Valve failure or dysfunction can result in diminished heart functionality, though the particular consequences are dependent on the type and severity of valvular disease.

[citation needed] Stenosis and insufficiency/regurgitation represent the dominant functional and anatomic consequences associated with valvular heart disease.

[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.

[5] Aortic insufficiency, or regurgitation, is characterized by an inability of the valve leaflets to appropriately close at the end systole, thus allowing blood to flow inappropriately backward into the left ventricle.

In these cases, the left ventricle of the heart becomes enlarged and causes displacement of the attached papillary muscles, which control the mitral.

[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.

[11] Tricuspid valve stenosis without co-occurrent regurgitation is highly uncommon and typically the result of rheumatic disease.

[12] In more severe cases it is a consequence of dilation of the right ventricle, leading to displacement of the papillary muscles which control the valve's ability to close.

[13] Dilation of the right ventricle occurs secondary to ventricular septal defects, right to left shunting of blood, eisenmenger syndrome, hyperthyroidism, and pulmonary stenosis.

[16] Auscultation may reveal a systolic murmur of a harsh crescendo-decrescendo type, heard in 2nd right intercostal space[15] and radiating to the carotid arteries.

[16] The murmur is heard best with the bell of the stethoscope[16] lying on the left side[15] and its duration increases with worsening disease.

[16] On auscultation of a patient with mitral stenosis, there may be a holosystolic murmur at the apex, radiating to the back or clavicular area,[16] a third heart sound,[16] and a loud, palpable P2,[16] heard best when lying on the left side.

[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] Patients with tricuspid regurgitation may experience symptoms of right-sided heart failure, such as ascites, hepatomegaly, edema and jugular venous distension.

[16] Signs of tricuspid regurgitation include pulsatile liver, prominent V waves and rapid y descents in jugular venous pressure.

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.

[24] This results in generalized inflammation in the heart, producing acute erosions and vegetations with fibrin deposition in the mitral valve that may be followed by chronic changes over years to decades, including shortening of the chordae tendinae and thickening or fusion of the mitral leaflets, leading to a severely compromised "buttonhole" or "fish mouth" valve.

[31] Typically the pump function of the heart during systole is normal, but an echocardiogram will show flow reversal during diastole.

[8] Chest x-ray in 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.

[8] 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.

[36] Any angina is treated with short-acting nitrovasodilators, beta-blockers and/or calcium blockers, although nitrates can drastically decrease blood pressure in patients with severe aortic stenosis and are therefore contraindicated.

[15] Any heart failure is treated with digoxin, diuretics, nitrovasodilators and, if not contraindicated, cautious inpatient administration of ACE inhibitors.

[8] Hypertension is treated in patients with chronic aortic regurgitation, with the anti-hypersensives of choice being calcium channel blockers, ACE inhibitors, or ARBs.

[15] In severe moderate/severe cases, patients should be followed with echocardiography and cardiac stress test and/or isotope perfusion imaging every 3–6 months.

[8] Anticoagulation is recommended for patients that have mitral stenosis in the setting of atrial fibrillation or a previous embolic event.

[39] This valve disease is primarily caused by aortic root dilation, but infective endocarditis has been an increased risk factor.

[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.