cv outcomes of smoking & hypertension

CV Outcomes Of Smoking And Hypertension

Nemencio A. Nicodemus Jr., MD, FPCP, FPSEDM Professor, UP College of Medicine

Vice-President, Philippine Society of Endocrinology, Diabetes & Metabolism

Learning Objectives

•  To discuss the potential mechanisms for smoking-mediated cardiovascular dysfunction

•  To discuss the burden of disease attributable to and prevalence of smoking and hypertension

•  To discuss the cardiovascular outcomes of smoking and hypertension

Cigarette Smoke Is Divided Into Two Phases

Tar Or Particulate Phase •  Material that is trapped

when the smoke stream is passed through the cambridge glass-fiber filter that retains 99.9% of all particulate material with a size >0.1 m

•  Contains >1017 free radicals/g

•  Radicals associated are long-lived (hours to months)

Gas Phase •  Material that passes

through the filter •  Contains >1015 free

radicals/puff •  Radicals have a shorter

life span (seconds)

PryorWA,StoneK.AnnNYAcadSci1993;686:12–28.

Mainstream Smoke

•  Cigarette smoke that is drawn through the tobacco into an active smoker’s mouth

•  Comprises 8% of tar and 92% of gaseous components

PryorWA,StoneK.AnnNYAcadSci1993;686:12–28.

Sidestream Smoke

•  Smoke emitted from the burning ends of a cigarette

•  Contains a relatively higher concentration of the toxic gaseous component than mainstream cigarette smoke

GlantzSA,ParmleyWW.CirculaDon1991;83:1–12.

Environmental Tobacco Smoke

•  Results from the combination of sidestream smoke (85%) and a small fraction of exhaled mainstream smoke (15%) from smokers

TaylorAE,JohnsonDC,KazemiH.CirculaDon1992;86:699–702.

The Ugly Truth!

•  Both active and passive (environmental) cigarette smoke exposure predispose to cardiovascular events

Amrose,JAandBaruaRS.JACCVol.43,No.10,2004:1731–7

Potential Mechanisms For Cigarette Smoking-mediated Cardiovascular Dysfunction

Amrose,JAandBaruaRS.JACCVol.43,No.10,2004:1731–7

Potential Mechanisms For Cigarette Smoking-mediated Cardiovascular Dysfunction

Amrose,JAandBaruaRS.JACCVol.43,No.10,2004:1731–7

Main Determinants Of The Acute Vascular Damage From Smoking

Active smoking Passive smoking Increased platelet

aggregation Impaired endothelium-

dependent vasodilatation Increased platelet

adhesiveness Reduced nitric oxide

production Changes in platelet form Increased systolic blood

pressure Thrombus formation Increased heart rate

Increased carboxyhemoglobin

Increased carboxyhemoglobin

LeoneA.JCardiolCurrRes2015,2(2):00057

Common Classes Of Antihypertensive Drugs And Their Response To Smoking

Drug Response to smoking Beta-blockers Highly reduced (+++) ACE-Inhibitors Highly reduced (+++) Calcium Antagonists Reduced (++/−) Diuretics Highly reduced (+++) Angiotensin receptor blockers

not yet known (−−/+ ?)

LeoneA.CardiologyResearchandPracDce.Volume2011,doi:10.4061/2011/264894

Burden Of Disease Attributable To 20 Leading Risk Factors In Both Sexes, 2010

LimSS,etal,Lancet.2012Dec15;380(9859):2224–2260

Burden Of Disease Attributable To 20 Leading Risk Factors In Men, 2010

LimSS,etal,Lancet.2012Dec15;380(9859):2224–2260

Burden Of Disease Attributable To 20 Leading Risk Factors In Women, 2010

LimSS,etal,Lancet.2012Dec15;380(9859):2224–2260

CV Risks With Smoking & Hypertension

FeiginV,etal.onbehalfoftheAsiaPacificCohortStudiesCollaboraDonStroke.2005;36:1360-1365.

Design •  Included Individual

participant data from 26 prospective cohort studies (total number of participants 306,620) that reported incident cases of SAH (fatal and/or nonfatal)

•  Median follow-up period of 8.2 years

FeiginV,etal.onbehalfoftheAsiaPacificCohortStudiesCollaboraDonStroke.2005;36:1360-1365.

Hypertension And Smoking Significantly Increase The Risk Of SAH

FeiginV,etal.onbehalfoftheAsiaPacificCohortStudiesCollaboraDonStroke.2005;36:1360-1365.

Findings From This Meta-analysis

•  Current smoking (HR, 2.4; 95% CI, 1.8 to 3.4) and SBP >140 mm Hg (HR, 2.0; 95% CI, 1.5 to 2.7) were significant and independent risk factors for SAH

•  Attributable risks of SAH associated with current smoking and elevated SBP (≥140 mm Hg) were 29% and 19%, respectively

•  The strength of the associations of the common cardiovascular risk factors with the risk of SAH did not differ much between Asian and Australasian regions

FeiginV,etal.onbehalfoftheAsiaPacificCohortStudiesCollaboraDonStroke.2005;36:1360-1365.

Design •  Individual level data from 543,694 (85% Asian;

36% female) participants from 32 cohorts in the Asia Pacific Cohort Studies Collaboration were included

•  Adjusted hazard ratios for mortality from HF were estimated separately for Asians and non-Asians for a quintet of cardiovascular risk factors: –  systolic blood pressure, diabetes, body mass index,

cigarette smoking and total cholesterol

•  3,793,229 person-years of follow-up

Huxleyetal.BMCCardiovascularDisorders2014,14:61

A 10 mm-Hg Increment In Systolic BP Increased The Risk Of Fatal HF By 13%

Huxleyetal.BMCCardiovascularDisorders2014,14:61

Hazard ratios for fatal heart failure associated with a 10 mm-Hg Increment in systolic blood pressure

Cigarette Smoking Increased The Risk Of Fatal Heart Failure By 30%

Huxleyetal.BMCCardiovascularDisorders2014,14:61

Hazard ratios for fatal heart failure associated with cigarette smoking (ever versus never)

Findings From This Meta-analysis

•  Most traditional cardiovascular risk factors including elevated blood pressure, obesity and cigarette smoking appear to operate similarly to increase the risk of death from HF in Asians and non-Asians populations alike

Huxleyetal.BMCCardiovascularDisorders2014,14:61

HypertensRes2007;30:1169–1175

Design •  8,912 Japanese men and women without a

history of stroke and heart disease •  Categorized into 4 groups:

–  Individuals who neither smoked nor had hypertension (HT)

– Current smokers – With HT – Current smokers with HT

•  Follow-up of 19 years •  Assessing risk of CVD and all-cause mortality

HozawaA,etal.HypertensRes2007;30:1169–1175

HR for CVD and All-cause Mortality According to BP or Smoking Status, age < 60 years

Normotensive Hypertensive Non-

smoker Current Non-smoker Current

Men HR for CVD

mortality 1 1.58

(0.63 – 3.97) 1.96

(0.73 – 5.22) 3.86

(1.62 – 9.19) HR for all-

cause mortality

1 1.4 (0.98 – 2.01)

1.21 (0.79 – 1.84)

1.69 (1.17 – 2.42)

Women HR for CVD

mortality 1 2.58

(0.75 – 8.93) 2.19

(1.13 – 4.22) 5.88

(2.07 – 16.72) HR for all-

cause mortality

1 1.63 (0.90 – 2.94)

1.07 (0.79 – 1.47)

1.77 (0.91 – 3.46)

AdaptedfromHozawaA,etal.HypertensRes2007;30:1169–1175

HR for CVD and All-cause Mortality According to BP or Smoking Status, age ≥ 60 years

Normotensive Hypertensive Non-

smoker Current Non-smoker Current

Men HR for CVD

mortality 1 1.02

(0.56 – 1.87) 1.27

(0.74 – 2.17) 1.72

(1.02 – 2.89) HR for all-

cause mortality

1 1.24 (0.87 – 1.76)

1.32 (0.95 – 1.82)

1.47 (1.07 – 2.02)

Women HR for CVD

mortality 1 0.46

(0.14 – 1.48) 1.23

(0.88 – 1.71) 2.01

(1.25 – 3.23) HR for all-

cause mortality

1 1.23 (0.75 – 2.01)

1.28 (1.03 – 1.59)

1.61 (1.15 – 2.26)

AdaptedfromHozawaA,etal.HypertensRes2007;30:1169–1175

Implications of this Study

•  Aggressive attempts to discourage smoking and to curb HT could yield large health benefits , particularly for those aged <60 years.

HozawaA,etal.HypertensRes2007;30:1169–1175

Implications of this Study

•  Efforts to warn about the adverse consequence of HT and smoking during adolescence and youth could yield the greatest health benefits, since positive behaviors adopted early are more easily continued into middle adulthood and later life

HozawaA,etal.HypertensRes2007;30:1169–1175

CV Outcomes Of Smoking And Hypertension: Summary

•  Smoking and hypertension both induce vascular damage that could lead to the initiation and progression of atherothrombotic diseases

•  Smoking and hypertension increase the risk of SAH and mortality from HF, CVD and all causes

•  Younger patients with HT and smoking are at higher risk for mortality and will benefit more with interventions, especially in our country where a significant number with risk these risk factors are young