with ARF, however, little evidence of benefit was found Since RHVD results from an abnormal immune response, therapies targeting immune system could be more effective to avert valvular damage. Therefore, more research is needed to find specific immune components associated with the RHVD pathogenesis that will provide a more precise and effective therapeutical interventions to treat this devastating condition.
All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Type of valvular heart disease requiring surgery in the 21st century: mortality and length-of-stay related to surgery.
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PubMed Abstract Google Scholar. Calcified rheumatic valve neoangiogenesis is associated with vascular endothelial growth factor expression and osteoblast-like bone formation. Reciprocal interactions between mitral valve endothelial and interstitial cells reduce endothelial-to-mesenchymal transition and myofibroblastic activation. J Mol Cell Cardiol. Leducq Mitral Transatlantic, Mitral valve disease—morphology and mechanisms. Nat Rev Cardiol. Heart valve structure and function in development and disease.
Annu Rev Physiol. Activated interstitial myofibroblasts express catabolic enzymes and mediate matrix remodeling in myxomatous heart valves. Kaplan MH. The concept of autoantibodies in rheumatic fever and in the postcommissurotomy state.
Ann N Y Acad Sci. Atherosclerosis and autoimmunity: a growing relationship. Int J Rheum Dis. Innate and adaptive immunity in cardiovascular calcification. Less commonly, the aortic valve can be involved; tricuspid valve involvement is rare, but reported.
Rheumatic fever acutely causes symptoms of pericarditis and congestive heart failure, depending on the degree of valvulitis and myocarditis present. Migratory polyarthritis is the most common symptom in acute rheumatic fever. Subcutaneous nodules arise over the bones and tendons, as well as a rash that starts on the trunk and extends to the limbs.
The rash has a characteristic erythematous ring with a pale center and is referred to as erythema marginatum. Sydenham's chorea St. Enlarge Rheumatic valvular disease is diagnosed predominantly via echocardiography. To find useful services to help you on your journey with heart disease, see our services and resources listing.
Donate now. Heart disease Conditions A-Z Rheumatic heart disease. What is rheumatic fever? What is rheumatic heart disease? Types of rheumatic heart disease Every part of the heart may be damaged by inflammation caused by rheumatic fever. Some heart problems linked to rheumatic fever are: valvular heart disease pericarditis endocarditis heart block The most common form of rheumatic heart disease affects the heart valves.
Valve stenosis occurs when there is narrowing of a valve, which restricts blood flow. Valve regurgitation is when blood leaks backward through a valve, instead of following its usual direction. The inflammation of rheumatic fever can damage the heart muscle itself.
Who is at risk? Symptoms 1. The symptoms of rheumatic fever include: fever painful joints migrating pain from joint to joint red, warm, swollen joints small, painless bumps beneath the skin chest pain heart murmur painless rash with a jagged edge erythema marginatum jerky movements unusual behaviours accompanying the movements 2. The symptoms of heart valve problems — which are often the result of rheumatic heart disease — can include: chest discomfort or pain irregular or rapid heartbeats heart palpitations shortness of breath fatigue or weakness light-headedness, dizziness or near fainting swelling of the stomach, feet, or ankles If you have one or more of these symptoms, see your doctor.
Tests that will check your heart for damage include: echocardiogram chest X-ray.
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