Rheumatic heart disease
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Rheumatic heart disease
Cardiovascular system
Vascular disorders
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
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Coronary steal syndrome
Peripheral artery disease
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Congenital heart defects
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Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Coarctation of the aorta
Atrial septal defect
Cardiac arrhythmias
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Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
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Premature ventricular contraction
Long QT syndrome and Torsade de pointes
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Bundle branch block
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Valvular disorders
Tricuspid valve disease
Pulmonary valve disease
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Aortic valve disease
Cardiomyopathies
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Heart failure
Cor pulmonale
Cardiac infections
Endocarditis
Myocarditis
Rheumatic heart disease
Pericardial disorders
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Cardiac tumors
Cardiovascular system pathology review
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
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Rheumatic heart disease
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Carditis
rheumatic fever p. 321
Hypersensitivity reactions p. 110-111
rheumatic fever p. 320
M protein
rheumatic fever and p. 134
Penicillin
for rheumatic fever p. 321
Pharyngitis
prophylaxis (rheumatic fever) p. 195
Rheumatic fever p. 321
chorea with p. 537
heart murmur with p. 298
Streptococcus pyogenes p. , 134
streptolysin O p. 131
type II hypersensitivity p. 110
Type II hypersensitivity reactions
rheumatic fever p. 320
Transcript
Contributors
Tanner Marshall, MS
Jake Ryan
Robyn Hughes, MScBMC
“Rheumatism” is used to describe inflammation in the joints, muscles, and the fibrous tissue, so rheumatic fever is a type of inflammatory disease that can damage the heart tissue, and lead to rheumatic heart disease.
Rheumatic fever develops after streptococcal pharyngitis, inflammation of the throat due to Streptococcus pyogenes where pyogenes literally means “makes pus”. The bacteria is sometimes referred to as “Group A beta hemolytic” streptococcus, and the infection itself is most often just called Strep throat. This particular group of streptococcus has an antigen that lumps it into a group called “group A”, and it also produces an enzyme called streptolysin, that completely lyses nearby red blood cells, or causes them to rupture—rupturing red blood cells is called hemolysis, right? And when those red blood cells rupture and are destroyed, it’s called beta-hemolysis—as opposed to alpha-hemolysis, where cells aren’t actually destroyed, they’re just damaged or bruised.
Some of these strep bacteria have a protein on their cell wall called “M protein”, and this particular protein is highly antigenic, meaning that the immune system sees it and recognizes it as a foreign molecule, and mounts an immune response, which rightfully so, produces antibodies against these proteins. Those antibodies, though, are thought to cross-react with proteins on some of our body’s own cells, like cells in the myocardium (or heart muscle) and heart valves, but also cells in the joints, the skin and the brain.
This phenomenon, where antibodies accidentally target proteins on our own cells because they look like the proteins on foreign cells, is called molecular mimicry, and is an example of what’s called a type 2 hypersensitivity reaction. Once bound to cardiac tissue, the antibodies activate nearby immune cells, which causes a cytokine-mediated inflammatory response and tissue destruction.
Summary
Rheumatic heart disease is a condition that develops as a complication of rheumatic fever, which is an inflammatory disease that can occur as a complication of streptococcal infections such as strep throat. This occurs due to the antibodies against streptococcal M proteins that cross-react with proteins in the myocardium, heart valves, joints, skin, and brain.
Rheumatic heart disease is characterized by heart tissue scarring that damages the heart valves, leading to problems such as mitral stenosis, and aortic regurgitation. Symptoms of rheumatic heart disease include shortness of breath, fatigue, chest pain, and heart palpitations. Treatment may involve antibiotics to prevent further streptococcal infections, and surgery to repair or replace damaged heart valves.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "Acute rheumatic fever" The Lancet (2005)
- "Rheumatic fever & rheumatic heart disease: the last 50 years" Indian J Med Res (2013)
- "Rheumatic heart disease" The Lancet (2012)
- "Rheumatic Heart Disease: Causes, Symptoms, and Treatments" Cell Biochemistry and Biophysics (2015)
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