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OJHAS Vol. 9, Issue 3:
(Jul - Sep, 2010) |
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| Cardiovascular
Risk Factors in Normolipidemic Acute Myocardial
Infarct Patients on Admission – Do Dietary Fruits and Vegetables
Offer Any Benefits? |
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Arun Kumar,
Assistant Professor,
Department of Biochemistry, College of
Medicine & JNM Hospital, The West Bengal
University of Health Sciences, Kalyani, Nadia,
West Bengal India,
Ramiah Sivakanesan,
Professor and Head, Department of Biochemistry, Faculty of Medicine, University of Peradeniya, Sri Lanka
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Address For Correspondence |
Department of Biochemistry,
College of
Medicine & JNM Hospital,
The West Bengal
University of Health Sciences,
Kalyani, Nadia,
West Bengal India.
E-mail:
arun732003@gmail.com |
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Kumar A, Sivakanesan R. Cardiovascular
Risk Factors in Normolipidemic Acute Myocardial
Infarct Patients on Admission – Do Dietary Fruits and Vegetables
Offer Any Benefits? Online J Health Allied Scs.
2010;9(3):3 |
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Submitted: Aug 9, 2010;
Accepted:
Sep 28, 2010; Published: Oct 15, 2010 |
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| Abstract: |
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Background:
Myocardial Infarction (MI) is a leading cause
of death in India. Whether dietary vitamins could reduce risk of cardiovascular
disease among Indians is still not clear and very few studies have addressed the association between dietary vitamin acting
as an antioxidant or pro-oxidant and its effect on risk reduction or
aggravation in normolipidemic AMI patients. Objective:
The goal of the current study was to address the association between
dietary vitamin and cardiovascular risk in normolipidemic acute myocardial
infarct patients compared with healthy controls. Design:
Dietary intake of vitamins was assessed by 131 food frequency questionnaire
items in both AMI patients and age/sex-matched controls. The associated
changes in risk factors due to antioxidant vitamins intake was also
assessed in normolipidemic acute myocardial patients and was compared
with controls. Results: Dietary intake
of vitamin A, B1, B2, B3 was significantly higher in AMI patients compared
to healthy controls but the intake of vitamin C was significantly higher
in controls compared to AMI patients. Even though the vitamins intake
was higher in patients, the associated cardiovascular risk factors were
not reduced compared to controls. The total cholesterol, LDL-c, TAG were
significantly higher (p<0.001) in AMI patients except HDL-c which
was significantly higher (p<0.001) in controls. The endogenous
antioxidants were found to be significantly lowered in patients compared
to controls in spite of higher vitamin intake. Similarly the enzymatic
antioxidants were also significantly lowered in patients. The mean serum
Lipoprotein (a) malondialdehyde (MDA) and conjugated diene (CD) levels
in patients were significantly elevated compared with controls. The
levels of caeruloplasmin, C-reactive protein, fibrinogen, ischemia-modified
albumin were significantly higher but arylesterase activities were lowered
in patients. Conclusion:
Diets rich in vegetables and fruits do not seem to reduce the cardiovascular
risk in normolipidemic AMI patients among Indians and Sri Lankans.
Key Words: Dietary vitamins; Acute myocardial infarction; Cardiovascular risk factors;
Normolipidemia; India; Sri Lanka
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Cardiovascular
disease (CVD) is a major cause of morbidity and mortality in the Western
World. In recent years, its steep rise has alarmed common man and
raised its importance internationally among scientists and researchers,
and it is going to be the major cause of mortality in the globe by 2020.1
It is a multifactorial disease associated with factors like
heredity, hyperlipidemia, obesity, hypertension, environmental and
life style variables like stress, smoking, alcohol consumption, etc.2
The World Health
Organization predicts that deaths due to CVD are projected to double between 1985 and 2015.3,4 Asian Indians living
abroad have a 40% higher risk of ischemic heart disease (IHD) mortality than that for Europeans.5
Researchers across the world are emphasizing their
researches to prevent or minimize this increase in the death rate due
to CVD. When it comes to prevention and regression of
this disease, dietary management comes as the first line of management
and emphasis is placed on a dietary regimen rich in antioxidants.6
It is believed that oxidative stress is involved in the pathogenesis
of atherosclerosis; while a variety of antioxidants have been used in
clinical trials and studies during the past few years, a very clear
cut message is still awaited from the studies.7 American
Heart Association has taken long standing commitment to provide information
related to nutritional role in risk reduction of future episodes of CVD.8
No clear cut dietary regimen in antioxidant vitamins have still been provided for prevention of this disease; even though
vitamins act as antioxidants, at times can also act
as pro-oxidants and nullify the antioxidant effect of other antioxidants
if consumed in the form of cocktail.9 In the present
study, the dietary antioxidant vitamins were assessed in AMI patients
and were compared with healthy controls. The study also aimed to observe
the variation in risk factors in patients and controls due to variation
in dietary vitamins intake which was estimated using three 24-hour dietary
records from the food stuffs which are generally consumed among Indians
and Sri Lankans. The study also measured anthropometric details among the two
groups along with risk factors which could be associated in causation of
myocardial infarction.
Cases: Eligible cases
were all patients aged 48-69 y hospitalized with
a diagnosis of first incident acute myocardial infarction (MI)
in Sharda Hospital, Greater Noida, India and Peradeniya Hospital, Faculty
of Medicine, Peradeniya, Sri Lanka from
12 September 2004 to 16 February 2007. The definitive diagnosis of AMI
was established according to diagnostic criteria: chest pain lasting
for ≤3 hours, electrocardiographic (ECG) changes (ST elevation ≥
2 mm in at least two leads) and elevation in enzymatic activities of
serum creatine phosphokinase and aspartate aminotransferase. The control
group consisted of 165 age/sex-matched healthy volunteers (123 men and
42 women).
Inclusion criteria
were patients diagnosed of AMI with normal lipid profile. Patients were
excluded if they had any previous history of MI or IHD (including bypass surgery, angina, or stroke)
because such prior diagnoses may alter behaviors,
including diet. Patients with diabetes mellitus, renal insufficiency,
hepatic disease or taking lipid lowering drugs or antioxidant vitamin
supplements were also excluded from the study. We also excluded patients
if they were pregnant, had a history of cancer, gastrointestinal
tract infection, or thyroid, because these conditions may have affected dietary intake. The patients
were interviewed on average 2–5 d after admission. The
eligibility criteria were met by 245 cases, and 165 were included
in the study. The reasons for exclusion were death (n = 19)
or discharge (n = 27) before the interviews could be completed,
being too sick to be interviewed (n = 16), and not giving consent
to participate (n = 18).
Controls: For each case subject, 2 control subjects matched by age (within
5 y), sex, and hospital were obtained from noncardiac outpatient
clinics or inpatient wards. The same exclusion criteria used
for cases were applied for control selection as well. We identified
≈ 165 eligible control subjects.
Controls were selected by using predominantly any of these two methods
depending on the hospital. In the first method, we accompanied a particular
physician during an outpatient clinic, according to a weekly
schedule of clinics and wards. At the end of each consultation,
the physician or the physician’s assistant invited the
patient to speak with us about his or her lifestyle and
diet. Patients matching the required age and sex profile were eligible
according to study criteria and were then informed
of the study and asked to participate. In these situations,
participation was 100%. In the second method, we independently identified
control patients from clinics and wards.
We attempted to approach all individuals present
during a particular outpatient clinic or in a specified ward.
In large clinics, patients were screened for eligibility and
invited to participate according to their queue number (highest
number first). This method was used to prevent bias in the selection
of controls. Overall participation was high, ≈ 98%. Basic demographic
information was collected from all persons who were approached.
If an individual fit the required age and sex profile and was
eligible, we briefly explained the study and asked
whether the person was willing to participate.
Criteria
for Normolipidemics: Normal lipid profile was defined if LDL was
<130mg/dL, HDL ≥ 35 mg/dL, Total cholesterol (TC) <200 mg/dL
and Triglycerides (TG) <150 mg/dL.10
Data Collection: Interviews
were conducted in the hospital wards or clinics by us and lasted ≈ 30
min. Informed consent was obtained from all study subjects.
This included various life style factors such as education, socio-economic
status, income and type of job. Details of major cardiovascular risk
factors such as smoking, alcohol intake, diabetes, obesity and hypertension
were also obtained. We also collected
data on socioeconomic status; smoking history; history of hypertension,
diabetes, and hypercholesterolemia; family history of cardiovascular
disease (including IHD, angina, MI, hypertension, diabetes,
stroke, sudden death, and bypass surgery); dietary intake; types
of fat or oils used in cooking; nutritional supplement use;
and physical activity.
Dietary
intake by 24-hour dietary record:11 The patients and controls were given the food
items which they were supposed to mark including the quantity consumed.
This was carried for three times in the same subjects to avoid bias
and to get more accuracy. The dietary intake was tabulated
and the amount of vitamins was calculated from the food consumed.
Anthropometric
measurements: Anthropometric measures (height,
weight, and hip and waist circumferences) were obtained and
body mass index (weight in kg divided by height in meters squared)
and waist-to-hip ratio were calculated. Their blood pressures were recorded. Height was measured in centimeters
and weight in kilograms using calibrated spring balance. Supine waist
girth was measured at the level of umbilicus with a person breathing
silently and standing hip girth was measured at inter-trochanteric level.
Waist and hip measures were assessed by using a standardized
tape measure, with waist
measures taken at the midpoint between the costal margin and
ileac crest and hip measures taken at the widest circumference.
Blood
Pressure:
The blood pressure was measured using standard mercury manometer. At
least two readings at 5 minutes intervals as per World Health Organization
guidelines were recorded.12 If high blood pressure (≥140/90
mmHg) was noted, a third reading was taken after 30 minutes. The lowest
of the three readings was taken as blood pressure.
Electrocardiogram: Electrocardiogram (12 lead) was performed on all persons using
proper standardization.
Collection
of Samples: Blood (10 ml)
was collected after overnight fasting in different containers.
EDTA vial:
5.0 ml of blood was taken. Red cells were washed 3-4 times with ice-cold
normal saline and used for estimation of glutathione peroxidase, superoxide
dismutase and catalase.
Plain vial:
Remaining blood was allowed to clot and serum separated by centrifugation
for 5 min at 5000 rpm and was used for determination of lipid profile,
malondialdehye and conjugated dienes, and other assays as described.
For IscMA analysis,
2 ml of blood was collected from the patients immediately after admission
to intensive care unit.
Lipid profile:
Total cholesterol, triglycerides, and HDL-cholesterol were estimated
by enzymatic methods using the kits obtained from Randox Laboratories
Limited, Crumlin, UK. Plasma LDL-cholesterol was determined from the
values of total cholesterol and HDL-cholesterol using the following
formulae:
LDL-C = TC -
(TG/5) – HDL-C (mg/dl)
All chemicals
of analytical grade were obtained from Sigma chemicals, India.
Serum Albumin: Serum Albumin was measured by Bromocresol green dye binding method.13
Serum Uric
acid: Serum uric acid was estimated by the method of Brown based
on the development of a blue color due to tungsten blue as phosphotungstic
acid is reduced by uric acid in alkaline medium.14
Serum total
bilirubin: Serum total bilirubin was estimated by Jendrassik and
Grof method.15
Glutathione
peroxidase: The glutathione peroxidase activity was determined
by the procedure of Paglia and Valentine.16
Superoxide
dismutase (SOD): Superoxide dismuatse enzyme activity was measured
by SOD assay kit using rate of inhibition of 2-(4-indophenyl)-(4-Nitrophenol)-5-phenyltetrazolium
chloride (I.N.T) reduction method modified by Sun et al.17
Catalase:
Catalase activity was measured spectrophotometrically as described by
Beutler.18,19
MDA: MDA levels were estimated by thiobarbituric acid
(TBA) reaction.20
Conjugated
dienes (CD): CD levels were measured by Recknagel and Glende method21 with little modification.
Serum Ceruoplasmin: The ceruloplasmin assay was done by p-phenylene diamine
method.22
All chemicals
of analytical grade were obtained from Sigma Chemicals, India.
Ischemia
Modified Albumin (IscMA): IscMA concentration was determined by
addition of a known amount of cobalt (II) to a serum sample and measurement
of the unbound cobalt (II) by the intensity of colored complex formed
after reacting with dithiothreitol (DTT) by colorimeter.23,24
Lipoprotein
(a), Lp(a): The Lp(a) levels were determined by Latex- Enhanced
Turbidimetric method.
Aryesterase/Paraoxonase assay: Serum Arylesterase/Paraoxonase
was estimated using Zeptometrix Assay Kit obtained from Zeptometrix Corp, New York, 14202 based
on the cleavage of phenyl acetate resulting in phenol formation. The
rate of formation of phenol is measured by monitoring the increase in
absorbance at 270 nm at 25°C.
Ascorbic
acid: Estimation of Vitamin C was carried out by Roe and Kuether
method.25
Measurement
of High sensitive C- Reactive protein
(hs-CRP): The hsCRP ELISA is based on the principle of a solid phase
enzyme-linked immunosorbent assay.
Plasma fibrinogen:
TEClot Fib
Kit 10 (TECO GmbH, Dieselstr. 1, 84088 Neufahrn NB Germany) was used
for the estimation of fibrinogen.
Dietary vitamins
intake was higher in AMI patients excepting for ascorbic acid which
was higher in controls as shown in Table 1. Anthropometric variables
in acute myocardial infarction (AMI) patients showed highly significant
differences in weight, BMI, waist circumference, hip circumference,
waist-hip ratio, mid-arm circumference, biceps and triceps skin fold
thickness as shown in Table 2. The total cholesterol, LDL-c, TG were
significantly higher (p<0.001) in AMI patients except HDL-c which
was significantly higher (p<0.001) in controls as shown in Table
3. The cardiac markers enzymes are shown in Table 4. The serum endogenous
antioxidants were significantly decreased in patients compared to controls.
Similarly the enzyme antioxidants were also significantly lowered in
patients. The mean serum Lipoprotein (a) malondialdehyde (MDA) and conjugated
diene (CD) levels in MI patients were higher compared with controls
as shown in Tables 5 and 6. Serum fibrinogen, ceruloplasmin, ischemia-modified albumin and C-reactive protein were significantly elevated
whereas arylesterase activities were significantly lowered in cases
compared with controls as shown in Table 7.
Table 1: Mean dietary
intakes of vitamins in Control and
AMI Patients |
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Control (n=165) |
AMI Patients (n=165) |
P value (95%CI) |
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Vitamin A
(μg) |
2102.3 ± 425.2
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2638.6 ± 154.3
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<0.01(2611.33-2665.87) |
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Vitamin B1
(mg) |
1.8 ± 0.3 |
2.2 ± 0.3 |
<0.05 (2.15-2.24) |
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Vitamin B2
(mg) |
1.7 ± 0.2 |
1.9 ± 0.3 |
<0.001(1.85-1.94) |
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Vitamin B3
(mg) |
19.0 ± 3.6
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25.3 ± 3.6
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<0.001 (24.79-24.80) |
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Vitamin
C (mg) |
460.8 ± 85.3 |
304.0 ± 101.5 |
<0.001(289.67-318.32) |
Table
2: Anthropometric data of control and
AMI patients (mean ± SD) |
| |
Control (n=165) |
AMI patients (n=165) |
P- value (95%CI) |
|
Age Range (years) |
60.5 ± 3.4 (48-69) |
61.8 ± 3.8 (48-69) |
0.0037 (61.26- 62.33) |
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Height (m) |
1.63 ± 0.04 |
1.64 ± 0.59 |
0.2919 (1.55-1.72) |
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Weight (
kg) |
68.34 ± 3.97 |
72.01 ± 5.37 |
<0.01 (71.25-72.76) |
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BMI ( kg/m2) |
25.40 ± 1.20 |
26.16 ± 1.45 |
<0.01 (25.95-26.36) |
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Waist Circumference
(cm) |
93.70 ± 3.63 |
100.77 ± 6.06 |
<0.01 (99.91-101.62) |
|
Hip Circumference
(cm) |
100.01 ± 3.16 |
105.72 ± 5.23 |
<0.01 (104.82-106.45) |
|
Waist-Hip
ratio |
0.93 ± 0.01 |
0.95 ± 0.01 |
<0.001 (0.94-0.95) |
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Mid Arm Circumference
(cm) |
29.70 ± 1.47 |
30.63 ± 1.87 |
<0.01 (30.36-30.89) |
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Biceps skin
fold thickness (mm) |
6.95 ± 1.05 |
7.5 ± 1.38 |
<0.001 (7.30-7.69) |
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Triceps skin
fold thickness (mm) |
11.97 ± 1.27 |
12.89 ± 1.69 |
<0.001 (12.65-13.12) |
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Systolic
blood pressure (mmHg) |
121.06 ± 4.19 |
134.32 ± 11.65 |
<0.05 (132.67-135.96) |
|
Diastolic
blood pressure (mmHg) |
79.90 ± 3.64 |
86.04 ± 4.25 |
<0.05 (85.44-86.63) |
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Table
3: Lipid profile in AMI patients and healthy controls (mean
± SD) |
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Variables |
Controls (n=165) |
AMI patients (n=165) |
P-value (95%CI) |
|
Age |
60.55 ± 3.98 |
61.84 ± 3.80 |
0.0037( 61.26-62.42) |
|
Total Cholesterol† |
168.58 ± 12.16 |
186.44 ± 13.95 |
<0.001(184.31-188.56) |
|
HDL-Cholesterol† |
50.51 ± 6.78 |
41.27 ± 4.62 |
<0.001(40.56-41.97) |
|
Triglycerides† |
107.84 ± 11.51 |
128.96 ± 12.19 |
<0.001(127.10-130.82) |
|
LDL-Cholesterol† |
83.59 ± 11.95 |
119.37 ± 14.05 |
<0.001(17.22-21.51) |
|
* ratio
† (mg %) |
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Table
4: Cardiac Enzyme Markers in Control subjects and AMI patients (Mean ± SD) |
| |
Control (n=68) |
AMI patients (n=97) |
P value ( 95%CI) |
|
Troponin
I (ng/ml) |
0.23 ± 0.11 |
1.56 ± 1.03 |
<0.0001(1.41-1.70) |
|
Troponin
T (ng/ml) |
0.04 ± 0.03 |
0.64 ± 0.42 |
<0.0001(0.58-0.69) |
|
Myoglobin
(ng/ml) |
20.64 ± 6.37 |
180.87 ± 120.31 |
<0.0001(163.89-197.87) |
|
CK-Total
(IU/L) |
0.97 ± 0.53 |
314.78 ± 221.13 |
<0.0001(283.57-345.98) |
|
CK-MB (IU/L) |
0.13 ± 0.07 |
67.11 ± 54.64 |
<0.0001(59.39-74.82) |
Table
5: Antioxidant status in Control subjects and AMI patients (Mean ± SD) |
| |
Control (n=165) |
AMI patients (n=165) |
P value (95%CI) |
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Serum albumin
(mg/dl) |
4.4 ± 0.3 |
4.2 ± 0.3 |
<0.0001(4.15-4.24) |
|
Serum uric
acid (mg/dl) |
5.8 ± 1.2 |
4.3 ± 0.9 |
<0.0001(4.17-4.42) |
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Serum ascorbic
acid (mg/dl) |
5.3 ± 1.2 |
2.8 ± 0.7 |
<0.0001(2.70-2.89) |
|
Serum Total
bilirubin (mg/dl) |
0.8 ± 0.2 |
0.7 ± 0.2 |
<0.0001(0.67-0.72) |
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Serum superoxide
dismutase (U/gHb) |
1826.5 ± 31.9 |
813.9 ± 208.9 |
<0.0001(784.42-843.37) |
|
Serum glutathione
peroxidase (U/gHb) |
61.3 ± 3.9 |
42.6 ± 6.3 |
<0.0001(41.71- 43.48) |
|
Serum catalase
(k/gHb) |
256.2 ± 26.7 |
193.1 ± 35.9 |
<0.0001(188.03-198.16) |
Table
6: Lp(a) and Lipid Peroxidation levels in Control subjects and AMI patients
(Mean ± SD) |
| |
Control (n=165) |
AMI patients (n=165) |
P value (95%CI) |
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Serum Lipoprotein
(a) (mg/dl) |
3.0 ± 1.1 |
10.9 ± 2.2 |
<0.0001 (10.58-11.21) |
|
Serum malondialdehyde
(nmol/L) |
5.7 ± 1.0 |
14.8 ± 1.7 |
<0.0001(14.56-15.03) |
|
Serum conjugated
dienes (µmol/L) |
31.0 ± 2.7 |
48.3 ± 5.5 |
<0.0001(47.52-49.07) |
Table 7:
Other Biochemical parameters in Control subjects and AMI patients (Mean ± SD) |
| |
Control (n=165) |
MI patients (n=165) |
P value (95% CI) |
|
Plasma fibrinogen
(mg/dl) |
237.5 ± 17.4 |
357.8 ± 23.2 |
<0.0001 (354.52 -361.07 |
|
Serum caeruloplasmin
(mg/dl) |
20.4 ± 2.3 |
51.5 ± 2.4 |
<0.0001 (51.16-51.83) |
|
Serum Arylesterase
activity (kU/L) |
98.4 ± 6.2 |
69.7 ± 10.0 |
<0.0001(68.28-71.11) |
|
Serum Ischemia
modified albumin (U/ml) |
81.9 ± 3.9 |
97.5 ± 11.7 |
<0.001(95.84-99.15) |
|
Serum C-reactive
protein (mg/dl) |
1.1 ± 0.3 |
3.0 ± 1.1 |
<0.0001(2.84-3.15) |
Coronary artery
disease (CAD) remains the major cause of morbidity and mortality in
all developed and developing countries in the world including India.26 Various risk factors have been identified among which dyslipidemia
is one of the major modifiable risk factors.27-29
The coronary
artery disease risk factors do not predict the occurrence of acute
myocardial infarction (AMI) as variation in risk factors is observed
in South Asian population due to varied dietary habits and life style.30
The search for various conventional risk factors among Asians
could be helpful as
there are always some missing links between cardiovascular disease (CVD) and
risk factors associated with them. This prompted us to
identify the newer risk factors and to observe the variations in known risk
factors such as variation in antioxidant vitamins intake, with respect
to Indian and Sri Lankan population.
Even though
antioxidants and vitamins are efficient in cardio-protection and delay
the progression of CVD, the search for the newer risk factors continues and now investigations
are on the line to exploit the role of inflammatory markers and other
potential risk factors which could link with acute myocardial infarction
(AMI).
In this prospective
case-control study, only normolipidaemic acute myocardial infarction
(AMI) patients were selected. The study was designed to identify and
evaluate potential risk factors in normolipidaemic acute myocardial
infarction (AMI) patients with respect to their antioxidants intake.
The subjects selected for the study comprised of 165 controls, 48-69
y and 165 acute MI patients, 48-69 y.
Antioxidants
intake
The current
study observed higher antioxidant vitamins consumption in patients compared
to controls, excepting for vitamin C which was higher in controls. It is
therefore debatable why the antioxidant status was comparatively
lower in patients and risk factors observed were higher in them compared
to controls, even though they had higher exogenous intake of antioxidants
through the food. The basis could be partially explained with
the nullifying effect of these vitamins by various inter-plays of oxidants
and pro-oxidants which could have been higher in patients, that failed
to provide adequate protection from oxidants.31 Earlier
studies have emphasized to increase the antioxidants in diet and clinical
trials have shown effective results. Though a beneficial role for vitamins
in CVD has long been explored but the data are still inconsistent and
it is not affirmative with several findings. Studies show that
intake of fruits and vegetables do not prevent but can instead cause metabolic
syndrome and type II diabetes, which are considered as a major risk factor
in cardiovascular diseases.32 The beneficial effects of antioxidants, though supported
by observational studies and randomized controlled clinical trials, have
not yet supported their role in the prevention of CVD and some studies have rather indicated higher mortality
in those with late-stage atherosclerosis.33
Studies have
suggested that a combination therapy is superior over single supplementation
but ongoing trials are yet to confirm.34 Further studies have indicated
that beta-carotene neutralizes the beneficial effects mediated by other
vitamins as it acts as a pro-oxidant when given in supplementation cocktail.
The trials that used a combination of vitamins that include beta-carotene
have been disappointing.35 However, ascorbic acid along with vitamin E
in combination have shown some good results as long term anti-atherogenic
effects but their combined effect on clinical endpoints has been
inconsistent.36 Research data suggest that vitamins would be beneficial
to individuals who are deficient of antioxidants or exposed to increased
levels of oxidative stress such as in smokers, diabetics and elderly
patients. Through defining the right population group and the optimal
vitamin combination we could potentially find a future role for vitamins
in CVD.
Anthropometric
variables:
Anthropometric
variables in acute myocardial infarction (AMI) patients showed highly
significant differences in waist/hip ratio and biceps skin fold thickness.
It has been reported37 that waist / hip ratio is a dominant,
independent and predictive variable of cardiovascular disease and coronary
heart disease deaths in Australian men and women. Megnien et al38 also reported high hip circumference relative to weight and
waist circumference as a better predictor of low incidence of cardiovascular
disease and coronary heart disease. The present study is in good agreement
with the observations of the above studies. Among Indians, the cardiovascular
risk is high even if the prevalence of obesity is minimal.38
In the present study, the mean body mass index and waist / hip ratio in
all subjects was 26.56 and 0.96 respectively, showing a significantly higher body mass index and weight
/ hip ratio in patients compared with controls.
Based on the
observations of the aforementioned studies and further supported by
the present study, it could be concluded that weight/hip ratio is a better
predictor of cardiovascular disease (CVD) than body mass index. So it
is a better,
non-invasive, tool for
identifying the future risk of acute myocardial infarction.
Observations
on lipid profile
The mean total
cholesterol level of the controls compared with acute myocardial infarction
patients (186.44 ± 13.95 mg/dL) was significantly (p<0.001) higher
compared with controls (168.58 ± 12.16 mg/dL). The mean high density
lipoprotein-cholesterol level in the patients was significantly lower
(p<0.001) compared with controls. Triglyceride (TG) values observed
in AMI patients was (129mg/dL) significantly
higher than controls (107.8mg/dL). The mean low density lipoprotein-cholesterol
(LDL-c) levels in patients was (119.4mg/dL), significantly higher than
controls (83.6 mg/dL). The total cholesterol / high density lipoprotein
– cholesterol ratio in acute myocardial infarct patients (4.6) was
significantly (p<0.001) higher compared with controls (3.4). The
present study observed significantly higher ratio (2.9) in acute myocardial
infarction patients compared with controls (1.9).
Earlier studies
on lipid profile analysis conducted in acute myocardial infarction patients39-50 observed higher total cholesterol,
triglyceride, low-density lipoprotein–cholesterol and lower levels
of high-density lipoprotein-cholesterol in patients compared to controls.
Also higher
ratio of total cholesterol to high density lipoprotein-cholesterol,
low-density lipoprotein-cholesterol to high-density cholesterol-lipoprotein
and higher triglyceride to high-density cholesterol-lipoprotein were
observed in the present study. The present study concludes the importance
of assessing the lipid ratios even in normolipidemic subjects as it
is one of the atherogenic factors for development of myocardial infarction
and other coronary complications. The practice of computing the ratio
should be implemented even in a normal health check up packages. In
the final analysis it appears that myocardial infarction and coronary
artery disease are not always associated with an elevated serum total
cholesterol concentration. The major concern of this observation is
that subjects who maintain desirable total cholesterol concentration
also are targets for myocardial infarction and coronary artery
disease and therefore analysis of other risk factors that are
non-conventional and newly emerging will be of immense important in
the eventual assessment of the risk status. The existing literature
and the results of the present study all point out that acute myocardial
infarction and coronary artery disease patients have significantly higher
total cholesterol concentration whether the values are in the desirable
range or elevated.
Antioxidant
status
The serum endogenous
antioxidants were decreased in acute myocardial infarction compared
to controls. Similarly the enzyme antioxidants were also significantly
lowered in patients.
Studies conducted51,52 in acute myocardial infarction patients reported significantly
lower (p<0.0001) albumin and bilirubin (p<0.0001), whereas lower
levels of uric acid48-50 and ascorbic acid40,56-59 have
also been
reported in acute
myocardial infarct patients.
The aforementioned
studies suggest that the expected risk of acute myocardial infarction is
increased where these endogenous antioxidants are lowered due to enhanced
utilization during oxidative stress in patients. Though uric acid is
a well established antioxidant, at times it can also act as a pro-oxidant,
which might increase the risk of myocardial infarction. Aulinskas et
al,60 established the role of ascorbic acid as up-regulator
of low density–lipoprotein (LDL) receptors, facilitating the clearance
of low density–lipoprotein (LDL). The low levels of ascorbic acid
in acute myocardial infarction patients in the present study might
be due to enhanced utilization of ascorbic acid during oxidative stress
in patients.
The enzymatic
antioxidants, namely superoxide dismutase, catalase and glutathione peroxidase,
are also lowered in patients compared with controls. The findings of
the present study concurs with earlier studies40,48,57,61-64 that
reported lower activities of superoxide dismutase,
catalase and glutathione peroxidase. Other studies42,49,61,63-65 also reported reduced activities of glutathione
peroxidase in patients compared with controls. These studies are based
on the hypothesis of decreased antioxidants due to oxidative insult
in myocardial infarct patients. Thus it is indicative that low levels
of both endogenous and enzyme antioxidants in circulation may be due
to its increased utilization to scavenge toxic lipid peroxides.
Lipoprotein
(a) and lipid peroxidation:
The mean serum
Lipoprotein (a) malondialdehyde (MDA) and conjugated diene (CD) levels
in MI patients were higher compared with controls. Earlier studies conducted44,63,66,67
also observed higher Lipoprotein (a) in AMI patients
where as Nascetti et al,68 did not observe any change in Lipoprotein
(a) levels in cardiovascular disease patients and
concluded that lipoprotein (a) should not be considered as an independent risk
factor in CVD patients.
Other studies40,42,49,57,58,61,64
have also reported higher levels of malondialdehyde
(MDA) in myocardial infarct patients, as in our study.
Other biochemical
parameters
The levels
of ceruloplasmin, C-reactive protein, fibrinogen, ischemia-modified
albumin were higher and arylesterase activities were lowered in patients.
Other studies65,69-71 also observed significantly higher (p<0.001) levels of ceruloplasmin
and higher levels of C-reactive
protein47,72-75 in patients. Shukla et al,76
reported elevated levels
of ceruloplasmin as a risk factor for acute myocardial infarction.
The reactive oxygen species disrupts copper binding to ceruloplasmin,
thus impairing its antioxidant property and further promoting oxidative
pathology. Other studies conducted on plasma fibrinogen levels in acute myocardial
infarct patients23,24,47,77-79 also reported rise in plasma fibrinogen as
in the present study. Studies on arylesterase activities in acute myocardial infarct patients80-86 also observed lower activities,
concurring with the current study. Increased C-reactive protein (CRP)
concentrations in patients with unstable angina and acute myocardial
infarction might induce the production by the monocytes of the tissue factor
which initiates the coagulation process. C-reactive protein, together
with fibrinogen, acts as a chemotactic factor. Fibrinogen is responsible
for the adhesion of macrophages to the endothelial surface for their
migration into the intima. The elevated c-reactive protein levels have
been found to be related to the occurrence of cardiovascular complications
such as sudden cardiac death or AMI.87
Our study has concluded
that dietary vitamins do not decrease the risk of acute
myocardial infarction. There might be a number of additional risk factors
interplaying in acute myocardial infarction patients, which have not
been adequately protected against by the higher vitamin intake.
The sample size is not adequate to draw definitive
conclusion. Future studies should be carried out with large scale patients
sample size.
The authors do not have any conflict
of interests from the
study.
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