Valvular heart disease

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Valvular heart disease
Classification and external resources
ICD-10 I34-I37, I05-I08, Q22-Q23
ICD-9 394-396, 424, 746
MeSH D006349

Valvular heart disease is any disease process involving one or more of the four valves of the heart (the aortic and mitral valves on the left and the pulmonary and tricuspid valves on the right). Collectively and anatomically, the valves are part of the dense connective tissue makeup of the heart known as the cardiac skeleton. Valve problems may be congenital (inborn) or acquired (due to another cause later in life). Treatment may be with medication but often (depending on the severity) involves valve repair or replacement (insertion of an artificial heart valve). Specific situations include those where additional demands are made on the circulation, such as in pregnancy.[1]

Types[edit]

Phonocardiograms from normal and abnormal heart sounds.png
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[edit]

These are termed left heart diseases.

Pulmonary and tricuspid valve disorders[edit]

Pulmonary and tricuspid valve diseases are right heart diseases. Pulmonary valve diseases are the least common heart valve disease in adults.[2]

The most common types of pulmonary valve diseases are:

  • pulmonary valve stenosis
  • pulmonary valve insufficiency
    • pulmonary valve incompetence
    • pulmonary valve regurgitation

The International Statistical Classification of Diseases classifies non rheumatic pulmonary valve diseases as I37.

Both tricuspid and pulmonary valve diseases are less common than aortic or mitral valve diseases due to the lower pressure those valves experience.[2]

Dysplasia[edit]

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.[1]

Rheumatic disorders[edit]

Valvular heart disease resulting from rheumatic fever is referred to as "rheumatic heart disease". 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 and there has been a resurgence in efforts to eradicate the diseases in these populations. Inflammation of the heart valves due to any cause is called endocarditis; this is usually due to bacterial infection but may also be due to cancer (marantic endocarditis), certain autoimmune conditions (Libman-Sacks endocarditis) and hypereosinophilic syndrome (Loeffler endocarditis). Certain medications have been associated with valvular heart disease, most prominently ergotamine derivatives pergolide and cabergoline.[3]

In pregnancy[edit]

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 an intercurrent 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.[4] 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.[4] 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.[4] 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.[4] 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 increases in systolic and diastolic blood pressure.[4]

Valvular heart lesions associated with high maternal and fetal risk during pregnancy include:[4]

  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

[4]

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.

Comparison[edit]

The following table includes the main types of valvular stenosis and regurgitation. Major types of valvular heart disease not included in the table include mitral valve prolapse, rheumatic heart disease and endocarditis.

Valvular disease Mitral stenosis Aortic stenosis Aortic regurgitation Mitral regurgitation Tricuspid regurgitation
Prevalence Most common valvular heart disease in pregnancy[5] Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85[6] 2% of the population, equally in males and females.[7]
Main causes and risk factors Almost always caused by rheumatic heart disease[8]

Hypertension, diabetes mellitus, hyperlipoproteinemia and uremia may speed up the process.[9]

Acute

Chronic

Acute

Chronic

Hemo
dynamics

/
Patho-
physiology
Progressive obstruction of the mitral ostium causes increased pressure in the left atrium and the pulmonary circulation.[9] Congestion may cause thromboembolism, and atrial hypertension may cause atrial fibrillation.[9] Obstruction through the aortic ostium causes increased pressure in the left ventricle and impaired flow through the aorta Insufficiency of the aortic valve causes backflow of blood into the left ventricle during diastole. Insufficiency of the mitral valve causes backflow of blood into the left atrium during systole. Insufficiency of the tricuspid valve causes backflow of blood into the right atrium during systole.
Symptoms

Symptoms increase with exercise and pregnancy[8]

Medical signs

Signs increase with exercise and pregnancy[8]

In acute cases, the murmur and tachycardia may be only distinctive signs.[9]

Diagnosis
  • Chest X-ray showing calcific aortic valve, and in longstanding disease, enlarged left ventricle[8][9] and atrium[8]
  • ECG showing left ventricular hypertrophy and left atrial abnormality[8]
  • Echocardiography is diagnostic in most cases, showing left ventricular hyperthrophy, thickened and immobile aortic valve and dilated aortic root,[8] but may appear normal if acute[9]
  • Cardiac chamber catheterization provides a definitive diagnosis, indicating severe stenosis in valve area of <0.8 cm2 (normally 3 to 4 cm2). It is useful in symptomatic patients before surgery.[8]
  • Chest X-ray showing left ventricular hypertrophy and dilated aorta[8]
  • ECG indicating left ventricular hypertrophy[8]
  • Echocardiogram showing dilated left aortic root and reversal of blood flow in the aorta. In longstanding disease there may be left ventricular dilatation. In acute aortic regurgitation, there may be early closure of the mitral valve.[8]
  • Cardiac chamber catetherization assists in assessing the severity of regurgitation and any left ventricular dysfunction[8]
  • Chest X-ray showing dilated left ventricle[8]
  • Echocardiography to detect mitral reverse flow, dilated left atrium and ventricle and decreased left ventricular function[8]
Treatment

No therapy is required for asymptomatic patients. Diuretics for any pulmonary congestion or edema.[8] If stenosis is severe, surgery is recommended.[8] Any atrial fibrillation is treated accordingly.[8]

No treatment in asymptomatic patients.[8]

Medical therapy and percutaneous balloon valvuloplasty have relatively poor effect.[8]
- Any angina is treated with short-acting nitrovasodilators, beta-blockers and/or calcium blockers[9]
- Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers[9]
- Any heart failure is treated with digoxin, diuretics, nitrovasodilators and, if not contraindicated, cautious inpatient administration of ACE inhibitors[9]

Also, endocarditis prophylaxis is indicated before dental, gastrointestinal or genitourinary procedures.[8]

Follow-up
  • In moderate cases, echocardiography every 1–2 years, possibly complemented with cardiac stress test.[9] Immediate revisit if new related symptoms appear.[9]
  • In severe cases, echocardiography every 3–6 months.[9] Immediate revisit or inpatient care if new related symptoms appear.[9]
  • In mild to moderate cases, echocardiography and cardiac stress test every 1–2 years[9]
  • In severe moderate/severe cases, echocardiography with cardiac stress test and/or isotope perfusion imaging every 3–6 months.[9]
  • In mild to moderate cases, echocardiography and cardiac stress test every 1–3 years.[9]
  • In severe cases, echocardiography every 3–6 months.[9]

References[edit]

  1. ^ a b Bonow RO, Carabello BA, Kanu C, et al. (2006). "ACC/AHA 2006 guidelines 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 (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons". Circulation 114 (5): e84–231. doi:10.1161/CIRCULATIONAHA.106.176857. PMID 16880336. 
  2. ^ 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.
  3. ^ Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E (2007). "Dopamine agonists and the risk of cardiac-valve regurgitation". N. Engl. J. Med. 356 (1): 29–38. doi:10.1056/NEJMoa062222. PMID 17202453. 
  4. ^ a b c d e f g Bonow, RO; Carabello, BA; Chatterjee, K; De Leon Jr, AC; Faxon, DP; Freed, MD; Gaasch, WH; Lytle, BW et al. (2008). "2008 focused update incorporated into the ACC/AHA 2006 guidelines 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 (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Journal of the American College of Cardiology 52 (13): e1–142. doi:10.1016/j.jacc.2008.05.007. PMID 18848134. 
  5. ^ Gelson, E.; Gatzoulis, M.; Johnson, M. (2007). "Valvular heart disease". BMJ (Clinical research ed.) 335 (7628): 1042–1045. doi:10.1136/bmj.39365.655833.AE. PMC 2078629. PMID 18007005.  edit
  6. ^ Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol. 1997; 29: 630-634.
  7. ^ The Cleveland Clinic Center for Continuing Education > Mitral Valve Disease: Stenosis and Regurgitation Authors: Ronan J. Curtin and Brian P. Griffin. Retrieved September 2010
  8. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by bz ca cb cc cd ce cf cg ch ci cj ck cl cm cn co cp cq cr cs ct cu cv cw cx cy cz da db dc dd Chapter 1: Diseases of the Cardiovascular system > Section: Valvular Heart Disease in: Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6. 
  9. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au 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

External links[edit]