A.ht & Downstream Effects

7/28/2019 A.ht & Downstream Effects

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Kriengkrai Hengrussamee MD.

Central Chest Institute

Nonthaburi, Thailand

[email protected]

HT&

Downstream

Effects

Whattolookforinanoutpatient

clinic

1 HT & Downstream effects&OPD


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THE CARDIOVASCULARCONTINUUM

5

DM,HT & IR

Endothelialdysfunction

Vasculardisease

Constriction,inflammation,Hypertrophy,hyperplasia,atherogenesis,thrombosis

Tissue injuryMI,stroke,glomerular

ischemia

PathologicalremodellingLVH,LVE,glomerulosclerosis

Target-organdysfunction

HF,nepropathy

End-stageorgan failur

Death

Maladaptive remodeling

In-hospital management of HF-KK


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The prevalence of HT in adult~30-40%


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HT & Downstream effects&OPD


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Hypertension,theglobal majorhealthproblem

Downstreameffectsof HTWhattolookfor inanoutpatientclinic

Headlines

HT & Downstream effects&OPD17


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DefinitionDownstream effect

= Relating to or happening at a later

stage in a process

HT and downstream effect

=HT and its complication or target

organ damage18 HT & Downstream effects&OPD


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Downstream Effects of HT

Sub-

clinical/Asymptomatic

CVD (LVH) CVA (Increasecarotid IMT) Renaldiseases

(MAU/AU/CKD)

PAD (abnormalABI)

Clinical/Symptomatic

CVD (HTCVD,CAD,CHF) CVA Renaldiseases PAD



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Healthy artery vs. Artery in HT(Atherosclerosis)



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HT is a significant riskfactor for:

cerebrovascular

disease

coronary arterydisease

congestive heart

failure

renal failure peripheral vascular

disease

dementia

atrial fibrillation


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Learn more from ADHERE

25

Figure 3: Aetiology and co-morbidity

-

10

20

30

40

50

60

70

Coronary Artery

Disease

A-fib/flutter Hypertension Diabetes

%o

fpatients Thai ADHERE

RiksSvikt

EHFS I

EHFS II

A Thai ADHEREcomparison to Europe (in press)


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Causes of HF in THAI(THF registry)

management of CHF 2008

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What to look for in an outpatient

HT clinic

Subclinical

CVD (LVH) CVA (Increase

carotid IMT) Renaldiseases

(MAU/AU/CKD) PAD (abnormal

ABI)

Clininical

CVD CVA Renaldiseases PAD

Comobidities

& OtherCV

riskfactors

DM Dyslipidemia Cigarettesmoking Mets



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30 HT & Downstream effects&OPD ESC CVD Prevention


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LIFE Study Change in Cornell Voltage

Duration Product and Sokolow-Lyon

-18

-16

-14

-12

-10

-8

-6

-4

-2

0Cornell Product Sokolow-Lyon

Changefrombase

line(%)

LosartanAtenolol

P


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HT & LVHACEI orARBinduceregressionof

LVHdecreasesadverse

cardiovasculareventsandimproves

overallsurvival.

Whenmodifyingmedicationsin

hypertensivepatients, itisimportant

torememberthatthetreatmentof

LVHisnotsynonymouswithblood

pressurecontrol.33 HT & Downstream effects&OPD


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Carotid B-Mode Ultrasonography

Measurement of intimal medial thickness

Non-invasive, inexpensive, no radiation

Well-established as an indicator of cardiovascular

risk from epidemiologic studies

Published clinical trials on utility of carotid IMT as

measure of progression of atherosclerosis and

effects of therapy

Accuracy of assessments depends on experience

of those interpreting scans

ACCF/AHA 2010 Guideline: CIMT

measurement may be reasonable for CV risk

assessment in asymptomatic adults at

intermediate risk (Class IIa-B)


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C di l H lth St d C bi d


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Cardiovascular Health Study: Combinedintimal-medial thickness predicts total MIand stroke

Cardiovascular Health Study (CHS) (aged 65+): MI or stroke rate 25% over 7 years in

those at highest quintile of combined IMT (OLeary et al. 1999)


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CVATIA/RIND/Ischemicstroke

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ESC CVD Prevention 2012


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FromabnormalABI to PAD 43HT & Downstream effects&OPD


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ABI and Total Mortalty(ABI Collaboration, JAMA 2008)


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Definitions of abnormalities in albumin excretion

Category24 hour

collection

(mg/24h)

Timed collection

(g/min) Spot collection(g/mg Cr)Normal < 30 < 20 < 30

Microalbuminuria

30-299 20-199 30-299

Clinical

albuminuria 300 200 300

Because of variability in urinary albumin excretion, 2 of 3 specimens

over

3-6 should be abnormal before considering diagnostic threshold

positive

False positive: exercise < 24 hours, fever, CHF, marked hyperglycemia,

marked HTN, pyuria and hematuria.


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E l CKD i HT


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Early CKD in HT




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Assessmentof HT Patients

HT

Confirm

Diagnosis

Detect

TargetOrgan

Damage&CVD

Cardiovascular

riskcalculation

Loof for

Secondary

Causes



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BENEFITS OF LOWERING BP

(12/6 mmHg) Stroke 35-40%

MI 20-25%

CCF 50%

Stage 1 with 1 risk factor, SBP 12 mmHg

for 10 years prevents 1 death for 11 treated

Stage 1 plus TODonly 9 patients



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HT & Downstream effects&OPD 66

Ri k F t


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RiskFactors 1



Ri k F t


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RiskFactors 2

68HT & Downstream effects&OPDESC CVD Prevention 2012


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RiskFactors 3



C di l M t lit Ri k D bl ith E h


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1X risk2X

risk

Cardiovascular mortality risk

0

2

4

8

115/75 135/85 155/95 175/105

6

Systolic BP/Diastolic BP (mmHg)

*Individuals aged 4069 years

4X

risk

8X

risk

Cardiovascular Mortality Risk Doubles with Each

20/10 mmHg Increase in Systolic/Diastolic BP*

Lewington et al. Lancet 2002;360:190313


Cardiovascular Mortality Risk Doubles with


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Lewington et al. Lancet 2002;360:190313

Each 20/10 mmHg Increment in

Systolic/Diastolic BP*

Cardiovascular mortality risk

0

2

4

8

115/75 135/85 155/95 175/105

6

Systolic BP/Diastolic BP (mmHg)

*Individuals aged 4069 years

2X

risk

4X

risk

8X

risk

1X risk

BenefitBenefit not established

The closer to target

the less reliable to

office BP becomes


CV Risk in Men With Hypertension Rises


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CV Risk in Men With Hypertension RisesWith Other Additional CV Risk Factors

4

6

10

14

21

40

0

6

12

18

24

30

36

42

SystolicBP 150-160

Cholesterol240-262

SystolicBP 150-160

SystolicBP 150-160

Cholesterol240-262

HDL-C 33-35

SystolicBP 150-160

Cholesterol240-262

HDL-C 33-35

Diabetes

SystolicBP 150-160

Cholesterol

240-262

HDL-C 33-35

Diabetes

Smoking

SystolicBP 150-160

Cholesterol240-262

HDL-C 33-35

Diabetes

Smoking

ECG-LVH

A combination of high BP and high serum cholesterol increases the risk of CHD,

especially in men

Adapted from Kannel.Am J Hypertens. 2000;13:3S-10S.

10-Year%

Probab

ilityofEvent


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Table 5. Reynolds Risk Score Applied to Population of U.S. Men.


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Tattersall MC, Gangnon RE, Karmali KN, Keevil JG (2012) Women Up, Men Down: The Clinical Impact of Replacing the

Framingham Risk Score with the Reynolds Risk Score in the United States Population. PLoS ONE 7(9): e44347.

doi:10.1371/journal.pone.0044347

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044347 76 HT & Downstream effects&OPD
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044347http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044347http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044347http://www.plosone.org/article/info:doi/10.1371/journal.pone.0044347


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A cohort of patients with high risk forcardiovascular events : CORE Thailand)



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Patients characteristicsN=4981(%)

CV risk factorsDM 3157 (63.4)HT 4131 (82.9)Dyslipidemia 4261 (85.5)Smoking (current) 292 (5.9)CKD 981 (19.7)FHx of premature athero 406 (8.2)



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Awareness Treatment Control

HT Managemnet


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Undertreatment of Risk Factors in PatientsW ld id *1


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Worldwide*1

159

65 64

34

4344 43

17

40

28

53

43

17

60

48

21

56

1513

52

24

7

56

0

20

40

60

80

100

Elevated blood

pressure (140/90 mm

Hg)

Elevated cholesterol

(200 mg/dL)

Continued smoking (5

cigarettes/d)

Patientsnotachievingtarget(%) North AmericaLatin America

Western EuropeEastern EuropeMiddle EastAsiaAustraliaJapan

*Data shown may differ slightly from published abstracts owing to a subsequent database lock.

1. Bhatt DL et al, on behalf of the REACH Registry Investigators.JAMA 2006; 295(2): 180-189.

Patients not achieving target

(% of regional population)1


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Hypertension,theglobal majorhealthproblem

Downstreameffectsof HTWhattolookfor inanoutpatientclinic


Diseases Attributable to


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Hypertension

Hypertension

Heart failureStrokeCoronary heart disease

Myocardial infarction

Left ventricular

hypertrophy

Aortic aneurysmRetinopathy

Peripheral vascular disease

Hypertensive

encephalopathy

Chronic kidney failure

Cerebral hemorrhage

Adapted from: Arch Intern Med 1996; 156:1926-1935.

All

Vascular90


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HT& Target Organ Damage

HT

AtherosclerosisVasoconstriction

Carotid IMT & bruit

Vascular hypertrophy

Endothelial dysfunction

Ankle brachial index

LV hypertrophy

Fibrosis

Remodeling

Apoptosis

GFR Proteinuria ALdosterone releaseGlomerular sclerosis

Stroke

Hypertension

Heart failure

MI

Renal failure

Death

Adapted from Willenheirrer et al. Eur Heart J 1999,20:997; Jahlof. J Hum Hypertens.1995;9(suppl6):S37;Daugherty et al. J Clin Invest 2000; 105:1605; Fynrquist

et al. J Hum Hypertens. 1995; 9(suppl5): S19Bcoz and Baker. Heart Fail Rev. 1998; 3: 125; Beers and Berkow, eds. The Merck Manual of DiagnosisAnd

Therapy; Andersor. Exp Nephrol 1996;4(suppl1):34; Fogo. Am J idney Dis. 2000;36:179.


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How to approach HT patients?

History Clinical signs & symptoms Lab;

Urine strip test for blood and protein

Blood electrolytes and creatinine, and eGFR

Blood glucose & lipid (LDL-C, TG,HDL)

Serum total and HDL cholesterol

CXR12 lead ECG

UA, MAU, renal function test (eGFR)93 HT & Downstream effects&OPD

Important Aspects of the Physical Examination in the


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p p y

Hypertensive Patient

Accurate measurement of blood pressure General appearance: distribution of body fat, skin

lesions, muscle strength, alertness

Fundoscopy

Neck: palpation and auscultation of carotids, thyroid

Heart: size, rhythm, sounds

Lungs: rhonchi, rales

Abdomen: renal masses, bruits over aorta or renalarteries, femoral pulses

Extremities: peripheral pulses, edema

Neurologic assessment


Clinical Signs of LV Dysfunction


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Clinical Signs of LV Dysfunction

Hypotension

Pulsus alternans

Reduced volume

carotid LV apical

enlargement/displace

ment

Sustained apex - to

S2

Soft S1

Paradoxically split S2

S3 gallop

(not S4 = impairedLV compliance)

Mitral regurgitation

Pulmonarycongestion

rales


Investigation of all patients with hypertension:


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g p yp

1. Urinalysis

2. Complete blood cell count

3. Blood chemistry (potassium, sodium andcreatinine)

4. Fasting glucose

5. Fasting total cholesterol, high-density

lipoprotein (HDL) cholesterol, low-density

lipoprotein (LDL) cholesterol, triglycerides

6. Standard 12 ECG

7. CXR

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Target Organ damage detection Left ventricular hypertrophy(ECG: Sokolow-Lyons>38 mm

Echo ; LVMI ; M 125,F 110 g/m2)

Vascular ultrasound

Carotid IMT 0.9 mm or positive atheroscleroticplaque

Microalbuminuria

(30-300 mg/24 h; albumin-creatinine ratio M 22,W

31 mg/g) Slight increase in serum creatinine

(M1.3-1.5 , W 1.2-1.4 mg/dl)


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The Heart Association of Thailand underthe Royal Patronage of H.M. the King


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y g g

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A.ht & Downstream Effects