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Left atrial function and ventricular filling in hypertensive patients with paroxysmal atrial fibrillation
~y~e~ens~on may alter the diastolic pro the cQ~tractile(2,3) and electrical (4,5), sometimes evolving toward paroxysmal or sustained atrial fi~riilat~on(6,7).Loss ofatria! contraction may decrease cardiac output (8) or left vent ular ejection fraction (9). The anatomic and f~nctiQ~a~ atrial and ventricular characteristics associated with the develo ment of atrial fibrillation in human hypertension have not been investigated; the main question of whether the occurrence of atrial fibrillationis associated with distinct patterns of ventricular filling and atrial contractile activity remains unanswered. From the Istituto di Cardiologiadell’llniversiti degli Stuai, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricercbe. Centro Cardiolokw-Fondazione “I. Monzino”-IRCCS,Milan, My. Manuscript received September27, 1993;revised manuscriptreceived February 18, 1994,acceptedFebruary 25, 1994. Address for correw: Dr. Paolo Barbier, lstituto di Cardiologia, via Parea, 4,20138.Milano,Italy. 81994by the AmericanCollegeof Cardiology
e investigated patie ts with essential hy~e~ension and rillation because t eralds the onset of chronic atrial fib~llation (HI), ecause a study like this would not be feasible in chr atrial fibrillation because of the variability of the cardiac cycle (1I).
Hypertensive patients from a group of 280 untreated consecutive sttbjects ad stitute because of ressure were screened for inclusi aroxysmal atrial fib~llatio~(lastingfr 2 weeks and occurring not late admissions had been documented p them. Thirty-four subjects without atrial arrhythmias were selected patients and were matched for age and gender patients with the arrhythmia. Seventeen normal s similarage and gender were also investigated.The 07351097/94/$7.@0
1
BAXBIERETAL. PAROXYSMALATRIALFIBRILLAT~ONiNHYPERTENSlON
JAW
%I
July 1
,No.
1
K&i0
approvedby the EthicalCommitteeof our Institute and was illustrated to all subjectsinvolved. Diagnosis of essential
o be associated with excessive alcohol consumptton
sample volume (length, valve lea&t tip level
itral annulus endcm) diamethe same view from inner edge to inner edge of the basal insertion of the mitral leafletsand We lit transmiti flow. The following left ventricular variables were c&Mated: end-diastolic and end-systolic postet’ohtteralwall thickness (PWd and PWs, respectively, cm)and in+-cavitary diameters (LVDD and LVSD, respecl
The followingindexes were measured: isovolumic relaxation time (ms), as the time interval between the first high frequency deflectionof the second heart sound and the onset of mitral flow in early diastole; early late diastolic velocities (cm/s); Doppler dia early/l velocity ratio; deceleration time of early velocity (ms); velocity-time inte1sof early and late Doppler velocities (cm): and derived transmittal flow rates in early and late diastok, calculated, respectively, as early velocity-timeintegral x [~A~NS/2)2x 3.141,late velocity-time integral x [(ANND/2P x 3.141and earlynate ratio of transmitral flow. At any heart rate, when deceleration of the early diastolic wave was not linear, the
6llB 62 2 9 63 r 9* 193 f 23
1082 13 4.9t 0.5 2.82 0.4 1 L 0.3 1.1c 0.21 131r 58f 42 c 8.5 57.1k 20.6
ode and Two-Dimensional
Bchocardiographic bl
LADS (mm) LADa (mm)
37.8r 6 31 + 3.6
Left Atrial WI
EH 37.9f 4.c
44.6-c6.9*t
34.j e
40.4+ w’$
5-f
LADd (mm) Factional sbo~e~i~g (%)
27.6 i: 2.8 10.8 f 4.4
29.5 f 4.9 14.6 f 5.st
36.8 2 9.3’t 9.3 + 5.3*
E~&systolic area (cm*) End-diastolic area (cm*)
18.4 2 28 12.8 2: 2.3
20.6 + 5.1 14.9 f 4.5
26.1 2 3.9*$
Transport function (%)
29.5 k 13.2
28.6 2 11
31.6 2 85
Il.9
+ 5t
*p < 0.05 versus the EH group. tp c 0.05. &I c 0.001 versus normal subjects. LADa = M-mode left atria1 anteroposterior diameter before atria1 contractiw LADd = M-mode minimal left atrial anteroposterior diameter at the end of atria! contraction; LADs = M-mode maximal left atrial anbroposterior diameter at end-systole; other abbreviations as in Table 1.
BARBlERETAL. PAROXYSMALATRiAL FlBRILLATlONIN HYPERTENSION
I
”
JACC Vol. 24,No.I July Isw4:i65-7Q
eq~e~cy of episodes of e left atrial diameters and fractional shorten-
*p < U.QS, hypertensivepatientskth versus without arrhyth#p < 0.05, hypertensive patientswithoutarrhythmiaversus normalsubjects.LAFS = left atrial fractionalshorteni itiesandE/A ratio flow rates. *p < 0.05 and **p K’ 0.001, hypertensive s without arrhythmia. $7~e 0.05, hypertensive out arrhythmia versus normal subjects. Ap = peak v&city of A wave; Ep = peak velocity of E wave: EfrlAfr = ratio of transmitral flow rates: other abbreviations as in Figure 1.
tion or fractionai shorteningand left ventricular mass or wall thickness, end-systolic wall stress or fictional
ode echocardiogramsto have a high he evaluation of atria! co~t~cti~ity. Atrial diameter modificationsevaluated with this technique reflect left atria1volume variations in patients without thoracic:deformities, mitral valve disease or markedly dilated left atrium (14).
In hyperearly velocity and early/late ratio of peak velocities and of flow rates were reduced, whereas peak late velocity and flow rate were increased in norms!ensive subjects. In those with the arrhytharia, peak early velocity and ratio of early to late peak velocities were not dilTerentfivrn those of control subjects, but were increased significantly in hypertensive patients
eccentric hypertrophy seems to be a stronger precursor of chronic atrial fibrillation than arterial by~~e~sio~ alone (6.7).Myocardialdamage has been suggested to precede the onset of chronic atria1 fibrillation (7). Unlike results from previous studies using larger groups of ~aticnts with chronic atrial fibrillation(6,7), we were reasonably able to exclude left ventricular systolic dysfunction, decreased inotropic state, increased wdl stress or concentric Lypertrophy as
.2).
JAW Voll. 24, No. I July 1994: 164-70
without the arrbyt~m~a~as eter before atrial co~tractio~ rvatiotls have been atsuzaki et al. (2) in ttents, unselected for age.
atsuda et al. (41 and
Doppler flow pattern. In fact, left atria1 diameters were greater than in hypcrtetxive patients without the a~~~t~~ia, and atrial contractile function and left ventricular rapid range, were, respectively, filling,although within the with high blood pressure lower and greater than in without the arrhythmia. These diversities were unrelated to ventricular anatomy, wall stress and systolic funcart rate might have accounted partially for these owever, wbett patieentswith similar heart ences in tra~s~~tra~Doppler rates were compared, d vocal. Paroxysmalatrial fibrilvelocity patterns were un lation was associated invariably with altered atria1fractional shortening and was unrelated to the time interval from the last episode of arrhythmia. tlvc’.Reduced active "Nordi y' Duppler atria1emptying leads to Increased atrial residual volume at
mec~a~~~rn§ linking these three vari es remaia e~§~~t~a~~y that patiems whose undefined, one interpretation may atria1muscle fibers are more susce le to i~crea§edload, wall stress or inotropic stimulation (2) develop atrial tissue alterations facilitating depression of atria1 function, “normalization” of the ventricular fillingpattern aradfrag~~emtathe electrical impuIse con In hypertensive atria%fibrillation,enlargement and fr ression of the left atrium are associated with ventricular inflow during early dias
or consequence of paroxysmal atria1fibrillationremains to be determined.
170
BARBIER ET AL. PAROXYSMAL ATRIAL FIBRILLATION
JACC Vol. 24, No. I July 1994~165-70
IN HYPERTENSION
in mhral stenosis:factors influencingtheir relationship. Circukttion 1973;
I. Snider AR, Gidding SS, Rocchini AP, et al. Doppler evaluation of left ventricular diastolic tilling in children with systemic hypertension. Am J chrdid 1985;~:921-0. 2. Matsuraki M. Tami:ani M. Toma Y, et al. Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by letI atria! pressuretiension relation. Am J Cardiol 1991; 67:1121-6. 3. Matsuda Y. Toma Y, Moritani K, et al. Assessment of leftattial function in with-~<.hvoertensive heatt disease. Hypertension 1986;8:779-85. ---oatients r-.4. Loakii A, Pepi M, Agostoni PG, et al. Card& rhythm in hypilension assessed through 24 hour ambulatory electrocardiogaphic monitoring. Effects of Joad manipulation with atenolol, veraparnil, and nifedipinee. Rr Heart J 1!%3;~Ukll8--26. 5. Mcsserli FH, Ventuta HO. Mardi DJ, Dunn FG, Frohtich ED. Hy tension and sudden death. Increased ventricular ectopic activity in ventricular hypertrophy. Am J Med 1 6. Kannel WB, Abbo1t RD. Savage DD, ~~N~~ PM. Epidemiologic features of chronic atrial hhrillation. The F~min~h~ Study. N Et@ J 7. Gnundarson PT, ~or~eirsson G, JonmundssonE, SigfussonN, Hardarson T. Chronic atria! ~b~llati~epidcmio~o~i~ features and 14 year follow-up: a case control study. Eur Heart J I%7;8521-7. ynamic role of the atria with and tl. Carieton RA, Graettinger JS. The h
48: 1282-7. 20. Petersen P. Kastrup J. Brincb K, Godtfredsen J, between left atrial dimension and duration of atri Cardiol 1%7;60:382-4. Sheehan hi, et al. P,%-ialeol~eme~t as a 21. ion. A prospective ec~~~~iogm~~i~ study. Circulation 1930$32792-7. PA. 22. Brand FN. Abbott RI), Kannel prognosisof lone atriai fibrillation. 23. Benjamin EJ. Levy D. Anderson indexes of left ventricular diastohc function in normal subjects @be Framingham Heart Study). Am J Cardiol~~2;?~5~-~§. 24. 25.
26. 27. Shapiro El), ERron MR. Lima S, Ouyang P, Siu CO, atrial dysfu~~tiu~ after 28.
9.
Ration in patients initially believed to have dilated cardiomyopathy. Am J Cardiil 1992;69:15703. 10. Seizer A. Atrial fibrillation revisited. N Et@ J Wed 1982;306:1@44-5. Il. Karhner JS, Gauh JH, Rouchard RJ, Holzer 3. Factors influencing I ejection fraction and the mean rate of cirmrmferenlial tibre shortening durine atrial fibrillation in man, Cardiovasc Res 1974;8:18-25. 12. Takahashi N. Seki A, Imataka K, Fujii J. Clinical features of paroxysmat atrial fibrillation. An observation of ?4 patients. Jpn Heart 3 1 143-9. 13. Manning WJ. Leeman DE. Gotch PJ. Come PC. Pulsed Doppler evaluaelectrical caruioversion of atrial fibrillation. J Am Coil 17-23. II. Strunk BL, Fitqerald pp RL, Barry WH. The posterior aortic wall echocardiogram: its mla1ionshipto left atrial vohune change. Circulation 1976;58:744-50. r SL. Kwan OL, et at. Accuracy of ech~ardio~~~ phy versus ele~t~ar~io~mphy in detecting left ventricular hypertrophy: comparison with pod-mortem mass measurements. J Am Colt Cardiii 19832305-11. 16. Reich& N, Wilson J, St. John Suttou M, Plappetl TA, Hirshfeld JW. Noninvasive determination of left ventricular method and initial application. Cii th J, Pearlman AS. et al. Relation between echocarrmined left atrial sire and atrial fibrillation. Circulation N, Imataka K, Seki A, Fujii J. LeR atrial enlargement in th paroxysmal attial fibrillation. Jpn Heart J 1952;23:677-83. 19. Pr si.stP, Goldschlager N, Seizer A. Lefi atrial size and atrial fibrillation
29. Alam M, worsting C. Left veutricular function in patients with atriai fibrillatioa before and after ca~ioversi~~. Am J Cardiol 1~2;6~6~-6. 30. 31.
LC, Abi~a~er EG. ntricular pacemakers. Am 3
32.
, et al.The~m~rta~t role of left V~ntri~M~~ pressure in the left ventricular filling velocity
33.
of ~ppler~e~ve~ indexes of left ventricular diastolic function in humans. J Am Coil Cardiol 1%7;10:8 34. Thomas JD. Choong CYP. Aaehskampf FA, Weymao AK Analysis of the early lransmitral Doppler velocity curve: effect of primary phys changesand compensatory preload adjustmeet. 3 Am Coil Cardio 16:644-55.
35. Appleton CP. Natle LK, Popp RL. Relation of transmitral Row velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiopraphic study. J Am Co11 Cardiol19iJ8tl2:426-40. 36. Suzuki M, Hamada M, Sekiya M, Fujiwara Y, Sumimoto T. Hiwada K. Shortened deceleration time of early peak flow velocity in apparent normal transmitral Doppler flow in patients with dilated cardiomyopathy. Am J Noninvas Cardiol lW2;6:252-6.
e investigated patie ts with essential hy~e~ension and rillation because t eralds the onset of chronic atrial fib~llation (HI), ecause a study like this would not be feasible in chr atrial fibrillation because of the variability of the cardiac cycle (1I).
Hypertensive patients from a group of 280 untreated consecutive sttbjects ad stitute because of ressure were screened for inclusi aroxysmal atrial fib~llatio~(lastingfr 2 weeks and occurring not late admissions had been documented p them. Thirty-four subjects without atrial arrhythmias were selected patients and were matched for age and gender patients with the arrhythmia. Seventeen normal s similarage and gender were also investigated.The 07351097/94/$7.@0
1
BAXBIERETAL. PAROXYSMALATRIALFIBRILLAT~ONiNHYPERTENSlON
JAW
%I
July 1
,No.
1
K&i0
approvedby the EthicalCommitteeof our Institute and was illustrated to all subjectsinvolved. Diagnosis of essential
o be associated with excessive alcohol consumptton
sample volume (length, valve lea&t tip level
itral annulus endcm) diamethe same view from inner edge to inner edge of the basal insertion of the mitral leafletsand We lit transmiti flow. The following left ventricular variables were c&Mated: end-diastolic and end-systolic postet’ohtteralwall thickness (PWd and PWs, respectively, cm)and in+-cavitary diameters (LVDD and LVSD, respecl
The followingindexes were measured: isovolumic relaxation time (ms), as the time interval between the first high frequency deflectionof the second heart sound and the onset of mitral flow in early diastole; early late diastolic velocities (cm/s); Doppler dia early/l velocity ratio; deceleration time of early velocity (ms); velocity-time inte1sof early and late Doppler velocities (cm): and derived transmittal flow rates in early and late diastok, calculated, respectively, as early velocity-timeintegral x [~A~NS/2)2x 3.141,late velocity-time integral x [(ANND/2P x 3.141and earlynate ratio of transmitral flow. At any heart rate, when deceleration of the early diastolic wave was not linear, the
6llB 62 2 9 63 r 9* 193 f 23
1082 13 4.9t 0.5 2.82 0.4 1 L 0.3 1.1c 0.21 131r 58f 42 c 8.5 57.1k 20.6
ode and Two-Dimensional
Bchocardiographic bl
LADS (mm) LADa (mm)
37.8r 6 31 + 3.6
Left Atrial WI
EH 37.9f 4.c
44.6-c6.9*t
34.j e
40.4+ w’$
5-f
LADd (mm) Factional sbo~e~i~g (%)
27.6 i: 2.8 10.8 f 4.4
29.5 f 4.9 14.6 f 5.st
36.8 2 9.3’t 9.3 + 5.3*
E~&systolic area (cm*) End-diastolic area (cm*)
18.4 2 28 12.8 2: 2.3
20.6 + 5.1 14.9 f 4.5
26.1 2 3.9*$
Transport function (%)
29.5 k 13.2
28.6 2 11
31.6 2 85
Il.9
+ 5t
*p < 0.05 versus the EH group. tp c 0.05. &I c 0.001 versus normal subjects. LADa = M-mode left atria1 anteroposterior diameter before atria1 contractiw LADd = M-mode minimal left atrial anteroposterior diameter at the end of atria! contraction; LADs = M-mode maximal left atrial anbroposterior diameter at end-systole; other abbreviations as in Table 1.
BARBlERETAL. PAROXYSMALATRiAL FlBRILLATlONIN HYPERTENSION
I
”
JACC Vol. 24,No.I July Isw4:i65-7Q
eq~e~cy of episodes of e left atrial diameters and fractional shorten-
*p < U.QS, hypertensivepatientskth versus without arrhyth#p < 0.05, hypertensive patientswithoutarrhythmiaversus normalsubjects.LAFS = left atrial fractionalshorteni itiesandE/A ratio flow rates. *p < 0.05 and **p K’ 0.001, hypertensive s without arrhythmia. $7~e 0.05, hypertensive out arrhythmia versus normal subjects. Ap = peak v&city of A wave; Ep = peak velocity of E wave: EfrlAfr = ratio of transmitral flow rates: other abbreviations as in Figure 1.
tion or fractionai shorteningand left ventricular mass or wall thickness, end-systolic wall stress or fictional
ode echocardiogramsto have a high he evaluation of atria! co~t~cti~ity. Atrial diameter modificationsevaluated with this technique reflect left atria1volume variations in patients without thoracic:deformities, mitral valve disease or markedly dilated left atrium (14).
In hyperearly velocity and early/late ratio of peak velocities and of flow rates were reduced, whereas peak late velocity and flow rate were increased in norms!ensive subjects. In those with the arrhytharia, peak early velocity and ratio of early to late peak velocities were not dilTerentfivrn those of control subjects, but were increased significantly in hypertensive patients
eccentric hypertrophy seems to be a stronger precursor of chronic atrial fibrillation than arterial by~~e~sio~ alone (6.7).Myocardialdamage has been suggested to precede the onset of chronic atria1 fibrillation (7). Unlike results from previous studies using larger groups of ~aticnts with chronic atrial fibrillation(6,7), we were reasonably able to exclude left ventricular systolic dysfunction, decreased inotropic state, increased wdl stress or concentric Lypertrophy as
.2).
JAW Voll. 24, No. I July 1994: 164-70
without the arrbyt~m~a~as eter before atrial co~tractio~ rvatiotls have been atsuzaki et al. (2) in ttents, unselected for age.
atsuda et al. (41 and
Doppler flow pattern. In fact, left atria1 diameters were greater than in hypcrtetxive patients without the a~~~t~~ia, and atrial contractile function and left ventricular rapid range, were, respectively, filling,although within the with high blood pressure lower and greater than in without the arrhythmia. These diversities were unrelated to ventricular anatomy, wall stress and systolic funcart rate might have accounted partially for these owever, wbett patieentswith similar heart ences in tra~s~~tra~Doppler rates were compared, d vocal. Paroxysmalatrial fibrilvelocity patterns were un lation was associated invariably with altered atria1fractional shortening and was unrelated to the time interval from the last episode of arrhythmia. tlvc’.Reduced active "Nordi y' Duppler atria1emptying leads to Increased atrial residual volume at
mec~a~~~rn§ linking these three vari es remaia e~§~~t~a~~y that patiems whose undefined, one interpretation may atria1muscle fibers are more susce le to i~crea§edload, wall stress or inotropic stimulation (2) develop atrial tissue alterations facilitating depression of atria1 function, “normalization” of the ventricular fillingpattern aradfrag~~emtathe electrical impuIse con In hypertensive atria%fibrillation,enlargement and fr ression of the left atrium are associated with ventricular inflow during early dias
or consequence of paroxysmal atria1fibrillationremains to be determined.
170
BARBIER ET AL. PAROXYSMAL ATRIAL FIBRILLATION
JACC Vol. 24, No. I July 1994~165-70
IN HYPERTENSION
in mhral stenosis:factors influencingtheir relationship. Circukttion 1973;
I. Snider AR, Gidding SS, Rocchini AP, et al. Doppler evaluation of left ventricular diastolic tilling in children with systemic hypertension. Am J chrdid 1985;~:921-0. 2. Matsuraki M. Tami:ani M. Toma Y, et al. Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by letI atria! pressuretiension relation. Am J Cardiol 1991; 67:1121-6. 3. Matsuda Y. Toma Y, Moritani K, et al. Assessment of leftattial function in with-~<.hvoertensive heatt disease. Hypertension 1986;8:779-85. ---oatients r-.4. Loakii A, Pepi M, Agostoni PG, et al. Card& rhythm in hypilension assessed through 24 hour ambulatory electrocardiogaphic monitoring. Effects of Joad manipulation with atenolol, veraparnil, and nifedipinee. Rr Heart J 1!%3;~Ukll8--26. 5. Mcsserli FH, Ventuta HO. Mardi DJ, Dunn FG, Frohtich ED. Hy tension and sudden death. Increased ventricular ectopic activity in ventricular hypertrophy. Am J Med 1 6. Kannel WB, Abbo1t RD. Savage DD, ~~N~~ PM. Epidemiologic features of chronic atrial hhrillation. The F~min~h~ Study. N Et@ J 7. Gnundarson PT, ~or~eirsson G, JonmundssonE, SigfussonN, Hardarson T. Chronic atria! ~b~llati~epidcmio~o~i~ features and 14 year follow-up: a case control study. Eur Heart J I%7;8521-7. ynamic role of the atria with and tl. Carieton RA, Graettinger JS. The h
48: 1282-7. 20. Petersen P. Kastrup J. Brincb K, Godtfredsen J, between left atrial dimension and duration of atri Cardiol 1%7;60:382-4. Sheehan hi, et al. P,%-ialeol~eme~t as a 21. ion. A prospective ec~~~~iogm~~i~ study. Circulation 1930$32792-7. PA. 22. Brand FN. Abbott RI), Kannel prognosisof lone atriai fibrillation. 23. Benjamin EJ. Levy D. Anderson indexes of left ventricular diastohc function in normal subjects @be Framingham Heart Study). Am J Cardiol~~2;?~5~-~§. 24. 25.
26. 27. Shapiro El), ERron MR. Lima S, Ouyang P, Siu CO, atrial dysfu~~tiu~ after 28.
9.
Ration in patients initially believed to have dilated cardiomyopathy. Am J Cardiil 1992;69:15703. 10. Seizer A. Atrial fibrillation revisited. N Et@ J Wed 1982;306:1@44-5. Il. Karhner JS, Gauh JH, Rouchard RJ, Holzer 3. Factors influencing I ejection fraction and the mean rate of cirmrmferenlial tibre shortening durine atrial fibrillation in man, Cardiovasc Res 1974;8:18-25. 12. Takahashi N. Seki A, Imataka K, Fujii J. Clinical features of paroxysmat atrial fibrillation. An observation of ?4 patients. Jpn Heart 3 1 143-9. 13. Manning WJ. Leeman DE. Gotch PJ. Come PC. Pulsed Doppler evaluaelectrical caruioversion of atrial fibrillation. J Am Coil 17-23. II. Strunk BL, Fitqerald pp RL, Barry WH. The posterior aortic wall echocardiogram: its mla1ionshipto left atrial vohune change. Circulation 1976;58:744-50. r SL. Kwan OL, et at. Accuracy of ech~ardio~~~ phy versus ele~t~ar~io~mphy in detecting left ventricular hypertrophy: comparison with pod-mortem mass measurements. J Am Colt Cardiii 19832305-11. 16. Reich& N, Wilson J, St. John Suttou M, Plappetl TA, Hirshfeld JW. Noninvasive determination of left ventricular method and initial application. Cii th J, Pearlman AS. et al. Relation between echocarrmined left atrial sire and atrial fibrillation. Circulation N, Imataka K, Seki A, Fujii J. LeR atrial enlargement in th paroxysmal attial fibrillation. Jpn Heart J 1952;23:677-83. 19. Pr si.stP, Goldschlager N, Seizer A. Lefi atrial size and atrial fibrillation
29. Alam M, worsting C. Left veutricular function in patients with atriai fibrillatioa before and after ca~ioversi~~. Am J Cardiol 1~2;6~6~-6. 30. 31.
LC, Abi~a~er EG. ntricular pacemakers. Am 3
32.
, et al.The~m~rta~t role of left V~ntri~M~~ pressure in the left ventricular filling velocity
33.
of ~ppler~e~ve~ indexes of left ventricular diastolic function in humans. J Am Coil Cardiol 1%7;10:8 34. Thomas JD. Choong CYP. Aaehskampf FA, Weymao AK Analysis of the early lransmitral Doppler velocity curve: effect of primary phys changesand compensatory preload adjustmeet. 3 Am Coil Cardio 16:644-55.
35. Appleton CP. Natle LK, Popp RL. Relation of transmitral Row velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiopraphic study. J Am Co11 Cardiol19iJ8tl2:426-40. 36. Suzuki M, Hamada M, Sekiya M, Fujiwara Y, Sumimoto T. Hiwada K. Shortened deceleration time of early peak flow velocity in apparent normal transmitral Doppler flow in patients with dilated cardiomyopathy. Am J Noninvas Cardiol lW2;6:252-6.