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„Hypertension”

„Hypertension”. Prof. Dr. János Borvendég CHMP member Hungary. Definitions and Classification of Blood Pressure levels (mmHg). Category Systolic Diastolic Optimal  120  80 Normal 120-129 80-84 High normal 130-139 85-89

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„Hypertension”

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  1. „Hypertension” Prof. Dr. János Borvendég CHMP member Hungary

  2. Definitions and Classification of Blood Pressure levels (mmHg) Category Systolic Diastolic Optimal  120  80 Normal 120-129 80-84 High normal 130-139 85-89 Grade 1 Hypertension 140-159 90-99 -”- 2 -”- 160-179 100-109 -”- 3 -”-  180  110 Isolated Systolic Hypertension  140  90

  3. The significance of hypertension • The number of patients with hypertension is growing(!)1988-1991 43,2 mill/US1999-2000 60,0 mill/US - the population ages  - obesity  - diabetes  • Hypertension is the most common risk factor for heart attack and stroke

  4. The significance of hypertension: (cont.) • Only ≈ 34 % of patients with hypertension have their blood pressure controlled.- the HBP remains asymptomatic for long period of time- lack of adherence with the therapy- side effects of the antihypertensive- poor access to medications

  5. Factors influencing the prognosis Risk Factors: S/D BP levels 180/ 110 mmHg Diabetes mellitus Age (M  55 y. F  66 y) Dyslipidemia Abdominal obesity Metabolic syndrome Smoking Snoring / sleep apnoea

  6. Obesity: • Body weight • Increased waist circumference M : 102 cm W: 88 cm • Increased body mass index body weight (kg) / height2(m) overweight  25 kg/m2 obesity  30 kg/m2

  7. Complications: • heart failure • Left ventricular hypertrophy • MI • sudden cardiac death • stroke • intracerebral haemorrhage • chronic renal insufficiency hypertensive nephrosclerosis • retinopathy

  8. Laboratory Investigations: fasting plasma glucose/tolerance test se total cholesterol se LDL se HDL fasting se triglycerides se uric acid se creatinine creatinin clearance Hgb/Htc urine analysis (quantitative microalbiminuria) se electrolytes

  9. Determinants of arterial pressure Stroke volumen Cardiac output Heart rate Arterial pressure Vascular structure Perip. resistance Vascular function

  10. Essential (primary hypertension) Pathogenesis: • increased sympathetic neural activity, with enhanced beta-adrenergic activity • increased Angiotensin II. activity and mineral corticoid excess • genetic factors (≈ 30 %) • reduced nephron mass (genetic factors? intra uterine developmental disturbances)

  11. Search for secondary hypertension Measurement of: renin aldosterone, corticosteroids catecholamines arteriographies renal / adrenal ultra sound CT MRI

  12. Goals of Treatment: • Primary goal: to achieve maximum reduction in the long-term total risk of cardiovascular disease • BP should be reduced: 140/90 mmHg (in all hypertensive patients) 130/80 mmHg (in diabetics and in high risk patients) • Antihypertensive th. shouldbe initiated before significant CV damage develops

  13. Antihypertensive agents

  14. Mechanism of Action of Antihypertensive Agents Diuretics: (?) • Na+ excretion  • Plasma volume  • Smooth muscle Na+ conc.  Outcome: perif. resist.  -blockers: • 1/2blocking • 1blocking • MSA (Membrane Stabilisig Activity) • ISA (IntrinsicSympatheticActivity) Outcome: heart ratecardiac outputplasma RAresetting of baro receptors

  15. Mechanism of Action of Antihypertensive Agents (cont.) Alfa antagonists • Selective post synapticic1 blockade Outcome: peripherialresist.  preload  Ca channel antagonists: • Blockade of voltage sensitive Ca channels • Outcome: peripherial. resist  (relax the arterial smooth muscle)

  16. RAS (Renin-Angiotensin-System Kidneys beta blocking agents renin aliskiren Angiotensinogen Angiotensin I ACEiACE Angiotensin II ARB AR aldosteron secretionsympathic activity Vasoconstriction BP

  17. The ACEi-s • inhibition:- the LVH (Left Ventricular Hypertrophy)- the myocardial ischemia- glomerular hypertrophy- production of procollagen • mitigate/decrease:- deposition of mesangial macromolecules- impairment tubule-interstitial tissues- the endothelial impairment • improve:- the cardiac function- the rheological properties of the blood - the lipid profile- endothelial function- insulin sensitivity

  18. Pharmacological effects of ARB-s Blockade of AT1 receptors: Outcome: • vasodilatation- TPR (total Peripheral Resistance)  • aldosteron secretion: - Na reabsorption- H2O reabsorption- plasma volume - cardiac output  • intra glomerular pressure  • release of NA from the synapses - sympathetic tone, neurotransmission  • endothelin production  • production of A II and renin secretion  • stimulation of AT2 receptors (indirectly)

  19. Pharmacological effects of ARB-s(cont.) Blockde of AT1 receptors: Outcome: • decrease/mitigate:- LVH (LeftVentricularHypertrophy)- albuminuria (microalbuminuria!)- progression of renalimpairment • protect (?)- CHF- diabeticnephropathy- stroke

  20. Pharmacological effects of ARB-s(cont.) Blockade of AT1 receptors: Outcome: • decrease/mitigate:- LVH (LeftVentricularHypertrophy)- albuminuria (microalbuminuria!)- progression of renalimpairment • protect (?)- CHF- diabeticnephropathy- stroke

  21. Pharmacological effects of RI-s Direct blockade of renin enzyme activity • PRA (Plasma Renin Activity) (tissue renin activity ?) • Plasma AT1/AT2 • Aldosterone secretion  • BP  • - PRC (plasma cc. of renin) 

  22. ReninInhibitors: Outcome: • vascular effects:- neointima formation - thickening in carotid intima (?) • renal effects (specific uptake of the drug by the kidney?)- renal vascular resistance - renal blood flow - proteinuria  • ccardiac effects:- beneficial hemodynamic effects(LV end diastolic pressure stroke volume systemic vascular resistance )

  23. ?Effects of RI-s on target organ damage Cardiac:- preventive (cardio protective): LVH- curative: CHF Vascular: - protective: endothelial dysfunction against atherogenesis, stroke- improve the elasticity of the large arteries Renal: - nephroprotective (in diabetic nephropathy) Metabolic:- improve: insulin sensitivitydyslipidemy

  24. Monotherapy versus Combination • Use of more than one agent is necessary to achieve target BP in the majority of patients • Initial treatment can be monotherapy or combination of two drugs (at low doses) with a subsequent increase in doses • Combination of two drugs should be preferred as first step treatment in patients with grade 2/3 range or with high CV risk • In patient with severe hypertension combination of three or more drugs is required

  25. Monotherapy versus Combination strategies Mild/moderateMarked BP elevation BP elevation CV highrisk Singleagent (lowdose) Two-drugcombination (lowdose) previousswitchtodiff. Previous add a third agent (fulldose) agent (lowdose) comb.(fulldose) drug (lowdose) two/three drugcombination mono th. (fulldose) (fulldose) two /threedrug combination (fulldose)

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