Valvular heart disease

Source: Wikipedia, the free encyclopedia.
Valvular heart disease
Phonocardiogram of normal and abnormal heartbeats.
SpecialtyCardiology
Diagnostic methodChest radiograph
Mitral Valve Prolapse murmur
Heart sounds of a 16-year-old girl diagnosed with mitral valve prolapse and mitral regurgitation. Auscultating her heart, a systolic murmur and click are heard. Recorded with the stethoscope over the mitral valve.
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Valvular heart disease is any

rheumatic heart disease and pregnancy.[2]

Anatomically, the valves are part of the dense connective tissue of the heart known as the

valve repair or valve replacement
.

Classification

This diagram shows the valves of the heart. The aortic and mitral valves are shown in the left heart, and the tricuspid and pulmonic valves are shown in the right heart.

Stenosis and insufficiency/regurgitation represent the dominant functional and anatomic consequences associated with valvular heart disease. Irrespective of disease process, alterations to the valve occur that produce one or a combination of these conditions. Insufficiency and regurgitation are synonymous terms that describe an inability of the valve to prevent backflow of blood as leaflets of the valve fail to join (coapt) correctly. Stenosis is characterized by a narrowing of the valvular orifice that prevents adequate outflow of blood. Stenosis can also result in insufficiency if thickening of the annulus or leaflets results in inappropriate leaf closure.[3]

Valve involved Stenotic disease Insufficiency/regurgitation disease
Aortic valve
Aortic valve stenosis
Aortic insufficiency
/regurgitation
Mitral valve
Mitral valve stenosis
Mitral insufficiency
/regurgitation
Tricuspid valve Tricuspid valve stenosis
Tricuspid insufficiency
/regurgitation
Pulmonary valve Pulmonary valve stenosis
Pulmonary insufficiency
/regurgitation

Aortic and mitral valve disorders

Aortic and mitral valve disorders are

right heart due to the higher pressures in the left heart.[4]

Stenosis of the aortic valve is characterized by a thickening of the valvular annulus or leaflets that limits the ability of blood to be ejected from the left ventricle into the aorta. Stenosis is typically the result of valvular calcification but may be the result of a congenitally malformed bicuspid aortic valve. This defect is characterized by the presence of only two valve leaflets. It may occur in isolation or in concert with other cardiac anomalies.[5]

Aortic insufficiency, or regurgitation, is characterized by an inability of the valve leaflets to appropriately close at the end

systemic lupus erythematosus, respectively. Processes that lead to aortic insufficiency usually involve dilation of the valve annulus, thus displacing the valve leaflets, which are anchored in the annulus.[5]

Mitral stenosis is caused largely by rheumatic heart disease, though is rarely the result of calcification. In some cases, vegetations form on the mitral leaflets as a result of endocarditis, an inflammation of the heart tissue. Mitral stenosis is uncommon and not as age-dependent as other types of valvular disease.[1]

Mitral insufficiency can be caused by dilation of the left heart, often a consequence of heart failure. In these cases, the left ventricle of the heart becomes enlarged and causes displacement of the attached papillary muscles, which control the mitral.[7]

Pulmonary and tricuspid valve disorders

Pulmonary and tricuspid valve diseases are

right heart diseases. Pulmonary valve diseases are the least common heart valve disease in adults.[1][4]

Pulmonary valve stenosis is often the result of congenital malformations and is observed in isolation or as part of a larger pathologic process, as in Tetralogy of Fallot, Noonan syndrome, and congenital rubella syndrome. Unless the degree of stenosis is severe, individuals with pulmonary stenosis usually have excellent outcomes and better treatment options. Often patients do not require intervention until later in adulthood as a consequence of calcification that occurs with aging.[citation needed]

Pulmonary valve insufficiency occurs commonly in healthy individuals to a very mild extent and does not require intervention.[8] More appreciable insufficiency is typically the result of damage to the valve due to cardiac catheterization, intra-aortic balloon pump insertion, or other surgical manipulations. Additionally, insufficiency may be the result of carcinoid syndrome, inflammatory processes such a rheumatoid disease or endocarditis, or congenital malformations.[9][10] It may also be secondary to severe pulmonary hypertension.[11]

Tricuspid valve stenosis without co-occurrent regurgitation is highly uncommon and typically the result of rheumatic disease. It may also be the result of congenital abnormalities, carcinoid syndrome, obstructive right atrial tumors (typically lipomas or myxomas), or hypereosinophilic syndromes.[citation needed]

Minor tricuspid insufficiency is common in healthy individuals.

pulmonary stenosis. Tricuspid insufficiency may also be the result of congenital defects of the tricuspid valve, such as Ebstein's anomaly.[14]

Signs and symptoms

Aortic stenosis

Symptoms of

angina pectoris,[16] and syncope, usually exertional.[16]

Medical signs of aortic stenosis include pulsus parvus et tardus, that is, diminished and delayed

2nd right intercostal space[15] and radiating to the carotid arteries.[16]

Aortic regurgitation

Patients with

circulatory shock.[16]

Medical signs of aortic regurgitation include increased

water hammer pulse, Austin Flint murmur, and a displaced apex beat down and to the left.[16] A third heart sound may be present[16]

Mitral stenosis

Patients with

paroxysmal nocturnal dyspnea, palpitations, chest pain, hemoptysis, thromboembolism, or ascites and edema (if right-sided heart failure develops).[16] Symptoms of mitral stenosis increase with exercise and pregnancy[16]

On

jugular venous distension, hepatomegaly, ascites and/or pulmonary hypertension (presenting with a loud P2).[16] Signs increase with exercise and pregnancy.[16]

Mitral regurgitation

Patients with

paroxysmal nocturnal dyspnea,[16] palpitations,[16] or pulmonary edema.[16]

On auscultation of a patient with mitral stenosis, there may be a

P2,[16] heard best when lying on the left side.[15] Patients also commonly have atrial fibrillation.[16] Patients may have a laterally displaced apex beat,[16] often with heave[15] In acute cases, the murmur and tachycardia may be only distinctive signs.[15]

Tricuspid regurgitation

Patients with

jugular venous distension.[16]

Signs of tricuspid regurgitation include

left lower sternal border (LLSB)[16] and a blowing holosystolic murmur at LLSB, intensifying with inspiration, and decreasing with expiration and Valsalva maneuver.[16] Patients may have a parasternal heave along LLSB.[16] Atrial fibrillation is usually present in patients with tricuspid regurgitation[16]

Causes

Calcific disease

hyperlipoproteinemia and uremia may speed up the process of valvular calcification.[15]

Dysplasia

Heart valve dysplasia is an error in the development of any of the heart valves, and a common cause of congenital heart defects in humans as well as animals; tetralogy of Fallot is a congenital heart defect with four abnormalities, one of which is stenosis of the pulmonary valve. Ebstein's anomaly is an abnormality of the tricuspid valve, and its presence can lead to tricuspid valve regurgitation.[16][18] A bicuspid aortic valve[16] is an aortic valve with only 2 cusps as opposed to the normal 3. It is present in about 0.5% to 2% of the general population and causes increased calcification due to higher turbulent flow through the valve.[17]

Connective tissue disorders

Marfan's Syndrome is a connective tissue disorder that can lead to chronic aortic or mitral regurgitation.[16] Osteogenesis imperfecta is a disorder in formation of type I collagen and can also lead to chronic aortic regurgitation.[16]

Inflammatory disorders

Inflammation of the heart valves due to any cause is called valvular

systemic lupus erythematosus) and hypereosinophilic syndrome (Loeffler endocarditis). Endocarditis of the valves can lead to regurgitation through that valve, which is seen in the tricuspid, mitral, and aortic valves.[16] Certain medications have been associated with valvular heart disease, most prominently ergotamine derivatives pergolide and cabergoline.[19]

Valvular heart disease resulting from

chordae tendinae and thickening or fusion of the mitral leaflets, leading to a severely compromised "buttonhole" or "fish mouth" valve.[25]

In 70% of cases rheumatic heart disease involves only the mitral valve, while 25% of cases involve both the aortic and mitral valves. Involvement of other heart valves without damage to the mitral is exceedingly rare.[23] Mitral stenosis is almost always caused by rheumatic heart disease.[16] Less than 10% of aortic stenosis is caused by rheumatic heart disease.[15][16] Rheumatic fever can also cause chronic mitral and aortic regurgitation.[16]

While developed countries once had a significant burden of rheumatic fever and rheumatic heart disease, medical advances and improved social conditions have dramatically reduced their incidence. Many developing countries, as well as indigenous populations within developed countries, still carry a significant burden of rheumatic fever and rheumatic heart disease

secondary prophylaxis against additional streptococcal infections, which can contribute to progression of rheumatic heart disease.[27] In people with severe valvular disease, however, short-term risks of cardiovascular compromise after intramuscular injections may outweigh the benefits, and oral therapy may be considered instead of IM injections in this subset of patients.[28]

Diseases of the aortic root can cause chronic aortic regurgitation. These diseases include syphilitic aortitis, Behçet's disease, and reactive arthritis.[16]

Heart disease

Tricuspid regurgitation is usually secondary to right ventricular dilation

myxomatous degeneration.[16]

Diagnosis

Aortic stenosis

ECG showing left ventricular hypertrophy, these findings may be present in aortic stenosis.

Patients with

ECG typically shows left ventricular hypertrophy in patients with severe stenosis, but it may also show signs of left heart strain.[30] Echocardiography is the diagnostic gold standard, which shows left ventricular hypertrophy, leaflet calcification, and abnormal leaflet closure.[30]

Diagnostic classification of aortic stenosis[30]
Classification Valve area
Mild aortic stenosis 1.5-2.0 cm2
Moderate aortic stenosis 1.0-1.5 cm2
Severe aortic stenosis <1.0 cm2

Aortic regurgitation

echocardiogram can be helpful in determining the root cause of the disease, as it will clearly show aortic root dilation or dissection if it exists.[31] Typically the pump function of the heart during systole is normal, but an echocardiogram will show flow reversal during diastole.[31] This disease is classified using regurgitant fraction (RF), or the amount of volume that flows back through the valve divided by the total forward flow through the valve during systole. Severe disease has an RF of >50%, while progressive aortic regurgitation has an RF of 30–49%.[8]

Mitral stenosis

mitral stenosis will typically show an enlarged left atrium, and may show dilation of the pulmonary veins.[32] ECG can show left atrial enlargement, due to increased pressures in the left atrium.[32] Echocardiography is helpful in determining the severity of the disease by estimating the pulmonary artery systolic pressure.[32] This test can also show leaflet calcification and the pressure gradient over the mitral valve.[32] Severe mitral stenosis is defined as a mitral valve area <1.5 cm2.[8] Progressive mitral stenosis has a normal valve area but will have increased flow velocity across the mitral valve.[8]

Mitral regurgitation

mitral regurgitation can show an enlarged left atrium, as well as pulmonary venous congestion.[33] It may also show valvular calcifications specifically in combined mitral regurgitation and stenosis due to rheumatic heart disease.[33] ECG typically shows left atrial enlargement, but can also show right atrial enlargement if the disease is severe enough to cause pulmonary hypertension.[33] Echocardiography is useful in visualizing the regurgitant flow and calculating the RF.[33] It can also be used to determine the degree of calcification, and the function and closure of the valve leaflets.[33] Severe disease has an RF of >50%, while progressive mitral regurgitation has an RF of <50%.[8]

Treatment

Some of the most common treatments of valvular heart disease are avoiding smoking and excessive alcohol consumption, antibiotics, antithrombotic medications such as aspirin, anticoagulants, balloon dilation, and water pills.[34] In some cases, surgery may be necessary.

Aortic stenosis

Treatment of aortic stenosis is not necessary in asymptomatic patients, unless the stenosis is classified as severe based on valve hemodynamics.

cardiovascular death, hospitalization with heart failure due to progression of aortic valve stenosis, or aortic valve replacement surgery).[37] In patients with non-severe asymptomatic aortic valve stenosis and no overt coronary artery disease, the increased troponin T (above 14 pg/mL) was found associated with an increased 5-year event rate of ischemic cardiac events (myocardial infarction, percutaneous coronary intervention, or coronary artery bypass surgery).[38]

Aortic regurgitation

isotope perfusion imaging every 3–6 months.[15]

Mitral stenosis

For patients with symptomatic severe mitral stenosis, percutaneous balloon mitral valvuloplasty (PBMV) is recommended.[8] If this procedure fails, then it may be necessary to undergo mitral valve surgery, which may involve valve replacement, repair, or commisurotomy.[8] Anticoagulation is recommended for patients that have mitral stenosis in the setting of atrial fibrillation or a previous embolic event.[8] No therapy is required for asymptomatic patients. Diuretics may be used to treat pulmonary congestion or edema.[16]

Mitral regurgitation

Surgery is recommended for chronic severe mitral regurgitation in symptomatic patients with left ventricular ejection fraction (LVEF) of greater than 30%, and asymptomatic patients with LVEF of 30-60% or left ventricular end diastolic volume (LVEDV) > 40%.[8] Surgical repair of the leaflets is preferred to mitral valve replacement as long as the repair is feasible.[8] Mitral regurgitation may be treated medically with vasodilators, diuretics, digoxin, antiarrhythmics, and chronic anticoagulation.[15][16] Mild to moderate mitral regurgitation should be followed with echocardiography and cardiac stress test every 1–3 years.[15] Severe mitral regurgitation should be followed with echocardiography every 3–6 months.[15]

Epidemiology

In the United States, about 2.5% of the population has moderate to severe valvular heart disease.[39] The prevalence of these diseases increase with age, and 75 year-olds in the United States have a prevalence of about 13%.[39] In industrially underdeveloped regions, rheumatic disease is the most common cause of valve diseases, and it can cause up to 65% of the valve disorders seen in these regions.[39]

Aortic stenosis

Aortic stenosis is typically the result of aging, occurring in 12.4% of the population over 75 years of age, and represents the most common cause of outflow obstruction in the left ventricle.[1] Bicuspid aortic valves are found in up to 1% of the population, making it one of the most common cardiac abnormalities.[40]

Aortic regurgitation

The prevalence of aortic regurgitation also increases with age. Moderate to severe disease has a prevalence of 13% in patients between the ages of 55 and 86.[39] This valve disease is primarily caused by aortic root dilation, but infective endocarditis has been an increased risk factor. It has been found to be the cause of aortic regurgitation in up to 25% of surgical cases.[39]

Mitral stenosis

rheumatic heart disease, and has a prevalence of about 0.1% in the United States.[39] Mitral stenosis is the most common valvular heart disease in pregnancy.[41]

Mitral regurgitation

Mitral regurgitation is significantly associated with normal aging, rising in prevalence with age. It is estimated to be present in over 9% of people over 75.[1]

Special populations

Pregnancy

The evaluation of individuals with valvular heart disease who are or wish to become

pregnant is a difficult issue. Issues that have to be addressed include the risks during pregnancy to the mother and the developing fetus by the presence of maternal valvular heart disease as a pre-existing disease in pregnancy
. Normal physiological changes during pregnancy require, on average, a 50% increase in circulating blood volume that is accompanied by an increase in cardiac output that usually peaks between the midportion of the second and third trimesters.[42] The increased cardiac output is due to an increase in the stroke volume, and a small increase in heart rate, averaging 10 to 20 beats per minute.[42] Additionally uterine circulation and endogenous hormones cause systemic vascular resistance to decrease and a disproportionately lowering of diastolic blood pressure causes a wide pulse pressure.[42] Inferior vena caval obstruction from a gravid uterus in the supine position can result in an abrupt decrease in cardiac preload, which leads to hypotension with weakness and lightheadedness.[42] During labor and delivery cardiac output increases more in part due to the associated anxiety and pain, as well as due to uterine contractions which will cause an increase in systolic and diastolic blood pressure.[42]

Valvular heart lesions associated with high maternal and fetal risk during pregnancy include:[42]

  1. Severe aortic stenosis with or without symptoms
  2. Aortic regurgitation with
    NYHA
    functional class III-IV symptoms
  3. Mitral stenosis with NYHA functional class II-IV symptoms
  4. Mitral regurgitation with NYHA functional class III-IV symptoms
  5. Aortic and/or mitral valve disease resulting in severe pulmonary hypertension (pulmonary pressure greater than 75% of systemic pressures)
  6. Aortic and/or mitral valve disease with severe LV dysfunction (EF less than 0.40)
  7. Mechanical prosthetic valve requiring anticoagulation
  8. Marfan syndrome with or without aortic regurgitation

[42]

In individuals who require an artificial heart valve, consideration must be made for deterioration of the valve over time (for bioprosthetic valves) versus the risks of blood clotting in pregnancy with mechanical valves with the resultant need of drugs in pregnancy in the form of anticoagulation.[citation needed]

References

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  2. ^ Pregnancy and contraception in congenital heart disease: what women are not told. Kovacs AH, Harrison JL, Colman JM, Sermer M, Siu SC, Silversides CK J Am Coll Cardiol. 2008;52(7):577.
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  4. ^ a b Ragavendra R. Baliga, Kim A. Eagle, William F Armstrong, David S Bach, Eric R Bates, Practical Cardiology, Lippincott Williams & Wilkins, 2008, page 452.
  5. ^ a b "Thoracic Aortic Aneurysms". The Lecturio Medical Concept Library. 28 September 2020. Retrieved 30 June 2021.
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  7. ^ "Mitral Regurgitation". The Lecturio Medical Concept Library. Retrieved 11 August 2021.
  8. ^ a b c d e f g h i j k l m n o 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, O'Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD. J Am Coll Cardiol. 2014;63(22):e57.
  9. ^ Isolated pulmonic valve infective endocarditis: a persistent challenge.[citation needed] Hamza N, Ortiz J, Bonomo. Infection. 2004 Jun;32(3):170-5.
  10. ^ Carcinoid heart disease. Clinical and echocardiographic spectrum in 74 patients. Pellikka PA, Tajik AJ, Khandheria BK, Seward JB, Callahan JA, Pitot HC, Kvols LK. Circulation. 1993;87(4):1188.
  11. ^ "What Is Pulmonary Hypertension?". NHLBI – NIH. 2 August 2011. Archived from the original on 28 July 2017. Retrieved 30 July 2017.
  12. Zoghbi WA
    , Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto CM, Quinones MA, Rakowski H, Stewart WJ, Waggoner A, Weissman NJ, American Society of Echocardiography. J Am Soc Echocardiogr. 2003;16(7):777.
  13. ^ Impact of tricuspid regurgitation on long-term survival. Nath J, Foster E, Heidenreich PA. J Am Coll Cardiol. 2004;43(3):405.
  14. ^ "Facts About Critical Congenital Heart Defects | NCBDDD | CDC". www.cdc.gov. 2017-06-27. Retrieved 2017-10-12.
  15. ^ a b c d e f g h i j k l m n o p q r s t u v w VOC=VITIUM ORGANICUM CORDIS, a compendium of the Department of Cardiology at Uppsala Academic Hospital. By Per Kvidal September 1999, with revision by Erik Björklund May 2008
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  20. ^ National Center for Immunization and Respiratory Diseases, Division of Bacterial Diseases (27 June 2022). "Acute Rheumatic Fever". Centers for Disease Control and Prevention. Retrieved 19 September 2022.
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  23. ^ a b Vinay, Kumar (2013). Robbin's Basic Pathology. Elsevier Health Sciences. pp. Chapter 10: Heart.
  24. ^ "Rheumatic heart disease". Heart & Stroke. Heart and Stroke Foundation of Canada. 2022.
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  26. ^ AIHW. "Australia's health 2020: data insights". Australian Institute of Health and Welfare. Australian Government. Retrieved 29 January 2021.
  27. ^ "Rheumatic Heart Disease". World Health Organization. 6 November 2020. Retrieved 20 September 2022.
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  39. ^ a b c d e f Chambers, John B.; Bridgewater, Ben (2014). Otto, CM; Bonow, RO (eds.). Epidemiology of Valvular Heart Disease (4th ed.). Saunders. pp. 1–13. {{cite book}}: |work= ignored (help)
  40. ^ Braverman AC. The Bicuspid Aortic Valve and Associated Aortic Disease. In: Valvular Heart Disease, 4th, Otto CM, Bonow RO. (Eds), Saunders/Elsevier, Philadelphia 2013. p.179.
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