prof. dr. sarma vsn rachakonda

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

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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 !

4

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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

9

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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

11

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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?

34

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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 ??

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

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

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

78

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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

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

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

90

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 www.drsarma.in

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