diastolic mitral regurgitation - heart · valve closure during late diastole. atrial fibrilla-tion...

Brit. Heart ., 1969, 31, 468.

Diastolic Mitral RegurgitationHaemodynamic and Angiographic Correlation

MAYLENE WONG

From Cardiovascular Diagnostic Laboratory, Wadsworth Hospital, Veterans Administration Center, Los Angeles,California, U.S.A.

A better understanding of the factors involved inensuring competence of the mitral valve based onknowledge of the function of the leaflets, chordaetendineae, and papillary muscles has expanded theclinical range of systolic mitral regurgitation. Forall this, diastolic mitral regurgitation remains acuriosity. Late diastolic mitral regurgitation hasbeen described together with reversal of the leftatrioventricular pressure gradient in experimentaland clinical studies (Williams et al., 1968; Rutis-hauser et al., 1966; Lochaya, Igarashi, and Shaffer,1967). In these reports the mitral valve was estab-lished or judged to be normal, and, therefore, in-complete closure of the valve was a causal factor ofmitral regurgitation. A diseased mitral valve un-able to close tightly during systole might be regurgi-tant during diastole as well if left ventricular pres-sure were to exceed left atrial pressure. In the pastyear we have recognized systolic and diastolic refluxacross abnormal mitral valves in 4 patients whorepresent a spectrum of valvular heart disease. Wewish to present the haemodynamic and angio-graphic evidence for diastolic mitral regurgitation.Its incidence in 4 of 50 consecutive patients studiedfor rheumatic heart disease is frequent enough tomake it something to consider in any patient withmitral valve disease.

SUBJECTS AND METHODSEach patient was selected for pre-operative cardiac

catheterization on the basis of his clinical condition.The need for premedication was decided individually,and Cases 1, 2, and 3 received hydroxyzine hydrochloride("Vistaril" 100 mg.) intramuscularly before the study.Right heart catheterization was performed using No. 7Goodale-Lubin catheters passed from an antecubitalvein. The left heart was catheterized with No. 8

Received January 14, 1969.468

Lehman or Gensini catheters introduced from a brachialarteriotomy or percutaneously from a femoral artery.Cardiac output was determined from either duplicateindocyanine-dilution curves or by the Fick method.Simultaneous pulmonary artery wedge and left ven-tricular pressures were measured immediately beforeand within two minutes after the injection of contrastmedia for angiography. The pressures were obtainedusing Statham P23D strain-gauges and were recorded bya Sanborn multichannel photographic recorder. Thecalibrations and sensitivities of the gauges were matched;and the zero levels of each gauge were referred to themid-chest plane. Baselines were checked against thezero reference before and during each recording. Leftventriculograms were obtained on 35 mm. cinefilm at30 or 60 frames per second with the patient lying in theright anterior oblique position. Aortograms were takenwith the same technique with the patient lying in the leftanterior oblique position. Injections of 70 to 100 ml.of 76 per cent Hypaque were used for each exposure andwere delivered in 2 to 3 seconds with a Cordis injector.

RESULTSIn Table I the pertinent clinical data are sum-

marized, and anatomical findings observed at openheart operation are indicated.The reported auscultatory findings represent the

agreed observations of several examiners. All thepatients had atrial fibrillation.At operation the mitral valves showed typical

rheumatic changes with shrunken leaflets. In Case 1the anterior leaflet was flail; in Cases 2 and 3 thevalve was stenotic as well as regurgitant. All 3patients required mitral and aortic valve prostheses.Operation was not recommended at the time ofstudy for Case 4.The catheterization and angiography data are

listed in Table II. Two sets of heart rates andpressures are given for each patient. The uppersets are averaged values observed before the ven-

on June 8, 2020 by guest. Protected by copyright.

http://heart.bmj.com

/B

r Heart J: first published as 10.1136/hrt.31.4.468 on 1 July 1969. D

ownloaded from

http://heart.bmj.com/

Diastolic Mitral Regurgitation 469

TABLE IDIASTOLIC MITRAL REGURGITATION-CLINICAL AND SURGICAL FINDINGS

Case No., Aetiology Final Functional Auscultatory findings Electrocardiograms Surgical findingssex, age diagnoses class

1 M 43 Rheumatic Aortic and III-IV S, accentuated and pal- Atrial fibrillation, Mitral valve: attenuation ofheart mitral pable, S2 single and QRS-60', left ven- both leaflets, flail an-disease regurgitation loud, S3, opening snap tricular hyper- terior leaflet, nodular

inconstant, ASM 1/6, trophy, digitalis edges, no calciumADM 3/6, MSM 2/6, effect Aortic valve: rolled inver-MDM 2/6 ted edges, no calcium

2 M 41 ,, Aortic and III S, normal intensity, Atrial fibrillation, Mitral valve: fibrosis andmitral re- aortic closure absent, QRS + 30', digitalis heavy calcification ofgurgitation S3, no opening snap, effect both leaflets, area] 1-25and stenosis ASM 4/6, ADM 3/6, Cm.2

MDM 1/6 Aortic valve: extensive cal-cification of all leaflets,area 1-0 Cm.2

3 M 34 ,, ,, III S diminished, aortic clo- Atrial fibrillation, Mitral valve: fibrotic,sure absent, pulmonary QRS + 75°, left thickened, and stenoticclosure loud, S3, no ventricular hyper- Aortic valve: fused cuspsopening snap,ASM 4/6, trophy, digitalis and inverted edgesADM 3/6, MSM 2/6, effectMDM 1/6

4 M 44 ,, Mitral regur- II-III S, normal intensity, S2 Atrial fibrillation, Operation not performedgitation widely split, pulmonary QRS + 60', tall R

closure accentuated, S3, waves, digitalisno opening snap, MSM effect3/6, MDM 2/6, ASM1/6 transmitted? noADM

ASM, aortic systolic murmur; ADM, aortic diastolic murmur; MSM, mitral systolic murmur; MDM, mitral diastolic murmur; QRS,mean axis in frontal plane.

TABLE IIDIASTOLIC MITRAL REGURGITATION-CATHETERIZATION AND ANGIOGRAPHY FINDINGS

Case Body Cardiac Heart Pressures (mm. Hg) AngiogramstNo. surface index rate*

area (l./ (beats/ Rt. Rt. Puln. Pulm. Lt. Aortic Lt. Lt. Mitr. Aortic(mi.2) min./ min.) atrial ventr. art. art. ventr. atrial ventr. regurg. regurg.

m.2) wedge vol. vol. (syst.)

1 2 14 1-7 67 72 18 86/25 88/35 (55) 54/22 (30) 155/26 155/57 3+ 3+ 2+ 3+77 62/22 (32) 153/25 153/60

2 1-80 2-4 48 56 14 57/8 55/24 (33) 31/16 (2-0) 124/24 85/52* 2+ 2+ 1+ 2+53 198/44 127/78

3 1*80 2-4 54 54 5 36/4 36/15 (24) 24/14 (18) 150/13 122/51* 2 + 2+ 2 + 2 +73 56/26 (35) 198/15 156/54

4 1-66 2-5 81 83 3 3 12/4 (7) 121/5 1+ 2+ 2+ -

- 85 6 31/5 31/15 (20) 24/10 (14) 141/11 141/79

* Figures in left hand column refer to heart rates during left ventricular opacification.t Chamber volume and severity of valvular regurgitation are graded on 1 + to 4 + scale.* Brachial artery pressure.

triculographic studies; the lower sets, values ob-served after. Fig. 1 to 4 are representative of thetracings from which the upper set of pulmonaryartery wedged and left ventricular pressures werederived. The pulmonary artery wedge was treatedas a measurement of left atrial pressure, and com-pared with the left ventricular pressure tracing it isdelayed by 004 to 008 second. All four tracingsshow that in at least one cardiac cycle in each, leftventricular pressure exceeded pulmonary arterywedge during late diastole. The reversal of themitral diastolic gradient is less convincing in the

illustration from Case 3 because it is small andoccurs in only one cycle; other tracings from thesame patient recorded at four times greater sensi-tivity, however, also showed an occasional reversalof pressures during late diastole. High left ven-tricular end-diastolic pressures were recorded inonly 2 patients. In Cases 3 and 4, end-diastolicleft ventricular pressure was normal or only slightlyraised before and after the injection of contrastmedia. Heart rate influenced the reversed gradientin all the patients; the slower the rate, the greaterthe reversal. The reversed mitral gradient per-



/B


ownloaded from


Maylene Wong

FIG. I FIG. 3

FIG. 2 FIG. 4

FIG. 1 to 4.-Simultaneous pulmonary artery wedge (PAWP) and left ventricular (LVP) pressure tracingsrecorded in Cases 1 to 4, respectively. See text.

sisted after angiography in Cases 1 and 4. In Case 2,though the post-injection pulmonary artery wedgepressure was not recorded, the reversed atrio-ventricular gradient probably remained in view ofthe continued slow heart rate and extremely highend-diastolic pressure of 44 mm. Hg. In Case 3only, the heart rate accelerated after the angio-graphic study and pulmonary artery wedge pressureincreased, producing a forward mitral gradientwhich persisted throughout diastole.

Angiographic estimation of left ventricular andleft atrial volumes revealed a variation from markedenlargement in Case 1 to slight enlargement inCase 4. Aortic valvular regurgitation was shown in3 patients but was severe only in Case 1. In Case 4an aortogram was not performed because aortic

regurgitation was clinically absent. Systolic mitralregurgitation occurred in all 4 patients and wasminimal to moderate. In all patients a small butdefinite jet of contrast media regurgitated across themitral valve during late diastole in one to five cardiaccycles, and was not associated with ventricular pre-mature beats. In Case 2, the diastolic regurgitantjet appeared to be larger than the systolic jet. Theheart rates during ventricular opacification, trans-lated from mean R-R intervals, approximated pre-injection heart rates. Fig. 5 illustrates the diastolicmitral regurgitation in Case 4.

DISCUSSIONDiastolic mitral regurgitation resulting from in-

complete closure of a normal mitral valve has been

470



/B


ownloaded from


:........ .;.........

FIG. 5.-Case 4. Retrograde left ventricular cine-angiogram in RAO projections. Late systole: the leftatrium is opacified by mitral regurgitation and is delineated anteriorly by the anterior mitral leaflet (AML);the regurgitant jet occurs near the postero-medial commissure. Late diastole, 0 3 sec. later: left atrialopacification is lighter due to the preceding rapid emptying of left atrial contents; the posterior fornix (PF),lying between the posterior mitral leaflet and basilar endocardium of the ventricle, is continuous with a

small diastolic regurgitant jet in the left atrium.



/B


ownloaded from


Maylene Wong

demonstrated in experimental and clinical heartblock. Williams et al. (1968) analysed, with a video-densitometer, left ventricular injections of contrastmedia, and detected small amounts of left atrialopacification. Similarly, Rutishauser et al. (1966),using thermodilution methods, injected cold salineinto the ventricle and recorded temperature dropsin the atrium. In both studies diastolic mitral re-gurgitation occurred after every atrial systole whichwas not followed after a normal interval by ven-tricular systole, when a reversed atrioventricularpressure gradient of 2 to 4 mm. Hg was recorded.

Reversal of late diastolic pressure between theleft ventricle and atrium or wedged pulmonaryartery has been recorded in patients with aorticregurgitation in normal sinus rhythm, first degreeAV block, and atrial fibrillation (Meadows et al.,1963; Oliver, Gazetopoulos, and Deuchar, 1967;Rees et al., 1964). Distinctive features were severeaortic reflux and high left ventricular end-diastolicpressures. The reversal of the atrioventriculargradient was related by some authors to increasedventricular inflow and reduced ventricular distensi-bility. Its significance was thought to be that itwould produce premature closure of the mitralvalve. Again in patients with severe aortic regur-gitation, Lochaya et al. (1967) demonstrated, angio-graphically, diastolic mitral regurgitation which wasassociated with a reversed atrioventricular gradient,and Aldridge, Lansdown, and Wigle (1966), in apublished abstract, reported similar findings. Theformer group did not see systolic mitral reflux, andsuggested that the diastolic mitral reflux was aconsequence of incomplete valve closure.

In the past year, we have recognized late diastolicmitral regurgitation in 4 patients, and in each therewas an associated reversal of the atrioventriculargradient. We have not seen the one without theother. Unlike the previous reports, aortic regurgi-tation was not uniformly severe in our cases, and theleft ventricular end-diastolic pressures were not in-variably or inordinately raised. Indeed, in 1patient aortic regurgitation was clinically absent,and in 2 patients the end-diastolic pressures werenormal, or nearly so. Notably, the mitral valveswere anatomically abnormal in all 4 patients.

Anatomical incompetence of the mitral valvesin these patients is adequate basis for the defectivevalve closure during late diastole. Atrial fibrilla-tion excludes an atrial mechanism producing thediastolic mitral regurgitation. Therefore, themechanism of the diastolic reflux in our patientsbecomes a question of the validity of the atrioven-tricular gradient. Strict equivalence of pulmonaryartery wedge pressure and left atrial pressures,

recorded through catheter-manometer systems ofidentical dynamic characteristics, is precluded bythe transmission of the pulmonary artery wedgepressure through the pulmonary vessels. Pressuresrecorded through a wedged catheter-manometersystem tend to be overdamped and the amplitudebetween the peaks and valleys of the pulmonaryartery wedge pressure compared to the left atrialpressure may be less (Connolly, Kirklin, and Wood,1954). The "y" point of the pulmonary arterywedge pressure would then be falsely high and morelikely to conceal a reversed gradient than to produceone as an artefact. For these reasons we feel thatif left ventricular end-diastolic pressure exceedspulmonary artery wedge pressure, it very likelyexceeds left atrial pressure.Large injections of contrast media made into the

left ventricle under pressure alter ventricular per-formance immediately (Hallermann, Rastelli, andSwan, 1964). It is, therefore, speculative to con-sider that atrioventricular pressure relationships arecomparable before and during the angiographicstudy. However, we are arguing from the positionthat despite any probable alteration, the angiogra-phic events agreed with the pressure data measuredimmediately before the injection. In addition,soon after the injection the reversed mitral gradientpersisted in 2 patients and probably did in a thirdwhose heart rates did not change significantly.Furthermore, if forceful left ventricular injectionsof contrast media alone produced artefactual dia-stolic mitral reflux, we should see it more frequentlythan we do.The appearance and magnitude of the reversed

diastolic atrioventricular gradient are dependent inpart upon the diastolic pressure-volume characteris-tics or distensibility of the ventricle. To whatpoint on its pressure-volume curve the ventricleprogresses in diastole is determined by the ventricu-lar filling rate and the length of the diastolic fillingperiod. Recent observations in experimental ven-tricular asystole have shown that the left ventriculardiameter reaches its maximal dimension within onesecond of asystole and does not increase furthereven when asystole is prolonged to 30 seconds (VanCitters and Ruttenberg, 1967). In patients withincreased ventricular filling rates due to either aorticregurgitation or systolic mitral regurgitation, thedistension limits of the ventricle may possibly bereached at normal heart rates. The reversed atrio-ventricular gradients are also influenced by theability of the atrium to empty and to relax. In thisregard the reversed mitral gradient observed withcompletely normal pressures in Case 4 is pertinent.The smallness of the left atrium plus its rapid

472



/B


ownloaded from


Diastolic Mitral Regurgitation

evacuation by cine-angiographic estimation prob-ably effected the low "y" point of the pulmonaryartery wedge pressure. We presume that bothrapid ventricular filling and rapid atrial emptyingmust concur in reversing the atrioventricular gra-dient at normal levels of pressure.The studies from these 4 patients show that

anatomically incompetent mitral valves permit re-gurgitation whenever, in the cardiac cycle, systoleor diastole, left ventricular pressure even minimallyexceeds left atrial pressure. Left ventricular end-diastolic pressure need not be greatly increased toreverse the atrioventricular gradient. The feasi-bility of a small gradient producing mitral regurgita-tion illustrated in these patients is consistent withthe earlier studies on heart block.Our inability to quantify the diastolic mitral re-

gurgitation makes its haemodynamic and clinicalsignificance conjectural. In these patients thereversed atrioventricular gradients were small andthe amount of diastolic reflux was not large, andprobably did not compromise effective strokevolume. However, in Case 2, the amount of dia-stolic regurgitation appeared to be at least equivalentto the systolic reflux and, therefore, the reductionof forward stroke flow from diastolic mitral regurgi-tation is potentially important in patients with highend-diastolic pressures. Additionally, in patientswith severe aortic regurgitation, mitral valve in-competence in diastole allows raised diastolic pres-sures to be reflected into the lungs (Welch, Braun-wald, and Sarnoff, 1957). The possible detrimentof diastolic mitral reflux in patients with normalventricular pressures and volumes would be adecrease in ventricular end-diastolic fibre stretch,with resultant loss in stroke volume.

SUMMARY

Late diastolic mitral regurgitation associated witha reversal of the left atrioventricular pressure gradi-ent occurred in 4 patients with mitral valve disease.Aortic regurgitation was severe in only one patientand absent in another. Left ventricular end-diastolic pressures were not invariably and inordin-ately raised. The incidence of diastolic mitral

reflux in this experience was 4 in 50 patients con-secutively studied for rheumatic heart disease.

It is concluded that anatomically incompetentmitral valves permit regurgitation in both systoleand diastole whenever left ventricular pressureexceeds left atrial pressure.

The author wishes to thank Drs. John Ellis, VictorLewin, Michael Wong, and Richard Ziemba for helpwith the catheterizations; and to acknowledge technicaland nursing assistance from Jim Beazell, Carl Robinson,Sam Snyder, Leonard Steris, Beverly Mills, and MillieWilliams.

REFERENCESAldridge, H. E., Lansdown, E. L., and Wigle, E. D. (1966).

Diastolic mitral insufficiency. Circulation, 34, Suppl. 3,p. 42.

Connolly, D. C., Kirklin, J. W., and Wood, E. H. (1954). Therelationship between pulmonary artery wedge pressureand left atrial pressure in man. Circulat. Res., 2, 434.

Hallermann, F. J., Rastelli, G. C., and Swan, H. J. C. (1964).Effects of rapid injection of heparinized blood into rightand left ventricles in dogs. Radiology, 83, 647.

Lochaya, S., Igarashi, M., and Shaffer, A. B. (1967). Latediastolic mitral regurgitation secondary to aortic regur-gitation: Its relationship to the Austin Flint murmur.Amer. Heart_J., 74, 161.

Meadows, W. R., Van Praagh, S., Indreika, M., and Sharp,J. T. (1963). Premature mitral valve closure. Ahemodynamic explanation for absence of the first soundin aortic insufficiency. Circulation, 28, 251.

Oliver, G. C., Jr., Gazetopoulos, N., and Deuchar, D. C.(1967). Reversed mitral diastolic gradient in aorticincompetence. Brit. Heart3J., 29, 239.

Rees, J. R., Epstein, E. J., Criley, J. M., and Ross, R. S.(1964). Haemodynamic effects of severe aortic regur-gitation. Brit. Heart_J., 26, 412.

Rutishauser, W., Wirz, P., Gander, M., and Luthy, E. (1966).Atriogenic diastolic reflux in patients with atrioventricu-lar block. Circulation, 34, 807.

Van Citters, R. L., and Ruttenberg, H. D. (1967). Left ven-tricular function in ambulatory dogs during experi-mental Adams-Stokes seizures. Amer. 7. Cardiol., 20,350.

Welch, G. H., Jr., Braunwald, E., and Sarnoff, S. J. (1957).Hemodynamic effects of quantitatively varied experi-mental aortic regurgitation. Circulat. Res., 5, 546.

Williams, J. C. P., O'Donovan, T. P. B., Vandenberg, R. A.,Sturm, R. E., and Wood, E. H. (1968). Atriogenicmitral valve reflux: Diagnostic mitral incompetencefollowing isolated atrial systoles. Circulat. Res., 22, 19.

473



/B


ownloaded from


diastolic mitral regurgitation - heart · valve closure during late diastole. atrial fibrilla-tion...

Documents