Drug-,toxin-,orradiation-inducedvascularobstruction
Hypertensiveheartdiseasecanaffecteithertheleftventricleortherightventricle;inthelattercase,thedisorderismostoftenduetoprimarypulmonarydiseaseandiscalledcor pulmonale. Elevatedpressuresinducemyocytehypertrophyandinterstitialfibrosisthatincreaseswallthicknessandstiffness.
Thechronicpressureoverloadofsystemichypertensioncausesleftventricularconcentrichypertrophy,oftenassociatedwithleftatrialdilationduetoimpaireddiastolicfillingoftheventricle.Persistentlyelevatedpressureoverloadcancauseventricularfailurewithdilation.
Corpulmonaleresultsfrompulmonaryhypertensionduetoprimarylungparenchymalorvasculardisorders.Hypertrophyofboththerightventricleandtherightatriumischaracteristic;dilationalsomaybeseenwhenfailuresupervenes.
always due to a primary cuspal abnormality stemming from a chronic process (e.g., calcification or valve scarring).
• Insufficiency results from failure of a valve to close completely, thereby allowing regurgitation (backflow) of blood. Valvular insufficiency can result from either intrinsic disease of the valve cusps (e.g., endocarditis) or disruption of the supporting structures (e.g., the aorta, mitral annulus, tendinous cords, papillary muscles, or ventricular free wall) without primary cuspal injury. It can appear abruptly, as with chordal rupture, or insidiously as a consequence of leaflet scarring and retraction.
Stenosis or regurgitation may occur alone or together in the same valve. Valvular disease can involve only one valve (the mitral valve being the most common target), or more than one valve. Turbulent flow through diseased valves typically produces abnormal heart sounds called murmurs; severe lesions can even be externally palpated as thrills. Depending on the valve involved, murmurs are best heard at different locations on the chest wall; moreover, the nature (regurgitation versus stenosis) and severity of the valvular disease determines the quality and timing of the murmur (e.g., harsh systolic or soft diastolic murmurs).
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The outcome of valvular disease depends on the valve involved, the degree of impairment, the tempo of its development, and the effectiveness of compensatory mechanisms. For example, rapid destruction of an aortic valve cusp by infection can cause massive regurgitation and the abrupt onset of cardiac failure. By contrast, rheumatic mitral stenosis usually progresses over years, and its clinical effects are well tolerated until late in the course.
Valvular abnormalities can be congenital or acquired. By far the most common congenital valvular lesion is a bicuspid aortic valve, containing only two functional cusps instead of the normal three; this malformation occurs with a frequency of 1% to 2% of all live births, and has been associated with a number of mutations, including those affecting proteins of the Notch signaling pathway. The two cusps are of unequal size, with the larger cusp exhibiting a midline raphe resulting from incomplete cuspal separation (
Fig. 11.17B ). Bicuspid aortic valves are generally neither stenotic nor incompetent through early life; however, they are more prone to early and progressive degenerative calcification that gives rise to stenosis (see later).
The most important causes of acquired valvular diseases are summarized in
Table 11.4 ; acquired stenoses of the aortic and mitral valves account for approximately two thirds of all valve disease.
Degenerative valve disease is a term used to describe changes that affect the integrity of valvular ECM. Degenerative changes include the following:
Calcifications, which can be cuspal (typically in the aortic valve) (