(Circulation. 2000;101:158.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Destabilizing Effects of Mental Stress on Ventricular Arrhythmias in Patients With Implantable Cardioverter-Defibrillators
From the Yale University School of Medicine, New Haven, Conn.
Correspondence to Rachel Lampert, MD, Yale University School of Medicine, Section of Cardiovascular Medicine, FMP 3, 333 Cedar St, New Haven, CT 06520. E-mail rachel.lampert{at}yale.edu
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Abstract |
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Background—The incidence of sudden cardiac death increases in populations who experience disasters such as earthquakes. The physiological link between psychological stress and sudden death is unknown; one mechanism may be the direct effects of sympathetic arousal on arrhythmias. To determine whether mental stress alters the induction, rate, or termination of ventricular arrhythmias, we performed noninvasive programmed stimulation (NIPS) in patients with defibrillators and ventricular tachycardia (VT), which is known to be inducible and terminated by antitachycardia pacing, at rest and during varying states of mental arousal.
Methods and Results—Eighteen patients underwent NIPS in the resting-awake state (nonsedated). Ten underwent repeat testing during mental stress (mental arithmetic and anger recall). Induced VT was faster in 5 patients (P=0.03). VT became more difficult to terminate in 5 patients during mental stress; 4 required a shock (P=0.03). There was no change in ease of induction with mental stress. There was no evidence of ischemia on ECG or continuous ejection fraction monitoring. Eight patients received a shock in the resting-awake state and did not perform mental stress. Four underwent repeat NIPS after sedation; 3 then had induced VT terminated with antitachycardia pacing. All patients with an increase in norepinephrine of >50% had alterations in VT that required shock for termination (P<0.01).
Conclusions—Mental stress alters VT cycle length and termination without evidence of ischemia. This suggests that mental stress may lead to sudden death through the facilitation of lethal ventricular arrhythmias.
Key Words: stress • tachyarrhythmias • tachycardia • cardioversion • defibrillation
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Sudden cardiac death increases in populations suffering disasters such as earthquake or war.1 2 3 Potential physiological mechanisms linking psychological stress and sudden death include coronary ischemia and direct modulation of arrhythmia via changes in autonomic tone. Mental stress can induce ischemia, both in laboratory protocols4 5 6 7 and in daily life.8 Whether mental stress influences arrhythmias, however, remains unknown.
Indirect evidence suggests that sympathetic arousal can trigger arrhythmic events. Ventricular tachycardia (VT), like sudden death, occurs more frequently in the morning, at the time of peak catecholamine levels,9 and of lowest vagal tone,10 as demonstrated in patients with implantable cardioverter-defibrillators (ICDs).11 12 VT occurs more frequently on Mondays in working patients with ICDs,13 suggesting a role for stress. In addition, atrial and ventricular ectopy and nonsustained arrhythmias increase during the stress of being on-call in house officers14 and during exposure to a hostile environment in animals.15 In invasive studies in animals,16 17 stress facilitates the induction of VT.
The population of patients with ICDs provides a unique opportunity to evaluate the effects of mental stress on human arrhythmias. Many patients have arrhythmias with well defined, reproducible characteristics. In addition, their devices allow the performance of noninvasive serial electrophysiological (EP) studies. To determine whether increased sympathetic activation alters the induction, rate, or termination of ventricular arrhythmias, we performed noninvasive EP studies in patients with ICDs and sustained VT, at rest and during varying states of mental arousal and stress.
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Methods |
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Patients
Eighteen patients with third-generation ICDs (Ventak PRxI, II, or Mini; Guidant/CPI) were invited to participate in the protocol. All provided written informed consent. The study was approved by the Yale University Human Investigation Committee.
In all patients, monomorphic VT had been induced and terminated with antitachycardia pacing (ATP) at least twice during previous noninvasive programmed stimulation (NIPS) performed with routine sedation (midazolam and fentanyl). Antiarrhythmic therapy at entry into the present study was unchanged from prior testing. Patients in whom ATP had failed to terminate induced VT were excluded, as were those with decompensated congestive heart failure or other active medical or psychiatric illness or those who were not fluent in English.
Study Protocol
Figure 1
illustrates the study
protocol. All studies were carried out in the morning after an
overnight fast. No sedatives or analgesics were administered. Two
venous cannulas were placed. After blood pool labeling with
99mTc, the miniature radiation detector (c-VEST)
was positioned on the chest for continuous left ventricular
ejection fraction (LVEF) monitoring. At least 30 minutes after
intravenous line and c-VEST placement, baseline
measurements of heart rate, blood pressure, ECG, and LVEF were
obtained. In the initial design of the protocol, each patient was to
undergo NIPS under 3 conditions: resting-awake, mental arithmetic, and
anger recall. These conditions were separated by a brief recovery
period, during which vital signs returned to baseline levels. The NIPS
protocol was initiated 3 minutes into each stage, after the
determination of vital signs, ECG, and LVEF. NIPS was continued until
the induction of an arrhythmia requiring termination by the ICD
or completion of the protocol. Venous blood for
catecholamine measurements was obtained continuously
throughout each stage of the protocol. Ten patients underwent the
mental stress protocol (group 1).
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In 8 patients, NIPS unexpectedly evoked an arrhythmia that
required a shock for termination in the resting-awake state, and these
patients were not asked to perform mental stress (group 2). Because
this outcome was unanticipated, the first 3 such patients did not
undergo further testing. The subsequent 5 were asked to undergo repeat
testing after sedation with fentanyl and midazolam; 4 agreed, and they
formed group 2a (Figure 1
).
The unexpected behavior of the group 2 patients suggested that the awake state itself may have altered arrhythmic characteristics. To further evaluate this possibility, we retrospectively compared the 18 study patients with a clinically similar cohort of control patients identified from the Yale Electrophysiology Database. Control subjects consisted of patients with ICDs who had reproducibly inducible, pacer-terminated VTs at an initial NIPS and underwent a later study while receiving the same antiarrhythmic regimen, both while under conscious sedation (group 3). The records of all patients with ICDs with ATP programmed (n=111) were reviewed to extract the control group of 40 patients who met these criteria. Temporal variability in VT characteristics was compared between the control group and the 18 study patients.
For comparisons among the groups, "state of arousal" was defined based on the protocol administered: from least aroused (sedated) to resting-awake to most aroused (mental stress).
Programmed Stimulation
A standard NIPS protocol was performed with drive cycle lengths
(CLs) of 500 and 400 ms with up to 3 programmed extrastimuli (PES).
Device settings, including ATP algorithms, programmed at prior NIPS,
remained unchanged throughout the study protocol.
Ventricular effective refractory periods were determined.
The ease of VT induction was quantified ordinally on the basis of the
level of the pacing protocol at which sustained VT was induced: level 1
indicates induction at either CL with 1 PES; level 2, induction with 2
PESs; level 3, induction with 3 PESs; and level 4, completion of
protocol without induction of sustained VT (noninducible). The ease of
termination was also quantified ordinally: level 1 indicates
self-terminating (nonsustained VT [NSVT]); level 2, pacer terminated;
and level 3, shock terminated.
Mental Stress Protocol
The mental stress protocol was administered by a clinical
psychologist (M.M.B.) as previously described.6 Room
lights were dimmed, and a quiet state was maintained. For the
resting-awake stage, patients were encouraged to relax by thinking
about past relaxing situations. During the mental arithmetic stage,
subjects were asked to serially subtract 7 from a 3-digit number. They
were reminded to respond rapidly, and mistakes were corrected harshly.
For anger recall, patients were asked to discuss an annoying or
frustrating event, as the interviewer requested further details and
asked irritating questions.
Radionuclide Angiography
Red blood cells were labeled with 20 to 25 mCi
99mTc according to the standard labeling
technique.18 A gamma camera with a general all-purpose
collimator interfaced with a minicomputer was positioned in the left
anterior oblique view to measure baseline LVEF through the use of
equilibrium radionuclide angiography. The miniature detector of an
ambulatory left ventricular function monitoring device
(C-Vest; Capintec) was then positioned over the left
ventricular blood pool. The device was held in place with a
semirigid plastic vest-like garment. Counts were acquired at 32
s-1 and analyzed off-line with the use
of a dedicated minicomputer to obtain 30-second averaged continuous
trends of LVEF.19 The LVEF reported was the average value
during the first 3 minutes of each stage, before the start of NIPS.
Catecholamine Analysis
Venous blood was continuously withdrawn at a rate of 1 mL/min
with an exfusion pump (Dakmed). Separate samples were collected during
each study phase and immediately placed on ice. Samples were spun and
stored at -70°C at the Yale General Clinical Research Center.
Norepinephrine levels were determined with radioenzymatic
assay or high-performance liquid
chromatography. All samples from a given subject were
analyzed in the same batch. Correlations of
catecholamine levels with arrhythmia
characteristics were based on the sample before arrhythmia (the
1.5 mL within the tubing at the onset of the arrhythmia).
Statistical Analysis
Continuous variables were compared with the use of paired
and unpaired t tests or repeated measures 2-way ANOVA as
appropriate. Ordinal variables were compared with the use of the
nonparametric sign test. Dichotomized variables were
compared with the use of 
2 and Fisher’s exact
tests.
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Results |
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Patient Characteristics
The clinical characteristics of the 3 patient groups are shown in Table 1
. There were no differences in any
demographic or clinical variable between groups.
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Resting-Awake Programmed Stimulation
In the resting-awake state, induced VT terminated with ATP or
spontaneously in 10 patients (group 1) but required shock for
termination in 8 patients (group 2). The baseline
norepinephrine level was 3.06±0.50 nmol/L (518±84 pg/mL)
in group 2 patients (levels were available in 4) and 2.78±0.41 nmol/L
(471±69 pg/mL) in group 1 patients (levels were available in 6)
(P=NS). However, during NIPS (before arrhythmia
induction and shock delivery), norepinephrine increased by
34% in group 2 patients but only 10% in group 1 patients
(P=0.01).
Patients Undergoing Mental Stress Protocol (Group 1)
Physiological Changes With Mental
Stress
Heart rate and blood pressure increased and
ventricular refractory periods decreased significantly with
mental stress (Table 2).
Norepinephrine levels rose during stress (Table 2),
with return to baseline levels between stress states (2.94+ 0.41
nmol/L, P=NS versus baseline).
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Changes in Arrhythmia Behavior During Mental
Stress
VT was induced earlier in the protocol during mental stress in 3
of the 10 patients (2 with only NSVT induced during resting-awake, had
sustained VT provoked by 2 PES during stress). In 6 patients, there was
no change, and in 1 patient, induction occurred 1 stage later (Figure 2, P=NS). The mean induction
stage at rest was 2.4±0.3; with stress, it was 2.0±0.2.
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VT CLs decreased during mental stress: 5 patients (50%) had a decrease
in CL of 
20 ms (P=0.03). The mean CL was 353±24 ms in the
resting-awake state and 314±20 ms with mental stress
(P=0.12).
VT termination became more difficult during mental stress in 5 of the
10 patients (P=0.03) (Figure 3). This occurred in 1 patient during
mental arithmetic, 3 during anger recall, and 1 during each of the
stress tasks. One patient had NSVT at rest and pacer-terminated VT with
stress. Four patients had pacer-terminated VT (3) or NSVT (1) induced
at rest but VT induced during mental stress that required shock for
termination. Of these, 1 required shock due to failure of ATP, 1
required shock due to induction of VT in a shock-only zone (Figure 4), and 2 received a shock after ATP
during stress-accelerated VT, of whom 1 had VT of identical CL and
morphology as that terminated with pacing in the resting state (Figure 5). (The other accelerated patient had
NSVT at rest.) In the remaining 5 patients, VT was terminated with ATP
both at rest and during mental stress. The mean stage of termination
was 1.8±0.1 at rest and 2.4±0.1 with stress.
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LVEF and ECG Changes
There were no ST or T-wave changes with mental stress in any
patient. Mean LVEF was 35±6% at baseline and did not change with
mental stress (Table 2). Only 1 of the 10 patients had a fall in
LVEF of >5% (this patient did not show alterations in any
parameter with mental stress).
Patients Studied Awake and Sedated (Group 2a)
Four patients who received a shock at baseline underwent repeat EP
testing after receiving sedation. There was no change in induction
stage (Figure 2). Induced VT was significantly slower after
sedation (CL 295±36 ms awake and 370±23 ms sedated,
P=0.05). In 3 patients, the VT CL increased by >20 ms.
After sedation, 3 of the 4 patients had induced VT effectively
terminated with ATP (in 1, the same VT had failed pacer termination
awake, in 2, faster VTs had been induced awake). One of the 4 patients
again required shock while sedated (Figure 3).
Relation of Catecholamine Levels to Arrhythmia
Characteristics
Comparisons between changes in norepinephrine levels
and changes in arrhythmia characteristics were made in the 9
patients with catecholamine levels available in 2 different
states of arousal: 6 group 1 patients (mental stress versus
resting-awake) and 3 group 2a patients (resting-awake versus sedation)
(Table 3). Overall, in these patients,
mean norepinephrine levels, which were measured during NIPS
before the induction of VT, were higher in the more aroused state.
Earlier induction and faster VT tended to correlate with a greater rise
in catecholamine levels with arousal. The ease of VT
termination correlated strongly with extent of arousal-induced
catecholamine rise, as shown in Table 3. When
patients were dichotomized based on change in
norepinephrine level, all 5 patients with a >50% increase
in norepinephrine level in the aroused state (before VT
induction) had induced VT that required shock for termination, whereas
VT in the 4 patients with a smaller increase in
norepinephrine remained pacer terminated
(P<0.001).
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Retrospective Comparison Awake Versus Sedated States
Temporal variability in VT characteristics was compared between
the study patients (groups 1 and 2), who had undergone a previous
sedated study and the awake study protocol, and the control subjects
(group 3), who had undergone 2 sedated studies on different days. All
were receiving the same antiarrhythmic medications for both
studies.
State of arousal did not influence VT induction, which occurred earlier in the second study in 17% of awake patients and 28% of sedated patients (P=NS). Mean VT CL decreased at the second study by 65±17 ms in the awake versus 17±12 ms in the sedated patients (P=0.03). Arousal state strongly influenced VT termination. Although all patients had pacer-terminated VT at the first, sedated, study, termination of VT at the second study required shock in 8 of 18 (44%) of the awake patients but only 4 of 40 (10%) of the sedated patients (P=0.002).
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Discussion |
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This study shows that mental stress shortens CL and renders induced VT more difficult to terminate. Similarly, arrhythmias induced in the awake state are faster and more difficult to terminate than those induced in the sedated state in the same patient. These alterations in VT characteristics were associated with increased norepinephrine levels, which are known to rise during mental stress,20 21 but with no evidence of ischemia on ECG or LVEF. In these patients with a defined VT substrate, mental arousal destabilized the circuit, creating a potentially more dangerous arrhythmia. This suggests that psychological stress may facilitate sudden cardiac death by increasing the lethal potential of arrhythmias in susceptible patients.
Unexpectedly, despite the inclusion of only patients with reproducible termination of VT by ATP at previous sedated noninvasive EP study (and no change in antiarrhythmic medications), 40% received shocks for induced VT in the "resting" awake state. To evaluate whether the awake state itself altered VT, 4 patients receiving shocks while awake underwent repeat testing after sedation; 3 again had pacer-terminated VT. The environment of the EP laboratory and the ongoing NIPS protocol may have produced anxiety or fear in some patients, changing the "resting" awake state to that of heightened arousal. The far greater increase in norepinephrine during NIPS (before VT induction) in patients proceeding to receive shocks supports this hypothesis, underscoring the influence of sympathetic tone on arrhythmia behavior. Although a pharmacological effect of the sedating agents cannot be excluded, studies in isolated tissue preparations or denervated hearts, which evaluated the effects of drugs in the absence of autonomic mediation, have not shown either midazolam or fentanyl to alter ventricular refractory periods or other EP parameters.22 23
To exclude the possibility that the unexpected changes in arrhythmia behavior were due only to day-to-day variability of response to EP testing,24 we retrospectively compared the consistency of response to NIPS over time in a group of similar patients (with inducible pacer-terminated VT) who had undergone 2 NIPS while sedated. The results of NIPS varied minimally between 2 sedated studies, unlike the dramatic changes seen with a second study in the awake state, again suggesting that due to lack of sedation, a higher state of arousal increased the lethal potential of VT.
The results of previous studies in animals support our findings. Both Lown et al,16 in a healthy canine model, and Kirby et al,17 in a porcine model of scar-related VT, found VT to be more readily inducible and faster in animals stressed by being lifted in a sling. The present study demonstrates that not only the primitive fight-or-flight responses of animals but the more complex human emotions of anger, anxiety, and performance stress alter arrhythmias. In addition, although these studies induced only rapid VTs or NSVTs, the selection of patients with stable monomorphic VT in the present study allowed an evaluation of the mode of VT termination as well.
Although multiple epidemiological studies have shown an increase in sudden cardiac death in populations undergoing the stress of natural disaster or war,1 2 3 the physiological link between stress and sudden cardiac death remains unexplained. Ischemia is often hypothesized to precipitate stress-induced cardiac events. Mental stress testing in the laboratory setting can induce ischemia,4 5 6 7 and anger can precipitate myocardial infarction.25 To evaluate whether ischemia might underlie stress-induced changes in arrhythmia, both ECG and ambulatory LVEF (a more sensitive indicator of ischemia than repolarization changes4 ) were monitored. No changes were seen in 9 of the 10 patients, suggesting that direct effects of the sympathetic nervous system on the VT circuit, rather than ischemia, effected the stress-related changes in VT behavior. This further implies that stress may directly cause arrhythmic sudden death in susceptible patients through the facilitation of lethal arrhythmias.
Stress-induced changes in EP properties such as repolarization time and conduction velocity may underlie the effects on arrhythmias seen in the present study. Toivonen et al26 showed changes in repolarization in healthy house officers exposed to the sudden stress of an on-call alarm. Repolarization also exhibits diurnal variation, further suggesting an influence of changing adrenergic tone.27 The signal-averaged ECG has shown changes with both mental stress28 and time of day,29 implying sympathetic effects on conduction. Analogous changes in the reentrant circuit in patients with monomorphic VT may explain the changes seen in the present study. Although refractory periods, conduction times, and the excitable gap of the VT circuit cannot be measured without invasive mapping, the changes seen in CL and response to overdrive pacing may reflect changes in these properties of the VT circuit.
Study Limitations
Patients who received a shock at baseline did not undergo mental
stress because we believe that the risk of delivering a second shock
with the patient awake was not acceptable. We cannot exclude the
possibility that the changes seen could reflect regression to the mean
as an artifact of the protocol (ie, would the patients who received a
shock at baseline have been pacer terminated with mental stress?).
However, three fourths of the patients who received a shock who
underwent testing while sedated then had pacer-terminated VT, and
catecholamine levels correlated with arousal state;
artifactual changes in response seem highly unlikely. Similarly, the
order of testing was not randomized. However, catecholamine
levels returned to baseline between stressors, suggesting that the
stressor itself, rather than a cumulative effect of testing, was
responsible for the changes seen.
Only 1 woman was enrolled in the study (5%). Whether the effects of mental stress and arousal state on arrhythmia differ in women requires further evaluation.
Conclusions and Implications
Mental stress alters VT CL and termination, suggesting that
autonomic arousal may lead to sudden death through the facilitation of
lethal ventricular arrhythmias. Whether these
results can be extrapolated to patients without a preceding history of
VT is unknown. In patients with defibrillators, as well as in all
patients at risk for ventricular arrhythmias,
therapies aimed at blocking the sympathetic response to stress may
decrease the frequency and lethality of arrhythmic events.
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Acknowledgments |
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The analysis of catecholamines was supported by NIH/NCRR/GCRC program grant RR-00125.
Received April 30, 1999; revision received August 5, 1999; accepted August 17, 1999.
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P. Taggart, P. Sutton, C. Redfern, V. N. Batchvarov, K. Hnatkova, M. Malik, U. James, and A. Joseph The Effect of Mental Stress on the Non-Dipolar Components of the T Wave: Modulation by Hypnosis Psychosom Med, May 1, 2005; 67(3): 376 - 383. [Abstract] [Full Text] [PDF]
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M. M. Burg, R. Lampert, T. Joska, W. Batsford, and D. Jain Psychological Traits and Emotion-Triggering of ICD Shock-Terminated Arrhythmias Psychosom Med, November 1, 2004; 66(6): 898 - 902. [Abstract] [Full Text] [PDF]
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R. Lampert, C. A. McPherson, J. F. Clancy, T. L. Caulin-Glaser, L. E. Rosenfeld, and W. P. Batsford Gender differences in ventricular arrhythmia recurrence in patients with coronary artery disease and implantable cardioverter-defibrillators J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2293 - 2299. [Abstract] [Full Text] [PDF]
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W. J. Kop, D. S. Krantz, B. D. Nearing, J. S. Gottdiener, J. F. Quigley, M. O'Callahan, A. A. DelNegro, T. D. Friehling, P. Karasik, S. Suchday, et al. Effects of Acute Mental Stress and Exercise on T-Wave Alternans in Patients With Implantable Cardioverter Defibrillators and Controls Circulation, April 20, 2004; 109(15): 1864 - 1869. [Abstract] [Full Text] [PDF]
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A. R. Schwartz, W. Gerin, K. W. Davidson, T. G. Pickering, J. F. Brosschot, J. F. Thayer, N. Christenfeld, and W. Linden Toward a Causal Model of Cardiovascular Responses to Stress and the Development of Cardiovascular Disease Psychosom Med, January 1, 2003; 65(1): 22 - 35. [Abstract] [Full Text] [PDF]
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R. Lampert, T. Joska, M. M. Burg, W. P. Batsford, C. A. McPherson, and D. Jain Emotional and Physical Precipitants of Ventricular Arrhythmia Circulation, October 1, 2002; 106(14): 1800 - 1805. [Abstract] [Full Text] [PDF]
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R. Lampert, S. J. Baron, C. A. McPherson, and F. A. Lee Heart Rate Variability During the Week of September 11, 2001 JAMA, August 7, 2002; 288(5): 575 - 575. [Full Text] [PDF]
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T. M. Ramahi, M. D. Longo, A. R. Cadariu, K. Rohlfs, S. A. Carolan, K. M. Engle, H. Samady, and F. J. T. Wackers Left ventricular inotropic reserve and right ventricular function predict increase of left ventricular ejection fraction after beta-blocker therapy in nonischemic cardiomyopathy J. Am. Coll. Cardiol., March 1, 2001; 37(3): 818 - 824. [Abstract] [Full Text] [PDF]
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