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Statinlarning hayotni uzaytirish nuqtai nazaridan qanday foydalari bor?

Statinlarning hayotni uzaytirish nuqtai nazaridan qanday foydalari bor?



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Yaqinda Buyuk Britaniya hukumati 50 yoshdan oshgan barcha kattalarga, istisnosiz, statinlarni qabul qilishdan foyda ko'rishni taklif qildi.

Menda keksa ayol qarindoshim bor, u kichik yurak xurujiga uchragan yoki bo'lmasligi mumkin (tashxis haligacha) va qon bosimi past. Ularga statinlardan foyda ko'rishlari taklif qilingan va mendan (sobiq biolog) ko'proq ma'lumot olishimni so'rashgan.

Men aniq ko'rinadigan harakat mexanizmlarini ko'rib chiqdim. Ammo klinik ma'lumotlar biroz chalkash.

Ko'rinib turibdiki, biz aniq aytishimiz mumkinki, foydalanuvchilarning kichik, ammo sezilarli soni nisbatan kichik nojo'ya ta'sirlar haqida xabar beradi va juda ozchilikda jiddiy holatlar mavjud.

Biroq, imtiyozlar nuqtai nazaridan, rasm unchalik aniq emas. Men yurak xastaliklarini qanday kamaytirishi haqida turli xil statistik ma'lumotlarni topdim, ammo bu hayot davomiyligi va hayot sifati nuqtai nazaridan nimani anglatishi aytilmagan.

Men ko'rib chiqqan bir maqolada, yurak xastaligi xavfi yuqori bo'lgan odamlarga statinlarni 30 yil davomida qabul qilish o'rtacha 9 oy davom etishi taklif qilingan.

Bu sayt muallifining sotadigan kitobi bor va boltasi bo'lishi mumkin. Ammo u erda bir nechta boshqa maqolalar mavjud - masalan, bu, bu va bu - statinlar klinik sinovlarga qaraganda xavfsizroq va kamroq foydali ekanligi haqida tashvishli da'volarni keltirib chiqaradi. Ayniqsa, ayollarga foyda keltiradigan juda cheklangan dalillar mavjud.

Men ularni xavotirli bema'nilik deb bilishga moyilman - ularda ularda isteriya hissi bor. Ammo mualliflar qonuniy ko'rinishini hisobga olsak, klinik tadqiqotlar ma'lumotlari bir -biriga mos kelmaydigandek (masalan, nojo'ya ta'sirlar haqida xabar bergan foydalanuvchilar foizi har xil) va bu qarindosh ekan, men ikkinchi fikrni olmoqchi edim. .

Xo'sh, kimdir raqamlarni aniqlab berishi mumkinmi va menga statinlardan foydalanishning hayot yillari va hayot sifati nuqtai nazaridan qanday foydalari borligini ayta oladimi? Yurak kasalligi bo'lgan yoki bo'lmagan ayollar uchun foyda bormi? Va ulardan foydalanish bilan bog'liq ba'zi tashvishlarga asos bormi?


O'ylaymanki, siz xohlaganingizcha ko'p sonlarni kesmayman, lekin bu erda asosiy fikrlar:

  • Statinlar qondagi llipid profilini yaxshilashning aniq qobiliyatini ko'rsatdi.
  • Ularni yurak xastaliklari uchun birlamchi/ikkilamchi profilaktikada qo'llanishi, qon lipidlari kamroq bo'lsa, arteriyalar tiqilib qolishi uchun lipidlar kamroq qoladi, degan ishonch bilan oqlanadi. Bu eski paradigma va u munozara qilinmoqda, hatto agar biz bugungi kunda haqiqatan ham barcha yurak potentsial bemorlariga statinlar bersak. Ushbu dorilarning ijobiy ta'siri haqida dalillar mavjud, ammo bu shubhasiz emas.
  • Statinlardan katta miqdordagi pul ishlab chiqariladi va farmatsevt ulardan foydalanish uchun juda qattiq harakat qiladi.
  • Ular istalmagan ta'sirga ega, lekin ular asosan erta ko'rinadi, shuning uchun bemorlar odatda ular uchun yaxshi kuzatiladi va ular hech qanday xavf tug'dirmaydi.

Ayollar mavzusida: menopauza oldidan ayollar o'zlarining gormonal profiliga ko'ra yurak kasalliklaridan himoyalangan va shuning uchun o'sha paytda statinlardan juda kam foyda olishlari mumkin. Menopauzadan so'ng, ayollarda erkaklar kabi yurak xavfi mavjud. Men bilmaymanki, tadqiqotlar postmenopozal ayollarda statinlar natijasida farq ko'rsatganmi yoki yo'qmi. Agar siz ko'proq bilmoqchi bo'lsangiz, men uni Pubmedda qidirishni maslahat beraman

Ogohlantirish: Yuqoridagilar professional tibbiy maslahatni anglatmaydi va muhokama qilinadi.


Xolesterolni kamaytiradigan statin preparatlari haqida 3 ta afsona

Agar siz yomon odatlaringizni almashtirsangiz (salom, kechqurun ovqatlanish va sevimli dasturini tomosha qilish), masalan, yugurish va uyda sog'lom ovqat tayyorlash kabi yaxshi odatlarga, siz xolesterin miqdorini me'yorda ushlab turish yoki to'g'ri yo'lda topasiz. diapazon.

Ammo ba'zida turmush tarzini o'zgartirish xolesterolni kamaytirish uchun etarli. Shunda shifokoringiz dori-darmonlarni tavsiya qilishi mumkin.

Statin preparatlari xolesterinni kamaytiradigan va Qo'shma Shtatlarda o'limning asosiy sababi bo'lgan yurak-qon tomir kasalliklarining oldini oladigan retsept bo'yicha dori-darmonlardir. Ko'pincha turmush tarzini o'zgartirgandan so'ng terapiyaning birinchi liniyasi bo'lgan statinlar insult, yurak xuruji va hatto yurak-qon tomir kasalliklaridan o'lim xavfini 25 foizga yoki undan ko'proq kamaytirishi mumkin. Agar siz allaqachon yurak-qon tomir kasalliklarini boshdan kechirgan bo'lsangiz, statinlar takrorlanish ehtimolini kamaytirish uchun uzoq muddatli profilaktik terapiyaning asosidir.

Statinlar yurak-qon tomir kasalliklari xavfi yuqori bo'lganlarga foyda keltirsa-da, ko'p odamlar ushbu toifadagi dori-darmonlarni qabul qilishdan xavotirda. &ldquoUmuman olganda,&rsquos statinlar xavfini bo'rttirib ko'rsatdi&rdquo, deydi Set Martin, M.D., M.H.S., Jons Xopkins universiteti tibbiyot fakultetining tibbiyot professori va Advanced Lipid Disorders Center direktori. & ldquoStatins ishonchli rekordga ega. O'nlab yillar davomida statinlarni qabul qilgan odamlarni kuzatib, biz ularning xavfsizligini aniqladik va ko'pchilik ularga hech qanday muammosiz toqat qilishini aniqladik. Lekin baribir, bu noto'g'ri tushunchalar saqlanib qolmoqda. & Rdquo


Xolesterin, statinlar va 70 yoshdan 90 yoshgacha bo'lgan uzoq umr ko'rish

Fon: Keksa odamlar, ayniqsa qariyalar orasida xolesterinning xavf omili sifatida ahamiyati munozarali. Giperkolesterolemiya tibbiy tashvishga sabab bo'ladimi yoki yo'qmi va statinlar juda keksa odamlar uchun foydalimi, hal qilinmagan umumiy klinik dilemmalar. Ushbu tadqiqot umumiy xolesterin (TC) ortishi 70 yoshdan 90 yoshgacha bo'lgan o'lim darajasining oshishi bilan bog'liqmi yoki yo'qmi va statinlar himoya ta'siriga egami yoki yo'qligini tekshiradi.

Usullari: Quddus bo'ylama kohort tadqiqotining (1990-2010) vakili namunasi (1920-1921) ochlik zardobidagi TC, past zichlikdagi (LDL) va yuqori zichlikdagi lipoproteinlar (LDL) uchun 70, 78 va 85 yoshda baholandi. triglitseridlar statinlaridan foydalanish ijtimoiy, funktsional va tibbiy sohalar va barcha sabablarga ko'ra o'lim ma'lumotlari (1990-2010). TC uzluksiz (10 mg/dL o'sish) yoki dichotomous o'zgaruvchi (yuqori TC & gt200 mg/dL) sifatida tahlil qilindi. Koks proportsional xavf modellari o'lim xavfi nisbatlarini (HR), TC, statinlar bilan davolash, jins, o'z-o'zidan baholangan salomatlik, chekish, gipertoniya, diabet, yurak ishemik kasalligi, neoplazma, tana massasi indeksi, albumin va triglitseridlarni aniqladi.

Natijalar: 70, 78 va 85 yoshda yuqori TC tarqalishi 75% (n = 344), 65% (n = 332) va 34% (n = 237), statinni ishlatish esa 0%, 17.9% va 45.4 ni tashkil etdi. %, mos ravishda. 70 dan 78 gacha, 78 dan 85 gacha va 85 dan 90 gacha bo'lgan TC >200 mg/dL ga nisbatan ≤200 mg/dL ga teng bo'lgan sub'ektlar orasida omon qolish (sezilarli darajada emas) oshdi: 79,1% ga nisbatan 73,3% (log darajasi P = .16) , 68.7% ga nisbatan 61.5% (P = .10) va 73.4% ga nisbatan 70.3% (P = .45). 78 dan 85 yoshgacha bo'lgan statinlar bo'lmagan bemorlar orasida omon qolish darajasi sezilarli darajada oshdi (74.7%, 64.3%, log darajasi P = .07) va 85 dan 90 gacha (76.2% - 67.4%, P = .01). Tuzatishdan so'ng, TC (uzluksiz yoki dixotomik) 70 dan 78 gacha, 78 dan 85 gacha yoki 85 dan 90 gacha bo'lgan o'lim bilan bog'liq emas edi. Aksincha, 85 yoshdagi statinlar 85 yoshdan 90 yoshgacha bo'lgan o'limning kamayishi bilan bog'liq edi (HR 0,61, 95% ishonch oralig'i 0,42-0,89).

Xulosa: Keksa odamlarda xolesterin darajasi 70-90 yoshidagi o'lim bilan bog'liq emas edi. Statinlarning himoya ta'siri, keksa odamlarda kuzatilgan.

Kalit so'zlar: Xolesterinning uzoq umr ko'rish bo'ylama kohorti eng qadimgi eski statinlarni o'rganadi.

Mualliflik huquqi © 2013 American Medical Directors Association, Inc. Elsevier Inc tomonidan nashr etilgan. Barcha huquqlar himoyalangan.


Yangi tadqiqot shuni ko'rsatadiki, statinlar o'pka saratoni bilan og'rigan bemorlarga foyda keltirmaydi

Yangi tadqiqotga ko'ra, kimyoterapiya bilan birgalikda ishlatiladigan xolesterinni kamaytiradigan dorilar o'pka saratoni bilan kasallangan bemorlarni davolash natijalariga ta'sir qilmaydi.

Statinlar bo'yicha so'nggi tadqiqotlar saraton rivojlanishining oldini olish yoki bir nechta keng tarqalgan saraton kasalliklari, shu jumladan o'pka saratoni bilan og'rigan bemorlarning omon qolish muddatini uzaytirishda dorilarning rolini da'vo qildi va shu sababli tibbiyot hamjamiyatida katta qiziqish uyg'otdi. Ammo London Imperial kolleji va UCL (London universiteti kolleji) jamoasi tomonidan e'lon qilingan dalillar shuni ko'rsatadiki, bu dorilar o'pka saratoni bilan kasallangan bemorlarga umuman foyda keltirmaydi.

Tadqiqot guruhi yangi dalillar shunchalik jozibadorki, saraton kasalligini davolashda statinlardan foydalanish bo'yicha mavjud yoki yangi rejalashtirilgan sinovlar qayta ko'rib chiqilishi kerak.

Cancer Research UK tomonidan moliyalashtirilgan tadqiqot jurnalida chop etilgan Klinik Onkologiya jurnali.

Statinlar bemorlarda xolesterin miqdorini pasaytirish orqali ishlaydi va odatda shifokorlar tomonidan yurak xuruji yoki insultning oldini olish uchun buyuriladi. So'nggi besh yil ichida chop etilgan bir qator kichik tadqiqotlar statinlarning saraton hujayralarining o'sishi va omon qolishini cheklash imkoniyatlarini o'rganib chiqdi.

Xolesterin hujayra o'sishi xabarlarida asosiy rol o'ynaganligi sababli, dastlab xolesterin darajasini pasaytirish saraton hujayralarining rivojlanishi va o'sishiga putur etkazishi mumkin deb o'ylangan. Xolesterin, shuningdek, davolanish tugagandan so'ng, saratonning qaytalanishini kechiktirishiga ishonishdi. Birgalikda bu ta'sirlar saraton kasallarining hayotini yaxshilaydi deb ishonilgan.

Immunitet guruhi saraton kasalligida statin terapiyasining eng katta randomizatsiyalangan sinovida kichik hujayrali o'pka saratoni bilan og'rigan bemorlarda pravastatin deb nomlangan etakchi statin ta'sirini o'lchadi - o'pka saratonining ayniqsa agressiv shakli, bu erda yangi davolash usullari juda zarur. .

Tadqiqot Buyuk Britaniyadagi 91 kasalxonadan 846 bemorni o'z ichiga oldi va UCL Saraton Institutidagi Cancer Research UK & UCL Cancer Trials Centerda o'tkazildi. Bemorlar tasodifiy ravishda statin yoki platsebo qabul qilish uchun tanlab olindi va ular ikki yil davomida kuzatildi. Natijalar shuni ko'rsatdiki, statinlarni qabul qilishning salbiy ta'siri bo'lmasa-da, afzalliklari ham yo'q.

"Xolesterin miqdori yuqori bo'lgan bemorlarda statinlarni qabul qilish odatiy holga aylanib bormoqda va ko'plab saraton kasallariga bu dorilar saraton kasalligini davolashdan alohida -alohida buyuriladi yoki buyuriladi", - tushuntiradi London Imperial kolleji tibbiyot fakulteti professori Maykl Sekl. tadqiqot. "Odamlar xolesterinni boshqarish uchun statinlarni qabul qilishni to'xtatishlari uchun hech qanday sabab yo'q, ammo kichik hujayrali o'pka saratoni bilan og'rigan bemorlar uchun statinlarni qabul qilish ularning saraton kasalligini davolash natijalariga hech qanday ta'sir ko'rsatishi ehtimoldan yiroq emas. Chunki barcha statinlar shunga o'xshash tarzda ishlaydi. xolesterin miqdori past bo'lsa, Pravastatindan boshqa statinlar boshqacha foydali ta'sir ko'rsatishi ehtimoldan yiroq emas.

Imperatorlik tadqiqotchilari statinlarning hujayra darajasida qanday ishlashini o'rganishni davom ettirishni rejalashtirmoqdalar, ammo ishonishadiki, yangi o'tkazilgan sinovlar keraksiz bo'lishi mumkin.

"Bizning natijalarimiz saratonning har xil turlarini tekshiradigan boshqa tasodifiy tadqiqotlar natijalariga to'g'ri keladi, lekin ular bizning tadqiqotlarimizdan ancha kichik edi va ular saraton kasalligini davolashda statinlardan foydalanishdan hech qanday foyda ko'rmadi", deydi direktor o'rinbosari, katta muallif professor Allan Xakshou. Saraton tadqiqotlari Buyuk Britaniya va UCL saraton sinovlari markazi. "Birgalikda, bu dalillar ishonarli ko'rinadi."

"Boshqa saraton turlari bo'yicha davom etayotgan statin sinovlari foyda keltirishi mumkin va shuning uchun ularning topilmalari mavjud bo'lganda ko'rish qiziq bo'lar edi. Biroq, menimcha, tadqiqotchilar saraton kasalligining bir qismi sifatida yangi statin sinovini boshlash yoki yo'qligini diqqat bilan o'ylab ko'rishlari kerak. davolash, biznikiga o'xshash keyingi yirik tadqiqotlar natijalarisiz.


Statin terapiyasidan nimani kutish kerak

Xolesterinni kamaytiradigan statinlar bir necha o'n yillar davomida yurak-qon tomir kasalliklarini davolashda birinchi o'rinda turadi. Nega? Bu ’s, chunki katta miqdordagi tadqiqotlar yurak xuruji va qon tomir xavfini kamaytirishda ularning afzalliklarini qo'llab -quvvatlaydi.

Klivlend klinikasi-notijorat akademik tibbiyot markazi. Saytimizdagi reklama bizning vazifamizni qo'llab -quvvatlashga yordam beradi. Biz Cleveland Clinic bo'lmagan mahsulotlar yoki xizmatlarni ma'qullamaymiz. Siyosat

Dori -darmonlar shu qadar keng qo'llanila boshladiki, agar sizga hali statin buyurilmagan bo'lsa, ehtimol, siz bir paytlar shunday bo'lasiz.

Profilaktik kardiolog Lyuk Laffin, tibbiyot fanlari doktori, statinlar LDL (yoki "yomon") xolesterinni kamaytiradi, bu esa aterosklerotik yurak-qon tomir kasalliklari xavfini kamaytiradi. (Bu arteriyalaringizning ichki devorlarida xolesterin, yog 'hujayralari va yallig'lanish birikmalarining to'planishi, ya'ni arteriyalarning "qattiqlashishi" yoki "tiqilib qolishi").

"Bundan tashqari, statinlar yallig'lanishni kamaytiradi, biz bilamizki, bu ateroskleroz va yurak -qon tomir kasalliklarini keltirib chiqaradi", deydi doktor Laffin.

Shunga qaramay, ularning ko'pgina afzalliklariga qaramay, statinlar (barcha dorilar kabi) siz bilishingiz kerak bo'lgan muhim yon ta'sirga ega. Shunday qilib, shifokoringiz bilan ushbu muhim dori -darmonlarning xavf -xatarlarini ko'rib chiqing va statin terapiyasiga bo'lgan ehtiyojingizni muhokama qiling.

Statinlarning afzalliklari qanday?

Statinlar jigarda xolesterin ishlab chiqarish uchun mas'ul bo'lgan ferment ta'sirini inhibe qiladi. Bu jarayonda ular LDL va umumiy xolesterinni sezilarli darajada kamaytiradi, shu bilan birga HDL (“yaxshi ”) xolesterin, triglitseridlar va yallig'lanishga foydali ta'sir ko'rsatadi. Ba'zi dalillar shuni ko'rsatadiki, yuqori intensivlikdagi statin terapiyasi arteriyalarda tiqilib qoladigan aterosklerotik blyashka o'sishini sekinlashtirishga va aksincha qaytarishga yordam beradi. Ular, shuningdek, ularni yorilishga kamroq moyil qilib, infarkt va insultga olib kelishi mumkin.

Doktor Laffin: "Biz LDLni qanchalik ko'p tushirishimiz mumkin bo'lsa, qon tomirlari va yurak xurujlari kabi yurakdagi salbiy hodisalar xavfini kamaytiramiz", deb tushuntiradi.

Statinlarning barchasi bir xil dorilar sinfiga mansub bo'lsa -da, ular qanchalik kuchli va LDL xolesterin miqdorini kamaytirishi bilan farq qiladi.

Sizning shifokoringiz Amerika kardiologiya kolleji/Amerika yurak assotsiatsiyasi xavf kalkulyatori va boshqa omillar kabi aterosklerotik yurak-qon tomir kasalliklari xavfini aniqlash uchun sizga statin terapiyasi kerak yoki yo'qligini aniqlash uchun asbobdan foydalanadi.

Statinlar odatda kuniga bir marta olinadi va umumiy shakllarda mavjud. "Atorvastatin va rosuvastatin haqiqatan ham hozirgi vaqtda kardiologiya va statinlarning ishchi otlari ekanligini ta'kidlash muhim", - deya qo'shimcha qiladi doktor Laffin. "Ko'pgina dorixonalarda odatda yuqori intensivlikdagi statinlardan biri bo'ladi. Ularni arzon va olish oson. Mening tajribamga ko'ra, sug'urta kompaniyalarining 99% hech bo'lmaganda bittasini, 75% dan ko'prog'i ikkalasini ham qamrab oladi.

Siz statinga nomzodmisiz?

Amerika Kardiologiya kolleji va Amerika yurak assotsiatsiyasining ko'rsatmalari quyidagi hollarda statin terapiyasini tavsiya qiladi:

  • O'rnatilgan aterosklerotik yurak-qon tomir kasalliklari bo'lgan odamlarda ikkilamchi profilaktika.
  • Genetik holat tufayli LDL xolesterin darajasi 190 milligramm desilitr (mg/dL) yoki undan yuqori bo'lgan odamlar.
  • LDL darajasi 70 mg/dL dan yuqori bo'lgan va aterosklerotik yurak -qon tomir kasalliklari bo'lmagan 40-75 yoshli diabetli odamlar.
  • Qandli diabetga chalingan kattalar 40-75 yoshda, 20% yoki undan yuqori aterosklerotik yurak-qon tomir kasalliklari rivojlanish ehtimoli yaqin 10 yil ichida (yuqori xavfli bemorlar).
  • LDL darajasi 70 dan 189 mg/dL va 10 yillik ASCVD xavfi 7,5% dan 20% gacha (oraliq xavf) bo'lgan 40-75 yoshdagi diabetga chalingan bemorlar, agar xavfni baholasa va ba'zi xavfni oshiruvchi omillar bo'lsa. * davolanishni afzal ko'rish.

* Bu omillar oila tarixida ASCVD, LDL darajasi doimiy ravishda ≥160 mg/dL, triglitseridlar darajasi doimiy ravishda ≥175 mg/dL, surunkali buyrak kasalligi, etnik kelib chiqishi, yallig‘lanish kasalliklari, metabolik sindrom va (agar o‘lchangan bo‘lsa) natijalarni o‘z ichiga oladi. Yuqori sezuvchanlikdagi C-reaktiv oqsil, lipoprotein (a) va apolipoprotein B. Eslatma: Ko'rsatmalar statin bilan davolanishni boshlash to'g'risida qaror qabul qilinmagan, xavfi o'rtacha bo'lgan odamlar uchun koronar arter kaltsiyini baholashni tavsiya qiladi.

Statinlarning yon ta'siri qanday?

Jigar fermentlarining ko'payishi. Bosh og'rig'i va ko'ngil aynishi kabi keng tarqalgan yon ta'sirlardan tashqari, statinlar vaqti-vaqti bilan jigar fermentlarining ko'payishiga olib kelishi mumkin, bu jigar yallig'lanishini ko'rsatadi. Biroq, ACC/AHA ning so'nggi ko'rsatmalari jigar fermentlarini tekshirishni faqat yuqori xavf ostida bo'lgan yoki jigar toksikligini ko'rsatishi mumkin bo'lgan statinli foydalanuvchilar uchun tavsiya qiladi. Bundan tashqari, statinlar qon shakarining ozgina ko'tarilishiga olib kelishi mumkin, bu ba'zi odamlarni 2-toifa diabetga olib kelishi mumkin. "Ammo, biz bilamizki, statinlarning foydasi ko'p populyatsiyalarda qondagi glyukoza o'sishining o'sishidan ustundir", deydi doktor Laffin.

Ruhiy xiralik. Ba'zi tadqiqotlar statinlarning kognitiv funktsiyaga ijobiy ta'sirini aniqlagan bo'lsa -da, ba'zi foydalanuvchilar preparatni to'xtatgandan so'ng o'tib ketadigan ruhiy xiralik va unutuvchanlik kabi muammolar haqida xabar berishgan. Umuman olganda, keng ko'lamli klinik tadqiqotlar statinni ishlatish bilan bog'liq kognitiv muammolarning ko'payishini ko'rsatmaydi, deydi doktor Laffin.

Mushaklardagi og'riq. Statin terapiyasi bilan bog'liq eng diqqatga sazovor nojo'ya ta'sirlardan biri mushaklarning og'rig'i va qattiqligidir, bu statin dozasi va quvvati ortishi bilan yanada og'irroq bo'lishi mumkin va ba'zi odamlarda dorilarga toqat qilmasligi mumkin. Ayrim statinlar - xususan, atorvastatin va simvastatin - bu yon ta'sirlarni keltirib chiqarishi ehtimoli ko'proq, boshqalari esa, rosuvastatin va pravastatin kabi, kam ta'sir ko'rsatadi.

Yon ta'sirlarni qanday kamaytirish mumkin

Ba'zi davolash mumkin bo'lgan sharoitlar (qalqonsimon bezning disfunktsiyasi va jiddiy D vitamini etishmovchiligi kabi) statinlarga nisbatan murosasizlikka yordam berishi mumkin. Shuning uchun ko'p miqdorda greyfurt (yoki sharbat) iste'mol qilish va ba'zi dori-darmonlarni qabul qilish mumkin. Ushbu omillarni bartaraf etish statin bilan bog'liq mushaklar ta'sirini engillashtirishi yoki oldini olishi mumkin. Bundan tashqari, ba'zi odamlar koenzim Q10 qo'shimchalarini qabul qilish yordam berishi mumkinligini aniqladilar, garchi ACC/AHA ko'rsatmalari ulardan foydalanishni tavsiya etmasa ham.

Statinni qabul qilishni to'xtatmaslik va mushaklarning yon ta'siri haqida doktoringizga xabar berish muhim. Shifokoringiz sizni kuchsizroq statinga o'tkazishi, dozani o'zgartirishi yoki boshqa dozalash strategiyalarini o'rganishi mumkin. Bu dori -darmonlarni har kuni yoki kamroq qabul qilishni o'z ichiga olishi mumkin. Bir oz sabr -toqat bilan, siz va sizning shifokoringiz sizga mos keladigan statin rejimini ishlab chiqa olasiz.

Doktor Laffin shunday deydi: "Odatda, siz hech bo'lmaganda haftasiga ikki marta bo'lsa ham, odamlar bardosh beradigan statin dozasini topishingiz mumkin". "Agar siz statinni har qanday dozada toqat qila olmasangiz, bizda boshqa dori -darmonlar bor, masalan, ezetimibe (Zetia ®) yoki PCSK9 ingibitorlari deb nomlanuvchi yangi dorilar: alirocumab (Praluent ®) va evolokumab (Repatha ®).

Katta yoshli odamlarda statinni qo'llash haqida nimalarni bilishingiz kerak

Aterosklerotik yurak -qon tomir kasalliklari uchun eng muhim xavf omili yoshdir. Shu bilan birga, statinlarning xavfi va foydasi keksa odamlarda, ayniqsa sog'lig'i muammosi bo'lgan odamlarda diqqat bilan ko'rib chiqilishi kerak.

Keksa odamlar, umuman olganda, statinlarning jiddiy yon ta'sirini yosh hamkasblariga qaraganda ko'proq boshdan kechirishlari mumkin. Ko'pgina keksalar bir nechta dori-darmonlarni qabul qilishadi, bu esa statinlar bilan salbiy dori ta'sirini boshdan kechirish ehtimolini oshiradi. Muhimi, boshqa kasalliklarga chalingan keksalar, umr ko'rish davomiyligini qisqartirsa, statin terapiyasining samarasini olmaydilar.

Shunday qilib, agar siz 75 yoshdan oshgan bo'lsangiz va ayniqsa sog'ligingizda boshqa muammolar bo'lsa - shifokor bilan statin terapiyasining ijobiy va salbiy tomonlarini muhokama qiling, deydi doktor Laffin.

"Statinlarning ta'siri odatda uzoq muddatli bo'ladi - biz yurak -qon tomir kasalliklari xavfini kamaytirish borasida besh yildan 10 yilgacha gaplashamiz", deb tushuntiradi u. "Shunday qilib, siz boshqa dori -darmonlarni qabul qilish xavfini muvozanatlashingiz kerak, shu 5-10 yil ichida siz boshqa narsadan o'lasizmi? Menimcha, boshqa raqobatdosh komorbidiyalari bo'lgan odam uchun statinlarni bekor qilish haqida gapirish juda o'rinli.

Ushbu maqola birinchi marta paydo bo'lgan Klivlend klinikasi erkaklar sog'liqni saqlash bo'yicha maslahatchisi.


Statinlarning qo'llanilishi va xavflari

Statinlar - bu qonda xolesterin miqdorini kamaytiradigan dorilar guruhi. Ular buni jigarda xolesterin ishlab chiqarish uchun zarur bo'lgan fermentni blokirovka qilish orqali amalga oshiradilar.

Xolesterin hujayra va tananing normal ishlashida muhim rol o'ynaydi. Ammo juda yuqori darajalar aterosklerozga olib kelishi mumkin. Bu arteriyalarda xolesterin o'z ichiga olgan blyashka to'planishiga va qon oqimining to'silishiga olib keladi.

Qonda xolesterin miqdorini kamaytirib, statinlar, shuningdek, angina deb ataladigan yurak xuruji, qon tomir va ko'krak og'rig'i xavfini kamaytiradi.

Tadqiqotchilarning hisob-kitoblariga ko'ra, Qo'shma Shtatlardagi 40 va undan katta yoshdagi odamlarning qariyb 30 foizi statinning qandaydir shaklini oladi. Quyida biz ushbu dorilarning qo'llanilishi, xavfi va mumkin bo'lgan afzalliklarini tasvirlaymiz.

Shifokorlar odatda qondagi xolesterolni pasaytirish uchun statinlarni buyuradilar. Ushbu dorilar xolesterin ishlab chiqarishga yordam beradigan jigar fermenti ta'sirini bloklaydi. Ular HMG-CoA reduktaza inhibitörleri sifatida ham tanilgan.

Statinlar tanadagi past zichlikdagi lipoprotein (LDL) xolesterin miqdorini kamaytirishi mumkin. Ba'zida odamlar bu turni "yomon" xolesterin deb atashadi. Statinlar yuqori zichlikdagi lipoprotein (HDL) yoki "yaxshi" xolesterin darajasini ham ko'tarishi mumkin.

Bundan tashqari, statinlar qondagi triglitseridlar deb ataladigan yog'lar miqdorini kamaytirishi mumkin.

  • atorvastatin (Lipitor)
  • fluvastatin (Lescol)
  • lovastatin (Mevakor)
  • pitavastatin (Livalo, Livazo)
  • pravastatin (Pravachol)
  • rosuvastatin (Crestor)
  • simvastatin (Zokor)

Atorvastatin va rosuvastatin eng kuchli, fluvastatin esa eng kam ta'sir ko'rsatadi.

Kombinatsiyalangan dorilar ham mavjud. Masalan, Vytorin - bu statin bo'lgan simvastatin va xun xolesterolining so'rilishini kamaytiradigan ezetimib preparatining kombinatsiyasi.

Simvastatin, atorvastatin yoki lovastatinni qabul qiladigan odamlar o'zaro ta'sir qilish xavfini kamaytirish uchun greyfurt va greyfurt sharbatidan voz kechishlari kerak.

Statinlarni qabul qiladigan ko'pchilik odamlar, agar mavjud bo'lsa, kichik yon ta'sirga ega. Kichik yon ta'siri quyidagilarni o'z ichiga olishi mumkin.

Ikkita jiddiy yon ta'sir - bu jigar etishmovchiligi va skelet mushaklarining shikastlanishi. Bular kamdan -kam uchraydi.

Xususan, statinlar har yili ushbu turdagi dori -darmonlarni qabul qiladigan har 10 ming odamdan birida mushaklarning shikastlanishiga olib kelishi mumkin. Odam statin qabul qilishni to'xtatgandan so'ng, zarar odatda qaytariladi.

Yana kamdan-kam hollarda, rabdomiyoliz deb ataladigan mushak shikastlanishining og'ir turi paydo bo'lishi mumkin, har yili bu turdagi dori-darmonlarni qabul qiladigan 100 000 kishidan 2-3 tasida.

Bundan tashqari, ba'zi tadqiqotlar statinlardan foydalanishni katarakt bilan bog'ladi. Biroq, 2017 yilda o'tkazilgan tadqiqotlar buning aniq dalillarini topa olmadi.

Bundan tashqari, statinlar odamning 2 -toifa diabet xavfini biroz oshirishi mumkin.

Va nihoyat, statinlar xotira muammolari bilan bog'liq bo'lishi mumkin, ammo dalillar aralashtiriladi. 2018 yilgi sharhga ko'ra, statinlar vaqtinchalik xotira buzilishiga olib kelishi mumkin, ammo ular yoshga bog'liq kognitiv pasayishdan himoya ta'siriga ham ega bo'lishi mumkin. Bu borada tadqiqotlar davom etmoqda.

Rabdomiyoliz nima?

Rabdomiyoliz dastlab mushaklarning og'rig'iga sabab bo'ladi va mushaklarning sezilarli buzilishi yoki buyrak etishmovchiligiga olib kelishi mumkin. Kamdan kam hollarda o'limga olib kelishi mumkin.

Bu holat, statinni rabdomiyoliz xavfiga olib keladigan yoki qondagi statin darajasini ko'taradigan boshqa dori bilan birgalikda qabul qiladigan odamlarda ko'proq uchraydi.


Statinlar bo'yicha statistika: 50 yoshdan oshgan sog'lom kattalar ularni qabul qilishi kerakmi?

50 yoshdan oshgan har bir kishi xolesterinni pasaytirish uchun statinlar qabul qilishi kerak, deb o'tgan hafta tahririyatda ta'kidlangan. Lancet. Ushbu maqola o'z tavsiyasini xuddi shu nashrda chop etilgan 27 ta klinik sinovning meta-tahliliga asoslangan bo'lib, statinlar sog'lom odamlarda yurak xuruji va boshqa yurak-qon tomir kasalliklari xavfini sezilarli darajada kamaytiradi, degan xulosaga keldi. Meta-tahlil va#39s topilmalari haqida xabar beradigan keyingi maqolalar nashrda chop etildi Qo'riqchi, Forbes va Buyuk Britaniya Telegraf. Ammo raqamlarga asoslanib, ko'plab mutaxassislar hali ham dorilarning foydalari ularning xavflaridan ustun ekanligiga ishonchlari komil emas.

Statinlar yurak -qon tomir kasalliklari bo'lgan odamlarga buyurilganda hayotni saqlab qolishiga hech qanday shubha yo'q. Ammo dori-darmonlarni yuqori xolesterin yoki boshqa yurak-qon tomir xavf omillari bo'lmagan sog'lom odamlarga ham berish kerakmi, uzoq vaqtdan beri va munozarali savol bo'lib kelgan. 2008 yilda JUPITER nomi bilan ma'lum bo'lgan yirik klinik tadqiqotlar rosuvastatin (Crestor) sog'lom odamlarda yurak xurujlari va boshqa hodisalar xavfini 44 foizga kamaytiradi, ammo ekspertlar o'sha paytdan boshlab uning metodologiyasi haqida savol tug'dirishdi, chunki sinov erta to'xtatilgan, bu esa mumkin. dorining foydasini haddan tashqari baholash samarasini yaratdilar. Hozirgi meta-tahlil muammoni hal qilishga yordam berish uchun yaratilgan. & quot; Bizning maqsadimiz-mavjud bo'lgan barcha dalillarni to'plash edi & quot;-tushuntiradi Angliya Oksford universiteti epidemiologi Kolin Baigent.

165 149 kishi ishtirok etgan 27 ta sinov natijalarini birlashtirgandan so'ng, meta-tahlil shuni ko'rsatdiki, odamlarda xolesterin kutilgan miqdorda pasayganidan keyin yurak xuruji, insult yoki bypass jarrohligi kabi jiddiy qon tomirlari bilan kasallanish ehtimoli 21 foizga kamroq. bir yil davomida statinlarni qabul qilgandan keyin, xuddi shunga o'xshash, tabletkalarni qabul qilmaydigan odamlarga qaraganda. Ammo sog'lom odamlarda bunday natijalar kamdan-kam uchraydi, shuning uchun xavfning kamayishi kichik klinik foyda keltirdi va umumiy xavfni yiliga 4,04 foizdan 3,27 foizga, farq 0,77 foizga qisqartirdi.

Boshqacha qilib aytadigan bo'lsak, faqat bitta istalmagan sog'liq oqibatining oldini olish uchun taxminan 130 kishi bir yil davomida statinlarni qabul qilishi kerak va bitta o'limning oldini olish uchun 500 kishi ularni qabul qilishi kerak. & quot; Agar siz juda past darajadagi xavf darajasiga tushib qolsangiz, foyda juda kichik bo'ladi & quot; Baigent tan oladi.

Mutaxassislar meta-tahlilga kiritilgan mavzular haqida ham savollar berishadi. Ko'rib chiqish qon tomir kasalliklari xavfi past bo'lgan odamlarda statinlarning ta'sirini baholash uchun mo'ljallangan bo'lsa-da, aslida uning ishtirokchilarining 60 foizi allaqachon bor edi qon tomir kasalligi. & quot; Nega yurak xastaligi bilan og'rigan odamlarni birlashtirmaslik kerak? Bu haqiqatan ham chalg'itadi, - deydi Londonning Sent -Jorj universiteti kardiologi Kausik Rey. 2010 yilda Rey va uning hamkasblari yurak-qon tomir kasalliklari bo'lmagan 65 229 ta sub'ektni o'z ichiga olgan 11 ta statin klinik tadkikotining meta-tahlilini e'lon qilishdi va statinlar sog'lom odamlarda o'lim xavfini kamaytirmaydi degan xulosaga kelishdi. (Qon tomir kasalliklari bo'lgan odamlarni qo'shib, Lanset Meta-tahlil statinlar va 39-sonli imtiyozlarni ortiqcha baholadi: kichik guruh tahlillari shuni ko'rsatadiki, qon tomir kasalligi bo'lmagan odamlar orasida statinlar yurak-qon tomir kasalliklarining mutlaq xavfini yiliga 0,4 foizga kamaytiradi.)

Va yon ta'siri haqida nima deyish mumkin? Statinlar gemorragik insult, mushaklarning og'rig'i va boshqa og'ir (lekin kamdan -kam uchraydigan) mushaklar va jigar asoratlari xavfini oshirishi uzoq vaqtdan beri ma'lum. 2012 yil fevral oyida AQSh oziq-ovqat va farmatsevtika idorasi iste'molchilarni dorilar diabet va xotira yo'qotish xavfini oshirishi mumkinligi haqida ogohlantirdi. Shunga qaramay, Lanset tahlillar shuni ko'rsatadiki, bu nojo'ya ta'sirlarning ehtimoli juda past, har 2000 davolangan odamdan faqat bittasi gemorragik insultga uchraydi. "Foydalar xavf-xatarlardan sezilarli darajada kattaroqdir, hatto juda past darajadagi xavflarda ham", - deydi Baigent.

Shunga qaramay, ba'zi ekspertlar topilmalar haqiqiy xavfni kam baholaydilar. San -Frantsiskodagi Kaliforniya universiteti kardiologi va bosh muharriri Rita Redbergning so'zlariga ko'ra Ichki kasalliklar arxivi, tahlilga kiritilgan sinovlardan birining boshlanishidan oldin, potentsial sub'ektlarga qanchalik yaxshi toqat qilishlarini ko'rish uchun bir necha hafta davomida statinlar berildi. Agar biron bir odam yon ta'sirga duch kelgan bo'lsa, ular sud jarayoniga taklif qilinmagan. Oldindan ko'rishning bu turi "toza fan emas", deydi Vinay Prasad, Shimoli -g'arbiy universiteti Feinberg tibbiyot maktabining internisti, chunki bu dorilar haqiqatdan ham xavfsizroq ko'rinadi.

Moliyalashtirish va tarafkashlik masalasi ham bor. Meta-tahlilga kiritilgan deyarli barcha sinovlar qisman farmatsevtika kompaniyalari tomonidan moliyalashtirildi va meta-tahlillarning hammualliflari ham dori kompaniyalaridan mukofot oldi. Garchi bu faktlar natijalarning haqiqiy emasligini anglatmasa ham, 2003 yilda nashr etilgan Britaniya tibbiyot jurnali Dori kompaniyalari tomonidan moliyalashtiriladigan sinovlar mustaqil tashkilotlar tomonidan moliyalashtiriladigan sinovlarga qaraganda, ularning mahsulotlari haqida ijobiy natijalar haqida xabar berish ehtimoli ko'proq ekanligini ko'rsatadi. "Sanoatdan o'z tadqiqotlarini o'tkazishni so'rash, rassomdan o'z ishining mukofotga sazovor bo'lishi yoki yo'qligi haqida o'z ishini baholashini so'rashga o'xshaydi", deydi Prasad. & quot; Bu shubhalanishning yana bir sababi. & quot

Agar meta-tahlil natijalari aniq va nojo'ya ta'sirlar kamdan-kam bo'lsa ham, & quot; millionlab odamlarni ozgina foyda keltiradigan dori-darmonlarga sarflash iqtisodiy jihatdan samarasizmi? Bostondagi Brigham and Women 's kasalxonasida dori. Dori-darmonlarning arzon narxlardagi umumiy versiyalari mavjud va mdashWalmart bir oyda past dozali lovastatinni 4 dollarga sotadi, lekin ko'p iste'molchilar qimmatroq tovar nomlari variantlarini tanlaydilar. Masalan, 2011 yilda amerikaliklar AstraZeneca 's Crestor -ga 4,4 milliard dollar, Pfizer va Lipitor -ga esa 7,7 milliard dollar sarflashgan.

Shunday qilib, sog'lom odamlar ko'proq statinlarni olishlari kerakmi? Baigentning ta'kidlashicha, bunday qilish millionlab odamlarning hayotini saqlab qolishi mumkin, chunki ko'p yurak xurujlari xavfi past bo'lgan odamlarda uchraydi. Lekin qanday narxda? "Ko'p odamlar statinlarni qabul qilishadi, ulardan hech qanday foyda yo'q va ular juda ko'p noxush hodisalarga duch kelishadi", deydi Redberg.


Statinlar hech kimga foyda keltirmaydi

LDL xolesterolini kamaytirish yomon fikr

Ko'pchilik tibbiy veb -saytlarda LDL xolesterinining ko'payishiga olib kelishi ma'lumsan'at kasalligi. Biroq, bu yolg'on. Bugungi kunda bu noto'g'ri ekanligini tasdiqlovchi ko'plab tadqiqotlar mavjud, ammo bu tushuncha saqlanib qolmoqda. Kichik LDL zarrachalari hajmi yurak kasalligi bilan bog'liq, shuning uchun homosistein, CRP, yuqori insulin, yuqori glyukozalangan oqsillar, A1c yuqori Lp(a), pishmagan HDL zarralari, yuqori temir zahiralari va boshqalar. Yurak kasalligi rivojlanishi bilan bog'liq bo'lgan narsalar ro'yxati uzoq va ularning hech biri dispozitiv emas. Qizig'i shundaki, past xolesterin depressiyadan saratongacha bo'lgan hamma narsa bilan bog'liq. Statistika bo'yicha kechirim so'raganlar buni ko'p bahonalar bilan baholaydilar, ammo xolesterin miqdori pastligi va boshqa kasalliklar o'rtasida qanday bog'liqlik borligini hech kim bilmaydi.

Amerika tibbiyoti 40 yildan beri xolesterinni pasaytiradigan haqiqiy salib yurishida. Odamlarga xolesterin miqdori past bo'lgan taomlarni iste'mol qilish va xolesterinni kamaytiruvchi dori-darmonlarni, xususan statinlarni qabul qilish buyurilgan. Tananing kasallikni davolashga qanday intilishlarini bilganimdek, men har doim bunga shubha qilardim. Agar tanada xolesterin miqdori past bo'lsa, hamma narsa bir xil bo'lsa, u allaqachon bo'lar edi - tabletka kerak emas.

Darhaqiqat, 2002 yilda dori sanoati ezetinib (Zetia, Vytorin) deb ataladigan xolesterinni kamaytiradigan statin o'rnini bosuvchi vositani ishlab chiqdi. U statinlarga toqat qilmaydigan odamlar yomon xolesterinni kamaytirishi uchun maxsus ishlab chiqilgan. Ammo, eksetimiba, agar yolg'iz ishlatilsa, nafaqat yurak xurujining oldini olmagan, balki saratonni ham sezilarli darajada oshirgan. Ko'rinib turibdiki, bu tibbiy xato, FDAga hali ham mavjud bo'lgan va keng tarqalgan retsept bo'yicha yuborilgan dori -darmonlarni olish uchun etarli emas edi. So, whatever the merits of lowering cholesterol as evidenced by statins lowering cholesterol, it was not as simple as ‘lower cholesterol and everything will be fine.’ The failure of this drug should have put the simple ‘lipid hypothesis’ to rest. By the way ‘the lipid hypothesis’ is the generic term for the whole cholesterol model of disease.

“BUT, BUT, BUT, statins reduce heart ‘events’. There’s surely a benefit.” This is true, but who benefits? If you consider ‘all cause mortality’, rather than considering just heart events, the picture is not so sanguine. No category of women, with or without pre-existing heart disease is helped overall. For men with no pre-existing heart disease, no benefit either. For men over 80, no benefit. We have now ‘sliced and diced’ the benefit group down to “men, under 80, with pre-existing heart disease may get benefit from statins.” For that group, maybe. Even this is controversial. Not quite the wonder drug hoped for. More than that, there is an increase in non-heart related deaths. Hmmmm.

Are there positive uses for statins? Ha. The most striking example, and the secret of its use revealed, is this: if atorvastatin is infused at the time of a coronary catheterization then there are fewer heart complications, including death, from the procedure. Now this immediate benefit is obviously not from lowering cholesterol. It is from calming ‘endothelial inflammation:’ the metabolic fire in the lining of damaged arteries is dampened. This is a good thing. Congratulations statins!

We know that unstable plaque, the damaged area of an artery, is the source of the clotting trigger that brings on a heart attack. We further know that inflammation is what destabilizes these areas of damage. Decrease the intimal inflammation and you get fewer heart attacks and bingo you also now know the real benefit of statins.

However, are the 30,000,000 Americans currently taking statins receiving benefit? In almost all cases, the answer is ‘no benefit:’ by any measure no more than 1 or 2 per hundred and probably much less than that in most populations.

Recent studies show 20% percent of statin users report side effects: 10% have muscle pain and damage, sometimes permanent, the rest are divided between liver damage, kidney damage, adult onset diabetes, cataracts, depression and memory loss.

Summary: Statins are effectively proven to be of no benefit to most, if not all, segments of the population. There are some specific uses, and that’s that.

Even though I question whether any of you would benefit from statin therapy, almost all of you could benefit from inflammation reduction. Do you need to address this? Quantitative Medicine can easily answer that one. C-Reactive Protein, or CRP, is a quite general inflammation marker, easily determined with a blood draw. Is yours high? If so, something is amiss. Could be heart disease. Could be allergy, genetics, cancer, a cold, or a lot of other things. However, you need to figure out the bad actors and reduce them to see if CRP goes down. Diet and exercise can play a strong role here. If you do reduce it, you reduce your heart attack risk enormously, far more than even the wildest dreams of the statin manufacturers. Do your own heavy lifting – don’t outsource it to statins.


Common Side Effects of Statins

The most commonly reported side effects of statins include:

  • bosh og'rig'i
  • belching or excessive gas
  • ich qotishi
  • croaky voice or hoarseness
  • uxlash qiyinligi
  • heartburn, indigestion, nausea, or stomach discomfort
  • lower back or side pain, tenderness around the eyes or cheekbones
  • nasal congestion or stuffiness, or a runny nose
  • slight muscle pain
  • terlash.

Other side effects, such as liver damage, are rare, and it is not necessary to have ongoing liver tests while you are taking a statin once you have had a baseline liver function test done.


Tarkibi

Statins are usually used to lower blood cholesterol levels and reduce risk for illnesses related to atherosclerosis, with a varying degree of effect depending on underlying risk factors and history of cardiovascular disease. Clinical practice guidelines generally recommend people start with lifestyle modification through a cholesterol-lowering diet and physical exercise. For those unable to meet their lipid-lowering goals through such methods, statins can be helpful. [14] [15] The medication appears to work equally well regardless of sex, [16] although some sex-related differences in treatment response were described. [17]

If there is an underlying history of cardiovascular disease, it has a significant impact on the effects of statin. This can be used to divide medication usage into broad categories of asosiy va ikkinchi darajali prevention. [18]

Primary prevention Edit

For the primary prevention of cardiovascular disease, the United States Preventive Services Task Force (USPSTF) 2016 guidelines recommend statins for those who have at least one risk factor for coronary heart disease, are between 40 and 75 years old, and have at least a 10% 10-year risk of heart disease, as calculated by the 2013 ACC/AHA Pooled Cohort algorithm. [18] [19] [20] Risk factors for coronary heart disease included abnormal lipid levels in the blood, diabetes mellitus, high blood pressure, and smoking. [19] They recommended selective use of low-to-moderate doses statins in the same adults who have a calculated 10-year cardiovascular disease event risk of 7.5–10% or greater. [19] In people over the age of 70, statins decrease the risk of cardiovascular disease but only in those with a history of heavy cholesterol blockage in their arteries. [21]

Most evidence suggests that statins are also effective in preventing heart disease in those with high cholesterol but no history of heart disease. A 2013 Cochrane review found a decrease in risk of death and other poor outcomes without any evidence of harm. [4] For every 138 people treated for 5 years, one fewer dies for every 49 treated, one fewer has an episode of heart disease. [10] A 2011 review reached similar conclusions, [22] and a 2012 review found benefits in both women and men. [23] A 2010 review concluded that treatment without history of cardiovascular disease reduces cardiovascular events in men but not women, and provides no mortality benefit in either sex. [24] Two other meta-analyses published that year, one of which used data obtained exclusively from women, found no mortality benefit in primary prevention. [25] [26]

The National Institute for Health and Clinical Excellence (NICE) recommends statin treatment for adults with an estimated 10 year risk of developing cardiovascular disease that is greater than 10%. [27] Guidelines by the American College of Cardiology and the American Heart Association recommend statin treatment for primary prevention of cardiovascular disease in adults with LDL cholesterol ≥ 190 mg/dL or those with diabetes, age 40–75 with LDL-C 70–190 mg/dl or in those with a 10-year risk of developing heart attack or stroke of 7.5% or more. In this latter group, statin assignment was not automatic, but was recommended to occur only after a clinician-patient risk discussion with shared decision making where other risk factors and lifestyle are addressed, the potential for benefit from a statin is weighed against the potential for adverse effects or drug interactions and informed patient preference is elicited. Moreover, if a risk decision was uncertain, factors such as family history, coronary calcium score, ankle-brachial index, and an inflammation test (hs-CRP ≥ 2.0 mg/L) were suggested to inform the risk decision. Additional factors that could be used were an LDL-C ≥ 160 or a very high lifetime risk. [28] However, critics such as Steven E. Nissen say that the AHA/ACC guidelines were not properly validated, overestimate the risk by at least 50%, and recommend statins for patients who will not benefit, based on populations whose observed risk is lower than predicted by the guidelines. [29] The European Society of Cardiology and the European Atherosclerosis Society recommend the use of statins for primary prevention, depending on baseline estimated cardiovascular score and LDL thresholds. [30]

Secondary prevention Edit

Statins are effective in decreasing mortality in people with pre-existing cardiovascular disease. [31] Pre-existing disease can have many manifestations. Defining illnesses include a prior heart attack, stroke, stable or unstable angina, aortic aneurysm, or other arterial ischemic disease, in the presence of atherosclerosis. [18] They are also advocated for use in people at high risk of developing coronary heart disease. [32] On average, statins can lower LDL cholesterol by 1.8 mmol/L (70 mg/dL), which translates into an estimated 60% decrease in the number of cardiac events (heart attack, sudden cardiac death) and a 17% reduced risk of stroke after long-term treatment. [33] A greater benefit is observed with high-intensity statin therapy. [34] They have less effect than the fibrates or niacin in reducing triglycerides and raising HDL-cholesterol ("good cholesterol"). [35] [36]

No studies have examined the effect of statins on cognition in patients with prior stroke. However, two large studies (HPS and PROSPER) that included patients with vascular diseases reported that simvastatin and pravastatin did not impact cognition. [37]

Statins have been studied for improving operative outcomes in cardiac and vascular surgery. [38] Mortality and adverse cardiovascular events were reduced in statin groups. [39]

Older adults who receive statin therapy at time of discharge from the hospital after an inpatient stay have been studied. People with cardiac ischemia not previously on statins at the time of admission have a lower risk of major cardiac adverse events and hospital readmission two years post-hospitalization. [40] [41]

Comparative effectiveness Edit

While no direct comparison exists, all statins appear effective regardless of potency or degree of cholesterol reduction. [22] Simvastatin and pravastatin appear to have a reduced incidence of side-effects. [5]

A comparison of simvastatin, pravastatin, and atorvastatin, based on their effectiveness against placebos, found no differences in reduction of cardiovascular disease or lipid levels in the blood. [42] A 2015 Cochrane systematic review update reported that rosuvastatin is more than three-fold more potent than atorvastatin. [43]

Females Edit

According to the 2015 Cochrane systematic review, atorvastatin showed greater cholesterol-lowering effect in females than in males compared to rosuvastatin. [43]

Children Edit

In children statins are effective at reducing cholesterol levels in those with familial hypercholesterolemia. [44] Their long term safety is, however, unclear. [44] [45] Some recommend that if lifestyle changes are not enough statins should be started at 8 years old. [46]

Familial hypercholesterolemia Edit

Statins may be less effective in reducing LDL cholesterol in people with familial hypercholesterolemia, especially those with homozygous deficiencies. [47] These people have defects usually in either the LDL receptor or apolipoprotein B genes, both of which are responsible for LDL clearance from the blood. [48] Statins remain a first-line treatment in familial hypercholesterolemia, [47] although other cholesterol-reducing measures may be required. [49] In people with homozygous deficiencies, statins may still prove helpful, albeit at high doses and in combination with other cholesterol-reducing medications. [50]

Contrast-induced nephropathy Edit

A 2014 meta-analysis found that statins could reduce the risk of contrast-induced nephropathy by 53% in people undergoing coronary angiography/percutaneous interventions. The effect was found to be stronger among those with preexisting kidney dysfunction or diabetes mellitus. [51]

Choosing a statin for people with special considerations [52]
Vaziyat Commonly recommended statins Tushuntirish
Kidney transplantation recipients taking ciclosporin Pravastatin or fluvastatin Drug interactions are possible, but studies have not shown that these statins increase exposure to ciclosporin. [53]
HIV-positive people taking protease inhibitors Atorvastatin, pravastatin or fluvastatin Negative interactions are more likely with other choices [54]
Persons taking gemfibrozil, a non-statin lipid-lowering drug Atorvastatin Combining gemfibrozil and a statin increases risk of rhabdomyolysis and subsequently kidney failure [55] [56]
Persons taking the anticoagulant warfarin Any statin The statin use may require that the warfarin dose be changed, as some statins increase the effect of warfarin. [57]

The most important adverse side effects are muscle problems, an increased risk of diabetes mellitus, and increased liver enzymes in the blood due to liver damage. [5] [58] Over 5 years of treatment statins result in 75 cases of diabetes, 7.5 cases of bleeding stroke, and 5 cases of muscle damage per 10,000 people treated. [31] This could be due to the statins inhibiting the enzyme (HMG-CoA reductase), which is necessary to make cholesterol, but also for other processes, such as CoQ10 production, which is important for muscle function and sugar regulation. [59]

Other possible adverse effects include neuropathy, [60] pancreatic and liver dysfunction, and sexual dysfunction. [61] The rate at which such events occur has been widely debated, in part because the risk/benefit ratio of statins in low-risk populations is highly dependent on the rate of adverse events. [62] [63] [64] A Cochrane meta-analysis of statin clinical trials in primary prevention found no evidence of excess adverse events among those treated with statins compared to placebo. [4] Another meta-analysis found a 39% increase in adverse events in statin treated people relative to those receiving placebo, but no increase in serious adverse events. [65] The author of one study argued that adverse events are more common in clinical practice than in randomized clinical trials. [61] A systematic review concluded that while clinical trial meta-analyses underestimate the rate of muscle pain associated with statin use, the rates of rhabdomyolysis are still "reassuringly low" and similar to those seen in clinical trials (about 1–2 per 10,000 person years). [66] A systematic review co-authored by Ben Goldacre concluded that only a small fraction of side effects reported by people on statins are actually attributable to the statin. [67]

Cognitive effects Edit

Multiple systematic reviews and meta-analyses have concluded that the available evidence does not support an association between statin use and cognitive decline. [68] [69] [70] [71] [72] Statins have been shown to decrease the risk of dementia, Alzheimer's disease, and improve cognitive impairment in some cases. [73] [ needs update ] Additionally, both the Patient-Centered Research into Outcomes Stroke Patients Prefer and Effectiveness Research (PROSPER) study [74] and the Health Protection Study (HPS) demonstrated that simvastatin and pravastatin did not affect cognition for patients with risk factors for, or a history of, vascular diseases. [75]

There are reports of reversible cognitive impairment with statins. [76] The U.S. Food and Drug Administration (FDA) package insert on statins includes a warning about the potential for non-serious and reversible cognitive side effects with the medication (memory loss, confusion). [77]

Muscles Edit

In observational studies 10–15% of people who take statins experience muscle problems in most cases these consist of muscle pain. [6] These rates, which are much higher than those seen in randomized clinical trials [66] have been the topic of extensive debate and discussion. [31] [78]

Serious muscle problems such as rhabdomyolysis (destruction of muscle cells) and statin-associated autoimmune myopathy occur in less than 0.1% of treated people. [79] Rhabdomyolysis can in turn result in life-threatening kidney injury. The risk of statin-induced rhabdomyolysis increases with older age, use of interacting medications such as fibrates, and hypothyroidism. [80] [81] Coenzyme Q10 (ubiquinone) levels are decreased in statin use [82] CoQ10 supplements are sometimes used to treat statin-associated myopathy, though evidence of their efficacy is lacking as of 2017 [update] . [83] The gene SLCO1B1 (Solute carrier organic anion transporter family member 1B1) codes for an organic anion-transporting polypeptide that is involved in the regulation of the absorption of statins. A common variation in this gene was found in 2008 to significantly increase the risk of myopathy. [84]

Records exist of over 250,000 people treated from 1998 to 2001 with the statin drugs atorvastatin, cerivastatin, fluvastatin, lovastatin, pravastatin, and simvastatin. [85] The incidence of rhabdomyolysis was 0.44 per 10,000 patients treated with statins other than cerivastatin. However, the risk was over 10-fold greater if cerivastatin was used, or if the standard statins (atorvastatin, fluvastatin, lovastatin, pravastatin, or simvastatin) were combined with a fibrate (fenofibrate or gemfibrozil) treatment. Cerivastatin was withdrawn by its manufacturer in 2001. [86]

Some researchers have suggested hydrophilic statins, such as fluvastatin, rosuvastatin, and pravastatin, are less toxic than lipophilic statins, such as atorvastatin, lovastatin, and simvastatin, but other studies have not found a connection. [87] Lovastatin induces the expression of gene atrogin-1, which is believed to be responsible in promoting muscle fiber damage. [87] Tendon rupture does not appear to occur. [88]

Diabetes Edit

The relationship between statin use and risk of developing diabetes remains unclear and the results of reviews are mixed. [89] [90] [91] [92] Higher doses have a greater effect, but the decrease in cardiovascular disease outweighs the risk of developing diabetes. [93] Use in postmenopausal women is associated with an increased risk for diabetes. [94] The exact mechanism responsible for the possible increased risk of diabetes mellitus associated with statin use is unclear. [91] However, recent findings have indicated the inhibition of HMGCoAR as a key mechanism. [95] Statins are thought to decrease cells' uptake of glucose from the bloodstream in response to the hormone insulin. [91] One way this is thought to occur is by interfering with cholesterol synthesis which is necessary for the production of certain proteins responsible for glucose uptake into cells such as GLUT1. [91]

Cancer Edit

Several meta-analyses have found no increased risk of cancer, and some meta-analyses have found a reduced risk. [96] [97] [98] [99] [100] Specifically, statins may reduce the risk of esophageal cancer, [101] colorectal cancer, [102] gastric cancer, [103] [104] hepatocellular carcinoma, [105] and possibly prostate cancer. [106] [107] They appear to have no effect on the risk of lung cancer, [108] kidney cancer, [109] breast cancer, [110] pancreatic cancer, [111] or bladder cancer. [112]

Drug interactions Edit

Combining any statin with a fibrate or niacin (other categories of lipid-lowering drugs) increases the risks for rhabdomyolysis to almost 6.0 per 10,000 person-years. [85] Monitoring liver enzymes and creatine kinase is especially prudent in those on high-dose statins or in those on statin/fibrate combinations, and mandatory in the case of muscle cramps or of deterioration in kidney function.

Consumption of grapefruit or grapefruit juice inhibits the metabolism of certain statins. Bitter oranges may have a similar effect. [113] Furanocoumarins in grapefruit juice (i.e. bergamottin and dihydroxybergamottin) inhibit the cytochrome P450 enzyme CYP3A4, which is involved in the metabolism of most statins (however, it is a major inhibitor of only lovastatin, simvastatin, and to a lesser degree, atorvastatin) and some other medications [114] (flavonoids (i.e. naringin) were thought to be responsible). This increases the levels of the statin, increasing the risk of dose-related adverse effects (including myopathy/rhabdomyolysis). The absolute prohibition of grapefruit juice consumption for users of some statins is controversial. [115]

The U.S. Food and Drug Administration (FDA) notified healthcare professionals of updates to the prescribing information concerning interactions between protease inhibitors and certain statin drugs. Protease inhibitors and statins taken together may increase the blood levels of statins and increase the risk for muscle injury (myopathy). The most serious form of myopathy, rhabdomyolysis, can damage the kidneys and lead to kidney failure, which can be fatal. [116]

Osteoporosis and fractures Edit

Studies have found that the use of statins may protect against getting osteoporosis and fractures or may lead to getting osteoporosis and fractures. [117] [118] [119] [120] A cross-sectional retrospective analysis of the entire Austrian population found that the risk of getting osteoporosis is dependent on the dose used. [121]

Statins act by competitively inhibiting HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Because statins are similar in structure to HMG-CoA on a molecular level, they will fit into the enzyme's active site and compete with the native substrate (HMG-CoA). This competition reduces the rate by which HMG-CoA reductase is able to produce mevalonate, the next molecule in the cascade that eventually produces cholesterol. A variety of natural statins are produced by Penitsilium va Aspergillus fungi as secondary metabolites. These natural statins probably function to inhibit HMG-CoA reductase enzymes in bacteria and fungi that compete with the producer. [123]

Inhibiting cholesterol synthesis Edit

By inhibiting HMG-CoA reductase, statins block the pathway for synthesizing cholesterol in the liver. This is significant because most circulating cholesterol comes from internal manufacture rather than the diet. When the liver can no longer produce cholesterol, levels of cholesterol in the blood will fall. Cholesterol synthesis appears to occur mostly at night, [124] so statins with short half-lives are usually taken at night to maximize their effect. Studies have shown greater LDL and total cholesterol reductions in the short-acting simvastatin taken at night rather than the morning, [125] [126] but have shown no difference in the long-acting atorvastatin. [127]

Increasing LDL uptake Edit

In rabbits, liver cells sense the reduced levels of liver cholesterol and seek to compensate by synthesizing LDL receptors to draw cholesterol out of the circulation. [128] This is accomplished via proteases that cleave membrane-bound sterol regulatory element binding proteins, which then migrate to the nucleus and bind to the sterol response elements. The sterol response elements then facilitate increased transcription of various other proteins, most notably, LDL receptor. The LDL receptor is transported to the liver cell membrane and binds to passing LDL and VLDL particles, mediating their uptake into the liver, where the cholesterol is reprocessed into bile salts and other byproducts. This results in a net effect of less LDL circulating in blood.

Decreasing of specific protein prenylation Edit

Statins, by inhibiting the HMG CoA reductase pathway, inhibit downstream synthesis of isoprenoids, such as farnesyl pyrophosphate and geranylgeranyl pyrophosphate. Inhibition of protein prenylation for proteins such as RhoA (and subsequent inhibition of Rho-associated protein kinase) may be involved, at least partially, in the improvement of endothelial function, modulation of immune function, and other pleiotropic cardiovascular benefits of statins, [129] [130] [131] [132] [133] [134] as well as in the fact that a number of other drugs that lower LDL have not shown the same cardiovascular risk benefits in studies as statins, [135] and may also account for some of the benefits seen in cancer reduction with statins. [136] In addition, the inhibitory effect on protein prenylation may also be involved in a number of unwanted side effects associated with statins, including muscle pain (myopathy) [137] and elevated blood sugar (diabetes). [138]

Other effects Edit

As noted above, statins exhibit action beyond lipid-lowering activity in the prevention of atherosclerosis through so-called "pleiotropic effects of statins." [132] The pleiotropic effects of statins remain controversial. [139] The ASTEROID trial showed direct ultrasound evidence of atheroma regression during statin therapy. [140] Researchers hypothesize that statins prevent cardiovascular disease via four proposed mechanisms (all subjects of a large body of biomedical research): [139]

  1. Improve endothelial function
  2. Modulate inflammatory responses
  3. Maintain plaque stability
  4. Prevent blood clot formation

In 2008, the JUPITER trial showed statins provided benefit in those who had no history of high cholesterol or heart disease, but only elevated high-sensitivity C-reactive protein (hsCRP) levels, an indicator for inflammation. [141] The study has been criticized due to perceived flaws in the study design, [142] [143] [144] although Paul M. Ridker, lead investigator of the JUPITER trial, has responded to these criticisms in length. [145]

Click on genes, proteins and metabolites below to link to respective articles. [§ 1]

As the target of statins, the HMG-CoA reductase, is highly similar between eukaryota and archaea, statins also act as antibiotics against archaea by inhibiting archaeal mevalonate biosynthesis. This has been shown in vivo and in vitro. [146] Since patients with a constipation phenotype present with higher abundance of methanogenic archaea in the gut, the use of statins for management of irritable bowel syndrome has been proposed and may actually be one of the hidden benefits of statin use. [147] [148]

The statins are divided into two groups: fermentation-derived and synthetic. Some specific types are listed in the table below. Note that the associated brand names may vary between countries.

LDL-lowering potency varies between agents. Cerivastatin is the most potent, (withdrawn from the market in August, 2001 due to risk of serious rhabdomyolysis) followed by (in order of decreasing potency), rosuvastatin, atorvastatin, simvastatin, lovastatin, pravastatin, and fluvastatin. [160] The relative potency of pitavastatin has not yet been fully established, but preliminary studies indicate a potency similar to rosuvastatin. [161]

Some types of statins are naturally occurring, and can be found in such foods as oyster mushrooms and red yeast rice. Randomized controlled trials have found these foodstuffs to reduce circulating cholesterol, but the quality of the trials has been judged to be low. [162] Due to patent expiration, most of the block-buster branded statins have been generic since 2012, including atorvastatin, the largest-selling [ iqtibos kerak ] branded drug. [163] [164] [165] [166] [167] [168] [169]

Statin equivalent dosages
% LDL reduction (approx.) Atorvastatin Fluvastatin Lovastatin Pravastatin Rosuvastatin Simvastatin
10–20% 20 mg 10 mg 10 mg 5 mg
20–30% 40 mg 20 mg 20 mg 10 mg
30–40% 10 mg 80 mg 40 mg 40 mg 5 mg 20 mg
40–45% 20 mg 80 mg 80 mg 5–10 mg 40 mg
46–50% 40 mg 10–20 mg 80 mg*
50–55% 80 mg 20 mg
56–60% 40 mg
* 80-mg dose no longer recommended due to increased risk of rhabdomyolysis
Starting dose
Starting dose 10–20 mg 20 mg 10–20 mg 40 mg 10 mg 5 mg if hypothyroid, >65 yo, Asian 20 mg
If higher LDL reduction goal 40 mg if >45% 40 mg if >25% 20 mg if >20% 20 mg if LDL >190 mg/dL (4.87 mmol/L) 40 mg if >45%
Optimal timing Istalgan vaqtda Evening With evening meals Istalgan vaqtda Istalgan vaqtda Evening

The role of cholesterol in the development of cardiovascular disease was elucidated in the second half of the 20th century. [170] This lipid hypothesis prompted attempts to reduce cardiovascular disease burden by lowering cholesterol. Treatment consisted mainly of dietary measures, such as a low-fat diet, and poorly tolerated medicines, such as clofibrate, cholestyramine, and nicotinic acid. Cholesterol researcher Daniel Steinberg writes that while the Coronary Primary Prevention Trial of 1984 demonstrated cholesterol lowering could significantly reduce the risk of heart attacks and angina, physicians, including cardiologists, remained largely unconvinced. [171] Scientists in academic settings and the pharmaceutical industry began trying to develop a drug to reduce cholesterol more effectively. There were several potential targets, with 30 steps in the synthesis of cholesterol from acetyl-coenzyme A. [172]

In 1971, Akira Endo, a Japanese biochemist working for the pharmaceutical company Sankyo, began to investigate this problem. Research had already shown cholesterol is mostly manufactured by the body in the liver with the enzyme HMG-CoA reductase. [11] Endo and his team reasoned that certain microorganisms may produce inhibitors of the enzyme to defend themselves against other organisms, as mevalonate is a precursor of many substances required by organisms for the maintenance of their cell walls or cytoskeleton (isoprenoids). [123] The first agent they identified was mevastatin (ML-236B), a molecule produced by the fungus Penicillium citrinum.

A British group isolated the same compound from Penicillium brevicompactum, named it compactin, and published their report in 1976. [173] The British group mentions antifungal properties, with no mention of HMG-CoA reductase inhibition. [ tibbiy ma'lumotnoma kerak ] Mevastatin was never marketed, because of its adverse effects of tumors, muscle deterioration, and sometimes death in laboratory dogs. P. Roy Vagelos, chief scientist and later CEO of Merck & Co, was interested, and made several trips to Japan starting in 1975. By 1978, Merck had isolated lovastatin (mevinolin, MK803) from the fungus Aspergillus terreus, first marketed in 1987 as Mevacor. [11]

In the 1990s, as a result of public campaigns, people in the United States became familiar with their cholesterol numbers and the difference between HDL and LDL cholesterol, and various pharmaceutical companies began producing their own statins, such as pravastatin (Pravachol), manufactured by Sankyo and Bristol-Myers Squibb. In April 1994, the results of a Merck-sponsored study, the Scandinavian Simvastatin Survival Study, were announced. Researchers tested simvastatin, later sold by Merck as Zocor, on 4,444 patients with high cholesterol and heart disease. After five years, the study concluded the patients saw a 35% reduction in their cholesterol, and their chances of dying of a heart attack were reduced by 42%. [11] [174] In 1995, Zocor and Mevacor both made Merck over US$1 billion . [11]

Though he did not profit from his original discovery, Endo was awarded the 2006 Japan Prize, and the Lasker-DeBakey Clinical Medical Research Award in 2008, for his pioneering research. [175] Endo was also inducted into the National Inventors Hall of Fame in Alexandria, Virginia in 2012. Michael C. Brown and Joseph Goldstein, who won the Nobel Prize for related work on cholesterol, said of Endo: "The millions of people whose lives will be extended through statin therapy owe it all to Akira Endo." [176]

As of 2016 [update] misleading claims exaggerating the adverse effects of statins had received widespread media coverage, with a consequent negative impact to public health. [31] Controversy over the effectiveness of statins in the medical literature was amplified in popular media in the early 2010s, leading an estimated 200,000 people in the UK to stop using statins over a six-month period to mid 2016, according to the authors of a study funded by the British Heart Foundation. They estimated that there could be up to 2,000 extra heart attacks or strokes over the following 10 years as a consequence. [177] An unintended effect of the academic statin controversy has been the spread of scientifically questionable alternative therapies. Cardiologist Steven Nissen at Cleveland Clinic commented "We are losing the battle for the hearts and minds of our patients to Web sites. " [178] promoting unproven medical therapies. Harriet Hall sees a spectrum of "statin denialism" ranging from pseudoscientific claims to the understatement of benefits and overstatement of side effects, all of which is contrary to the scientific evidence. [179]

Lovastatin (Mevacor) was approved as a generic drug in the US in December 2001. [180]

Pravastatin (Pravachol) was approved as a generic drug in the US in April 2006. [181]

Simvastatin (Zocor) was approved as a generic drug in the US in June 2006. [182]

Atorvastatin (Lipitor) was approved as a generic drug in the US in November 2011. [183] [184]

Fluvastatin (Lescol) was approved as a generic drug in the US in April 2012. [185]

Pitavastatin (Livalo) and rosuvastatin (Crestor) were approved as generic drugs in the US in 2016. [186] [187]

Ezetimibe/simvastatin (Vytorin) and ezetimibe/atorvastatin (Liptruzet) were approved as generic drugs in the US in 2017. [188]

Clinical studies have been conducted on the use of statins in dementia, [189] lung cancer, [190] nuclear cataracts, [191] hypertension, [192] [193] and prostate cancer. [194] There is no high quality evidence that statins are useful for pneumonia. [195] The small number of available trials do not support the use of statins as an adjunctive therapy or as a monotherapy in multiple sclerosis. [196]