The systemic
veins may be arranged into three groups: (1) The veins of
the heart. (2) The veins of the upper extremities, head,
neck, and thorax, which end in the superior vena
cava. (3) The veins of the lower extremities, abdomen, and pelvis, which
end in the inferior vena cava.
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The
Veins of the Heart
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Coronary
Sinus (sinus coronarius)
Most of the veins of
the heart open into the coronary sinus. This is a wide venous channel about
2.25 cm. in length situated in the posterior part of the coronary sulcus, and
covered by muscular fibers from the left atrium. It ends in the right atrium
between the opening of the inferior vena cava and the atrioventricular
aperture, its orifice being guarded by a semilunar valve, the valve
of the coronary sinus (valve of Thebesius).
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Tributaries.—Its tributaries are the great, small, and
middle cardiac veins, the posterior vein of the left ventricle, and the
oblique vein of the left atrium, all of which, except the last, are provided
with valves at their orifices.
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1. The Great
Cardiac Vein (v. cordis magna; left coronary vein) begins at
the apex of the heart and ascends along the anterior longitudinal sulcus to
the base of the ventricles. It then curves to the left in the coronary
sulcus, and reaching the back of the heart, opens into the left extremity of
the coronary sinus. It receives tributaries from the left atrium and from
both ventricles: one, the left marginal vein, is of
considerable size, and ascends along the left margin of the heart.
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2. The Small
Cardiac Vein (v. cordis parva; right coronary vein) runs in
the coronary sulcus between the right atrium and ventricle, and opens into
the right extremity of the coronary sinus. It receives blood from the back of
the right atrium and ventricle; the right marginal vein ascends
along the right margin of the heart and joins it in the coronary sulcus, or
opens directly into the right atrium.
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3. The Middle
Cardiac Vein (v. cordis media) commences at the apex of the
heart, ascends in the posterior longitudinal sulcus, and ends in the coronary
sinus near its right extremity.
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4. The Posterior
Vein of the Left Ventricle (v. posterior ventriculi sinistri)
runs on the diaphragmatic surface of the left ventricle to the coronary
sinus, but may end in the great cardiac vein.
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5. The Oblique
Vein of the Left Atrium (v. obliqua atrii sinistri[Marshalli]; oblique
vein of Marshall) is a small vessel which descends obliquely on the back
of the left atrium and ends in the coronary sinus near its left extremity; it
is continuous above with the ligament of the left vena cava (lig.
venæ cavæ sinistræ vestigial fold of Marshall), and the two structures
form the remnant of the left Cuvierian duct.
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The following cardiac
veins do not end in the coronary sinus:
The anterior
cardiac veins, comprising three or four small vessels which collect
blood from the front of the right ventricle and open into the right atrium;
the right marginal vein frequently opens into the right atrium, and is
therefore sometimes regarded as belonging to this group;
The smallest
cardiac veins (veins of Thebesius), consisting of a number of
minute veins which arise in the muscular wall of the heart; the majority open
into the atria, but a few end in the ventricles.
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Vein Of Interest
The Vein of Marshall, oblique vein of
Marshall or the oblique vein of the left atrium is
a small vein that descends on and drains the posterior wall of the left
atrium. It drains directly into the coronary sinus at the same
end as the great cardiac vein, marking the origin of the sinus. It
represents the persistent left horn of the sinus venous (left SVC) and is
important prenatally, but is of little importance postnatally.
Source of Focal AF
In humans, the sinus node is not
the only pacemaker. Boineau et al demonstrated widely distributed atrial
pacemaker complexes in the human heart. In the isolated, perfused canine right
atrium, ectopic pacemaker activity was most often found near the sinus node or
the crista terminalis. These pacemakers may exhibit different responses to
norepinephrine and acetylcholine. Scherlag et al reported that sympathetic
stimulation could also induce left atrial ectopic activity. To study the source
of these ectopic activities, we performed a computerized mapping study in the
isolated-perfused canine left atrium. Isoproterenol can cause automatic rhythm
with this preparation. On the basis of these findings, hypothesized that the Marshall
bundle may serve as a source of focal AF in humans.
In the present study, they
successfully cannulated the Vein of Marshall and
recorded sharp potentials directly from the catheter within the Vein of
Marshall. Because the Vein of Marshall is an
epicardial structure and the recording site was not close to the pulmonary
veins, it is unlikely that these sharp second potentials originated from the
extension of the atrial musculature into the pulmonary veins. Rapid activation
of the Marshall bundle might serve as a trigger of atrial arrhythmias,
including AF. Finally, they were able to use the Vein of Marshall catheter
as a guide for radiofrequency ablation. A radiofrequency lesion placed in the
posterolateral left atrium between the Marshall bundle insertion and the ostium
of the left inferior pulmonary vein resulted in successful treatment of the
focal AF. This finding suggests that the trigger of the focal AF episodes
resides not within the pulmonary veins, but in the Marshall bundle.
Vein of Marshall And Recurrent AF.
Atrial
fibrillation (AF) or flutter can recur after pulmonary vein (PV) antral
isolation (PVAI). The Vein of Marshall has been linked to the genesis of AF. The most accepted
strategy for catheter ablation of atrial fibrillation (AF) is pulmonary vein
(PV) antral isolation (PVAI), since the PVs or neighboring tissues are thought
to provide the source of AF-initiating ectopic beats. The vein of Marshall and
its associated myocardial fibers and nerves have been implicated in the genesis
of AF by multiple mechanisms: as a source of ectopic beats initiating AF,as a
connection pathway with neighboring myocardium and left PVs,and as a source of
arrhythmogenic autonomic innervation. Given its location on the epicardial surface
of the left atrial ridge, it is unclear whether a conventional PVAI reaches the
Vein of Marshall sufficiently to ablate it. Therefore, we hypothesized that Vein of Marshall-dependent mechanisms may play a role in AF recurrences after
PVAI.
Vein of Marshall as
a Mechanism of AF Recurrence
Although a wealth of
animal data supports the potential arrhythmogenic role of the Vein of
Marshall, its role in human AF
has been more elusive. Reports of paroxysmal AF initiating from Vein of
Marshall-dependent triggers
are abundant in the literature. Based on the potential role of the Vein of
Marshall triggering AF; its
well-documented sympathetic and parasympathetic innervation that can
create a pro-AF physiological state in the atria; and the Vein of
Marshall 's fibers connecting
to the PVs, which could bypass endocardial ablation lesions and lead to PV
reconnections, we had hypothesized that the Vein of Marshall could play a role in PVAI failures. However,
aside from atrial ectopic beats and Vein of Marshall tachycardia in a minority of patients, we
could not demonstrate AF initiation from Vein of Marshall triggers. This may reflect lack of
arrhythmogenicity from the Vein of Marshall, but it also could be due to limitations in
the stimulation techniques (isoproterenol, adenosine) used to unmask Vein of
Marshall triggers.
Reference
