The attached in the Appendix A. 2.2.2.1

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  The first discovery of cardiovascular
beneficial effect of omega-3 was in 1975, through a study conducted on
Greenland Eskimos showed that they had lower lipids levels and incidence of
cardiovascular due to their high polyunsaturated fatty acids diets (Dyerberg et al., 1975).  From this, a lot
of studies have been performed to study the mechanism and benefits of omega-3.

2.2.3 Cardioprotective mechanisms of omega-3 fatty acids

 

Omega-3
supplement is another way to obtained enough this fatty acid as suggested by
guidelines (European Society of Cardiology, 2017; Kris-Etherton et al.,
2002; Ministry of Health Malaysia, 2014; National Heart Foundation of
Australia, 2008; WHO, 2003). Supplement can be in capsule or liquid form which
contain various dosage according to manufacturer, which usually stated on the
product itself (Covington, 2004). The
types of sources, even type of fish, used to manufacture omega-3 supplement
also differ in different manufacturer (Covington, 2004). Though the source of this
supplement is through nature, some of this omega-3 are processed to produce
high quality supplement with free contaminant and can give higher doses of
fatty acids easily as compared through diet (Kris-Etherton
et al., 2002).

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2.2.2.2 Supplement omega-3 fatty acids

Different type of omega-3 can be obtained
depending on their sources (Covington, 2004; Kris-Etherton et al.,
2000; Lavie et al., 2009). EPA and DHA can be obtained directly through
marine-based sources and ALA through plant-based sources, which can be
metabolised by human body to EPA and DHA (Covington,
2004; Kris-Etherton et al.,
2000; Lavie et al., 2009; Simopoulos, 1991). A list of plant-based and marine-based
sources with their amount of omega-3 content is attached in the Appendix A.

2.2.2.1 Diet omega-3 fatty acids

2.2.2 Sources of omega-3 fatty acids

 

Figure 2.1

Omega-3 is an unsaturated fatty acid under the
category polyunsaturated fatty acid (PUFA) (Covington,
2004; Simopoulos, 1991). This means that
omega-3 has double bond in its fatty acid chain and its location differentiate
omega-3 with omega-6, another type of PUFA (Simopoulos, 1991). Omega-3 also
known as alpha-linolenic acid (ALA), which can be converted to eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA) (Covington,
2004; Lavie et al., 2009; Kris-Etherton et al.,
2000; Simopoulos, 1991). As omega-3 is an essential fatty acid,
human can only obtained it exogenously (Covington, 2004; Simopoulos, 1991).

2.2.1 Definition

2.2 Omega-3 fatty acids

 

Among the non-pharmacological preventions of
myocardial infarction,             one of
them is to consume omega-3 fatty acids which can be obtained            through diet or supplement (European Society of Cardiology, 2017; Kris-          Etherton et al., 2002; Ministry of Health
Malaysia, 2014; National Heart                   Foundation
of Australia, 2008; WHO, 2003). Some of the guidelines
stated      the amount of fatty acid need
to be consumed, which range from 1g to 2g          per
day, and the source of omega-3 either by increase intake of fish and      nuts, using vegetable oils or through
supplement (ACCF & AHA, 2011;                   National Heart Foundation of
Australia, 2008; National Heart Foundation        of Australia, 2012). Other guidelines
stated to increase fatty acids           generally
or specifically omega-3 fatty acids by incorporating fish and nuts     into diet or by taking omega-3 supplement (ESC,
2017; Ministry of Health                   Malaysia,
2014; Ministry of Health Malaysia, 2017).

2.1.3.2 Non-pharmacological prevention

              Statin is a 3-hydroxy-3-methylglutarylcoenzyme
A (HMG-CoA) reductase blocker (Stancu & Sima, 2001). It was introduced in
1998 to be used in preventing cardiovascular events (Teeling et al., 2004). Statin needed to manage risk factors and prevent
myocardial infarction by reducing the cholesterol levels (ACCF & AHA, 2011;
ESC, 2016, Ministry of Health Malaysia, 2017; National Heart Foundation of
Australia, 2012; NICE, 2013). Different kind of statin have different intensity
in lowering the lipid levels, which 40mg to 80mg of atorvastatin is high
intensity therapy compared to other types and doses of statins (ACC & AHA,
2013b)

              b) Lipid-lowering therapy: Statin

              In 1950, the first
evidence of aspirin ability in reducing myocardial infarction detected (Godley
& Hernandez-Vila, 2016). Aspirin the first choice in antiplatelet class
(ACCF & AHA, 2011; ESC, 2016, Ministry of Health Malaysia, 2017; National
Heart Foundation of Australia, 2012; NICE, 2013). Aspirin blocks the enzyme
cyclooxygenase (COX) irreversibly, thus blocking platelet aggregation (Dai
& Ge, 2012).

              a) Antiplatelet: Aspirin

              Across national and international guidelines,
these following drugs are often used as prevention of myocardial infarction
(ACCF & AHA, 2011; ESC, 2016, Ministry of Health Malaysia, 2017; National
Heart Foundation of Australia, 2012; NICE, 2013).

2.1.3.1 Pharmacological prevention

Prevention of myocardial infarction involved
prevention of myocardial incidence itself and management of the risk factors
like diet, physical inactivity, weight, lipids levels, smoking habit, and other
disease like hypertension, which need beta-blocker or
angiotensin-converting-enzyme (ACE) inhibitor and diabetes, which need oral
antidiabetic drug (OAD) or insulin (ACCF & AHA, 2011; ESC, 2016, Ministry
of Health Malaysia, 2017; National Heart Foundation of Australia, 2012; NICE,
2013). The needs of primary prevention of myocardial infarction usually determined
by cardiovascular risk assessment like Framingham Risk Score (ACC &
AHA, 2013a; ESC, 2016, Ministry of Health Malaysia, 2017)

2.1.3 Primary and secondary prevention of myocardial infarction

 

      Most
common imaging technique used is echocardiography which detect abnormality in function and structure of heart and help to           confirm diagnosis or myocardial
infarction and rule out other possible      causes
(ACC & AHA, 2014; ACCF & AHA, 2013; ESC, 2015; ESC,       2017; Ministry of Health Malaysia, 2011;
Ministry of Health           Malaysia;
2014; Thygesen
et al., 2012).

d) Imaging

ECG is
one major and most common diagnostic tools for myocardial          infarction which needs to be conducted
within 10 minutes of clinical         manifestation
of myocardial injury and repeated (ACC & AHA, 2014;     ACCF & AHA, 2013; ESC, 2015; ESC, 2017; Ministry of Health   Malaysia, 2011; Ministry of Health Malaysia;
2014; Thygesen
et al.,             2012). Abnormality of ST-segment, mainly, PR segment,
QRS      complex, Q-waves or presence of
left bundle branch block (LBBB) indicates
cardiac injury (ACC & AHA, 2014; ACCF & AHA, 2013;           ESC, 2015; ESC, 2017; Ministry of
Health Malaysia, 2011; Ministry of         Health
Malaysia; 2014; Thygesen et al., 2012). The ST-segment     readings differentiate ST-elevation
myocardial infarction (STEMI)             from
non-ST-elevation myocardial infarction (NSTEMI), where ST-   elevation can range from ?1.0mm to 2.0mm in
STEMI and ST-      depression or T-wave
inversion in NSTEMI (ACC & AHA, 2014; ACCF & AHA, 2013; ESC, 2015; ESC, 2017;
Ministry of Health   Malaysia, 2011;
Ministry of Health Malaysia; 2014; Thygesen
et al.,        2012)

c) ECG

CKMB is an isoenzyme of creatine kinase, was
one the earliest method to detect cardiac injury within 2 to 3 hours (Collinson & Chamberlain; 2001). It has less sensitivity and
specificity to myocardial infarction as CKMB can be found in skeletal muscle,
gastrointestinal tissue and uterus, and can rise for other clinical problems
like renal failure, trauma and rhabdomyolysis (Babuin & Jaffe, 2005). Since it is elevated for shorter period
compared to Troponin (I or T), it is useful to detect reinfarction (ACC &
AHA, 2014; ACCF & AHA, 2013; ESC, 2015; ESC, 2017; Ministry of Health
Malaysia, 2011; Ministry of Health Malaysia; 2014).

ii) Creatine kinase-MB (CKMB)

     This test is the most vital diagnostic
measures in the current         guidelines
that can be detected within 3 to 4 hours after myocardial incidence (ACC & AHA, 2014; ACCF & AHA,
2013; ESC, 2015;         ESC, 2017;
Ministry of Health Malaysia, 2011; Ministry of Health      Malaysia; 2014; Thygesen et al., 2012). Troponin (I or T) are found        in actin filament of myocardium and released to blood after          myocardium injury (Babuin & Jaffe,
2005). As Troponin (I or T)          only
found in cardiac muscle, released into the blood with greater      percentage and remain elevated days, compared
to CKMB, this    make   them a better sensitivity and specificity test
to myocardial   infarction (Babuin &
Jaffe, 2005; Panteghini et
al., 1999; Thygesen            et
al., 2012).  

i) Troponin (I or T)

This is the most prominent detection and
diagnostic tools for myocardial infarction as clinical symptoms and
abnormal ECG may be absence in some myocardial cases (Babuin & Jaffe, 2005; Thygesen
et al., 2012). Detection for cardiac injury is when an increase
of one measurement above the 99th percentile of URL (ACC
& AHA, 2014; ACCF & AHA, 2013; ESC, 2015; ESC, 2017; Ministry of Health
Malaysia, 2011; Ministry of Health Malaysia; 2014; Thygesen
et al., 2012). The two types of cardiac biomarkers usually
tested are Troponin (I or T) and CKMB (Thygesen et al., 2012).

b) Blood cardiac biomarkers

Most
common ischaemic symptom for myocardial infarction is chest           pain with sudden onset, which can be
felt as pressured, tightness or           burning,
which can be last for more than 10 minutes and can radiate to            other part like left arm, jaw, back
and shoulder (ACC & AHA,      2014; ACCF & AHA, 2013; ESC, 2015; ESC, 2017; Ministry of      Health Malaysia, 2011; Ministry of Health
Malaysia; 2014;         Thygesen
et al., 2012).  Other symptoms include shortness of breath,   nausea and vomiting, dizziness, weakness, and
sweating (ACC & AHA,     2014; ACCF & AHA, 2013; ESC, 2015; ESC, 2017; Ministry of        Health Malaysia, 2011; Ministry of Health
Malaysia; 2014;    Thygesen
et al., 2012).

a) Ischaemic symptoms

The definition and diagnostic measures in the
recent national and international guidelines on myocardial infarction mostly correlates
with the third universal definition of myocardial infarction was published by
the ESC, ACCF, AHA and WHF which was published on 2012 (Thygesen
et al., 2012).
The main diagnostic measures is to detect myocardial necrosis which was the
elevation of cardiac troponin with addition of at least one other clinical
manifestation of myocardial infarction such as ischaemic symptoms, abnormal ECG
readings of the ST segment, T-wave, or Q-wave, and imaging (Thygesen et al., 2012). Detection before
possible incidence of myocardial infarction included in this document which are
Q-wave abnormality and imaging findings (Thygesen
et al., 2012).
Revascularisation related myocardial infarction diagnostic measures and other
imaging technique like magnetic resonance imaging (MRI) are highlighted as well
(Thygesen et al., 2012).
The four main diagnostic measures in the national and international guidelines
are as following:

2.1.2.2 Current definition and diagnostic measures of myocardial
infarction

In 2007, another document was published on
2007 as the second universal myocardial infarction definition which they
added various ECG abnormalities which involved the ST segment, T-waves, PR
segment and QRS complex (Thygesen
et al., 2007). One of the main new
information added in this article was the five classification of myocardial
infarction which were segregated according to different aetiology, severity and
revascularisation complication (Thygesen
et al., 2007). 

By the year 2000, new document with more
details definition and diagnosis methods of myocardial infarction published by
the Joint European Society of Cardiology (ESC) and American College of
Cardiology (ACC) Committee (Alpert et al.,
2000). In this new report, any cardiac necrosis due to ischaemia considered as
infarct and this can be classified into sizes and pathologic aspect whether
acute, healing or healed (Alpert et al., 2000). Apart from common
symptom of chest pain, additional symptoms for myocardial infarction added were
radiating chest pain to jaw, arm, shoulder or back of chest, shortness of
breath, nausea and vomiting, dizziness and weakness (Alpert et al., 2000). The most prominent
different from previous report were addition of more precise cardiac biomarker which
were the Troponin I or Troponin T, and more detailed interpretations of cardiac
biomarker which was an increase of one measurement above the 99th percentile of
upper reference limit (URL) (Thygesen et al., 2012). Besides that, addition of non-ST elevation in ECG readings, and imaging
techniques like echocardiography, angiography and myocardial perfusion single
photon emission computed tomography (SPECT) (Alpert et al., 2000).

Following this, WHO released a special report
for definition and diagnosis criteria in ischaemic heart disease in 1979, which
commonly known as first universal definition on myocardial infarction (WHO,
1979).  In this revision, ischaemic heart
disease was termed as myocardial impairment resulting from coronary circulation
changes that leads to imbalance in cardiac requirements with the coronary blood
flow (WHO, 1979). Additional diagnostic approach included in this report where patient’s
history of ischaemic symptoms like chest pain and changes in enzymes, creatine
kinase (CK) and its isoenzyme from myocardiac (CKMB), in addition to abnormal ECG
readings (Eggers, 2015; WHO, 1979).

The first
document that standardised the definition of myocardial infarction was proposed
by the WHO in their 168th Technical Report Series in 1959 (WHO, 1959). In this
report, the myocardial infarction was one of the classification under the
coronary heart disease category which can be identified by severe chest pain
with sudden onset and the main diagnosis method by using 12 leads, or at least
7 leads, electrocardiography (ECG) (WHO, 1959). A list of changes in ECG
readings, mostly on Q-waves, that occurred in myocardial infarction        was explained for proper diagnosis (WHO,
1959).

2.1.2.1 Evolution of definitions and diagnostic measures of myocardial                        infarction

Definition of myocardial infarction goes hand
in hand with the diagnostic measures for this disease. Throughout the years,
the definition and diagnostic tools of myocardial infarction have been revised and
changed as new, better and more accurate diagnostic tools and measures emerged.

2.1.2 Definitions and diagnostic measures of myocardial infarction

 

Death due to cardiovascular diseases becoming the
leading cause of global death according to World Health Organization (WHO) (WHO,
2017). One of the main cause of death in cardiovascular disease is myocardial
infarction, which is part of coronary disease, causing 40% of death within
cardiovascular deaths (WHO, 2017). Recent data show that approximately 7
million deaths due to ischaemic heart disease and this number expected to
increase to 23 million by 2030 (Mozaffarian et al.,
2015, WHO, 2017). In Malaysia, the highest amount of death in noncommunicable
diseases is due cardiovascular disease (WHO, 2014).

2.1.1 Prevalence

2.1 Myocardial infarction

2.     
LITERATURE REVIEW

 

 

 

 

 

 

 

 

 

 

 

Several systematic
reviews and meta-analysis
have been published to assess the cardiovascular benefits of omega-3
(Delgado-Lista et al., 2012; Enns et al., 2014; Kotwal et al., 2012; Kwak et al., 2012; Rizos et
al., 2012). However, these systematic reviews have mixed and contradictory
results and focused on peripheral arterial disease (Delgado-Lista et al., 2012; Enns et al., 2014; Kotwal et al.,
2012; Kwak et al., 2012; Rizos et al., 2012). Additionally these
reviews, included open-label studies or studies with secondary prevention or
trials which considered omega-3 source from supplement only or marine source
alone (Delgado-Lista et al., 2012;
Enns et al., 2014; Kotwal et al., 2012; Kwak et al., 2012; Rizos et al.,
2012). The aim of the study will be to assess the effects of omega-3, from all
sources and as primary and secondary prevention, on risk of myocardial
infarction by conducting meta-analysis on randomised controlled trials. The findings of this systematic review will provide updated
evidence and determine the presences and
extent of usefulness of omega-3 administration in people with myocardial
infarction and those with risk of the disease.

 

Omega-3 is a type of polyunsaturated fatty acid and
also an essential fatty acid as human is unable to synthesize it and it can
only be obtained exogenously (Covington, 2004; Simopoulos, 1991). It is an alpha-linolenic acid (ALA) that
can be metabolized by human into commonly known components, eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA) (Covington, 2004; Simopoulos, 1991). Human can obtain
EPA and DHA directly through their diet of fish, and ALA through vegetable oils
(Covington, 2004; Kris-Etherton et al., 2000). Though it can be acquired through diet, omega-3
supplements is another option for people to obtain adequate amounts of EPA and
DHA as suggested by the guidelines (Kris-Etherton
et al., 2002; Kris-Etherton et al., 2000). Several studies reported that omega-3 exerts
cardioprotective effects mainly through its antiinflammatory and antithrombotic
properties plus alteration of endothelial cells, cell membrane, ion channels,
plasma lipoproteins, lipid metabolism and others (Jain et al., 2015; Jin
& Makoto, 2016; Mozaffarian & Wu, 2011; Nestel et al., 2015).

 

World Health Organization (WHO) states that
approximately 7 million people died due to ischaemic heart diseases which
include myocardial infarction, making it the leading cause of global death,
accounting for 40% of death in cardiovascular diseases cases (WHO, 2017).
Myocardial infarction, also known as heart attack, is characterized by clinical
manifestations comprising of ischaemic symptoms, changes in electrocardiogram
(ECG) readings and level of cardiac biomarkers, and imaging (Thygesen
et al.,
2012). One of the major complications of myocardial infarction is sudden
cardiac death (Huikuri et al., 2001). By 2030, 23
million deaths are expected due to cardiovascular diseases, partly due to
myocardial infarction (Mozaffarian et al., 2015). Global burden of
ischaemic heart diseases increases as population and aging group expands (Moran
et al., 2014). Healthcare expenditure
and patients’ morbidity rise while patients’ productivity decreases due to
incapability to work (Heidenreich et al., 2011; Johansson et
al., 2017; Likosky et al., 2013;
Oksak & Golovanova,
2017). Thus, it is important to have prevention and proper management of
myocardial infarction through various approaches that are tailored according to
patient’s needs and conditions (American College of
Cardiology Foundation & American Heart Association, 2013). One of the measures proposed by national and
international guidelines and cardiology bodies worldwide, is to consume omega-3
fatty acids either through diet or supplements (European Society of Cardiology,
2017; Kris-Etherton et al.,
2002; Ministry of Health Malaysia, 2014; National Heart Foundation of
Australia, 2008; WHO, 2003).

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