Diagnosis and Management of Dyslipidemia in Family Practice

SPECIAL THEME
Diagnosis and Management of Dyslipidemia in Family Practice
Abigael C. Andal-Saniano, MD, FPAFP; Noel M. Espallardo, MD, Msc, FPAFP; Jane Eflyn Lardizabal-Bunyi, MD, FPAFP;
Djhoanna Aguirre-Pedro, MD, FPAFP; Daisy M. Medina, MD, FPAFP; Teri Marie P. Laude, MD, FPAFP;
Nicolas R. Gordo Jr., MD, MHA, CFP and Irmina Concepcion-Beltran, MD, FPAFP
Background: Atherosclerotic cardiovascular disease (ASCVD) is a top cause of mortality in the Philippines. A known modifiable
risk factor for ASCVD is dyslipidemia. Thus, proper diagnosis and management of dyslipidemia in family practice clinic could
significantly decrease the burden of cardiovascular disease in the country.
Objectives: This clinical pathway was developed to guide family and community physicians on the diagnosis and management
of dyslipidemia.
Methods: To develop evidence -based recommendations, the authors searched for the latest guidelines of reputable international
and local societies. They also searched PubMed using the terms “dyslipidemia”, “diagnosis”, “therapeutics”, “family” and
“community medicine”. The more rigorous meta-analysis of clinical trials and observational studies were prioritized over low-
quality trials in the formulation of the recommendations.
Recommendations: Thorough ASCVD risk assessment for all adults should be done during initial visit in family practice. The
physician should review patient’s present medication; probe regarding lifestyle habits; conduct complete physical examination;
use family assessment tools; and assess risk for ASCVD using calculators or risk factor counting method. For patients ≥ 45 years
old and all adult patients regardless of age at increased ASCVD risk the following should be requested: lipid profile, urinary
albumin- creatinine ratio/ urinary dipstick test, alanine transaminase (ALT), 12-lead electrocardiography (12-L ECG) and fasting
blood sugar (FBS). During subsequent visits, re-assessment of ASCVD risk; checking compliance to non-pharmacologic intervention;
and review of medication adherence and adverse effects should be performed. Repeat measurement of lipid profile should be
done 6-8 weeks after initiation of statin therapy; 8-12 weeks after dose adjustment; and biannually for patients with controlled
lipid levels. For individuals on statin therapy who have already achieved their low-density lipoprotein cholesterol (LDL-C) goal,
compute for non- high density lipoprotein cholesterol (non-HDL C). Repeat ALT 6-8 weeks after initiation of statin therapy for
those at high risk of statin-induced liver injury. Request creatine kinase (CK) if with development of muscle symptoms while on
statin therapy. For primary prevention, start low-moderate intensity statins for following: individuals with diabetes mellitus (DM)
Type 2 without ASCVD; individuals with mild-moderate chronic kidney disease (CKD); and individuals without ASCVD aged ≥ 45
years old with LDL -C ≥ 130 mg/dl AND with ≥ 2 risk factors. Start high intensity statins for individuals diagnosed with Familial
Hypercholesterolemia. Give high intensity statins as secondary prevention for individuals with established ASCVD. For individuals
with ASCVD on maximally tolerated statin therapy not meeting target LDL-C, ezetimibe could be added to their regimen. Low
saturated fat diet rich in fruits and vegetable; regular exercise; and smoking cessation should be advised for all adult patients.
The physician should also engage other family members to adopt healthy lifestyle. Formation of a community-based lifestyle
intervention program to reduce cardiovascular risk should also be supported by the family physician.
Implementation: Adherence to pathway recommendations that are graded as either A-I, A-II or B-I is strongly advised. However,
the authors also recommend using sound clinical judgment and patient involvement in the decision making before applying
the recommendations.
VOL. 59 NO. 2 DECEMBER, 2021 215

Introduction publication on the management of patients with dyslipidemia in family
and community practice. The recommendations are time-bound tasks
Diseases of the heart and the vascular system are the top causes
on patient care processes, in terms of history and physical examination,
of mortality in the Philippines. In 2015, these diseases led to almost
laboratory tests, pharmacologic and non-pharmacologic interventions.
200,00 deaths (35.3% of all deaths), causing more deaths among
Filipino men (111,403) than women (86,674).1 Atherosclerosis in the The group adopted several strategies in developing the
arteries remains as the major underlying pathology of cardiovascular recommendations. The first strategy is emphasizing on evidence-based
diseases (CVD). In the coronary vessels, atherosclerosis causes recommendations as recommended assessments and interventions.
myocardial ischemia. In the arteries supplying the brain, it leads to The second strategy is recognition of potential variations between-
stroke and cerebrovascular ischemia. In the peripheral circulation, it patient and between specific practice settings. The third strategy is the
causes claudication in the lower limbs.2 recognition of “stakeholder groups” in family and community practice
A well-established modifiable risk factor for atherosclerosis with careful attention to getting their opinion and support but without
is dyslipidemia or lipid disorders. Lipid disorders are derangements sacrificing the objectives of the clinical pathway’s implementation. The
in plasma lipoproteins and abnormalities in lipid metabolism. fourth strategy is emphasis on the commitment to establishment of the
Lipoproteins, specifically those containing Apolipoprotein B (ApoB), goal of improving the effectiveness, efficiency, and quality of patient
have an integral role in the development of atherosclerosis. ApoB care in family and community practice.
containing lipoproteins include low density lipoprotein- cholesterol For the first strategy, the authors searched for the latest guidelines
(LDL-C), intermediate density lipoprotein cholesterol (IDL-C), very low- of reputable international and local societies including but not limited
density lipoprotein cholesterol (VLDL-C) and the chylomicrons.3 The to American Heart Association, American College of Cardiology,
main initiating process to development of atherosclerosis is the entry European Society of Cardiology, European Atherosclerosis Society,
and retention of ApoB lipoproteins in the subendothelium of the arterial Philippine Lipid and Atherosclerosis Society and Philippine Heart
walls. This accumulation of ApoB lipoproteins in the arterial walls which Association. They also searched PubMed using the terms “dyslipidemia”,
depends on sustained plasma levels of ApoB lipoproteins, will trigger “diagnosis”, “therapeutics”, “family” and “community medicine”
a localized macrophage and t-cell- mediated inflammatory response. Retrieval of articles was focused on the following type of clinical
This will lead to subsequent steps of atheroma development or plaque publications: clinical practice guidelines, meta-analysis, randomized
formation.4 LDL-C, the most numerous among the ApoB-containing controlled trials and clinical trials. The more rigorous meta-analysis
lipoproteins, has consistently been proven to be associated with risk of clinical trials and observational studies were prioritized over low-
of ASCVD. Lowering the plasma LDL-C reduces the risk of developing quality trials in the formulation of the recommendations. The evidence
ASCVD and more.5 for the patient care processes were reviewed and summarized as notes
Almost 1 out of 2 Filipinos has increased serum total cholesterol to justify the recommendations. The second strategy was to present
(≥ 200mg/dl) and LDL-C (≥ 130mg/dl) - 47.2% and 47.5%, respectively. the recommendations to the PAFP Research Committee who acted as
According to the 2013 National Nutrition Survey Clinical Health Survey, panel of experts and discussed potential variations in different setting
women are more affected than men with 21.9% of them having LDL-C of family practice. As part of the third strategy, the clinical pathway
≥ 160mg/dl. Disease awareness, treatment and control of dyslipidemia will then be disseminated to the selected PAFP chapters and members
remain poor.6,7,8
and other stakeholders for consensus development. Dissemination
A multi-center, observational study done among 1868 participants
will be publication in the Filipino Family Physician Journal, conference
identified as having a need for preventive treatment for ASCVD showed
presentations (PAFP Annual Convention) and focused group discussions.
that among 1482 (79.3%) in secondary prevention group, only 67.5% were
As a fourth strategy, the implementation of clinical pathways to
prescribed with statin and only 18% met the recommended LDL-C goal.
be adopted by the PAFP will be quality improvement activities in a form
Among the 386 (20.7%) into the primary prevention group, only 30.1%
received statin therapy and only 10% met the recommended LDL-C goal.9 of patient record reviews, audit, and feedback. Audit standards will
be the assessment and intervention recommendations in the clinical
Objectives pathway. Implementation of clinical pathways will be at the practice
level and the organizational level. Practice level can be a simple count
This clinical pathway was developed to guide family and community of family and community medicine practitioners using and applying
physicians on the diagnosis and management of dyslipidemia. the clinical pathways. Organizational outcomes can be activities of
It provides recommendations to the following clinical decisions: the PAFP devoted to the promotion, development, dissemination, and
1) clinical history and physical examination; 2) laboratory and ancillary implementation of clinical pathways.
procedures to be requested; 3) pharmacologic interventions; 4) non-
pharmacologic interventions; and 5) patient outcomes to expect. Grading of the Recommendations
Methods of Development and Implementation Chosen members of the PAFP Research Committee met as a panel
and graded the recommendations as shown in Table 1. The grading
Members of the Philippine Academy of Family Physician (PAFP) system was a mix of the strength of the reviewed published evidence
Publication Committee reviewed the published medical literature and the consensus of a panel of experts. In some cases, the published
to identify, summarize, and operationalize the evidence in clinical evidence may not be applicable in Philippine family and community
216 THE FILIPINO FAMILY PHYSICIAN

practice setting, so a panel grade based on the consensus of clinical C - Panel members were divided that the recommendation
experts was also used. Thus, if the recommendation was based on a should be adopted and is not sure if it will be applicable in
published evidence that is a well done randomized controlled trial and many areas or will benefit many patients.
the panel of expert voted unanimously for the recommendation, it was
given a grade of A-I. If the level of evidence is based on an observational Evidence Grade Levels
study but the panel still unanimously considered the recommendation,
the grade given was A-II and if the level of evidence is just an opinion I - The best evidence cited to support the recommendation is
and the panel still unanimously recommended it, the grade was A-III. a well-conducted meta-analysis and randomized controlled
trial. The CONSORT standard may be used to evaluate a well-
Table 1. Grading of the recommendations. conducted randomized controlled trial.
II - The best evidence cited to support the recommendation is
Panel Grade Level Evidence Grade Level a well-conducted observational study i.e., match control or
1 2 3 before and after clinical trial, cohort studies, case control
studies and cross-sectional studies. The STROBE statement
A A-I A-II A-III
B B-I B-II B-III may be used to evaluate a well-conducted observational
C C-I C-II C-III study.
III - The best evidence cited to support the recommendation is
based on expert opinion or observational study that did not
Panel Grade Levels meet the criteria for level II.
A - All the panel members agree that the recommendation In the implementation of the clinical pathways, the PAFP Quality
should be adopted because it is relevant, applicable and will Assurance (QA) committee recommend adherence to guideline
benefit many patients. recommendations that are graded as either A-I, A-II or B-I. However,
B - Majority of the panel members agree that the the committee also recommend using sound clinical judgment and
recommendation should be adopted because it is relevant, patient involvement in the decision making before applying the
applicable in many areas and will benefit many patients. recommendation
Pathway Recommendations
Pathway Tasks
Visit History and Physical Examination Laboratory Pharmacologic Intervention Non-pharmacologic Intervention Patient Outcomes
First Visit • Perform thorough ASCVD risk • Request the following for • No pharmacologic Patient Interventions • Awareness of
assessment for all adults (Refer patients ≥ 45 years old and intervention if with no • Recommend low saturated fat diagnosis and risks
to Table 1) (A -I) all adult patients regardless of compelling indication (A-I) diet rich in fruits and vegetables (A-II)
age at increase cardiovascular (A-I) • Understanding
• Review patient’s present risk: NOTE: See variation • Prescribe regular exercise with and agreement
medications (A-I) a. Lipid Profile (B-I) below for pharmacologic appropriate frequency and to diagnostic,
b. Urine albumin-to- treatment. intensity (A-I) pharmacologic
• Probe regarding lifestyle creatinine ratio/ Urine • Advise smoking cessation (A-I) and non-
habits (diet, physical activity, protein dipstick test (A-I) pharmacological
smoking) (A-I) c. Alanine Transaminase Family Intervention treatment (A-II)
(ALT) (A-I) • Engage other family members,
• Conduct complete physical d. 12-L-ECG (A-I) especially spouses, to also
examination including the e. FBS (A-I) adopt the lifestyle interventions
following for assessment of prescribed (A-II)
cardiovascular risk (A-I): • Request for other
a. BP measurement laboratory examinations as Community-Level Intervention
b. Waist Circumference/BMI recommended by pathways/ • Promote the formation of a
c. Signs of ASCVD guidelines appropriate for the community-based lifestyle
patient with co-morbidities intervention program to reduce
• Utilize family assessment tools such as hypertension, diabetes cardiovascular risk (A-I)
(A-II) mellitus (DM) and ASCVD
Follow-up visit: Within 1- 2 weeks
• Assess risk for ASCVD using (III-A)
either calculator (B-I) or risk
factor counting method (A-I)

Pathway Tasks
Variation Proceed to second visit table if

patient (A-I):
• Already has laboratory
results
• Diagnosed with the
following:
o ASCVD
o Diabetes Mellitus (DM)
o Familial
Hypercholesterolemia
o Moderate-Severe
Chronic Kidney disease
(CKD)
Second Visit • Ask for symptoms pertaining to • Repeat lipid profile 6-8 weeks In the absence of Patient Interventions • Adherence to
development of ASCVD (A-I) after initiation of statin contraindications, start statin • Recommend low saturated fat lifestyle change
therapy (A-III) for the following: diet rich in fruits and vegetables (A-I)
• Check for compliance to (A-I) • Adherence to
agreed non-pharmacologic • Repeat ALT 6-8 weeks after • Give low-moderate • Prescribe regular exercise with diagnostic,
intervention (A-I) starting statin therapy for intensity statins as appropriate frequency and pharmacologic
high-risk patients (A-III) primary prevention for the intensity (A-I) and non-
• Repeat complete physical following: • Advise smoking cessation (A-I) pharmacological
examination with focus on the • Request CK if with myalgia o Individuals with DM • Discuss barriers and treatment, and
following (A-I): (A-I) (A-I) misperceptions to lifestyle other management
o BP measurement o Individuals with mild to change (A-III) plan (A-I)
o Waist Circumference/BMI moderate CKD (A-I) • Explain the dose, frequency, • Awareness of
o Signs of ASCVD o Individuals without intended effect, possible side symptoms to watch
ASCVD aged ≥ 45 years effects of medications and out for and adverse
• Review laboratory results (A-I) old with LDL -C ≥ 130 importance of medication effect of statins
AND with ≥ 2 risk adherence (A-III) (A-II)
• Reassess risk for ASCVD using factors (A-I) or • Awareness of goal
either calculators (B-I) or risk depending on the result Family Intervention LDL-C, target BMI
factor counting method (A-I) of the risk calculator • Engage other family members, and understands
(B-I) especially spouses, to also the importance of
adopt the lifestyle interventions achieving it (A-II)
• Give high intensity prescribed (A-II)
statins for individuals
diagnosed with Familial Community-Level Intervention
Hypercholesterolemia (A-I) • Promote the formation of a
community-based lifestyle
• Give high intensity statins intervention program to reduce
as secondary prevention for cardiovascular risk (A-I)
individuals with established
ASCVD (A-I) Follow-up visit:
• Immediately if with
development of muscle
symptoms while on statin
therapy or if with any adverse
event from medication (A-I)
• 6-8 weeks after initiation
of statin therapy if with no
development of adverse event
from medication (A-III)
Variations

Pathway Tasks
Continuing • Ask for symptoms pertaining to • Repeat lipid profile 8-12 weeks • For individuals already on Patient Interventions • Adherence to
Visit development of ASCVD (A-I) after dose adjustment (A-III) statin therapy and meeting • Recommend low saturated fat diagnostic,
target LDL-C, continue diet rich in fruits and vegetables pharmacologic
• Check for compliance to • Request CK if with myalgia statin therapy (A-I) (A-I) and non-
agreed non-pharmacologic (A-I) • Prescribe regular exercise with pharmacological
intervention (A-I) • For individuals already appropriate frequency and treatment, and
• For individuals on statin on statin therapy but are intensity (A-I) other management
• Repeat complete physical therapy who have already not meeting target LDL-C, • Advise smoking cessation (A-I) plan (A-I)
examination with focus on the achieved their LDL-C goal, increase dose of statin (A-I) • Discuss barriers and
following (A-I): compute for non-high-density misperceptions to lifestyle • Reduction in LDL-C
o BP measurement lipoprotein cholesterol (non- • Dose adjustment of statin change (A-III) level and CVD
o Waist Circumference/BMI HDL-C). (A-I) should be done for patients • Explain the dose, frequency, events (A-I)
o Signs of ASCVD with muscle symptoms intended effect, possible side
• For those patients who already depending on severity of effects of medications and • Improved quality of
• Review laboratory results (A-I) achieved target lipid levels, symptoms and results of importance of medication life (A-I)
repeat measurement should laboratory tests. (Refer to adherence (A-III)
• Reassess risk for ASCVD using be done bi-annually (B-III) Figure 3) (A-I) • Improved patient
either calculators (B-I) or risk Family Intervention satisfaction (A-I)
factor counting method (A-I) • For individuals with ASCVD • Engage other family members,
on maximally tolerated especially spouses, to also
• Check for compliance to lipid statin therapy not meeting adopt the lifestyle interventions
lowering agent and other target LDL-C add ezetimibe prescribed (A-II)
medications (A-I) (A-I)
Community-Level Intervention
• Check for drug-related • For patients with persistent • Promote the formation of a
adverse effects. For individuals hypertriglyceridemia community-based lifestyle
prescribed with statin, ask ≥ 500 mg/dl despite intervention program to reduce
about statin- induced muscle addressing lifestyle factors cardiovascular risk (A-I)
symptoms (A-I) and secondary causes of
elevated triglycerides, start Referral
fibrate therapy (A-I) • For patients uncontrolled on dual
therapy (statin and ezetimibe)
and lifestyle modifications, refer
patient to specialist (A-III)
Follow-up visit:
• Immediately if with
development of muscle
symptoms while on statin
therapy or if with any adverse
event from medication (A-I)
• If with no adverse event from
medication:
o 8-12 weeks after dose
adjustment of statin therapy
(A-III)
o biannually after patient
achieved target lipid levels
(B-III)
Variations

Notes On The Recommendations and carotid pulses should be determined to check for signs of ASCVD.
Advanced evaluation such as cardiac evaluation; vascular bruits; and
First Visit ankle-brachial index may be conducted. Physical manifestations of
dyslipidemia can also be assessed by looking for presence of tendon
Clinical History and Physical Examination xanthomas, eruptive xanthomas, , corneal arcus, lipemia retinalis and
xanthelasma.3,10,12,14,17
Most patients with dyslipidemia are asymptomatic and it is often With the findings that are obtained during the history taking and
discovered during a routine blood test. It can, however, lead to ASCVD physical examination, the individual’s risk for ASCVD can be assessed
which may manifest with symptoms (i.e., chest pain in coronary artery and become the basis of screening and management of dyslipidemia in
disease and leg pain when walking in peripheral arterial disease). the patient. The risk factors identified in the different clinical practice
History taking is essential in identifying individuals with high guidelines are summarized in Table 1: .3,11,12,13,14,15,16,17
risk for ASCVD.10 Medical conditions that increase a patient’s risk of
dyslipidemia and/or atherosclerotic cardiovascular disease include
abdominal aortic aneurysm, autoimmune or inflammatory disease Table 1. Risk factors for atherosclerotic cardiovascular disease from various clinical
(e.g., human immunodeficiency virus [HIV] infection or acquired practice guidelines on dyslipidemia.
immunodeficiency syndrome [AIDS], lupus, rheumatoid arthritis [RA],
periodontal disease, psoriasis), blood coagulation abnormalities, • Age (40-75 years)
chronic kidney disease, chronic obstructive pulmonary disease (COPD), • Sex (Male)
depression, erectile dysfunction, hypertension, hypertensive diseases of • Race (South Asian ancestry)
pregnancy or pre-eclampsia, impaired fasting glucose (IFG) or glucose • Lack of exercise
tolerance (IGT), diabetes, hepatitis C, metabolic syndrome, non- • History of smoking or tobacco use
alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis • IFG, IGT
(NASH), overweight or obesity, primary hypercholesterolemia, stress, • Elevated HbA1c
a history of pancreatitis, and prior cardiovascular or cerebrovascular • Diabetes
events.3,11,12,13,14,15,16,17 • Hypertension
Medications and medication classes have also been reported
• Blood coagulation abnormalities
to cause dyslipidemia.18 Anabolic steroids, selective estrogen
• Chronic Kidney Disease (eGFR 15–59 mL/min/1.73 m2)
receptor modulators, oral estrogens and progestins, highly active
• Chronic Inflammatory Conditions (HIV infection/AIDS, Lupus, Psoriasis, RA)
antiretroviral agents such as protease inhibitors for the treatment of
HIV, immunosuppressive medications (e.g., cyclosporine, mammalian • COPD
target of rapamycin [mTOR] kinase inhibitor), glucocorticoids, retinoids, • Depression
interferon, taxol derivatives, L-asparaginase, cyclophosphamide, • Metabolic syndrome (elevated waist circumference, elevated triglycerides, elevated blood
atypical antipsychotic agents, beta-blockers and thiazide diuretics are pressure, elevated glucose, and low HDL-C; total of 3 makes the diagnosis)
some of the medications noted to negatively affect lipid levels. Bile acid • Post-menopausal women
sequestrants, which are used mainly for reduction of cholesterol, may • Primary Hypercholesterolemia (LDL-C 160–189 mg/dL; non–HDL-C 190–219 mg/)
also elevate triglycerides and should be used cautiously in patients with • Stress
increased triglyceride levels.12 • History of ASCVD
Family history would also provide data that would help identify • History of Premature Menopause (before age 40)
high-risk individuals such as patients whose family members have
• History of Pre-eclampsia
dyslipidemia, hypertension, premature ASCVD (males < 55 years;
• Family History of premature ASCVD (males <55 years; females < 65 years)
females < 65 years.3,11,12,13,14,15,16,17 These findings, together with the
• Overweight or Obesity
other clinical and laboratory parameters, are among the criteria that
will help identify patients with familial hypercholesterolemia, which • Reduced ankle–brachial index
would warrant aggressive lipid management. • Elevations in apolipoprotein B (may be especially useful if hypertriglyceridemia
Social history should focus on lifestyle – use of tobacco, alcohol >2.3 mmol/L [>200 mg/dL] persists)
intake, diet and activity. These factors can contribute as secondary • High sensitivity C-reactive protein levels of 19.0476 nmol/L (2.0 mg/L) or higher
causes of dyslipidemia. In developed nations, high carbohydrate diet • LDL-C levels of 4.1 mmol/L (160 mg/dL) or higher
and sedentary lifestyle leads to dyslipidemia. Dyslipidemia is also • Lipoprotein(a) levels with elevations above 125 nmol/L (50 mg/dL) (especially useful in
caused by high alcohol intake and high saturated fat diet.12 those with a family history of premature ASCVD)
The focus of the physical examination are the anthropometric • Triglyceride levels persistently elevated above 2.0 mmol/L (175 mg/dL)
measurements and the cardiovascular system. The height and weight • Left ventricular hypertrophy
should be determined for the computation of the body mass index
• Microalbuminuria
[BMI] or the waist circumference should be measured to determine
• Proteinuria
if the patient is obese or overweight. The blood pressure, peripheral

The four major risk factors remain the same across the different LDL particles are the most abundant of the Apo-B containing
cited guidelines – dyslipidemia, diabetes, hypertension, and tobacco lipoproteins. Plasma LDL-C measure the cholesterol carried by LDL
use. The other factors are considered minor or risk enhancers, which particles. Thus, it mirrors the amount of LDL level in the circulation.
may be used to aid the clinician individualize the plan in managing TG-rich VLDL particles and their remnants carry most of the circulating
dyslipidemic patients. TGs. Therefore, the plasma TG concentration estimates the levels of
Besides the assessment of ASCVD risk, the different guidelines also circulating ApoB-containing TG-rich lipoprotein.3
recommend the use of risk assessment tools or calculators to compute A study which used two sets of single-nucleotide-polymorphism
for the 10-year ASCVD risk. The computed 10-year ASCVD risk is used to (SNP) genetic variants for Mendelian randomization analysis of causal
supplement the identified risk factors to serve as guide as to which type factors for coronary artery diseases showed that LDL-C was strongly
of therapy should be employed to the patient. There are several ASCVD associated with increased risk for CAD. It also demonstrated that HDL-C
risk assessment tools available, and they are as follows: Framingham was strongly associated with reduced risk for CAD. It was demonstrated
Risk Assessment Tool; Multi-Ethnic Study of Atherosclerosis (MESA) that TG is not a causal risk factor for CAD.21
10-year ASCVD (atherosclerotic cardiovascular disease) Risk with
Coronary Artery Calcification (CAC) Calculator; Reynolds Risk Score; Urine Albumin-to-Creatinine Ratio (ACR)/ Urine Protein Dipstick Test
UK Prospective Diabetes Study (UKPDS) Risk Engine for patients with
type 2 diabetes and; American College of Cardiology/American Heart In the Philippine guideline for dyslipidemia (2020), proteinuria
Association pooled-cohort ASCVD Risk Estimator.12 was considered as a risk factor for ASCVD.19 Proteinuria could be assessed
However, these risk calculators were not validated for the by measuring the urine albumin to creatinine ratio or by using urine
Filipino population. The 2020 Clinical Practice Guidelines (CPG) for the protein dipstick test. A meta-analysis published in 2011 showed a linear
Management of Dyslipidemia in the Philippines recommended the use association between log albuminuria and log risk for all-cause mortality
Risk Factor Counting as the method in identifying the risk of the Filipino without thresholds. Similar findings were demonstrated in studies with
individual for cardiovascular disease. The following are the risk factors dipstick data. The study concluded that in high-risk population, higher
to take in consideration: smoker, male, post-menopausal women, albuminuria and lower eGFR and are risk factors for cardiovascular
family history of premature coronary heart disease (CHD), BMI 25 and all-cause mortality independent of each other and of other
kg/m2, hypertension > 140/90 mmHg , proteinuria and left ventricular cardiovascular risk factors.22 Another similar meta-analysis published in
hypertrophy.19 2015 demonstrated that in the general population there is significant
improvement in the determination of cardiovascular outcomes with
Laboratory the addition of eGFR and ACR. Demonstrated improvement was larger
with ACR than with eGFR, and more apparent for heart failure and
Age for Dyslipidemia Screening cardiovascular mortality compared to coronary disease and stroke.
Smaller improvement was seen when dipstick proteinuria is used. The
In estimating the ASCVD risk, age is considered as part of the discrimination improvement with eGFR or ACR was especially apparent
major independent risk factors as noted in the pooled cohort used by for individuals with diabetes or hypertension but remained significant
the American Heart Association (AHA) Clinical Practice Guideline on with ACR for cardiovascular mortality and heart failure in those without
Dyslipidemia (2018). The age considered for dyslipidemia screening either of these diseases.23
in US population starts at 40 years old to 75 years old.20 However, in
the local setting, the recommended cut-off age for starting statin for Alanine Transaminase (ALT)
primary prevention is 45 years old for patients with no DM or CKD.19
This cut-off age is based on epidemiology of dyslipidemia among A study published in 2018 revealed that odds ratio for occurrence
Filipinos.17 of liver injury during statin therapy was 1.18 (95% confidence interval
In many primary prevention studies, 45 years was also the cut off (CI): 1.01-1.39).24 To identify patients where treatment may be
age for inclusion. Most of these studies also require the presence of at contraindicated or may need close follow-up, measurement of ALT as a
least two risk factors in their participants.17 marker of hepatocellular damage may be done. The European guideline
Hence, the authors recommend dyslipidemia screening for all on management of dyslipidemia recommends measurement of ALT
patients ≥45 years old and adult patients with two or more risk factors, before starting statin therapy.3
regardless of age, but with increased ASCVD risk.
12-Lead Echocardiography (12-L ECG)
Lipid Profile
Left ventricular hypertrophy (LVH) is a risk factor for ASCVD.17 LVH
Measurement of lipids and lipoproteins are needed to estimate could be assessed using 12L-ECG. A study published in 2012 showed
the risk of ASCVD. They are used to guide therapy. Apolipoprotein-B that independently of other cardiovascular risk factors, participants
(ApoB) -containing lipoproteins play a central role in the initiation and with ECG LVH had increase probability of experiencing any CVD event
progression of atherosclerosis. ApoB-containing lipoprotein are VLDL, before non-CVD death over 15 years of follow up. The study also showed
TG-rich remnant particles, and LDL.3 that coronary heart disease/nonfatal myocardial infarction is the most

probable first event among men with ECG LVH was. In contrast, heart focused on Mediterranean diet (consisting mainly of vegetables, fruits,
failure, followed closely by coronary heart disease/nonfatal myocardial whole grains, and healthy fats) found that an increase in adherence
infarction were the most probable events in women.25 score to the Mediterranean diet by 2 points resulted in 8% lowering
of overall mortality (RR 0.92 [0.91-0.93]), a 10% lower risk of CVD
Fasting Blood Sugar (FBS) (RR 0.90 [0.87-0.92]). The benefit of Mediterranean diet which was
characterized by high loadings of olive oil, non-starchy vegetables and
Presence of diabetes mellitus (DM) is an indication for giving cheese was also seen in meta-analysis done in 2019 that showed an
statin therapy as primary prevention for cardiovascular disease.19 inverse association of dyslipidemia and this type of diet (Odds Ratio
Macrovascular complications of DM include cerebrovascular (OR) 0.53, [0.30-0.95]).29 A more recent meta-analysis published in
disease, coronary heart disease, arrhythmias and sudden death, 2021 which included 37 guidelines, 108 systematic reviews, and 20
cardiomyopathy, and peripheral artery disease. The leading cause of randomized controlled trials (RCTs) found that foods rich in unsaturated
death among patients with DM is cardiovascular disease. Thus, to assess fat and contain only small amounts of saturated and trans-fatty acids
cardiovascular risk, we should screen for diabetes in adults.26 According in addition to plant sterols/stanols and high in soluble fiber caused at
to American Diabetes Association guideline in 2021, start of testing is at least moderate (i.e. 0.20-0.40 mmol/L) reductions in LDL-C.30
age 45 for the general population. However, it could be started earlier The 2020 Philippine CPG recommend use of Pinggang Pinoy for
for adults who are overweight or obese and have one additional risk Filipinos with dyslipidemia.19 Pinggang Pinoy is a food guide that
factor for DM.27 demonstrate the advisable amount by food group: Go, Grow and Glow
to take for each meal. The plate is divided into the following: ½ consist
Non-Pharmacologic Intervention of Glow foods including fruits and vegetables; 1/6 consist of Grow foods
such as meats, eggs, poultry, ﬁsh, beans and legumes and 1/3 consists
Patient- Centered Intervention of Go foods like rice, corn, bread, oatmeal, bread, and root crops (see
figure below).31
Diet and Physical Activity Increase physical activity is advocated for decreasing
cardiovascular risk by several guidelines on dyslipidemia.3 For Filipinos,
Several guidelines on management of dyslipidemia emphasized at least 150 minutes of moderate to high-intensity exercise per week is
the vital role of healthy diet in lowering LDL-C and decreasing ASCVD recommended.19
risk.3,19,20 A meta-analysis published in 2012 found that there is a Several studies have already proven the benefit of exercise on
reduction in the risk of cardiovascular events by 14% ( Relative Risk (RR) cardiovascular health. A meta- analysis published in 2015 found that
0.86, 95% CI 0.77-0.96) with the reduction of saturated fat done by exercise significantly raised absolute and relative cardiorespiratory
reducing and/or modifying dietary fat.28 Another meta-analysis which fitness among adults without cardiovascular disease. People in
Figure 1. Pinggang Pinoy Food Guide

Image from: Food and Nutrition Research Institute – Department of Health

the exercise intervention had lower triglycerides; higher HDL-C Family-Focused Intervention
and apolipoprotein A1; and lower fasting insulin and glycosylated
hemoglobin A1c.32 Another study published in 2016 showed that there There is limited number of studies focusing on family focused
is lower risk of CVD mortality by 23% (RR 0.77[0.71–0.84]), CVD interventions for patients with dyslipidemia. Studies focused mainly
incidence by 17% (RR 0.83 [0.77– 0.89]), and T2DM incidence by 26% on effect of spouses on lifestyle choices of patients. A cohort study
(RR 0.74 [0.72–0.77]) with an increase from being inactive to achieving published in 2015 showed positive association between individual
recommended physical activity level (150 minutes of moderate- changes and spousal changes in the sport/exercise and leisure indices.
intensity aerobic activity per week).33 The study demonstrated that the odds that an individual would meet
A meta-analysis done for US Preventive Services Task Force physical activity recommendation is higher if their spouse met these
showed that the behavioral interventions demonstrated a small, recommendations.39 A cross-sectional study published in 2018 showed
statistically significant between-group mean differences for systolic that there is correlation between sedentary behaviors with each other
blood pressure (−1.26mmHg [95%CI, −1.77 to −0.75]), diastolic blood among middle aged and older couples. These correlations were not
pressure (−0.49mmHg [0.82 to −0.16]), LDL-C (−2.58mg/dL [−4.30 moderated by attachment to one’s spouse. The concordance for physical
to −0.85], total cholesterol level (−2.85mg/dL [−4.95 to −0.75]), and activity was weaker than that for sedentary behavior.40 Another cohort
body mass index (−0.41 [−0.62 to −0.19] at 6 to 12 months among study published in 2018 aimed to determine the correlation of ideal
adults with no cardiovascular risk factors. The interventions also cardiovascular health variables among spousal or cohabitating partner.
showed small-to-modest associations with dietary and physical activity This study found that there was a low prevalence of ideal cardiovascular
behaviors.34 A similar but more recent meta-analysis which focused on health. The greatest concordances in achievement of ideal factor status
adults with cardiovascular risk factors showed that there is reduction were for the following: non-smoking (26.1%), ideal fruit and vegetable
of cardiovascular events, blood pressure, low-density lipoproteins, and consumption (23.9%), and ideal fasting blood glucose (35.6%). The
adiposity-related outcomes with the use of the medium- and high- highest odds of intracouple concordance were for smoking (OR, 3.6;
contact multisession behavioral counseling interventions for patients 95% CI, 1.9–6.5), fruit and vegetable consumption (OR 4.8; 95% CI
who have hypertension and dyslipidemia.35 2.5–9.3) and blood pressure (OR 3.0 [1.2–7.9]). It was also noted that
In patients with dyslipidemia who are overweight or obese, a person had 3-fold higher odds of attaining ≥3 ideal cardiovascular
weight reduction of even 5–10% of basal body weight lead to health variables if he or she had a partner who attained ≥3 components
improvement in lipid levels and positively affects the other (OR 3.0 [1.6–5.6]).41
cardiovascular risk factors. 3
Community-Oriented Intervention
Smoking Cessation
Community-based interventions to reduce cardiovascular risk have
Smoking cessation is beneficial to decrease cardiovascular disease been done in the past. One of this is the Complete Health Improvement
risk. An individual participant data meta-analysis published in 2006 Program (CHIP). It was formerly known as Coronary Health Improvement
showed that in men with diabetes, the hazard ratio (HR) comparing Project as it initially only targeted cardiovascular disease. However,
current smokers with non-smokers was 1.42 (1.10-1.83) for coronary because many studies have shown its efficacy in improving other chronic
heart disease, 1.10 (0.88-1.37) for total stroke and 1.15 (0.98-1.35) diseases, such as DM Type 2 and even depression, it was renamed in
for total CVD. Similar findings were demonstrated in men without 2012 the Complete Health Improvement Program.42 The first study
diabetes with the following hazard ratios computed: 1.47 (1.33-1.61) on the effectiveness of community- based CHIP was done in Rockford,
for coronary heart disease, 1.27 (1.16-1.39) for total stroke and 1.35 Illinois. The study’s intervention is a 40-hour educational curriculum
(1.27-1.44) and for total CVD. Irrespective of diabetes status, smoking delivered over a period of 30 days. Before and after intervention, clinical
cessation was found to lead to a 19% reduction in CVD risk.36 A and nutritional assessments were done. This study found that after
meta-analysis published in 2015 showed an increased risk of with the intervention, there is significant lowering in total cholesterol, LDL,
cardiovascular mortality (HR 2.07 [95% CI 1.82 to 2.36)]) for current triglycerides, blood glucose, blood pressure and weight with notably
smokers and for former smokers (HR 1.37[1.25 to 1.49]) compared with the greatest improvements among those at greatest risk. The authors
never smokers among people aged 60 year and older. Among smokers , concluded that well-designed community-based intervention programs
excess risk is increased with cigarette consumption in a dose-response can lead to improvement in lifestyle choices and reduction of coronary
manner. Among former smoker, excess risk decreases with time since risk factors.43 After this study, several other communities adopted CHIP. A
smoking cessation.37 study in Canada involving 1003 people enrolled in 27 CHIP interventions
A study done in 2019 showed a dose-response relationship hosted in community settings found that after 30 days, there were
between pack-years of smoking and three ASCVD namely peripheral significant overall reductions in the following parameters: BMI (-3.1%),
artery disease (PAD), coronary heart disease (CAD) and stroke. systolic BP (-7.3%), diastolic BP (-4.3%), total cholesterol (-11.3%), low-
The strongest relationship was seen in PAD. Lower risk of the three density lipoprotein cholesterol (-12.9%), triglycerides ([TG] -8.2%), and
ASCVD was seen with longer time from smoking cessation. However, FBS (-7.0%).44 Another study done in Appalachian patients showed that
significantly increased risk persisted up to 30 years following smoking after the CHIP intervention, participants had significant reduction in TC
cessation for PAD and up to 20 years for CHD or stroke.38 levels, HDL-C, LDL-C, FBG levels, BMI, and systolic blood pressure.45

Patient Outcomes Table 2. Target lipid levels.
After the initial consultation, the family physician must confirm

that the patient understood the disease, risks and agree to the diagnosis
and treatment plan. Patients’ awareness and understanding is an
important surrogate outcome of the effectiveness of health education
intervention. This can be measured in a form of patient recall. This is
asking the patient to repeat key information he/she learned from the
health education advice. This outcome was measured in an observational
study within a randomized controlled trial. In the trial patients recalled
43% (alcohol), 52% (diet) to 70% (exercise) of the discussions. This
active patient engagement and explicit conversations about the illness
and medications are associated with improved treatment information
recall.46 Understanding and adherence to the planned diagnostic and
management strategies may also be affected by the patient’s trust to
their family doctor. This trust rating been measured in some trials on
health coaching to patients with DM, hypertension or dyslipidemia.47
Table from: Executive Summary of the 2020 Clinical Practice Guidelines for the
Second Visit Management of Dyslipidemia in the Philippines17
Clinical History And Physical Examination ALT measurement 6-8 weeks after start of therapy for patients at high
risk for statin-induced liver injury. A study done in 2018 showed that
On the patient’s follow-up visit, evaluate the patient for that Fluvastatin and statin dose over 40 mg/daily significantly increased
occurrence of ASCVD from the initial consultation. Check for compliance the risk of hepatic injury with odds ratio of 3.50 (95% CI: 1.07–11.53)
to medications and the agreed non-therapeutic interventions. Ask for and 3.62 (95% CI: 1.52–8.65), respectively. Other patients that may
possible drug-related adverse effects. If statin was started during the be at high risk for statin-induced liver injury are elderly patients and
first visit, ask about statin-induced myopathy. Ask for concomitant patients with active liver disease with inflammation.24
intake of gemfibrozil; niacin; cyclosporine; azole antifungals;
macrolide antibiotics; HIV protease inhibitors; verapamil and diltiazem; Creatine Kinase (CK)
amiodarone and grapefruit juice for these may enhance the myopathy.13
Review and interpret the laboratory results if there are any and re-assess One of the adverse effects of statin therapy is statin-associated
the patient’s ASCVD risk taking the subjective and objective findings. muscle symptoms (SAMS). It is described as muscular pain and
tenderness without major functional loss.48 Another adverse effect
Laboratory of therapy with statin is myositis. It is defined as muscle symptoms
in association with a substantially high serum creatine kinase (CK)
Repeat Measurement of Lipid-Levels concentration. This adverse effect occurs rarely. CK elevations >10×
the upper limit of normal (ULN) occur in 1 per 1000 to 1 per 10 000
As mentioned above, lipoproteins are associated with ASCVD risk. people per year, depending on the statin, its dose, and the presence
They are used to guide therapy and have target levels for different of other risk factors.49 Patient at risk for myopathy include very elderly
patient groups (see Table 2). The European guideline recommend that with comorbidities, those with previous muscle symptoms and patients
for those patients on statin therapy not experiencing muscle symptoms, receiving interacting drugs.3
repeat lipid measurement should be done 4-12 weeks after starting Routine monitoring of creatinine kinase is not recommended.3,18
statin therapy or after dose adjustment. However, evidence concerning It should be monitored if previous CK was requested for an indication.
frequency of monitoring of lipids are limited and the guideline Check CK immediately in all patients who develops myalgia while on
recommendation come from consensus rather than evidence.3 In this statin therapy.3
pathway, it is recommended to repeat measurement of lipid profile 6-8
weeks after starting statin therapy. Pharmacologic Intervention
ALT Level Measurement Statins remain as the major lipid lowering therapy in conjunction
with lifestyle interventions.20 Statins lower cholesterol production in
Routine monitoring and control of ALT during treatment is not the liver by competitive inhibition of the enzyme HMG-CoA reductase
recommended but should be requested if indicated.3 Frequency of repeat which is needed for cholesterol biosynthesis. Lower levels of cholesterol
liver enzyme measurement to check for statin-induced liver injury varies intracellularly promote increased LDL receptor (LDLR) expression at the
across different guidelines. In this pathway, it is recommended to repeat hepatocytes’ surfaces. Consequently, there will be increased uptake of

LDL from the circulation and reduction of plasma concentrations of LDL- primary prevention studies in terms of the relationship between the
and other Apo B-containing lipoproteins.3 LDL-C difference and the event reduction rate.55
Statins are generally safe and well-tolerated. In a statement by
the American Heart Association published last 2018 the risk of adverse Statins for Patients with Mild to Moderate Chronic Kidney Disease (CKD)
effects of statins are the following: serious muscle injury (which
includes rhabdomyolysis) - <0.1%; serious hepatotoxicity is ≈0.001%; A meta-analysis done in 2014 investigated the effect of statin
and newly diagnosed diabetes mellitus ≈0.2% per year depending on therapy in patients with mild-moderate CKD. Statin therapy was
the underlying risk. There is a possible increased hemorrhagic stroke demonstrated to lead in the reduction of risk of the following: CVD
risk in patients with cerebrovascular disease, but the risk is clearly (24% reduction), total mortality (21% reduction), MI (34% reduction),
outweighed by the higher reduction in atherothrombotic stroke risk. stroke (30% reduction) and cardiovascular mortality (17% reduction).
There is no conclusive evidence that statins cause cancer, cognitive No statistically significant drug-related adverse events were noted in
dysfunction, cataracts, erectile dysfunction, peripheral neuropathy, and the study.56
tendonitis.50 More recently, a meta-analysis determined the effect of the
Statin could be subdivided into three categories based on how different statins on cardiovascular complications in patients with
much they lower LDL-C levels: High-intensity statins lowers LDL-C chronic kidney disease. The studies included mostly used moderate
levels by 50%, moderate-intensity statins by 30% to 49%, and low- intensity statins. Pravastatin (40 mg/day) was shown to significantly
intensity statins by <30% (Table 3).3 reduce patient mortality (OR 0.66 [0.46–0.91]) compared to placebo.
However, it must be noted that there are some racial differences in The following statins showed significant reduction in cardiac events:
lipid lowering effects of statins. In some Asian populations, lower doses Atorvastatin 80mg, Fluvastatin 40mg, Lovastatin 20mg, Pravastatin
of statins are needed to achieve the same percentage of lipid lowering 40mg, and Simvastatin 40mg. Pravastatin showed the best effect at
compared to the Western population.51 all-cause mortality rate in rank probability. Lovastatin, Fluvastatin, and
The beneficial effects of statins on cardiovascular disease Pravastatin showed good effects with the 1st, 2nd, and 3rd ranks in
prevention are already well-established.3,52 cardiac events.57
Statins for Patients with Diabetes Mellitus (DM) Statins for Patients with Multiple Cardiovascular Risk Factors
Cholesterol Treatment Trialists’ Collaborators conducted a meta- There are several meta-analyses done which revealed that
analysis in 2008 that was focused on the diabetic population. It showed statin therapy in patients at increased risk reduces all-cause
that statin therapy leads to a reduction in myocardial infarction (MI) or mortality, major coronary events, major cerebrovascular events,
coronary death (RR 0.78; 99 % CI: 0.69–0.87), coronary revascularization and revascularizations.58,59,60,61 A meta – analysis study done in 2019
(RR 0.75 [0.64–0.88]), and stroke (RR 0.79 [0.67–0.93]). Diabetic patients which investigated the effectiveness and safety of statins for primary
had similar effects of statin therapy regardless of prior cardiovascular prevention of CVD showed statistically significant reductions in the risks
disease (CVD) and other baseline characteristics. The authors concluded for following: non-fatal MI (risk ratio [RR] 0.62, 95% CI 0.53-0.72),
that statin should be given to all individuals with DM who have elevated non-fatal stroke (RR 0.83 [0.75-0.92]), ]), unstable angina (RR 0.75
risk of vascular events.53 In 2013, another meta-analysis reported that [0.63-0.91]), CVD mortality (RR 0.80 [0.71-0.91]), all-cause mortality
statins given for DM patients as primary prevention strategy lowered the (RR 0.89 [0.85-0.93]) and composite major cardiovascular events (RR
risk of CVD with pooled odds ratio of 0.757 (95% CI 0.676 -0.847).54 0.74 [0.67-0.81]).62
A recent randomized controlled trial conducted among Japanese Factors to take in consideration in risk assessment for
patients who have hypercholesterolemia and diabetic retinopathy in cardiovascular disease in Filipino patients as recommended by the
the primary prevention setting showed similar findings with previous Philippine Heart Association are as follows: male, post-menopausal
Table 3. Classification of statins
Boldface type indicates specific statins and doses that were evaluated in RCTs and the Cholesterol Treatment Trialists’ 2010 meta-analysis.
†LDL-C lowering that should occur with the dosage listed below each intensity. Individual responses to statin therapy varied in the RCTs and should be expected to vary in clinical practice.
‡Evidence from 1 RCT only: down titration if unable to tolerate atorvastatin 80 mg in the IDEAL (Incremental Decrease through Aggressive Lipid Lowering) study.
§Although simvastatin 80 mg was evaluated in RCTs, initiation of simvastatin 80 mg or titration to 80 mg is not recommended by the FDA because of the increased risk of myopathy, including
rhabdomyolysis.
Taken from: 2018 AHA/ACC/AACVPR/AAPA/ ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol20

women, smoker, family history of premature coronary heart disease, Statins for Patients with Atherosclerotic Vascular Disease (ASCVD)
BMI 25 kg/m2, hypertension > 140/90 mmHg proteinuria and left
ventricular hypertrophy.17 A meta-analysis done in 2013 found that statins produce
significant reduction in all-cause mortality (OR 0.82, 95% CI 0.75–0.90)
Statins for Patients with Familial Hypercholesterolemia (FH) and major coronary events (OR 0.69 [0.62–0.77]) compared to control
in patients with cardiovascular disease.65 In 2017 another meta-analysis
Familial hypercholesterolemia (FH) is an autosomal dominant on statins as secondary prevention strategy showed that statins were
disorder resulting from mutations in genes that encode proteins needed beneficial in terms of reduction in major vascular events. In terms of
in the LDL receptor endocytic and recycling pathways. These mutations types of intervention done in the studies, trials comparing statin vs. no
lead to reduced cellular uptake of LDL leading to higher levels of statin had RR 0.77 (95% CI 0.71–0.83) while trials of more-statin vs.
plasma LDL-C. People with heterozygous FH have 2x higher LDL-C levels less-statin had RR 0.88 (95% CI 0.82–0.93).66
compared to general population. Those with homozygous FH have A recent randomized controlled study investigated the effect
4x higher LDL-C levels. People with untreated FH has higher risk for of high-dose vs low-dose statin on the Asian population specifically
premature coronary artery disease (CAD) and stroke. 63 The Dutch Lipid Japanese patients who have stable CAD. The study compared high-dose
Network criteria could be used to identify individuals with Familial Pitavastatin (4mg/day) with low-dose Pitavastatin (1 mg/day.)67 A
Hypercholesterolemia.3 composite of nonfatal myocardial infarction, unstable angina requiring
emergency hospitalization, nonfatal ischemic stroke, and cardiovascular
death is the primary end point of this research. Reduction in this
Table 4. Dutch Lipid Clinic Network diagnostic criteria for familial hypercholesterolemia. endpoint was found with the use of high-dose Pitavastatin (HR 0.81;
95% CI, 0.69–0.95).67
Non-Pharmacologic Intervention
Patient-Intervention
There is only indirect evidence in the effectiveness of patient

education in medical adherence to therapy. A meta-analysis published
in 2019 which included 18 RCTs demonstrated a low to moderate
quality evidence on the improvements of medication adherence
with educational interventions. Education interventions benefited
participants with DM type 2 but not those with hypertension. No RCTs
were found for participants with hyperlipidemia since none fit the
eligibility criteria.68
Follow-up Visits
As mentioned above, myositis is a rare adverse effect of statins.

Thus, it is recommended that patients with muscle symptoms follow-
up immediately with their physicians for proper evaluation and
management.
For those patients on statin therapy not experiencing muscle
symptoms, follow-up could be done at the same time that repeat lipid
Taken from: 2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid measurements will be done: 6-8 weeks after starting statin therapy.
modification to reduce cardiovascular risk3
Patient Outcomes
After the second consultation, the family physician after providing

initial counselling and health education can already measure adherence
A systematic review and meta-analysis of epidemiologic studies to the advice on diet and lifestyle. Adherence to the interventions is
done in 2015 showed that participants with FH had a lower odd for very important to achieve the expected clinical outcome. Lifestyle
stroke following the general use of statin therapy (OR 0.251, 95% CI: and dietary changes are often difficult to follow especially with low-
0.176-0.358).63 In addition a cohort done in 2016 showed that giving intensity counselling which is often the only feasible method in
moderate to high intensity statins to patients with heterozygous FH family practice. However, in a simple clinical trial, measurement of
decreased the risk of CAD and mortality by 44%.64 adherence to diet is feasible. Dietary adherence can be evaluated by

using simple questionnaire or checklist. In the trial mentioned, this was A landmark randomized controlled trial done in 2015 which
associated with decreases in LDL-C levels.69 Aside from dietary changes, included 18,144 patients stabilized after acute coronary syndrome
improvement in physical activity can also be measured in the short term. demonstrated that significantly more patients given ezetimibe and
In one clinical trial, the participants exhibited a significant increase in simvastatin, in comparison with simvastatin alone, met LDL-C and high
physical activity and a borderline significant decrease in body weight.70 sensitivity C reactive protein (hs-CRP) targets. It was also shown after
In general, objectively measured and self-reported changes in diet and multivariable adjustment that reaching these targets was associated
physical activity are concordant with intermediate and clinical outcome with improved outcomes.73
findings. Lifestyle and dietary changes counselling have been associated A meta-analysis published in 2020 which compared combination
with other favorable clinical outcomes like lowering of CVD risks and ezetimibe and statin vs statin monotherapy on patients with ASCVD
events. But these findings can be realised during the continuing visits. demonstrated higher absolute reduction of LDL-C with combination
If pharmacologic intervention is prescribed during the second visit therapy (mean difference − 21.86 mg/dL; 95% CI − 26.56 to − 17.17)
awareness of the goals of treatment and the side effects must also be after 6 months of treatment or at a timepoint closest to 6 months.74
assured. The process of checking for the awareness has been described Another meta-analysis done in the same year focused on determining
in the patient outcome during the first visit. the efficacy of statin with ezetimibe therapy as secondary prevention
strategy in Asians. Combination therapy showed greater reduction
Continuing Visit of the following in comparison with control group: LDL-C (weighted
mean difference (WMD) − 0.39 mmol/L, 95% CI − 0.73 to − 0.05),
Laboratory triglycerides (WMD - 0.23 mmol/L [ − 0.33 to − 0.13]), and total
cholesterol (WMD − 0.31 mmol/L, [− 0.45 to − 0.17]). However, the
Non-High-Density Lipoprotein Cholesterol (Non- HDL-C) combination therapy had minimal effects on HDL-C and no effect hs-
CRP biomarkers in ASCVD.75
Non-HDL-C is a measure of the total cholesterol (TC) carried by all
atherogenic ApoB containing lipoproteins. This includes tryglyceride-
rich particles in VLDL and their remnants. It could be calculated as:
TC – HDL-C.3 A meta-analysis published in 2012 showed that among
statin-treated patients, there is an association between risk of future
major cardiovascular events and levels of LDL-C, non-HDL-C, and ApoB.
However, the strength of this association was greater for non-HDL-C
than for LDL-C and apoB.71 Another meta-analysis published in the same
year demonstrated that non-HDL-C decrease modestly outperformed
ApoB decrease for prediction of coronary heart disease (CHD) and CVD.72
Non- HDL C could be used as an additional target to decrease
cardiovascular risk for statin treated patients who already reached goal
LDL-C. Target non-HDL in various guidelines is set at 30 mg/dL above
target LDL-C.19
Frequency of Lipid Level Measurement
Guidelines differ on frequency of monitoring of lipid levels once

target is reached. It may range from 6-12 months.3 In this pathway,
it is recommended to repeat lipid measurement 8-12 weeks after dose
adjustment and bi-annually for those already on target lipid levels.
Pharmacologic Intervention
Management of Statin–Induced Elevation of Transaminases and Statin-

Associated Muscle Symptoms (SAMS)
Ezetimibe for Individuals with ASCVD on Maximally Tolerated Statin

Figure 2. Algorithm for patients who are on statins with elevated liver enzymes
Ezetimibe prevents intestinal uptake of dietary and biliary Taken from: 2015 Updated Clinical Practice Guidelines for the Management of Dyslipidemia
cholesterol leading to a reduction in the amount of cholesterol delivered in the Philippines15
to the liver. This causes the liver to upregulate LDLR expression which
leads to higher clearance of LDL from the circulation.3

Statin induced muscle symptoms should be managed as follows:19 493.0 (337-736.3) mg/dL. Findings were independent of lipid-lowering
medication(s) and prior nutrition counseling.76
Reduction of cardiovascular events is the primary goal of
pharmacotherapy for patients with dyslipidemia. Since studies have
demonstrated strong evidence that this reduction is achieved by
lowering LDL-cholesterol levels, the first step in the management
of patients with hypertriglyceridemia is to attempt to achieve the
target LDL cholesterol level. Statins could be used for this purpose.77
In addition, statins are also known to decreased triglycerides levels.
A study done in 2016 using data from VOYAGER meta-analysis which
included individuals treated with rosuvastatin, simvastatin and
atorvastatin showed that statin therapy results in mean triglyceride
reductions of -15.1% to -31.3%.78
Most patients with severe hypertriglyceridemia have elevated
VLDL and chylomicrons. Patients do not only have elevated risk of
ASCVD but also acute pancreatitis. Thus, therapies that target both
lipoproteins should be given. Statin therapy could be given. Persistence
of severe hypertriglyceridemia even after addressing lifestyle factors
and secondary causes of increased levels of triglycerides, fibrate therapy
could be initiated to prevent acute pancreatitis. If fibrate therapy is
needed in a patient already on statin, it is better to use fenofibrate than
gemfibrozil because of lower risk of severe myopathy.20
A meta-analysis published in 2014 showed that combination
therapy of statin and fibrate provided significantly higher reductions
in total cholesterol (Standard difference in means (SE) = 0.430; 95%
CI 0.315-0.545), LDL cholesterol (SE = 0.438 [0.321-0.555]) and
triglycerides (SE = 0.747 [0.618-0.876]). Combination therapy also
leads to significantly higher increase in HDL cholesterol (SE = 0.594
[0.473-0.715]) than treatment with statin alone. In the analysis of
safety, statin monotherapy was associated with a significant reduction
of the numbers for the following adverse event: liver-related adverse
events (RR = 0.396 [0.206-0.760]) kidney-related adverse events (RR
= 0.146 [0.075-0.285]) and total adverse events (RR = 0.665; 95% CI
0.539-0.819).79
Figure 3. Algorithm for Statin-induced Myopathy
Taken from Executive Summary of the 2020 Clinical Practice Guidelines for the Management Non-Pharmacologic Intervention
of Dyslipidemia in the Philippines19
Follow-up Visit:
Management of Persistent Severe Hypertriglyceridemia For those patients on statin therapy not experiencing muscle
symptoms, follow-up could be done at the same time that repeat lipid
Management of hypertriglyceridemia is dependent on the measurements will be done: 8-12 weeks after dose adjustment of statin
level of triglyceride elevation. Moderate hypertriglyceridemia is therapy and biannually for patient who already reached target lipid
diagnosed when fasting or non-fasting triglycerides 175-499 mg/dL levels.
(2.0-5.6 mmol/L). Diagnosis of severe hypertriglyceridemia requires a
fasting triglycerides ≥ 500 mg/dL (≥5.6 mmol/L). Before considering Patient Outcomes
pharmacologic treatment for hypertriglyceridemia, the following
should first be addressed/ treated: lifestyle factors (obesity and Measurement of intermediate and clinical outcomes can be done
metabolic syndrome), secondary factors (diabetes mellitus, chronic during the continuing visits. Lifestyle counselling in persons with
liver or kidney disease and/or nephrotic syndrome, hypothyroidism), CVD risk factors lead to reductions in total cholesterol, LDL-C, blood
and medications that increase triglycerides.20 pressure, fasting glucose, diabetes incidence, and weight outcomes.
A study published in 2015 showed that among those with severe Overall, counselling leads to a reduction in total cholesterol by an
hypertriglyceridemia who underwent nutritional intervention, there average of 4.48 mg/dL (95% CI, 6.36 to 2.59), and LDL cholesterol by
is reduction in triglycerides from median of 961.5 (611.5-1785.3) to 3.43 mg/dL (95% CI, 5.37 to 1.49). Counselling also reduces clinical CVD

Medicines For Dyslipidemia
Table 3. Pharmacologic options for management of dyslipidemia.
HMG-CoA reductase inhibitors/Statins - Lower total cholesterol, LDL, and triglyceride concentrations while increasing HDL concentrations80
Drug Dose Contraindications, Administration Considerations and Side Effects
Atorvastatin Usual initial dose: 10-40 once daily Contraindications: active hepatic disease or unexplained persistent
Max: 80 mg/day81 elevations in aminotransferase levels, pregnancy, and breastfeeding
Fluvastatin Usual initial dose: 20-40 mg once daily Administration considerations:

Max: 80 mg/day • Coadministration of simvastatin and gemfibrozil is contraindicated
Dose Adjustments: • Giving some statins in the evening is the recommended (e.g.,
• Mild-moderate renal impairment: No dosage adjustment needed Fluvastatin, Lovastatin, Pravastatin, and Simvastatin)
• Avoid administration of two 40 mg conventional cap at one time82
• Avoidance of grapefruit juice should be done with some statins
Pitavastatin Usual initial dose: 1-4 mg once daily to decrease CYP3A4 interactions that could lead in higher serum
concentrations
Dose Adjustments:
• Moderate – severe renal impairment and end stage renal disease • Coadministration of CYP3A4 substrate statins (atorvastatin,
(ESRD): Initial:1 mg once daily; Max 2 mg once daily lovastatin, and simvastatin) with medications that are potent 3A4
• If given with erythromycin or rifampicin, max dose of 1 mg or 2 mg inhibitors may lead to increased serum concentrations. Reduction of
respectively83 dose is recommended.
Rosuvastatin Usual initial dose: 5-10 mg once daily • Caution is advised when given with other drugs associated with
myopathy
Max: 20 mg once daily; a max of 40 mg once daily may be used only in
patients with severe hypercholesterolemia at high CV risk • Dose restrictions are recommended with the coadministration of
gemfibrozil or other fibrates with statins, and the use of more than
Dose Adjustments: one statin is not recommended
• CrCl 30-60 ml/min: Initially 5 mg once daily; Max of 20 mg once daily
• CrCl <30: contraindicated Side effects: myopathy, rhabdomyolysis (rare), hepatotoxicity (rare),
• Those with predisposing factors to myopathy or patients with Asian and diabetes mellitus80
ancestry: Initially, 5 mg once daily. 40 mg dose is contraindicated.84
Simvastatin 10 – 40 mg once daily

Max: 80 mg daily
Adjust dose according to patient response at intervals of at least 4 weeks
Dose Adjustments:
• CrCl<30 ml/min: Initially 5 mg once daily with close monitoring
• Patients taking fibrates (except fenofibrate): Max: 10 mg daily
• Patients taking amiodarone, amlodipine, ranolazine, verapamil,
diltiazem, elbasvir, grazoprevir: Max: 20 mg daily
• Patients taking lomitapide: Max: 40 mg daily85
Cholesterol absorption inhibitors - Reduce total cholesterol, LDL, Apo B, and non-HDL86
Drug Dose Contraindications, Administration Considerations and Side Effects
Ezetimibe 10 mg once daily87 Contraindications: Hypersensitivity to any ingredient of the formulation;

Concomitant use with an HMG-CoA reductase inhibitor among those
with active liver disease or unexplained persistent elevations in serum
transaminases, pregnant and breastfeeding patients; moderate to severe
hepatic impairment
Administration considerations:
• If co-administered with bile acid sequestrant: Take it at least 2 hours
before or 4 hours after taking bile acid sequestrants
Side effects:
Headache, runny nose, sore throat, body aches, back pain, chest pain,
diarrhea, joint pain, fatigue, weakness, rhabdomyolysis (rare)86

Peroxisome proliferator-activated receptor-α (PPAR-α) agonist/Fibrates- Reduce total cholesterol, LDL, triglycerides, and Apo-B. It increases HDL88
Drug 1-2 g daily in 2 divided doses Contraindications, Administration Considerations and Side Effects
Gemfibrozil Alternate dosing: 900 mg as a single dose in the evening Contraindication: Known hypersensitivity to the drug class, active
liver disease, active gall bladder disease, severe renal dysfunction,
• Should be given 30 mins before meals89 lactation88,89
Dose Adjustments: Administration considerations:

• Mild to moderate (GFR 30-80 mL/min/1.73m2): Initially, 900 mg daily • Gemfibrozil should not be used concomitantly with statin
• Severe Renal impairment: Contraindicated • When fenofibrate is to be used with statin, monitor serum creatinine
levels and renal function
Fenofibrate Standard micronised formulation:
• Initially, 67 mg tid or 200 mg once daily. Side effects: Deranged AST, ALT levels; infrequent elevations in serum
• May reduce to 67 mg bid, or increase to 67 mg 4 times daily, or 267 CPK (creatinine phosphokinase) levels; increase serum creatinine and
mg once daily according to response homocysteine levels; myopathy, cholelithiasis; venous thrombosis (rare)88
Non-micronised formulation:
• Initially 200-300 mg daily given in divided doses
• May be adjusted to 200-400 mg daily according to response
Improved bioavailability formulation:

• 40-160 mg once daily
• Should be taken with food90
outcomes. In one early good-quality trial, counselling in combination are included. Within PAFP chapters, peer group discussions, individual
with a protocol to start medication led to reduction in CVD events at 6.6 feedback and quality improvement reports are the main components.
years compared with usual care (relative risk [RR], 0.71 [95% CI, 0.51 to This model has been shown to improve the care process for urinary
0.99]). It also showed improvement on selected QOL measures. Adverse problems in one randomized clinical trial. This trial showed that
events are not common in counselling interventions.91 In several meta- prescribing of first choice appropriate management increased in the
analysis on statin treatment, CVD events, CVD risk levels i.e., LDL-C intervention group from but remained the same in the control group.94
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Diagnosis and Management of Dyslipidemia in Family Practice

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SPECIAL THEME

Diagnosis and Management of Dyslipidemia in Family Practice

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Variation Proceed to second visit table if

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Figure 1. Pinggang Pinoy Food Guide

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After the initial consultation, the family physician must confirm

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Table 3. Classification of statins

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There is only indirect evidence in the effectiveness of patient

As mentioned above, myositis is a rare adverse effect of statins.

After the second consultation, the family physician after providing

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Frequency of Lipid Level Measurement

Guidelines differ on frequency of monitoring of lipid levels once

Management of Statin–Induced Elevation of Transaminases and Statin-

Ezetimibe for Individuals with ASCVD on Maximally Tolerated Statin

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Table 3. Pharmacologic options for management of dyslipidemia.

Fluvastatin Usual initial dose: 20-40 mg once daily Administration considerations:

Simvastatin 10 – 40 mg once daily

Adjust dose according to patient response at intervals of at least 4 weeks

Drug Dose Contraindications, Administration Considerations and Side Effects

Ezetimibe 10 mg once daily87 Contraindications: Hypersensitivity to any ingredient of the formulation;

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Dose Adjustments: Administration considerations:

Improved bioavailability formulation:

• Should be taken with food90

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