(2021) 73:107
Taha et al. The Egyptian Heart Journal
https://doi.org/10.1186/s43044-021-00235-9
The Egyptian Heart
Journal
Open Access
REVIEW
Egyptian practical guidance
in hypertriglyceridemia management 2021
Hesham Salah El Din Taha1*, Hossam Kandil1, Nabil Farag2, Abbas Oraby3, Magdy El Sharkawy2,
Fouad Fawzy1, Hossam Mahrous1, Juliette Bahgat1, Mina Samy1, Mohamed Aboul1, Mostafa Abdrabou1 and
Mirna Mamdouh Shaker1
Abstract
Hypertriglyceridemia (HTG) is a very common, yet underappreciated problem in clinical practice. Elevated triglyceride
(TG) levels are independently associated with atherosclerotic cardiovascular disease (ASCVD) risk. Furthermore, severe
HTG may lead to acute pancreatitis. Although LDL-guided statin therapy has improved ASCVD outcomes, residual risk
remains. Recent trials have demonstrated that management of high TG levels, in patients already on statin therapy,
reduces the rate of major vascular events. Few guidelines were issued, providing important recommendations for
HTG management strategies. The goal of treatment is to reduce the risk of ASCVD and acute pancreatitis. The management stands on lifestyle modification, detection of secondary causes of HTG and pharmacological therapy, when
indicated. In this guidance we review the causes and classification of HTG and summarize the current methods for risk
estimation, diagnosis and treatment. The present guidance provides a focused update on the management of HTG,
outlined in a simple user-friendly format, with an emphasis on the latest available data.
Keywords: Hypertriglyceridemia, Dyslipidemia, Practical guidance, Atherosclerotic cardiovascular disease
Background
Hypertriglyceridemia (HTG) prevalence in adults varies
between 10 and 29% according to the studied population
[1]. HTG is classified as primary; due to genetic causes,
or may be secondary to particular diseases, drugs or metabolic disorders [2].
Dyslipidemia itself usually causes no symptoms but can
lead to symptomatic vascular disease, including coronary artery disease (CAD), cerebrovascular disease and
peripheral arterial disease (PAD). In hereditary lipid disorders, a patient may present with the variants of cutaneous xanthoma. Eruptive xanthomas at pressure sites
on the elbows, buttocks, and knees may be indicative of
hypertriglyceridemia. High levels of TG (> 500 mg/dL)
can cause acute pancreatitis. Higher TG levels can also
*Correspondence: heshsalt@yahoo.com
1
Department of Cardiology, Faculty of Medicine, Cairo University, 27
Nafezet Sheem El Shafae St Kasr Al Ainy, Cairo 11562, Egypt
Full list of author information is available at the end of the article
cause dyspnea, hepatosplenomegaly lipemia retinalis and
neurological manifestations such as confusion, transient
memory loss, paresthesias and rarely, focal neurologic
deficits. Extremely high lipid levels also give a lactescent
(milky) appearance to blood plasma [3–5].
HTG is an underappreciated risk factor that is often
overshadowed by low-density lipoprotein cholesterol
(LDL-C) and other chronic conditions [6]. Studies have
shown that despite the use of statin therapy, atherosclerotic cardiovascular disease (ASCVD) event rates remain
high in patients with elevated TG [7]. The importance
of lowering plasma levels of TG is currently considered
an integral part of residual cardiovascular risk reduction strategies [8]. The American College of Cardiology/
American Heart Association cholesterol guidelines list
HTG as a risk-enhancing factor for cardiovascular disease (CVD) [9].
Dietary TGs are carried via the intestinal lymphatics in chylomicrons, while endogenous TGs produced by the liver are transported in very low density
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Taha et al. The Egyptian Heart Journal
(2021) 73:107
lipoproteins (VLDL) [10]. Large triglyceride-rich lipoproteins (TRL) particles such as nascent chylomicrons
are unable to infiltrate the vessel wall [11]. However,
cholesteryl-ester (CE)-enriched smaller TRLs (‘remnants’) can penetrate the subendothelium promoting
atherogenesis through pro-inflammatory and prothrombotic pathways [12].
Therefore, ASCVD risk mediated by TRLs appears
to be determined by the circulating concentration of
apo B-containing particles rather than their TG content. An estimate for all apo B-containing lipoproteins is non-HDL-C [calculated as total cholesterol
(TC) − HDL-C], hence its importance [13].
In addition, HTG is frequently associated with pathological high-density lipoprotein (HDL) particles that
may add to the ASCVD risk [12].
Furthermore, HTG is believed to be causative in up
to 10% of episodes of acute pancreatitis [14]. The risk
of acute pancreatitis is a continuum with mild hypertriglyceridemia associated with a low long-term risk
[15, 16], while more severe HTG is associated with
progressively increased risk [16, 17].
We have previously published a consensus statement
on the management of lipids [18]. We felt that there
was a need to address an ignored and frequently overlooked part in the management of dyslipidemia which
was hypertriglyceridemia. The following guidance is
based on the best scientific evidence available till present and expert opinion considerations.
Scope of the article
The goal of this article is to provide practical guidance for clinicians in situations not covered by the current lipid guidelines, in a world with rapidly evolving
evidence.
There are current gaps in care for high-risk patients
with mild to moderate as well as severe forms of HTG.
There are also limited data on management of patients
at low to moderate atherosclerotic cardiovascular risk
and moderately elevated triglycerides.
The evidence from clinical trials on triglyceride riskbased agents for ASCVD risk reduction is evolving and
newer medications are soon coming into play. In this
document, we aim to fulfill the following aspects:
Page 2 of 10
Definitions and classifications
Hypertriglyceridemia is defined as a fasting plasma/
serum TG level > 150 mg/dL or a non-fasting TG
level > 175 mg/dL. We endorse the definition proposed by
the American College of Cardiology on persistent hypertriglyceridemia; Fasting triglycerides ≥ 150 mg/dL following a minimum of 4–12 weeks of lifestyle intervention, a
stable dose of maximally tolerated statin therapy when
indicated, as well as evaluation and management of secondary causes of hypertriglyceridemia [7].
Patients with HTG can be categorized according to
their fasting TG level as shown in Table 1.
Causes of hypertriglyceridemia
HTG may be either secondary to a variety of medical
conditions or medications, or primary due to genetic
causes [2]. Potential secondary causes for hypertriglyceridaemia [7] are listed in Table 2.
While secondary factors more frequently cause mild
to moderate HTG, severe forms of HTG are more commonly primary in nature [10]. The causes of primary
HTG are listed in Table 3 [19–22].
Who and when should we screen?
The age at which screening is recommended differs
according to the level of risk as illustrated in Table 4.
Screening for HTG should also be considered in
patients with [7]:
• Acute pancreatitis
• Suspected primary HTG:
• Presence of tuberous xanthomas in the patient or
family member
• Family history of HTG
• Severely elevated TG levels
• Premature ASCVD in the patient or family member
• Secondary causes for HTG
Table 1 Categories of hypertriglyceridemia and goals of therapy
1.
2.
3.
4.
Definition and categories of HTG
Role of lifestyle intervention in patients with HTG
Role of statin therapy in patients with HTG
Triglyceride risk-based non-statin therapies; when
and how to give them?
5. Providing practical algorithms for HTG management
Category of HTG
Fasting TG
level (mg/dl)
Goals
Mild
150–199
Moderate
200–499
Reduce ASCVD risk and risk of
pancreatitis
Severe
≥ 500
Very severe
≥ 1000
Taha et al. The Egyptian Heart Journal
(2021) 73:107
Page 3 of 10
Table 2 Secondary causes of hypertriglyceridemia
Secondary causes of hypertriglyceridemia [7]:
Diseases
Uncontrolled diabetes mellitus, chronic kidney disease, nephrotic syndrome, hypothyroidism, Cushing’s disease
Metabolic and dietary disorders
Overweight/obesity, metabolic syndrome, sedentary lifestyle, alcohol abuse or alcohol excess, diets high in
saturated fat, sugar, or high-glycemic index foods, total parenteral nutrition with lipid emulsions
Drugs
Propofol, beta blockers, diuretics, thiazide and loop diuretic agents, bile acid sequestrants, glucocorticosteroids, anabolic steroids, oral estrogens, tamoxifen, HIV protease inhibitors, atypical antipsychotics, tacrolimus,
sirolimus, cyclosporine, interferons
Pregnancy
Especially in the third trimester
Table 3 Different types of familial HTG [19–22]
FCH
(Type IIB)
FCS
(Type I)
MFCS
(Type IV)
FHTG
(Type V)
FD
(Type III)
Lipoprotein change
↑VLDL, LDL
↑Chylomicrons
↑VLDL
↑VLDL, chylomicrons
↑IDL
Lipid change
↑TG, TC
↑TG
↑TG
↑TG, TC
↑TG, TC
Incidence
1/100–200
1/500,000–1,000,000 1/600–1000
Genetics
Polygenic (TG, LDL raising
alleles)
Monogenic
homozygous (autosomal recessive)a
Monogenic heterozygous
(autosomal dominant)a
Polygenic
1/500
1/10,000
Monogenic heterozygous
(autosomal dominant)a
Polygenic
Monogenic
homozygous
(defect in APOE
gene)
Time of presentation All in adulthood (earlier with secondary causes) except for FCS (type I) in childhood
Specific for diagnosis Combination of:
ApoB > 120 mg/dL
TGs > 133 mg/dL
FH of premature CVD
TG > 885 mg/dl
Creamy appearance
of the blood
Failure to thrive,
Recurrent abdominal pain, nausea,
vomiting
Acute pancreatitis
(60–80% lifetime
risk)
Tuberous xanthoma
Lipemia retinalis
Hepatosplenomegaly
TG 150–885 mg/dl
or
> 885 mg/dl with secondary insult
Responsive to standard
therapy
Require an aggravating
effect
TG 150–885 mg/dl
Require an aggravating
effect
Lower risk of pancreatitis
Palmer crease
xanthomas
are pathognomonic
FCH familial combined hyperlipidemia, FCS familial chylomicronemia syndrome, FD familial dysbetalipoproteinaemia, FHTG familial HTG, GPIHBP1
glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein-1, MFCS multifactorial chylomicronemia syndrome, LDL low density lipoprotein, LMF1
Lipase maturation factor 1, LPL lipoprotein lipase, TC total cholesterol, TG TG, VLDL very low-density lipoprotein, FH family history
a
Defect in LPL, APOC2, APOA5, GPIHBP1 or LMF1 genes
Table 4 Recommendations for screening [18]
Primary prevention
All adults ≥ 40 years, however
earlier screening at the age of
20 years can be considered
Secondary prevention
All patients with ASCVD, (e.g.,
CAD, CVD, PAD), or multiple
major risk factors
Family history of early CVD or familial
dyslipidemia
As early as the second year of life
How should we screen?
For screening, lipid testing should include total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C),
high-density lipoprotein cholesterol (HDL-C), TG and
non-HDL-C. It can generally be done using a non-fasting blood sample. The postprandial rise in TG is usually
small, between 12 and 27 mg/dL. Fasting lipid testing is
preferred in patients with metabolic syndrome, family
history of premature ASCVD or genetic lipid disorders,
non-fasting TG ≥ 400 mg/dL and to assess adherence to
lifestyle interventions and lipid lowering medications [7,
9, 18, 23, 24].
Management of HTG in patients without ASCVD
or diabetes mellitus (DM)
Limited data are available on ASCVD risk reduction
using TG risk-based non-statin therapies for primary
prevention in non-diabetic patients with persistent
Taha et al. The Egyptian Heart Journal
(2021) 73:107
mild to moderate HTG [7]. Management of these
patients is described in Fig. 1. However, patients with
more severe forms of HTG have a relatively higher
incidence of acute pancreatitis [7]. Management of
these patients is described in Fig. 2.
Management of HTG in patients with ASCVD
Individuals with persistent moderate to severe HTG
may be at increased risk of premature CVD. Few studies have shown an independent relationship, although
small, between HTG and CVD. Studies have suggested
that the ApoB-containing particles and/or lipoprotein (a), rather than the TG content of TRLs and their
remnants are the cause of ASCVD risk [25, 26]. Management of HTG in ASCVD patients is illustrated in
Fig. 3.
Management of HTG in patients with DM
The leading cause of mortality in diabetes mellitus is
CVD. Diabetic patients have higher risk of developing ASCVD and much of this risk can be attributed to
the development of atherogenic dyslipidemia, in which
HTG is an essential component.
In well-controlled DM, the lipid profile may be normal, while in poorly controlled DM, the lipid profile
shows a triad of HTG, increased levels of small dense
LDL, and low HDL [27]. The management algorithm
of HTG in diabetic patients is shown Figs. 2 and 4.
Page 4 of 10
Management of HTG in patients with chronic kidney
disease (CKD)
HTG is frequently encountered in the setting of CKD,
especially in association with nephrotic syndrome and
in patients on peritoneal dialysis [28]. The exact mechanisms through which CKD causes HTG are not exactly
known, however, increased catabolism of VLDL [due to
increased lipoprotein lipase (LPL) inhibitors as apo-C
III] and increased VLDL production have been suggested [29]. Risk factors for development of HTG in
CKD include DM, the degree of glomerular filtration rate
(GFR) affection, severity of proteinuria, the modality of
renal replacement therapy (peritoneal dialysis more than
hemodialysis), nutritional status of the patient, and the
presence of other comorbidities [14].
The aim of treatment is to primarily reduce the
patient’s cardiovascular (CV) risk and in patients with
severe HTG, reduce the risk of pancreatitis [14]. Nonpharmacological treatment is indicated as in patients
without CKD, but diet modification is not recommended
in malnourished patients. Statins are the cornerstone of
treatment and are recommended to all patients with nondialysis-dependent stage 3 or higher CKD, or recipients
of renal transplantation. They should not be started in
dialysis-dependent patients but should be continued if
already on statins before being dialysis-dependent [23].
Caveats of statin use in CKD include the need for dose
adjustment of some statins and the higher risk of rhabdomyolysis when used with cyclosporine or fibrates [11].
Icosapent Ethyl should be considered if HTG persists
on statin therapy [30]. Whether there is a net benefit
Fig. 1 Management of HTG in patients without ASCVD or DM. *ASCVD risk-enhancing factors including family history of premature ASCVD,
persistently elevated LDL-C ≥ 160 mg/dL, chronic kidney disease, metabolic syndrome, inflammatory diseases (especially rheumatoid arthritis,
psoriasis), biomarkers (persistently elevated fasting triglycerides ≥ 150 mg/dL, hs-CRP ≥ 2.0 mg/L) [7].
Taha et al. The Egyptian Heart Journal
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Page 5 of 10
Fig. 2 Management of HTG ≥ 500 mg/dl in patients without ASCVD or DM
or not on CV outcomes with fibrate use in CKD is still
unknown. Fibrates are therefore not recommended for
the reduction of CV risk in CKD patients [14]. They may
be considered in patients with severe HTG who are at
high risk of pancreatitis under specialist consultation.
Fibrates should be adjusted to GFR. Fibrates may lower
cyclosporine levels in patients with renal transplants [14].
Lomitapide may be considered in patients with severe
HTG who are at high risk of pancreatitis, with dose
adjustment to GFR [31].
Management of HTG in patients with familial
hypertriglyceridemia (FHTG)
There are five different types of FHTG classified according to the type of elevated lipoprotein and associated lipid
changes including: familial combined hyperlipidemia
(FCH), which is the commonest, familial chylomicronemia syndrome (FCS), familial dysbetalipoproteinaemia
(FD), familial HTG (FHTG), and multifactorial chylomicronemia syndrome (MFCS) (Table 3) [19–22].
Pharmacologic management is frequently needed in
FHTG to prevent pancreatitis and/or reduce risk of CVD.
Medications commonly used for TG lowering are icosapent ethyl, fibrates, and Niacin [32]. In individuals who
are unresponsive to treatment, plasmapheresis has been
used.
There has been considerable interest in developing
new TG lowering agents, especially for treatment of
FHTG, using approaches targeting LPL and its regulators because of the central role they play in TRL metabolism. Volanesorsen is an antisense oligonucleotide that
binds to apolipoprotein C3 (APOC3) mRNA preventing
APOC3 translation. It has been shown to lower circulating APOC3 levels by 70–90% and TG levels by 56–86%
in clinical trials involving both FCS and non-FCS patients
with moderate to severe HTG. A reduction in the number of episodes of pancreatitis was also reported. The
Taha et al. The Egyptian Heart Journal
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Page 6 of 10
Fig. 3 Management of HTG in patients with ASCVD
monoclonal antibody evinacumab that blocks the action
of angiopoietin-like protein 3 (ANGPTL3) has been
found to lower TG levels up to 80% in patients with mild
to moderate HTG, as well as LDL-C levels [33, 34].
Lifestyle interventions
HTG is closely associated with a sedentary lifestyle and
visceral adiposity. Weight loss is considered the most
effective lifestyle intervention to lower TG levels; the
effect of weight loss on lowering TGs is variable [35].
Five to ten percent reduction in body weight is associated with a 20% decrease in TG [34]. Higher-fat, lower
carbohydrate diets have better effect on TG levels compared with lower-fat, higher carbohydrate diets [36]. The
reduction in TG was greater for the very low carbohydrate regimens (in which carbohydrates represent < 10%
of calories) [37]. A higher-protein (31% of caloric intake)
versus a standard-protein (18% of caloric intake) weightloss diet results in more weight loss and TG lowering
[38].
There are different types of fasting, as shown in Table 5.
Weight loss and greater TG lowering were noticed with
alternate day fasting. A summary of nutrition recommendations for patients with HTG is shown in Table 6.
Taha et al. The Egyptian Heart Journal
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Page 7 of 10
duration, and intensity of activity. In addition, smoking cessation should be advocated as a part of lifestyle
intervention.
Pharmacological management [32]
Classes of medications commonly used in the management of HTG include omega-3 fatty acids, fibric acid
derivatives and niacin. High doses of a strong statin (simvastatin, atorvastatin, rosuvastatin) also lower TG by up
to 30%. The effect of different drugs on different lipid
components is illustrated in Table 7.
Fibrates [39]
Fig. 4 Management of HTG in diabetic patients without ASCVD
Alcohol is an important cause of elevated TG levels;
patients with HTG are advised to abstain completely.
Physical activity and exercise reduce TG levels by
7–30%; the response is variable depending on the type,
Fibrates are commonly used to treat HTG. They increase
the activity of LPL through peroxisome proliferator activated receptor (PPAR) alpha receptor agonist action,
which hydrolyzes TG in TRL.
Fibrates may be associated with a reversible increase in
serum creatinine; therefore the dose should be lowered in
patients with mild-to-moderate renal disease (about one
third of the usual dose) and should be avoided in severe
renal impairment. Risk for myopathy/ rhabdomyolysis
increases with renal impairment or concurrent use of
HMG-CoA reductase inhibitors. Rarely, severe anemia,
leukopenia, thrombocytopenia may occur so periodic
blood counts are recommended.
Table 5 Types of fasting [34–38]
Alternate day fasting
3 to 4 days/week, consumption of < 25% of energy needs
during a 24-h period
Periodic fasting
Fasting 1 or 2 days/week
Time restricted eating
Food intake is limited to a specific window of time each day
Table 6 Summary of nutrition recommendations for patients with HTG [7, 34–38]
Nutrient
Encourage
Limit/restrict
Stop completely
If TG < 500 mg/dl
If TG > 500 mg/dl
Fruits
Can be included but individualize
3–4 servings per day
1 serving per day if TG > 1000
Vegetables
Encourage most vegetables
Vegetables with high glycemic
index (carrots, potatoes,..)
Canned vegetables
Vegetable juices
Limit full-fat dairy
Sugar-sweetened dairy products
Full fat dairy if TG > 1000 mg/dl
Sugar-sweetened beverages
Legumes
Encourage
Fish—sea food
Encourage fatty or lean fish at least 2
servings/week
Poultry—lean meats
Encourage instead of red meat
Dairy products
Fiber-rich whole grains
Encourage 4–6 servings per day
Nuts and peanuts
Encourage in moderation
Desserts
Limit if TG > 1000 mg/dl
May be used occasionally if TG
500–999 mg/dl
Avoid if TGs > 1000 mg/dl
Taha et al. The Egyptian Heart Journal
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Table 7 Lipid effects of different drugs:
Drug
Lipid effects
Fenofibrate
LDL ↓: 20.6% (145 mg)
HDL ↑: 11% (145 mg)
TG ↓: 23.5–50.6% (greatest drop is in
patients with highest TG) (145 mg)
IPE
HDL ↑: 9.1% (4 g/day)
TG ↓: 45% (4 g/day)
Niacin
LDL ↓: 14–17% (2 g/day)
HDL ↑: 22–26% (2 g/day)
TG ↓: 20–50%
Ezetimibe
LDL ↓: 18% (10 mg/day)
HDL ↑: 1% (10 mg/day)
TG ↓: 8%
Statins
LDL ↓: 30–50% (dose, and drug dependent)
HDL ↑: 1–10%
TG ↓: 10–30%
Omega 3 fatty acids [40]
Icosapent ethyl and docosahexaenoic acid (DHA)
are the active constituents of the omega 3 fatty acids.
Higher doses of icosapent ethyl (2–4 g) significantly
reduce the levels of TGs. Omega 3 fatty acids reduce
hepatic VLDL-TG synthesis and secretion. They also
increase plasma LPL activity that in turn enhances TG
clearance from circulating VLDL particles. Caution
should be exercised in patients allergic to fish. Recurrent atrial fibrillation or flutter has been reported with
administration of high doses. Omega 3 fatty acids may
increase liver alanine transaminase (ALT), therefore it
should be monitored. They may prolong bleeding time;
therefore, caution is needed in patients at high bleeding
risk.
Niacin [32]
Niacin reduces VLDL synthesis, and may increase chylomicron TG removal from plasma. Caution is used in
patients with gout, DM, gall bladder disease, CVD, renal
or hepatic impairment, if the patient is taking anticoagulants or HMG-CoA reductase inhibitors or if symptoms
of myopathy occur (monitor creatine phosphokinase).
Statins [32]
Statins are competitive inhibitors of the activity of
HMG-CoA reductase enzyme. This results in the
reduction of the levels of LDL. Statins reduce TG possibly through upregulation of the VLDL uptake by hepatocytes, as well as a reduction in the production rate of
VLDLs. Statin-associated muscle symptoms (SAMs)
may occur in 10–15%. Liver function tests should be
checked at baseline, and when clinically indicated.
Page 8 of 10
Conclusions
Management algorithms proposed in this document for
the management of hypertriglyceridemia are simple,
cover the clinical situations most commonly observed in
routine practice and are designed to improve the quality of care. In all patients with HTG, risk stratification is
mandatory and an attempt should be made to identify a
cause or association. All patients with HTG should have
an assessment of their LDL-C and non-HDL-C levels.
The goal of therapy is to reduce ASCVD risk, as well as
risk of pancreatitis. The first step of treatment involves
implementing lifestyle changes and management of
secondary causes, if present. Proper control of other
ASCVD risk factors is recommended. Statins are advised
as first line agent for ASCVD risk reduction. For patients
with persistently elevated TG levels after non-pharmacologic interventions and despite maximally tolerated LDLguided therapy, we suggest introducing additional drug
therapy when indicated. Pharmacological management in
persistent, as well as severe HTG, is centered on omega-3
fatty acid therapy and fenofibrate.
Future directions
HTG and its impact on ASCVD remain an underexplored frontier in lipidology. Research is needed to
uncover the molecular basis and the dynamics of the different atherogenic particles in this disease process.
A risk stratification algorithm for acute pancreatitis in
patients with severe HTG is needed.
More RCT-based evidence is needed for the use of
fibrates to reduce CV risk in various subgroups e.g.: CKD
patients and the elderly.
More data regarding the efficacy of IPE in reducing
CV risk without concomitant statin use (e.g.: in patients
intolerant to statins) is needed.
Further safety and efficacy data on novel drugs acting
on existing pharmacological targets (e.g.: the novel selective PPAR alpha modulator-pemafibrate), or novel pharmacological targets (e.g.: apoC-III and ANGPTL-3) is
needed.
Abbreviations
ACC: American College of Cardiology; ANGPTL3: Angiopoietin-like protein
3; ApoB: Apolipoprotein-B; ApoC: Apolipoprotein-C; ASCVD: Atherosclerotic
cardiovascular disease; CAD: Coronary artery disease; CE: Cholesteryl-ester;
CKD: Chronic kidney disease; CV: Cardiovascular; CVD: Cardiovascular
disease; CYP2CA: Cytochrome-P 2CA; DGAT: Diacylglycerol acyltransferase;
DM: Diabetes mellitus; FCH: Familial combined hyperlipidemia; FCS: Familial
chylomicronemia syndrome; FD: Familial dyslipoproteinemia; FHTG: Familial
hypertriglyceridemia; GFR: Glomerular filtration rate; GPIHBP1: Glycosylphosphatidylinositol-anchored high density lipoprotein binding protein-1;
HDL-C: High density lipoprotein-cholesterol; HIV: Human immunodeficiency
virus; HMG-CoA: Hydroxymethylglutaryl coenzyme-A; Hs-CRP: Highlysensitive C-reactive protein; HTG: Hypertriglyceridemia; IDL-C: Intermediate
density lipoprotein-cholesterol; IPE: Icosapent ethyl; LDL-C: Low density
Taha et al. The Egyptian Heart Journal
(2021) 73:107
lipoprotein-cholesterol; LMF1: Lipase maturation factor 1; LPL: Lipoprotein
lipase; MCT: Medium-chain triglyceride; MFCS: Multifactorial chylomicronemia
syndrome; mRNA: Messenger ribonucleic acid; PPAR: Peroxisome proliferator
activated receptor; PTT: Partial thromboplastin time; SAM: Statin-associated
muscle symptom; SPPARMa: Selective PPAR alpha modulator; T1DM: Type-1
diabetes mellitus; T2DM: Type-2 diabetes mellitus; TC: Total cholesterol;
TG: Triglyceride; TRL: Triglyceride-rich lipoprotein; VLDL-C: Very low density
lipoprotein-cholesterol.
Page 9 of 10
8.
9.
Acknowledgements
None.
10.
Authors’ contributions
HT: main author, put the idea behind this review and wrote, revised and
edited the manuscript. HK, NF, AO, MS, FF, HM, JB, MS, ME, MA, MM: contributed to the writing of this manuscript and has read and approved the final
manuscript.
11.
12.
Funding
None.
Availability of data and materials
The dataset supporting the results and conclusions of this article will be available from the corresponding author on request.
Declarations
Ethics approval and consent to participate
This research involved human subjects and was performed in accordance
with the Declaration of Helsinki and approved by Cairo University Ethical Committee with reference number–Egypt.
13.
14.
15.
16.
Consent for publication
Not applicable.
17.
Competing interests
No conflict of interest.
18.
Author details
1
Department of Cardiology, Faculty of Medicine, Cairo University, 27 Nafezet
Sheem El Shafae St Kasr Al Ainy, Cairo 11562, Egypt. 2 Ain-Shams University,
Cairo, Egypt. 3 Suez Canal University, Ismailia, Egypt.
19.
20.
Received: 24 August 2021 Accepted: 14 December 2021
21.
22.
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