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Comments Description Download ESSENTIALS OF ECHOCARDIOGRAPHY #2 Transcript ESSENTIALS OF ECHOCARDIOGRAPHY #2Diseases of the Heart ValvesJoseph A. Kisslo, MDDavid B. Adams, RDCSGraham J. Leech, MAThis unit covers the application of both M-mode and two-dimensional echocardiography in theinvestigation of acquire diseases of the heart valves, discussing the advantages and disadvantagesof each technique. Subsequent units will discuss the applications of echocardiography in heartmuscle disease and congenital disease. The Atrioventricular ValvesMitral StenosisIn mitral stenosis, fusion of the commissures between the mitral valve leaflets causes obstructionto left ventricular inflow. The leaflets also become infiltrated with fibrous tissue, whichproduces shrinkage, thickening and immobility, particularly at the tips of the leaflets (Fig. 1). Over a longer period, the fibrotic tissue may calcify and eventually the valve becomes a funnel-shaped structure that impedes blood flow as much by its rigidity as by actual stenosis of theorifice. Chronic elevation of left atrial pressure in mitral stenosis usually causes the chamber to dilate,although the extent to which this occurs depends additionally on atrial wall stiffness. Elevatedfilling pressure also results in pulmonary venous hypertension, and hence a rise in pulmonaryartery pressure. If severe, this leads eventually to right ventricular hypertrophy and thedevelopment of tricuspid regurgitation. The pathological changes in the valve apparatus produce dramatic alterations to theechocardiographic images (Fig. 2). On the M-mode recording, thickening of the leaflets andreduction in their mobility can be appreciated. Commissural fusion alters the motion of theposterior leaflet; instead of moving in the opposite direction to that of the anterior, it is pulledforward when the valve opens at the beginning of diastole. In the normal valve, rapid earlydiastolic filling of the left ventricle means that the valve can partially close in mid-diastole, and itthen reopens during atrial systole. This sequence produces the characteristic “M” shape of the recording, with the down slope of the“M” designated as the “E-F slope”. With mitral stenosis, however rapid filling is not possible, sothe valve leaflets have to remain as widely separated as they can throughout diastole, and the“M” disappears. Another reason for a different pattern of leaflet motion is that atrial fibrillationis frequently present, and this eliminates the late diastolic reopening. These changes are also apparent on two-dimensional recordings. Fig. 3 shows commissuralfusion causing the valve leaflets to assume a dome shape in diastole, with the anterior leafletforming a characteristic “elbow” due to its tethering to the posterior leaflet. The hallmark ofrheumatic mitral valve disease is the restriction of motion of the anterior mitral valve leaflet tip. Abrupt halting of the early diastolic opening motion coincides with the opening snap evident onauscultation. Echocardiography is a very sensitive method for detecting mitral stenosis and simple inspectionof the recordings (Fig. 4) can often differentiate between mild and very severe stenosis. Quantification of severity has, however, proved more difficult by M-mode. Early attemptsmeasured the “E-F slope”, which indicates the difference between early and mid-diastolic leafletposition, but these proved unsatisfactory because the E-F slope is influenced by factors such asstroke output and ventricular stiffness. Traditional approaches for the calculation of mitral valve area involve cardiac catheterization. The value of cardiac catheterization methods for assessing a patient with mitral stenosis isquestionable; the end-diastolic valve gradient is influenced by heart rate, stroke volume, and thepresence of mitral aortic regurgitation, which also invalidate estimation of valve orifice area bythe “Gorlin” formula. Two-dimensional echocardiography is able to visualize the mitral orifice directly in diastole, thusproviding information previously available only to the surgeon. Using the parasternal short-axisview, it is possible to differentiate between various orifice shapes that are indistinguishable byM-mode (Fig. 5). Planimetry of a still-frame image (Fig. 6) allows the mitral valve orifice areato be measured. Great care is needed to ensure that the image selected is accurate. If the scanplane transects the valve obliquely, above or below the region of maximum constriction, theorifice will appear too large; if the wrong part of the cardiac cycle is used, it will appear toosmall. Other technical difficulties arise from limitations of lateral resolution of the instrument,and from multiple reverberations produced by valve calcification. In spite of these problems, inthe hands of an experienced operator two-dimensional echocardiography has proved the bestmethod available for preoperative estimation of mitral valve area. Thoughtful clinical uses of thetwo-dimensional echocardiographic data will obviate the need for cardiac catheterization in mostpatients. In the setting of previous mitral valve commissurotomy, however, caution should be exercised. Such direct planimetric methods have not been shown to be as reliable in this setting. Doppler echocardiographic methods have also been shown to be useful for estimation of mitralvalve area using the pressure half-time method and for the estimation of mean mitral gradient. Such methods are particularly useful in a patient with previous commissurotomy and also serveto double-check the direct planimetric approaches. Of course, with significant mitral stenosis, the left atrium will dilate. Such dilatation can beobserved in any view of the left atrium (Fig. 7). Estimation of left atrial size usingechocardiography is very important. The normal left atrial size is below 4 cm in adults anddilates with chronic mitral stenosis, insufficiency, or atrial fibrillation. Patients with severe leftatrial dilatation are usually very difficult to convert to normal sinus rhythm with cardioversion. The echocardiogram helps to select patients in which cardioversion might or might not besuccessful Mitral Annulus CalcificationIn the elderly patient, calcium is sometimes present in the mitral valve annulus (Fig. 8) and itproduces a dense band of echoes behind the posterior valve leaflet adjacent to the annulus. However, the leaflets themselves remain thin, and there is no commissural fusion, so theyseparate normally in diastole. Since the calcium absorbs, or reflects, much of the ultrasoundenergy an area of shadowing may be seen posterior to the calcific ring. Mitral valve annular calcification can also be detected on M-mode. Due to lack of spatialinformation, however, the M-mode recordings are difficult to interpret except by experiencedobservers. Atrial Tumors and ClotsAn uncommon but important condition is a left atrial tumor, most frequently a myxoma, whichpartially bocks the mitral orifice and can, therefore, be indistinguishable from mitral stenosis onclinical examination. In most cases, M-mode recordings are diagnostic of this condition. As Fig. 9 shows, the tumorproduces an amorphous cloud of echoes that appears behind the mitral valve leaflet shortly afterthe valve opens. Depending on the mobility of the tumor, other recordings will show it in the leftatrium during systole, and descending into the body of the left ventricle later in diastole. Theanterior mitral leaflet is usually normal in thickness in this situation. The opening of the normalmitral leaflet in diastole, followed by the appearance of the mass lesion an instant later serves todifferentiate the M-mode appearance of mitral stenosis and atrial myxoma. The spatial presentation of echocardiographic data offered by two-dimensional echocardiographymakes the diagnosis of left atrial myxoma quite easy in most cases (Fig. 10). The size, mobility,and point of attachment of the tumor can be determined with some accuracy. Its motion exhibitsa “rocking” action about the point of attachment, normally to the interatrial septum just behindthe anterior mitral leaflet. Indeed, if it appears to be attached elsewhere it is more likely to be amalignant myosarcoma or lymphoma. Additional two-dimensional short-axis and four-chamber views (Fig. 11) not only provide furthergraphic evidence of the tumor, but also greatly reduce the chance of accidentally missing thediagnosis because of small tumor size, lack of mobility, or abnormal attachment point. As aresult, echocardiography obviates the need for invasive and dangerous techniques such asangiography. Such left atrial tumors have, infrequently, been reported to the bilateral. The usual mechanismfor extension into the right atrium is growth of the tumor through the fossa ovalis (Fig. 12). Careful examination of both the left and right atria as well as the interatrial septum are requiredin such patients as it gives useful information to the surgeon in planning the surgical approach. Surgical removal of atrial myxoma requires resection of the atrial septum at the point ofattachment to prevent regrowth of the myxoma (Fig. 13). Myxomas may occur in any cardiac chamber and on any cardiac valve. The second mostcommon area of occurrence after the left atrium is the right atrium (Fig. 14). As with left atrial locations such tumors often prolapse into the valve orifice in diastole, impeding forward flow ofblood through the heart (Fig. 15). Wherever their location, the echocardiographic identificationof such mass lesions is indication for surgical removal in suitable surgical candidates due to theirpropensity for obstruction to flow and the high rates of embolization of such tumors. Tricuspid StenosisOrganic tricuspid stenosis is an unusual but important finding. The clinical signs can easily bemasked by those of the mitral valve disease with which it is almost invariably associated. Because of the low pressures in the right side of the heart, significant tricuspid stenosis canproduce transvalvular pressure gradients of 1mmHg or less, which are hard to detect by cardiaccatheterization, even when suspected in advance. Echocardiography, in contrast, is a very sensitive method for detecting tricuspid stenosis, andexamination of the tricuspid valve should always be included in all patients, particularly inpatients with rheumatic aortic or mitral valve disease. Fig. 16 shows an M-mode scan fromtricuspid to mitral valve in a patient with both mitral and tricuspid stenosis. Similar changes areevident in both valves, namely reduced mobility, leaflet thickening, and reduced or reversedmotion of the posterior leaflet. Clear two-dimensional visualization of the stenotic tricuspid orifice is not as easy as with themitral valve. This is due to the lack of an appropriate window by which to access the plane ofthe open tricuspid valve. In fact, it is a rare patient where the severity of tricuspid stenosis maybe planimetered. As with mitral stenosis, the severity of tricuspid stenosis may be estimated byDoppler methods and has been shown to be quite helpful in this regard. The apical four-chamber view, however, will reveal tethering of the tricuspid leaflet tips inpatients with tricuspid stenosis, Fig. 17 shows fusion of both the tricuspid and mitral valve leaflettips during diastole in tricuspid and mitral stenosis. Mitral RegurgitationWithout the use of Doppler, there are no specific signs of mitral regurgitation by either M-modeor two-dimensional echocardiography. Nevertheless, echocardiography can contributesignificantly to the assessment of a patient with mitral regurgitation by indicating thehemodynamic severity and by determining the pathogenesis, both of which have importantprognostic implications. The primary echocardiographic features of mitral regurgitation are volume overloading of boththe left atrium and the left ventricle. This results from the transfer of a proportion of the strokevolume back and forth between the two chambers. Wall thickness is normal (though by virtue ofenlargement, wall mass increases). Left ventricular volume overload is recognized by an end-diastolic dimension greater than 5.5 cm, and hyperdynamic wall motion, most noticeable on theinterventricular septum (Fig. 18). Such profound changes noted by echocardiography requirethat the hemodynamic load from mitral regurgitation be severe. It is axiomatic that severe mitral regurgitation must cause some enlargement of the left atriumand pulmonary veins, since they have to accommodate the regurgitant blood in addition to normal left side inflow. Unfortunately, however, the proportion of the additional volume storedin the atrium and the veins varies, as does the relative duration of systole and diastole, soquantification of regurgitation from measurement of atrial size has not been useful. In cases ofacute, severe mitral regurgitation, the left atrium is rarely noted to be enlarged even in the face ofmarked elevation of atrial pressures. Changes in left atrial volume are reflected as motion of the aortic root. This is because theposterior atrial wall is firmly anchored to the lungs by the pulmonary veins. This forms one ofthe major supports of the whole heart, and the posterior atrial wall consequently moves verylittle. Expansion of the atrium therefore causes its anterior wall, which is echocardiographicallyindistinguishable from the posterior wall of the aortic root, to be pushed forward. Thus, vigorousmotion of the aortic root indicates high left atrial stroke volume and is a feature of mitralregurgitation (though it is also seen in severe mitral regurgitation in the presence of abnormalventricular function). Quantification of aortic root motion suffers from the same limitations asmeasurement of left atrial dimension. Thus, without Doppler echocardiography, the severity of mitral regurgitation can only bededuced from the M-mode or two-dimensional echocardiographic recordings. Direct imaging ofthe valves, however, frequently reveals the etiology of the regurgitation and provides very usefulinformation for planning surgical approaches. Now that primary valvular reconstruction, ratherthan replacement is possible, a surgeon experienced in interpretation of echocardiographic datamay precisely identify disordered valvular anatomy and predict patient suitability for surgicalvalvuloplasty. Rheumatic Mitral RegurgitationSome degree of regurgitation frequently accompanies rheumatic mitral stenosis. Thepathological changes in the valve described earlier indicate the rheumatic etiology, but thepresence of mild regurgitation usually cannot be detected by echocardiographic studies and it isbest diagnosed by auscultation or by Doppler. However, extreme enlargement of the left atrium,especially if accompanied by a heavily calcified valve and enlargement of the left ventricle(which is normally small in pure stenosis, reflecting low cardiac output), should give strongsuspicion of significant regurgitation. When regurgitation is dominant, with little or no stenosis, the rheumatic changes in the mitralvalve may be minimal and are frequently confined to a restriction of posterior leaflet motion, butwithout frank reversal of motion direction. In such cases, two-dimensional parasternal long-axisand apical four-chamber views are helpful for showing the shortened, immobile posterior leaflet,which is the cause of the incompetence. Mitral Valve ProlapseThe origin of the auscultatory finding of a mid-systolic click, often with a late-systolic murmurwas, until recently, widely held to be extra-cardiac. Echocardiography has been responsible forshowing that these findings are most commonly caused by prolapse of part of the mitral valveinto the left atrium. The click occurs when the prolapsing motion is suddenly halted by therestraining chordae tendineae and is analogous to the opening snap of mitral stenosis. Themurmur indicates the presence of mitral regurgitation. Mitral valve prolapse usually occurs in a “floppy” mitral valve (Fig. 19) that has an abnormallylarge leaflet area and lengthened chordae tendineae due to abnormal collagen synthesis. It ishistologically identical to the “myxomatous degeneration” associated with Marfan’s disease. The incidence has been said to be as high as 20% in young females, though there is nowindependent pathological evidence from routine necropsies to support the view that mitral valveprolapse is present in some 3-5% of all adult females and 0.5% of adult males, the incidencerising with age in both sexes. Mitral prolapse usually manifests either as a sudden posterior buckling (Fig. 20) associated witha mid-systolic click and/or late-systolic murmur (Fig. 21), or a pan-systolic “hammock” patternof the closed leaflets during systole (Fig. 22). The nature and timing of the prolapse pattern isdetermined to a large degree by ventricular dimensions, and hence is influenced by strokevolume. Thus, for example, lowering stroke volume by standing a patient up reduces ventricularfilling and, with a smaller chamber, the elongated chordae restrain the valve even less, allowingit to prolapse earlier. This can often turn a mid-systolic prolapse into the pan-systolic“hammock” type. Although M-mode echocardiography, especially when aided by a simultaneousphonocardiogram, is a reliable method for detecting most cases of mitral prolapse, it does suffersome disadvantages. Firstly, it is not possible to distinguish an abnormal prolapse motion fromthe overall movement of the mitral annulus during systole. This shows a small degree ofposterior displacement during the isovolumic contraction period, followed by a steady anteriormovement. An arbitrary criterion has been proposed, which defines prolapse as a posteriordisplacement of more than 2 mm below a straight line joining the “C” and “D” points, but clearlythe apparent incidence of the condition is greatly influenced by the value chosen. Minor degreesof prolapse can be detected best by M-mode, but false positives can be produced by incorrectultrasound beam angulation (transducer too low on the chest) or by abnormal overall motion ofthe heart, as found in pericardial effusions. Use of the two-dimensional parasternal long-axis view improves specificity because it shows themotion of the leaflets better in relation to that of the annulus (Fig. 23). The mitral valve consistsof two leaflets. The smaller, posterior of these comprises three “mini-cusps”. Because the twopapillary muscles are situated beneath the major commissures, the central “mini-cusp” of theposterior leaflet is less well supported by the chordae and the part most commonly affected byprolapse. It is clearly visualized by M-mode and two-dimensional echocardiography in theparasternal long-axis view. However, prolapse is sometimes confined to the lateral sections nearthe commissures, and can then easily be missed by M-mode. In such cases the two-dimensionalexamination, utilizing the apical four-chamber view, permits visualization of these areas. In thisway, the use of the combined techniques provides superior sensitivity and specificity to thatoffered by either one alone. Bacterial EndocarditisBacterial endocarditis infection of the mitral valve can present in several ways, depending on thetype of organism and the route by which the infection is carried. Primary infection is usuallyassociated with a valve abnormality, (e.g., floppy or rheumatic valve). Secondary infection canarise as a result of a jet of blood from a leaking, infected aortic valve striking a normal mitralvalve. In the former case, vegetations are most commonly present on either or both valve leaflets, whereas in the latter, perforation of the anterior leaflet or erosion of the chordaetendineae are also found. Vegetations can be detected by M-mode (Fig. 24), but are much more readily seen by two-dimensional echocardiography. Using both long-axis and short-axis parasternal views, thelocation and approximate sizes of the masses can be determined (Fig. 25). Additional echocardiographic signs appropriate to the preexisting floppy or rheumatic mitralvalve will be present. A possible source of confusion can arise from the redundant leaflet tissueand chordae of a floppy valve, which can give a “clubbed” appearance to the leaflet that isindistinguishable from that of a small vegetation. Caution must therefore be exercised in makingthe diagnosis of vegetations on a floppy valve. Thus, echocardiography can detect the presenceof an abnormality, but knowledge of the clinical setting provides the observer with very usefulinformation as to whether the abnormality is likely to be due to infective endocarditis. The images of vegetations are very striking, and their violent motions often give the impressionof imminent embolization. Even in the face of successful medical therapy these lesions rarelyresolve quickly and may persist for years. Once the infection is controlled, however, theavailable evidence is that the mere presence of such masses does not indicate a need for surgicalremoval. When infection causes perforation of a mitral leaflet, and if there are no vegetations,the only echocardiographic sign may be rapid fluttering of the cusps during systole that isdetectable on M-mode recordings. Echocardiography is particularly useful for evaluating the complication of acute vegetativeendocarditis such as valve ring abscess, leaflet rupture, or for determining the presence ofsecondary vegetations. Fig. 26 shows a secondary vegetation due to mitral regurgitation on theposterior left atrial wall in a young girl with fever and multiple embolic strokes. Carefulangulation of the interrogating beam revealed the mass to be in two parts (Fig. 27). In thispatient, Doppler echocardiography showed only mild mitral regurgitation. Because of themultiple embolic strokes, the vegetation was surgically removed and showed a morphologystrikingly similar to that noted by two-dimensional echocardiography (Fig. 28). Careful echocardiographic examination in the clinical setting of endocarditis always requirescomplete evaluation for the presence of complications. Fig. 29 demonstrates a necropsyspecimen of an infected mitral valve with erosion and thrombus on the posterior wall of the leftatrium where the regurgitant jet was likely to have been directed. Infection of a tricuspid valve can also be primary, with vegetations on the valve or can be causedby a jet lesion from a ventricular septal defect that frequently ruptures chordae. Unlike the caseof the mitral valve primary infection, tricuspid valve primary infection does not imply anyabnormality of the valve itself. Vegetations are most clearly visualized in the apical four-chamber view or right ventricular inlet view. A patient with rupture of the tricuspid valve leafletis seen in Fig. 30 where the anterior leaflet of the tricuspid valve is seen to flail into the rightatrium in systole. At surgery (viewed from over the patient’s head and through the right atriuminto the right ventricle) the flail tricuspid leaflet is seen held by a surgical instrument coming infrom the right (Fig. 31). Ischemia and Rupture of the Valve Support Apparatus Mitral regurgitation can result from ischemic dysfunction of the papillary muscles. Thissometimes manifests as a lengthening, or failure to shorten, of the valve support apparatus. Froman echocardiographic viewpoint, ischemic mitral regurgitation is indistinguishable from mitralvalve prolapse. More commonly, however, ischemia causes retraction of the papillary muscle,with the result that the leaflets fail to coapt adequately in systole. Mitral regurgitation associated with a floppy mitral valve or papillary muscle ischemia isnormally only mild. Echocardiographically there are few signs of papillary muscle dysfunctionexcept for the presence of an underlying wall motion abnormality. However, if all support to aportion of the valve is lost due to fracture of some of the chordae (Fig. 32), or if one of thepapillary muscle heads ruptures following myocardial infarction (Fig. 33), severe regurgitationusually results. The echocardiographic findings vary according to the site and degree of damage to the valveapparatus. M-mode recordings generally show irregular or discordant motion of either or bothvalve leaflets (Fig. 34). Additional echoes may be generated by fractured chordae that show asshort lines randomly superimposed on the valve pattern. Echoes from parts of the valve leafletsmay be seen in the left atrium as they are carried up into it during systole. In such a setting, partial flail of one or both of the mitral valve leaflets is noted. Flail portions ofthe valve apparatus are much better appreciated on two-dimensional recordings, since they allowthe abnormal motions to be followed for more of the cardiac cycle. In the setting of acute myocardial infarction, the appearance of a new murmur suggests thepresence of a ventricular septal defect or mitral regurgitation due to disordered mitral valveleaflets. The auscultatory findings in such patients may be quite confusing and V waves arepresent in both situations by pulmonary capillary wedge pressure recordings. Echocardiographyis quite helpful in detecting and differentiating these potential complications. Fig. 35 shows aflail posterior mitral valve leaflet in diastole that is seen to move entirely into the left atrium insystole (Fig. 36). Functional Mitral RegurgitationGross enlargement of the left ventricle can dilate the mitral valve annulus to the point where thevalve becomes incompetent. This is not easy to detect either clinically or echocardiographically,particularly since there is frequently concomitant tricuspid regurgitation. Because of the verypoor left ventricular function, volume overload is not apparent, and any left atrial enlargementcould be ascribed to chronic elevation of ventricular filling pressure. However, in patients withleft ventricular failure who have considerable atrial enlargement, functional mitral regurgitationmay be suspected. Tricuspid RegurgitationAs with the mitral valve, there are no specific signs of tricuspid regurgitation onechocardiographic recordings. With the widespread use of Doppler echocardiography it has beenlearned that small degrees of tricuspid regurgitation are quite common, being present in over65% of otherwise normal individuals. Such patients have little, or no, evidence of murmur byauscultation. When tricuspid insufficiency is severe, changes are noted echocardiographically. In the majorityof these cases, most functional tricuspid regurgitation is secondary to pulmonary hypertension. Other causes include infective endocarditis and/or abnormalities of the valve itself, such asEbstein’s anomaly. The primary echocardiographic manifestation of tricuspid regurgitation is volume overload of theright ventricle. The right ventricle becomes enlarged, and the direction of the interventricularseptal motion appears to become reversed or “paradoxical”. In fact, the left ventricle contractsnormally, but superimposed on its motion is the greater movement of the hyperdynamic rightventricle (Fig. 37). Contrast echocardiography has been shown to help in the detection of tricuspid regurgitation ifDoppler echocardiography is not available. When a bolus of liquid, usually sterile saline, isinjected rapidly into a peripheral vein, microbubbles of gas are released. On a two-dimensionaldisplay, echoes from these microbubbles can be seen to pass back and forth across the tricuspidvalve and also seen passing retrograde into the enlarged hepatic veins; they often continue forseveral minutes before they are eventually cleared into the pulmonary artery. M-mode recordingsshow that the contrast echoes first appear in the inferior vena cava during systole, and can beseen passing retrograde into the enlarged hepatic veins (Fig. 38). The Semilunar ValvesAortic Valve StenosisCauses of left ventricular outflow obstruction include aortic valve stenosis and subvalvular andsupravalvular obstructions. Subvalvular obstruction can be further divided into the discretediaphragmatic or fibromuscular ring types, and obstruction secondary to septal hypertrophycaused by hypertrophic cardiomyopathy. Only primary valve leaflet pathology will be discussedhere and the others dealt with in subsequent units. Aortic valve stenosis can be present from birth due to malformation of the valve, or can developin later life as a result of calcification either of a congenitally bicuspid valve (Fig. 39) or of avalve inflamed by rheumatic disease. A congenitally stenotic valve may be grossly dysplastic, and in such cases its echocardiographicappearance is usually abnormal. Fig. 40 demonstrates a short-axis of a bicuspid aortic valve insystole with a slit-like orifice. Alternatively, the valve cusps may be thin, either with one commissure imperfectly formed, orconsisting essentially of a diaphragm with a small hole through which the blood must pass.During ventricular ejection, such a valve is pushed upward to form a dome shape; while this maybe apparent on a long-axis two-dimensional view, it cannot be appreciated by M-modeechocardiography, which frequently gives normal recordings in cases of severe stenosis. Eventwo-dimensional echocardiography can fail to detect any abnormality. The absence ofechocardiographic evidence cannot, therefore, rule out the presence of congenital aortic stenosis. Mild congenital defects of the aortic valve are common, occurring in about 1% of the population. In most cases, the valve is “bicuspid”, either with two equal-sized cusps or with three cusps, twoof which are fused together. The patient is usually asymptomatic and there may be little or nomurmur. Typically, the M-mode diastolic closure line is eccentrically placed within the aorticlumen (Fig. 41), and there are often multiple echoes in diastole, arising from corrugations on thecusp edges or from the raphe. There is, however, an aortic ejection sound, generated as the valve is suddenly halted as it opensand forms the “dome” shape described above. High-speed M-mode echocardiograms recordedsimultaneously with a phonocardiogram show the coincidence of the ejection sound withmaximal valve opening and provide a reliable method for detecting bicuspid valves (Fig. 42). Inmany cases, the valve itself appears abnormal. The doming action of the valve during systole cansometimes be seen on two-dimensional recordings, but it is not easy to obtain technicallyadequate images from the thin cusps (Fig. 43). In adult life, though rarely before the age of forty, some bicuspid valves calcify and becomeprogressively more stenotic. Although histological examination can usually distinguish suchcases from rheumatic aortic stenosis, the echocardiographic appearances of the valves areidentical due to the severe fibrosis with calcification in both entities. In mild cases, fibrousthickening of the cusps is apparent, and their separation in systole is restricted. Here it may bepossible to estimate the orifice area using the two-dimensional short-axis view. Assuming thelumen to be circular, the reduction in orifice diameter, which increases the gradient from 40 to100 mmHg, is only 2mm. Bearing in mind the probable irregular shape of the hole, and thepresence of reverberation echoes from the calcium, visualization of this is, at present, beyond thecapability of current techniques. Nevertheless, if two-dimensional echocardiography shows that a substantial orifice exists, thereis unlikely to be severe stenosis. This can be very helpful, for example in eliminating aorticstenosis as the primary pathology in a patient who presents in a moribund state with a systolicmurmur. Two-dimensional echocardiography is also useful for detecting changes associated with chronicrheumatic or degenerative aortic stenosis. In such cases, the aortic cusps are immobile, or onlypartially mobile and are markedly thickened (Fig. 44). A rough correlation exists between the severity of calcification and the pressure gradient acrossthe valve. Echocardiographic estimations of calcification are, however, not very reliable asreverberations from small regions of calcium tend to obscure the entire aorta, giving a misleadingimpression of the overall severity. Echocardiography is a very precise method for assessing left ventricular hypertrophy, and thismeans that some helpful information about the effect of aortic stenosis on the myocardium can beobtained (Fig. 45). M-mode recordings permit measurement of ventricular wall thickness andindication of their stiffness is obtained from the rate of diastolic filling. The relative dimensionsof the ventricular cavity and wall thickness can also be used to estimate wall stress using theformula:Wall Stress (S) = LVP x (r/h),where LVP = peak LV pressure; r = cavity radius; h = mean wall thickness. Thus, assuming the ventricle hypertrophies to maintain constant wall stress:LVP – (constant) x (h/r)If peak pressure can thus be estimated and systemic arterial pressure measured by a cuff aroundthe brachial artery, it ought to be possible to determine the valve gradient. Several reports havesuggested that this is the case, but not all researchers can produce adequate correlations to permituseful prediction in individual cases. Left ventricular hypertrophy may also be detected withtwo-dimensional echocardiography (Fig. 46). Doppler echocardiography provides the most reliable noninvasive means for determining aorticvalve peak and mean gradients, as does estimating valve orifice area by the continuity equation. The primary echocardiographic signs of aortic regurgitation are volume overload of the leftventricle combined with a rapid fluttering, either of the anterior mitral valve leaflet, or the septalendocardial, in the region of the left ventricular outflow tract, or both (Fig. 47). Rarely, and onlyin patients with dilated ventricles, it may not be possible to detect this fluttering. Somedetectable abnormality of the aortic root or valve is normally found combined with these signs. In cases of acute, severe regurgitation, premature closure of the mitral valve may be seen (Fig.48) and is usually an ominous prognostic sign. This is caused by extremely high end-diastolicpressures in an uncompensated ventricle, and is associated with a loud mid-diastolic (AustinFlint) murmur. Aortic RegurgitationIf aortic regurgitation is the sole lesion, its severity may be gauged from the degree of leftventricular volume overload, but the duration and severity of the mitral or septal flutter are of nohelp in this regard. It has long been appreciated that most patients tolerate even quite severe aortic regurgitation formany years, but that deterioration is rapid once left ventricular failure occurs. Thus, a majorcontribution of echocardiography to the management of aortic regurgitation is in determining thepathogenesis, and in providing a noninvasive method for monitoring left ventricular function. As with other flow lesions, Doppler echocardiography is now the noninvasive standard fordetecting the presence and severity of aortic regurgitation. In rheumatic heart disease, the most common presentation after pure mitral stenosis is acombination of this with aortic regurgitation. The changes in the aortic valve can be minimal,causing only slight thickening of the cusp echoes. The aortic root diameter, measured at the levelof the cusps, is normal. Evidence of the etiology comes from the mitral valve, which almostalways shows some echocardiographic signs of rheumatic disease. The mitral valve abnormalitymay be confined to slight reduction in amplitude of the posterior leaflet motion without anyclinical manifestations (Fig. 49). If, on the other hand, the mitral valve is heavily calcified, anyflutter caused by aortic regurgitation may be difficult to detect. Magnified views of the valve andinterventricular septum, recorded by M-mode using higher paper speed and low gain settings,may help to demonstrate diastolic fluttering. Where vegetations on the aortic valve result from the infection, they are best detected by usingtwo-dimensional long-axis and short-axis views, shown in Fig. 50. Vegetations larger than 2-3mm can usually be visualized clearly and their approximate size can be determined, along withthe cusps to which they are attached. Aortic valve endocarditis is sometimes complicated by the development of a mycotic aneurysm,which can rupture into one of the other cardiac chambers, or by the spread of the infection to thetricuspid valve. Although M-mode recordings may demonstrate the resulting hemodynamicchanges, direct visualization of such defects is normally possible only by two-dimensionalechocardiography (Fig. 51). In many cases, however, endocarditis infection of an aortic valve does not produce vegetations,but rather causes erosion of the cusp tissue that leads to rupture or perforation. Theechocardiographic sign of such lesions is rapid fluttering of the aortic cusps during diastole,caused by a turbulent jet of blood passing through a defect in the otherwise closed valve. Many infected aortic valves also appear to be bicuspid, and it is well known that any abnormalityof the valve greatly increases its susceptibility to infection. But only about one percent of thepopulation has a bicuspid valve, and roughly half of the patients requiring valve replacement forsevere aortic regurgitation caused by endocarditis have a normal three-cusp configuration. Not infrequently, the regurgitant jet of blood spreads the infection to the mitral valve, producingthe signs described previously. Aortic Root DiseaseUnlike the mitral valve, the aortic cusps have no supporting apparatus; they withstand theconsiderable diastolic pressure in the aorta by their shape, and by virtue of the fact that they restagainst each other with some 30% of each cusp overlapping its neighbors. However, if theregion of the aorta where the cusps are attached is dilated or distorted by disease, the cusps mayfail adequately to withstand aortic diastolic pressure and regurgitation will occur. Fig. 52 shows a diagram of the aortic root. Between the aorta proper and the lower annulus,which forms part of the fibrous skeleton of the heart, is a tube comprised mainly of collagen,which bulges outward to form the sinuses of valsalva and to which the aortic cusps are attached. Dilation of the fibrous annulus is rare. Dilation of the ascending aorta is commonly found in patients with aortic stenosis, but does notnormally affect the valve cusps (otherwise almost all patients with aortic stenosis would haveregurgitation). Dilation of the supra-aortic ridge at the point where the aorta meets the top of thecollagen sleeve, however, pulls the cusps apart and reduces their mutual support (Fig. 53). Inthis way, an enlargement in this area by as little as 2mm above the normal range can be sufficientto cause regurgitation severe enough to require valve replacement. Such dilation is readilydetected by echocardiography, since it is at this level that the echoes from the cusps are routinelyrecorded. Aortic root disease can be divided into those characterized by an inflammatory reaction, forexample syphilis, Reiter’s disease, ankylosing spondylitis, and giant cell aortitis, and those inwhich the elastic within the aorta is partially destroyed, as in Marfan’s disease. In nearly all cases, echocardiography shows a dilated aortic root, though in some cases of syphilis, valveincompetence results from distortion of the cusps rather than dilatation. It may also be possibleto infer the presence of inflammation or calcium from dense aortic wall echoes. The cuspsthemselves often generate multiple echoes in diastole, similar to those frequently found withbicuspid valves (Fig. 54). This is probably due to the thickening of the cusp edges caused bytheir rubbing against each other as they partially prolapse under the stress or aortic pressure. This“functional prolapse” should be distinguished from that of the mitral valve, and occasionally theaortic valve, in which the cusps themselves are abnormal. One of the features of Marfan’s disease is the destruction of the elastic in the aortic media,causing the root to dilate and the valve to become incompetent (Fig. 55). However, manypatients with aortic regurgitation have dilated aortic roots, biopsies from which are histologicallyidentical to those of Marfan’s disease but have none of the other clinical or echocardiographicstigmata of this condition. This “idiopathic root disease” is in fact the most common cause ofsevere aortic regurgitation in western countries where rheumatic fever is now rare. Interestingly,it is frequently found in patients with aortic regurgitation who also have bicuspid aortic valves. Aortic DissectionIn its most severe form, loss of structural strength in the aortic walls leads to aneurismal dilationand/or dissection of the intima. The dilation is at best documented by two-dimensionalechocardiography, using the parasternal long-axis view to visualize the ascending aorta and thesuprasternal position to see the aortic arch.In cases where there is gross dilation at the valve level, the aortic cusps may show a pattern ofearly partial closure and fluttering indistinguishable from that characteristic of subvalvar aorticstenosis. This is probably caused by turbulent eddies of blood in the sinuses of valsalvaproduced by the high ejection velocity into the dilated aorta. With careful technique and goodapparatus, high success has been reported in detecting dissection by two-dimensionalechocardiography and in classifying it according to the DeBakey criteria. The use of M-mode alone, however, leads to many false positives because of the difficulty inobtaining correct beam angulation and an inability to distinguish, for example, a true dissectionfrom a double echo generated by the bulbous sinuses of valsalva or the transverse sinus of thepericardium posteriorly. Even more productive is the use of transesophageal echocardiography where a small transducer,mounted on a flexible endoscope is inserted into the esophagus. Using this approach providessuperior images of the ascending aorta and proximal transverse aortic arch in almost all patients. Fig. 56 shows a short-axis transesophageal image of the proximal aorta where true and falselumens are easily visualized. Pulmonary StenosisIn cases of mild pulmonary stenosis, no abnormality is detectable either by M-mode or two-dimensional echocardiography. With a more severe obstruction, it may be possible to detectright ventricular hypertrophy, but echocardiography is not a very sensitive method for diagnosingthis. Another sign that has been reported, but in our experience is confined to patients with severe obstruction, is an exaggerated “a-dip” on the pulmonary valve echocardiogram. Thisarises from the fact that the hypertrophied right atrium forcefully injects blood into an alreadyfull and stiff right ventricle during atrial systole. Pulmonary artery pressure is low, and so thesudden increase in right ventricular pressure is sufficient to partially open the pulmonary valve(Fig. 57). Echocardiography can assist phonocardiography in the diagnosis of pulmonary valve stenosis byconfirming the origin of the early systolic ejection sound (Fig. 58). A recording showingpulmonary valve closure may also help confirm the timing of the later pulmonary component ofthe second heart sound, although such recordings are routinely possible only in small children. Now that Doppler echocardiography is available, it has been shown to be able to detect, andreliably quantitate, pulmonary stenosis. Pulmonary RegurgitationPulmonary regurgitation causes volume overloading of the right ventricle, indicated on theechocardiogram by enlargement of the right ventricle and reversal of septal motion, as describedearlier for tricuspid regurgitation following surgery for pulmonary stenosis. The combination ofresidual right-sided hypertrophy with overfilling of the right ventricle due to regurgitation gives avery deep pulmonary valve a-dip, and may even open the valve fully before the onset of systole(Fig. 59). Doppler, again, has been shown to be quite sensitive in detecting and quantitating theseverity of pulmonic regurgitation. Pulmonary HypertensionPulmonary hypertension causes right ventricular hypertrophy, which may be coupled withvolume overload due to associated pulmonary or tricuspid regurgitation. Where pulmonaryhypertension develops as a result of a large left-to-right shunt, it reduces the volume of the shunt,eventually reversing it (Eisenmenger physiology). The echocardiographic signs thus reflect boththe primary pathology and the degree of pulmonary hypertension. In cases of severe pulmonary hypertension, the right ventricle compresses the left ventricularseptum posteriorly, resulting in a characteristic “flattening” of the septum (Fig. 60). The degreeof flattening does not, however, correlate in a useful fashion with the severity of the pulmonaryhypertension. Elevation of pulmonary artery pressure reduces the amount by which right atrial systole causesthe pulmonary valve leaflets to dome upward, and so the a-dip on the M-mode echo recording isreduced. Provided the patient is in sinus rhythm, absence of the a-dip is a fairly reliable sign ofpulmonary hypertension. Using high-speed M-mode recordings, it is possible to perform right ventricular systolic timeinterval studies and to measure, for example, pre-ejection period and ejection time. Pulmonaryhypertension prolongs right ventricular isovolumic contraction time, and delays pulmonary valveopening at the onset of systole. The technique is difficult and measurements should be made at aconstant point in the respiratory cycle to eliminate variations caused by changes in strokevolume. Provided that other causes of abnormal right ventricular dynamics such as right bundle branch block and right ventricular failure can be eliminated, such methods permit quantitativeestimation of pulmonary artery pressure. Doppler echocardiography can detect the presence of pulmonary hypertension by a rapid time topeak of the systolic pulmonary waveform. Using tricuspid regurgitation, Doppler can alsoestimate peak right ventricular systolic pressure. Prosthetic ValvesGeneral PrinciplesEchocardiography is sometimes a useful tool for the management of patients who have one ormore prosthetic valves. The aim of the echocardiogram study is to visualize the valve itself,along with its surrounding structures, and also to evaluate left ventricular function. There veryhigh M-mode sampling rate generally makes it preferable to two-dimensional echocardiographyfor this purpose, although the latter can permit more rapid location of the valve and may assist inleft ventricular studies. When studying a prosthetic valve, it is necessary to direct the ultrasound beam in such a way thatit detects motion of the prosthesis. Thus, for an aortic ball valve, either the apical or rightsupraclavicular transducer positions must be employed. Mitral ball prostheses are also bestvisualized from the apical region. Pivoting disk (e.g., Bjork-Shiley) and tissue xenograft valvescan normally be seen from the parasternal position. Because changes in echocardiograms may be so subtle with prosthetics, every patient having avalve replacement should be studied while still in the hospital, about two weeks after theoperation. This provides a baseline against which to compare any later recordings. Since cardiacfunction in such patients remains abnormal, alterations in their hemodynamic status must bededuced from changes in the echocardiographic parameters, rather than their absolute values. Fig. 61 shows a diagram of the motion of a Starr-Edwards aortic prosthesis, as viewed from anapical transducer position, and Fig. 62 is an actual recording. The echo-free space below thetransducer reverberations represents the left ventricle. The first echo encountered from theprosthesis arises from the sewing ring (SR). Its motion is paralleled by the echo that arises fromthe top of the valve cage (C). Immediately below the sewing ring is the echo from theventricular aspect of the ball (PB). A second echo (AB), having similar motion, is seenposteriorly to the cage; this actually arises from the top of the ball, which is inside the cage, butbecause ultrasound travels more slowly within the ball, this echo takes longer to return to thetransducer and thus appears to the machine to have come from further away. A similar analysis, taking into account the inverted position of the valve, applies to a mitral ballprosthesis when viewed from the apex (Fig. 63). One important difference is that the pressuregradient across an aortic valve is high both in systole and diastole, so its movements are rapidand it stays fully open throughout systole and fully closed throughout diastole. A mitral valve, incontrast, has a high gradient across it is systole, but only a small gradient in diastole, and by theend of the filling period this should be nearly zero. Consequently, a correctly functioning mitralprosthesis is often seen to partially close toward the end of diastole (Fig. 64). A normal Bjork-Shiley disk aortic prosthesis is shown in Fig. 65. During diastole, the valve isclosed and presents no target to the ultrasound beam from the parasternal position. When thevalve opens in systole, it is encountered in the center of the aorta, and forms an intense echo,usually with multiple reverberations behind it (Fig. 66, left). Similar recordings are obtainedfrom a mitral disk prosthesis (Fig. 66, right – note the partial closure in the last diastole). Tissue heterografts are normally mounted in a coronet-shaped frame or stent. They are aorticvalves and so, in the aortic position, appear essentially normal, except for the heavy echoes fromthe stent. For use as a mitral replacement the valve is inverted, and thus the patient appears tohave two aortic valves, one of which opens in systole, and the other in diastole (Fig. 67). Differential Diagnosis of Prosthesis MalfunctionMalfunction of an artificial prosthesis is relatively rare nowadays. When it does occur, it isusually associated with rapid deterioration of the patient’s condition. The main signs of prosthetic valve obstruction are: 1. Delayed, reduced, incomplete, or intermittent valve opening or closing. Multiple echoes around the valve, suggestive of organized thrombus or fibrous tissue impeding its motion. Other signs, such as ventricular hypertrophy, or reduced filling rate, are generally unhelpful unless they are definitely of recent appearance. Failure of tissue prosthesis tends to be more gradual, involving development of mildregurgitation or stenosis secondary to calcification. The exception is infection, which can rapidlydestroy the prosthesis. They may be seen as fluttering of the cusps during the closed phase,indicating perforation, or by the classical appearances of vegetations. Partial dehiscence of a prosthetic valve, due to failure of its fixing sutures, produces grossincompetence. This is rare in the case of an aortic valve, but when it does occur it causes severeventricular volume overload and high end-diastolic pressure evidenced by premature mitral valveclosure. The most common cause of dehiscence is erosion of the surrounding tissue by infectionand other signs indicating this may be present. Dehiscence of a mitral valve is more common, and causes severe mitral regurgitation that can bedifficult to detect clinically. Sometimes it is possible to obtain direct evidence of dehiscence(Fig. 68). It should be suspected whenever the motion of the mitral stent appears undulyvigorous; in this respect, two-dimensional studies can be of assistance. Such dehiscence isreadily detected by two-dimensional echocardiography. In addition, Doppler echocardiographyhas been shown to be helpful in detecting even small degrees of prosthetic valvular insufficiencyand moderate degrees of stenosis. Septal Motion in Patients with Mitral ProsthesesVery useful information about mitral valve prosthesis function can be obtained from the analysisof septal motion. Immediately following surgery, septal motion is flat, or perhaps slightlyreversed. The cause of this is not clear, but it is probably due to alteration of cardiac dynamics as a result of opening the pericardium, and relative ischemia during cardiopulmonary bypass. Provided recovery is satisfactory, and in the absence of surgically induced conduction defects,septal motion essentially returns to normal within a year of surgery. If the patient remains in chronic right heart failure, the associated tricuspid regurgitationproduces right ventricular enlargement and reversed septal motion. Valve function, leftventricular cavity size, and posterior ventricular wall motion should all be normal. When right heart failure is caused by mitral obstruction, the best evidence comes from theprosthesis motion. As described earlier, partial or hesitant opening or multiple echoes around thevalve suggest buildup of tissue around the valve. Late diastolic partial closure is no longer seen(if it is present, stenosis is highly unlikely). Ventricular filling rate may be observed to be veryslow. Severe mitral regurgitation causes left ventricular volume overload, with vigorous, normal septalmotion. Thus, a patient who, clinically, has evidence of right heart failure, but whose septalmotion is normal, probably has significant left ventricular volume overload. If other causes canbe eliminated (for example, ventricular septal defect or aortic regurgitation) the finding of normalseptal motion in a patient with know tricuspid regurgitation is evidence of a mitral paraprostheticleak. Finally, when the right-sided failure is accompanied by left ventricular failure, the left ventriclewill become dilated and hypokinetic, showing the appearances typical of cardiomyopathy. Diseases of the Heart Valves (Figure Legends)Fig. 1 Stenotic mitral valve viewed from the left atrium showing thickened leaflets and partial commissural fusion. Fig. 2 M-mode recording of a normal mitral valve (left) and a stenotic mitral valve (right). Note the “M” shapedescribed by the normal valve. The restricted mobility of the thickened anterior leaflet and the forward movementof the posterior leaflet in the stenotic valve are clearly seen. Fig. 3 2-D parasternal left ventricular long-axis view of a stenotic mitral valve during diastole. Note the leaflet tipand left atrial enlargement typical of rheumatic mitral stenosis. Fig. 4 M-mode recordings of mild (left) and severe (right) mitral stenosis. With severe stenosis the leaflets arecalcified and show almost no movement. Fig. 5 Diagram showing how 2-D echocardiograms (left and right) can differentiate between mitral orifices ofvarious shapes that would appear identical on an M-mode recording (center)Fig. 6 2-D parasternal short-axis view at the mitral valve orifice in a patient with rheumatic mitral stenosis. Notethe smaller area and irregular shape of the stenotic valve orifice. Fig. 7 2-D parasternal short-axis view at the aortic valve level during systole. The left atrial enlargement andbowing of the interatrial septum towards the right atrium is typical of high left atrial pressures in patients withmitral stenosis. Fig. 8 2-D parasternal left ventricular long-axis view showing a calcified/fibrotic mitral annulus (arrowed). Fig. 9 M-mode slow scan recording of a left atrial tumor. A dense cloud of echoes appears behind the anteriormitral valve leaflet shortly after diastolic opening. Fig. 10 2-D parasternal left ventricular long-axis view in a patient with a left atrial myxoma. Fig. 11 2-D apical four-chamber view showing a large left atrial myxoma in diastole. Fig. 12 2-D parasternal short-axis view at the aortic valve level in a patient with a large left atrial myxoma. Notethe tumor extension through the fossa ovalis into the right atrium. Fig. 13 Pathological specimen of a left atrial myxoma after resection. Fig. 14 2-D apical four-chamber view in a patient with a right atrial myxoma during systole. Fig. 15 2-D apical four-chamber view of the same right atrial myxoma as is in Fig.14. With diastole the tumormoves through the tricuspid valve causing severe obstruction. Fig. 16 M-mode scan in a case of mitral and tricuspid stenosis. Note the similar leaflet motions of the abnormaltricuspid (upper left) and mitral (lower right) valves. Fig. 17 2-D apical four-chamber view in a patient with rheumatic mitral and tricuspid valvular stenosis. Fig. 18 M-mode recording of the left ventricle in a case of mitral regurgitation. The left ventricular cavity isenlarged and wall motion hyperdynamic. Fig. 19 Postmortem preparation showing the prolapse of the central scallop of the posterior mitral leaflet, viewedfrom the left atrium. Prolapse has been induced by filling the left ventricle with water to physiological pressure; aregurgitant jet (arrowed) is escaping from the base of the domed prolapsed section. Fig. 20 M-mode recording of a floppy mitral valve showing sudden posterior buckling when prolapse occursduring late systole (arrowed). Fig. 21 Magnified high-speed M-mode recording of the same case as Fig.20 with simultaneous phonocardiogramillustrating the relationship of the click (X) and later systolic murmur (SM) to the movement of the prolapsed valve. Fig. 22 Magnified M-mode recording showing the “hammock” posterior movement associated with pan-systolicprolapse. Fig. 23 2-D parasternal left ventricular long-axis view showing marked prolapse of the posterior mitral valveleaflet. Fig. 24 M-mode recordings of a mitral valve showing echoes from vegetations attached to the anterior leaflet. Inthe magnified high speed view (right) the echoes from the vegetations are arrowed. The phonocardiogram shows apan-systolic murmur and a diastolic filling murmur. Fig. 25 2-D parasternal left ventricular long-axis view in a patient with bacterial endocarditis. Note the vegetativemass lesion of the mitral valve seen within the left atrium. Fig. 26 2-D parasternal left ventricular long-axis view showing a secondary vegetative lesion on the free wall ofthe left atrium. The secondary lesion was due to a jet of mitral regurgitation striking the posterior left atrial wall. Fig. 27 2-D parasternal left ventricular long-axis view with oblique angulation demonstrating two distinct parts ofthe vegetative lesion seen in Fig.26. Fig. 28 Pathologic specimen of the vegetative lesion seen in the previous two figures. Fig. 29 Pathological specimen at autopsy of an infected mitral valve showing erosion and thrombus on theposterior wall of the left atriumFig. 30 2-D parasternal right ventricular inflow view in a patient with a flail tricuspid valve leaflet. Fig. 31 Photograph taken during surgery of a patient with a flail tricuspid leaflet. The flail leaflet is held by asurgical instrument coming in from the right. Fig. 32 Ruptured chordae tendineae (arrowed). Fig. 33 Ruptured papillary muscle. Fig. 34 M-mode recording of a mitral valve showing the extreme posterior movement during systole and anteriormovement during diastole (arrowed) of the flail posterior leaflet. Fig. 35 2-D apical four-chamber view during diastole of a patient with flail posterior mitral valve leaflet. Fig. 36 2-D apical four-chamber view in systole of the same patient in Figure 2.35. Note that the posterior mitralleaflet is now entirely within the left atrium. Fig. 37 M-mode recording showing the reversed, or paradoxical systolic motion of the interventricular septum in apatient with tricuspid regurgitation. Fig. 38 M-mode recording of the inferior vena cava (IVC) in a patient with tricuspid regurgitation. Following aperipheral venous injection of saline, microbubbles are seen to appear in the IVC after the QRS complex, in latesystole. Fig. 39 Specimen of a calcified bicuspid aortic valve. Fig. 40 2-D parasternal short-axis view of the aorta in a patient with a bicuspid aortic valve. Note the slit-likeorifice seen during systoleFig. 41 M-mode recording of a bicuspid valve showing the eccentrically placed diastolic closure line (arrowed). Fig. 42 Magnified high-speed M-mode recording of a bicuspid aortic valve with phonocardiogram showing thecoincidence of the ejection sound (X) with maximal valve opening. Fig. 43 2-D parasternal left ventricular long-axis view in a patient with a bicuspid aortic valve. Note the doming ofthe aortic valve leaflets during systole. Fig. 44 2-D parasternal left ventricular long-axis view in a patient with calcified aortic stenosis. The aortic leafletsare markedly thickened and demonstrate reduced mobility during systole. Fig. 45 M-mode recordings of a normal left ventricle (left) and in a case of left ventricular hypertrophy (right). Symmetrical thickening of the walls and reduced early diastolic filling rate are evident. Fig. 46 2-D parasternal left ventricular short-axis view at the papillary muscle level in a patient with concentricleft ventricular hypertrophy. Fig. 47 M-mode recording showing the rapid fluttering (arrowed) of the anterior mitral valve leaflet and septalendocardium as a result of aortic regurgitation. Fig. 48 M-mode recording with phonocardiogram showing presystolic closure of the mitral valve resulting fromacute, severe aortic regurgitation. Mitral closure is silent and “X” indicates the ejection sound of a bicuspid aorticvalve. Fig. 49 M-mode recording showing anterior leaflet flutter and reduced posterior leaflet motion, indicating that theaortic regurgitation has rheumatic etiology. Fig. 50 2-D parasternal left ventricular long-axis view during diastole. Note the aortic valve vegetation prolapsinginto the left ventricular outflow tract. Fig. 51 2-D parasternal left ventricular short-axis view of the aorta of the same patient as in Figure 2.50. Thevegetative mass lesion is now seen to involve both the aortic and tricuspid valves. Fig. 52 Diagram of the aortic root showing the manner in which the aortic cusps are suspended in the bulboussleeve that forms the sinuses of Valsalva. Fig. 53 Diagram illustrating the means by which dilation of the supra-aortic ridge pulls the aortic cusps apart andcauses aortic regurgitation. Fig. 54 M-mode recording of aortic root disease showing thickened aortic cusp edges resulting from their rubbingtogether as a result of partial prolapse. Fig. 55 2-D parasternal left ventricular long-axis view in a patient with Marfans disease. Note the markeddilatation of the aortic root. Fig. 56 Short-axis transesophageal image of the proximal transverse aorta in a patient with aortic dissection. Notethat both the true and false lumens are usually identified using this echocardiographic approach. Fig. 57 M-mode recording of severely stenotic pulmonary valve showing its partial opening during right atrialcontraction. Fig. 58 Magnified, high-speed recording that demonstrates the coincidence of the early systolic ejection sound (X)with maximal pulmonary valve opening. Fig. 59 High-speed M-mode recording showing premature opening of the pulmonary valve during inspiration(arrowed) causing the disappearance of the ejection sound (X). Fig. 60 2-D parasternal left ventricular short-axis view at the papillary muscle level in a patient with pulmonaryhypertension. Note the characteristic "flattening" of the interventricular septum. Fig. 61 Diagram of the motion of a Starr-Edwards ball aortic prosthesis, as viewed from an apical transducerposition. Fig. 62 M-mode recording of a Starr-Edwards ball aortic prosthesis. Fig. 63 Diagram of the motion of a Starr-Edwards ball mitral prosthesis viewed from the apex. Fig. 64 M-mode recording of a ball mitral prosthesis viewed from the apex, showing partial closure toward end ofdiastole (arrowed). Fig. 65 Diagram of the motion of a Bjork-Shiley disk aortic prosthesis viewed from the parasternal position. Fig. 66 M-mode recordings of a Bjork-Shiley disk aortic prosthesis (left) and mitral prosthesis (right). Note thepartial closure of the mitral prosthesis in late diastole. Fig. 67 M-mode recording of a tissue mitral prosthesis. Echoes from the closed cusps are seen during systole. Fig. 68 Diagram and M-mode recording of a partially dehisced prosthetic valve. As shown in the diagram andarrowed on the M-mode recording, the posterior part of the sewing ring is swinging freely to and fro.
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Bolesti srčanih zalistaka – kako ih razlikovati? Bolesti srčanih zalistaka su bolesti koje zahvaćaju jedan ili više srčanih zalistaka. One mogu biti prirođene (kongenitalne) ili stečene (posljedica neke bolesti ili stanja). Srce ima dvije pretklijetke i dvije klijetke. Svaka klijetka ima valvulu, jednosmjerni ventilni otvor kroz koji ulazi krv, te valvulu kroz koju krv izlazi. Ponekad se ventilni otvori ne otvaraju i zatvaraju ispravno, te narušavaju protok krvi kroz srce i tijelo. Stanje koje nazivamo stenoza jest ono u kojem se ventil ne može ispravno otvoriti. Regurgitacija (insuficijencija) je pak, stanje kada se ventil ne zatvara ispravno te propušta krv. Bolesti srčanih zalistaka uključuju: - Aortalnu stenozu i regurgitaciju - Mitralnu stenozu i regurgitaciju - Trikuspidalnu stenozu i regurgitaciju - Plućnu stenozu i regurgitaciju Bolesti aortnih zalistaka Bolesti aortnih zalistaka su stanja u kojem ventil između glavne crpne komore srca (lijeve klijetke) i glavne arterije u tijelu (aorte) ne radi ispravno. Takva bolest može biti kongenitalna ili stečena. Vrste: - Aortalna stenoza – u tom stanju, aortalni ventilni otvor je sužen. To sužavanje sprječava otvaranje ventila u potpunosti, što ometa dotok krvi iz srca, aorte i ostatka tijela. - Aortalna regurgitacija – u tom stanju, aortalni ventilni otvor se ne zatvara ispravno, uzrokujući da krv teče natrag u lijevu klijetku. Bolesti mitralnih zalistaka Kod bolesti mitralnih zalistaka, mitralni ventil, koji se nalazi između lijeve srčane komore (lijevi atrij i lijeva klijetka), ne radi ispravno. - Mitralna stenoza – u tom stanju, ventil postaje debeo ili tvrd. To rezultira suženim otvorom i smanjenim protokom krvi iz lijevog atrija u lijevu klijetku. - Mitralna regurgitacija – u tom stanju, mitralni ventil se ne zatvara dobro, što uzrokuje da krv teče natrag u lijevi atrij srca. Ako se ne liječi, može doći do oštećenja srčanog mišića. Bolesti plućnih zalistaka Bolesti plućnih zalistaka se odnose na bilo koji poremećaj plućnog ventila, koji je odgovoran za čuvanje krvi te pravilan protok iz srca prema plućima. Bolesti se mogu odnositi na propuštanje ventila (plućno povraćanje) i suženje ventila (pulmonalna stenoza). Liječenje ovisi o vrsti bolesti te njenoj težini. Bolesti trikuspidalnih zalistaka Bolesti trikuspidalnih zalistaka su stanja u kojem ventil između desne klijetke i desne pretklijetke ne radi ispravno. Često se javlja kod drugih problema srčanih zalistaka. - Trikuspidalna stenoza – u tom stanju, trikuspidalni ventil je sužen, smanjuje količinu krvi koja može teći kroz njega iz desne pretklijetke u desnu klijetku. - Trikuspidalna atrezija – u tom stanju, nema komunikacije između desne pretklijetke i desne klijetke. - Ebsteinova bolest – predstavlja urođenu manu trikuspidalnih zalistaka.