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Journal of Human Hypertension (2012) 1 -- 5
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ORIGINAL ARTICLE
Inflammatory markers are associated with left ventricular
hypertrophy and diastolic dysfunction in a population-based
sample of elderly men and women
S Masiha1, J Sundström2 and L Lind2
Markers of inflammation have previously been related to left ventricular (LV) hypertrophy (LVH) in uremic and hypertensive
patients. The present study investigated inflammatory markers in relation to LV geometry and diastolic function in a population
of elderly persons. In the population-based Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study (1016 men
and women 70 years of age), echocardiograms to determine relative wall thickness (RWT), LV mass index (LVMI) and the
E/A-ratio were obtained. Based on RWT and LVMI, four geometric subgroups were defined; normal, concentric remodeling,
eccentric and concentric LVH. In all, 10 circulating inflammatory markers were measured. Higher levels of high sensitive
C-reactive protein (hsCRP) and E-selectin were seen in the three abnormal geometry groups than in the normal group adjusting
for gender, body mass index, systolic and diastolic blood pressure and use of antihypertensive medication. Higher level of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1) and P-selectin were only seen in concentric
LVH. Levels of tumor necrosis factor-alpha, interleukin-6, l-selectin, monocyte chemotactic protein-1 and leukocyte count did
not differ between the LV groups. l-selectin and hsCRP were related to the E/A-ratio. The adhesion molecules; E-selectin,
ICAM-1, VCAM-1, P-selectin and hsCRP were elevated in elderly persons with abnormal LV geometry, especially in concentric
LVH, after adjusting for hypertension and obesity. l-selectin and hsCRP were related to LV diastolic function. Further studies are
motivated to investigate a pathogenetic role of inflammation for abnormal LV geometry and function.
Journal of Human Hypertension advance online publication, 12 January 2012; doi:10.1038/jhh.2011.113
Keywords: left ventricular hypertrophy; inflammation; echocardiography
INTRODUCTION
Geometric alterations of the left ventricle as an independent risk
factor for cardiovascular disease have been demonstrated in
several studies. Left ventricular (LV) hypertrophy (LVH) is
associated with subsequent cardiovascular events but the exact
mechanism is not fully understood.1 - 4
Involvement of inflammatory markers in fibrotic process as the
main component in ventricular remodeling process has previously
been suggested in several studies using animal models.5 - 8 We
conducted this study to investigate the hypothesis that biomarkers
of inflammation were even associated with LVH in humans.
A role for inflammatory markers as predictors of cardiovascular
diseases has been the theme of numerous studies during the past
decade. C-reactive protein (CRP) has been demonstrated to be a
strong and independent risk marker regarding both incident
diabetes and cardiovascular disease.9 - 16
The association between LVH and high sensitivity CRP (hsCRP)
values has recently been investigated. CRP values both at baseline
and after a 6-year follow-up were almost twofold higher than in
patients without LVH independently of cardiovascular and
metabolic risk factors.17
Several studies have demonstrated a relationship between
soluble cell adhesion molecules and LVH. An investigation of
plasma levels of inter-cellular adhesion molecule 1 (ICAM-1),
vascular cell adhesion protein 1 (VCAM-1) and E-selectin
in patients with uncomplicated essential hypertension suggested
a significant elevation of VCAM-1 in patients with LVH.18
Furthermore E-selectin, VCAM-1 and ICAM-1 levels have been
shown to be higher in hypertensive patients with concentric LVH
than those with eccentric LVH.19
Some recent studies have investigated the association
between the inflammatory biomarkers and LVH in patients with
renovascular disease. In adults with type 2 diabetes, LVH is
associated with susceptibility to atherothrombosis and increased
albuminuria, the latter being a marker of microangiopathy and
endothelial dysfunction that appears to be a relevant pathogenetic link between LVH and inflammation.20 Proinflammatory
cytokines, tumor necrosis factor-alpha (TNF-a) in particular have
been demonstrated to be associated with LVH in hemodialysis
patients.21
Previous studies have investigated a limited numbers of
inflammatory markers among specific populations suffering either
from hypertension or renal disease.
Our aim in the present study was to investigate the relations
between several inflammatory markers, LV geometry and
LV diastolic function in a population-based sample of elderly
men and women, the Prospective Study of the Vasculature in
Uppsala Seniors (PIVUS).
The hypothesis tested was that proinflammatory markers are
increased in persons with LVH and diastolic dysfunction.
1
Department of Cardiology, Uppsala University Hospital, Uppsala, Sweden and 2Departments of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
Correspondence: Dr S Masiha, Department of Cardiology, Uppsala University Hospital, SE-751 85 Uppsala, Sweden. E-mail: [email protected]
Received 1 September 2011; revised 29 November 2011; accepted 30 November 2011
Inflammatory markers associated with LVH and diastolic dysfunction
S Masiha et al
2
Inflammatory markers
METHODS
Sample
Eligible were all men and women aged 70 living in the community
of Uppsala, Sweden. The participants were chosen from the register of
community living and were invited in a randomized order from the start of
the study in April 2001 to the last included persons in June 2004. Potential
participants received an invitation by letter within 1 month of their 70th
birthday in order to standardize for age. Of the 2025 persons invited, 1016
were investigated giving a participation rate of 50.1%.
Participants with CRP410 mg l1 or leukocyte count 410 109 l1
(n ¼ 44) were excluded from the analysis in order not to include persons
with infections, chronic inflammatory disorders or some hematological
malignancies, which might distort the analysis. Characteristics of the
sample are given in Table 1.
The study was approved by the Ethics Committee of the University of
Uppsala and the participants gave informed consent.
Baseline investigation
The participants were asked to answer a questionnaire about their medical
history, smoking habits and regular medication.
All participants were investigated in the morning after an overnight fast.
No medication or smoking was allowed after midnight. After recordings of
height, weight (body mass index (BMI), calculated as weight (kg)/ height
(m2), abdominal and hip circumference, an arterial cannula was inserted in
the brachial artery for blood sampling and later regional infusions of
vasodilators. During the investigation, the participants were supine in a
quiet room maintained at a constant temperature.22
Blood pressure was measured by a calibrated mercury sphygmomanometer in the non-cannulated arm to nearest mm Hg after at least 30 min
of rest and the average of three recordings was used.
Approximately 10% of the cohort reported a history of coronary heart
disease, 4% reported stroke and 9% diabetes mellitus. Almost half the
cohort reported any cardiovascular medication (45%), with antihypertensive medication being the most prevalent (32%). In all, 15% reported use of
statins, whereas insulin and oral hypoglycaemic drugs were reported in 2%
and 6%, respectively.22
Table 1. Basic characteristics and major cardiovascular risk factors in
the total sample
Total sample
N
Females (%)
Height (cm)
Weight (kg)
Waist circumference (cm)
BMI (kg m2)
Waist/hip ratio
SBP (mm Hg)
DBP (mm Hg)
Heart rate (b.p.m.)
Serum cholesterol (mmol l1)
LDL-cholesterol (mmol l1)
HDL-cholesterol (mmol l1)
Serum triglycerides (mmol l1)
Fasting blood glucose (mmol l1)
Current smoking (%)
RWT
LVMI (g m2)
E/A-ratio
IVRT (ms)
1016
50.2
169±9.1
77±14
91±12
27.0±4.3
0.90±0.075
150±23
79±10
62±8.7
5.4±1.0
3.3±0.88
1.5±0.42
1.3±0.60
5.3±1.6
11
0.44±13
43±13
0.96±0.28
121±21
Abbreviations: BMI, body mass index; DBP, diastolic blood pressure; HDL,
high density lipoprotein; IVRT, isovolumic relaxing time; LDL, low density
lipoprotein; LVMI, left ventricle mass index; RWT, relative wall thickness;
SBP, systolic blood pressure. Means are given±s.d.
Journal of Human Hypertension (2012), 1 -- 5
hsCRP was measured in human serum by an ultrasensitive particle
enhanced immunoturbidimetric assay (Orion Diagnostica, Espoo, Finland)
on a Konelab 20 autoanalyser (Thermo Clinical Labsystems, Espoo,
Finland). The inter-assay coefficient of variation was 3.2%.
Cytokines, chemokines and adhesion molecules were analyzed on the
Evidence array biochip analyzer (Randox Laboratories Ltd, Crumlin, UK).
The functional sensitivity for the different inflammatory markers was as
follows: interleukin-6: 0.3 pg ml1, TNF-a: 1.8 pg ml1, MC-1: 19.4 pg ml1,
ICAM-1: 18.6 pg ml1, VCAM-1: 3 pg ml1, E-selectin: 3.1 pg ml1, P-selectin:
11.2 pg ml1, l-selectin: 32.8 pg ml1, CRP: 0.1 mg l1, Leukocyte count:
0.2 109 l1.
Echocardiography and Doppler
A comprehensive two-dimensional and Doppler echocardiography was
performed with an Acuson XP124 cardiac ultrasound unit (Acuson,
Mountain View, CA, USA). A 2.5-MHz transducer was used for the majority
of the examinations.
LV dimensions were measured with M-mode on-line from the
parasternal projections, using a leading edge to leading-edge convention.
Measurements included interventricular septal thickness, posterior wall
thickness, LV diameter in end diastole and end systole. LV relative
wall thickness (RWT) was calculated as (interventricular septal
thickness þ posterior wall thickness)/left ventricular diameter in end
diastole.
LV mass was determined from the Penn convention and indexed for
height 2.7 to obtain LV mass index (LVMI).
LV geometry was also divided into four categories according to Ganau
et al.23 A normal LV geometry was considered to be present if LVMI was
normal (o51 g m1 2.7) and RWT o0.45. Concentric LVH was defined as
LVMI above the threshold for LVH together with RWT 40.45, but if RWT was
below this cutoff for RWT eccentric LVH was present. If LVMI was normal
but RWT 40.44 the LV geometry was denoted as concentric remodeling.
The LV diastolic filling pattern of the mitral inflow was obtained from
the apical transducer position with the pulsed Doppler sample volume
between the tips of the mitral leaflets during diastole. The peak velocity of
the early rapid filling wave (E wave) and the peak velocity of atrial filling
(A wave) were recorded and the E to A ratio (E/A) was calculated in persons
with sinus rhythm. LV isovolumic relaxation time (IVRT) was measured as
the time between aortic valve closure and the start of mitral flow using the
Doppler signal from the area between the LV outflow tract and mitral flow.
Presence of a restrictive filling pattern was evaluated in persons with an
impaired LV systolic function. This pattern was considered to be present if
E/A-ratio was 41.5 and IVRT o96 ms.
Statistical analyses
Non-normally distributed variables (HOMA, CRP, E-Selectin, ProBNP, leptin,
adpinectin, PTH, aldosterone, renin, TNI) were log-transformed to achieve a
normal distribution. Differences between groups were evaluated with
ANOVA with Bonferroni post-hoc analysis (P ¼ 0.017 for significance for
comparisons of three abnormal LV geometric groups vs the normal group).
Relationships between pairs of variables were evaluated by Pearson’s
correlation coefficient. Multiple regression analysis was applied to relate
several independent variables to a dependent variable. Two-tailed
significance values were given with Po0.05 regarded as significant. The
statistical program package StatView (SAS inc., Cary, NC, USA) was used.
RESULTS
Inflammatory variables in relation to LV geometric groups
Differences between the LV geometry groups were found for CRP,
E-selectin, ICAM-1, VCAM-1 and P-selectin in ANOVA analysis
(Table 2). TNF-a, interleukin-6, l-selectin, monocyte chemotactic
protein-1 and leukocyte count did not differ between the groups
(Table 2).
In post-hoc analyses comparing the three abnormal LV
geometric groups with the normal group, CRP and E-selectin
& 2012 Macmillan Publishers Limited
Inflammatory markers associated with LVH and diastolic dysfunction
S Masiha et al
3
Table 2.
Inflammatory markers in four left ventricular geometry groups
Normal
N
TNF-a
IL-6
CRP
E-selectin
P-selectin
1-Selectin
MCP-1
VCAM-1
ICAM-1
Leukocyte count
3.6
3.6
1.0
13.5
100
735
395
527
349
5.6
403
(2.3 - 8.3)
(1.1 - 66)
(0.37 - 2.9)
(7.9 - 21)
(29)
(150)
(123)
(145)
(90)
(1.5)
Eccentric LVH
3.6
3.9
1.3
16.0
105
711
394
558
362
5.7
76
(2.2 - 6.9)
(1.6 - 56)
(0.41 - 4.1)
(10 - 25)***
(28)
(136)
(144)
(125)
(86)
(1.6)
Concentric remodeling
3.8
3.9
1.2
15.4
103
706
385
526
362
5.7
244
(2.4 - 6.5)
(1.4 - 65)
(0.42 - 4.2)**
(9.4 - 23)***
(27)
(135)
(132)
(128)
(94)
(1.5)
Concentric LVH
3.8
4.7
1.2
14.9
107
725
412
567
374
5.8
P-Anova
152
(2.3 - 6.5)
(1.4 - 56)
(0.45 - 4.9)***
(8.7 - 28)***
(33)**
(124)
(142)
(151)**
(102)**
(1.5)
0.76
0.74
0.47
0.13
0.02
0.39
0.34
0.18
0.25
0.87
Abbreviations: CRP, C-reactive protein; ICAM-1, inter-cellular adhesion molecule 1; IL-6, interleukin-6; LVH, left ventricular hypertrophy; MCP-1, monocyte
chemotactic protein-1; TNF-a, tumor necrosis factor-alpha; VCAM-1, vascular cell adhesion protein 1. Median with 10th to 90th percentile limits (first four rows)
or mean and s.d. (last six rows) for indices of inflammation on different left ventricular geometry groups. The stars given reflect the significance levels vs
normal group after adjustment for gender, BMI, systolic and diastolic blood pressure and use of hypertensive medication. P-ANOVA is given in the first right
column. ** ¼ P-valueo0.01, *** ¼ P-valueo0.001.
Table 3. Correlations between the indices of inflammation and two
measures of the left ventricular diastolic function
TNF-a
IL-6
CRP
E-selectin
P-selectin
1-selectin
MCP-1
VCAM-1
ICAM-1
Leukocytes count
E/A-ratio
IVRT
0.01
0.01
0.17 (0.0001)***
0.13 (0.0001)*
0.04
0.07 (0.032)*
0.03
0.01
0.01 (0.0033)
0.10 (0.0023)*
0.01
0.03
0.05
0.10 (0.003)
0.04
0.08 (0.023)
0.04
0.04
0.04
0.06
Abbreviations: CRP, C-reactive protein; ICAM-1, inter-cellular adhesion
molecule 1; IL-6, interleukin-6; IVRT, isovolumic relaxing time; MCP-1,
monocyte chemotactic protein-1; TNF-a, tumor necrosis factor-alpha;
VCAM-1, vascular cell adhesion protein 1. E/A-ratio and the isovolumetric
relaxation time (IVRT), given as correlation coefficients and P-values in
parenthesis if significant. These relationships exist when gender-adjusted
only. The stars given after some P-values reflect the significance level after
adjustment for gender, BMI, systolic and diastolic blood pressure and use
of hypertensive medications. * ¼ P-value o0.05, *** ¼ P-value o0.001.
were elevated in all of the three abnormal groups when compared
with the normal group (except for CRP in eccentric LVH, not
significant after Bonferroni correction) after adjustment for
gender, BMI, systolic and diastolic blood pressure and use of
antihypertensive medication (Table 2). Higher ICAM-1, VCAM-1
and P-selectin levels were only seen in the group with concentric
LVH after a similar adjustment.
Inflammatory variables in relation to LV diastolic function
In unadjusted models, hsCRP, E-selectin, l-selectin, ICAM-1 and
leukocyte count were all inversely related to the E/A-ratio. These
relations persisted after adjustment for gender, BMI, systolic and
diastolic blood pressure and use of antihypertensive medication,
although the relation to ICAM-1 was attenuated (Tables 3 and 4).
In multiple regression analysis with the E/A-ratio as dependent
variable and the above mentioned five inflammatory indices as
independent variables together with the potentially confounding
variables, gender, BMI, systolic and diastolic blood pressure and
use of antihypertensive medication, CRP (inversely) and l-selectin
were independently related to the E/A-ratio.
& 2012 Macmillan Publishers Limited
Table 4. Multiple regression analysis relating inflammatory indices to
the E/A-ratio as dependent variable
Gender
DBP
Hypertensive medications
BMI
1-Selectin
E-selectin
Leukocyte count
ICAM-1
CRP
Partial correlation
coefficient
t-Value
P-Value
0.02
0.20
0.04
0.09
0.08
0.05
0.05
0.03
0.10
0.66
4.75
1.12
2.62
2.39
1.30
1.35
0.68
2.68
0.50
0.0001
0.26
0.0090
0.017
0.19
0.18
0.50
0.0075
Abbreviations: BMI, body mass index; CRP, C-reactive protein; ICAM-1, intercellular adhesion molecule 1; DBP, diastolic blood pressure. The E/A-ratio is
used as dependent variable. Only inflammatory indices being significantly
associated with the E/A-ratio in table 3 were used as independent variables
together with potentially confounding variables gender, BMI, diastolic
blood pressure and use of hypertensive medications.
In unadjusted models, E-selectin and l-selectin (inversely) were
related to IVRT. However, none of these two relationships
persisted after adjustment for gender, BMI, systolic and diastolic
blood pressure and use of antihypertensive medication.
We even studied current smoking as a confounder in the
models and generally very little effect was seen. If anything, the
reported associations tended to become even stronger following
this additional adjustment.
DISCUSSION
Previous studies have investigated a limited numbers of
inflammatory markers which have been demonstrated to be
related to mainly concentric LVH in hypertensive or uremic
patients.19 - 21 In the present study, several markers of inflammation were studied and observed to be higher in elderly persons
with abnormal LV geometry, especially of the concentric
hypertrophy type, independently of hypertension and obesity,
two main drivers of abnormal LV remodeling.
Furthermore, some markers of inflammation were related to LV
diastolic dysfunction, a well-known consequence of abnormal LV
geometry, especially of the concentric hypertrophy type.
Journal of Human Hypertension (2012), 1 - 5
Inflammatory markers associated with LVH and diastolic dysfunction
S Masiha et al
4
Inflammatory variables in relation to myocardial fibrosis
Kuwahara F et al.5 examined the role of macrophages in
myocardial remodeling and cardiac dysfunction in pressure-overloaded hearts in rats. They could present that the pressureoverloaded heart of rats is a cardiac hypertrophy model
characterized by a rapid progression of reactive myocardial fibrosis
associated with diastolic dysfunction and that transforming growth
factor-b has a crucial role in the fibrotic process.5
Moreover, ICAM-1 was transiently induced on endothelial cells
of the intramyocardial arteries. Also, macrophages accumulated in
the area adjacent to the arteries showing ICAM-1 expression.6
The involvement of mast cells in the development of fibrosis in
rats with postmyocarditis-dilated cardiomyopathy has been
investigated and a significant correlation between myocardial
fibrosis and cardiac mast cell density was obtained. The findings
confirm the active participation of mast cells in the progression of
myocardial fibrosis in rats with postmyocarditis-dilated cardiomyopathy.7
Furthermore the role of TNF-a in progressive LV dysfunction
and remodeling in rats has been the subject of a study.8 The major
conclusion in experimental study was that sustained, pathophysiologically relevant circulating concentrations of TNF-a were
sufficient to provoke deleterious changes in LV structure and
function. The major finding with respect to myocardial function
was that a continuous infusion of TNF-a led to a time-dependent
depression in LV function that was evident at the level of the
intact ventricle as well as in the isolated cardiac myocyte itself.
Inflammatory variables in relation to LV geometric groups
VCAM-1 has been investigated in patients with uncomplicated
essential hypertension. The investigators found a significant
elevation of circulating levels of VCAM-1 in persons with LVH
compared with the persons with normal LV geometry. On the
other hand, there were not any significant differences regarding
sICAM-1 and sE-selectin levels between the same groups.18
Comparing middle-aged persons suffering from hypertension
with normotensive persons confirmed the previous findings.
Furthermore the levels of ICAM-1, VCAM-1 and E-selectin among
the patients with concentric LVH were higher compared with
persons with eccentric LVH.19
In 2003, Palmieri et al.20 investigated 1299 adults with type II
diabetes in order to study microangiopathy and albuminuria as a
marker of endothelial dysfunction and its impact on the relation of
LVH and inflammatory markers. They found a significant elevation
of hsCRP, fibrinogen and urinary albumin/creatinine among the
persons with LVH compared with those without LVH, independently of plasma creatinine levels and cardiovascular risk factors.
Fibrinogen and hsCRP levels were significantly higher in
participants with LVH among those without pathological levels
of urinary albumin indicating that the relation between the LVH
and the inflammatory response may proceed a clinically relevant
albuminuria.20
A study investigated the potential relationship between LVH and
proinflammatory cytokines in hemodialysis patients and the effect
of hemodialysis on cytokine production. There was a significant
association between the inflammatory markers, particularly TNF-a,
and LVH in patients with end-stage renal disease.21
In the present study when the different inflammatory indices
were related to LV geometry, significant elevations in CRP and
E-selectin were seen in all of the three abnormal groups compared
with the normal group except for CRP in eccentric LVH after
adjustment for gender, BMI, systolic and diastolic blood pressure
and use of antihypertensive medication.
For ICAM-1, VCAM-1 and P-selectin, increased levels were only
seen in concentric LVH.
The discrepancy between the result of our study and the
previous studies can probably be explained by the fact that all the
Journal of Human Hypertension (2012), 1 -- 5
previous studies evaluated groups of patients suffering from
specific disorders, such as renal failure or hypertension, although
our study was based on a general population of elderly persons.
Inflammatory variables in relation to diastolic dysfunction
As LV diastolic dysfunction generally is induced by an abnormal LV
geometry, especially of the concentric type, we also investigated
the relationships between markers of inflammation and two
indices of LV diastolic function, E/A-ratio and IVRT. To the best
of our knowledge no previous study has investigated the
relationship between the inflammatory markers and LV diastolic
function.
We observed that CRP, E-selectin, l-selectin, ICAM-1 (inversely)
and leukocyte count were inversely related to the E/A-ratio. These
relationships persisted after adjustment for gender, BMI, systolic
and diastolic blood pressure and use of antihypertensive
medication, except for ICAM-1.
In multiple regression analysis the levels of hsCRP and 1-selectin
were independently related to the E/A-ratio whereas none of the
inflammatory markers were related to IVRT following adjustment.
Potential mechanisms
Even though the relation between the inflammatory markers and
the LVH has been demonstrated in several studies in different
patient samples, the mechanisms underlying this association are
not known.
Some possible mechanisms have previously been suggested.
Plasma levels, as well as myocardial expression, of proinflammatory
cytokines, including TNF-a, are increased in patients with heart
failure.24,25 Cardiac-specific overexpression of TNF-a causes
myocardial inflammation and remodeling, resulting in the
development of congestive heart failure.26 As LVH might be
related to later heart failure, early myocardial overexpression of
proinflammatory cytokines might be one mechanism.
How CRP might drive LVH is not clear. It is possible that CRP
could induce direct myocardial effects, as CRP can cause intimal
hypertrophy both in vitro and in animal studies.27,28 Alternatively,
such effects may be indirect as studies of transgenic mice have
associated CRP with the development of hypertension29 and
perivascular fibrosis.30
The relationship between CRP genotype and human LVH was
investigated for the first time in a study by Mann et al.31 They
observed an association between a variant of the CRP gene with
exercise-induced LVH in young healthy males, undergoing an
identical 12-week physical training program. Homozygosity for the
T allele of the CRP þ 1444C4T gene variant was associated with
serum CRP levels, which were 0.68 mg l1 higher than carriers of
the C allele. These persons showed increased thickness of the LV
as a response to the training program. Thus, CRP might be a
physiological governor of LV adaptation to an increased load, such
as training or hypertension.31
Furthermore, the crucial role of transforming growth factor-b in
developing fibrosis and LV remodeling, involvement of mast cells,
ICAM-1 and the role of TNF-a in progressive LV dysfunction and
remodeling have been suggested as potential mechanisms in
some experimental studies.5 - 8
Strengths and limitations of the study
The present sample is a population-based sample of circa 1000
men and women, but it is limited to Caucasians aged 70. So,
caution should be made in drawing conclusions about other
ethnic and age groups. The present study had a moderate
participation rate. However, an analysis of non-participants
showed the present sample to be fairly representative of the
total population regarding most cardiovascular disorders and drug
intake.
& 2012 Macmillan Publishers Limited
Inflammatory markers associated with LVH and diastolic dysfunction
S Masiha et al
CONCLUSION
CRP and the adhesion molecules E-selectin, ICAM-1, VCAM-1 and
P-selectin were all elevated in elderly persons with abnormal LV
geometry, especially in concentric LVH, after adjustment for
hypertension and obesity. CRP and l-selectin were related to LV
diastolic function, further indicating a role for inflammation in
abnormal LV geometry and function.
What is known about this topic:
A role for inflammatory markers as predictors of cardiovascular
diseases has been the theme of numerous studies during the
past decade. C-reactive protein (CRP) has been demonstrated
to be a strong and independent risk marker regarding both
incident diabetes and cardiovascular disease.
What this study adds:
The adhesion molecules; e-selectin, ICAM-1, VCAM-1, P-selectin
and hsCRP were elevated in elderly persons with abnormal LV
geometry, especially in concentric LVH, after adjusting for
hypertension and obesity. l-selectin and hsCRP were related to
LV diastolic function.
CONFLICT OF INTEREST
The authors declare no conflict of interest.
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