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European Review for Medical and Pharmacological Sciences
2014; 18: 3737-3742
Comparison of cerebral-cardiac syndrome
caused by nonaneurysmal or aneurysmal
subarachnoid hemorrhage
W.-J. HUANG, W.-W. CHEN, X. ZHANG
Department of Neurology, Xuzhou Central Hospital, Xuzhou, Jiangsu Province, China
Abstract. – OBJECTIVE: To investigate the
difference between myocardial injuries caused
by nonaneurysmal subarachnoid hemorrhage
(SAH) or aneurysmal SAH.
PATIENTS AND METHODS: A total of 92 inpatients with SAH at early stage (within 48h),
who were treated in our hospital from 2008 to
2014 were enrolled in this study. Differences in
cerebral-cardiac syndrome seen in perimesencephalic subarachnoid hemorrhage (PMSAH),
non-perimesencephalic subarachnoid hemorrhage (n-PMSAH), and aneurysmal subarachnoid hemorrhage (aSAH) were recorded based
Hunt-Hess scores, electrocardiogram/echocardiography findings, and serum myocardial enzymes.
RESULTS: The Hunt-Hess grade was relatively lower in the PMSAH group (mainly at grades I
and II) than in aSAH group and n-PMSAH group.
The ECG score was significantly lower in the
PMSAH Group than in the aSAH or n-PMSAH
Group. In the PMSAH group, the left ventricular
function was normal; in contrast, the left ventricular end-systolic diameter, left ventricular
end-diastolic diameter, left ventricular wall
thickness, and left ventricular ejection fraction
showed certain abnormalities in the aSAH
group and n-PMSAH group. The myocardial enzymes remarkably increased only in the aSAH
group.
CONCLUSIONS: In PMSAH patients, the lower Hunt-Hess grade, milder ECG abnormalities,
less changes in cardiac enzymes and echocardiography are associated with better prognosis.
The clinical course and myocardial injuries are
poorer in n-PMSAH patients when compared
with the PMSAH patients but better than aSAH
patients.
Key words:
Perimesencephalic subarachnoid hemorrhage, Subarachnoid hemorrhage, Cerebral-cardiac syndrome,
PMSAH, n-PMSAH.
Introduction
Subarachnoid hemorrhage (SAH) is a common
acute cerebrovascular disease, with aneurysms
and cerebral vascular malformation as the main
etiology. However, no hemorrhagic evidences of
etiology for such aneurysms were found in approximately 5%-28% patients undergoing whole
cerebral angiography in clinical practice. Perimesencephalic regions were involved in certain
proportion of these SAH patients (1/3-2/3) with
negative whole cerebral angiography findings.
For these patients, there were unique clinical
manifestations, treatment and prognosis. Currently, this disease type is defined as perimesencephalic subarachnoid hemorrhage (PMSAH)1,
which is also known as benign subarachnoid hemorrhage. Since nonaneurysmal subarachnoid
hemorrhage was not restricted to the perimesencephalic region for a considerable number of patients, this disease species is defined as non-perimesencephalic subarachnoid hemorrhage (nPMSAH)2. Since Dozzi tried to explore the relationship between cardiac dysfunction and cerebrovascular disease in 19373, the importance of
cerebrovascular disease in the development of
myocardial injury, cardiac arrhythmia and acute
myocardial infarction has been confirmed by
many researchers4. Moreover, some patients died
of such fatal arrhythmias and cardiac arrest. In
clinical practice, this secondary heart damage induced by acute cerebrovascular disease is referred as cerebral-cardiac syndrome (CCS). In
the present study, enrolled patients were divided
into PMSAH, n-PMSAH and aneurysmal subarachnoid hemorrhage (aSAH) groups. HuntHess rating scale was employed to assess the extent of nerve damage. Changes of ECG, myocardial enzymes and cardiac ultrasound findings
were examined to compare the variance of cerebral-cardiac syndrome among these groups.
Corresponding Author: Xia Zhang, MD; e-mail: [email protected]
3737
W.-J. Huang, W.-W. Chen, X. Zhang
Patients and Methods
Clinical Data
Inclusion Criteria
According to the diagnostic criteria of subarachnoid hemorrhage formulated by the 4th National
Conference on Cerebrovascular Disease, 86 patients who were admitted to the Department of
Neurology of our hospital due to subarachnoid hemorrhage from February 2008 to February 2014
were included. Inclusion criteria were: no family
history of subarachnoid hemorrhage, not receiving
anti-platelet regimen, incident subarachnoid hemorrhage, and disease onset within 48 hours. All patients underwent emergency cranial CT examinations before or at admission and were diagnosed to
be SAH. The existence of any aneurysms was confirmed by computed tomography angiography
(CTA) or digital selective angiography (DSA) within one week. 26 Males and 34 females, aging from
42 to 78 years, were included, with the mean age of
56.4 years. According to the PMSA diagnostic criteria, enrolled patients were divided into three
groups: PMSAH Group (26 patients), n-PMSAH
Group (28 patients) and aSAH Group (32 patients).
Exclusion criteria:
(1) Subarachnoid hemorrhage induced by other
etiologies, such as trauma, intracranial hemorrhage, arteriovenous malformation, and aneurysm;
Figure 1. A cranial CT image of patients with nonaneurysmal subarachnoid hemorrhage.
3738
(2) documented heart disease before admission,
such as coronary heart disease, valvular heart disease, arrhythmias, etc.; (3) ECG abnormalities
within three months prior to admission; and (4)
hypertensive heart disease for patients with hypertension.
Diagnostic criteria for PMSA
According to the diagnostic criteria proposed
by Rinkel et al5: (1) patients underwent cranial
CT examination within 48 hours, with the hemorrhagic center located in the frontier of perimesencephalic region, downward extension to anterior
myelencephalon, and forward to posterior longitudinal fissure without fully occupied, outward to
the internal horizontal portion of lateral fissure
without external portion involved, excluding little
hemorrhage; (2) a small amount of depositing intraventricular hemorrhage; and (3) no parenchymal hemorrhage (Figure 1).
Diagnostic criteria for n-PMSAH
According to the diagnostic criteria proposed
by Gupta et al6: the majority of hemorrhage was
located at the intersection pool, exterior cistern
and interhemispheric pool, with some perimesencephalic regions involved. However, majority of
the hemorrhage was located at other brain pools
(Figure 2).
Figure 2. A cranial CT image of patients with perimesencephalic subarachnoid hemorrhage.
Comparison of cerebral-cardiac syndrome
Methods
lyzed by one-way ANOVA, and a p < 0.05 denotes the statistical significance of difference.
The basic information of patients was documented at admission to evaluate the extent of disease condition (Hunt-Hess Scale). After admission, bedside 12-lead ECG was performed within
24 hours and abnormalities were defined as follows: (1) Sinus tachycardia, heart rate >100 bpm,
absence of rhythm disorders; (2) Sinus bradycardia, heart rate < 60 bp, no rhythm disorder; (3)
QT prolongation (≥ 0.44s); (4) ST segment
changes: ST-segment elevation (≥ 0.1 mv), ST
segment depression (≥ 0.05 mv). Assessment was
based on Kawasaki et al scale criteria 7, and
scores represented the respective frequencies of
pathologic Q waves, ST segment elevation or depression, and T wave prolongation. Any of above
performance was counted as one point.
In the next morning of admission, venous blood
samples were collected and submitted to our laboratory. Biomarkers for cardiac injury, such as troponin I (TnI), and creatine kinase and its isozymes
(CK-MB), were quantitatively assayed by using
enzyme-linked immune-sorbent assays (ELISA).
For abnormalities of the first test, repeated tests
were performed on day-3 and day-7.
After admission, echocardiography examinations were performed within 48 hours. Variables
to determine include left ventricular end-systolic
diameter (LVESD), left ventricular end-diastolic
diameter (LVEDD), left ventricular wall thickness (LVPWH), left ventricular ejection fraction
(LVEF) and ventricular wall motion.
Statistical Analysis
Statistical analyses were performed on the
platform of SPSS 16.0 software (SPSS Inc.,
Chicago, IL, USA), with results represented as
mean ±SD. Pairwise mean comparison was analyzed between the two groups by t-test; and multiple mean comparisons were analyzed were ana-
Results
Stratified Hunt-Hess comparisons among
PMSAH, n-PMSAH and aSAH groups
The severity of condition was judged based on
the Hunt-Hess scale. As shown by the results,
less severity was observed in condition for patients with PMSAH, with Grade-I or -II for the
majority of patients; and more severity was observed in patients with aSAH, including 22 patients with Grade III-V. The condition of severity
of patients with n-PMSAH was between the
above two groups, as shown in Table I.
Comparisons of ECG results among
PMSAH, n-PMSAH and aSAH Groups
Based on the findings of ECG monitoring
changes, there were ECG abnormalities in all
three groups, but the frequency of abnormality
was higher in the PMSAH Group than in the
aSAH or n-PMSAH Group (Table II). Moreover,
the ECG score was significantly lower in the
PMSAH Group than in the aSAH or n-PMSAH
Group (1.6±0.8 vs 5.8±3.1; 4.3±1.1, p < 0.01).
These differences were statistically significant.
There was no significant difference in ECG
scores between aSAH and n-PMSAH Groups.
Comparisons of cardiac ultrasound
results among PMSAH, n-PMSAH
and aSAH Groups
All enrolled patients underwent cardiac ultrasound examinations. As shown by the results,
normal findings of left ventricular function were
observed in patients of the PMSAH Group, without reporting inner diameter expansion of heart
cavity and wall motion abnormalities. There
were abnormalities of LVESD, LVEDD, LVPWH
Table I. Comparisons of HUNT-HESS scores among the three groups (frequency, %).
Group
Group aSAH
Group n-PMSAH
Group PMSAH
Number
32
28
26
HUNT-HESS Grade
Grade I
Grade II
Grade III
Grade IV/V
3 (9.3)
4 (14.3)
3 (11.5)
7 (21.9)
19 (67.9)
22 (84.6)
14 (43.8)
2 (7.1)
1 (3.8)
8 (25.0)
3 (10.7)
0 (0)
3739
W.-J. Huang, W.-W. Chen, X. Zhang
Table II. Comparisons of ECG abnormality scores among three groups (± s).
Group
N
Number of ECG abnormalities (percentage)
ECG Scores
Group aSAH
Group n-PMSAH
Group PMSAH
32
28
26
Elevation of
ST segment
Depression of
ST segment
QT prolongation
Q wave
abnormalities
9 (28.13%)
7 (25.00%)
3 (11.54%)
13 (40.63%)
15 (53.57%)
12 (46.15%)
6 (18.75%)
4 (14.29%)
2 (7.69%)
2 (6.25%)
0 (0)
0 (0)
5.8±3.1
4.3±1.1
1.6±0.8*
Note: Compared with that of aSAH Group, *p < 0.05.
and LVEF to various extents in aSAH and n-PMSAH Groups. There were 9 and 4 cases of abnormal wall motion, respectively. See Table III for
details.
Comparison of troponin levels
among the three groups of PMSAH,
n-PMSAH and aSAH
In the next morning of admission, venous
blood samples were collected and submitted to
our laboratory for myocardial enzyme tests
(Table IV). As shown by the results, the highest
levels of TnI, CK and CK-MB of myocardial enzyme panel were observed for aSAH patients.
Only 7 cases of myocardial enzyme elevations
were observed in 26 PMSAH patients. The differences were statistically significant (p < 0.01).
Discussion
Van Gijin et al8 first proposed the concept of
PMSAH in 1985 based on the findings of imaging
examinations. In their reports, for patients with the
hemorrhage site located at the perimesencephalic
region, the clinical symptoms were relatively less
severe, and mild-to-moderate distending pain was
identified to be the main manifestations of
headache, with temporal or occipital regions most
commonly affected. The conditions were fully recovered after three months of onset. No relapse
was observed over the 18 months of follow-up.
Therefore, for the first time, these authors considered the perimesencephalic SAH with no
aneurysms or other abnormalities in angiography,
mild symptoms and favorable prognosis to be PMSAH. In this study, three groups of patients were
evaluated based on Hunt-Hess scales. The least
severity in neurological deficit was observed in
PMSAH patients, with Grade I/II for the majority.
Perimesencephalic regions include basal cistern, cerebral peduncle, ambient cistern and
quadrigeminal cistern. As a unique subtype of
subarachnoid hemorrhage, the cause of PMSAH
has not yet been fully understood. Possible etiologies include expansion and bleeding of veins or
capillaries, rupture of perforating artery, occult arteriovenous malformation, secondary bleeding induced by occlusion of small perforating branches.
The center of bleeding was concentrated around
perimesencephalic regions9. If there were diffuse
bleeding or blood clots in the merger longitudinal
or lateral cistern, non-PNSH origin of bleeding
should be considered. Although the clinical manifestations of such nervous system damage were
relatively less severe, patients might experience
other complications such as hyponatremia or
heart abnormalities10. Imaging changes and neurological injury have been highlighted in prior
PMSA related studies, and there were few investigations on the classification of myocardial injury
following PMSAH, n-PMSAH and aSAH. Therefore, the post-SAH cerebral- cardiac syndrome
has been investigated in this study.
Table III. Comparisons of cardiac ultrasound results among PMSAH, n-PMSAH and aSAH Groups (± s).
Group
N
LVESD
LVEDD
LVPWH
LVEF
Abnormal wall
motion (N)
Group aSAH
Group n-PMSAH
Group PMSAH
32
28
26
47.23±2.01
48.18±1.86
38.23±2.31*
49.76±3.69
50.23±2.82
40.19±3.08*
9.28±0.76
9.86±0.49
8.99±0.92*
42.17±2.48
43.15±1.59
53.23±1.24*
9
4
0
Note: Compared with that of aSAH Group, *p < 0.05.
3740
Comparison of cerebral-cardiac syndrome
Table IV. Comparisons of myocardial enzyme panel among these three groups (± s).
Group
N
TnI (ng/ml)
CK (U/L)
CK-MB (U/L)
Group aSAH
Group n-PMSAH
Group PMSAH
32
28
26
4.18±1.20
3.06±0.83
1.06±0.26*
389.12±60.41
293.56±50.39
198.67±45.23*
35.26±12.30
26.14±10.52
19.68±8.93*
Note: Compared with that of aSAH Group, *p < 0.05.
The cardiac injury post subarachnoid hemorrhage belongs to the scope of brain-heart syndrome, with ischemia changes such as ST segment elevation of depression, flat T-wave or inversion, Q-T prolongation as shown by ECG examinations within one week of SAH onset, ventricular contraction, sinus tachycardia, bradycardia or atrioventricular block arrhythmias and other changes persisting for several days or weeks as
the main manifestations. Its nature of functional
or organic changes remained controversial.
Based on above changes, ECG score has been recently employed to determine the post-SAH
ECG abnormalities. Kawasaki et al7 described
ECG score was an independent factor of SAH
patient mortality. In this study, ECG abnormalities were analyzed by ECG scores within 24
hours of admission, suggesting the presence of
ECG abnormalities to variable extent in patients
of three groups. However, the incidence of ECG
abnormality was lowest in PMSAH patients, with
an overt lower ECG score compared with those
of other two groups. ECG injury appeared to be
less severe in patients with mild neurological
damage (Hunt-Hess grade). Aneurysm rupture
induced hemorrhage mainly affected cerebral arterial circle (Willis circle). The result of direct
stimulation to the cardiovascular center, such as
the hypothalamus and brain stem and Willis circle induced certain region changes of cardiac autonomy was consistent to the pathological mechanism of ECG abnormalities.
Intra-cardiac structures, heart beat and blood
flow could be dynamically demonstrated by
echocardiography, which could be useful to detect
changes of cardiac function of early stages and to
formulate early interventions. Sugimoto et al11
conducted 2D-dimensional echocardiography in
47 SAH patients without prior heart diseases to
determine cardiac functions. As shown by the results of this study, for SAH patients with regional
wall motion abnormality (RWMA), higher HuntHess classification, and CK and CK-MB levels, as
well as higher initial heart rate were observed,
concomitant with a high incidence of inverted T
waves. In that study, a detailed classification comparison was conducted for SAH patients. As
shown by echocardiography among PMSAH, nPMSAH and aSAH patients, the variables of PMSAH patients were essentially in the normal range,
without the observation of regional wall motion
abnormality, and left ventricular expansion to variable extents and decrease of ejection fraction were
observed in n-PMSAH and aSAH patients, with
regional wall motion abnormalities reported in 4
and 9 cases respectively. However, no follow-up
re-examinations were implemented for patients
with echocardiography abnormalities in this study.
SAH patients often experienced concomitant elevation of myocardial enzymes in the early stages
of disease onset, suggestive of the presence of secondary myocardial damage. This injury was generally considered to be reversible and could be gradually recovered in response to the treatment of primary disease. As described by Der Bilt et al12, TnI
elevation was associated with increased risk of cardiopulmonary complications, delayed encephalopathy and death. However, there were relatively few studies dealing with myocardial injury
induced by non-aneurysmal or aneurysmal subarachnoid hemorrhage. The levels of CK, CK-MB
and TnI were examined in this study, in which TnI
level was one of specific indices for myocardial injury. As shown by the results, elevations of cardiac
enzyme panel to variable extents were observed in
patients of the three groups. The incidence of perimesencephalic subarachnoid hemorrhage and the
elevations of cardiac enzyme panel were relatively
low in extent. The severity of myocardial injury for
n-PMSAH patients was between that of PMSAH
patients and of aSAH patients.
Conclusions
Based on the four data sets of comparative
analyses, lower Hunt-Hess grades were associated with less changes of ECG findings, cardiac
3741
W.-J. Huang, W.-W. Chen, X. Zhang
enzymes and echocardiography, as well as more
favorable prognosis, for patients with PMSAH.
The clinical course and severity of myocardial
injury for patients with n-PNSAH were inferior
to those of patients with PMSAH. However,
these variables were more favorable than those of
patients with aneurysmal subarachnoid hemorrhage. Therefore, the severity of SAH was proposed to be positively proportional to cardiac
performance. Thus, changes of ECG and cardiac
enzyme panels should be actively monitored after
SAH attack. Early detection and intervention
were generally recommended.
–––––––––––––––––––-––
Conflict of interest
The Authors declare that they have no conflict of interests.
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