(Circulation. 1996;93:745-752.)
© 1996 American Heart Association, Inc.
Articles |
Initial Experience With an Implantable Hemodynamic Monitor
From the Department of Cardiology (D.M.S., R.L., D.R.B., Jr, L.H., D.C., L.F., R.L.), Mid America Heart Institute, University of Missouri-Kansas City School of Medicine; and Medtronic, Inc (A.M., T.B.), Minneapolis, Minn.
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Abstract |
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 Top Abstract IntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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Background Measurement of intracardiac hemodynamic parameters has been limited to brief periods in the acute care setting. We developed and evaluated an implantable hemodynamic monitor that is capable of measuring chronic right ventricular oxygen saturation and pulmonary artery pressure.
Methods and Results The device consists of an electronic controller placed subcutaneously and two transvenous leads placed in the right ventricle (reflectance oximeter) and pulmonary artery (variable capacitance pressure sensor). Implantation was performed in 10 patients with severe left ventricular dysfunction. Average implant pulmonary artery pressures were systolic, 52±16 mm Hg; diastolic, 29±11 mm Hg; and mean, 40±12 mm Hg. The mean right ventricular oxygen saturation at implant was 51%. Provocative maneuvers, including postural changes, sublingual nitroglycerin, and bicycle exercise, demonstrated expected changes in measured oxygen saturation and pulmonary artery pressures over time. At follow-up of 0.5 to 15.5 months, there were no significant differences between pulmonary artery pressures or oxygen saturation values transmitted from the device and simultaneous measurement with balloon flotation catheters. Four of the pulmonary artery leads dislodged and three demonstrated sensor drift, whereas two of the oxygen saturation sensors failed. Four patients died and four received transplants. Pathological study did not demonstrate injury to the right ventricular outflow tract or pulmonic valve.
Conclusions Chronic measurement of hemodynamic parameters in the outpatient setting with implantable sensor technology appears to be feasible. The devices are well tolerated without significant untoward effects, and the sensors generally function well over time, providing reliable information. Clinical usefulness remains to be established.
Key Words: monitors, hemodynamic • heart failure • devices, implantable
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Introduction |
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TopAbstractIntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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Despite advances that have caused a decline in the morbidity and mortality of heart disease, heart failure remains a significant problem. It is estimated that 9% of the population older than 65 years of age has heart failure, and ventricular decompensation accounts for nearly 2.4 million hospitalizations per year, with an average length of stay of 7.4 days.1 2 Not only does this imply substantial morbidity, but the annual mortality of patients with the diagnosis of heart failure remains high at 15% to 50% over 1 to 5 years, respectively.3 4 5 6 7 8 9 Any development that could decrease mortality, improve quality of life, or decrease need for hospitalization might have a significant impact on the disease. Over the past decade, implantable sensor technology has evolved for use in rate-responsive pacing systems in an attempt to match heart rate and metabolic need. Hemodynamic sensors have been used to measure a variety of intravascular parameters.10 11 12 13 14 With the availability of this sensor technology, we developed and evaluated a new implantable hemodynamic monitor that has the capability of measuring chronic absolute pressure in the pulmonary artery and blood oxygen saturation in the right ventricle.
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Methods |
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TopAbstractIntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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The hemodynamic monitor system consists of two transvenous leads and an electronic controller that is implanted subcutaneously, similar to the pulse generator of a permanent pacemaker (Fig 1A
).
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Right Ventricular Oxygen Saturation Lead
The right
ventricular oxygen saturation lead (model
6227, Medtronic) uses the principle of reflectance oximetry to measure
oxygen saturation as previously described (Fig
1B
).15 Two
light-emitting diodes are placed inside a sapphire glass tube
adjacent to a photodetector placed in a small separate chamber. Pulses
of light in the red spectrum (660 nm) are reflected by red blood cells
variably, depending on the percentage of oxygenated
hemoglobin, and are collected by the detector. Measurements are
converted to time signals and transferred to the electronic controller.
Sequential pulses of infrared light (890 nm), the reflection of which
does not vary with oxygen saturation, are used to "normalize" the
measurement, and the true oxygen saturation is computed as a ratio of
the red-to-infrared reflectance. This normalization makes the
measurements relatively immune to fluctuation caused by changes in
hemoglobin concentration, fibrin or fibrous tissue overgrowth, and
carboxyhemoglobin.15 Again, multifilar coils are used as
conductors, a stylet is used to place the lead, and tines are used to
stabilize the tip. The insulation is polyurethane, and the distal tip
contains an electrode to sense ventricular depolarization.
QRS synchronization allows the saturation measurement to be made at end
diastole.
Pulmonary Artery Pressure Lead
The pulmonary artery pressure
lead (model 6229,
Medtronic) uses the principle of variable capacitance to measure
absolute pressure (Fig 1C). Details of sensor operation have
been
described previously.13 In brief, a change in pressure
alters the distance between capacitor plates, and an integrated circuit
compares the resulting capacitance with a reference capacitor. The
waveform signal is converted to time, which can be measured by the
electronic controller for display. The coaxial lead consists of
silicone insulation around multifilar coils used as conductors. A
stylet is used to place the lead in the pulmonary artery under
fluoroscopic guidance. Large tines placed near the distal tip help
secure the lead, as does a sleeve sutured to the subcutaneous tissue in
the pectoral fascia.
Electronic Controller
The electronic controller (model 2507,
Medtronic) contains a
lithium manganese dioxide power supply as well as integrated circuitry
and a radiofrequency transmission coil hermetically sealed in a
titanium case. The device weighs 53 g and has dimensions of
52x60x10
mm. Time signals received from the leads are telemetered via
radiofrequency coupling link with a Medtronic model 9710 programmer
head and transmitted to a computer customized to digitize and display
the pressure waveforms and oxygen saturation data.
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Patient Recruitment |
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TopAbstractIntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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Between January and August 1993, 10 patients at the Mid America Heart Institute were recruited to receive the new device. Inclusion criteria were dilated or ischemic cardiomyopathy, ejection fraction of <20%, history of heart failure requiring hospitalization, symptoms of left ventricular decompensation (greater than or equal to class II, New York Heart Association), and willingness to participate in frequent follow-up as well as implantation and subsequent right heart catheterization. Patients were also selected from the cardiac transplantation list with the expectation that pathological evaluations could be performed at the time of surgery.
Exclusion criteria included inability to participate in follow-up
as well as pulmonary hypertension with pulmonary artery
resistance of 
7 Wood units. Patients who had heart failure less than
6 weeks after acute myocardial infarction were also excluded.
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Study Protocol |
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TopAbstractIntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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Evaluation before device implantation included physical examination, ECG, chest radiograph, and laboratory studies. Two-dimensional echocardiography with Doppler imaging, rest and exercise radionuclide ventriculography, and exercise cycle ergometry with measurement of maximum oxygen uptake were also performed. A 48-hour Holter monitor recording was obtained before and in the initial days (1 to 5 days) after device placement.
At implantation, right heart catheterization was performed with a standard fluid-filled balloon flotation catheter/pressure transducer system (PentaCath, Viggo Spectramed; Transpac II, Abbott Laboratories; VR12 Simultrace Recorder, Electronics for Medicine). Samples of blood were withdrawn for measurement of baseline supine right ventricular oxygen saturation with the use of a standard laboratory co-oximeter (model 482, Instrumentation Laboratory). Pulmonary artery pressure measurements were obtained simultaneously with recordings from the implantable monitor. The pulmonary artery pressure waveform of the implanted device was then calibrated to the balloon flotation pressure measurements.
Patients were evaluated every 2 weeks for 6 months in the outpatient
office setting. Pulmonary artery pressure and right
ventricular oxygen saturation values were transmitted in
the supine position as well as while sitting and standing. Values were
also measured after a 3-minute walk and after the administration of 0.4
mg nitroglycerin SL. Chest radiographs were obtained to
verify lead position. At the end of 3 and 6 months,
echocardiography,
O2 bicycle testing,
rest/exercise radionuclide ventriculography scans, and 48-hour Holter
monitor recordings were repeated. In addition, balloon
flotation right heart catheterization was also
performed with simultaneous telemetry of pulmonary
artery pressure and right ventricular oxygen saturation (2
to 62 weeks after implantation). After the 6-month intensive phase,
patients have been followed on a monthly basis for an additional 6
months and then on a quarterly basis. No patient has been lost to
follow-up.
The study protocol was approved by the Food and Drug Administration and the Institutional Review Board of St Luke's Hospital (Kansas City, Mo). Informed consent was obtained from all patients after full discussion of the potential risks involved. Data were analyzed with standard statistical techniques, including ANOVA, t tests for between-group mean values, and regression analysis. Bland-Altman plots were used to display oxygen saturation and pressure readings.
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Results |
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TopAbstractIntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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Patient Population
Eight men and two women (age range, 36 to 73 years) were enrolled in the study (Table
). All had a history of heart failure
requiring up to 9 hospitalizations for left ventricular
dysfunction over 8 years. Three were in New York Heart Association
class IV, five were in class III, and two were in class II. Six had
ischemic heart disease, and four had idiopathic
cardiomyopathy. Ejection fractions as assessed by
resting radionuclide ventriculography ranged from 8% to 18%, with a
mean of 13%. On bicycle ergometry, maximum oxygen uptake was 7.6 to
12.2
mL·kg-1·min-1
(mean, 10.6
mL·kg-1·min-1).
This corresponds to an average of 39.4% of the predicted maximum
oxygen uptake. All patients were monitored while receiving digoxin,
diuretics, and angiotensin-converting enzyme
inhibitors. Seven were on nitrates; seven, flosequinan;
three, L-dopa; and two, continuous or intermittent
intravenous positive inotropic agents.
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Four patients died at 14, 22, 42, and 48 weeks. Four received transplants at 5, 19, 23, and 74 weeks, and 2 patients continue to be followed at 18 and 22 months. With the exception of two patients who died, all completed the 6-month intensive protocol. All of the deaths were expected and secondary to refractory severe heart failure. Only one patient had sudden death (14 weeks). This patient had progressive heart failure and was taking flosequinan (100/50 mg alternating QOD), which is known to increase the risk of sudden death in this population.16 17 18 19 Sepsis may have contributed to the death of one patient at 11 months after implantation. This patient also had an implanted peripheral intravenous catheter terminating in the superior vena cava for continuous inotropic drug delivery. All four of the transplant patients have recovered successfully (5, 13, 15, and 18 months) with removal of the device during transplantation surgery.
Pulmonary Artery Pressure Recordings
At implantation,
pulmonary artery systolic
pressures averaged 52±16 mm Hg (31 to 77 mm Hg), and
diastolic pressures ranged from 19 to 52 mm Hg (average,
29±11 mm Hg). The average mean pulmonary artery pressure was
40±12 mm Hg (range, 26 to 62 mm Hg).
During follow-up, there
were four dislodgements of the
pulmonary artery lead, two of which were successfully
repositioned. Two of the four dislodgements occurred in our first two
patients. The incidence of lead dislodgement diminished once we learned
to place a loop of catheter in the right ventricular apex,
which stabilized the lead and directed its distal tip to the left
pulmonary artery. The chest radiograph shown in Fig 2
demonstrates this apical loop. Significant drift was
suspected in one sensor and confirmed in an additional two sensors at
the time of repeat right heart catheterization
performed 6 months after implantation. However, measurements made
before drift and on the stable sensors demonstrated appropriate
responses to provocations, including sitting, standing, exercise, and
nitroglycerin (Fig 3). In 2 to 16
repeated measurements in eight patients, mean pulmonary artery
pressures decreased an average of 10±4 mm Hg in response to sitting
(range, 6 to 18 mm Hg) and 15±7 mm Hg in response to standing upright
(range, 6 to 27 mm Hg). Systolic/diastolic
pressures fell 14±6/8±3 mm Hg with sitting and
20±11/11±5 mm Hg
with standing. Systolic, diastolic, and mean
pulmonary artery pressures increased by 5±5, 3±3, and 4±4
mm
Hg after a 3-minute walking protocol, whereas they decreased 11±9,
6±5, and 8±7 mm Hg, respectively, in response to
nitroglycerin. In patients with stable sensors (six),
systolic, diastolic, and mean pulmonary
artery pressures correlated well with pressures from a balloon
flotation catheter during right heart catheterizations
2 to 62 weeks (mean, 26.2 weeks) after device implantation (Fig
3). The
average differences in pulmonary artery systolic,
diastolic, and mean pressures from the implanted sensor and
the balloon flotation catheter were -0.2±6.8,
-0.2±5.3,
and 0.3±5.0 mm Hg, respectively (P>.05).
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), 4 to 6 months
(
), and 14 months (
).
Right Ventricular Oxygen Saturation
At implantation, supine
right ventricular oxygen
saturations varied from 25.7% to 69.4% (mean, 50.8%). Despite this
wide range between patients, there was no significant difference
between measurements from the device and those obtained from blood
samples withdrawn at the time of simultaneous right heart
catheterization (Fig 4). In
follow-up, two sensors failed at 2 and 26 weeks. One failure was
due to lead entrapment in the myocardial trabeculae,
documented after excision of the heart at transplantation, preventing
sensor exposure to blood flow. The second was due to
urethane-coating degradation, observed at autopsy. There were no
lead dislodgements or problems with sensing of ventricular
depolarization. All leads sensed QRS complexes appropriately at
sensitivity settings as low as 5.0 mV during follow-up
evaluations.
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), 16 to 26 weeks (
), and 46 to 62 weeks
(
). Note the high correlation coefficient of .84 and the small
differences obtained.Oxygen saturation measurements responded as expected to provocations of sitting, standing, walking, and nitroglycerin. In 2 to 17 repeated measurements in 10 patients, oxygen saturation fell an average of 4.7±3.0% in response to sitting (range, 0.2% to 9.6%), 8.0±4.8% with standing (range, 0.8% to 15.9%), and 21.0±11.6% after a 3-minute walking protocol (range, 1.0% to 35.6%). Oxygen saturation increased 9.2±5.8% (range, 1.4% to 16.9%) after administration of sublingual nitroglycerin in three to six repeated measurements in seven patients. In some patients, such slight activity as talking could lower baseline oxygen saturation as much as 5%.
The oxygen saturation sensors demonstrated no
significant drift at the
time of repeat right heart catheterization, an average
of 26.2 weeks (range, 2 to 62 weeks) after implantation. There were no
significant differences in measurements obtained
simultaneously from the device and blood withdrawn from
balloon flotation catheters (Fig 4).
Exercise Ergometry With Oxygen Consumption
Seven of the 10
patients conducted one or more maximal exercise
tests during upright bicycle ergometry (Fig 5) at 1 to
14 months after device implantation. On symptom-limited exercise
testing, heart rates increased from a mean of 92 to 154 beats per
minute, whereas oxygen consumption
(O2)
increased from 3.6±1.0 to 12.4±4
mL·kg-1·min-1.
During exercise, pulmonary artery systolic,
diastolic, and mean pressures increased 19±18, 7±3, and
14±11 mm Hg, respectively. Right ventricular oxygen
saturation transmitted from the implanted device decreased from an
average of 48±10% to 28±10%. Changes in all
physiological variables were significant
(P<.05).
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Pathology
Devices were recovered, and hearts were examined
from three of
four patients who died and four patients who received transplantations.
Findings were typical of those seen after implantation of permanent
pacemakers, including fibrin deposits and fibrous tissue overgrowth,
which were especially noted at points of contact with
myocardium or the tricuspid valve. As previously noted, one
right ventricular lead demonstrated entrapment of its
sapphire glass window within the myocardial trabeculae. One
patient had near-occlusion of the superior vena cava, found at the
time of postmortem examination. This patient had no clinical symptoms
or signs to suggest caval obstruction. He did have an indwelling
peripheral intravenous catheter that terminated
in the superior vena cava and a low-flow state preceding death.
Another patient had inflammatory tissue with bacteria noted on
histological examination 11 months after implantation,
raising the possibility of infection, perhaps related to a long
indwelling peripheral intravenous catheter.
Importantly, there was no evidence of injury to the pulmonic valve,
right ventricular outflow tract, or pulmonary
artery.
Ventricular Ectopic Activity
We obtained 48-hour ambulatory
monitoring before implantation and
at 3-month and 6-month follow-up. Based on paired t
tests, there was no significant difference in the mean number of
premature ventricular depolarizations per hour per patient
before implantation (186±316), at 3 months (110±101), or at 6
months
(91±124). In addition, there was no change in episodes of repetitive
forms preimplantation (289±936), at 3 months (54±110), or at 6
months
(82±218). One patient was placed on empiric amiodarone therapy
for complex ventricular ectopy that preceded device
implantation. As previously mentioned, one patient on flosequinan
experienced what was probably an arrhythmic death. This patient had
complex ventricular ectopy before and after device
implantation, an ejection fraction of 8% with pulmonary artery
pressures as high as 106/64 mm Hg, and oxygen saturation of 50%.
Clinical Observations
Although we were reluctant to use
unvalidated sensor measurements
to alter therapy, we made several unique observations during the study.
For example, patient 3 remained clinically stable for 8 months while
awaiting transplantation, with few changes in therapy.
Pulmonary artery pressures and oxygen saturation reflected
similar stability, varying only from 20/8 to 33/23 mm Hg and from 64%
to 72%. However, patient 9, who had a more unstable clinical course,
requiring frequent medication adjustments and intravenous
inotropes, had higher pressures and more volatile oxygen saturation
readings, ranging from 52/35 to 74/47 mm Hg and from 32% to 65%.
Changes in oxygen saturations in this patient, as in others, preceded
clinical deterioration. On one occasion, patient 9 presented to
the hospital with increasing dyspnea and cough. Oxygen saturation
values demonstrated a decline without elevation in pulmonary
artery pressures, suggesting an exacerbation of chronic obstructive
pulmonary disease rather than worsening left
ventricular decompensation. This patient was treated
successfully with bronchodilators and antibiotics rather than with
inotropes and large doses of diuretics. Similarly, patient 1
experienced an unstable clinical course requiring long-term
intravenous inotropes. Oxygen saturation values varied from
30% to 60%. Dislodgement of the pulmonary artery lead
provided right ventricular pressures ranging from 33/5 to
60/10 mm Hg. At week 16, this patient presented to the clinic
with increasing fatigue, weakness, and nonproductive cough
without fever. The decision to hospitalize for observation was reversed
after transmitted data demonstrated only a mild decrease in oxygen
saturation (49%).
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Discussion |
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TopAbstractIntroductionMethods Patient Recruitment Study Protocol ResultsDiscussion References |
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Since the advent of balloon flotation catheterization in 1970, measurements of pulmonary artery diastolic and wedge pressures as a close approximation to left atrial pressure have been useful in the management of heart failure.20 Similarly, mixed venous oxygen saturation as obtained from blood sampling in the pulmonary artery has been used as an index of cardiac output.21 22 23 24 25 However, these measurements have generally been made only in acutely ill patients hospitalized in the intensive care unit setting.
More recently, systems have been designed to allow ambulatory monitoring of hemodynamics in patients with heart failure or myocardial ischemia via the use of micromanometer-tipped catheters as well as traditional fluid-filled catheters and miniature recorders.26 27 28 29 30 31 32 33 Using such a system in 1990, Gibbs et al32 reported pulmonary artery pressure variations in nine men with heart failure during daily activities and exercise. This series demonstrated significant postural changes in pressure, with mean systolic pressures decreasing 10 mm Hg from lying to sitting and 15 mm Hg with standing. With exercise, mean systolic pressures increased approximately 30 mm Hg. These values are somewhat greater than our findings but are likely due to increased exercise duration as well as lower baseline pulmonary artery pressures in their study group.
Monitoring systems of this type have not been capable of recording simultaneous central oxygen saturation and have been limited to several days of measurement. In addition, there have been problems with external calibration in fluid-filled catheters as well as zero drift in micromanometer-tipped catheters. Accordingly, the usefulness of right heart catheterization has been limited to relatively brief periods due to technical considerations and expense as well as concerns regarding sepsis and thromboembolization.
To our knowledge, this study represents the first attempt at chronic monitoring of absolute pulmonary artery pressure and right ventricular oxygen saturation in the outpatient setting with a totally implantable device. Although the implantable hemodynamic monitor does not measure pulmonary artery wedge pressure or true mixed venous oxygen saturation, pulmonary artery pressures and right ventricular oxygen saturation are reasonable alternatives, offering similar diagnostic parameters and therapeutic end points.34 35
Device placement has been well tolerated and uses essentially the same methodology, resources, and expertise as permanent pacemaker implantation.36 Although stability of the lead systems proved to be somewhat problematic, the sensors generally performed as expected and provided reliable, accurate data over a wide range of pulmonary artery pressures and oxygen saturation values. There appear to be no significant complications of this type of monitoring, and in particular, the pulmonary artery lead appears to be well tolerated without injury to the pulmonic valve and surrounding structures or increase in ventricular ectopic activity. Redesign of the pulmonary artery lead and sensors will be required to facilitate placement and long-term sensor stability. Preferably, both sensors could be incorporated into one lead. The current system is also limited by the lack of memory capacity. Although the device transmits pressure waveforms and oxygen saturations continuously, the data are available only when in contact with the external programming head. Internal data storage that could be downloaded periodically would be a significant improvement. More importantly, ours was a feasibility study, and clinical usefulness will need to be demonstrated before any broad application can be made.
Despite these technological challenges, there is reason to be hopeful
that chronic hemodynamic monitoring might be
beneficial. To date, outpatient medical management of heart failure has
relied on symptoms, physical examination, and chest
roentgenography.37 However, several studies have
demonstrated the inability of physical signs to predict left
ventricular filling pressures in chronic heart
failure.38 39 40 In one study by
Stevenson and
Perloff,39 elevations in jugular venous pressure,
peripheral edema, and rales were absent in 18 of 43
patients (42%) whose pulmonary wedge pressures were greater
than 22 mm Hg and in 8 of 18 of those (44%) with wedge pressures of
>35 mm Hg. In a more recent study by Chakko et al40
involving 52 patients with chronic heart failure undergoing
evaluation for heart transplant, a poor correlation was found among
physical examination, chest radiograph, and pulmonary wedge
pressure findings. For example, radiographic
pulmonary congestion was absent in 8 of 15 patients (53%) with
mild to moderate elevation of wedge pressures (16 to 29 mm Hg) and in 7
of 18 patients (39%) with marked elevations (30 mm
Hg).40
Likewise, there is at least some suggestion that optimization of heart failure therapy may improve survival. Multiple trials of angiotensin-converting enzyme inhibitors have demonstrated a significant increase in life expectancy.41 42 43 In addition, carefully adjusted "tailored therapy" with initial invasive hemodynamic monitoring to reach specific hemodynamic goals has been used successfully to improve quality of life and perhaps extend survival. In one study by Stevenson,44 patients who had been stabilized for 1 year with such an approach were compared with a similar population 1 year after cardiac transplant and found to have no difference in exercise capacity, number of medications, or quality of life. A previous retrospective study by the same investigators before such careful systematic therapy was used demonstrated a high failure rate of medical therapy with sudden death or urgent transplantation required, even among patients considered initially too well to transplant.45
Although there have been no randomized studies demonstrating improved mortality in heart failure with therapy based on invasive hemodynamic monitoring, the assumption that such an approach would be helpful seems reasonable. Furthermore, the inference that more frequent measurements of hemodynamic parameters might be beneficial seems plausible.
Although implantable monitors are not without cost or morbidity, it is also conceivable that the information provided would decrease hospital use by improving outpatient management of heart failure. If so, the potential for a favorable effect on cost of therapy could be realized. One can certainly imagine that an implantable monitor might be used to adjust intravenous medications delivered through implantable pumps. For example, intermittent inotropic therapy adjusted to the individual hemodynamic state might avoid the tachyphylaxis that commonly accompanies such therapy. An implantable hemodynamic monitor might also be helpful in other processes, such as primary pulmonary artery hypertension, or even in the assessment of rejection after cardiac transplantation.
Finally, regardless of whether implantable monitoring will be broadly applicable in the treatment of disease states, the research implications of such a device are substantial. The ability to measure the effects of drugs and dosing intervals on hemodynamics in the outpatient setting should prove useful.
In summary, the early experience with this device is encouraging, and we believe chronic hemodynamic monitoring holds significant promise.
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Acknowledgments |
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This study was supported in part by a grant from the William T. Kemper Foundation, Kansas City, Mo. We gratefully acknowledge Drs Ben D. McCallister, James H. O'Keefe, Jr, Warren L. Johnson, Jr, and Spencer Kubo for critical review of the manuscript; Dr Amy Kragel for pathology expertise; George Pool for technical assistance; and Lori Maher for manuscript preparation.
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Footnotes |
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Reprint requests to David M. Steinhaus, MD, 4330 Wornall Rd, Ste 2000, Kansas City, MO 64111.
Received July 20, 1995; revision received September 14, 1995; accepted October 2, 1995.
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