*From the Division of Cardiology, Department of Internal Medicine, Stadtspital Triemli, Zürich, Switzerland.
Correspondence to: Barbara Naegeli, MD, Division of Cardiology, Department of Internal Medicine, Stadtspital Triemli, CH-8063 Zürich, Switzerland; e-mail: firstname.lastname@example.org
The management of congestive heart failure remains an issue of
great interest. Encouraging data emerged over the last 2 years
supporting the use of multisite pacing in patients with severe
congestive heart failure and intraventricular conduction delay. We
present a case of acute biventricular pacing in a 81-year old man with
dilated cardiomyopathy and symptomatic congestive heart failure. This
novel form of pacemaker treatment resulted in a rapid hemodynamic and
progress in the treatment of congestive heart failure (CHF), the
quality of life for patients in New York Heart Association class III
and IV remains poor and the prognosis is dismal.1Besides
continuous research to improve the medical management of CHF, there is
increasing interest in nonpharmacologic treatment options. In the early
1990s, dual chamber pacing (DDD) with short atrioventricular delay was
used to improve hemodynamics in these patients.2–4 The
promising results, however, could not be confirmed in subsequent,
controlled studies.5–7 One possible reason that the
expected hemodynamic improvement in these patients did not take place
is a lack of synchrony between left and right ventricle, which may even
have been worsened by conventional pacemaker treatment.8–
Attempts to achieve a more physiologic pattern of conduction by pacing
in the right ventricular outflow tract as opposed to the traditional
right apical pacing showed some hemodynamic
improvement.9–10 Since the mid 1990s, there is increasing
evidence that the synchrony of the ventricles can be restored by
biventricular pacing.11–13 Few long-term studies with
biventricular pacing have been conducted so far, all of which showed
improvement of symptoms.14–15
We report of a 81-year old man, who has been in an excellent
state of health until about 10 months ago when he developed progressive
CHF. Dilated cardiomyopathy was diagnosed, and he was referred for
further workup and treatment. On admission, the patient had signs and
symptoms of severe CHF (New York Heart Association functional class
IV). Treatment with angiotensin-converting enzyme inhibitors and
diuretics had been started before admission, but had to be stopped
temporarily due to nausea and vomiting. ECG showed sinus rhythm at 70
beats/min, a 220-ms PR interval, intraventricular conduction block (QRS
duration, 140 ms), multiple multifocal premature ventricular
contractions, and short nonsustained runs of ventricular tachycardia.
An echocardiography study revealed an ejection fraction of 10%.
In view of the promising results with cardiac pacing in similar
settings, it was decided to perform biventricular pacing to improve the
patient’s critical hemodynamic condition.
Three 6F bipolar temporary pacemaker leads (Bard
Electrophysiology, C.R. Bard; Billerica, MA) and a Swan-Ganz catheter
(Baxter Healthcare, Edwards Critical Care Division; Irvine, CA) were
inserted by left subclavian approach. Electrodes were placed at the
right atrial appendage, the right ventricular apex, and a
posterolateral vein over the left ventricular free wall through the
coronary sinus to pace the left ventricle (Fig 1
). An external, constant-current, dual chamber demand pacemaker
(Medtronic 5388; Medtronic; Minneapolis, MN) was set at a fixed rate
that was 20 beats/min greater than the intrinsic sinus rate. The four
pacing modes used were as follows: (1) atrial demand pacing (AAI); (2)
atrio-right ventricular; (3) atrio-left ventricular; and (4)
atrio-biventricular. Biventricular pacing was achieved by connecting
the two ventricular leads by a Y bifurcated adapter to the ventricular
port of the pacemaker. A standard atrioventricular delay interval of
150 ms was used for all pacing modes.
Hemodynamic studies were performed in a supine, nonsedated state after
10 min in each pacing mode and during intrinsic rhythm. Midchest
position was used for the zero reference level. Cardiac output was
measured by the continuous thermodilution method, which is a generally
accepted method (CCO method; Baxter Vigilance; Edwards Critical Care
Division; Irvine, CA).16
The hemodynamic changes were seen quite rapidly over the course of
2 to 3 minutes. The plateau was reached after 4 to 5 minutes. The
results of the invasive hemodynamic measurements in each pacing mode
are summarized in Table 1
. An increase in cardiac output was noted in all pacing modes; however,
the most striking improvement was seen during atrio-biventricular
pacing (Fig 2
). A slight decrease in pulmonary capillary wedge pressure (PCWP) was
noted with biventricular pacing (Fig 2). When compared to AAI pacing at
the same rate, biventricular DDD pacing increased the cardiac output by
48% and reduced PCWP by 7.7%. As a result of these changes an
increase in systolic BP (Fig 3
) and urine output as well as a decrease in systemic vascular resistance
(Table 1) were observed. This
hemodynamic stabilization was also reflected by a clear improvement of
the patient’s symptoms.
Since the early 1990s, there have been numerous approaches to
improve left ventricular function in patients with CHF by means of
cardiac pacing.2–7,9–15,17By far, the most
encouraging results have been shown over the last 2 years through the
introduction of biventricular pacing.11–15,17
The most probable mechanism is a restored synchrony of the left
and right ventricle and an improved filling time.18 Some
early uncontrolled small studies with chronic biventricular pacing
demonstrated that patients with severely impaired systolic function and
intraventricular conduction delay clearly experienced an improvement of
symptoms.13–14 In our case, we used temporary
biventricular pacing in a patient with a critical hemodynamic situation
to achieve improvement of myocardial contractile function within a
short period of time. In the future, biventricular pacing may have its
place in the acute as well as chronic treatment of patients with severe
CHF and intraventricular conduction delay. This mode of stimulation can
be seen as another tool in the management of patients with end-stage
heart failure. In some cases, it might even be used to bridge the time
to transplantation. However, further hemodynamic acute and long-term
studies are needed to establish optimal pacing sites and to develop
simplified implantation techniques.
Abbreviations: AAI = atrial demand pacing;
CHF = congestive heart failure; DDD = dual chamber pacing;
PCWP = pulmonary capillary wedge pressure
HR = heart rate; PAP = pulmonary artery pressure;
CO = cardiac output; SVR = systemic vascular resistance; see Figure 2 legend for other abbreviations.
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