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{{Tricuspid regurgitation}} | |||
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==Overview== | ==Overview== | ||
'''Tricuspid insufficiency''', a [[valvular heart disease]] also called '''Tricuspid regurgitation''', refers to the failure of the heart's [[tricuspid valve]] to close properly during [[systole]]. As a result, with each heart beat, a portion of the blood is pumped out from the right side of the heart backwards in the ''opposite'' direction into the [[right atrium]] rather than forwards into the [[right ventricle]]. | '''Tricuspid insufficiency''', a [[valvular heart disease]] also called '''Tricuspid regurgitation''', refers to the failure of the heart's [[tricuspid valve]] to close properly during [[systole]]. As a result, with each heart beat, a portion of the blood is pumped out from the right side of the heart backwards in the ''opposite'' direction into the [[right atrium]] rather than forwards into the [[right ventricle]]. | ||
==Classification== | |||
Tricuspid regurgitation (TR) can be classified into primary and secondary. Primary (or organic) TR results from an organic lesion of the [[tricuspid valve]] itself, whereas secondary (or functional) TR is caused by [[left heart failure]] or [[pulmonary hypertension]] without an intrinsic abnormality of the [[tricuspid valve]]. | |||
==Pathophysiology== | |||
Tricuspid regurgitation (TR) refers to the failure of the [[tricuspid valve]] to close properly during [[systole]]. As a result, with each heart beat some blood passes from the [[right ventricle]] to the [[right atrium]], the opposite of the normal direction. The pathophysiology of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the [[tricuspid valve]], such as the leaflets, [[chordae tendineae]], or [[papillary muscle]]s.<ref name="pmid19470900">{{cite journal| author=Rogers JH, Bolling SF| title=The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. | journal=Circulation | year= 2009 | volume= 119 | issue= 20 | pages= 2718-25 | pmid=19470900 | doi=10.1161/CIRCULATIONAHA.108.842773 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19470900 }} </ref> Secondary TR results from hemodynamic and structural changes in the [[right ventricle]] and [[tricuspid valve]] apparatus secondary to [[left heart failure]] and/or [[pulmonary hypertension]]. Tricuspid annular dilation is the most important factor in the pathophysiology of secondary TR. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR.<ref name="pmid22340261">{{cite journal| author=Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O| title=The growing clinical importance of secondary tricuspid regurgitation. | journal=J Am Coll Cardiol | year= 2012 | volume= 59 | issue= 8 | pages= 703-10 | pmid=22340261 | doi=10.1016/j.jacc.2011.09.069 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22340261 }} </ref> | |||
==Causes== | |||
Most cases of tricuspid regurgitation are due to dilation of the [[right ventricle]], although congenital causes exist. Such dilation leads to derangement of the normal anatomy and mechanics of the [[tricuspid valve]] and the muscles governing its proper function. The result is incompetence of the tricuspid valve. Common causes of right ventricular dilation include [[left heart failure]], [[pulmonary hypertension]], and right ventricular [[infarction]]. One notable exception to right ventricular dilation as a cause of tricuspid insufficiency occurs in right-sided [[endocarditis]] (i.e. infection affecting the right side of the heart). In that case, there is direct damage to the tricuspid valve as as a result of infection. | |||
==Differential Diagnosis== | |||
The blowing [[holosystolic murmur]] of tricuspid regurgitation must be distinguished from [[mitral regurgitation]] and a [[ventricular septal defect]]. | |||
==Epidemiology and Demographics== | |||
The prevalence of tricuspid regurgitation (TR) of a severity ≥ mild is approximately 15% in men and 18% in women.<ref name="pmid10190406">{{cite journal| author=Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL et al.| title=Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study) | journal=Am J Cardiol | year= 1999 | volume= 83 | issue= 6 | pages= 897-902 | pmid=10190406 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10190406 }} </ref> Secondary TR is more common than primary TR.<ref name="pmid3657250">{{cite journal| author=Cohen SR, Sell JE, McIntosh CL, Clark RE| title=Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. I. Prevalence, diagnosis, and comparison of preoperative clinical and hemodynamic features in patients with and without tricuspid regurgitation. | journal=J Thorac Cardiovasc Surg | year= 1987 | volume= 94 | issue= 4 | pages= 481-7 | pmid=3657250 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3657250 }} </ref> | |||
==Natural History, Complications and Prognosis== | |||
==Diagnosis== | |||
===Stages=== | |||
===History and Symptoms=== | |||
===Physical Examination=== | |||
===Chest X ray=== | |||
===Electrocardiogram=== | |||
===Echocardiography=== | |||
===Cardiac Stress Test=== | |||
===Cardiac MRI=== | |||
===Cardiac Catherization=== | |||
==Treatment== | |||
===Medical Therapy=== | |||
===Surgery=== | |||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
Overview
Tricuspid insufficiency, a valvular heart disease also called Tricuspid regurgitation, refers to the failure of the heart's tricuspid valve to close properly during systole. As a result, with each heart beat, a portion of the blood is pumped out from the right side of the heart backwards in the opposite direction into the right atrium rather than forwards into the right ventricle.
Classification
Tricuspid regurgitation (TR) can be classified into primary and secondary. Primary (or organic) TR results from an organic lesion of the tricuspid valve itself, whereas secondary (or functional) TR is caused by left heart failure or pulmonary hypertension without an intrinsic abnormality of the tricuspid valve.
Pathophysiology
Tricuspid regurgitation (TR) refers to the failure of the tricuspid valve to close properly during systole. As a result, with each heart beat some blood passes from the right ventricle to the right atrium, the opposite of the normal direction. The pathophysiology of TR depends on whether TR is primary or secondary. Primary TR results from an organic abnormality in one or more parts of the tricuspid valve, such as the leaflets, chordae tendineae, or papillary muscles.[1] Secondary TR results from hemodynamic and structural changes in the right ventricle and tricuspid valve apparatus secondary to left heart failure and/or pulmonary hypertension. Tricuspid annular dilation is the most important factor in the pathophysiology of secondary TR. In addition, tethering of the leaflets and inadequate leaflet coaptation also contribute to secondary TR.[2]
Causes
Most cases of tricuspid regurgitation are due to dilation of the right ventricle, although congenital causes exist. Such dilation leads to derangement of the normal anatomy and mechanics of the tricuspid valve and the muscles governing its proper function. The result is incompetence of the tricuspid valve. Common causes of right ventricular dilation include left heart failure, pulmonary hypertension, and right ventricular infarction. One notable exception to right ventricular dilation as a cause of tricuspid insufficiency occurs in right-sided endocarditis (i.e. infection affecting the right side of the heart). In that case, there is direct damage to the tricuspid valve as as a result of infection.
Differential Diagnosis
The blowing holosystolic murmur of tricuspid regurgitation must be distinguished from mitral regurgitation and a ventricular septal defect.
Epidemiology and Demographics
The prevalence of tricuspid regurgitation (TR) of a severity ≥ mild is approximately 15% in men and 18% in women.[3] Secondary TR is more common than primary TR.[4]
Natural History, Complications and Prognosis
Diagnosis
Stages
History and Symptoms
Physical Examination
Chest X ray
Electrocardiogram
Echocardiography
Cardiac Stress Test
Cardiac MRI
Cardiac Catherization
Treatment
Medical Therapy
Surgery
References
- ↑ Rogers JH, Bolling SF (2009). "The tricuspid valve: current perspective and evolving management of tricuspid regurgitation". Circulation. 119 (20): 2718–25. doi:10.1161/CIRCULATIONAHA.108.842773. PMID 19470900.
- ↑ Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O (2012). "The growing clinical importance of secondary tricuspid regurgitation". J Am Coll Cardiol. 59 (8): 703–10. doi:10.1016/j.jacc.2011.09.069. PMID 22340261.
- ↑ Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL; et al. (1999). "Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study)". Am J Cardiol. 83 (6): 897–902. PMID 10190406.
- ↑ Cohen SR, Sell JE, McIntosh CL, Clark RE (1987). "Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. I. Prevalence, diagnosis, and comparison of preoperative clinical and hemodynamic features in patients with and without tricuspid regurgitation". J Thorac Cardiovasc Surg. 94 (4): 481–7. PMID 3657250.