Abstract
Rheumatic heart valve disease (RHVD) is a post-infectious sequel of acute rheumatic fever resulting from an abnormal immune response to a streptococcal pharyngitis that triggers valvular damage. RHVD is the leading cause of cardiovascular death in children and young adults, mainly in women from low and middle-income countries. It is known that long-term inflammation and high degree of fibrosis leads to valve dysfunction due to anatomic disruption of the valve apparatus. However, since public and private investments in RHVD studies are practically inexistent the number of publications is scarce. This disease shows different natural history and clinical presentations as compared to other degenerative heart valve diseases. Although more than five decades passed after the pioneering studies on the pathogenesis of RHVD, it is still unclear how self-tolerance mechanisms fail in this disease, and how humoral and cellular inflammatory responses are interconnected. Despite that pathological mechanisms have been already proposed for RHVD, none of them are able to explain the preferential involvement of the mitral valve. This review focuses on pathophysiology and underlying mechanisms of RHVD.
Highlights
Rheumatic Heart Valve DiseaseHeart valve disease (HVD) is generic term that includes several etiologic entities with different pathophysiologic mechanisms that lead to anatomic disruption of the valve apparatus [1]
This review focuses on pathophysiology and underlying mechanisms of rheumatic heart valve disease (RHVD)
RHVD first occurs in childhood, its incidence peaks in adulthood, usually between the ages of 25–45 years [10]
Summary
Vanvitelli, Italy Paul “Li-Hao” Huang, Washington University in St. Louis, United States. Heart Valve Disease, a section of the journal Frontiers in Cardiovascular Medicine. Rheumatic heart valve disease (RHVD) is a post-infectious sequel of acute rheumatic fever resulting from an abnormal immune response to a streptococcal pharyngitis that triggers valvular damage. Since public and private investments in RHVD studies are practically inexistent the number of publications is scarce. This disease shows different natural history and clinical presentations as compared to other degenerative heart valve diseases. More than five decades passed after the pioneering studies on the pathogenesis of RHVD, it is still unclear how self-tolerance mechanisms fail in this disease, and how humoral and cellular inflammatory responses are interconnected.
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