To establish the hypothesis that cholesterol level affects the short term prognosis of acute myocardial infarction

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2. Apollo Medicine 2012 September
Volume 9, Number 3; pp. 263e267 Research Article
Role of lipid profile in the short term prognosis of acute myocardial
infarction in a rural hospital in South India
M.G. Binua,*, P. Manojb, C. Vinodinic
ABSTRACT
Background: Acute myocardial infarction is a major cause of morbidity and mortality, more so in Indians.
Aim: To establish the hypothesis that cholesterol level affects the short term prognosis of acute myocardial infarction.
Method: One hundred patients with acute myocardial infarction attending a rural tertiary care hospital were selected
randomly and assessed for complications their lipid profiles were measured and mean values calculated and
compared for complicated and uncomplicated groups.
Results: In the group without complications 79.1% had total cholesterol <250 mg/dl and 85.58% had non-HDL
cholesterol <160 mg/dl. In the group with complications 69.7% had total cholesterol >250 mg/dl and 75.76% had
non-HDL cholesterol >160 mg/dl. The mean non-HDLC values for the two groups were 124 10 and 189 8
respectively (p ¼ 0.08373).
Conclusions: The study shows strong relation between the short term prognosis of acute myocardial infarction and
baseline cholesterol values, especially non-HDL cholesterol.
Copyright © 2012, Indraprastha Medical Corporation Ltd. All rights reserved.
Keywords: Myocardial infarction, Total cholesterol, LDL cholesterol, Non-HDL cholesterol
INTRODUCTION
Increased levels of total cholesterol (TC), non-HDL choles-terol
and LDL cholesterol (LDL-C) disturbs the endothelial
function, while normalization of lipid profile improves its
activity.1e4 Thus it can be expected, that hypercholesterol-emia
found in some patients at the onset of acute myocardial
infarction (AMI) may unfavorably influence the course of the
disease and consequently the patients who display normal
lipid levels in AMI should have a more benign clinical
outcome. To the best of our knowledge this matter has not
yet been investigated in South Indian population. If the above
hypothesis proves to be correct, it would be a further argument
in favor of early administration of statins in AMI. Such
patients should then be also considered as high-risk and sub-jected
to more intensive management. This may also be
a strong indication for primary prophylaxis with statin.
AIM OF THE STUDY
The aim of our study was to test the hypothesis, which
states that patients in whom lipid levels are found to be
above normal during the first hours of AMI have an unfa-vorable
short term clinical outcome.
STUDY PATIENTS, METHODS
We included 100 consecutive patients (66 males) aged
66.2 12 years (from 34 to 85), with confirmed AMI,
who were admitted to hospital up to 24 h after the onset
of clinical symptoms (from 0.5 to 20 h; average
6.5 5.5). The exclusion criteria were: lipid lowering
treatment in the month prior to AMI, lung, liver, kidney
and thyroid diseases as well as cancer. Myocardial
aAssociate Professor of Medicine, Fatima Institute of Medical Sciences, Kadapa 516003, Andhra Pradesh, bAssociate Professor of Medicine, Sree
Gokulam Institute of Medical Sciences, Venjarammoodu, Kerala, cSenior Assistant Surgeon, GH, Kuzhithurai, India.
* Corresponding author. email: binumonglavil@hotmail.com
Received: 30.4.2012; Accepted: 30.6.2012; Available online: 8.7.2012
Copyright 2012, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2012.06.012

3. 264 Apollo Medicine 2012 September; Vol. 9, No. 3 Binu et al.
Table 1 Patient distribution into two groups.
complicat
ed
Uncompli
cated
Total Adverse events No adverse events
100 33 67
Group-I Group-II
infarction was diagnosed based on typical clinical history
and/or characteristic electrocardiographic changes and an
increased level of biochemical markers of myocardial
injury i.e. isoenzyme of creatine kinase CK-MB and/or
troponin I. All the patients in the study received thrombo-lytic
therapy. On the first day of hospitalization blood
samples for lipid profile were taken in the morning, while
fasting. Total cholesterol (TC), LDL-chol, HDL-chol and
triglycerides (TG) were determined using enzymatic
assay. Plasma LDL-chol was calculated by using the Frie-dewald
formula in all patients in whom TG level did not
exceed 400 mg/dl. The clinical course of AMI was consid-ered
complicated if there occured in-hospital death, recur-rent
acute myocardial ischemia, serious ventricular rhythm
Table 2 Adverse events.
death
PI Angina
CCF
VT
SVT
AF
CHB
Adverse event Number of patients
Death 8
Post infarction angina 10
Cardiac failure 8
Ventricular tachycardia after 24 h 4
Atrial fibrillation 1
Complete heart block 1
SVT 1
Table 3 Total cholesterol relations.
Complicat
ed
Uncompli
cated
Uncompli
Complicat
ed
cated
60
50
40
30
20
10
0
TC250 TC250
Total cholesterol (mg/dl) Group-I Group-II
250 23 14
250 10 53
Table 4 LDL cholesterol relations.
50
40
30
20
10
0
LDL130 LDL130
Group-I
Group-II
LDL (mg/dl) Group-I (complicated) Group-II (uncomplicated)
130 21 17
130 12 50
Table 5 Non-HDL cholesterol relations.
60
50
40
30
20
10
0
Non HDL160 Non HDL160
Gp-I
Gp-II
Non-HDL cholesterol (mg/dl) Group-I Group-II
160 25 11
160 8 56

4. Role of lipid profile in the short term prognosis Research Article 265
disturbances (ventricular tachycardia or ventricular fibril-lation
24 h after AMI), paroxysmal supraventricular tachy-cardia,
atrial fibrillation, new symptoms of heart failure
and/or 3rd degree A-V block requiring temporary pacing.
Out of 100 patients, 33 had an adverse clinical course of
AMI. The most frequent complications were recurrent
myocardial ischemia with ECG changes and new symp-toms
of heart failure. In-hospital mortality was 8%. Statis-tical
significance was tested using SPSS version17.
RESULTS
Patients were divided as those with adverse events
(Group-I) and those without adverse events. Total Choles-terol,
LDL Cholesterol and non-HDL Cholesterol of these
patients were compared with the patients who did not
develop complications (Group-II). 69.7% of group-I had
total cholesterol 250 mg% and 79.10% of group-II had
LDL cholesterol 250 mg%. Similar relationships were
seen with LDL and non-HDL cholesterol too. Among all
the relationship of non-HDL cholesterol with adverse
effects was strongest. 75.76% in group-I had non-HDL
cholesterol 160 mg/dl and 83.58% of group-II had
non-HDL cholesterol 160 mg/dl. All patients who died
had non-HDL cholesterol 160 mg/dl.
The same is further signified in Tables 1e6 which shows
a stronger p-value for non-HDL cholesterol relationship.
CONCLUSIONS
1. Serum cholesterol, especially non-HDL cholesterol is
significant in determining short term (as well as long
term) prognosis in acute myocardial infarction.
2. Patients with lower cholesterol values at onset have
a smoother course of disease and a better prognosis.
3. A higher level of total cholesterol is an independent
prognostic factor of in-hospital death or non-fatal new
infarction.
4. The results of our study strongly support the use of sta-tins
as early as possible in acute myocardial infarction.
5. Primary prevention with statin may not only help in
reducing incidence of acute myocardial infarction, but
reduce the complications of those myocardial infarctions
which do occur.
DISCUSSION
We found that an elevated level of TC and LDL-chol in the
first 24 h of AMI is associated with a complicated in-hospital
clinical course and in particular with increased
mortality and an increased rate of non-fatal infarction. To
the best of our knowledge this is the first report on the prog-nostic
value of lipid profile at the onset of AMI in south
Indian population.
In previous observations, where lipid profiles were
determined early in the acute phase of infarction, i.e.
during the first hours or days after the occurrence of symp-toms,
attention was paid to subsequent changes of lipid
levels, but not to the prognostic potential of the baseline
lipid values.5e8
It has been well established that enhanced lipid levels
constitute a major risk factor for the development of arterio-sclerosis
in the years to come.9,10 However, there is also
good evidence that increased serum cholesterol especially
its oxidized LDL fraction adversely influence endothelial
function. This phenomenon appears to be transient in nature
and may be reversed after lipid normalization.
It has been found LDL apheresis improves endothelium-dependent
vasodilation in hypercholesterolemic humans.11
Liao et al have shown that with an elevated level of
LDL-chol and its oxidized form, the activity of endothelial
nitric oxide (NO) synthase decreases, the production of
cytokines and dimethylarginine is augmented,12 Vergnani
et al3 documented that in these types of lipid disorders
the generation of free oxygen radicals is increased with
subsequent limitation of NO production. Hypercholesterol-emia
also stimulates the activity of renineangiotensin
system in the blood vessel wall13 and endothelin 1 produc-tion
in the endothelium,2 which increases vessel contrac-tility
resulting in the decrease of coronary perfusion. This
effect is multiplied by coagulation activation due to
a high level of LDL-chol, which augments adhesion and
aggregation of platelets and thromboxane A2 production.14
It can thus be expected that each of these mechanisms may
adversely influence the clinical course of AMI.
As it may be expected, in view of the above mentioned
findings, both experimental investigations and clinical trials
have documented that high level of cholesterol, especially
oxidized LDL cholesterol is one of the most important
factors that destabilizes the atherosclerotic plaque and
Table 6 Mean values.
Complicated MI (n ¼ 33) Uncomplicated MI (n ¼ 67) ‘p’ value
Total cholesterol 268 12 206 11 0.72872
LDL 176 14 108 13 0.32842
Non-HDLC 189 8 124 10 0.08373

5. 266 Apollo Medicine 2012 September; Vol. 9, No. 3 Binu et al.
thus leads to the development or aggravation of acute coro-nary
syndrome (ACS).15,16
Therefore, the high TC and LDL-chol found in our
patients with serious clinical course of MI may be, perhaps,
regarded not only as markers of more advanced atheroscle-rosis.
High lipid levels at the onset of MI are likely to
adversely modify endothelial function, per se, which may
influence clinical course of MI.
The results of our study strongly support the administra-tion
of statins as early as possible in MI. Laufs et al17 have
found in “in vitro” model that statins increase the activity
of endothelial NO synthase within a few hours after adminis-tration.
Kaesemeyer et al18 showed that an addition of statins
to endothelial cell culture stimulates activity of NO synthase,
thus increasing the production and release ofNOwithin a few
minutes. Dupuis et al4 observed in a clinical setting that
lowering of the cholesterol level causes quick improvement
of the endothelial function in patients with ACS.
After positive results of observational studies,19,20 the
first prospective, controlled trials have been published,
showing the beneficial effects of this therapy. Arntz
et al21 administered pravastatin (occasionally together
with cholestyramine or niacin) on the sixth day of AMI
whereas in the MIRACL trial atorvastatin was given 2e4
days after the onset of symptoms of unstable angina or
non-Q AMI.22 Lipid lowering therapy reduced the risk of
recurrent myocardial ischemia requiring hospitalization.
Results of our study suggest that aggressive lipid lowering
therapy should be commenced earlier even in the first hours
of MI together with aspirin.
CONFLICTS OF INTEREST
All authors have none to declare.
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