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2 Eka Fithra Elfi

Eka Fithra Elfi

Department of
Cardiology and Vascular Medicine
FK-UNAND
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Refferences

Drazner. Circulation. 2011;123:327-334

Diamond. Hypertens Res 2005; 28:191–202
Lip. European Heart Journal. 2000;21:1653–1665
Chobanian. Hypertension. 2003;42:1206-1252
Vikrant, Indian Academy of Clinical Medicine.
2001;(3):141-161
Oparil. Ann Intern Med. 2003;139:761-776
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Perhatian
Bahan ajar ini hanya sebagai panduan dan rangkuman
dasar dari materi kuliah pakar. Sebagai sumber
pengetahuan dan bahan untuk ujian silahkan membaca
referensi tersebut diatas.

Eka Fithra Elfi

Penulis
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Introduction
 Hypertension :
 Prevalence up to 1 billion individuals
world wide
 7.1 million deaths per year
 62 % of cerebrovascular disease and
49 % of ischemic heart disease
 Riskerdas 2013 : Indonesian
prevalence ± 25%, West Sumatera
22,6%
 Overall prevalence of worldwide
population 30-45%
 Most common, readily identifiable,
and reversible risk factor for
cardiovascular disease
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Definition
 Hypertension :
 BP 140/90 mmHg or higher (for every age!)
 JNC VII :
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Grade of Hypertension (latest)

 ESC Guideline Arterial Hypertension
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Mortality caused by hypertension

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Cardiovascular Continuum
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Blood Pressure Control

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Pathophysiology of Hypertension
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Essential Hypertension
 A high blood pressure for which an obvious secondary
cause cannot be determined (AKA idiopathic)
 Account for 95% of all hypertension
 Several factors contributed to essential (primary)
hypertension are obesity, excess alcohol and salt
intake, sedentary lifestyle, and diabetes
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Mechanism of Essential Hypertension

 Neural Mechanism
 Increased sympathetic activity
 Renal Mechanism
 Defect in renal sodium retention
 Vascular Mechanism
 Endothelial dysfunction
 Vascular remodeling
 Hormonal Mechanism : Renin-Angiotensin-
Aldosterone System (RAAS)
 Most important mechanism in hypertension
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Renal mechanism
of hypertension
 Volume-based hypertension
by retaining excessive
sodium and water due to :
 Failure to regulate renal
blood flow appropriately
 Ion channel defect (Na K
ATPase)
 Inappropriate hormonal
regulation
 Abnormality of renal
pressure natriuresis
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Neurohormonal mechanism
 Sympathetic nervous system is a major long and short
term BP controller
 Renal sympathetic nerves plays important role in long
term regulation of BP and pathogenesis of
hypertension
 Excessive renal sympathetic nerves
activation leads to sodium retention,
increased RAAS, and impaired
renal natriuresis
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Neurohormonal mechanism
 Baroreceptor reflexes buffering moment-to-
-moment changes in BP that varies during
daily activities.
 Baroreceptor detect sudden increase or
decrease of BP and causing reflex mechanism
through vagal stimulation and sympathetic
or parasympathetic activation.

 In obese patients, reflex sympathetic activation,

which used to increase burn fat, cause
hyperactivity in vascular vessel and kidney, thus
produce hypertension.
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Baroreceptor reflex
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Neurohormonal mechanism
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Vascular mechanism
 Endothelial cells of vascular
vessel have expresses nitric oxide
synthase which produce NO and
possess vasodilatation properties

 Several condition (i.e diabetes,

vascular inflammation, and
hypertension) cause
dysfunctional endothelium
characterized by impaired release
of NO and enhanced release of
endothelium-derived
constricting, proinflammatory,
prothrombotic, and growth factor
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Vascular mechanism
 Endothelial dysfunction and hypertension caused
vascular remodeling over time, which perpetuates
further hypertension
 Remodeling marked by an increase in the medial
thickness relative to lumen diameter in arteries
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RAAS
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RAAS
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RAAS
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Diagnostic of Essential
Hypertension
 Blood pressure measurement and monitoring
 Analysis of cardiovascular risk factors, target organ
damage, and comorbid
 Rule out secondary cause of hypertension
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Blood pressure measurement

 Clinic blood pressure
measurement

 Out-clinic blood
pressure monitoring
 Ambulatory BP
monitoring (ABPM)
 Home BP monitoring
(HBPM
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 ABPM  HBPM
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Category of Hypertension
Monitoring
Kategori TD sistolik TD diastolic

TD klinik ≥ 140 dan/atau ≥90

HBPM ≥ 135 dan/atau ≥85

ABPM

Daytime (or awake) ≥ 135 dan/atau ≥85

Nighttime (or asleep) ≥ 120 dan/atau ≥70

24 jam ≥ 130 dan/atau ≥80

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Investigation of hypertension
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Treatment of Hypertension

 Strategies :
 Life styles changes
 Monotherapy or combination antihypertension drugs
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Lifestyles changes
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Complication of hypertension
 Target organ Damage
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Complication of hypertension
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Hypertensive Heart Diseases

 Constellation of abnormalities of the heart with their
clinical manifestation due to hypertension
 Abnormalities ranging from LVH, systolic and
diastolic dysfunction
 Manifestation of HHD includes heart failure,
myocardial ischemia, and arrhythmias
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Burden of Hypertensive Heart

Disease
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Global Burden to Hypertensive

Heart Diseae
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Hypertensive Heart Disease

 What is the mechanism?
 Classic paradigm : LV wall thickens in response to
elevated blood pressure as a compensatory mechanism
to reduce wall stress
 Progressive changes to LV dilatation and reduction of
LV ventricular systolic function ( remember the
Cardiovascular continuum)
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From Hypertension to Heart Failure

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From Hypertension to Heart Failure

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From Hypertension to Heart Failure

Ventricular hypertrophy

•Increased wall stress leads to LVH

•Which leads to diastolic LV dysfunction
•Which can be followed by systolic LV dysfunction
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Diagnostic modality
 ECG
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Diagnostic modality
 Chest X ray
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Diagnostic modality
 Echocardiography
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Management
 Regression of LV Mass and reversing LV systolic and
diastolic dysfunction
 Several drugs are proven to reduce the hypertensive
heart disease progression
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Management
 Current Medication :
 ACE-I / ARB
 CCB
 β –blocker and α-blocker
 Diuretics

 Future perspectives
 cyclosporin
 HMG CoA reductase inhibitor
 Recombinant human B-type natriuretic peptide
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