Fig. 11.17A and B ) or annular (in the mitral valve) (
Fig. 11.17C and D ). Mitral annular calcification is usually asymptomatic unless it encroaches on the adjacent conduction system.
Alterations in the ECM. In some cases, changes consist of increased proteoglycan and diminished fibrillar collagen and elastin (myxomatous degeneration); in other cases, the valve becomes fibrotic and scarred.
Changes in the production of matrix metalloproteinases or their inhibitors
Degenerative changes in the cardiac valves are probably an inevitable aspect of aging related to the repetitive mechanical stresses to which valves are subjected—40 million beats per year, with each normal opening and closing requiring substantial valve deformation.
Calcific aortic degeneration is the most common cause of aortic stenosis. In most cases, calcific degeneration is asymptomatic and is discovered only incidentally by viewing
Table 11.4 Etiology of Acquired Heart Valve Disease (myocarditis,dilatedcardiomyopathy)Calcificationofmitralring
Fen-phen, Fenfluramine-phentermine.DatafromSchoenFJ:Surgicalpathologyofremovednaturalandprostheticvalves,Hum Pathol 18:558,1987.
Fig. 11.17 Calcificvalvulardegeneration.(A)Calcificaorticstenosisofapreviouslynormalvalve(viewedfromabovethevalve).NodularmassesofcalciumareheapedupwithinthesinusesofValsalva(arrow).Notethatthecommissuresarenotfused,asinrheumaticaorticvalvestenosis(see
Fig.
11.19C ).(B)Calcificaorticstenosisoccurringonacongenitallybicuspidvalve.Onecusphasapartialfusionatitscenter,calledaraphe(arrow).(CandD)Mitralcalcification,withcalcificnoduleswithintheannulus(attachmentmargin)ofthemitralleaflets(arrows). (C)Leftatrialview.(D)Sectiondemonstratingtheextensionofcalcificationintotheunderlyingmyocardium.Suchinvolvementofadjacentstructuresneartheinterventricularseptumcanimpingeontheconductionsystem.
http://ebooksmedicine.net calcifications on a routine chest radiograph or at autopsy. In other patients, valvular sclerosis and/or calcification can be severe enough to cause stenosis, necessitating surgical intervention. The incidence of calcific aortic stenosis is increasing in pace with longevity. In anatomically normal valves, it typically begins to manifest when patients reach their 70s and 80s; onset with bicuspid aortic valves is at a much earlier age (often 40 to 50 years of age).
Although simple progressive age-associated “wear and tear” is often invoked to explain the process, cuspal fibrosis and calcification also can be viewed as the valvular counterparts to age-related arteriosclerosis. Thus, chronic injury due to hyperlipidemia, hypertension, inflammation, and other factors implicated in atherosclerosis have been proposed as contributors to valvular degenerative changes, but firm evidence is lacking.
opening(Fig.
11.17AandB );commissuralfusion(usuallyasignofpreviousinflammation)isnotatypicalfeatureofdegenerativeaorticstenosis,althoughthecuspsmaybecomesecondarilyfibrosedandthickened.Anearlier,hemodynamicallyinconsequentialstageofthecalcificationprocessiscalledaortic valve sclerosis.