Cardiovascular Journal of Africa: Vol 23 No 6 (July 2012) - page 33

CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 6, July 2012
AFRICA
331
of pregnant women.
11
However, many non-placental sites of
PAPP-A production have also been identified. It is a member of
the metzincin metalloproteinase superfamily. Metalloproteinases
may contribute to the fragility of the lipid-rich atherosclerotic
plaque and eventually to its rupture by degrading the extracellular
matrix.
12
Recent studies by Bayes-Genis
et al.
reveal that it may
be a potential determinant of plaque instability by degrading
the extracellular matrix of the fibrous cap of the atherosclerotic
plaque.
13
C-reactive protein, determined by high-sensitivity techniques,
is the most widely studied marker of inflammation in the
field of atherosclerosis. Its role has been identified in the
initiation, progression and final outcome of the atherosclerotic
process. It is an acute-phase reactant and is an important
player in the inflammatory process observed to be active in
atherosclerosis. Studies have revealed that it is not an innocent
bystander and indicator of the inflammatory process; rather it
is actively involved in the pathogenic mechanisms underlying
atherosclerosis.
14,15
Lipoprotein (a) is a cardiovascular risk factor highly prevalent
in subjects with Asian Indian origin. It has both thrombogenic
and atherogenic properties. This is due to its homology to
plasminogen and its low-density lipoprotein (LDL)-like
properties. Hence it is known as a dual pathogen. It may play an
important role in the susceptibility of atherosclerotic plaques to
instability.
3
The present study aimed to evaluate these novel risk factors
and to look for interrelationships between them in the setting of
acute coronary syndrome.
Methods
The study was jointly conducted by the Departments of
Biochemistry and Medicine, Maulana Azad Medical College
and associated hospitals, New Delhi, India. The study involved
screening of 379 patients with symptoms of ‘chest pain’,
presenting to the medical emergency department during the
period between April and October 2010. These patients were
then further evaluated by electrocardiography. One hundred and
sixty-seven patients demonstrated ECG abnormalities such as ST
elevation, ST depression and T inversion. They were enrolled as
the study population.
Cardiac enzymes such as troponins and CK-MB levels were
evaluated in these patients. One hundred and five patients had
raised serum cardiac enzyme concentrations and hence depicted
the onset of acute coronary syndrome. These patients were
classified as cases and they were further evaluated by coronary
angiography.
Angiography was conducted by cardiologists using standard
techniques. The angiograms were done by two different
cardiologists who did not have any information regarding patient
identity and aetiology, to avoid any subjective bias. Those who
had normal cardiac enzyme concentrations were enrolled as
controls.
The inclusion criteria were:
AMI patients diagnosed by typical rise and gradual fall of
biochemical markers (troponins, CK-MB) of myocardial
necrosis with at least one of the following:
–– ischaemic symptoms
–– development of pathological Q waves on the ECG reading
–– ECG changes indicative of ischaemia (ST elevation or
depression)
–– coronary artery intervention (e.g. coronary angioplasty)
Unstable angina: chest discomfort at rest with either ST
depression of at least 0.1 mV or T-wave inversion in two
or more contiguous ECG leads, CK-MB levels normal and
angiographically confirmed coronary artery disease (CAD).
The exclusion criteria that were considered during the selection
of the study population were:
advanced kidney failure indicated by high serum urea and
creatinine
overt heart failure as diagnosed by echocardiography
history of major surgery/trauma within the previous month
suspected systemic inflammatory diseases
pregnancy
chronic stable angina (effort induced) diagnosed as chest pain
of at least six months’ duration, accompanied by severe CAD
on angiography (70% stenosis in any major artery).
A fasting blood sample (8–10 ml) was drawn prior to
angiography and the serum was extracted and stored at –70°C
until further testing. Fasting serum leptin, hs-CRP and PAPP-A
levels were estimated with ELISA kits provided by DRG
International, Germany.
Statistical analysis
The data were expressed as mean ± standard deviation. Student’s
t
-test was used to compare the values between the cases and
controls. Spearman’s correlation analysis was used to find
the association between the various parameters of our study.
A
p
-value < 0.05 was accepted as statistically significant.
Multivariate regression analysis was carried out to assess the
role of the different biomarkers in unstable CAD. All statistical
analyses were performed with the program Statistical Package
for the Social Science 12.0 (SPSS Inc, Chicago, Illinois).
Results
The demographic and risk-factor profiles of the study population
are shown in Table 1. One hundred and five patients fulfilled
the inclusion criteria for enrolment as cases (acute myocardial
infarction) while 62 were classified as controls (angina pectoris).
The mean age of the cases was higher than the controls (56.9 ±
11.1 vs 48.8 ± 10.9 years, respectively). Females comprised 18%
of the cases and 23% of the controls.
The body mass index and waist circumferences were higher
in the cases compared to the controls. The prevalence of
TABLE 1. DEMOGRAPHIC DETAILSAND RISK FACTOR
PROFILE OF THE STUDY POPULATION
Characteristics
Cases
(
n
=
105)
Controls
(
n
=
62)
p
-value
Age (years)
56.9 ± 11.1 48.8 ± 10.9 NS
Male/female
86/19
45/17
BMI (kg/m
2
)
28.5 ± 5.7 25.2 ± 5.3
Waist circumference (cm)
101.46 ± 10.2 88.9 ± 15.9 < 0.01
Smoking (%)
50 (48%)
9 (13%) < 0.01
Hypertension (%) or antihyperten-
sive drugs taken
55 (52%)
31 (50%)
NS
Diabetes (%) or hypoglycaemic
drugs
46 (44%)
4 (8%) < 0.001
Hypolipidaemic drugs
42 (40%)
15 (25%) < 0.01
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