Left atrial appendage systolic forward flow

Left Atrial Roberto

Appendage

accurate evaluation of anatomic structure and function of the left atria1appendage(LAA).2-4 Although it is well established that there is an association of LAA thrombi and left atria1 spontaneousecho contrast with a history of peripheral embolism,2 only recently has a study focused on LAA Doppler flow signals.3 Kortz et al3 reported a quadriphasic pattern of LAA flow in normal subjects without overlapptig of tachycardia-related waves: a diastolic forward flow just after mitral valve opening is followed by a diastolic backward flow due to LAA recoil; subsequently, a forward and a backward flow wave respectivCly due to LAA contraction and relaxation can be detected. ... We report our observations on a new LAA flow pattern characterized by the presenceof an additional systolic forward flow wave after LAA relaxation. After the first occasional observation of a systolic LAA flow wave, a study was undertaken to characterize this new tiding. TEE was prospectively performed in 62 consecutive patients with sinus rhythm. Reasons for the examinations were determination of source of embolism (62%), assessmentof suspectedendocarditis (lo%), detection of aortic and mitral valve disease(18%), and evaluation of valve prosthesis (10%). Ten patients were excluded from the sttidy becauseof inadequate representation of the LAA. The study group consistedof 12patients (mean age 51 f 16 years) in whom the presence of LAA systolic forward flow was observed. Anesthesia of the hypopharynx was p&formed with 10% lidocaine spray. For sedation, patients were given a mean intravenous dose of 2 mg of midazolam. TEE was performed using a Sonos 1500 (Hewlett-Packard, Andover, Massachusetts),a Sonolayer SSH 140-A (Toshiba, Tokyo, Japan),or a Domier (DeutscheAerospace, Munich, Germany) ultrasound system equipped with 5 MHz multiplane phased-array transducers. The LAA was mainly visualized in the longitudinal view and the probe adjusted to maximize its dimensions. Flow velocities were obtained by positioning the sample volume inside the left atria1 appendageat the point that offered the best alignment with its flow and avoided the noise signal due to wall motion. Furthermore, color M- and B-mode of the left atrial appendageflow were recorded. The presenceof systolic forward flow after LAA relaxation was assumedwhen there were concomitant pulsed Doppler signal and color B- and M-mode findings. Pulmonary venous velocity recordings were obtained with From the Department of Cardiology, University of Essen, Essen, Germany, and the Department of Cardiology, General Hospital, Viale delle Fosse 43, 36061 Bassano del Gra pa, Vicenza, Italy. Manurevise B manuscript received and script received May 3 1, 1994; accepted August 3 1, 1994.

THE AMERICAN

Forward

Zeppelini, MD, Frank SchGn, MD, Giuseppe Gheno, MD, Jaroslaw Anja Balzereit, MD, Francesco Cucchini, MD, and Raimund Erbel,

he adventof transesophagealechocardiography(TEE) T has greatly improved the ability to detect cardiac sourcesof embolism.1This technique allows an easy and

204

Systolic

JOURNAL

OF CARDIOLOGY@

VOL. 75

Flow Drozdz, MD

MD,

the sample volume in the left upper pulmonary vein 21 cm from the orifice into the left atrium. Transmitral flow was assessedby pulsed Doppler, with the sample volume just to the atria1 side of the coaptatioh point of the mitral leaflets. Transesophagealechocardiographic estimation of the left ventiicular ejection fraction was performed by biplane area-lengthmethod using 4 transverse and 2 longitudinal chamber views.5 All echo and Doppler findings were recorded on an SVHS video recorder with a speed of 100 mm/s. The followhig parameters were dssessedas averages of 5 consecutive beats: the time interval from the beginning of the QRS complex on the electrocardiogram to (1) the beginning of the systolic LAA forward flow, (2) the onset, (3) the peak of systolic pulmonary venous flow, and (4) Ihe time of mitral valve flow. LAA area was assessedby means of frame-by-frame analysis at the time of LAA contraction, at the time of systolic LAA forward flow, andjust before mitral valve opening. Ali pulsed-Doppler velocities, time intervals, 2nd appendage area changes were measured off-line with a commercially available software system (Echo-Corn System,PPG Hellige, Freiburg, Germany). The differences among means of studied parameters were calculated using Student’s t test for unpaired data. A p value co.05 was considered statistically significant. Table I lists the characteristicsand the LAA flow patterns of the study subjects; in 3 eatients, all with slow heart rates, a pentaphasicLAA flow pattern was detected. The time relation betweenLAA systolic forward flow and mitral and pulmonary flow are displayed in Table II. LAA systolic forward flow begins 235 f 52 nis before mitral valve flow (p
15,

1995

TABLE I Clinical Characteristics and iefi Atrial Appendage Doppler Data of the Study Subjects Patient Number 1 2 3 4 5 6 7 8 9 10 11 12 Mean +SD

Age (yd 87 Sex 65M 25F 48F 32F 25M 69M 48M 55M 55F 64F 63M 66M 51 + 16

RR hsl

EF% 35 70 65 60 65 33 20 50 58 65 53 54.6 & 15

CAD = coronoiy artery disease; ic left ventricular ejection fraction;

4.50 747 657 565 800 550 615 763 754 616 905 682 675 + 125

Peak DFFl km/s)

Peak DBF bdsl

Peak DFF2 km/s1

Peak SBF km/s1

Peak SFF km/s1

Flow Panein

0 40 0 30 42.5 0 0 25.3 0 0 28.1 36.7 33.7 i- 6.9

0 32 0 0 34.4 0 0 0 0 0 12 0 26.1 + 12.3

87.5 63.5 46 91.5 93.1 47.3 37.6 94.1 80.5 60.5 62.7 146 75.8 zt 29.6

62.5 70

79.3 42 23.5 22.4 46.6 24.5 34 49.8 26 30.2 30.1 56 37.5 i 16.1

3 5 3 3 5 3 3 4 3 3 5 4 -

DBF = diastolic backward flow; DFFl N = normal; RR = electrocardiographic

= i lrst d. lo&c RR intervals;

51.9

80 90 46.3 58.9 68.35 71.1 39 61.1 73.6 64.8 * 13.9

Diagnosis CAD N N N N Septic shock Aortic stenosis Mitral incompetence N N N CAD

forword flow; DFF2 = second dlostolic forward flow; EF% = echocardiogroph SBF = systolic backward flow; SFF = systolic forward f!ow

TABLE II Time Intervals Between Electrocardiographic Q Wave and Systolic Left Atrial Appendage Forward Flow, Pulmonary Venous Flow, and Mitral Valve Flow Intervals QSlAAF hsl Meon *SD

140 * 49

Q-PVF (msl 57* * 51

QPPVF lmsl

QMVF hl

191t * 70

382* * 47

QMVF = time intern between electrocardlogrophlc Q wove and the onset of mitral valve flow; QPPVF = time interval between electrocordlogrophlc Q wove and the peak of systolic pulmonary venous flow; QPVF = time interval beiween electrocardiographic Q wove and the onset of systolic pulmonary venous flow; QSLAAF = time interval bebeen electrocardlogrophic Q wove and the onset of systolic left atria1 appendage forword flow. p
l

relevance of this finding. The LAA area at the time of systolic forward flow is less than LAA areajust before mitral valve opening, but signikntly larger than the LAA area at the time of left atria1 appendagecontraction, although a short time interval exists between LAA contraction and systolic forward flow. This implies that at the time of the systolic forward flow, the LAA area has nearly reached its maximum. The LAA dimension curve after LAA contraction is characterized by an early rapid volumic restoration, followed by a very slow phase until mitral valve opening$ the deflection point that separatesthe 2 phases seemsto be related to systolic forward flow as indicated by analysis of the chronologic sequence of these changes. The LAA is a blind anatomic structure; as a consequence,when its maximal volume is reached after the rapid filling phase,the reflection coefficient can be expected to be very high and the occurrence of a reflection wave probable.7,s LAA systolic forward tlow was demonstratedin 18% of our patients. This low prevalence may be explained by severalarguments:first, anatomic LAA features,such as multilobate appearanceor pectinate muscles, could produce dispersion of reflecting sitesx9;moreover,relaxation velocity, left atria1 pressure, viscous-elastic properties, and the relatively high compliance of LAA could interact and modulate the reflection phenomena.6,9J0 The clinical significance of this new tiding is still completely

flow; b = second diastolic forward flow; c flow; LUPV = left upper pulmonary vein.

q

systolic backward

undefined. It was observed both in subjects without echocardiographic evidence of heart disease and in patients with low left ventricular ejection fraction. A noticeable common characteristic was the presence of good LAA systolic function, as suggestedby the high velocity of the second diastolic forward flow. The use of the longitudinal view to study LAA flow seemsto be a sensitive approach because the ultrasound beam is BRIEF REPORTS 205

quite parallel to the LAA flow, and this may explain some ination provides reliable information on LAA function, of the differences with other studies in which LAA sys- but further investigations are neededto elucidate the relatolic forward flow was not described.3,4Doppler exam- tions between flow pattern and anatomic or functional features of this stnicture. cm2 6-

6 --

i 4 -3 --

1. Pearson AC, Labavitz AJ, Tatineni S, Gomea CR. Superiority of tmnsesophageal echocardiography in detecting source of embolism in patients with cerebral ischemia of uncertain etiology. J Am Co11 Cardiol 1991;11:66-12. 2. Garcia-Femandez MA, Torrecilla EG, San Roman D, Azevedo J, Buena H, Mar Moreno M, Delcan JL. Left &al appendage Doppler flow pattern: implications on tbrombus formation. Am Heart J 1992,124:955-960. 3. Kortz RA, Debname BJ, Dantzig JM, Bot H, Kamp 0, Visser CA. Left atrial appendage blood flow determined by tramesophageal echocardiography in healthy subjects. Am J Cardiol 1993;71:97&981. 4. Jue I, Winslow T, Fazio G, Redberg RF, Foster E, Shiller NB. Pulse Doppler characterization of the left atrial appendage flow. .I Am Sot Echocardiogr 1993; 61237-244.

5. Hozumi T, Schakudo M, Shah PM. Quantitation of left ventricular volumes and ejection fraction by biplane tramesophageal echocardiography. AmJCardiol1993;

2 --

72~356362.

1 -c-

LAAmin

LAAsff

LAAmax

FIGURE 2. Left atria1 appendage (LAA) area changes. IAAmax = IAA area just before mitral valve opening; LAAmin = MA area at the time of left atrial appendage contraction; IA/M = LAA area at the time of systolic forword flow; *p<0.05 compared with LAAsff.

Systolic

6. Hoit BD, Walsh R. Regional atrial distensibility. Am J Physiol 1992262: H1356-H1360. 7. O’Rourke MF. Vascular impedance in studies of arterial and cardiac function. Physiol Rev 1982;62:57@623. 8. Westerhof N, Sipkema P, Van Den Bos GC, Elzinga G. Forward and backward . I - .^_^, _.^ _-_ waves

m tt~e menal

System.

LarU2OVasc

KeS lY/L;b:w8436.

9. Taylor MG. The input impedance of an assembly of randomly branching elastic tubes. Biophys J 1966$x29-51. 10. Alexander J, Burkoff D, Schipke J, Sagawa K. Influence of mean pressure. on mtic impedance and reflections in the systemic arterial system. Am J Physiol 1989;257:H969-H978.

and Diastolic Effects of Beta-Adrenergic Stimulation in Normal Humans

Peter Bruce

Mark

Clarkson, MRCP, Nigel Mark Wheeldon, and Thomas Maclennan MacDonald,

MD, Catherine MD

Macleod,

From the University Department of Clinical Pharmacolog Ninewells Y Hospital and Medical School, Dundee DO1 9SY, Scotand, United Kingdom. Manuscript received June 7, 1994; revised manuscript received and accepted August 30, 1994.

lead electrocardiography and echocardiography were normal in all subjects. Subjects were studied on 2 separatedays, at least 1 week apart, in a balanced, randomized, single-blind, placebo-controlled, crossoverstudy. Subjectswere asked to refrain from alcohol, caffeine, and cigarettes for 24 hours and to fast for 2 hours before each study day. On each study day, subjectsreported to the researchlaboratory, and after voiding urine remained supine and inactive for the entire study period. No food or fluids were consumeduntil the study was completed. Two l&gauge intravenous cannulas were inserted into forearm veins, 1 in the right arm for blood sampling, and 1 in the left arm for infusion of isoprenaline or placebo. After 1 hour of supine bed rest, values of systolic, diastolic, and mean arterial pressures were measured in triplicate using a semiautomatic sphygmomanometer (Dinamap Vital SignsMonitor 1846:Critikon, Tampa,Florida); heartrate was determined with electrocardiographic monitoring (Hewlett-Packard 78352% Andover, Massachusetts). Baseline echocardiographic measurementsof diastolic filling parameters and aortic stroke distance were also obtained at this time. A placebo infusion was begun and measurementsrepeated 15 minutes later. A continuous infusion of either placebo (5% dextrose) or isoprenaline (SaventrineIntravenous, PharmaxLimited, Bexley, Kent, United Kingdom) in an equivalent volume of 5% dex-

206

JAN.

timulation of cardiac p adrenoceptors allows the heart to meet the metabolic requirementsof the body S through augmentation of cardiac output; this is achieved through both increased heart rate and increased stroke volume. In addition to these effects, it has been demonstratedin severalstudies that P-adrenoceptorstimulation also increasesthe rate of myocardial relaxation. l-3 In animal preparations it has been shown that myocardial relaxation (lusitropy) is more sensitive than myocardial contraction (inotropy) to P-adrenergic stimulation,4T5but the relative sensitivity of theseeffects in normal humans is not known. This study is designed to test t& hypothesis that in normal humans, P-adrenoceptor stimulation with isoprenaline has effectson myocardial relaxation at doses that have no effect on chronotropic or inotropic responses. ... Ten normal male subjects (mean age [+ SD] 22 f 3 years) were studied. Each provided written informed consentand the study was approvedby the TaysideCommittee on Medical Research Ethics. Physical examination, hematologic and biochemical parameters,and 12-

THE AMERICAN

JOURNAL

OF CARDIOIOGYe

VOL. 75

15,

1995