Download Adaptive servo-ventilation suppresses elevation of C

ORIGINAL ARTICLE
Interactive CardioVascular and Thoracic Surgery 24 (2017) 27–33
doi:10.1093/icvts/ivw286 Advance Access publication 7 September 2016
Cite this article as: Hiraoka A, Suzuki K, Chikazawa G, Nogami S, Sakaguchi T, Yoshitaka H. Adaptive servo-ventilation suppresses elevation of C-reactive protein
and sympathetic activity in acute uncomplicated type B aortic dissection. Interact CardioVasc Thorac Surg 2017;24:27–33.
Arudo Hiraokaa,*, Kota Suzukia, Genta Chikazawaa, Shinsaku Nogamib, Taichi Sakaguchia
and Hidenori Yoshitakaa
a
b
Department of Cardiovascular Surgery, The Sakakibara Heart Institute of Okayama, Okayama, Japan
Department of Nursing, The Sakakibara Heart Institute of Okayama, Okayama, Japan
* Corresponding author. Department of Cardiovascular Surgery, The Sakakibara Heart Institute of Okayama, 2-5-1 Nakaicho, Kita-ku, Okayama 700-0804, Japan.
Tel: +81-86-2257111; fax: +81-86-2235265; e-mail: [email protected] (A. Hiraoka).
Received 15 April 2016; received in revised form 13 July 2016; accepted 28 July 2016
Abstract
OBJECTIVES: The aim of this prospective, randomized study was to investigate the effects of adaptive servo-ventilation (ASV), based on
haemodynamic parameters, sympathetic status and respiratory conditions in patients with acute uncomplicated type B aortic dissection.
METHODS: We enrolled 28 patients with acute uncomplicated type B aortic dissection requiring antihypertensive therapies, who had been
admitted within 24 h from onset. Study subjects were randomly assigned either to the ASV group (n = 14) or to the non-ASV group (n = 14).
RESULTS: Antihypertensive therapy at an acute phase led to significant reduction in blood pressure in both groups. Heart rate significantly
dropped in the ASV group. In the non-ASV group, noradrenaline (746 ± 343 to 912 ± 402 pg/ml, P = 0.033) and dopamine (30 ± 21 to 42 ± 28
pg/ml, P = 0.015) significantly increased at 1 h after admission. Low frequency/high frequency ratios significantly decreased in the ASV group
(2.1 ± 1.6 to 1.7 ± 1.1, P = 0.045). During follow-up at the subacute period, pleural effusion significantly increased in the non-ASV group
(649 ± 611 vs 190 ± 292%, P = 0.033). Peak C-reactive protein (CRP) had a significant positive correlation with pleural effusion volume
(P = 0.039) and was significantly greater in the non-ASV group (15.5 ± 6.3 vs 8.5 ± 6.1 mg/dl, P = 0.009).
CONCLUSIONS: In acute type B aortic dissection, ASV was considered to have suppressed the development of sympathetic nervous activity,
pleural effusion and elevation of peak CRP.
Keywords: Adaptive servo-ventilation • Dissection • Sympathetic nervous system • Aorta
INTRODUCTION
With the advent of thoracic endovascular aortic repair, the optimal
strategy for treating uncomplicated type B aortic dissection is currently under debate. In addition, the optimal timing of performing
thoracic endovascular aneurysm repair (TEVAR) is still controversial
[1, 2]. However, with regard to the initial therapeutic approach for
uncomplicated type B aortic dissection at an acute phase, conventional treatments of antihypertensive drugs are routinely administered. In the process of administering optimal medical treatment,
pleural effusion and oxygenation impairment are frequently
observed, and respiratory distress can lead to delayed rehabilitation
[3–5]. Although the mechanisms of pleural effusion and oxygenation impairment are not fully known, they should be recognized
as serious complications of aortic dissection. Administration of
high-dose oxygen can lead to risk of damage to the lungs. In
patients with aortic dissection, appropriate management for oxygenation impairment remains an undetermined issue.
Adaptive servo-ventilation (ASV) is a compact ventilator support
device designed to achieve synchronized support and comfortable
respiration. The efficacy of ASV in patients with heart failure and
sleep apnoea has been reported in several studies [6–8], and sleep
apnoea is recognized as a significant risk factor for aortic dissection
[9]. However, the influence of ASV therapy in patients with acute
aortic dissection has not yet been evaluated. The aim of this study
was to investigate the prompt effects of ASV based on haemodynamic parameters, sympathetic status and the respiratory condition in patients with acute uncomplicated type B aortic dissection.
MATERIALS AND METHODS
Study design and patient selection
This was a prospective, randomized open-label study. Between
October 2014 and June 2015, 32 consecutive patients with acute
© The Author 2016. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
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Adaptive servo-ventilation suppresses elevation of C-reactive protein
and sympathetic activity in acute uncomplicated type B aortic
dissection
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uncomplicated type B aortic dissection were admitted to a single
cardiovascular institute. Patients with pericardial effusion and
aortic aneurysmal size >60 mm were excluded from this cohort,
on account of the possibility of introducing urgent therapies. Two
patients who were transferred more than 24 h after onset were
excluded. Consequently, the remaining 30 patients with uncomplicated acute type B aortic dissection, who required an antihypertensive therapy, were admitted within 24 h from onset and
enrolled in this cohort (Fig. 1A). Antihypertensive therapy was
chosen at the acute phase as a primary therapeutic approach.
During follow-up, significant changes in the entire aortic diameter
>60 mm, rapid increase in aortic diameter (>5 mm for 6 months)
and enlargement of an ulcer-like projection were considered indications to treat urgently. For the descending aortic lesions, TEVAR
was performed as a first-line therapy. For distal aortic arch lesions,
surgical aortic arch reconstruction was primarily chosen. Thirty
patients were targeted as the participants for this randomized study
by the institutional review board. ASV usage was randomly assigned
to each patient with block randomization (block size = 2). Thus, the
ASV group (n = 15) and the non-ASV group (n = 15) were formed.
After randomization, 2 patients were excluded from each group
due to refusal of ASV introduction and the presence of dementia.
Thereafter, the ASV group (n = 14) and the non-ASV group (n = 14)
were statistically analysed. The study protocol complied with the
Declaration of Helsinki and was approved by the institutional
review board. The informed consent of all patients was obtained.
Patient demographics
The average age was 70.9 ± 15.0 years. Eleven females (39%) were
included in the cohort. The mean duration from onset to admission was 4.8 ± 3.2 h, and there were no significant differences
between the non-ASV group and the ASV group (5.2 ± 3.1 vs
4.4 ± 3.4 h, P = 0.492). The morphological features of a false lumen
were categorized in patients as follows: fully open false lumen in 3
(11%), ulcer-like projections in 3 (11%), complete thrombosis in 17
(61%) and partial thrombosis in 5 (18%). There were no significant
differences in baseline data for backgrounds, cardiac function,
morphological features of aortic dissection and laboratory findings
between patients with and without ASV therapy (Table 1). There
was no patient with atrial fibrillation in either group.
Adaptive servo-ventilation introduction,
antihypertensive therapy and evaluation of plasma
catecholamines
On admission, laboratory work, including serum concentration of
adrenaline, noradrenaline and dopamine, was initially evaluated.
Antihypertensive therapy (calcium antagonists, β-blocker, analgesics
and sedatives) was initiated as promptly as possible under
intra-arterial and electrocardiographic monitoring for strict maintenance of systemic blood pressure <120 mmHg. At 30 min after administering antihypertensive therapy, ASV (AutoSet CS, ResMed, Sydney,
NSW, Australia) support was introduced from the default setting
[positive end-expiratory pressure (PEEP): 5 cmH2O; minimum and
maximum pressure support (PS): 3 and 10 cmH2O] in the ASV group.
PEEP and minimum PS were adjusted according to patients’
symptom and could be reduced to 4 and 0 cmH2O, respectively. In
the ASV group, ASV was continuously used for no less than 30 min
on the day of admission by referring to a previous report [10]. On the
next day after admission, ASV was intermittently used for no less
than 30 min and continued for no less than 1 week. To obtain
patients’ cooperation, a multidisciplinary team consisting of a doctor,
nurse, public health nurse and physiotherapist intervened. The statuses of ASV usage and rehabilitation progression were discussed in
the team conference to continue reasonable use of ASV. The average
time of daily ASV usage was 287 ± 167 min. Plasma catecholamines
were investigated at 1 h after starting antihypertensive therapy to
evaluate the effects of continuous usage of ASV on the sympathetic
status. A flow chart of the present study is shown in Fig. 1B.
Spectral analysis of heart rate variability
Changes in heart rate and blood pressure were analysed under
electrocardiographic monitoring, and low frequency (LF) and high
frequency (HF) were calculated by using MemCalc/Tonam2C
(GMS, Tokyo, Japan) to evaluate sympathetic nervous activity
[11–13]. LF and HF were measured under electrocardiographic
monitoring at intervals of 5 s. The mean LF/HF ratios at 30 min
from admission and those between 30 min and 1 h after admission were respectively calculated. The differences were evaluated
in both groups (Fig. 1B).
Figure 1: (A) Flow diagram showing the patient selection process. (B) Flow chart of the present study. ASV: adaptive servo-ventilation; LF/HF: low frequency/high
frequency.
A. Hiraoka et al. / Interactive CardioVascular and Thoracic Surgery
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Variables
All (n = 28)
ASV (−) (n = 14)
ASV (+) (n = 14)
P-value
Age (years)
Female gender
Body surface area (m2)
Hypertension
Hyperlipidaemia
Diabetes mellitus
Smoking history
COPD
LVEF (%)
Onset time (h)
Aortic diameter (mm)
False lumen size (mm)
Lumen status
Fully open
Ulcer-like projections
Complete thrombosis
Partial thrombosis
Laboratory tests
WBC (102/μl)
Haemoglobin (g/dl)
Platelet (104/μl)
Creatinine (mg/dl)
Albumin (g/dl)
CRP (mg/dl)
D-dimer (μg/ml)
BNP (pg/ml)
70.9 ± 15.0
11 (39%)
1.64 ± 0.26
24 (86%)
7 (25%)
7 (25%)
16 (57%)
2 (7%)
66.4 ± 5.6
4.8 ± 3.2
39.5 ± 6.9
11.4 ± 5.4
71.1 ± 12.1
6 (43%)
1.61 ± 0.25
12 (86%)
3 (21%)
3 (21%)
7 (50%)
2 (14%)
67.7 ± 4.9
5.2 ± 3.1
39.1 ± 7.4
10.8 ± 4.1
70.7 ± 18.0
5 (36%)
1.67 ± 0.27
12 (86%)
4 (29%)
4 (29%)
9 (64%)
0 (0%)
65.1 ± 6.0
4.4 ± 3.4
39.9 ± 6.6
12.3 ± 7.0
0.942
1.000
0.544
1.000
1.000
1.000
0.704
0.482
0.227
0.492
0.781
0.504
0.158
3 (11%)
3 (11%)
17 (61%)
5 (18%)
1 (7%)
0 (0%)
9 (64%)
4 (29%)
2 (14%)
3 (21%)
8 (57%)
1 (7%)
103 ± 38
12.9 ± 1.9
17.9 ± 6.0
0.8 ± 0.3
3.9 ± 0.3
0.9 ± 2.6
12.5 ± 19.7
132.7 ± 249.1
109 ± 43
13.3 ± 1.8
17.7 ± 6.8
0.8 ± 0.3
3.9 ± 0.3
0.4 ± 0.7
18.5 ± 25.9
59.5 ± 55.7
96 ± 33
12.5 ± 2.0
18.1 ± 5.4
0.9 ± 0.3
3.9 ± 0.3
1.5 ± 3.6
6.6 ± 7.4
205.9 ± 338.1
0.351
0.346
0.872
0.417
0.985
0.305
0.110
0.122
ASV: adaptive servo-ventilation; COPD: chronic obstructive pulmonary disease; LVEF: left ventricular ejection fraction; WBC: white blood cell; CRP: C-reactive
protein; BNP: B-type natriuretic peptide.
Evaluation of pleural effusion and oxygenation
impairment
Follow-up enhanced computed tomography (CT) was examined
within 1 week (3–6 days) after admission, depending on patient
condition. Pleural effusion was estimated by a previously validated
technique [5, 14], using the following equations: left-side pleural
effusion volume (ml) = [0.108 × area of pleural effusion (mm2)] +
20.972 ml; right-side pleural effusion volume (ml) = [0.107 × area
of pleural effusion (mm2)] + 2.33 ml. Total volume of pleural effusion was defined as the summation of the left- and right-side effusion volume. The area of pleural effusion was calculated from an
enhanced 5 mm slice CT using ZIOSTATION 2 PLUS ZWS-2000
(Zio Software Inc., Tokyo, Japan). Oxygenation impairment in
patients with aortic dissection was defined as a ratio of the partial
pressure arterial oxygen/fractional inspired oxygen (PaO2/FIO2)
less than or equal to 200 mmHg. Since measurements of FIO2
under ASV support were not considered to be accurate, the PaO2/
FIO2 ratio was alternatively evaluated on admission and followed
under non-ASV support at 1 and 24 h after admission.
Statistical analysis
Continuous data are presented as mean ± standard deviation and
were analysed using two-tailed t-tests or compared with a Mann–
Whitney U-test for independent data, as appropriate. Categorical
variables are given as a count and percentage of patients and
compared using χ 2 or Fisher’s exact test. The correlation between
parameters was assessed using Pearson’s correlation coefficient.
Changes in sympathetic nervous activities, arterial blood gas data
and haemodynamic parameters between patients with and
without ASV therapy were analysed by multivariate analysis of
variance (MANOVA). A P-value <0.05 was considered statistically
significant. All data were analysed using the Statistical Analysis
Systems software JMP 9.0 (SAS Institute Inc., Cary, NC, USA).
RESULTS
Changes of haemodynamic parameters under
antihypertensive therapy
Antihypertensive therapy with Nicardipine was used in all
patients. The dosage used was equivalent in the non-ASV and ASV
groups (77.5 ± 52.1 vs 90.6 ± 58.7 mg/m2, P = 0.554). Landiolol and
Precedex were equally used for patients with tachycardia (heart
rate >100 per min) and discomfort in non-ASV and ASV groups
(29% [4/14] and 29% [4/14], P = 1.000 and 50% [7/14] and 36% [5/14],
P = 0.704, respectively). There were no significant differences in the
respective dosage between the non-ASV and ASV groups
(33.1 ± 64.4 vs 49.0 ± 106.0 mg/m2, P = 0.636 and 76.6 ± 114.0 vs
61.9 ± 105.9 μg/m2, P = 0.728). Systolic and diastolic blood pressure,
heart rate and respiratory rate were evaluated at baseline, 1, 6, 12
and 24 h after admission. In both groups, significant reduction in systolic and diastolic blood pressures was achieved. However, heart rate
significantly decreased in the ASV group, and no significant changes
were found in the non-ASV group. MANOVA analysis showed that
the changes in heart rate were much more significant in the ASV
group (P = 0.003). Although the respiratory rate significantly
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Table 1: Baseline characteristics between patients with and without adaptive servo-ventilation therapy
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decreased at 1 h after admission in the ASV group, there were no significant differences between patients with and without ASV support
(Fig. 2).
Pain was measured with the use of the numeric rating scale
(0–10). Pentazocine was equally used for patients with a pain
score ≥3 (4.3 ± 7.0 mg in the non-ASV group and 5.4 ± 6.9 mg in
the ASV group, P = 0.686) as a first-line, anti-pain therapy.
Compared with baseline, the pain score similarly decreased at 1,
6, 12 and 24 h after admission in both groups (from 2.4 ± 2.3 to
1.3 ± 1.7, 1.0 ± 1.4, 0.3 ± 0.8 and 0.2 ± 0.6, P = 0.008 in the non-ASV
group and from 2.5 ± 1.9 to 1.3 ± 1.3, 0.9 ± 1.8, 0.5 ± 1.3 and
0.4 ± 0.9, P = 0.002 in the ASV group).
In the ASV group, the average of the PaO2/FIO2 ratio at 1 h after
admission tended to be higher under the condition without ASV
support. The mean of the PaO2/FIO2 ratio and the overall incidence rate of oxygenation impairment at 24 h after admission
were 317 ± 92 and 14.3% (4/28), respectively. There were no significant differences in the PaO2/FIO2 ratio (309 ± 91 vs 325 ± 95,
P = 0.652) between the non-ASV and ASV groups. Oxygenation
impairment at 24 h after admission was found more frequently in
the non-ASV group (21% [3/14]) compared with the ASV group
(7% [1/14]), but the differences were not significant (P = 0.596).
ASV (r = 0.412, P = 0.033 and r = 0.418, P = 0.030). In the ASV
group, significant changes in plasma catecholamine concentration
were not observed between baseline and 30 min after initiating
ASV support (noradrenaline: 794 ± 350 to 839 ± 426 pg/ml,
P = 0.502; adrenaline: 178 ± 141 to 171 ± 166 pg/ml, P = 0.764;
dopamine: 35 ± 30 to 35 ± 24 pg/ml, P = 0.960). In patients
without ASV support, noradrenaline and dopamine significantly
increased at 1 h after admission, compared with baseline (noradrenaline: 746 ± 343 to 912 ± 402 pg/ml, P = 0.033; adrenaline:
216 ± 205 to 231 ± 178 pg/ml, P = 0.923; dopamine: 30 ± 21 to
42 ± 28 pg/ml, P = 0.015). Serum dopamine elevation was insignificantly greater in the non-ASV group (P = 0.061).
The mean baseline (from admission to 30 min) and later
(from 30 min to 1 h after admission) LF/HF were 2.2 ± 1.4 and
2.1 ± 1.9, respectively. In the non-ASV group, there were no significant changes in LF/HF (from 2.2 ± 1.3 to 2.5 ± 2.4, P = 0.234).
However, significant decreases in LF/HF were found in patients
with ASV therapy (from 2.1 ± 1.6 to 1.7 ± 1.1, P = 0.045).
MANOVA analysis showed that changes in LF/HF were significant
between the non-ASV and the ASV groups (P = 0.037). Figure 3
shows comparisons in terms of changes in sympathetic nervous
parameters.
Changes of status of sympathetic nervous
parameters
Pleural effusion and serum C-reactive protein
during follow-up at subacute phase
Heart rate was an independent parameter correlated with the
value of noradrenaline and dopamine at the baseline (r = 0.551,
P = 0.004 and r = 0.619, P = 0.001) and 30 min after introducing
At baseline, the overall mean estimated volume of right- and leftside pleural effusion was 24.0 ± 71.6 and 42.9 ± 72.3 ml, respectively.
A follow-up CT within several days after onset revealed significantly
Figure 2: (A and B) In both groups, significant reduction of systolic and diastolic blood pressures (BPs) was achieved. (C) However, heart rate significantly decreased in
the adaptive servo-ventilation (ASV) group; no significant change was found in the non-ASV group. (D) There was no significant difference in respiratory rate between
patients with and without ASV support.
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Figure 3: (A–C) In patients without adaptive servo-ventilation (ASV) support, noradrenaline and dopamine significantly increased at 1 h after admission compared
with baseline. (D) A significant decrease in the low frequency/high frequency (LF/HF) ratio was found in patients with ASV therapy. MANOVA analysis showed that the
change of LF/HF was significant between the non-ASV and the ASV groups.
greater left-side pleural effusion volumes, compared with those of
the right side (39.0 ± 57.3 vs 131.0 ± 101.2 ml, P < 0.001). Between
the non-ASV and ASV groups, there were no significant differences
in total volume of bilateral pleural effusion at baseline (75.3 ± 186.2
vs 57.1 ± 77.0 ml, P = 0.755) and follow-up (197.5 ± 135.2 vs
137.6 ± 140.4 ml, P = 0.300); however, a significantly lower rate of increase in the total volume of bilateral pleural effusion was observed
in the ASV group (649 ± 611 vs 190 ± 292%, P = 0.033) (Table 2).
Serum C-reactive protein (CRP) was measured at baseline and
followed 1, 2, 3, 4 and 6 days after admission. Although CRP similarly and significantly elevated in both groups (Fig. 4A), the peak
CRP level was significantly higher in the non-ASV group compared
to that of the ASV group (15.5 ± 6.3 vs 8.5 ± 6.1 mg/dl, P = 0.009)
(Fig. 4B). Additionally, the peak CRP level had a significant positive
correlation with total pleural effusion volume at follow-up (r =
0.434, P = 0.039). The duration of ASV support had no significant
impact on pleural effusion and serum CRP.
Clinical states in follow-up
Rehabilitation was planned and performed as scheduled for
patients in both groups. Bed rest was continued from admission to
the next day (initial 24 h). On the third day after admission, independent standing was begun; walking around the bed was
initiated on the fourth day. Follow-up CT at 2 weeks after admission showed no significant difference in the change of the aortic
diameter and morphological features between the non-ASV and
ASV groups. There were no significant differences in intensive care
unit and hospital stay between the non-ASV and ASV groups
(3.1 ± 1.1 vs 3.1 ± 1.3 days, P = 1.000; and 14.4 ± 4.4 vs 18.4 ± 7.8
days, P = 0.120). During 6 months of follow-up, TEVAR was performed for 2 patients in the non-ASV group and for 1 patient in
the ASV group. Two patients in the ASV group underwent surgical
repair (P = 0.305).
DISCUSSION
In general, acute aortic dissection is accompanied by severe and
unbearable back pain which can increase sympathetic nervous activity. Moreover, respiratory problems due to pleural effusion and
oxygenation impairment are additional factors that activate catecholamines and elevate blood pressure [3–5, 15, 16]. Inflammation
and aortic dilatation were reported as risk factors for pleural effusion in patients with acute type B aortic dissection [5]. Incidence of
oxygenation impairment in aortic dissection was reported to be
49–51%, and body mass index ≥22 kg/m2, maximum body temperature ≥36.5°C, patent false lumen and a lower PaO2/FIO2 ratio
were reported as risk factors [3, 4]. In addition, respiratory impairment can be induced by other causes such as hypoxic pulmonary
vasoconstriction due to vasodilators and sleep apnoea in patients
requiring antihypertensive therapy for acute aortic dissection [17,
18]. Based on these diverse backgrounds, positive pressure ventilation was thought to be helpful to prevent respiratory impairment
and suppress increased sympathetic nervous activity. ASV is
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Table 2: Comparison of change of pleural effusion between patients with and without adaptive servo-ventilation therapy
Variables
All (n = 28)
ASV (−) (n = 14)
ASV (+) (n = 14)
P-value
Right-side PE volume on admission (ml)
Left-side PE volume on admission (ml)
Right-side PE volume at follow-up (ml)
Left-side PE volume at follow-up (ml)
Change rate of PE volume (%)
24.0 ± 71.6
42.9 ± 72.3
39.0 ± 57.3
131.0 ± 101.2
439 ± 535
28.2 ± 92.7
47.1 ± 93.5
49.9 ± 60.6
147.6 ± 101.5
649 ± 611
19.1 ± 38.3
37.9 ± 38.7
26.0 ± 53.0
111.5 ± 102.1
190 ± 292
0.754
0.754
0.320
0.397
0.033
ASV: adaptive servo-ventilation; PE: pleural effusion.
Figure 4: (A) Serum C-reactive protein (CRP) significantly elevated in both the non-adaptive servo-ventilation (ASV) and ASV groups. (B) Peak CRP level was significantly higher in the non-ASV group than in the ASV group.
compact and simple to apply, and synchronized support of ocean
waveform type in AutoSet CS was expected to be more suitable for
patients with acute aortic dissection.
In the present study, ASV therapy can partially suppress the
increases in serum catecholamines and significantly control the
elevation of LF/HF. While blood pressures significantly decreased in
both groups by equivalent antihypertensive therapy, only in the
ASV group significantly decreased heart rates were achieved. Used
dosage of Landiolol and Precedex did not correlate with haemodynamic and sympathetic parameters. Considering that vasodilators
generally increase heart rate in return for antihypertensive effects,
our results may reflect the efficacy of ASV. Regarding oxygenation
impairment, the influence of ASV on oxygenation impairment
could not be precisely evaluated because of difficulty in the accurate measurement of FIO2 under ASV support. Considering that oxygenation impairment frequently occurred between 24 h and 3 days
after onset, evaluation of oxygenation impairment within 24 h after
admission was likely to be inadequate [15]. At 1 h after admission,
continuous ASV support tended to improve the PaO2/FIO2 ratio.
However, significant prevention of oxygenation impairment at 24 h
was not achieved. After 30 min of continuous use of ASV, it was
used intermittently. Time differences of use may have an influence
on results.
On the other hand, ASV was considered to help reduce development of pleural effusion. Peak CRP had a significant positive correlation with pleural effusion volume, and peak CRP was significantly
lower in patients with ASV therapy during early follow-up. CRP was
reported to be a good marker for risk of oxygenation impairment
and long-term outcomes in type B acute aortic dissection [3, 19, 20].
Peak CRP level ≥15 mg/dl was detected as an independent determinant in the development of oxygenation impairment, and the
long-term survival rate was significantly lower in patients with
higher peak CRP level (14.90–32.60 mg/dl) [3, 20]. Therefore, maintaining peak CRP level below 15 mg/dl is thought to be meaningful
in the treatment of acute uncomplicated type B aortic dissection. In
the present study, the peak CRP level was significantly lower in
patients with ASV therapy, and the mean peak CRP level was
8.5 ± 6.1. On the other hand, the mean peak CRP level was 15.5 ± 6.3
in the non-ASV group, and ASV therapy achieved the inhibition of
elevation of CRP ≥15 mg/dl. However, CRP is not a specific marker
and is influenced by many factors. Therefore, the results in the
present study could not markedly demonstrate the efficacy of ASV.
Based on the obtained results, non-invasive positive pressure ventilation by ASV helped to maintain respiratory conditions at the hyperacute phase in uncomplicated type B dissection. Decreases in pleural
effusion may be caused by optimized lung inflations with positive
pressure, and they helped to suppress the excessive sympathetic
nervous activity. Consequently, all these actions might induce the
suppression of elevation in peak CRP level in multifactorial ways.
Although optimal positive PS is reported to be required to resolve
pleural effusion increases, the mechanism is not completely determined, and several trials are ongoing [21, 22]. We, on the other hand,
could present positive impacts of ASV on uncomplicated type B
aortic dissection at hyper-acute phases. However, the clinical
benefits of ASV at follow-up periods were not fully obtained by the
present protocol. Therefore, further evaluation is required to reveal
whether the introduction of ASV, in addition to cardiovascular
rehabilitation and antihypertensive therapy, can truly contribute
to improve late outcomes of acute uncomplicated type B aortic
dissection.
Study limitations
Our study was a prospective, randomized investigation; however,
it has several limitations. First, it does not have a high statistical
power because of the small sample size. It has been difficult to
obtain a sufficient number of enrolled patients with uncomplicated
type B dissection in a single institute for a certain time. Second,
different onset times, the timing of follow-up CT and lumen type
may influence the data on haemodynamics, sympathetic nervous
activity and pleural effusion volume. Plasma catecholamines were
not measured several times. Deciding the severity of uncomplicated type B dissection was difficult. Although the usage of
Landiolol and Precedex were equal in both groups, these agents
influenced sympathetic nervous activity. Third, oxygen therapy
was begun in several patients before admission and these different
conditions affected the results. Additionally, the doses of oxygen
administration could not be evaluated uniformly between
non-ASV and ASV groups, and FIO2 in ASV support was not accurately evaluated. Different markers and cytokines of inflammation,
such as interleukin, were not evaluated. Finally, a comparison
between continuous, positive airway pressure and ASV was not
performed. Therefore, the advantages of ASV may have been
influenced by confounding variables.
CONCLUSIONS
In patients with uncomplicated acute type B aortic dissection, excessive sympathetic nervous activity, the development of pleural
effusion volume and elevation of peak CRP level were possibly suppressed under ASV therapy. The results suggest that ASV introduction may have the potential to contribute to a positive impact on
early clinical states of uncomplicated type B acute aortic dissection.
Conflict of interest: none declared.
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