DK2985_C000 1..28 - AlSharqia Echo Club

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10CardiomyopathyVICKY SOULIÈRE, PHILIPPE L.-L’ALLIER, ANIQUE DUCHARMEUniversity of Montreal, Montreal, CanadaI. Hypertrophic Cardiomyopathy 215A. Epidemiology 215B. Clinical Features 216C. Anatomical Features 216D. Pathophysiology of OutflowTract Obstruction 216E. Echocardiographic Features 2181. M-mode and Two-DimensionalImaging 2182. Doppler and Color Flow Imaging 2213. Diastolic Function 222F. Condition Simulating HypertrophicCardiomyopathy 2231. Hypertrophy 2232. SAM and LVOT Obstruction 223G. Monitoring Therapy 2231. Intensive Care Unit andNoncardiac Surgery 2232. Nonsurgical Septal Ablation 2243. Surgical Septal Myectomy 225II. Dilated Cardiomyopathy 227A. Epidemiology 227B. Clinical Features 228C. Echocardiographic Features 2281. Chambers Dilatation 2282. Ventricular SystolicDysfunction 2293. Diastolic Dysfunction 2304. Secondary Findings 230D. Noncompacted LV 2331. Epidemiology 2332. Clinical Features 2333. Anatomical Features(Pathoanatomic Findings) 2334. Echocardiographic Features 2345. Conclusion 234E. Nontransplant Surgery 234III. Restrictive and InfiltrativeCardiomyopathy 234A. Definition 234B. Clinical Findings 234C. Echocardiographic Features 235D. Difference Between RestrictiveCardiomyopathy andConstrictive Pericarditis 236E. Amyloidosis 237F. Sarcoidosis 237G. Hemochromatosis 238IV. Conclusion 238References 238I. HYPERTROPHIC CARDIOMYOPATHYA. EpidemiologyHypertrophic cardiomyopathy (HCM) is defined as anondilated heart with right, left (or both) ventricularhypertrophy without an obvious cause such as aorticstenosis (AS) or systemic hypertension (1). This disorderis transmitted as an autosomal dominant trait in abouthalf of the patients and more than 200 mutations on 10different genes have been identified. Most of these215
216 Transesophageal Echocardiographyencode for sarcomeric proteins (such as myosin heavychain and tropomyosin), resulting in myofibrillar disarrayand dysfunctional myocytes, which in turn trigger reactionalhypertrophy. The vast array of genetic defects andtheir variable penetrance accounts for the heterogeneityof this disease, even within the same family. The causeof HCM in the remainder of the patients is unknown.This disorder has an estimated prevalence of 1/500 individualin the general population (2), but can be found in0.5% of the patients referred for an echocardiogram.B. Clinical FeaturesThe clinical manifestations are quite diverse. Patients withHCM can be completely asymptomatic or present withheart failure, exertional dyspnea, angina, postexertionalsyncope or serious arrhythmias. Sudden death could bethe first manifestation in as many as 10% and the estimatedannual mortality rate is 1–2%. It is of clinical importanceto distinguish between the obstructive and nonobstructiveforms of HCM as management strategies are usually tailoredto the hemodynamic status. A common characteristicfeature of HCM (obstructive and nonobstructive) is diastolicdysfunction (3). Abnormal relaxation of the left ventricle(LV) results from excessive wall thickness andcauses impaired ventricular filling, increased left ventricularend-diastolic pressure (LVEDP), and consequently,pulmonary congestion and dyspnea which can be potentiatedby outflow tract obtruction. Angina can occurwithout epicardial coronary stenosis and is thought toresult from multiple mechanisms: inadequate capillarydensity, impaired coronary flow (secondary to the highleft ventricular diastolic pressure or by myocardial bridging),or small vessel disease with further increase in O 2demand when left ventricular outflow tract (LVOT)obstruction occurs. Exertional syncope may be due tohypotension, caused by the inability to increase cardiacoutput (CO) because of the obstruction, together withinappropriate vasodilatation or arrhythmia. Sudden deathusually results from malignant arrhythmia; patients withHCM have an arrhythmogenic substrate that predisposesthem to ventricular arrhythmias, with a variable rolefrom triggers such as hypotension, ischemia or supraventriculararrhythmias (4).C. Anatomical FeaturesThe anatomic hallmark of HCM is ventricular hypertrophywith increased myocardial mass, small left ventricularcavity size, and dilated left atrium (LA) secondary tohigh LVEDP (3). The increased wall thickness varies inseverity and distribution; the “classic” asymmetric hypertrophyof the septal wall represents 70–75% of cases(Fig. 10.1), followed by basal septal location (10–15%),concentric symmetrical (5%), apical (5%) and isolatedhypertrophy of the lateral wall (1–7%). The mitral valvemay be intrinsically abnormal: the papillary muscles canbe displaced anteriorly and the leaflets can be elongated.These abnormalities, associated with a hypertrophied andbulging basal septum, will maximize the reduction inLVOT width, providing a substrate for dynamic subaorticobstruction. Obstruction may also occur at themid-cavitary level involving anomalous papillary muscleinsertion, preferential mid-ventricular, or papillarymuscle hypertrophy, and malalignment.The left ventricular function is usually hyperdynamic.However, long-standing HCM might evolve, and thehypertrophic segments could be replaced by thinner, dysfunctionalfibrotic walls with increased left ventricularsystolic and diastolic dimensions. This end-stage HCMcould be indistinguishable from dilated cardiomyopathy(DCM), and occurs in 20% of patients.D. Pathophysiology of OutflowTract ObstructionAlmost a quarter of the patients with septal hypertrophywill have significant resting outflow tract obstruction. Inthe others, the obstruction may be absent at rest but canbe revealed by provocative maneuvers or changes inhemodynamic conditions. There is a general consensusthat a true mechanical impediment to the left ventricularejection exists and results from the mitral valve (MV)and its apparatus moving anteriorly, the systolic anteriormotion (SAM).Rapid left ventricular ejection from the hypertrophiedLV will increase the velocity of blood flow across the narrowedLVOT, producing a Venturi effect. These forces willdrag the abnormal mitral leaflets and support apparatustowards the septum (5), creating a defect in the closureof the MV; the point of coaptation will then occur in thebody of the elongated leaflets instead of at their tips asin normal. The portion of the anterior leaflet distal fromthe coaptation point is then free to move with the subaorticflow (anteriorly and superiorly), leading to mitral leafletseptumcontact. This contact causes further narrowing ofthe LVOT, resulting in a SAM (Fig. 10.2). The severityand duration of the SAM is highly related to the extentof the subaortic obstruction (5). The SAM also creates agap between the mitral leaflets, in which mitral regurgitation(MR) can develop; this occurs predominantly in midto-latesystole, reflecting the dynamic nature of this insufficiency.The jet of MR is usually directed posteriorly(59%), but central (38%) and anterior jets (3%) can alsobe found, owing to concurrent prolapse of the posteriorleaflet (6,7). This sequence of events follows the “eject–obstruct–leak” pattern described in earlier angiographic
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TransesophagealEchocardiographyMult
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Published in 2005 byTaylor & Franci
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ForewordThe use of transesophageal
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xPrefaceThere are several other ind
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ContentsForeword Jean-Francois Hard
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ContributorsRobert Amyot, MD, FRCPC
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ContributorsxviiFrançois Marcotte,
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xxAbbreviationsCNS central nervous
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xxiiAbbreviationsPMLPpaPPHPPHTNPraP
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How to Use the Transesophageal Echo
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1Principles of UltrasoundALAIN GAUV
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Principles of Ultrasound 3Table 1.1
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Principles of Ultrasound 5the ratio
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Principles of Ultrasound 7transduce
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Principles of Ultrasound 9(A)(B)Fig
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Principles of Ultrasound 11certain
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Principles of Ultrasound 13PULSERBE
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Principles of Ultrasound 152. Trans
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Principles of Ultrasound 17(A)(B)TV
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Principles of Ultrasound 19(A)(B)(E
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Principles of Ultrasound 21to the i
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24 Transesophageal Echocardiography
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3TransducersFRANÇOIS HADDADUnivers
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Transducers 43(A)(C)(B)Figure 3.3 (
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Transducers 45more frequencies than
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Transducers 47Figure 3.10 Beam focu
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Transducers 49sound that propagate
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Transducers 51(A)(B)(C)Figure 3.15
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5Quantitative EchocardiographyJEAN
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Quantitative Echocardiography 91dim
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Quantitative Echocardiography 93Fig
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Quantitative Echocardiography 101Fi
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Quantitative Echocardiography 105in
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Quantitative Echocardiography 115On
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Quantitative Echocardiography 117Ha
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Quantitative Echocardiography 119fl
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6Imaging Artifacts and PitfallsROBE
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Imaging Artifacts and Pitfalls 123F
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Imaging Artifacts and Pitfalls 125F
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Imaging Artifacts and Pitfalls 127(
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Imaging Artifacts and Pitfalls 1391
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142 Transesophageal Echocardiograph
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Page 292 and 293: Aorta 263GRADE 1:NORMALAoGRADE 2:IN
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Aorta 265(A)(B)LALMCARAAoRVRCAFigur
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Aorta 267Figure 12.9Short- (A, B) a
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Aorta 269(A)(B)AORTAMOBILEATHEROMA(
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Aorta 271diameter (22). Aneurysms o
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Aorta 273(A)(B)NCCRALARCCMPALCCANEU
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Aorta 275(A)(B)LAARTEFACT(C)AoARTEF
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Aorta 277(A)(B)AoLATVRAFL TLPVRV(C)
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Aorta 279(A)(B)AORTICHEMATOMAAo(C)A
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Aorta 281(A)(B)FLTLAo(C)(D)INTRALUM
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Aorta 28331. Bansal RC, Chandraseka
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14Perioperative Role of TEE in Mech
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TEE in Mechanical Circulatory Assis
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15Native Aortic ValveFRANÇOIS A. B
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Native Aortic Valve 331Figure 15.2
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Native Aortic Valve 333(A)(B)ARANTI
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Native Aortic Valve 335(A) (B) (C)
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Native Aortic Valve 337(A)(B)LAAoLV
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Native Aortic Valve 339(A)(B)MVAoVL
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Native Aortic Valve 341(A)(B)LAAoVL
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Native Aortic Valve 343(A)(B)SAMLAI
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Native Aortic Valve 345(A)(B)AoVLAT
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Native Aortic Valve 347Although the
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Native Aortic Valve 349substitution
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Native Aortic Valve 351(A)(B)AoVLVO
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Native Aortic Valve 353(A)(B)LARPAL
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Native Aortic Valve 355(A)(B)LAAoVR
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Native Aortic Valve 357In those pat
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Native Aortic Valve 359Table 15.4 E
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Native Aortic Valve 36111. Levine R
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17Mitral ValveANDRÉ SAINT-PIERRELa
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Mitral Valve 385(A)SCHEMATIC VIEW(B
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Mitral Valve 387Figure 17.5 Echocar
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Mitral Valve 389(A)(B)LVP3A2LAAA1Fi
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Mitral Valve 391(A)(B)(C)(D)A1LAP1L
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Mitral Valve 393(A)(B)LARALVRV(C)(D
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Mitral Valve 395(A)(B)AoVFLAIL P1LA
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Mitral Valve 397(A)(B)P3LALVLAAA1(C
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Mitral Valve 399(A)(B)LALAALV(C)(D)
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Mitral Valve 401Table 17.3Mitral Re
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Mitral Valve 403(A)(B)MITRAL VALVEV
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Mitral Valve 405(A)EKG(B)PVFPaSDRES
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Mitral Valve 407Table 17.4BVR Echoc
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Mitral Valve 409Left ventricular sy
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Mitral Valve 411(A)(B)LALVAoRV(C)TM
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Mitral Valve 413Table 17.8StenosisT
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Mitral Valve 415identification of a
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19Pulmonic and Tricuspid ValvesFRAN
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Pulmonic and Tricuspid Valves 449Ta
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Pulmonic and Tricuspid Valves 451(A
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Pulmonic and Tricuspid Valves 459ti
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Pulmonic and Tricuspid Valves 463AN
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Pulmonic and Tricuspid Valves 46939
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23Intracavitary ContentsMARIA DI LO
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Intracavitary Contents 499(A)(B)PFO
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Intracavitary Contents 501(A)(B)LAL
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Intracavitary Contents 503artery ca
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Intracavitary Contents 505(A)(B)MYX
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Intracavitary Contents 507(A)(B)LVL
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Intracavitary Contents 509(A)(B)THY
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Intracavitary Contents 511wall clos
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Intracavitary Contents 513(A)(B)LAR
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Intracavitary Contents 515(A)(B)PER
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Intracavitary Contents 517dysfuncti
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Intracavitary Contents 519endocardi
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Intracavitary Contents 521and angle
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Intracavitary Contents 52317. Lando
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25Indications for Perioperative Tra
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Indications for Perioperative TEE 5
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570 IndexAortic aneurysmclassificat
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572 IndexColor jet area, 402Commiss
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574 IndexHypotension, 491Hypothermi
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576 IndexMitral valve repair, 394,
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578 IndexRight atrial thrombus, 517
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580 IndexTricuspid leafletsanterior
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DK2985_C000 1..28 - AlSharqia Echo Club

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