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(BQ) Part 2 book Feigenbaum’s echocardiography has contents: Masses, tumors, and source of embolus, diseases of the aorta, congenital heart diseases, hypertrophic and other cardiomyopathies, dilated cardiomyopathies, stress echocardiography,.... and other contents.
Chapter 13 Infective Endocarditis Infective endocarditis remains a challenging and often fatal condition One reason for this is the difficulty of establishing an accurate diagnosis, particularly early in the course of the disease when proper management can be lifesaving As therapeutic approaches have become more successful, the importance of early and accurate diagnosis is self-evident Unfortunately, no single test or finding establishes the diagnosis in all cases Instead, a constellation of findings that constitutes the diagnostic criteria continues to evolve The central role that echocardiography plays in the diagnosis of endocarditis began in the early 1970s with the echocardiographic demonstration of a valvular vegetation by the M-mode technique With the advent of two-dimensional and Doppler modalities, echocardiography has become virtually indispensable in the diagnosis and management of these patients Today, echocardiographic findings are a central part of the diagnostic criteria for infective endocarditis CLINICAL PERSPECTIVE Despite improvements in therapy, infective endocarditis remains a potentially lethal disease with an incidence of to 8/100,000 patient-years Although the overall incidence has not increased appreciably over time, several factors have contributed to substantial recent changes in the epidemiology of the disease For example, Staphylococcus aureus is now the most common cause of endocarditis in most series, in part due to an aging population and the increasing prevalence of intracardiac devices, including prosthetic valves, conduits, pacing wires, and indwelling catheters This has led to the concept of “healthcare contact” as a recognized risk factor for the development of infective endocarditis Currently, approximately 25% of infective endocarditis cases in this country are attributable to a previous medical event or procedure, such as implantation of a prosthetic valve or pacemaker More recently, the opioid epidemic that has plagued the United States has been associated with a striking increase in the incidence of drug-dependence– associated endocarditis Such patients appear to have a particularly poor prognosis, in part due to the likelihood of recurrent infection following valve replacement therapy Infective endocarditis is defined as a localized infection anywhere on the endocardium, including the chamber walls, vessels, and within congenital defects The vast majority of vegetations, however, occur on valve leaflets Infection may also develop on any implanted or prosthetic material such as prosthetic valves, conduits, pacing electrodes, and catheters The process of developing endocarditis occurs in the setting of bacteremia or fungemia The initiating event usually requires the presence of a high-velocity jet, which may be due to a congenital anomaly such as a ventricular septal defect, a regurgitant valve, or a prosthetic valve It is thought that the jet interferes with the protective endothelial surface, allowing the blood-borne pathogens to adhere and coalesce As the nidus of infection organizes, masses of microorganisms attract platelets, fibrin, and other materials and become adherent to the endothelial surface to form a vegetation The vegetation will grow in size, either as a sessile clump or as a highly mobile and even pedunculated mass with the potential for embolization As the hallmark of endocarditis, the ability to detect the vegetation is the focal point of diagnosis This sequence of events offers a mechanism for development of endocarditis in patients with underlying heart disease However, since as many as 50% of patients who get endocarditis not have lesions associated with a high-velocity jet, some other set of conditions must be operational in these patients to explain the link between bacteremia and cardiac involvement ECHOCARDIOGRAPHIC CHARACTERISTICS OF VEGETATION The versatility of echocardiography in the evaluation of endocarditis is illustrated in Table 13.1 Among its important functions is the identification of underlying heart disease known to increase a patient’s risk of infection Although the absence of underlying disease does not confer protection against endocarditis, particular conditions, such as congenital heart disease, bicuspid aortic valve, and a myxomatous mitral valve, are known risk factors At the same time, these conditions often confound the diagnosis of endocarditis by creating abnormalities that mimic or conceal echocardiographic evidence of infection An essential first step in the echocardiographic evaluation is to search for evidence of acute ongoing infection Although there are several manifestations of endocarditis, including abscesses and fistulae, the most common and direct evidence of infective endocarditis is the vegetation Because a vegetation begins as a microscopic focus of infection and gradually grows into a conspicuous mass, its presence may or may not be evident on an imaging study Thus, echocardiography must be sensitive enough to detect the vegetation and specific enough to distinguish it from other echocardiographic abnormalities or artifacts As can be seen in Table 13.2, certain echocardiographic features can be used to either increase or decrease the probability that a visualized mass is due to endocarditis A vegetation is typically irregularly shaped, highly mobile, and attached to the free edge of a valve leaflet They tend to develop on the upstream side of the valve, that is, the ventricular side of the aortic valve and the atrial side of the mitral valve (Fig 13.1) Vegetations may be sessile or pedunculated but usually have motion that is independent of the valve itself Figure 13.2 is an example of endocarditis involving the tricuspid valve in a patient with a history of intravenous drug use The infectious process can be seen encasing the valve leaflets and chordae Severe tricuspid regurgitation was present Because vegetations often occur in the path of a high-velocity jet, their motion is frequently described as oscillating or fluttering The presence of significant mobility, or oscillating motion, is a classic feature of most vegetations In fact, the absence of mobility argues against the diagnosis and should suggest the possibility of an alternative diagnosis, including a healed vegetation The shape and size of vegetations are quite variable and may either increase (due to progression of disease) or decrease (due to healing or embolization) over time (Fig 13.3) Fungal vegetations tend to be larger than those caused by bacterial infections, and those involving the tricuspid valve tend to be larger compared with vegetations that affect the aortic or mitral valve (Fig 13.4) Table 13.1 COMPREHENSIVE ROLE OF ECHOCARDIOGRAPHY IN PATIENTS WITH ENDOCARDITIS Initial/early role: Identifies predisposing heart disease Early assessment in all cases of suspected IE Detects complications Assesses hemodynamic consequences Serial evaluation (assesses efficacy of therapy) Intraoperative assessment of extent of disease Prognosis (risk of complications) Establishes new baseline after therapy Repeat/follow-up role: TEE (after positive TTE) in patients at high risk for complications Repeat TEE (after negative initial TEE) if clinical suspicion persists Repeat TEE if suboptimal course during therapy (e.g., clinical deterioration, persistently positive blood cultures, worsening physical examination) FIGURE 13.1 An example of a large, mobile vegetation on the aortic valve that fills the left ventricular outflow tract, seen from the parasternal long-axis (A) and the apical views (B) Video 13-1a Video 13-1b Table 13.2 ECHOCARDIOGRAPHIC CRITERIA FOR DEFINING A VEGETATION Positive Feature Negative Feature Low reflectance High echogenicity Attached to valve, upstream side Nonvalvular location Irregular shape, amorphous Smooth surface or fibrillar Mobile, oscillating Nonmobile Associated tissue changes, valvular regurgitation Absence of regurgitation Although typically attached to a valve, vegetations may also attach to chordae, chamber walls, or any foreign body, such as a pacemaker lead, indwelling catheter, or prosthetic valve sewing ring Figure 13.5 is an example of endocarditis involving a porcine tricuspid valve as well as the pacing wire that extends through it The mass itself is typically homogeneous with echogenicity similar to that of the myocardium However, vegetations can occasionally be cystic or appear more dense and calcified The infectious process often alters valve structure and function As a result, some degree of regurgitation is associated with most cases of acute endocarditis In Figure 13.6, a patient with an aortic valve vegetation is shown The involvement is extensive, and the valve is partially flail There is severe aortic regurgitation A patient with significant mitral regurgitation associated with an extensive aortic valve vegetation is shown in Figure 13.7 Despite the presence of severe mitral regurgitation, neither a vegetation nor leaflet perforation were demonstrated Figure 13.8 shows a patient with intravenous drug use who presented early in the course of their endocarditis Small vegetations were noted on the aortic, mitral, and tricuspid valves These were not fully appreciated on transthoracic imaging FIGURE 13.2 Extensive infection involving the right heart from a patient with a history of intravenous drug use The vegetation involves the tricuspid valve (arrow) and chordae (arrowhead) Video 13-2 FIGURE 13.3 A: An example of disease progression from a patient with positive blood cultures, mild aortic regurgitation, and a sclerotic aortic valve but no definite vegetation (day 1) B: Two weeks later (day 14), a small vegetation is seen on the valve (arrow) C: By day 22, the vegetation has increased in size (arrow) and there is severe aortic regurgitation, despite antibiotic therapy Video 13-3a Video 13-3b Video 13-3c FIGURE 13.4 A very large fungal vegetation in an immunocompromised patient is shown Extensive involvement of the mitral valve is demonstrated in the apical long-axis (A) and four-chamber (C) views In B, the dimensions of the mass are recorded Video 13-4a Video 13-4c FIGURE 13.5 Transesophageal echocardiography shows a large mass (large arrow) attached to a pacemaker lead, most likely an infected thrombus There are also multiple small vegetations (small arrows) attached to the pacemaker wire in the right atrium Pericardial constriction, 124–125, 228–235, 236t echocardiographic diagnosis of, 229–232 annular velocities, 233–234 color Doppler M-mode recording, 233f Doppler echocardiographic findings, 232–234 exaggerated ventricular interdependence, 230–232 M-mode echocardiogram, 231f quantification of pericardial thickness, 224f, 229 effusive constrictive pericarditis, 234 restrictive cardiomyopathy and, 234–235, 236t Pericardial cysts, 239, 239f Pericardial diseases, 153 clinical overview, 217 congenital absence of pericardium, 239 criteria for use of echocardiography, 218t detection of, 218–224 echocardiography-guided pericardiocentesis, 237–239 etiology, 217t inflammatory processes of pericardium, 217 pericardial cysts, 217, 239 pericardial effusions, 217 postprocedural effusions, 236 Pericardial effusion, 441, 441f detection and quantification of, 218–220 M-mode echocardiographic view, 218, 218f small effusion, definition of, 218 three-dimensional echocardiographic view, 219, 222f two-dimensional echocardiographic view, 218 Pericardial space, 217 Pericardium, echocardiographic and multimodality, evaluation of, 218–224 differentiation of pericardial from pleural effusion, 224 direct visualization of, 220–224 pericardial fluid volume, 219–220 Period, definition of, 10t Peripartum cardiomyopathy, 516–517, 516f Piezoelectricity, definition of, 10t Point-of-care cardiac ultrasound, 94–95 advantages, 95 equiments, 94, 94f Polar video signal, 18 Porcine mitral prosthesis, 391f Postoperative cardiac motion, 125–126, 126f Postprocedural effusions, 236 Power, definition of, 10t Pregnancy, heart in, 723–724, 723f–724f cardiovascular and echocardiographic changes in, 723t Premature ventricular contraction (PVC), 123, 124f Pressure gradients, measuring, 201–205 Pressure half-time, 209–212 of aortic regurgitation jets, 211 of mitral stenosis jet, 210, 211f Pressure recovery, 204, 204f Prosthetic aortic valves, 390–395 range of normal values for Doppler evaluation of, 394t–393t Prosthetic mitral valves, 397–402 Prosthetic valve endocarditis, 364–367 transesophageal echocardiography of, 365–367, 365f Prosthetic valves approaches to repair, 378 complications, 405f, 405t acute rupture or fracture of calcified leaflet, 411 infective endocarditis, 411–418, 415f–420f mechanical failure, 418–421 obstruction, 402–411, 406f–407f, 411f prosthesis–patient mismatch, 402 thrombus formation, 408f–410f, 411 echocardiography of, 380f–382f, 387–388 appropriate use criteria for, 388t Doppler imaging, 383, 383f, 386–387, 386f–387f intraoperative transesophageal echocardiography of, 388t effective orifice area (EOA) of, 381, 387, 391 general approach to, 389–390 geometric orifice area (GOA) of, 387 normal function of, 379–387 recommendations for evaluation of, 379t right-sided, 421–423 types of, 377–378, 377t Proximal isovelocity surface area (PISA), 275 severity of mitral regurgitation, determining, 303–304, 306 Proximal isovelocity surface area method, 213–215 Pseudonormal diastolic dysfunction, 132f, 150f Pseudonormalization, 130–131, 147–149, 148f, 149t Pseudotumors, 689–690, 689f Pulmonary artery stenosis, 556 systolic pressure, 188 Pulmonary embolus, 712–713, 713f–715f Pulmonary hypertension, 188–189, 188f–189f, 288, 702–706 etiologies of, 702t Pulmonary regurgitation, 188–189, 190f, 208, 208f, 328, 330, 423, 593, 599 Pulmonary valve disease, 324t appropriate use criteria for echocardiography, 324t Doppler imaging of, 326–328, 328f flow, 199 infectious endocarditis of, 331 M-mode echocardiography of, 326–327, 327f normal, 324 regurgitation, 328–331, 329f–330f Doppler imaging of, 328–329, 329f flow velocity of, 330 severity of, 329 stenosis, 326–327, 554–556 congenital, 328f transesophageal echocardiography of, 326f vegetations, 368 Pulmonary vascular resistance (PVR), determination of, 208, 209f Pulmonary veins, 169–173, 219, 288 echocardiographic views, 86 flow in, 173f pulmonary venous flow factors affecting, 139 patterns, 137–140, 139f–140f transesophageal echocardiography of, 172f stenosis, 172, 172f, 550, 550f Pulse inversion harmonic imaging, 24 Pulse length, definition of, 10t Pulse repetition frequency, definition of, 10t Pulse, definition of, 10t Pulsed-Doppler imaging, 34 Pulsus paradoxus, 217 Q Quadricuspid aortic valve, 561f R R-theta, 18 Radiation-induced cardiac disease, 721–722, 721f–722f Radiation-induced mitral valve disease, 322 Rayleigh scatterers, 12 Raynaud phenomenon, 697 Regional left ventricular function, 112–118 mass, determination of, 116–117 cubed (Teichholz) formula, 116 M-mode calculations, 116 septal and posterior wall thickness, 116 quantitative techniques for analyzing, 115–116 wall motion abnormalities, evaluation of, 113–115, 114f, 114t, 124 nonischemic, 122t Regurgitant orifice area (ROA), 32 Regurgitant volume, 214 Remodeling, chronic, 112, 451–453 Renal transplantation, 695–696, 696f Resolution, definition of, 10t Restrictive cardiomyopathy, 234–235, 235f, 236t, 536–537 diagnosis of, 537–538 echocardiographic evaluation of, 537 idiopathic, 537 Restrictive filling, 131–132, 149 Restrictive physiology, 131–132f Retrograde atrial wave, 137, 139 Rhabdomyomas, 659–661, 661f Rheumatic mitral stenosis, 211f apical four-chamber view, 289f parasternal long and short-axis views, 289f, 292f transesophageal echocardiographic view of, 289f, 291f, 296f transesophageal echocardiography of, 289f transthoracic echocardiogram of, 289f, 291f Rheumatic mitral valve disease, 288, 288f Right atrial thrombi, 680, 682f Right atrium anatomic variants of, 174 blood flow, 178 compression of, 173, 174f diastolic pressure, 189, 190f right atrial appendage, 176 right atrial collapse, 226–227 right atrial dilation, 190f right atrial myxoma, 173, 174f right atrial pressure, 178 right atrial thrombi, 176 right ventricular systolic pressure (RVSP), 187–188 size and function, 173 volume, 173–173f Right ventricle, 179–192 collapse of, 225–226 echocardiographic evaluation/examination of, 546t right ventricular cardiomyopathy, 191 right ventricular enlargement, hypokinesis, and aneurysm formation, 192f right ventricular outflow tract, abnormality of, 554 right ventricular volume overload, 185–190 size and function, 191f Right ventricular hypertrophy, 185, 228 Right ventricular infarction, 442–444, 443f Right ventricular inflow, abnormalities of, 547–548, 548f–549f Right ventricular ischemia, 339 Right ventricular outflow tract abnormalities of, 331–332 definition of, 331 Ringdown artifact, 26 Ross procedure, 378, 423 S Sarcoidosis, 706–707, 707f Scleroderma, 697, 698f Sensitivity, definition of, 10t Septal thickness, measurement of, 100 Shadowing, 26, 26f, 58 from papillary muscle, 55 from prosthesis, 394 in color flow imaging, 34 Shone complex, 552, 553f Shunting atrial, 162, 164, 568, 685, 686f magnitude of, quantifying, 200, 201f right-to-left, 44–48, 443, 567, 686f, 699–700, 703, 714, 730–731, 754 Sickle cell anemia, 710–711, 711f Simpson rule, 103, 140, 431 Sinus of Valsalva, 240f aneurysms, 622–624 Sinus tachycardia diastolic dysfunction in, 153 impact on mitral inflow pattern, 135 Sinus venosus defects, 569 Sound wave, physics of A-mode signal, 18–19, 19f acoustic impedance, 11 acoustic mismatch, 11–12, 11f amplitude of, 10–11 B-mode signal, 18–19, 19f band of frequencies, 19 bandwidth, 19 frequency of, intensity of, 11, 35 interaction between tissue and ultrasound, 11–12 longitudinal waves, M-mode signal, 18–20, 19f–20f manipulation of ultrasound beam, 14–15 acoustic focusing, 15 dynamic transmit focusing, 15 focusing of, 14–15 relationship between intensity and beam width, 15, 16f using phased-array technology, 15f pulsing in ultrasound, 19, 19f reflection and refraction, 11–12 resolution, 15–18 axial, 15–16 contrast, 17 lateral, 16, 17f spatial, 15 temporal, 17 scattered echoes, 12 signal processing, 22–23 display options and, 20–21 spatial average (SA) intensity, 35 spatial peak (SP) intensity, 35 speckle tracking, 12 specular echoes, 12 time of flight, 19 ultrasound wave, wavelength of, 9–10 Spatial average (SA) intensity, 35 Spatial peak (SP) intensity, 35 Speckle tracking, 12, 105, 108, 141, 161 of right ventricular free wall, 186f strain and strain rate from, 109 Spectral analysis, 28 Spontaneous echo contrast, 680–682 Squamous cell lung cancer, 665, 667f Staphylococcus aureus endocarditis, 418 Starr–Edwards valve, 377, 379, 421, 422f Stenotic tricuspid valve, 562 Stentless bioprostheses, 377 Stimulated acoustic emission, 40 Strain and strain rate imaging of left ventricular systolic function, 108–112 global longitudinal strain (GLS), 109–110 in detecting abnormalities in myocardial contraction or deformation, 112, 112t limitation to, 110 longitudinal, circumferential, and radial dimensions, 109–110, 109f myocardial strain, 110 negative and positive strain, 109 with speckle tracking, 109 Stress echocardiography, 485t after myocardial infarction, 479–481 after revascularization, 481–482 appropriate use criteria for, 481t–483t clinical application of, 477–484 correlation with symptoms and electrocardiographic changes, 471–473, 473f detection of of coronary artery disease, 473–477 diastolic, 485–487 dobutamine, 454, 463–464, 484f, 535 of aortic stenosis, 261f in acute chest pain, 479 in nonischemic heart disease, 484–487 in women, 483 interpretation of, 466–470, 466f localization of coronary artery lesions, 471, 471f methodologies, 461–465 bicycle ergometry, 463 comparison of, 466t treadmill exercise, 461–462, 462f, 467f–468f physiologic basis for, 460–461 preoperative risk assessment, 482–483 prognostic value of, 477–479, 478t strain imaging, 470 stress modalities, 465–466 three-dimensional, 464–465, 465f types of stresors used in, 462t wall motion response to stress, 469–470, 469f Stroke volume, 198–199, 198f–199f calculation of, 198–199, 198f–199f, 277f in aortic regurgitation, 272 relation between ejection fraction (EF) and, 259, 262f relationship among pressure gradient, aortic valve area, and, 254–255, 255f Subvalvular aortic stenosis, 557–558, 558f–560f Superior vena cava, 44, 46–47, 65, 77, 176, 178–179, 181f, 235, 553, 564, 569, 594, 596, 604 Suprasternal views, 76–78 Supravalvular aortic stenosis, 563 Syncope, 720 Synovial sarcoma, 662, 663f Systemic diseases appropriate use criteria for echocardiography, 693t clinical presentations for, 711–715 echocardiographic findings in, 713–715, 713f–715f Systemic embolus, 682–689, 686f sources, 685t transthoracic vs transesophageal imaging, 685t Systemic lupus erythematosus, 696 Systemic venous connections, abnormal, 594–596 Systolic fraction, 137 T Takayasu arteritis, 649f, 650 Takotsubo syndrome, 719–720, 719f–720f Tardokinesis, 467, 467f Tei index, 118 Tetralogy of Fallot, 598–607, 600f–602f Thoracic aorta aneurysmal, 126 descending, 224, 611–616, 612f, 616f, 618, 626–627, 631–632, 637f, 754 echocardiography of, 86 Three-dimensional echocardiography, 87–94, 464–465, 465f cropping in, 92 degenerative aortic stenosis, 249f echocardiographic views multibeat acquisition, 89, 90f multibeat imaging, 90–91 multiplane imaging, 90, 92f real-time, 91–92 short-axis views, 90, 92f full-volume data sets, 91f image resolution in, 88–89, 89f left ventricular mass, 117 left ventricular systolic function, 106–108, 107f–108f limiting factor in, 88–89, 93 live 3D, 91–92 of left atrial volume, 160 proximal isovelocity surface area, 214 quantifying blood flow, 198 real-time, 91–93, 93f–94f size and distribution of pericardial effusion, 219, 222f stenotic orifice, 245, 249f transducers, 87–88, 90f visualization of stenotic orifice, 249f Thromboemboli, 176, 177f Tilting-disk prostheses, 377 Time velocity integral (TVI), 137, 195, 199–200, 212 of left ventricular outflow tract, 120–121, 122f Tissue Doppler imaging, 35, 35f color M-mode imaging of left ventricle, 118 Tissue Doppler mitral annular velocity, 135–137, 137f Tissue harmonic imaging, 23–24 application of, 24 features, 23 Total systolic time, 118 Training in echocardiography, 97t, 98 Transcatheter aortic valve replacement (TAVR), 378, 380, 382, 395, 397 Transcatheter mitral valve repair, 400–402, 400f–401f Transcutaneous mitral valve replacement (TMVR), 378 Transducers, 13 artifacts, importance of, 24–26 design, 14 effects on image appearance, 14f for real-time three-dimensional echocardiography, 15 linear array of elements, 15 far field or Fraunhofer zone, 14 phased-array, 15, 15f principles of, 13f–14f transmission of ultrasound energy, 18–20 dead time, 19 duty factor, 19 pulse length, 19 pulse repetition period, 19 ultrasound, 14 Transesophageal echocardiography, 82–84 biplane transesophageal echocardiogram, 83f data from, 82t degenerative aortic stenosis, 249f echocardiographic views, 84–87, 84f–87f bicaval view, 85, 86f four-chamber view, 84, 84f left atrial appendage, 85–86, 87f of aortic valve, 84, 85f of left atrium, 86 of mitral valve, 86, 89f of pulmonary veins, 86, 89f of thoracic aorta, 86, 88f of ventricles, 86–87, 90f short-axis views, 84, 85f, 86 morphology of abnormal aortic valves, 249f preparation of patient, 83 probes, 83–84 risks and contraindications for, 83t transducers for, 83, 84f Transposition of great arteries, 599–607 Transpulmonary shunting, 164, 167f Tricuspid annular plane systolic excursion (TAPSE), 705, 706f Tricuspid annulus, 332 Tricuspid aortic valve, 247f Tricuspid atresia, 607, 607f Tricuspid regurgitation (TR), 203f, 335–338 causes of, 337–338 pacemaker-related form of, 338 quantification of, 340–341, 340f–341f right atrial pressure, 343t right ventricular systolic pressure, 341–343, 342f–343f severity of, 335 echocardiographic and Doppler parameters of, 342t Tricuspid stenosis, 335 Tricuspid valve anatomy, 332 carcinoid heart disease of, 343–344, 344f disease, 324t appropriate use criteria for echocardiography, 324t Doppler evaluation of, 333–334 Ebstein anomaly of, 344–345 endocardial fibrosis of, 344, 345f prolapse, 336, 337f repair, 746–751 resection, 345–346, 345f–346f transthoracic and transesophageal imaging of, 332–333, 332f, 334f tumors of, 346 vegetation, 368 Tuberous sclerosis, 707, 709f U Uhl disease, 542, 543f Ultrasound wave, 9, 9f definition of, 10t diagnostic utility, disadvantages, Unicuspid aortic valve, 561f V Valsalva maneuver, 140–141, 147 Velocity definition of, 10t in air and tissues, 10t Ventricular assist devices, 509–514, 510f–514f Ventricular morphology, 546 Ventricular pacing, 124 Ventricular pre-excitation, 125 Ventricular pseudoaneurysms, 52 Ventricular remodeling, 451 Ventricular septal defect, 207, 207f, 445, 570–583, 580f–592f accuracy of echocardiography for detecting, 571 perimembranous defects, 572–573 Ventricular septal rupture, 446–448, 448f diagnosis of, 447 therapy for, 447–448 Ventricular septum, 118f, 122 Ventricular thrombus, 442 Ventricular torsion of systole, 112 Vertical tethering, 430 Visceral pericardium, 217 Volumetric flow, calculation of, 200–201 W Wall motion categorization, 469 response to stress, 469–470, 469f rest and stress, 467t subjective and nonquantitative nature, 467 Wall motion abnormality, 113–115, 114f, 114t, 429 analysis methods, 431–436, 431t 17-segment scheme, 433 assessment of ventricular geometry, 431, 432f left ventricular volume, 431–432 M-mode left ventricular measurements, 431, 432f myocardial thickening, 432 of segments, 433–434, 434f, 434t regional left ventricular function, 432 wall motion score index, 434, 434t associated with left bundle branch block, 122–123, 123f causes of, 461t Doppler tissue imaging, 435, 435f in constrictive pericarditis, 124–125f left bundle branch block or paced rhythm, 125 location of, 114–115 natural history of, 439 prognostic implications, 439–440 ST-segment elevation and/or Q waves in, 436 three-dimensional echocardiography of, 434–435, 434f treadmill echocardiography, 461–462, 462f Wall motion score index, 468 Wall stress, left ventricular, 120, 121f Wave See also Sound wave, physics of A wave, 160 E wave, 134 longitudinal, 10t P wave, 160–161 Q wave, 436 retrograde atrial, 137, 139 ultrasound, Wavelength, definition of, 10t Wolf–Parkinson–White syndrome, 125, 125f Z Zero crossing line, 300f ... vegetations can never rely on echocardiography alone but must take into account clinical factors FIGURE 13.6 Transesophageal echocardiography demonstrates a vegetation (arrow) on a partially disrupted... large, partially calcified mass (arrows) is seen on the mitral valve Video 13-17a Video 13-17b The value of three-dimensional echocardiography in this area continues to grow Figure 13 .20 is an... with transesophageal echocardiography, but the high accuracy of two-dimensional transesophageal echocardiography will make it difficult for three-dimensional transesophageal echocardiography to