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8/11/2019 Cardiovascular Wellness.pdf 06
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CardiovascularCardiovascularWellnessWellness
Dr Asri Bin SaidDr Asri Bin Said
PhysicianPhysician
Presentation LayoutPresentation Layout
ll Incidence of cardiovascular diseasesIncidence of cardiovascular diseases
ll Coronary heart diseaseCoronary heart disease
ll Risk factor for cardiovascular diseasesRisk factor for cardiovascular diseases
ll Guidelines for preventing cardiovascular diseaseGuidelines for preventing cardiovascular disease
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Incidence of Cardiovascular diseaseIncidence of Cardiovascular disease
ll Cardiovascular deaths account for 20Cardiovascular deaths account for 20--25% of25% of
hospital deaths from 2000 to 2005 in Malaysiahospital deaths from 2000 to 2005 in Malaysia
ll Ischaemic heart disease accounted for 25% to 33%Ischaemic heart disease accounted for 25% to 33%
of admissions and 27% to 35% of deathsof admissions and 27% to 35% of deaths
Incidence CVD in the WorldIncidence CVD in the World
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The story of Cardiovascular diseaseThe story of Cardiovascular disease
ll It doesnt start in old age, in factIt doesnt start in old age, in fact
ll Autopsy on 2876 persons age 15Autopsy on 2876 persons age 15--34 year old34 year old
ll 1515--19 year olds = 10% has fatty streaks19 year olds = 10% has fatty streaksll 3030--34 year olds = 40%34 year olds = 40%
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Positive remodelingPositive remodeling
ll Positive remodeling is an outwardPositive remodeling is an outward
compensatory remodeling (the Glagovcompensatory remodeling (the Glagov
phenomenon) in which the arterial wall bulgesphenomenon) in which the arterial wall bulges
outward and the lumen remainsoutward and the lumen remains
uncompromised. Such plaques grow further,uncompromised. Such plaques grow further,
although they usually do not cause anginaalthough they usually do not cause angina
because they do not become hemodynamicallybecause they do not become hemodynamically
significant for a long time. In fact, the plaquesignificant for a long time. In fact, the plaque
does not begin to encroach on the lumen until itdoes not begin to encroach on the lumen until it
occupies 40% of the crossoccupies 40% of the cross--sectional area. Thesectional area. The
encroachment must be 70% or greater to causeencroachment must be 70% or greater to cause
flow limitation. Such positively remodeledflow limitation. Such positively remodeled
lesions thus form the bulk of the vulnerablelesions thus form the bulk of the vulnerable
plaques, grow for years, and are more prone toplaques, grow for years, and are more prone to
result in plaque rupture and ACS than stableresult in plaque rupture and ACS than stableangina, as documented by intravascularangina, as documented by intravascular
ultrasound (IVUS) studies.ultrasound (IVUS) studies.
Negative remodelingNegative remodeling
ll Many fewer lesions exhibitMany fewer lesions exhibitalmost no compensatoryalmost no compensatoryvascular dilation, and thevascular dilation, and theatheroma steadily grows inward,atheroma steadily grows inward,causing gradual luminalcausing gradual luminalnarrowing. Many of the plaquesnarrowing. Many of the plaqueswith initial positive remodelingwith initial positive remodelingeventually progress to theeventually progress to thenegative remodeling stage,negative remodeling stage,
causing narrowing of thecausing narrowing of thevascular lumen. Such plaquesvascular lumen. Such plaquesusually lead to the developmentusually lead to the developmentof stable angina. They are alsoof stable angina. They are alsovulnerable to plaque rupture andvulnerable to plaque rupture andthrombosis.thrombosis.
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Acute ST elevation MIAcute ST elevation MI
ll Plaque rupture exposes the highly thrombogenic lipid core andPlaque rupture exposes the highly thrombogenic lipid core andstimulates the production of blood clots that tries to seal off thestimulates the production of blood clots that tries to seal off the
superficial crack. The clot also gets into the crack and causes itsuperficial crack. The clot also gets into the crack and causes itto rise and further obstruct the channel of the artery. Theto rise and further obstruct the channel of the artery. Thesudden increase in the obstruction caused by the raisedsudden increase in the obstruction caused by the raised
ruptured plaque and associated clot can transform a mildruptured plaque and associated clot can transform a mildblockage into a critical one within a matter of hours. This canblockage into a critical one within a matter of hours. This can
completely fill the open channel of the artery and cut off bloodcompletely fill the open channel of the artery and cut off bloodflow to the part of the heart muscle that it supplies. Withoutflow to the part of the heart muscle that it supplies. Without
oxygen and nutrients, the patient suffers from a heart attackoxygen and nutrients, the patient suffers from a heart attackand the involved heart muscle can get permanently damaged.and the involved heart muscle can get permanently damaged.
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So what are the risk factors for CAD?So what are the risk factors for CAD?
ll Hyperlipidemia (particularly LDL)Hyperlipidemia (particularly LDL)
ll High blood pressureHigh blood pressure
ll DiabetesDiabetes
ll Cigarette smokingCigarette smoking
ll Strong family history of CADStrong family history of CAD
ll Male gender, obesity, age above 50 years, lack of exercise,Male gender, obesity, age above 50 years, lack of exercise,
stress and tension can also predispose to the development ofstress and tension can also predispose to the development ofatherosclerosisatherosclerosis
ll In Malaysia, the prevalence of diabetesIn Malaysia, the prevalence of diabeteswas one to two per cent in 1960, 6.3 perwas one to two per cent in 1960, 6.3 percent in 1985, 8.3 per cent in 1996 andcent in 1985, 8.3 per cent in 1996 and
14.9 per cent in 200614.9 per cent in 2006
ll NHMS 2006 revealed thatNHMS 2006 revealed that 14.914.9 per centper centof Malaysians were diabetic,of Malaysians were diabetic, 42.642.6 perper
cent were hypertensive,cent were hypertensive, 29.129.1 per centper centwere overweight andwere overweight and 14.414.4 per cent wereper cent wereobeseobese
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10 Malaysia 11.6 | 10 Malaysia 13.8
Prevention of Cardiovascular diseasePrevention of Cardiovascular disease
ll Control your risk!!Control your risk!!
ll Good control of diabetesGood control of diabetesmellitus, blood pressuremellitus, blood pressureand cholesteroland cholesterol
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Change Our Life Style !!!Change Our Life Style !!!
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Dietary change: FatDietary change: Fat
ll Saturated fats raises LDLSaturated fats raises LDL
ll Unsaturated fats lowersUnsaturated fats lowersLDLLDL
ll TransTrans--fat increases LDLfat increases LDLand lowers HDLand lowers HDL
ll Reduce total fat to 30& ofReduce total fat to 30& ofcaloriescalories
ll Saturated fat
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Dietary change: Fruits andDietary change: Fruits and
vegetablesvegetablesll Observational studiesObservational studies
showed a reduction inshowed a reduction instroke, CHD and CVDstroke, CHD and CVD
ll WHO recommendsWHO recommends400 g /day400 g /day
Reduce weightReduce weight
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ll Epidemiological studies showedEpidemiological studies showedobesity is associated withobesity is associated withCardiovascular diseases.Cardiovascular diseases.
ll Weight reduction of 5kg reduceWeight reduction of 5kg reducesystolic BP 4.44 mmHg andsystolic BP 4.44 mmHg anddiastolic 3.57 mmHg.diastolic 3.57 mmHg.
Physical activityPhysical activity
ll Improves endothelial function,Improves endothelial function,enhances vasodilatation andenhances vasodilatation andvasomotor function in bloodvasomotor function in bloodvesselsvessels
ll WHO recommendsWHO recommends30 minute moderate30 minute moderateactivity/day or 150 minutes peractivity/day or 150 minutes perweekweek
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SmokingSmoking
ll Dont start! If you did,Dont start! If you did,then stop!!then stop!!
ll Coronary heart diseaseCoronary heart diseasemortality risk is reducedmortality risk is reducedto the same level asto the same level aspeople who never smokepeople who never smoke
after stopping for 10after stopping for 10yearsyears
ll Quit early!! Those whoQuit early!! Those whoquit between 35quit between 35--45 had45 hadsame survival as thosesame survival as thosewho never smokedwho never smoked
Alcohol IntakeAlcohol Intake
ll Protective effect ifProtective effect ifconsumed 0consumed 0--30 g/day (130 g/day (1--3u3u/day) (half in women)/day) (half in women)
ll Deleterious effect if > 89 gDeleterious effect if > 89 g/day/day
ll 1u = 150 ml wine = 250 ml1u = 150 ml wine = 250 mlbeer = 30beer = 30--50 ml spirit50 ml spirit
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ConclusionConclusion
ll Take control of your riskMake a change in yourTake control of your riskMake a change in your
lifestyle to reduce future risk of Cardiovascularlifestyle to reduce future risk of Cardiovascular
diseasedisease
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