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Central Aortic Pressure in management Hypertension state of the art BY ASHRAF OKBA PROF. OF INTERNAL MEDICINE AIN SHAMS UNIVERSITY

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Page 1: Ueda2016 symposium - central aortic pressure in management hypertension state of the art -ashraf okba

Central Aortic Pressure in

management Hypertension

state of the art

BY ASHRAF OKBA

PROF. OF INTERNAL MEDICINE AIN SHAMS UNIVERSITY

Page 2: Ueda2016 symposium - central aortic pressure in management hypertension state of the art -ashraf okba

Diseases Attributable to Hypertension

2

Hypertension

Heart failure

StrokeCoronary heart disease

Myocardial infarction

Left ventricular

hypertrophy

Aortic aneurysm

Retinopathy

Peripheral vascular disease

Hypertensive

encephalopathy

Chronic kidney failure

Cerebral hemorrhage

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

All

Vascular

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ESH-ESC 2013

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Global cardiovascular risk in all hypertensive

patients

201

4

91%

Rantala A, et al. J Intern Med 1999;245;163-74. Wannamethee S, et al. J Hum Hypertens 1998;12;735-41

Risk factors = Global CV risk

91% of hypertensive patients have at least 1 additional risk factor

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RAS BLOCKER

RAS BLOCKER

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RAS BLOCKER

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Page 14: Ueda2016 symposium - central aortic pressure in management hypertension state of the art -ashraf okba

RAS BLOCKER

RAS BLOCKER

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RAS BLOCKER

RAS BLOCKER

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“A man is as old as his

arteries.”Thomas Sydenham, 1624-1689

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“Arterial aging”• Every heart beat generates a pulse wave, which disperses in the

human body. Young and healthy vessels are absorbing the energy of the wave – vascular walls are cushioning.

• When vessels are ageing. Over time they are getting stiff – vascular walls are not cushioning anymore. The travel speed of the pulse wave is increasing (pulse wave velocity – PWV).

• Early detection of vascular aging is important to prevent CVD and Hypertension.

Blood pressure 137/91 mmHg

Blood pressure 137/91 mmHg – What is the difference?

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Why Measure Arterial Stiffness?

• Reflects the true arterial wall damage

• Has an independent predictive value for CV events(independent of the traditional risk factors)

• A marker of earlier TOD compared to LVH and

albuminuria

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Increased Arterial Stiffness cause

• Increases vascular afterload with a propensity to develop LVH

• Decreases coronary perfusion pressure

• Increases myocardial oxygen demand and sub-endocardial ischemia

• Increases flow turbulence, endothelial dysfunction & atherogenesis

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APWV measured was a significant predictor of cardiovascular

complications, above and beyond mean arterial pressure.

Prognostic Value of Aortic Pulse Wave Velocity as Index of Arterial

Stiffness in the General Population

(Circulation. 2006)

Vascular Stiffness Measurements as

a Prognostic Indicator

An increase in PWV by 1.0 m/sec increases

the risk of CV events by 14%

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Speed of the wave is related to the stiffness of the

artery it is traveling in

The stiffer the artery;

the higher the wave speed

Wave speed is proportional to the square

root of arterial stiffness

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Assessment of Arterial Stiffness

1. Pulse wave velocity (PWV) (The gold standard measurement of arterial stiffness)

1. Central aortic pressure

2. Augmentation index

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Pulse Wave Velocity (PWV)

• In young adults, arteries are distensible, thus wave travelvelocity is relatively low. The reflected wave is seen indiastole.

• In older people and in arteriosclerosis, the pulse wavevelocity is high, the reflected wave is fater &superimposed on the systolic wave leading to highersystolic pressure and shorter diastolic time.

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Pulse wafeformof 25 year

Pulse wafeformof 47 year

Pulse wafeformof 85year

Central aortic pulse waveform in different age groups

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PWV predicts overall survival in end-stage renal disease patients

Blacher et al. 1999

Probability of survival (all-cause mortality) in end-stage renal disease patients according to the level of aortic pulse wave velocity (PWV) divided in tertiles(P< .0001).

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What creates central BP?

• Stroke volume

• Aortic stiffness (compliance / Windkessel)

• Systemic vascular resistance (“runoff”)

• Reflected pressure wave

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The major organs (brain, heart, and kidney) see central arterial BP and not brachial BP.

Therefore, brachial systolic and pulse BPs measured are not always reliable measures of central aortic systolic and pulse BPs.

Central BP & PP

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• Among 3520 participants, central and brachial pulse pressures were more strongly related to vascular hypertrophy and extent of atherosclerosis than were systolic pressures.

• Central pulse pressure was more strongly related to all 3 arterial measures than was brachial pulse pressure .

• central pulse pressure predicted cardiovascular events more strongly than brachial pulse pressure

• In conclusion, central pulse pressure is more strongly related to vascular hypertrophy, extent of atherosclerosis, and cardiovascular events than is brachial blood pressure.

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Beta-blockers not effectively protect against cardiovascular events as it’s central systolic pressure

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Cardioalex 2015

ARTERIAL STIFFNESS IN DAILY CLINICAL PRACTICE

ESH - ESC CHARTS

BP 185/105 mmHgCOL-LDL 135 mg/dlLVM 125 g/m2

PWV 10,5 m/sWaist 104 cm

BP 135/88 mmHgCOL-LDL 135 mg/dlLVM 116 g/m2

PWV 10,1 m/sWaist 104 cm

BP 135/88 mmHgCOL-LDL 98 mg/dlLVM 105 g/m2

PWV 8,8 m/sWaist 101 cm

BP 185/105 mmHgCOL-LDL 135 mg/dlLVM 125 g/m2

PWV 10,5 m/sWaist 104 cm

Guidelines ESH - ESC 2013

Treatment of BP ALONE does notnecessarily reduce risk !!

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ARTERIAL STIFFNESS IN DAILY CLINICAL PRACTICE

ESH - ESC CHARTS

BP 142/88 mmHgABPM 136/86 COL-LDL 135 mg/dlWaist 104 cmECG, UAE: negative

Guidelines ESH - ESC 2013

Searching for TOD modifies treatmentdecisions !!

BP 142/88 mmHgABPM 136/86 COL-LDL 135 mg/dlWaist 104 cmLVM 126 g/m2

PWV 10,5 m/s

NO Treatment with drugs

Treatment: YES, BP and LDL !!

Patient with recently diagnosed HT, no previous treatment

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ARTERIAL STIFFNESS IN DAILY CLINICAL PRACTICE

ESH - ESC CHARTS

Guidelines ESH - ESC 2013

What is our target? Blood Pressure? TOD? How often?

BP 142/88 mmHgABPM 136/86 COL-LDL 135 mg/dlLVM 126 g/m2

PWV 10,5 m/s

Patient with Stage 1 HT, treatment

Valsartan is addedstatin is added

BP 138/85 mmHgABPM ? COL-LDL 98 mg/dlLVM ?PWV 10,1 m/s

3 months later, treatment Amlodipine/Valsartan 10/160 , statin

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WHEN YOU KNOW SMILE AND CUSTOMIZE

ASHRAF OKBA

35

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• At least 75% of patients will

require combination therapy to achieve contemporary BP targets.

.1Gradman AH, Basile JN, Carter BL, et al. Combination therapy in hypertension. J Am Soc Hypertens 2010; 4 (2): 90-8.

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Valsartan &amlodipine combination achieve An optimal control of BP with

different degree of hypertension included isolated systolic hypertensionReal-Life Safety and Effectiveness Adv Ther (2011) 28(2):134-149.

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Amlodipin based therapy achieve control of BP 24 hrswithout much variability

Rothwell PM, et al. Lancet Neurol. 2010;9:469-480.

RAS BLOKER

RAS BLOKER

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VAL /AMLOD

VAL /AMLOD

Valsarten /amlodipine proved less 24hrs. BP. VARIABILITY

compered with VALS. /HCZ

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Boutouyrie et al J Hypertens 2014; 32: 108-114

Effect of B.blocker/Amlodipine versus Valsartan/Amlodipine

on aPWV Adjusted for Changes in MAP and Heart Rate

BETA-BLOCKER

BETA-BLOCKER

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ARTERIAL STIFFNESS IN DAILY CLINICAL PRACTICE

CONCLUSIONS

1. Measuring TOD improves stratification of cardiovascular

risk

2. Central blood pressure is more strongly related to vascular

hypertrophy, extent of atherosclerosis, and cardiovascular

events.

3. Arterial stiffness appears to be a useful measure for TOD,

and must be used for monitoring patients

4. The effect of drugs on arterial stiffness seems to be

important e.g ARBs and CBBs

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