Download Effective Closure of the Mitral Valve without Atrial Systole

Effective Closure of the Mitral Valve without
Atrial Systole
By EUGENE BRAUNWALD, M.D., S. DAvID ROCKOFF, M.D.
H. NEWLAND OLDHAM, JR., M.D.,
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THE PRECISE mechanisms responsible
for closure of the atrioventricular valves
under various physiologic and pathologic
circumstances have not yet been completely
defined. The factors considered to be of importance have been summarized by McKusick' and include (1) elevation of pressure in
the ventricle to a level greater than that in the
atrium, (2) contraction of the myocardium
surrounding the atrioventricular valve, resulting in a reduction of the cross-sectional area
of the valve ring, (3) contraction of the papillary muscles, thus drawing the valve cusps
together, and (4) approximation of the valve
cusps in the wake of the jet produced by
atrial systole. During recent years there has
been particular interest in the role played by
atrial contraction, an interest that stems largely from the recent reappraisals of atrial function in experimental animals and man.2-'0 It
has been suggested that the decline in atrial
pressure during atrial relaxation plays an important role in closure of the atrioventricular
valves.2' 5, 6 The availability of relatively simple technics for abolishing atrial fibrillation
and other atrial arrhythmias," and of cardiac
pacemakers that permit maintenance of the
normal sequence of atrial and ventricular contraction in patients with atrioventricular
block12 have provided additional impetus for
defining the role of an effective, appropriately
timed, atrial contraction in mitral and tricuspid valve closure.
In the course of diagnostic studies in which
selective angiocardiograms with left ventricular injection were performed, we became impressed that the presence, or the development
AND
JoHN Ross, JR., M.D.
of various cardiac arrhythmias was not necessarily associated with perceptible mitral regurgitation. This observation, which was similar to that of Bjork and co-workers,13 is not
compatible with the view that atrial systole is
always necessary for mitral valve closure. In
order to determine the frequency of this occurrence, all of our angiocardiograms with
left ventricular opacification were reviewed.
Methods and Results
A review of 500 selective angiocardiograms in
which the left ventricle was opacified yielded 106
studies in which the mitral valve was competent.
In 43 of these studies the valve was competent
in the absence of an appropriately timed atrial
systole. Twenty-nine of these 43 studies were
biplane serial angiograms, made with Schonander
film changers, at rates of 4 to 12 films per second.
The other 14 were cineangiocardiographic studies
at film speeds of 30 frames per second, with
either 16 or 35-mm. films.
The diagnoses of the patients studied are
listed in table 1. The contrast material (Renovist)
was injected into the left ventricle in 26 patients;
Table 1
Diagnoses in the Patients Studied by Angiography
Diagnosis
No. of patients
A. Patients with sinus rhythm
Tetralogy of Fallot
Aortic valve disease
Ventricular septal defect
Atrial septal defect
Hypertrophic subaortic stenosis
Transposition of great arteries
Mitral stenosis
11
8
5
5
6
2
1
38
B. Patients with atrial fibrillation
Mitral stenosis
Postoperative atrial septal defect
Cardiomyopathy
From the Cardiology Branch and the Clinic of
Surgery, National Heart Institute, and the Diagnostic
X-ray Department, Clinical Center, National Institutes of Health, Bethesda, Maryland.
3*
1
1
5
*Two of these patients had associated aortic valve
disease.
404
Circulation, Volume XXXIII, March 1966
CLOSURE OF MITRAL VALVE
405
in 19 of them the catheter was introduced
retrograde through the aortic valve, while in the
other seven patients transseptal left ventricular
catheterization was carried out.14 In 14 patients
the injection was made into the right ventricle,
the left ventricle being well opacified through a
large ventricular septal defect. In three patients
with severe aortic regurgitation the left ventricle
was opacified following injection into the ascending aorta.
In each instance the angiocardiogram
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was of
excellent quality, the left ventricle was densely
opacified and no detectable opacification of the
left atrium occurred (figs. 1-3). Special attention was directed to the area of the left atrium
and mitral valve to ensure that the projection
and exposure factors would have allowed recognition of even small amounts of regurgitated contrast material; angiocardiograms of less than excellent quality were not included in the analysis.
Standard lead II of the electrocardiogram was
recorded on a multichannel recorder before, during, and after the injection of contrast material.
When biplane serialographic studies were performed, the exposure of each film was recorded
together with the electrocardiogram. With the
cineangiographic studies precise synchronization
of the electrocardiogram with each cine frame
was made possible by a mechanical marker in
the radiologic field whose movement was triggered by the electrocardiogram. In some studies,
the Cinetrace,* a device which permits recording
of the electrocardiogram and other oscilloscopic
data directly on the cine film,15 was used.
Normal sinus rhythm was present prior to the
injection in 38 patients; 27 of them developed
multiple (three to five) ventricular extrasystoles,
while the other 11 exhibited brief bouts of ventricular tachycardia during the exposure of the
angiocardiogram (figs. 1 and 2). Atrial fibrillation was present in the other five patients prior
to the injection of the contrast material. No
ventricular extrasystoles occurred in two of them
(fig. 3); one patient developed multiple premature ventricular contractions during the exposure of the angiocardiogram, while the other two
developed ventricular tachycardia (six or more
consecutive ventricular extrasystoles).
Discussion
The results of many experiments in the anesthetized dog with an open chest, and usually
with an open pericardium, support the view
that atrial contraction can result in complete
*Electronics for Medicine, North White
New York.
Circulation, Volume XXXIII, March 1966
Plains,
closure of the atrioventricular valves.2,5-8 Using indicator-dilution methods, Daley et al.demonstrated in dogs that mitral incompetence develops with the onset of atrial fibrillation, Friedman and co-workers showed that
extrasystoles frequently induced mitral regurgitation,l'6 while Skinner et al. demonstrated
in dogs with heart block that mitral regurgitation was present when atrial systole was
improperly timed8 or when atrial fibrillation
was present.'7 In addition, Grant et al.18
showed in patients with complete atrioventricular block that a small reversed pressure
gradient (ventricular pressure exceeding that
in the atrium) existed across the tricuspid
valve following a prolonged diastole and suggested that the tricuspid valve had been
closed as a result of atrial activity. These
workers postulated that atrial relaxation reverses the atrioventricular pressure gradient
and is important in closing the tricuspid valve.
Alterations in the atrial pressure pulse, which
indicate that tricuspid regurgitation occurs
commonly in patients with atrial arrhythmias,7 19 20 have also been reported. As a
result of these experimental and clinical studies, the view that a properly timed atrial contraction is essential for complete closure of
the atrioventricular valves in early systole has
become widely accepted.
On the other hand, a number of investigators, using indicator-dilution methods with
left ventricular injection and left atrial sampling, have shown that atrial fibrillation or
multiple ventricular premature contractions
that alter the temporal relationship between
atrial and ventricular contraction do not induce mitral regurgitant flow in the dog.2'-24
Similarly, Paul et al., utilizing selective angiocardiography with left ventricular injection,
found no evidence for mitral regurgitation in
dogs with atrial fibrillation,25 while Vandenberg, Sturm, and Wood, working with a
videodensitometer to detect reflux of contrast
material, found that isolated ventricular extrasystoles were not associated with significant regurgitation.26 Both Conn and co-workers2' and Burchell9 have observed patients
with atrial fibrillation in whom indicator in-
BRAUNWALD ET AL.
406
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Figure 1
Lateral roentgenograms from a biplane serialographic left ventricular (L.V.) angiocardiogram
in a 27-year-old patient with valvular aortic stenosis. Panel A shows film with transseptal cathCirculation, Volume XXXIII, March 1966
CLOSURE OF MITRAL VALVE
407
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Figure 2A
Frames from a cineangiocardiogram performed in the left posterior oblique projection through
a retrograde left ventricular (L.V.) catheter in a 45-year-old patient with pure mitral stenosis,
during an arrhythmia superimposed upon atrial fibrillation (see fig. 2B). Note the absence of
regurgitation of contrast material into the left atrium (L.A.). The mechanical marker (C.M.)
was activated by the R wave of the electrocardiogram. Ao. = aorta.
jected into the left ventricle could not be
detected in the left atrium.
The present study was undertaken because
of the above controversy and the lack of information concerning the role played by atrial
contraction in closure of atrioventricular
valves in man. Forty-three patients with various forms of congenital and acquired heart
disease were found to have no detectable
mitral regurgitation in the presence of cardiac
arrhythmias in which the normal sequence
of atrial and ventricular contraction was disturbed. The arrhythmias in which the mitral
valve appeared to be competent included
atrial fibrillation alone (fig. 3), atrial fibrillation associated with frequent ventricular extrasystoles, sinus rhythm with multiple extrasystoles, and ventricular tachycardia (figs. 1
and 2). The angiocardiographic technic is a
sensitive one, and when technically excellent
films are available even trivial degrees of regurgitation can be detected. From these observations, it is concluded that a properly
timed atrial contraction is not always essential for mitral valve closure in man. In addition, the finding that mitral regurgitation was
eter in place, before contrast material has appeared. B and C are films exposed during systole
(note closed mitral valve) during arrhythmias, and D during diastole (note open mitral
valve). The left atrium (L.A.) does not opacify. Ao. = aorta. The electrocardiogram recorded
during the angiocardiogram and the timing of the roentgenograms are shown at the bottom.
Circulation, Volume XXXIII, March 1966
BRAUNWALD ET AL.
408
not present in seven patients in whom the
catheter was introduced into the left ventricle
through the mitral valve, indicates that transseptal left ventricular catheterization does not
necessarily interfere with complete closure
of the mitral valve.
From these observations we do not intend
to suggest that atrial systole never plays a role
in mitral valve closure, or that atrioventricular
dissociation, such as occurs with ventricular
ECG
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ECG
LI
CINE
MARKERi
B
B
A D
BA.
mm
Hg
INJECTION
0
T ME secs
Figure 2B
Oscillographic data recorded simultaneously with cineangiocardiogram reproduced in figure 2A, identifying
the cardiac cycle from which the cine frames are
presented. ECG = electrocardiogram. The position of
the frames from which panels A and D of figure 2A
were made are indicated. Panels C and D were exposed at equal time intervals between panels A and
B. The brachial arterial pressure (B.A.) is also shown,
as is the beginning of the injection of contrast material.
premature contractions, cannot result in valvular regurgitation. Indeed, we have observed
a large number of patients whose angiocardiograms exhibited mitral regurgitation in the
presence of atrial arrhythmias or atrioventricular dissociation, and the possibility cannot
be excluded that the absence of an appropriately timed atrial systole played a role in the
regurgitation that was present. Since all of
these patients had organic heart disease, it is
also possible that an abnormality of the mitral
valve was wholly or partly responsible for the
observed regurgitation. Thus, analysis of the
left ventricular angiocardiograms in which'
mitral regurgitation occurred provided no
definitive information concerning the importance of atrial systole in mitral valve closure,
and consequently conclusions cannot be
drawn concerning the relative incidence of
mitral regurgitation during various arrhythmias. The demonstration in 43 patients, however, that mitral regurgitation did not occur
in the absence of an appropriately timed
atrial contraction does allow the conclusion
that such an atrial contraction need not occur
for effective closure of the mitral valve to
take place.
Summary
There has been considerable dispute concerning the role of atrial contraction in the
closure of the atrioventricular valves. Selective angiocardiograms with left ventricular
Figure 3
Representative frames from a cineangiocardiogram performed in the left posterior oblique
projection through a catheter introduced retrograde through the aortic valve in a 41-year-old
patient with severe aortic regurgitation, aortic stenosis, and mitral stenosis. The basic rhythm
was atrial fibrillation and no ventricular arrhythmia occurred during the angiocardiogram.
No opacification of the left atrium (L.A.) occurred after there was, dense opacification of the
left ventricle (L.V.) as a consequence of the aortic regurgitation. Panel A, ventricular diastole; panel B, early systole; panel C, late systole.
Circulation, Volume XXXIII, March
1966
CLOSURE OF MITRAL VALVE
opacification in 43 patients having a variety
of arrhythmias that resulted in the absence of
atrial systole, or in an abnormal temporal
relationship between atrial and ventricular
contractions, revealed no evidence of mitral
regurgitation. From this observation it is concluded that a properly timed atrial contraction is not always essential for effective closure of the mitral valve in man.
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Effective Closure of the Mitral Valve without Atrial Systole
EUGENE BRAUNWALD, S. DAVID ROCKOFF, H. NEWLAND OLDHAM, JR.
and JOHN ROSS, JR.
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Circulation. 1966;33:404-409
doi: 10.1161/01.CIR.33.3.404
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