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124 Triglyceride And Cardiovascular Risk Whats New???

si-linetherapy in patients with mild –to-moderate hy- by 20-50% administration of 3 to 4 g/d of EPA plus
pertriglycerdemia.side effects of stains are reported DHA is required.
in about 10% of patients. They include muscle cramps,
weakness, and muscle aches. Rhabdomyolysis is Newer Hypolipidaemic Drugs:
very rare. Howeverstatins should be used with cau- Classification – Newer Drugs
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tion in elderly renal failure , and in the presence of
acute illness. Proprotein convertase subtilisin / kexintype 9 (pcsk9)
inhibitors Evolocumab,bococizumab, Alirocumab
Fibrates: Fibrates are PPAR-α agonists fibrates re-
duce triglyceride levels by 50%.Various trials with Apolipoprotein B synthesis inhibitor – Mipomersen
fibrates have shown reduction of Cv risk in patients Microsomal triglyceride transfer protein (MTTP)inhib-
with dyslipidemia. itor- Lopitamide
Fibrates reduces triglyceride levels through several
mechanisms Thyromimetic- Eprotirome

Increased fatty acid oxidation Cholestryl ester transfer protein (CETP) Ainhibitors-
Torcetrapib, dalcetrapib
Increased LPL synthesis
Dual peroxisome proliferator- activated Receptors
Reduced apo C-III expression Alpha /Gamma Agonist Saroglitazar: Saroglitazar(Li-
The net effect is a decrease in VLDL triglyceride pro- paglyn)
duction and an increase in catabolism of triglycer- In clinical studies,saroglitazar has demonstrated re-
ide-rich lipoproteins in moderate and severe hyper- duction of triglycerides (TG) LDL cholesterol,VLDL
triglyceridemia fibrates generally decrease triglycer- cholesterol,non –HDL cholesterol a characteristic
ide levels by 30-50% and sometimes increase HDL hallmark of atherogenic diabetic dyslipidemia(ADD)
cholesterol.
Saroglitazar is the only drug approved by Drug con-
Common adverse effects with fibrates are gastroin- troller general of india (DCGI).It is approved for the
testinal disturbances, rash, headache, pancreatitis, treatment of diadetic dyslipidemia and hupertriglycer-
myalgia, and myotoxicity, combining fibrates with idemia with T2DM not controlled on statin therapy.
48
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stains increases the myopathies 5.5% . Preexisting
severe renal dysfunctions, severe liver sysfunction, Other Measures:
and gall bladder disease are contraindications to ad-
ministration to fibrates. In patients with refractory hypertriglycerdemia com-
binations of statins,fibrates,nicotinic,acid and fish oil
Niacin: Niacin lowers triglyceride levels and increases may be used. Patients with marked symptoms with
HDL cholesterol levels. acute pancreatitis and hypertriglycerdemia have been
At doses of 500 to 2000 mg/d, niacin lowers tri- treated with plasma exchange/plasmapheresis. 49
glyceride by 10-30%, increases HDL cholesterol by In patients with type V hyperlipoproteinemia and
10-40%,and lowers LDL cholesterol by 5-20%. very high triglyceride levels refractory to therapies,
Also has Lp(a)- lowering effect. a study on five patients suggested benefit from orli-
stat. Orlistat is minimally adsorption of approximately
Complications of niacin therapy- hepatotoxicity im- 30% of ingested fat,and reduces intestinal chylomi-
paired glucose tolerance or hyperuricemia requiring corn synthesis. 50
laboratory monitoring
N-3 Fatty Acids: Many studies have demonstrated a Monitoring Response to Pharmacological
dose – dependent triglyceride- lowering effect of long management:
chain marine Omega-3 fatty acids(eicosapentaenoic Pharmacological therapies vary in time taken to re-
acid or EPA and docosahexaenoic acid or DHA).How- duce triglyceride levels.Effects with nicotinic acid is
ever, no studies using high –dose n-3 fatty acids in seen in 6 weeks, with fish oil in 2 weeks and a re-
hypertriglycerdemic patients have demonstrated any sponse to fibrates is seen as early as 2 weeks into
beneficial cardiovascular outcomes to date.
therapy with a maximal effect in 6-8 weeks. 51
Omega-3 fatty acids may be considered for treatment
of severe and very sever hupertriglyceridemia(>1,000
mg/dl), and to achieve a reductions of triglyceridemia

GCDC 2017