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Atovastatin is a slctiv, comptitiv inhibit3-hydoxy-3-mthylglutayl-conzym A (HMG-CoA) ductas, th at-limiting nzym that convts 3-HMG-CoA tmvalonat, a pcusstols, including cholstol. Cholstol and tiglycids (TG) ciculat in th bloodstam as pat lipopotin complxs. With ultacntiugation, ths complxs spaat inthigh-dnsity lipopotin (HDL), intmdiat-dnsity lipopotin (IDL), low-dnsity lipopotin (LDL) and vy-low-dnsity lipopotin (VLDL) actions. TG and cholstol in th liv a incopoatd intVLDL and lasd intth plasma dlivy tpiphal tissus. LDL is omd om VLDL and is catabolizd pimaily though th high-ainity LDL cpto.
Myopathy should b considd in any patint with dius myalgias, muscl tndnss waknss, and/makd lvation CPK. Patints should b advisd tpot pomptly unxplaind muscl pain, tndnss, waknss, paticulaly i accompanid by malais v i muscl signs and symptoms psist at discontinuing ATOLIP CV . ATOLIP CV thapy should b discontinud i makdly lvatd CPK lvls occu myopathy is diagnosd suspctd.
Th dosag clopidogl in unstabl angina (UA) / Non-ST-lvatd myocadial inaction (NSTMI) is 75 mg daily at a singl loading dos. In patints with STMI, cnt MI, stok piphal aty disas, th commndd dos clopidogl is 75 mg onc daily.
Atovastatin, as wll as som its mtabolits, a phamacologically activ in humans. Th liv is th pimay sit action and th pincipal sit cholstol synthsis and LDL claanc. Dug dosag, ath than systmic dug concntation, colats btt with LDL-C duction. Individualization dug dosag should b basd on thaputic spons.
In animal modls, atovastatin lows plasma cholstol and lipopotin lvls by inhibiting HMG-CoA ductas and cholstol synthsis in th liv and by incasing th numb hpatic LDL cptos on th cll suac tnhanc uptak and catabolism LDL; atovastatin alsducs LDL poduction and th numb LDL paticls.
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