prof. dr. sarma vsn rachakonda
DESCRIPTION
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. www.drsarma.in. - PowerPoint PPT PresentationTRANSCRIPT
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Prof. Dr. Sarma VSN RachakondaM.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
www.drsarma.in
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What is new and imperative in Hypertension
Based on the latest recommendations of
JNC VII, ISH, ESH, WHO, NICE, HWG
Hypertension High lights
A COMPREHENSIVE APPROACH
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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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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!
Many Avoidable HT Deaths !
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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
1. International cardiovascular disease statistics. Am Heart Assoc. 2004.6
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The New Paradigm of CVD
CVD
7
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Integrated Approach A Paradigm Shift in Management
• Clustering of two or more risk factors (RFs) was found to be associated with cardiovascular disease.
Individual Risk Factor Approach vs. More Integrated Strategies
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.
Volpe M. J Hum Hypertens. 2008;22(2):154157. 8
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CMR and CVD Paradigm
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1
2
3
COST
75 %
25 %
Percent of CV Events v/s Cost
EVENTS
10
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Cardio Metabolic Continuum
REGRESSR
ETAR
D
Target organ damageAsymptomatic
Target organ damage
Symptomatic
Death
CVDNew risk factors
Risk factorsCardiometabolic risk
PREV
ENT
Atherosclerosis
CVD
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REGRESSRETA
RD
Target organ damage
Asymptomatic
CVDNew risk factors
Risk factorsCardiometabolic risk
PREV
ENT
Target organ damage
Symptomatic
Death
Atherosclerosis
CVD
Cardio Metabolic Continuum
12
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HYPERTENSION
The Truth is
It is only a marker of the bigger problem
Hypertension is a multi-organ systemic disease
What we record as B.P.
The Problem is
Hypertension is asymptomatic in 85% of cases
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How to be wise in HT?
The Truth is
To consider Hypertension as an isolated disease
Hypertension, DM, Dyslipidemia, Obesity often coexistThey are the 4 pallbearers to the grave of CHD, CVD
For all of them
Primary and secondary prevention by TLC is the answerAfflicted with one, must be screened for all other thieves
It is wrong
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Where are we moving ?
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Hypertension Approach: JNC 7 vs. HWG
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). 16
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Hypertension Approach: JNC 7 vs. HWG
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). 17
CV risk factors and target organ damage are not the components of classification of blood
pressure in JNC 7.
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Treatment Goal
The Truth is
Keep B.P. < 140/90 mm Hg in each patientThis may be revised to 120/80 may be ? 110/70 MRFIT’s cut off values are 115/75 mm Hg
It is essential to keep the B.P at or below the goalBut, It also matters how the goal B.P. is achieved !
Goal BP
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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) 2004Normal 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 ?
Stage 1 SBP 140 to 159 DBP 90 to 99
Stage 2 SBP 160 and moreDBP 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
Stage 1 SBP 130 to 149 DBP 80 to 89
Stage 2 SBP 150 and moreDBP 90 and more
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Hypertension Optimal Treatment (HOT) Study
Lancet 1998; 351: 1755–62
p=0.005 (DM)
0
5
10
15
20
25
Ev
ents
/10
00 p
t-y
ears
<90 <85 <80
Target diastolic BP
DM
non-DM
Reduction in CV events
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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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Normotensives (78%)Normotensives (78%)
Hypertensives (22%)
Under control (40%)
(7.5% of the total hypertensives)
Uncontrolled hypertension
(60%)
Diagnosed HT
Diagnosed HT Under
treatment (50%)
Under treatment
(50%)
Undiagnosed HT
How many are really Dx. and Rx.ed ??
37%
63%
Un Rx. 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
Normal
ISH
DHT
S&DHT
40 + yrs
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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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0
5
10
15
20
00 100100 200200 300300
5 Y
ea
r R
isk
(%
)
Stroke
Myocardial Infarction
Systolic Blood Pressure (mmHg)
HT- RR of stroke and MI
Brown, M.J. Lancet 2000; 355: 659 - 660
20 40 60 80 120 140140 160 180 220 240 260 280
Normotensives Hypertensives
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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 5-year risk of diabetes by about 5%)
• Sedentary lifestyle • Raised pulse rate• Family history of premature coronary
heart disease (CHD) or stroke in first-degree relatives (male aged <55 years, female <65 years)
• Socioeconomic deprivation
http://www.who.int/cardiovascular_diseases/guidelines/Chart_predictions/en/index.htm Accessed on: 21 March 2013.
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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 thepatients of hypertension with –
One drugTwo drugsThree drugsCan’t control
In most of the patients of hypertension Two drugs are required for adequate controlMore 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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What are the so called CHD risk factors ?
What are known as CHD risk equivalents ?
What is Framingham risk score ?
CVD Risk Factors
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Global Risk Profile and HT
25)
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HT combined with other CHD RF
Framingham offspring study, subjects aged 17 – 84
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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
CVD Risk Factors
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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 ?
Target Organ Damage
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Diseases Attributable to 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.
AllVascular
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Target Organ Damage (TOD)
• Heart Left ventricular hypertrophy (LVH)Angina or prior myocardial infarction (CHD)Prior Coronary revascularization PTCA or
CABGHeart 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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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, ABIOptional tests • X-Ray Chest PA• 24 hr. urine albumin excretion or ACR• More extensive testing is not generally indicated
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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
Target Organ Damage
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It is not just ↓B.P.
Paradigm Shift in HT Therapy
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
TODAY we must strive to
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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 ?
Target Organ Damage
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Transverse Section of HEART - LVH
10 mm 25 mm
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Echocardiography of Heart - LVH
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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
1.00
0.99
0.98
0.97
0.96
0.95
0.94
0.9320 4 6 8 10 12 14 16 18
Survival Time (Years)
Hypertensive-LVH
Normotensive-LVH
Hypertensive-No LVH
Nomotensive-No LVH
Port
ion
Surv
ivin
g
Source : Am Hear J, 2000; 140 (6) : 848-856.
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LVH is the Single Most important predictor
-90
-80
-70
-60
-50
-40
-30
-20
-10
0
D A B C A + D
Can LVH be reduced at all ??
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-60
-50
-40
-30
-20
-10
0
CHF CVA LVH CVD CHD
Combined results of 17 RCTs ( n = 48,000)
Hebert 1993, Moser 1996
Will Treatment Help ??
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Value of excellent vs. good blood pressure control in NIDDM(144/82 vs. 154/87mmHg)
0
10
20
30
40
0 1 2 3 4 5 6 7 89
Pat
ient
s W
ith E
vent
s (%
) Less tight controlTight control
Years From Randomisation
UKPDS, BMJ 1998;317:703-713.
Reduction in risk with tight control 32% (95% CI 6% to 51%) (P=0.019)
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MAU as a Predictor of Morbidity and Mortality
Retinopathy
Diabetes+
MAU
LVH
Non-fatal cardiovascular
diseaseAll-cause mortality
Nephropathy
Peripheral/autonomic neuropathy
Parving HH. J Hypertens 1996;14 Suppl 2:S89-S94.
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Definitions of abnormalities in albuminuria
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 (macro) albuminuria
300 200 300
Because of variability in urinary albumin excretion, 2 of 3 specimens over3-6 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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Eastman RC, Keen H. Lancet 1997;350 Suppl 1:29-32.
Microalbuminuria
10
8
6
4
2
0
10.02
Smoking Hypertension
CHD Odds Ratio
6.52
Cholesterol
2.323.20
Relative Importance of MAU
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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
Target Organ Damage
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Clinical Signs of LV Dysfunction
HypotensionPulsus alternansTrigeminy, BigeminyReduced volume of carotidLV apicalEnlargement/displacementSustained heave of apex – Change in heart sounds
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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What is this pattern in HT – Dippers and Non-dippers ?
What is its significance and clinical relevance ?
Dippers & Non Dippers
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Dippers & Non Dippers
Non - dippers
Dippers
24 hours clock time
Sys
toli
c B
loo
d P
ress
ure
(m
m H
g)
110
120
130
140
150
160
6 8 10 12 14 16 18 20 22 24 2 4
Systolic Blood Pressure
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Dippers & Non Dippers
Non - dippers
Dippers
24 hours clock time
Dia
sto
lic
Blo
od
Pre
ssu
re (
mm
Hg
)
70
80
90
100
6 8 10 12 14 16 18 20 22 24 2 4
Diastolic Blood Pressure
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1. Less than 10% circadian variation in SBP and DBP2. Essential hypertension patients are – usually ‘Dippers’3. Non dippers are Dx. by ABPM – They are usually
1. Secondary HT cases2. More end organ damage3. More LVH4. More responsive to salt restriction5. Diabetics are non dippers6. Diuretics convert a non dipper to dipper
Dippers & Non Dippers
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Ambulatory Blood Pressure Monitoring - ABPM
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1. 24 hour B.P monitoring (every 15 minutes)2. Today - 24 hour B.P. control is essential3. Identifies dippers and non-dippers4. Excludes white coat hypertension
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Pulse Wave Velocity (PWV) – Arterial Stiffness
Systole Diastole
Sphygmocor
PulseTrace PCA
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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
Indications for ABPM
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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
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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 Approximate BP reduction(range)
Weight reduction 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
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 clinical trials of repute
Five international societies on HT
Seven JNC guidelines so far, 8th is ready
Multiple target organs damage
Many co-morbidities
Varied outcomes of interest
Cost constraints
No significant change in the proportion of HT under control
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The Many Faces of HT Therapy Today
Centrally acting agentsCentrally acting agents
DiureticsDiuretics
Beta blockers
Beta blockers
CCBsCCBs
ARBsARBs
ACE – inhibitorsACE – inhibitors
HypertensionHypertension
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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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-Blockers
ACE Inhibitors
AT1 Blockers
Direct renin inhibitors
1-Blockers
2-Agonists
All CCBs
Diuretics
Sympatholytics
Vasodilators
-Blockers
Non-DHPCCBs
Diuretics
BloodBloodPressurePressure == CardiacCardiac
OutputOutput
ACE = angiotensin-converting enzyme; AT1 = angiotensin type 1;CCBs = calcium channel blockers; DHP = dihydropyridine
Antihypertensive Drug Classes: Action Sites
Total PeripheralTotal PeripheralResistanceResistance
Ant
ihyp
erte
nsiv
e D
rug
Ant
ihyp
erte
nsiv
e D
rug
Cla
sses
Cla
sses
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Anti Hypertensive drug classes
TheA, B, C, D approach
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D
Diuretics
A
ACEI, ARB
B
β-Blockers
C
Ca-Blockers
D A
B C
The A B C D classes
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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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AGEAGE
Younger (< 55)Younger (< 55)High Renin HTHigh Renin HT
Renin
AB/CD Rule – HT Treatment
ACEi, Beta-blockerACEi, Beta-blocker Ca++-blocker, Diuretic)Ca++-blocker, Diuretic)(AB/CD(AB/CD =
Dickerson et al. Lancet 353:2008-11;1999
Resistant HT /Intolerance
Add / substitute alpha blockerRe-consider 20 causes trial of spironolactone
IV:IV:V:V:
Older (> 55)Older (> 55)Low Renin HTLow Renin HT
ACEi BB
A + B A + B + D
DiureticCCB
D + C + A D + C
I
II
III III
II
I
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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 effectwww.drsarma.in
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Drugs in Each Class
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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%88
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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 early89
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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
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