Transcript Slide 1

Prof. Dr. Sarma VSN Rachakonda
M.D., M.Sc., (Canada), FCGP, FICP, FIMSA, FRCP (G), FCCP & FACP (USA)
Adjunct Professor Tamilnadu Dr. MGR Medical University
Sr. Consultant Physician & Cardio-metabolic Specialist
Honorary National Professor of Medicine, CGP
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Hypertension High lights
A COMPREHENSIVE APPROACH
What is new and imperative in Hypertension
Based on the latest recommendations of
JNC VII, ISH, ESH, WHO, NICE, HWG
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Globally Renowned HT Societies
1. JNC VII – Joint National Committee on HT, USA
2. ISH – WHO International Society on HT
3. AHA – American Heart Association, USA
4. ACC – American College of Cardiologist
5. BHS – British Hypertension Society
6. NIHLB – National Inst. Heart Lung & Blood vessels
7. EHS – European Hypertension Society
8. CHS – Canadian Hypertension Society
9. NKF – National Kidney Foundation, USA
10.AKA – American Kidney Association, USA
11.HWG – Hypertension Writing Group, USA
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Many Avoidable HT Deaths !
On April 12, 1945, US President Franklin D. Roosevelt died
of cerebral hemorrhage, a consequence of HT. It was a
devastating illness for him.
By current standards, President Roosevelt’s death was
unnecessary. President Roosevelt was never treated with
Anti-hypertensive drugs.
Modern treatment would have controlled his BP and
prolonged his life.
Arch Int Med, Sept, 23,1996
. . . so also of many others!
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Friends, Let Us Reflect in Us
• How many of us routinely check blood pressure at each clinic visit
• How many of us screen asymptomatic patients for hypertension
• How many of us are focused on evaluating for target organ damage (TOD)
• How many of us look for ‘Co-Thieves’ like DM, Lipids, MS, CAD, CKD
• How many us offer correct combination of treatment for HT
• How many of us insist on continued therapy and follow up
• How many of us educate of Total Lifestyle Change (TLC)
• How many of us achieve ‘Goal Blood Pressure’
• By doing all of the above, do we know how much good we do!!
• If negligent, Almighty is taking note and will sure punish us!!
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Indian Statistics
• Currently, CVD is more common
in India and China as compared to
all economically developed
countries in the world added
together.1
• Compared to 2000, the number of
years of productive life lost to
CVD will have increased in 2030
by only 20% in USA, whereas for
India, the figure is 95%.1
• For India, hypertension is
projected to increase from 16.3%
to 19.4% between 1995 and
2025.1
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1. International cardiovascular disease statistics. Am Heart Assoc. 2004.
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The New Paradigm of CVD
DM
Lipids
HT
DM
CVD
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Lipids
CVD
MS
HT
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Integrated Approach
A Paradigm Shift in Management
Individual Risk Factor Approach vs. More Integrated Strategies
• Clustering of two or
more risk factors (RFs)
was found to be
associated with
cardiovascular disease.
Individual
RFs
Total risk
approach
INTERHEART study showed that sum
of smoking, dyslipidemia, arterial
hypertension and diabetes mellitus
was responsible for about 90% of
the risk of acute myocardial
infarction.
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Volpe M. J Hum Hypertens. 2008;22(2):154157.
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CMR and CVD Paradigm
CAD
Stroke
CAD
CKD
CMRStroke
CKD
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PAD
PAD
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Percent of CV Events v/s Cost
1
EVENTS
75 %
2
3
25 %
COST
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Cardio Metabolic Continuum
REGRESS
Target organ damage
Asymptomatic
CVD
New risk factors
Atherosclerosis
Target organ damage
Symptomatic
Risk factors
Cardiometabolic risk
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CVD
Death
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Cardio Metabolic Continuum
REGRESS
Target organ damage
Asymptomatic
CVD
New risk factors
Atherosclerosis
Target organ damage
Symptomatic
Risk factors
Cardiometabolic risk
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CVD
Death
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HYPERTENSION
What we record as B.P.
It is only a marker of the bigger problem
The Truth is
Hypertension is a multi-organ systemic disease
The Problem is
Hypertension is asymptomatic in 85% of cases
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How to be wise in HT?
It is wrong
To consider Hypertension as an isolated disease
The Truth is
Hypertension, DM, Dyslipidemia, Obesity often coexist
They are the 4 pallbearers to the grave of CHD, CVD
For all of them
Primary and secondary prevention by TLC is the answer
Afflicted with one, must be screened for all other thieves
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Where are we moving ?
Arm Blood Pressure to Blood Vessel
A Systemic Vascular Disease
A Cardiovascular Disease
CV and Endocrine Disease
CV, Endocrine and Metabolic Disease
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Hypertension Approach: JNC 7 vs. HWG
Joint National Committee
(JNC 7)1
Relies primarily on BP Threshold
Early markers of CVD and
target organ damage are not
considered
Does not clearly define
moderate- to high-risk
subgroups prone to CV events
in prehypertension group
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Hypertension Writing Group
(HWG)2
Priority to CV risk factors
Early markers of CVD, target
organ damage and overt CVD
are considered
Classifies patients as either
normal or hypertensive
1. The Seventh report of the Joint National Committee on the Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure (JNC 7).
2. Giles TD, et al. J Clin Hypertens. 2005;7(9).
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Hypertension Approach: JNC 7 vs. HWG
Joint National Committee
(JNC 7)1
Relies primarily on BP Threshold
Hypertension Writing Group
(HWG)2
Priority to CV risk factors
CV risk factors and target organ damage are
not the components of classification of blood
Early markers of CVD and
Early markers of CVD, target
in JNC
target organ damage arepressure
not
organ7.
damage and overt CVD
considered
Does not clearly define
moderate- to high-risk
subgroups prone to CV events
in prehypertension group
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are considered
Classifies patients as either
normal or hypertensive
1. The Seventh report of the Joint National Committee on the Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure (JNC 7).
2. Giles TD, et al. J Clin Hypertens. 2005;7(9).
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Treatment Goal
Goal BP
Keep B.P. < 140/90 mm Hg in each patient
This may be revised to 120/80 may be ? 110/70
MRFIT’s cut off values are 115/75 mm Hg
The Truth is
It is essential to keep the B.P at or below the goal
But, It also matters how the goal B.P. is achieved !
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Definitions
As per JNC VII and ISH (WHO) 2004
1. What is normal B.P ?
2. What is pre hypertension ?
As per JNC VII and ISH (WHO) 2004
Normal SBP < 120 and DBP < 80
Pre HT SBP 120 to 139 mm Hg
DBP 80 to 99 mm Hg
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Definitions
1. What is stage 1 HT ?
2. What is stage 2 HT ?
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Stage 1
SBP 140 to 159
DBP 90 to 99
Stage 2
SBP 160 and more
DBP 100 and more
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Definitions
Are the values same for Diabetics , CKD?
No, for DM, IHD and CKD the criteria
are more stringent
The cut off values are 10 mm lower
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Stage 1
SBP 130 to 149
DBP 80 to 89
Stage 2
SBP 150 and more
DBP 90 and more
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Hypertension Optimal Treatment (HOT) Study
Reduction in CV events
25
p=0.005 (DM)
DM
non-DM
Events/1000 pt-years
20
15
10
5
0
<90
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<85
<80
Target diastolic BP
Lancet 1998; 351: 1755–62
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Rule of Halves
What is this rule of halves in HT ?
•
•
•
•
•
•
•
For every 800 adults in the community
400 are HT (either ↑ SBP or ↑ DBP or both)
Of them only 200 are diagnosed HT
Of them only 100 are started on treatment
Of them only 50 are on correct drug
Of them in only 25 the goal B.P. is attained
Means 25 ÷ 400 = 6% only have goal BP
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How many are really Dx. and Rx.ed ??
Under control (40%)
Diagnosed
HT
37%
Hypertensives
(22%)
Normotensives (78%)
63%
Under
Un Rx.
treatment
HT
(50%)
(7.5% of the total
hypertensives)
Uncontrolled
hypertension (60%)
Undiagnosed
HT
A study from Europe on 23,339 patients
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Isolated Systolic Hypertension
1. What is ISH ? –
2. What percentage of 65+ aged have ISH ?
3. Which is more harmful – ↑ SBP or DBP ?
4. Why is ISH important ?
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Relative prevalence of SBP and DBP
40 + yrs
ISH
S&DHT
DHT
Normal
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R R for CVD - SBP and DBP
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ISH is universal after 65+
Persons who are normo-tensive at age 55
have a 90% lifetime risk for developing HTN.
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HT- RR of stroke and MI
20
5 Year Risk (%)
Normotensives
Hypertensives
15
10
Stroke
Myocardial
Infarction
5
0
0
20
40
60
80
100
120
140
160
180
200
220
240
260
280
300
Systolic Blood Pressure (mmHg)
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Brown, M.J. Lancet 2000; 355: 659 - 660
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Is SBP more dangerous or DBP ?
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Practice Points for Using
WHO/ISH Scoring System
CVD risk may be higher than indicated by the charts if following are seen
• Already on antihypertensive therapy
• Raised triglyceride level
• Premature menopause
• Low HDL
• Approaching the next age category or
systolic blood pressure category
• Raised levels of HsCRP, fibrinogen,
homocysteine, apoB or Lp(a), IFG, IGT
• Obesity (including central obesity)
• Micro albuminuria (increases the 5year risk of diabetes by about 5%)
• Sedentary lifestyle
• Raised pulse rate
• Family history of premature coronary
heart disease (CHD) or stroke in firstdegree relatives (male aged <55 years,
female <65 years)
• Socioeconomic deprivation
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http://www.who.int/cardiovascular_diseases/guidelines/Chart_predictions/en/index.htm Accessed on: 21 March 2013.
Isolated Systolic Hypertension
1. What is ISH ? –
SBP 140+ , DBP < 90
2. What percentage of 65+ aged have ISH ?
More than 90%
3. Which is more harmful – ↑ SBP or DBP ?
Of course ↑ SBP
4. Why is ISH important ?
Because of ↑↑ CVA and CHD mortality
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For adequate control of B.P.
Do you think we can control most of the
patients of hypertension with –
One drug
Two drugs
Three drugs
Can’t control
In most of the patients of hypertension
Two drugs are required for adequate control
More so if the initial BP is 20/10 above the goal
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TODAY’S PARADIGM
Gone are the days of monotherapy
It is the era of combination therapy
Why is it so?
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CVD Risk Factors
What are the so called CHD risk factors ?
What are known as CHD risk equivalents ?
What is Framingham risk score ?
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Global Risk Profile and HT
25)
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Dr.Sarma@works
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HT combined with other CHD RF
Framingham offspring study, subjects aged 17 – 84
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CVD Risk Factors
What are the so called CHD risk factors ?
List discussed in previous slide
What are known as CHD risk equivalents ?
DM, PVD, CVA, Nephropathy, Retinopathy
What is Framingham 10 CHD risk estimate ?
10 year CHD risk estimate based on age,
sex, smoking, TC, HDL, SBP, Rx. for HT
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Target Organ Damage
Why is there TOD in HT ?
What are the organs targeted for damage ?
What is the basis of TOD ?
What tests we need to do to assess HT ?
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Diseases Attributable to Hypertension
Coronary heart disease
Stroke
Heart failure
Cerebral hemorrhage
Myocardial infarction
Left ventricular
hypertrophy
Hypertension
Chronic kidney failure
Hypertensive
encephalopathy
Aortic aneurysm
Retinopathy
Peripheral vascular disease
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Adapted from: Arch Intern Med 1996; 156:1926-1935.
All
Vascular
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Target Organ Damage (TOD)
• Heart
Left ventricular hypertrophy (LVH)
Angina or prior myocardial infarction (CHD)
Prior Coronary revascularization PTCA or CABG
Heart failure (Systolic / Diastolic dysfunction)
• Brain
CVA Stroke or Transient Ischemic Attack (TIA)
• Kidney : Chronic kidney disease and CRF
• Vessels : Peripheral arterial disease PVD
• Eyes : Hypertensive Retinopathy
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Atherosclerosis – Time line
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Dr.Sarma@works
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Endothelial NO Balance
NO
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Target Organ Damage - Assessment
Routine Tests
• Electrocardiogram, Echocardiography (desirable)
• Urinalysis for proteinuria, Microalbuminuria
• Blood glucose (F and PP), and Hematocrit
• Serum Na and K, Creatinine or GFR, Calcium
• Lipid Profile complete, Eye examination, ABI
Optional tests
• X-Ray Chest PA
• 24 hr. urine albumin excretion or ACR
• More extensive testing is not generally indicated
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Target Organ Damage
Why is there TOD in HT ?
It is a disease of blood vessels.
What are the organs targeted for damage ?
Heart, brain, kidney, eye, peripheral vessel
What is the basis of TOD ?
ED, Arterial stiffness and Atherosclerosis
What tests we need to do to assess TOD ?
List discussed
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Paradigm Shift in HT Therapy
It is not just ↓B.P.
TODAY we must strive to
1. Alter the modifiable risk factors
2. Keep the SBP < 140 and DBP < 90
3. Prevent or halt or reduce TOD –
• LVH, CHD, CHF, CVA, CRF, PVD & Retino.
4. Prevent or control DM (as HT + DM is hazardous)
5. Prevent or control Dyslipidemia (Endothelial Dysf.)
6. Reduce morbidity and mortality
7. Improve QUALY – Quality Adjusted Life Years
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Target Organ Damage
What is single most imp. predictor of CHD, HF, Death ?
What time course of HT to LVH to LVF to death ?
Can LVH be regressed at all ?
Will drugs help to regress LVH and ↓TOD ?
How important is Micro-albuminuria ?
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Transverse Section of HEART - LVH
10 mm
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Dr.Sarma@works
25 mm
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Echocardiography of Heart - LVH
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Dr.Sarma@works
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ECG and Left Ventricular Hypertrophy
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Chest PA view of Heart - LVH
C/T ratio > 50%
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Progression of HT to LVH to HF
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Survival Rate HT + LVH v/s NT + LVH
Source : Am Hear J, 2000; 140 (6) : 848-856.
1.00
0.99
Nomotensive-No LVH
Portion Surviving
0.98
0.97
Hypertensive-No LVH
0.96
Normotensive-LVH
0.95
Hypertensive-LVH
0.94
0.93
0
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2
4
6
8
10
12
Survival Time (Years)
14
16
18
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Can LVH be reduced at all ??
0
-10
-20
-30
-40
-50
-60
-70
-80
-90
D
A
B
C
A+D
LVH is the Single Most important predictor
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Will Treatment Help ??
0
-10
-20
-30
-40
-50
-60
CHF
CVA
LVH
CVD
CHD
Combined results of 17 RCTs ( n = 48,000)
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Hebert 1993, Moser 1996
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Value of excellent vs. good blood pressure control in NIDDM
(144/82 vs. 154/87mmHg)
Patients With Events (%)
40
Less tight control
Tight control
30
20
10
0
0
9
1
2
3
4
5
6
Years From Randomisation
7
8
Reduction in risk with tight control 32% (95% CI 6% to 51%) (P=0.019)
UKPDS, BMJ 1998;317:703-713.
MAU as a Predictor of Morbidity and Mortality
Retinopathy
LVH
All-cause
mortality
Diabetes
+
MAU
Nephropathy
Non-fatal
cardiovascular
disease
Peripheral/autonom
ic neuropathy
Parving HH. J Hypertens 1996;14 Suppl 2:S89-S94.
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Definitions of abnormalities in albuminuria
Category
24 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 (macro)
albuminuria
 300
 200
 300
Because of variability in urinary albumin excretion, 2 of 3 specimens over
3-6 mon 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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Relative Importance of MAU
10.02
10
8
6.52
6
CHD Odds
Ratio
4
3.20
2.32
2
0
Microalbuminuria
Smoking
Hypertension
Cholesterol
Eastman RC, Keen H. Lancet 1997;350 Suppl 1:29-32.
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Target Organ Damage
What is single most imp. predictor of CHD, HF, Death ?
LVH – LV mass index
What is the time course of HT to LVH to LVF to death ?
The chart is explained
Can LVH be regressed at all ?
Very much Yes. ACEi/ARBs, Diuretics are the best
Will drugs help to regress TOD ?
Yes. All TOD regresses; LVF and CVA most
How important is Micro-albuminuria ?
The most important prognostic indicator of TOD
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Clinical Signs of LV Dysfunction
Hypotension
Pulsus alternans
Trigeminy, Bigeminy
Reduced volume of carotid
LV apical
Enlargement/displacement
Sustained heave of apex –
Change in heart sounds
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Soft S1
Paradoxically split S2
S3 gallop
S4 impaired LV compliance)
Mitral regurgitation
Pulmonary congestion rales
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Ankle-Brachial Index
Resting and post exercise SBP in ankle and arm.
1. Normal ABI > 1 (Ankle BP more than the arm BP)
2. ABI < 0.9 has 95% sensitivity for angiographic PVD
3. ABI of 0.5- 0.84 correlates with claudication
4. ABI < 0.5 indicates advanced ischemia
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Dippers & Non Dippers
What is this pattern in HT – Dippers and Non-dippers ?
What is its significance and clinical relevance ?
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Dippers & Non Dippers
Systolic Blood Pressure
Systolic Blood Pressure (mm Hg)
160
150
140
Non - dippers
130
Dippers
120
110
6
8
10
12
14
16
18
20
22
24
2
4
24 hours clock time
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Yonsei, Med J, Vol 43, No 3: 2002
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Dippers & Non Dippers
Diastolic Blood Pressure (mm Hg)
Diastolic Blood Pressure
100
90
Non - dippers
80
Dippers
70
6
8
10
12
14
16
18
20
22
24
2
4
24 hours clock time
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Yonsei, Med J, Vol 43, No 3: 2002
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Dippers & Non Dippers
1. Less than 10% circadian variation in SBP and DBP
2. Essential hypertension patients are – usually ‘Dippers’
3. Non dippers are Dx. by ABPM – They are usually
1.
2.
3.
4.
5.
6.
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Secondary HT cases
More end organ damage
More LVH
More responsive to salt restriction
Diabetics are non dippers
Diuretics convert a non dipper to dipper
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Ambulatory Blood Pressure Monitoring - ABPM
1.
2.
3.
4.
24 hour B.P monitoring (every 15 minutes)
Today - 24 hour B.P. control is essential
Identifies dippers and non-dippers
Excludes white coat hypertension
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Pulse Wave Velocity (PWV) – Arterial Stiffness
Systole
Diastole
PulseTrace PCA
Sphygmocor
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Indications for ABPM
 Unusual variability of Blood Pressure
 To confirm ‘White Coat’ hypertension
 Evaluation of nocturnal hypertension
 Evaluation of drug resistant hypertension
 To determine efficacy of drugs over 24 hours
 Diagnosis and Rx. of hypertension in pregnancy
 Evaluation of symptomatic hypotension
 Informing equivocal treatment decisions
What is MOST essential ??
 Not that ‘my drug is superior to yours’
 Not that ‘this trial is better than that’
 Nor ‘this combination is better than that’
 But to get AS MANY PEOPLE as we
can to goal SBP < 140 & DBP < 90
 And prevent or halt TOD.
 Of course, tailor the treatment as per
individual patient’s co-morbidities.
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Morbidity and Mortality in HT
Most of the morbidity and mortality of HT is due to
 LVH – LV diastolic and systolic dysfunction
 Increased risk of Coronary Artery Disease
 Increased risk of Cerebral Vascular Disease
 Hypertensive heart failure
 Chronic Renal Disease of hypertension
 Hypertensive vascular damage
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The correct Approach to HT
• Are all patients screened for hypertension?
Step1 • Are all hypertensives correctly identified?
• Are they evaluated for co-morbidities/TOD?
Step 2 • Are they assessed for CHD risk factors?
• Are the correct drug combinations prescribed?
Step 3 • What is the compliance for medicines & f/u?
• Is the goal B.P. achieved and maintained?
Step 4 • Are there any complications/ side effects?
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Lifestyle Modification
1. Life style modification is the sheet anchor
in the management Hypertension.
2. This surely reduces the number of drugs
used and their dosage in controlling HT.
3. Any drug treatment has value only when
coupled with Life style modification.
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Lifestyle Modification
Modification
Weight reduction
Approximate BP reduction
(range)
5–20 mm/10 kg wt loss
Adopt DASH eating plan
8–14 mmHg
Dietary sodium reduction
2–8 mmHg
Physical activity
4–9 mmHg
Abstinence from alcohol
2–4 mmHg
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All put together reduce BP by 20 to 55 mmHg
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What to choose from the ocean
 16 different classes of drugs
 117 approved molecules as on date
 Innumerable drug combinations
Over 1800 clinicalchange
trials of repute
Nosignificant
in the
 Five international
proportion
of HTsocieties
underon HT
control
 Seven JNC guidelines so far, 8th is ready
 Multiple target organs damage
 Many co-morbidities
 Varied outcomes of interest
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 Cost constraints
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The Many Faces of HT Therapy Today
Hypertension
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Physicians’ Bias in HT
 Isolated SHT is often dubbed as ‘aging factor’
 To consider HT is only in the ‘ARM’ and not in the body
 No concept of ‘pulse pressure’ – Not seeing the whole
 Worry about side effects – Need to watch, not to worry
 OK, some control is achieved – why attain goal BP ?
 Not insisting on compliance with drugs and assessments
 Pressure from patients – B.P. How much ? How much ?
 Concentrating on the pill and not on the ill – TLC forgotten
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Antihypertensive Drug Classes: Action Sites
Antihypertensive Drug Classes
Blood
Pressure
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=
Cardiac
Output
-Blockers

Total Peripheral
Resistance
-Blockers
ACE Inhibitors
AT1 Blockers
Direct renin inhibitors
1-Blockers
2-Agonists
Non-DHP
CCBs
All CCBs
Diuretics
Sympatholytics
Diuretics
Vasodilators
ACE = angiotensin-converting enzyme; AT1 = angiotensin type 1;
CCBs = calcium channel blockers; DHP = dihydropyridine
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Anti Hypertensive drug classes
The
A, B, C, D
approach
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The A B C D classes
D
A
Diuretics
ACEI, ARB
D A
B C
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B
C
β-Blockers
Ca-Blockers
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Anti Hypertensive drug classes
 ACEi – Angiotensin converting enzyme
inhibitors – Ramipril- let us call them ‘A’
 ARB – Angiotensin Receptor Blockers –
Losartan - Let us call them also as ‘A’
 BB – Beta Receptor Blockers – Metoprolol,
Carveidilol, Nebivolil - let us call them ‘B’
 CCB – Calcium channel blockers – Amlodepine
Cilnidepine, Diltiazem - let us call them ‘C’
 Diuretics – Hydrochlor Thiaz.- Furosemide,
CTH, Spiranolactone - let us call them ‘ D ’
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AB/CD Rule – HT Treatment
(AB/CD = ACEi, Beta-blocker
Ca++-blocker, Diuretic)
AGE
Renin
Younger (< 55)
High Renin HT
I ACEi
II
BB
A+B
Resistant HT /
Intolerance
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III
Older (> 55)
Low Renin HT
III
A+B+D
D+C+A
CCB
Diuretic I
D + C II
IV: Add / substitute alpha blocker
V: Re-consider 20 causes  trial of spironolactone
Dickerson et al. Lancet 353:2008-11;1999
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Hypertension – Why Combinations ?
 It is imperative to consider 2 drugs – not monotherapy
 Complimentary to each other - help achieve the goal BP
 Two agents sometimes nullify each others side effects
 Fixed dose combinations will reduce the no. of tablets
 Once daily formulations are good for compliance
 Nocturnal dosing – Chronotherapy – reduces CV events
 Sustained release or LA formulations for 24 h BP control
 Use of triple drug therapy if goal B.P is not achieved
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Drug Combinations
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ABCD Compare & Contrast
Parameter
Diuretic
ACEi, ARB
βblocker
Ca+ Blocker
Ischemia
No effect
Improves
Improves
Negative
LVH, LVF
Improves
Improves
Improves*
Negative
CV Mortality
Improves
Improves
Improves
Increases
Heart rate
No effect
No effect
Bradycardia
Tachycardia
Use in DM
Negative
Excellent
Negative
Negative
Lipid effects
Negative
Excellent
Negative
Neutral
Fluid & Na
Enhances
No effect
Vasoconstr.
Vasodilatory
K ex / bronchi Enhances
No effect
Bronchospa
No effect
UA / Conduct. ↑ Uric acid
No effect
↓conduction
No effect
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Drugs in Each Class
DIU
•
•
•
•
•
•
•
HCZ
Chlortha
Indapami
Furosemi
Torsemid
Spirono
Triamter
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ACEi
•
•
•
•
•
•
•
Ramipril
Enalapril
Lisinopril
Perindopr
Quinapril
Captopril
Benazopr
ARB
•
•
•
•
•
•
•
Losartan
Olmesartan
Telmisartan
Valsartan
Irbesartan
Candesart
Eprosartan
BB
•
•
•
•
•
•
•
•
Metoprol
Carvedio
Nebivol
Bisoprol
Labetolol
Pindolol
Proprano
Atenelol
CCB
•
•
•
•
•
•
•
Amlodipine
Cilnidipine
Nefidipine
Felodipin
Nitrendipin
Verapamil
Diltiazem
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Persistence with hypertensive therapy
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Take Home Points in Hypertension
1. High B.P recorded is only a clinical marker of CV disease
2. HT is a multi-organ disease, often asymptomatic
3. Not to consider in isolation- Must look for ‘Co-Thieves’
4. Today’s goal BP is 140/90 – It will sure be less tomorrow
5. It matters to attain goal; matters more how it is attained
6. In DM, CKD, IHD the cut off values are 10 mm less
7. Remember rule of ½ in HT– Adequate control only in 7%
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Take Home Points in Hypertension ..
8. ↑ SBP is more important than ↑ DBP; Often ignored it is !
9. Wide pulse pressure (SBP-DBP) signifies arterial damage
10. Day’s of monotherapy have gone; Combined Rx replaces
11. All HT must be screened for CHD risk factors & addressed
12. Target organ damage (TOD) must be investigated and Rx.
13. LVH is the single most predictor of mortality and morbidity
14. ABI, MAU, ABPM, PWV etc., identify high risk cases early
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Mandatory Ten Commandments
 Check and Screen every one of 20+ for hypertension
 Diagnose early, treat early, prevent the onslaught
 Screen for associated CV Risk factors – a must
 Evaluate TOD – Do not stop short at arm B.P recording
 Insist on compliance, follow up and achieve Goal B.P
 Consider Ambulatory BP monitoring – Dippers/Non/WC
 Use at 2 drugs with complimentary actions, step up
 Chronotherapy – nocturnal dosing to avoid CVD
 Put every hypertensive on vascular protection – BP to BV
 Patients of DM, CAD, CKD & PAD – be more comprehensive
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Many Gulfs to be Bridged
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