Download Blood Velocity and Endocarditis

Blood Velocity and Endocarditis
By
SIAION RODBARD,
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DESPITE the successful use of anitibioties
in the treatment of infective endocarditis, the failure of therapy in perhaps onre
third of the patients with this condition keeps
it in the forefront as a major threat in heart
disease.1 2 The increasing incidence of endocarditis following cardiac surgery has also
provided an unexpected and disturbing feature of progress in cardiac management.3In addition to the practical problems of
management of this disease a number of per
plexing clinical and laboratory questions re
main. Thus, the argument as to whether the
locus of the infection requires previous
trauma, inflammation, vascularization,6 or
deformity7 remains undecided. The mechanisms in the progression of verrucae and
uleerationis, the formationi of thrombi, the
validity of spontaneous cures, and the tendency to recurrence, demand re-evaluationi.
It is curious that extremnely large quantities
of antibiotics are required to halt the growth
of inifective agents at the valve, while a thousandth of these concentrations (calculated for
extracellular body water) miay destroy the
same organisms in other sites in the body or
in vitro.Y2 The antibody titers for some of
the antigens of the infecting organism mav
have little or no inhibitory effect on the
mnicrobial growth at the infected valve or
artery.'3-1 5There can be little doubt that the
circulation is seeded continually by organisms that are swept as emboli from a nidus to
all the tissues of the body, with the production of local vascular occlusions; vet these
pathogenic showers seldom produce local infections or abscesses. If some of these prob-
M.D.,
Pn.D.
lems could be resolved, it might become possible to approach the management of the
disorder in a more adequate manner.
Some of these questions have been re-exainiimed on the basis of findings of pathologic
anatonlv and of studies of flow through specially prepared tubes. As a result, the point
of view has been developed that the hydro-dvnamics of the blood stream in the region
of a lesion can account for many of the special
characteristics of the endocarditides.
Theories of Infective Endocarditis
The pathogenesis of infective endocarditis
has been a favored topic of manv investigators. Primary points of departure have been
that the lesion is engrafted most commonly at
sites of edema. iniflaimmation, injury or vaseularization, thrombosis, or congenital anomalxv. Numerous workers have suggested that
tibe hvdraulies of the blood stream played a
key role in the pathogenesis of endocarditis.
Particular emphasis has been given to the
contact of the blood with the involved site, the
volume of flow, the presence of eddies, or the
force with which the apposing walls are com-
pressed.
1. Contact with the Blood. The likelihood
of involvement of a site has been considered
byr Allen6 -18 to be proportional to the volume
of blood in contact with the surface. lie
tlhought that bacterial localization was favored
by the impact of the blood streain against a
fibroplastic deformity or a congenital anomalv. The atrial surfaces of the mitral valves
and the ventricular surfaces of the aortic
v-alves were believed to be in better contact
with the blood than were other sites. The
oreatest volume of blood, however, flows during ejeetion when the mitral leaflets are closed.
the aortic leaflets are widely separated, and
xv,hen, as a consequence, the quantity of blood
im direct contact with the valves is minimal.
Similarly. the mitral valves are widely open
Froml the Puiblic Healtlh Resear chl TIustitute for
Chlroniic Disease, State UVii-eirsitv of Ne\w York at
Buffalo, New York. The Public Health Researeh
Institute for Chronic Disease is supported in part
by the New York State Department of Health.
Aided by grant H-2271 from the National HIeart
Institute, U. Se Public Health Service.
18
Circuiation, Volume XXVII. January 196.?
BLOOD VELOCITY AND ENDOCARDITIS
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during diastolic filling and the blood in contact with these leaflets must also be relatively
small.
2. Increased Flow. An increased stroke output, as in aortic insufficiency or following the
production of large peripheral arteriovenous
fistulas or in chronic hypoxia, is known to
enhance the tendency to endocarditis even
in the absence of direct trauma to a valve.
Highman and Altland"9 found proliferative
changes on the mitral and aortic valves in
young rats that were exposed repeatedly to
simulated altitudes of 25,000 feet; such a
situation can be expected to result in hypoxia
and an increased cardiac output. Intravenous
injection of bacteria resulted in infective endocarditis in some of these animals. The occasional failure of the combination of hypoxia
and bacteremia was explained by these workers as due to trauma or other hydraulic factors.
3. Blood Currents. Swirling currents and
increased pulse pressures in conditions such
as patent ductus arteriosus may stretch and
modify the vessel wall, with the production
of intimal thickening on the wall opposite the
entrance of the ductus. The infective process
is considered to occur on the damaged surface.20 The buffetinog proeess, however, probably involves all segments of the tract while
only a specific segment of the ductus becomes
the seat of the endocarditic lesions.
4. Compression. Since the line of valve closure is compressed repetitively as the leaflets
serve their normal function, endocarditis has
been attributed to a compressive process, especially when a subendothelial inflammatory
focus is present.2' Lepeschkin22 analyzed statisties of the incidence of endocarditis and
showed it to occur in direct proportion to the
pressures that act on a given valve. The highest pressures operate against the mitral valve
while those acting on the aortic valve are
somewhat less and the pressures on the valves
of the right heart are lowest. Endocarditis
occurs commonly, however, at sites that probably do not suffer compression, as at a ventricular septal defect or a patent ductus
arteriosus. Further, the specific locus of the
Cireulation, Volume XXVII, January 196S
19
lesions is always on the low pressure side of
the valve, as discussed below.
A Hydrodynamic Approach
Recent studies of the effect of blood flow
on the structure of vessels have indicated that
certain aspects of the development and normal structure of the blood vessels, as well as
their pathologic states, can be attributed to the
response of the vascular connective tissues to
the hydraulic forces of the blood stream.23 24
Thus, the strengthening of the arterial and
venous walls by the accretion of ground substance, collagen, reticulin, and elastin, the
genesis of valves, the progression of stenoses
and ectasias, as well as other vascular changes,
have been analyzed in terms of the potential
interactions between the physical forces of
the stream and the strains imposed on the tissues of the vessel wall.
Evidence for the role of hydrodynamic
forces in the genesis and maintenance of infective endocarditis is provided in a review
of the pertinent literature, in studies on the
effect of flow on the growth of bacteria, in
chemical reactions in the walls of specially
designed tubes, and in the deformative effects
of a stream on a nonrigid wall.
Present Concept
Endocarditis appears only when a high
pressure source (e.g., aorta) extrudes blood
at critical velocities through a narrow orifice
(patent ductus arteriosus) into a low pressure
sink (pulmonary artery) (table 1, fig. 1).
The velocity of the stream is a function of
the pressure gradient from source to sink. If
the orifice were wide, the large flow across it
would quickly dissipate the gradient; however,
when the orifice is narrow, the volume of the
shunt will be small and a large pressure gradient and a high velocity will persist.
As fluid enters an orifice, momentum causes
the streamlines to continue to converge, with
the result that the velocity is greatest a short
distance beyond the anatomic constriction, at
the vena contracta. This appears to be the
consistent locus of the endocarditic process.
It is at this point that hydrodynamic factors
operate through two discrete mechanisms to
20*;
R( MDBARD
-educe the colntact of streamuborne materials
wvitlh tlue vessel walls, i.e., bv thNe pattern of
streamxYline flow and byr eductio iii the raue
of vascular perfusion.
The quanltity of nultritive and defensive
inaterials passinog from the blood stream-t to
the vascular lining depends in large part oii
the conatact of stream-borne muaterials with the
eiidothelituti and the rate of fliltration:of
C.
1
t
p)lasina eoinpolienits into tlle imtini.a. 'When the
0~~~~~
CCC~~~~~~~~~~~~~C
t C;+@|5 .~~~~~~~~~~~~~~~~~°' + 9C
i
t 05=
U
X;_'
',C
C "
0
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~ t~ Ct-
5r
I
-I
speed+to each
j> i t>
siiiootllly w-ith. rev-
other, as occurs in miost norilal
b lood vessels only the boulndarv lamniilacomties
!71)100r
40;Uconitaet witlh the wvall. Thlis rlelatively slow
XZ; ginto
< t > -_
io,
lll0sin0g layer briings only a ver. limiited quiami-
w :t > C '>
5
lavers of tile streaiii imove
_V V
-
-
titv of streambornie iimaterials to the wall.
Streamiilines passing through a niozzle conitinue
to coanverer for a sliort distance bexvond the
orifice because of uomnentumn: as a, result a
small seetor of thIe vessel at the -venta colitracta
have olily negligille conta(t vs itli tlhe matfterials of the streani. );
The lateral pressFure eolntribuLtes to the inu-
vvill
c:
.rCL
2
ftritioi- of tlhe inormal vessel wall as well as to
its remuarkable resistance to infection and
-prbablv determiles certain aspects of its
struclture. Thus the lligh pressure in arteries
eolinpresses anid conidenises the tissu-es of the
_-Z rlitilno layers alil Ttl y thdereby inihibit the
rC
O developumienit of the x asa vasortum in the intima anid inner miedia. At sites of highch
locity, however, the pressure nmay be very low.
even iii ani arterial system. rrlis is because
the total onrergy of a h-ydraulic svstem is the
~~~~~~~~~~~~~~~~~~C)
!_
1 <
sum of the lateral j)erfusiolnl1 pressure plus
the energy imaniLfested in the x elocity of thie
strean-i. Lateral pressure and perfusioni are
,m¢+.;i.axhitnalwhere flow is arrested since tIme entire hydratulic eimergv of the systeml distenlds
the vessel ai-id perf uses its wall. With flow,
solme of the hydraulie emiergy appears as
>
>
>u
-I
umO
ovemeut (kinletic energy) and the local perfalls.
ft-Lfsion
>=
pressure
.
CZ7r; Q
g
}Wheim the distending- pressure oii a segi-i'ent
of vessel wall- falls below aibient values
|
a localized suction xvill result and the fluiid
p)erfusiimg this segmne1it of tIme arterial wall or
x ! , -;4 > G f
X-alve lininig mnay8T tno longer comne (lirectly frotm
the hiood streain. Ilvstead. fluid from the mer4
C
L
itr
-4-
4=
4-
~D0
V flS
(Cl, 'rcu1atUi'
X X V IL J( rf(eh
21
BLOOD VELOCITY AND ENDOCARDITIS
SOURCE"
VENA CONTRACTA/
Figure 1
Flow through a p,ermeable tube. A high pressure source (at left) drives fluid through
an orifice into a low pressure sink. The curved arrows leaving the stream and entering
the wall in the upstream segment represent the normal perfusion of the lining layer.
Velocity is maximal and perfusing pressure is low immediately beyond the orifice
where the momentum of the stream converges the streamlines to form a vena contracta.
The low pressure in this segment results in reduced perfusion and may cause a
retrograde flow from the deeper layers of the vessel into the flowing stream.
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dia of adjacent segments of the wall where
perfusion persists, will tend to pass retrograde and to re-enter the blood stream at the
point of highest velocity (fig. 1). The intima
at this site would thus be perfused with a
fluid despoiled of its oxygen and nutrients
and surcharged with accumulated metabolic
end-products. Retrograde perfusion also may
diminish the facility with which leukocytes,
antibodies, and antibiotics can enter the site,
and may contribute to the deformation of
valve leaflets or vessel walls.23 27
This concept of retrograde flow is supported by catheterization data that demonstrate that the lateral pressure at a narrowing
may fall to "zero " levels or lower. Studies
on specially designed analogues also show that
the interaction of the stream and the wall is
minimal at the vena contracta.25 Certain effects of flow on lining materials in the walls
of a tube have been demonstrated in studies
of the effect of flow on bacterial deposition
and growth. In these experiments, nebulized
suspensions of Serratia marcescens were
blown through tubes of agar (fig. 2). When
the caliber of the agar tubes was uniform, a
few random colonies appeared on the agar
wall at the end of 16 hours of growth. Introduction of a nebulized suspension into the air
stream flowing through a venturi-shaped agar
tube resulted in a marked deposition on the
downstream segment of the throat. Bacterial
growth was so marked in this region as to
Cirulation, Volume XXVII, January 1963
form a thick raised collar in the lumen. These
results demonstrated that flow can determine
the site of deposition and the rate of growth
of bacteria on the walls of a tube. Similar
hydrodynamic effects may contribute to the
determination of the locus of deposition and
growth of organisms in infective endocarditis.
Sites of Clinical Endocarditis
A number of situations can be cited as
demonstrating that the lesion of endocarditis
requires only a sufficient velocity in a given
direction. For exanmple, in nonvalvular endocarditis and endarteritis, the process is consistently on only the downstream side of the
orifice.
Nonvalvular Endocarditis
Coarctation. Endarteritis is associated
quite frequently with coaretation of the
aorta,28-31 the lesion being found on the lips
of the stenosis immediately distal to the narrowing. When the orifice of the coaretation is
oriented so that the stream is directed against
the aortic wall, a satellite lesion may also develop beyond the coaretation.
Fistula. Systemic arteriovenous fistulas are
relatively vulnerable to infection.32 3 The
artery leading to the fistula is commonly enlarged, consistent with the increased flow
through it, and the pressure gradient across
the fistula is high. Fistulas often exhibit small
pedunculated vegetations (satellite lesions)
on the adjacent vein wall.33 The development
RODBARl)
V1 a tricitlar Septal Defect. Endocarditis
occurs in ventricular septal defects only wlheni
the abnormal orifice is relatively small and a
large pressure gradient persists. The lesions,
appearing invariably on the right side of the
eommnunication, may extend to the tricuspid
valve. There is, however, little or no involvemnent of the left ventricular surfacee
Valvular Endocarditis
Figure 2
and bacterial deposition. In jection of an?
Into the airstreamn pjassing from left to right th roagh ca venturi tu be re
slt. in a m(ximal deposition immediatelyi beyoncd
orifice. A collar of thick growth is seen consist entil at this point. Colonwis arranaged in streak
lines ai-e also seen on the wall beyond this point.
part of the supporting
The vertical bars ar)'e
*rStrrtch'I of the agar tube.
F'lo
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aw rosol containini-g bacter-ia
a
I.
of nuiiierous collateral vessels adjacent to the
fistuila makes it difficult to establish the exact
.:1lynani relation-ships of the endarteritis. The
(.cure, however, of this form of enidocarditis
w-henl the hydraulic basis is elirninated bv
surgery33 einphasizes the potential role of
ioigh velocity flow in the inifective process.
I)ictits Arteriosits. The ineidence of iiifece
tive enidocarditis at patent ductus arteriosus
is relatively high.37 40 In these, the vegetations
are f ound alimost always in. t lie pulmonary
arterv iiimmediately beyond the junction with
the ductus, i.e.. at the site of the vena contracta and the miiaximnal stream -velocity. The
aorta is seldom involv,ed by' these endocarditie
processes.
Endocarditis probablv occurs in. a ductus
unIlxIywheni its diameter is small. The high
veloeity of the jet stream-l produced by flow
thlrouigl-h the small duetal orifice mnay also inv-olve a portion of the wall of the pulnionary
arterv, The direetion. of flow of the shunit is
inflicated by the faet that miultiple snmall enboli in th-e systemni ecircuit are relatively unlc-omrnmorn in patent ductus arteriosus, whereas
nllibhi to the lun:gs oeeur commonly.
The infective lesions discussed in the foregooing sections provide examples in whiech
there ean be little doubt about the relationi
of the direction of blood flow and the locationof the lesion. In involvement of the cardiac
v,alves, the directioni of blood flow inivolved
itn tl-he local infectioii is less certain. An anial
vsis of the location of the valvular lesions,
however, permits the suggestioon that, as with1
the abnorrmalities noted above, the infectioun
appears on the dowv-nstreain side of an orifice
through which a high pressure gradient extrudes a regurgitanit stream of blood at high
velocities. This situation is observed most
clearlv when a fenestration develops in a cardiae valve.
Fenastration. Flow through aii aortic fenestration- probably does not occur during systole,
Since the leaflets are blown aside by the
stream; in diastole, flow through the fenestration is necessarilv from aorta to ventricle and
a loud diastolic murnur and otlher sign-is of
aortic valvular insufficieney mnav be present.
Characteristie of clinical and animnal findings,
a doughnut of inflamimatory mnaterial on the
ventricular surface of the orifice attests to the
regurgitant character of the flow; essentially
similar patterns emerge when an aneurysnm
of thie sinus of Valsalva ruptures into the
right atrium or another low pressure sink.4'- 42
Pr( dilectioon for Incompetent Yalves. It is
niot alwrays appreciated that the frequency of
bacterial endocarditis is mueh higher in th e
presenee of valvular incomupeteniee than in:
stenosis. For example, 10 of 30 cases in one
selected series of hospital cases of pure incoompetence were reported to have endocarditis.43 Cutler et al.44 have also noted that in
rheumatie heart disease, baeterial. vegetationis
(irrulatnov, Volxrne XX Vfi, January 1963
23
BLOOD VELOCITY AND ENDOCARDITIS
generally are found on incompetent mitral
and aortic valves, whereas pure acquired stenotic lesions are rarely sites of bacterial invasion.
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Mitral and Tricuspid VaZves. Perhaps the
most common site of endocarditis is on the
mitral valves.45 Examination of such valves,
especially in the acute process, reveals that
the lesion is characteristically on the atrial
surface adjacent to the line of closure. Considerable evidence may be cited to demonstrate that the process is associated with an
insufficiency rather than a stenosis. Endocarditis occurs fairly commonly in valves that
show no significant stenosis; especially is this
so in patients after only a few episodes of
rheumatic fever, long before stenotic processes
become manifest. Indeed, infective endocarditis is not a common finding in patients with
severe stenosis.
The hydrodynamic process may thus be
viewed as resulting from the high pressure
source of the left ventricle, which drives blood
at high velocities through the nearly closed,
but insufficient valves, to the low pressure
chamber of the left atrium. Satellite lesions
on the left atrial wall support this point of
view, as indicated below. The structure and
alignment of the polypoid exerescences on the
leaflets have been shown to extend in the direction of the left atrium as if they had been
pulled in this retrograde direction by a regurgitant flow.46
Aortic Valves. The aortic valve is involved
fairly commonly. In almost every instance,
the infective process is situated on the ventricular surface of the leaflets in line with a
high velocity regurgitant stream. Such lesions
are seen particularly in bicuspid valves, the
aortic insufficiency of syphilitic heart disease,
and in rheumatic fever. In these instances,
as well as in aortic valvular fenestration mentioned above, the dynamics may be explained
as due to the extrusion of blood by the high
pressure aortic source through the nearly
closed but insufficient aortic valve to the low
pressure sink of the relaxed left ventricle.
Lesions in the Right Heart. In accord with
the knowledge that the right ventricle norCirculation, Volume XXVII, January 196S
mally develops only a low pressure,47 primary
endocarditis of the tricuspid and pulmonic
valves occurs relatively rarely.20' 48-50 Disease
in some other part of the heart is usually present to account for abnormal pressure gradients.
The pulmonary valve is rarely the site of
bacterial endocarditis. Elevated right ventricular systolic pressures, however, as in
patent ductus arteriosus, pulmonary emphysema, left ventricular failure, or congenital
anomalies, may be sufficient to generate endocardial lesions on the ventricular surfaces of
the pulmonic valves or the atrial surfaces of
the tricuspid valve. Endocarditis of the tricuspid valve is associated with high right
ventricular pressures secondary to pulmonic
stenosis or pulmonary arterial hypertension.
Satellite Lesions
A high velocity stream can produce effects
at a distance from the orifice, as noted in several sections above. Such a stream through an
insufficient mitral valve may impinge upon
and roughen an adjacent segment of atrium.
producing a MacCallum patch. Similar involvement of adjacent areas is seen in aortic
insufficiency where the primary lesion is on
the ventricular surfaces of the aortic leaflets.
The high velocity regurgitant flow, which
streams in the direction of the chordae tendineae and their muscular attachments, may
generate local mechanical disturbances that
can open the way to rupture of these guy lines
of the mitral valve leaflets (fig. 3).
The rush of blood from an aortic insufficiency may also generate pseudovalvular
formations.51 When the jet impinges on the
wall of the aorta, a ductus, or the pulmonary
artery, local aneurysms may become evident.24
Endocarditis in Previously Normal Structures
Any distortion of a valve that permits insufficiency of the proper degree may serve as
a nidus for infective endocarditis.52 5 Even
when the valve is histologically normal, regurgitation because of high velocity flow can
provide the mechanical basis for an infective
process. Koletsky54 reported five cases of combined syphilitic heart disease and bacterial
,;;J4
)1'A I'd
2D
H)
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cardial infaretion with rupture of a papillary
muscle. The valvular insufficieney that resulted from the abnorimal positiont of the ni:
tral leaflet provided a basis for endocarditie
in;volvement of the presumptivelv previously
normal atrial surfaces of the mitral valves,
Secondary Endocarditis. Somrie evidence in
dicates that a primary infective endocarditis
miav lead to involvement of a second site. This
is documented in a number of eases of arteriivenous enidarteritis: infected fistuilas tenid to
enilarge with time and the flow throulgl thli
communication resuilts in an irnicreased strolwe
outtput and cardiae dilatation'. stt-l An aortle
diastolic murmu-lr, indicatinog valv fIar in sufficiency, may then appear in association Ax ith:
involvement of the aoirtic valve, whichl mavI
showv progression even after remova] of 4heb
peripheral fistula.34-31
Surgical Approaches
Figure 3
)epresentatiaon of the high reiocit, streams in.
mnitr((l and aortic insuffieieneij ancn siteUs of endocardtitL iesion.. Arrow at left indiecates a h igh arteri!l p,ressure th(ut qene rates regcurgitcmt flow, from.
r
aortit to rentricle. The ena contracta and the
endocarditic lesions appear at the reentricula r sturface of the ciortic vocles. The straom through the
iiieonipetent caortic valcle mai produee lesionas on
the rhordae tendineae of the aortic leaf of the
mitrafl oalie. If the maitral caires caniot seat properlq71 during ventricular s/ystole, the reqitrgitant
stream (arrow at riqht) irill pass to the sin k o f
the left aftrium and endocarditis wicill tend to bethe atrial surfacie of the mitrl
enrgrfted
t
n(-,ulocardiutm i;n line i'ithi the revale. The aal
on
conic
urqrita nt str?
m aij
a
shoir
fibrous
re
tio n.
etndocarditis; in one of these, the syphilitic
as confined to the root of the aorta
proeess
w
and the aeute bacterial endocarditis
parexitlv superinmposed
oni a
was ap-
normal aortic
valve. Another instructive case, without prevrious pathology of the -valve, was reported bv
Lehmann55 in
a
patient who suffered
a
nyo-
Success in eliminating en darteritis asso
eiated with systemic arteriovenous fistulas.3
together with improvements in anesthesia, the
sulfonamnide drugs, and transfusions, opened
the possibility 25 years ago that ligation of a
duetus might affect the theni inenirable endarteritides. Early workers57 who attempted this
approach feared that even if the ligation
were successful, vegetations persisting in thle
stumps of the duetus would continue to serv%e
as a source of emboli and bacteremnia. After
the first successful ligation of an uninfeeted
patent ductus arteriosus by Gross and Hubbard,58 Touroff and Vesell59, 60 ligated the
ductus in several eases of endoearditis and
aehieved prompt recovery from the infection}
AIore recently, surgical cure of endocarditis
by means of open-heart surgery of a ventrienlar septal defect has been achievedc.1 The
blood stream is freed of microorganisms immediatelv after closure of the defect, eveen
though bacteria may persist in the lesion andl
in contact with the blood. The prompt recovery of these patients and the absenee of recurrenee. emphasize the role of hydraulie
factors iin the genesis aind persistence of en]doearditis. since congenital abnormalities of the
vessel wall may be expected to persist despite
occlusion of the abnormal openinga
Circulation, Volume XXVI!.January 1196,7
BLOOD VELOCITY AND ENDOCARDITIS
Postsurgical Endocarditis. While surgical
technics have contributed to the treatment of
endocarditis, they have also led to this infection in patients subjected to heart surgery.61-65 For example, surgically induced
narrowing of the aorta, as at the site of placement of a Hufnagel valve, has been shown to
be the seat of endarteritis.66
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The Absence of Endocarditis
If anatomic abnormalities played a role in
the pathogenesis of endocarditis, this condition might be expected to be as common at
atrial septal defects and at larger ventricular
septal defects or widely patent ductus arteriosus, as it is when the communications are
small. Endocarditis, however, does not occur
in congenital defects that have a cross section
area large enough to abolish the pressure
gradient.
A survey of available data indicates that
endocarditis is associated with shunts of relatively small volume. The relatively high incidence of endocarditis in patients with small
ventricular septal defects contrasts sharply
with the rarity of the disease when the defect
is large. Such a conclusion can be drawn from
the data of Wood,67 which attributed the
causes of death in 53 necropsied cases of pulmonary hypertension with a shunt to the left
(Eisenmenger's complex) to hemoptysis, cardiac failure, fibrillation, or surgical intervention. It is of particular interest that no mention is made of bacterial endocarditis in any
of these cases. Berger et al.40 and others
failed to note endocarditis in patients with
Eisenmenger's complex. Dailey et al.68 have
recently noted the absence of endocarditis in
patent ductus arteriosus with reversed shunt.
The reduction in pressure gradient between
the two ventricles with its reduced tendeney
to high velocity flow can account for the absence of endocarditis in such patients. This
fact also challenges the direct pathogenic contribution of anatomic congenital abnormalities
in the production of endocarditis.
Atrial Septal Defect. Even though atrial
septal defeet69' 70 is a most common congenital
cardiac malformation, bacterial endocarditis
rarely complicates it. This absence of endoCirctlation, Volume XXVII, January 1963
25
carditis may result because the thin-walled
atria do not generate the high pressure gradient required for the development of the
process. Further, the defect is usually quite
large or multiple.
Shunting of a large volume of blood through
an atrial septal defect increases flow through
other orifices and may thereby contribute to
an increased susceptibility at another site.
Thus, in a few cases of endocarditis that have
been reported in patients with atrial septal
defect, the infective process has involved the
pulmonic, tricuspid, or mitral valves,'1 while
the atrial defect itself was not infected.
Aorta. Attention may be called to the absence of endocarditis in the aorta where high
pressures and pulses abound. Even when the
aortic and arterial walls are clearly damaged,
as in severe atherosclerosis, these abnormal
sites do not support endocarditic lesions. To
date, no report has appeared of endarteritis
at an aortic or arterial site subsequent to retrograde catheterization or arterial puncture.
Veins. It is worthy of note that lesions like
endocarditis do not occur in veins or their
valves even though these often serve as the
seats of inflammatory and thrombotic processes. The venous connection of an arteriovenous fistula may show involvement, but the
presence of a high pressure gradient abrogates
the normal characteristics of flow through
veins.
Reduced Cardiac Output. When the cardiac
index is reduced, the tendency to endocarditis
is diminished. Thus, many clinicians have
commented that endocarditis is relatively uncommon in chronic heart failure, especially in
mitral stenosis with atrial fibrillation. This
may be another instance where a weakened
heart or a reduced stroke output prevents the
development of the high velocities necessary
for the induction and persistence of the endocarditic process. On the other hand, endocarditis often precipitates acute failure by progressive damage to valves. The apparent
absence of endocarditis in myxedema may
also be noted.72
Spontaneous Heating. Prior to the advent
of specific therapy, oeeasional spontaneous
RODBARD
-?. iz
,..dw
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cUIrT's Of enidocarditis were reported. Eveir
tlhouo1i somne of these may have represented
diagnostic errors, others were probably true
eases of infective endocarditis.j3, 74 Olesen and
Fabricius,75 for example, described a patient
with gonococcal endocarditis who continued
to have pulmionary valvular regurgitation for
2-7 years, as indicated by clinical history and
(atheterization data. Morhous76 has doeuInelite(l a case of endocarditis of a patenit duetus arteriosus that cleared spontaneouslv and
in which the characteristic murmur disappeared. Spontaneous healing may result from
1losure of the orifice as a result of continued
iHAtinial proliferation, with the elimination of
the high velocity jet. The tenidenye to proglressive closure of stenotic lesions has been
demoonstrated in experimental studies.2i More
recentlyv catheterization data have beeome
aivalable to indicate that smiall orifices, as i
veitricular septal defects and patent ductus
arteriosusn may close in the natural history
o)f the condition.77 This belief is supported
an(I I illistrated by the cures noted above that
followed surgical occlusion of infected fistu
las. It is also gradually becoming appreciated
tlbat the static anatomic lesion exposed at
autopsy whieh formis the basis for pathologi(
liagnosis and classification of the ease, does
hiot necessarily reflect the dynainically changinig picture of the lesioni. Tllus, orifices may
increase in size relative to the chambers that
tlhey connect,24 or they m-ay unidergo stenotic
processes that mnay lead to physiologic or even2
anatomic closure."2
When progressive enlargenment of an orifice
takes )lace, the augmented flow places an iinereased ]oad on the heart and this miay lead
to .:ongestive failure. As the orifice is eii
ltir-ed, however the hemodynamic conditions
necessary for the persistenee of infective ei(docarditis mnay vanish and the process is
'eured " even though the cardiac failure mnay
ensu'e.
that drives blood at high velocities through a
narrow orifice coaretation, ductus arteriosus
ventricular septal defect, insufficient aortic or
mitral valve) into a low pressure sink (pulnmonary artery, atrium).
The high velocity of the streamii iminediately
beyoond the orifice is associated with a marked
drop in lateral pressure, and perfusion of the
intimua of this segment of the vessel is reduced: this is also the characteristic site of
the inlfective process. The inifrequeiney of peripheral niidatioin and abscess formation despite recnrrent bacteremia, and the rapid
clearing after surgical correctioln of high velocitv jets, as in ligation of a patent ductus
arteriosus, are in accord with the hvdrody
namie concept. An analysis of the literature
and experimental studies of the effects of flow
on deforminable channels and onl bacterial
growth anid chemical reactions are cited iin
support of this concept.
1.
2.
3.
4.
5.
6.
7.
8.
Summary and Conclusions
Exainination of the problemr of inifective
a hvdrodynamic point of
view indicates that it is associated with a high
p)eess-Lre source (aorta, left ventriele. etc.
ti11docarditis from
9.
10.
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C'renTation, T"lur XX H!!
rat oriy ti
Blood Velocity and Endocarditis
SIMON RODBARD
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Circulation. 1963;27:18-28
doi: 10.1161/01.CIR.27.1.18
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