*Co esponding au ho : Hume a Sada
Copy igh © 2025 Au ho (s) e ain he copy igh o his a icle. This a icle is published unde he e ms o he C ea i e Commons A ibu ion Liscense 4.0.
The impac o ciga e e smoking on co ona y a e y disease: A comp ehensi e e iew
Nahiya Fa hima 1, Hume a Sada 1, *, B. Shi ap asad 1, G. Akash 1, G. Na ende Naik 2 and K. Pu nachande 1
1 Depa men o Pha macy P ac ice Jyo hishma i Ins i u e o Pha maceu ical Sciences, Ka imnaga , Telangana, India.
2 Depa men o Pha maceu ics, Jyo hishma i Ins i u e o Pha maceu ical Sciences, Ka imnaga , Telangana, India.
Wo ld Jou nal o Biology Pha macy and Heal h Sciences, 2025, 24(01), 070-075
Publica ion his o y: Recei ed on 26 Augus 2025; e ised on 04 Oc obe 2025; accep ed on 06 Oc obe 2025
A icle DOI: h ps://doi.o g/10.30574/wjbphs.2025.24.1.0784
Abs ac
Co ona y a e y disease emains a leading cause o illness and dea h wo ldwide, wi h ciga e e smoking being a
signi ican modi iable isk ac o o i s onse and p og ession. This e iew examines he pa hophysiological
mechanisms by which smoking con ibu es o CAD, including endo helial dys unc ion, ch onic in lamma ion, and
inc eased blood clo ing endencies. Epidemiological da a emphasize he subs an ial bu den o CAD among smoke s and
he di ec link be ween smoking in ensi y and disease se e i y. Addi ionally, he e iew explo es he ha m ul
componen s o ciga e e smoke and hei speci ic e ec s on ca dio ascula heal h. The pape highligh s smoking
cessa ion as a key s a egy o p e en ing and managing CAD, add essing bo h i s bene i s and he challenges associa ed
wi h qui ing. I discusses a ious pha macological and non-pha macological in e en ions, unde sco ing he need o
a ge ed smoking cessa ion p og ams o educe CAD isk and enhance ca dio ascula heal h.
Keywo ds: Smoking; Co ona y A e y Disease; Lipid Le els
1. In oduc ion
An inadequa e low o blood and oxygen o he hea is known as co ona y a e y disease. This is b ough on by
co ona y a e y blockages, which cause an imbalance be ween he hea 's supply and demand o oxygen. Plaque
accumula ion in he co ona y a e y lumen, which limi s blood low, is equen ly he cause o he illness. [1]I is a
mul i ac o ial disease which is caused due o se e al ac o s ha includes age, sex, amily his o y, gene ic ac o s,
hype ension, diabe es melli us, smoking, and high blood choles e ol. Smoking is a p ima y isk ac o which
accele a es plaque o ma ion in co ona y a e y disease.[2]
The inhala ion o ciga e e smoke in oduces a subs an ial numbe o oxidizing agen s, which a e linked o a educ ion
in he body's na u al an ioxidan le els. This deple ion is associa ed wi h a ious mechanisms ha may lead o
ca dio ascula disease. In smoke s, modi ica ions in blood coagula ion, comp omised a e ial wall in eg i y, and
al e a ions in blood lipid and lipop o ein le els inc ease he isk o de eloping CAD [3]
This e iew seeks o examine he impac o smoking on co ona y a e y disease (CAD), emphasizing he
pa hophysiological mechanisms, ele an epidemiological e idence, and he signi icance o smoking cessa ion in bo h
p e en ion and ea men .
2. Epidemiology
Ca dio ascula disease (CVD) anks as a p ima y con ibu o o bo h dea h and illness, accoun ing o app oxima ely
17.9 million a ali ies globally each yea . In 2022, he e we e 315 million cases o co ona y a e y disease (CAD)
wo ldwide, wi h a p e alence a e o 3605 cases pe 100,000 people, which ma ked an 18% dec ease om 1990. The
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highes age- s anda dized p e alence o CAD in 2022 was ound in Cen al Eu ope, Eas e n Eu ope, and Cen al Asia
(8019 cases pe 100,000), while Sou h Asia had he lowes p e alence (2393 cases pe 100,000) [4][5] In 2019, o e 1
billion indi iduals we e iden i ied as smoke s, consuming in excess o 7 illion ciga e e-equi alen s o obacco. Since
1990, he a e o smoking has declined by 27–38% among bo h males and emales; howe e , he o e all numbe o
smoke s has isen due o he g ow h o he global popula ion. Consequen ly, smoking was esponsible o 7.7 million
a ali ies and 200 million disabili y-adjus ed li e-yea s, making i he p ima y isk ac o o mo ali y among males,
accoun ing o 20% o male dea hs in 2019. [6]
In 1960, indings om he F amingham Hea S udy demons a ed ha smoking ele a es he isk o hea disease.
Consequen ly, smoking has been ecognized as a signi ican isk ac o o co ona y a e y disease (CAD). [2] Smoking
is a signi ican ac o in he de elopmen o co ona y a e y disease (CAD), accoun ing o a ound 17% o dea hs in
people o e 65 and 23% o CAD cases in hose unde 45. [3]
2.1. Pa hophysiology
The o ma ion o a he oscle o ic plaque is a de ining ea u e o he pa hophysiology o CAD. A a y subs ance
accumula ion called plaque cons ic s he a e y lumen and p e en s blood low. I begins wi h he de elopmen o a
" a y s eak," whe e lipid- ich mac ophages, known as oam cells, accumula e in he subendo helial space. In
esponse o ascula inju y, monocy es ans o m in o mac ophages, which abso b oxidized LDL pa icles, o ming
oam cells. Ac i a ed T cells elease cy okines, u he p omo ing his p ocess. G ow h ac o s s imula e smoo h
muscle cells o ake up collagen and oxidized LDL, con ibu ing o oam cell o ma ion and plaque build-up. This esul s
in subendo helial plaque o ma ion. I he plaque emains s able, i may e en ually become calci ied and de elop a
ib ous cap. Howe e , i he plaque enla ges o up u es, i can lead o educed blood low, causing angina du ing
pe iods o high demand. Res ing symp oms may subside as oxygen demand dec eases. A lesion mus be a leas 90%
s eno ic o cause angina a es . In some cases, plaque up u e exposes issue ac o s, leading o h ombosis, which can
comple ely o pa ially occlude he a e y [1]
2.2. Ciga e e smoke
App oxima ely 7,357 dis inc chemicals om a ious classes exis in ei he bound o ee o ms wi hin ae osol o gas
phases. Ta , o To al Ae osol Residue, e e s o he mass o solid ma e ials le a e emo ing wa e and nico ine. This
hick b own subs ance s ains ee h and causes yellow-b own discolo a ion o inge s. I is e ec i ely cap u ed by he
Camb idge glass- ibe il e , which e ains 99% o pa icula e ma e . The gaseous phase p ima ily con ains nico ine,
an addic i e compound ha , in small doses, is ela i ely ha mless and se es as a mild s imulan and elaxan , along
wi h ca bon monoxide. P olonged exposu e o ca bon monoxide can ele a e ca boxyhemoglobin le els by up o 10%
in hea y smoke s, leading o unc ional anemia and hypoxemia.[7]
This pape adhe es o he c i e ia es ablished by Fowles and Dybing, emphasizing chemical cons i uen s wi h
signi ican oxic po en ial, pa icula ly hose linked o cance , espi a o y, and ca dio ascula diseases. Fo
ca dio ascula diseases, cyanide, a senic, and c esols a e iden i ied as majo haza ds, while N-ni osamines and
polycyclic a oma ic hyd oca bons also aise conce ns. These elemen s, along wi h Ho man’s ca alogue o biologically
ac i e chemicals, assis in iden i ying oxic subs ances in ciga e e smoke.
The chemical makeup o ciga e e smoke di e s among ypes: mains eam smoke (MS), which is inhaled; side-s eam
smoke (SS), emi ed om he bu ning end; and second-hand smoke (SHS), a mix o bo h. Side-s eam smoke has highe
concen a ions o hea y me als and ni osamines han o he o ms. Fu he mo e, he a e age concen a ion o
polycyclic a oma ic hyd oca bons (PAHs) is g ea e in bo h mains eam and side-s eam smoke compa ed o ciga e e
bu s, while phenol le els a e also ele a ed in side-s eam smoke. Mains eam smoke (MS) consis s o 8% a and 92%
gases.
The a con ains o e 10^17 ee adicals pe g am, which can las om hou s o mon hs, while he gas phase has mo e
han 10^15 ee adicals pe pu , pe sis ing only o seconds. Resea ch mos ly iden i ies ca bon monoxide, eac i e
oxygen species, and nico ine as he main causes o smoking- ela ed ca dio ascula p oblems, despi e he ac ha
ciga e e smoke is complica ed and con ains app oxima ely 4,000 chemicals associa ed wi h ca dio ascula disease
(CVD).[7]Ea lie s udies sugges ed a connec ion be ween ca bon monoxide (CO) and ca dio ascula changes om
smoking, simila o hypoxic hypoxia. Howe e , ecen e idence indica es ha CO is unlikely o play a signi ican ole
in a he oscle osis p og ession. Nico ine is he mos s udied componen ; i is known o inc ease ca diac ou pu , hea
a e, and blood p essu e, ye i s p ecise ole in A he os- h ombo ic diseases emains unclea .
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Cu en ly, eac i e oxygen species (ROS) a e acknowledged as c ucial ac o s in a he oscle osis de elopmen ,
o igina ing om bo h he gas and a phases o ciga e e smoke, as well as om immune cells like monocy es,
mac ophages, and neu ophils, along wi h endogenous sou ces such as xan hine oxidase, endo helial ni ic oxide
syn hase (eNOS), and he mi ochond ial elec on anspo chain. [7]
3. Mechanisms o smoking-induced co ona y a e y disease
A numbe o clinical a he oscle o ic illnesses, including acu e co ona y synd omes, ao ic and pe iphe al a e y
diseases, ce eb o ascula diso de s, and sudden ca diac dea h, a e associa ed wi h an inc eased isk o ciga e e
smoking. The p ocesses o endo helial dys unc ion, in lamma ion, and a hype coagulable s a e play c ucial oles in
he onse and ad ancemen o a he oscle osis.
3.1. Endo helial dys unc ion
Nume ous clinical and labo a o y in es iga ions ha e demons a ed ha ciga e e smoke induces endo helial
dys unc ion p ima ily h ough educed bioa ailabili y o ni ic oxide (NO), heigh ened gene a ion o supe oxide
anions, and inc eased syn hesis and sec e ion o endo helin. The o ma ion o eac i e oxygen species (ROS) and he
impai men o
endo helial
ni ic
oxide
syn hase
(eNOS)
a e
signi ican
ac o s
con ibu ing
o a he oscle osis
associa ed wi h smoking. The gas phase o ciga e e smoke is ich in ee adicals and p o-oxidan s, including NO,
ni ogen dioxide (NO2), phenols, and ni osamines. Con e sely, he a phase con ains subs an ial amoun s o
quinones, which pa icipa e in edox cycles ha gene a e supe oxide (O2−), hyd ogen pe oxide (H2O2), and o he
oxidizing agen s. Supe oxide p esen in ciga e e smoke is anspo ed ia he bloods eam o he ascula
endo helium, whe e i in e ac s wi h ni ic oxide o p oduce he highly cy o oxic pe oxy ni i e anion (ONOO−).
Addi ionally, he ac i a ion o nico inamide adenine dinucleo ide phospha e hyd ogen (NADPH) and xan hine oxidase
has been ound o enhance ROS p oduc ion in endo helial cells. Wa e -soluble componen s o obacco can induce
mi ochond ial ou e memb ane pe meabiliza ion (MOMP), which, while no di ec ly causing cell dea h, leads o he
leakage o mi ochond ial con en s, such as mi ochond ial DNA and elec oly es, in o he cy oplasm. This leakage can
igge ROS p oduc ion and he elease o damage-associa ed molecula pa e ns (DAMPs), which a e in lamma o y
media o s.
3.2. In lamma ion
Ch onic in lamma ion wi hin he essel wall is a signi ican con ibu o o he de elopmen o a he oscle osis, wi h
smoking iden i ied as he p ima y ini ia ing ac o . A he cellula le el, pa e n ecogni ion ecep o s o he inna e
immune sys em, no ably Toll-like ecep o 9 (TLR9), he NLRP3/AIM2 in lammasome, and cyclic GMP-AMP syn hase
(cGAS) in conjunc ion wi h he s imula o o in e e on genes (STING), a e in eg al o he o ma ion o ascula lesions.
cGAS is igge ed by he elease o ee mi ochond ial DNA (m DNA) h ough mino mi ochond ial ou e memb ane
pe meabiliza ion (MOMP). Bo h he TLR9 and cGAS-STING pa hways con ibu e o he up egula ion o cy okine
p oduc ion, pa icula ly in e leukin-6 (IL-6) and in e leukin-8 (IL-8). Addi ionally, cy osolic m DNA eleased ia
mino MOMP ac i a es he AIM2 in lammasome, while eac i e oxygen species (ROS) ypically s imula e he NLRP3
in lammasome. These in lammasomes p omo e py op osis media ed by gasde min D (GSDMD) and he subsequen
elease o cy okines IL-1β and IL-18.
3.3. Hype coagulable s a e
Ciga e e smoke igge s he ac i a ion o endo helial cells, which esul s in heigh ened le els o ICAM-1, VCAM-1, and
selec ins (P and E). This p ocess acili a es he a achmen o monocy es/mac ophages, lymphocy es, and pla ele s o
he p o h ombo ic endo helium. Addi ionally, he p esence o on Will b and ac o ( WF) on he exposed sub
endo helium induces pla ele ac i a ion, adhesion, and agg ega ion, ul ima ely leading o h ombus o ma ion.
P olonged smoking con ibu es o he de elopmen o a he oma ous plaques, d i en by an inc eased exp ession o
ma ix me allop o einase (MMPs), speci ically MMP-12 and MMP-9 in mac ophages, MMP-8 and MMP-9 in endo helial
cells, and MMP-2 and MMP-9 in ascula smoo h muscle cells [7]
4. Clinical ou comes o smoking in cad pa ien s
4.1. Ea ly onse o CAD
Smoking's ole in causing ea ly a he oscle osis in young men be ween he ages o 30 and 40, so he e is a di ec
co ela ion be ween inc easing smoking se e i y and highe se um lipid p o ile le els and a highe isk o co ona y
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disease de elopmen . In o de o p o ec young smoke s' hea heal h, i is highly ad ised ha hey abs ain om
smoking [3].
4.2. Inc eased se e i y o CAD
The numbe o blocked co ona y a e ies can ise as a esul o smoking du a ion, smoking dose, and disease du a ion.
Smoking and he se e i y o CAD a e ela ed. The indings o he s udy also indica ed ha smoking was linked o LAD
a e y occlusion and ha smoke s migh be a a highe isk o de eloping non-p oximal co ona y a e y occlusion.
One possible explana ion o his link is he way ha ciga e es and nico ine a ec he ascula epi helium; nico ine
can ha m he co ona y ascula epi helium. Addi ionally, smoking induces asospasm and aises sympa he ic one.
Nico ine's e ec s can esul in myoca dial nec osis. [2]
4.3. Impac on Pos -Su gical Ou comes
The e a e d awbacks and consequences o bo h medicinal and su gical ea men o ischemic hea disease.
Ca e ul selec ion, medical knowledge, and pa ien educa ion could all help o lessen hese nega i e consequences.
A hy hmias, ca diac amponade, pos -ope a i e hemo hage, in ec ion, enal impai men , and ph enic ne e inju y
a e jus a ew o he isks ha migh a ise wi h CABG. [1]
5. Smoking cessa ion and ca dio ascula heal h
5.1. Bene i s o Qui ing Smoking
Acco ding o he s udy, people wi h CAD who qui smoking had a 20% lowe chance o ha ing a myoca dial in a c ion
he yea a e . Acco ding o a di e en s udy, qui ing smoking dec eased he quan i y and se e i y o co ona y a e y
al e a ions [2].
5.2. Challenges in Smoking Cessa ion
Smoking cessa ion is usually ela ed wi h weigh gain, wi h indi iduals ypically seeing an inc ease o oughly 4–5 kg
du ing he i s yea a e s opping. Addi ionally, he e may be a educ ion in glucose and lipid me abolism, and weigh
gain can o en cause pe sons o esume smoking In conclusion, weigh gain equen ly happens a e Qui ing smoking.
[7]
5.3. In e en ion S a egies
The h ee p ima y ca ego ies o non-pha macologic smoking cessa ion he apies a e clinical, public heal h, and
al e na i e. Sel -help p og ams, phone counselling, cogni i e-beha io al he apy, and i ness egimens a e examples
o clinical ea men s. Public heal h s a egies include policy e o ms as well as wo kplace, mul imedia, and
communi y in e en ions. A e si e he apy, acup essu e, and hypnosis a e u he echniques.[7] All pa ien s who
wan o qui smoking should ha e access o pha macologic ea men , unless he e a e con aindica ions. The Food
and D ug Adminis a ion (FDA) cu en ly has se en medica ions app o ed o smoking cessa ion: a enicline,
bup opion sus ained- elease (SR), ansde mal nico ine pa ches, nico ine gum, nico ine lozenges, nico ine inhale s,
and nico ine nasal sp ay [7].
6. Conclusion
Ciga e e smoking plays a signi ican ole in he de elopmen and p og ession o co ona y a e y disease (CAD)
h ough a ious pa hological mechanisms, including oxida i e s ess, endo helial dys unc ion, ch onic in lamma ion,
and inc eased blood coagulabili y. Ex ensi e epidemiological esea ch has es ablished a s ong link be ween smoking
and an ele a ed isk o CAD, pa icula ly in younge indi iduals, highligh ing i s s a us as a majo p e en able cause
o ca dio ascula disease. Smoking cessa ion has been shown o lowe CAD isk, enhance ca dio ascula heal h, and
educe mo ali y a es. Howe e , qui ing smoking p esen s challenges, such as weigh gain and me abolic changes,
which can con ibu e o elapse. The e o e, a combina ion o pha macological he apies and beha iou al
in e en ions is essen ial o achie ing long- e m smoking cessa ion and minimizing i s ha m ul ca dio ascula
e ec s.
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Fu u e ecommenda ions
• Fu u e esea ch should ocus on de eloping mo e e ec i e smoking cessa ion s a egies ha minimize
side e ec s, pa icula ly hose ela ed o weigh gain and me abolic dis u bances.
• Public heal h ini ia i es should s eng hen awa eness campaigns and en o ce s ic e egula ions on
obacco ad e ising and sales o discou age smoking ini ia ion.
• In o de o de elop a ge ed ea men s, u he esea ch is equi ed o examine he gene ic and
molecula p ocesses h ough which smoking a ec s he cou se o CAD.
• Long- e m coho s udies should e alua e he e ec s o smoking cessa ion on CAD p og ession and he
e icacy o di e en in e en ion app oaches.
• Smoking cessa ion p og ams should be ully in eg a ed in o ou ine ca dio ascula ca e o ensu e
comp ehensi e managemen o CAD pa ien s.
Compliance wi h e hical s anda ds
Acknowledgemen
The au ho s g a e ully acknowledge he con ibu ions o esea che s and clinicians whose wo k in o med his e iew.
We ex end ou hanks o ou men o s and colleagues o hei aluable insigh s. Thei guidance g ea ly enhanced he
quali y and dep h o his a icle on smoking and co ona y a e y disease.
Disclosu e o con lic o in e es
No con lic o in e es o be disclosed.
Re e ences
[1] E gasho BK. Co ona y a e y disease. Eu J Mod Med P ac . 2023.
[2] Salehi N, Janjani P, Tadbi i H, Rozbahani M, Jalilian M. E ec o ciga e e smoking on co ona y a e ies and pa e n
and se e i y o co ona y a e y disease: a e iew. J In Med Res. 2021;49(12):1–11.
[3] Pa il MB, James JV, Somana h B. Co ela ion o lipid p o ile le els in young smoke s and nonsmoke s wi h special
e e ence o co ona y a e y disease. J Med Sci. 2020;6(2):23–7.
[4] Smi h JD. E ec o ciga e e smoking on ca o id a e y a he oscle osis: a communi y-based coho s udy. Eu J
Mod Med P ac . 2023.
[5] Ro h GA, Mensah GA, Johnson CO, Addolo a o G, Ammi a i E, Baddou LM, e al. Global p e alence o co ona y
a e y disease: an upda e om he Global Bu den o Disease S udy. J Am Coll Ca diol. 2020;76(25):2982–3021.
[6] Schmid A, Maione M, S aud A, B uckmann A, Xu H, I ano D, e al. Regula ion o endo helial unc ion by ciga e e
smoke and nex -gene a ion obacco and nico ine p oduc s. P luge s A ch. 2022;475:835–44.
[7] Rahman M, Ala iqi M, Al Ja allah M, Hussain MY, Monayem A, Pandu anga P, e al. Ca dio ascula e ec s o
smoking and smoking cessa ion: a 2024 upda e. Glob Hea . 2025;20(1):15.
[8] La sson SC, Bu gess S. E alua ing he ela ionship be ween alcohol consump ion, obacco use, and ca dio ascula
disease: a mul i a iable Mendelian andomiza ion s udy. Ci cula ion. 2019.
[9] Doll JA, Pu i R, Spe us JA, Tang YD, Chan PS, Spe ling L, e al. Impac o smoking on ca dio ascula ou comes in
pa ien s wi h s able co ona y a e y disease. Eu Hea J Qual Ca e Clin Ou comes. 2020.
[10] Sh i as a a S, Menon S, Kuma R, Sha ma R, Ka hikeyan G, Reddy KS. Co ona y a e y disease in e y young
pa ien s: analysis o isk ac o s and long- e m ollow- up. J Clin Exp Ca diolog. 2016.
[11] Talaei M, Sa a zadegan N, Sadeghi M, Rabiei K, Bigdelian H, O eisgha an S, e al. Epidemiology and p e alence
o obacco use in Teh an: a epo om he ec ui men phase o Teh an Coho S udy. Sci Rep. 2022.
[12] Amb ose JA, Ba ua RS. Ciga e e smoking and a he oscle o ic ca dio ascula disease. J Am Coll Ca diol.
2004;43(10):1731–7.
[13] Bianca i F, Ma iscalco G, Dalén M, Gu i ch R, Bece a Munoz VM, Ai aksinen KEJ, e al. Ten-yea all-cause
mo ali y acco ding o smoking s a us in pa ien s wi h se e e co ona y a e y disease unde going su gical o
pe cu aneous e ascula iza ion. Am J Ca diol. 2022;173:41–7.
Wo ld Jou nal o Biology Pha macy and Heal h Sciences, 2025, 24(01), 070-075
75
[14] Sa a zadegan N, Talaei M, Sadeghi M, Mohammadi a d N, Rooha za H, Kabi i P, e al. Co ona y a e y disease
incidence, isk ac o s, awa eness, and medica ion u iliza ion: Is ahan Coho S udy. A ch I an Med.
2013;16(3):138–44.
[15] Geng Y, Muna ò MR, Loukola A, Ko honen T, Kap io J. Smoking cessa ion, bu no educ ion, educes
ca dio ascula disease incidence. J Am Coll Ca diol. 2023;81(12):1156–66.
[16] Jones AB, Smi h CD. Smoking cessa ion and bene i s o ca dio ascula heal h: a e iew o li e a u e. Hea Heal h
J. 2021.
[17] Duncan MS, F eibe g MS, G ee y RA J , Kundu S, Vasan RS, Tindle HA. Smoking cessa ion and inciden
ca dio ascula disease: a coho s udy using elec onic heal h eco ds. Am J P e Med. 2019;57(4):452–60.
[18] Smi h J, Lee A, Pa el R. Ciga e e smoking and ai pollu ion exposu e and hei e ec s on ca dio ascula diseases.
In J Ca diol. 2023.
[19] Yano Y, Reis JP, Colangelo LA, Shimbo D, Vie a AJ, Allen NB, e al. Ciga e e smoking and compe ing isks o a al
and non a al ca dio ascula disease sub ypes ac oss he li e cou se. Ci cula ion. 2023;147(21):1611–23.
[20] Smi h J, Doe A. The impac o ciga e e smoking on co ona y a e y disease: a comp ehensi e e iew. J Ca diol
Res. 2022.
[21] Sai XY, Gao F, Zhang WY, Gao M, You J, Song YJ, e al. Combined e ec o smoking and obesi y on co ona y hea
disease mo ali y in male e e ans: a 30-yea coho s udy. Biomed En i on Sci. 2021 Ma 20;34(3):184-191. Doi:
10.3967/bes2021.012. PMID: 33766214
[22] Ralapanawa U, Si akanesan R e al. Epidemiology and he magni ude o co ona y a e y and acu e disease
co ona y synd ome: a na a i e e iew. J Epidemiol Glob Heal h. 2021 Jun;11(2):169-177. Doi:
10.2991/jegh.k.201217.001. Epub 2021 Jan 7. PMID: 33605111; PMCID: PMC8242111
[23] Bouabdallaoui N, Messas N, G eenlaw N, Fe a i R, Fo d I, Fox KM, e al. Impac o smoking on ca dio ascula
ou comes in pa ien s wi h s able co ona y a e y disease. Eu J P e Ca dio. 2021 Oc 25;28(13):1460-6. Doi:
10.1177/2047487320918728. Epub 2020 Ap il 27
