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Primary Hypertension
   2. Pathophysiology


   Prof. Dr. med. Günter Hennersdorf
                Germany
       SES consultant cardiologist
Pathophysiology of Hypertension

• Primary Hypertension 90%
      – Prevalence about 60% (age 60+)
      – Prevalence about 15-25% (age 25+)
      – Prevalence mean 35%
• Secondary Hypertension 10%
      – but: may normalize by special treatment (surgery,
        hormone treatment)!



April 2013             ghennersdorf SES FESC DGK
Pathophysiology of Hypertension



                   Primary Hypertension
             H. without primary organic cause




April 2013              ghennersdorf SES FESC DGK
Pathophysiology of Hypertension
                        Mean SBP
                                                              Female
                                                               Male




      Normal course
of blood pressure over age



                             Mean DBP        age



                                                             male
                                                             female


                                             age
 April 2013                      ghennersdorf SES FESC DGK
Cardiovascular risk factors
• not modifyable
      – Ethnic-genetic risk (black people)
      – Age
      – Gender
• modifyable
      –      Hypertension
      –      Hyperlipidemia (Cholesterol, TGs)
      –      Smoking
      –      Diabetes
      –      Overweight
      –      Inactivity (physical)
      –      Stress




April 2013                        ghennersdorf SES FESC DGK
Specific hypertension risks
• not modifyable
      – Ethnic-genetic risk (black people)
      – Age
      – Gender
• modifyable
      –      Diabetes
      –      Overweight
      –      Alcohol
      –      Salt intake
      –      combination



April 2013                 ghennersdorf SES FESC DGK
Prevalence of risk factors
             within western populations
             (FRAMINGHAM-Trial 1998):

             Hypertension                    20 %
                  >65 J.:                    65%

             Smoking                         31 %

             Overweight                      54 %

             Hyperlipidemia                  50 - 60 %

April 2013                  ghennersdorf SES FESC DGK
Pathophysiology of Hypertension: risks




             mortality risk and blood pressure
April 2013         ghennersdorf SES FESC DGK
Factors inducing Hypertension
•    Renin-angiotensin system RAS, RAAS
•    Sympathetic nervous system
•    Insuline resistance
•    Overweight
•    Stiff vessel walls (endothelial dysfunction)
•    Vasoactive substances (NO, Endotheline)
•    Kallikrein secretion
•    Natriuretic peptides

April 2013              ghennersdorf SES FESC DGK
Factors inducing Hypertension
• Neurohumoral system dysbalance
      – Renin-angiotensin system RAS, RAAS
      – Sympathetic nervous system




                Most important hypertension cause!




April 2013              ghennersdorf SES FESC DGK
Pathophysiology of Hypertension


Heart Rate      x   Stroke volume




      cardiac output                x   Peripheral resistance       =   Blood pressure


                                    Basic equation according to
                                    Law of OHM:

             Current I              x      Resistance R             =     Voltage U




April 2013                              ghennersdorf SES FESC DGK
Neuro-humoral Regulation of Hypertension

    Heart rate x stroke volume   x   Peripheral resistance        =     Blood pressure

                                        alpha1
               beta1




               Norepinephrine                    Angiotensin II




              Nervous system                   Humoral RAAS*

                                             *RAAS or RAS: renine angiotensine aldosterone system



April 2013                           ghennersdorf SES FESC DGK
Pathophysiology of Hypertension




             The role of endothelium
             and the RAAS cascade




April 2013         ghennersdorf SES FESC DGK
Pathophysiology of Hypertension
                                                        prorenine, katecholamines


                             Angiotensinogene
                                           Renin         Pathway of RAAS in the
Pathway of RAAS in the
Organism (kidney, heart,                                 Tissues: e.g.
                                Angiotensin I
Vessels) to maintain                                     Vessel wall
Fluid volume control,                       ACE
Adjustment of CO and
Resistance.                     Angiotensin II           Competition of receptors:
If regulation fails, high                                AT1 vasoconstriction
                                                         AT2 vasodilatation
blood pressure occurs


                                   receptor

                            AT1                AT2
April 2013                  ghennersdorf SES FESC DGK
Pathophysiology of Hypertension:
    Angiotensin II Stimulation
                                      Sodium, renine




                                       Kidney




                                       Ang II*         *Ang II effects mediated by AT1




                         Hypophysis                      Adrenal gland


                Hormone release                                      Aldosterone, katecholamines




   April 2013                         ghennersdorf SES FESC DGK
Pathophysiology of Hypertension:
     Angiotensin II Effects

                                                 synaptic conduction
                                     Brain

vasoconstriction


                     vessels         Ang II             Heart          hypertrophy



                     constriction




AT1 mediated effects of              Uterus      contraction
Angiotensin II

        April 2013                  ghennersdorf SES FESC DGK
Pathophysiology of Hypertension


                 basic structure and contents of the vessel intima
endothelium
                                                        Contents
                                                        Smooth muscle cells
intima            SMC                                   SMC
media                                                   Collagenes
                                                        Thrombocytes
Outer layer                                             Ox-LDL
                                                        NO
                                                        Kinines
                                                        Enzymes
                                                        coagulation factors
                                                        platelet activation factors
                                                        thromboxane
   April 2013                                           prostacycline
                                ghennersdorf SES FESC DGK
Pathophysiology of Hypertension
                                               ACh
    Vasoconstriction                                                        Vasodilatation

                               NE                               Vessel dilatation;
                          NE                                    endothelium intact
                    NE




                                               ACh

                               NE
NE=Norepinephine
Ach=Acetylcholine         NE

                    NE                                          no dilatation;
                                                                endothelium removed
  Furchgott‘s basic experiment (1980): key role of endothelium
   April 2013                       ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

                                  platelets




                 growth factors




Endothelial dysfunction causing atherosclerosis and vasoconstriction, infarction
    April 2013                          ghennersdorf SES FESC DGK
Angiotensin II Actions
                               on endothelium and
                                NO =nitric oxide




                       AT1                                   AT2

             AT1 stimulation                            AT2 stimulation
                  leads to:                                    leads to:
                  growth+
              vasoconstriction                              differentiation
                                                            vasodilatation
                                vasoactivity
       NO inhibition                                                    NO
                              Smooth muscle cell
                                   growth

April 2013                      ghennersdorf SES FESC DGK    modified acc. to Unger T et al 1996
Pathophysiology of Hypertension


                               constriction




                           vascular resistance



             Endothelial dysfunction causing hypertension
April 2013                 ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

               Heart rate x stroke volume   x    Peripheral resistance      =   Blood pressure




                              n.sympathicus                              RAAS*




                          Stress                 Genetic/Familial                      Vasoconstriction
                           social                    ethnic
                           familial                  Hereditary                             Endothelial
                                                     salt sensitivity                       dysfunction
*renine angiotensine aldosterone system

  April 2013                                    ghennersdorf SES FESC DGK
Pathophysiology of Hypertension



                   Conclusion:
                   Conclusion:
             Primary Hypertension
             Primary Hypertension
          is a target disease mainly
           is a target disease mainly
 of the RAAS -- intima -- endothelium system!
 of the RAAS intima endothelium system!

                   the endothelium is the major player


April 2013                 ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

                               time course of hypertension development
                 no symptoms             Nonspecific Symptoms:
                                             Head ache,
                                             Palpitation,
Onset,Trigger        Chronic stage           Exertional dyspnea   target organ damage     death




        3                  4                        5                      6            6+ (x10th years)




                                 accelerated course
   April 2013                        ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

              Trigger example: Obesity, Hyperinsulinism, Type-2-
                                  Diabetes


                                  Hypertension



                           Metabolic syndrome (X)




April 2013                    ghennersdorf SES FESC DGK
Pathophysiology of Hypertension


    Heart rate x stroke volume     x   Peripheral resistance       =      Blood pressure

                                                     AT2 -
        beta1                                                          + (NO )
                                                     AT1 +
                          alpha1
      Norepinephrine                       Angiotensin II               Hyperinsulinemia




        Sympathicus                             RAAS


April 2013                             ghennersdorf SES FESC DGK
Pathophysiology of Hypertension




April 2013             ghennersdorf SES FESC DGK
Pathophysiology of Hypertension



                    Target organ damage
                          followed by
                     arterial hypertension




April 2013              ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

   • Target organ damage:
         – Brain: Stroke (ischemic, hemorrhagic)
         – Heart: CAD, Heart failure (mainly diastolic)
         – Vessels:
              • Peripheral arterial disease
              • Central arterial disease: aortic dissection, aneurysm
              • Renovascular disease




April 2013                   ghennersdorf SES FESC DGK
Typical target organ damages following arterial hypertension

                           CAD


                                                        stroke




     LV hypertrophy




                           Peripheral artery disease:
                           necrosis, gangrene

April 2013                   ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

                       Left ventricular
                       hypertrophy
                       Coronary Atherosclerosis
                                                            Heart failure
                                                         (prevalence ~50%)

       Main target lesions

                                                            Brain: Stroke
                                                         (prevalence ~20%)
                        Wall damage
                        Cerebral Atherosclerosis


                                                         Renovascular damage


April 2013                   ghennersdorf SES FESC DGK
Pathophysiology of Hypertension




             Left ventricular hypertrophy      remodeling
             (w. anterior wall infarction)                      Heart failure



April 2013                          ghennersdorf SES FESC DGK
Heart failure and hypertension

             Diastolic Heart failure: stiffness and relaxation disturbances




u



             normal                     Early stage                   Late stage
                           Ultrasound appearance of mitral flow patterns (EA relation)


    April 2013                     ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

                   Survival rate in relation to renal damage (by renal albuminuria)




               Survival rate%                                            Alb. < median
                                                                         Alb. > median

                                                                         Median 7,52 µg/min
                                                                         P=0,0078




April 2013                         ghennersdorf SES FESC DGK
Pathophysiology of Hypertension



                Secondary Hypertension
              H. with primary organic cause




April 2013             ghennersdorf SES FESC DGK
Pathophysiology of Hypertension:
                                           secondary H.

             •   Renal 5%
                  –   Parenchymal
                  –   Renovascular (0,3%) (corrected to normal by balloon treatment or surgery!)
                  –   Tumors
                  –   Little‘s disease
             •   Endocrine
                  –   Thyroid dysfunction (1%)
                  –   Adrenal (0,3%)
                  –   Carcinoid
                  –   hormones
             •   Aortic coarctation
             •   Pregnancy
             •   Neurogenic (brain tumor, lead, porphyria, sleep apnea)
             •   Acute stress (including surgery)
             •   iv. volume increase
             •   Alcohol abuse

    Some may induce primary hypertension, so that the relationships sometimes are weak
April 2013                                ghennersdorf SES FESC DGK
Pathophysiology of Hypertension



            Systolic Hypertension
(H. of the aged w. or w/o. diastolic lowering




 April 2013             ghennersdorf SES FESC DGK
Pathophysiology of Hypertension: Isolated
                      systolic Hypertension (ISH).


      • Rigidity of the aorta (aged aorta)
      • Increased cardiac output
             – Aortic Valve regurgitation
             – AV fistula
             – Thyreotoxic crisis
             – Paget‘s disease (bone vessel fistulas)
             – Beriberi (Vit. B deficiency)
             – Hyperkinetic circulation (young, unfit)

April 2013                 ghennersdorf SES FESC DGK
Definition of arterial Hypertension AH*
                        systolic blood pressure      diastolic blood pressure

   Normal               <140                   and   <90
   (diabetic            <130                         <80)
   mild AH              140-179             and/or
                                                     90-104
   borderline AH        140-159                      90-94
   intermediate         >=180               and/or   >=105
   severe AH
   isolated             >=160                  and   <90
   systolic AH          140-159
   (ISH)
April 2013               ghennersdorf SES FESC DGK                  *WHO 2000
Pathophysiology of Hypertension:
                 Systolic Hypertension.




April 2013          ghennersdorf SES FESC DGK
Pathophysiology of Hypertension:
                 Systolic Hypertension.




April 2013          ghennersdorf SES FESC DGK
Pathophysiology of Hypertension:
                       Systolic Hypertension (SAH).

      • Risk of SAH in the elderly (SHEP, SYST-EUR Trials)

             – Stroke            20% Reduction)
             – Heart failure     54% Reduction)
             – Death             24%



             These results were maintained over 5 years observation




April 2013                     ghennersdorf SES FESC DGK
Pathophysiology of Hypertension: Morning
              Hypertension.



               Blood pressure

               Heart rate
               Resistance
               Cardiac output
               Renal function




April 2013    ghennersdorf SES FESC DGK
Increased cardiovascular morning risk
               Increased cardiovascular morning risk
                                                     Morning BP rise
             Stroke /2h
             Infarction /1 h




             6 pm                     0:00             6 am            12 am




April 2013                     ghennersdorf SES FESC DGK
Pathophysiology of Hypertension:
                          diastolic blood pressure DBP
                                                                       Prognosis
                 Stroke risk and DBP                       CAD risk and DBP

4,0                                       4,0

                                          2,0

1,0                                       1,0




           76   84   91   98 105                     76      84   91   98 105


  April 2013                   ghennersdorf SES FESC DGK
Pathophysiology of Hypertension

             understand
                          Save lives and improve life quality

                    diagnose



                                    treat




                                               control

April 2013                     ghennersdorf SES FESC DGK
Cardiovascular Diseases
    Hypertension Management
              part I
          The End

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Hypertension 2013 Pathophysiology

  • 1. Primary Hypertension 2. Pathophysiology Prof. Dr. med. Günter Hennersdorf Germany SES consultant cardiologist
  • 2. Pathophysiology of Hypertension • Primary Hypertension 90% – Prevalence about 60% (age 60+) – Prevalence about 15-25% (age 25+) – Prevalence mean 35% • Secondary Hypertension 10% – but: may normalize by special treatment (surgery, hormone treatment)! April 2013 ghennersdorf SES FESC DGK
  • 3. Pathophysiology of Hypertension Primary Hypertension H. without primary organic cause April 2013 ghennersdorf SES FESC DGK
  • 4. Pathophysiology of Hypertension Mean SBP Female Male Normal course of blood pressure over age Mean DBP age male female age April 2013 ghennersdorf SES FESC DGK
  • 5. Cardiovascular risk factors • not modifyable – Ethnic-genetic risk (black people) – Age – Gender • modifyable – Hypertension – Hyperlipidemia (Cholesterol, TGs) – Smoking – Diabetes – Overweight – Inactivity (physical) – Stress April 2013 ghennersdorf SES FESC DGK
  • 6. Specific hypertension risks • not modifyable – Ethnic-genetic risk (black people) – Age – Gender • modifyable – Diabetes – Overweight – Alcohol – Salt intake – combination April 2013 ghennersdorf SES FESC DGK
  • 7. Prevalence of risk factors within western populations (FRAMINGHAM-Trial 1998): Hypertension 20 % >65 J.: 65% Smoking 31 % Overweight 54 % Hyperlipidemia 50 - 60 % April 2013 ghennersdorf SES FESC DGK
  • 8. Pathophysiology of Hypertension: risks mortality risk and blood pressure April 2013 ghennersdorf SES FESC DGK
  • 9. Factors inducing Hypertension • Renin-angiotensin system RAS, RAAS • Sympathetic nervous system • Insuline resistance • Overweight • Stiff vessel walls (endothelial dysfunction) • Vasoactive substances (NO, Endotheline) • Kallikrein secretion • Natriuretic peptides April 2013 ghennersdorf SES FESC DGK
  • 10. Factors inducing Hypertension • Neurohumoral system dysbalance – Renin-angiotensin system RAS, RAAS – Sympathetic nervous system Most important hypertension cause! April 2013 ghennersdorf SES FESC DGK
  • 11. Pathophysiology of Hypertension Heart Rate x Stroke volume cardiac output x Peripheral resistance = Blood pressure Basic equation according to Law of OHM: Current I x Resistance R = Voltage U April 2013 ghennersdorf SES FESC DGK
  • 12. Neuro-humoral Regulation of Hypertension Heart rate x stroke volume x Peripheral resistance = Blood pressure alpha1 beta1 Norepinephrine Angiotensin II Nervous system Humoral RAAS* *RAAS or RAS: renine angiotensine aldosterone system April 2013 ghennersdorf SES FESC DGK
  • 13. Pathophysiology of Hypertension The role of endothelium and the RAAS cascade April 2013 ghennersdorf SES FESC DGK
  • 14. Pathophysiology of Hypertension prorenine, katecholamines Angiotensinogene Renin Pathway of RAAS in the Pathway of RAAS in the Organism (kidney, heart, Tissues: e.g. Angiotensin I Vessels) to maintain Vessel wall Fluid volume control, ACE Adjustment of CO and Resistance. Angiotensin II Competition of receptors: If regulation fails, high AT1 vasoconstriction AT2 vasodilatation blood pressure occurs receptor AT1 AT2 April 2013 ghennersdorf SES FESC DGK
  • 15. Pathophysiology of Hypertension: Angiotensin II Stimulation Sodium, renine Kidney Ang II* *Ang II effects mediated by AT1 Hypophysis Adrenal gland Hormone release Aldosterone, katecholamines April 2013 ghennersdorf SES FESC DGK
  • 16. Pathophysiology of Hypertension: Angiotensin II Effects synaptic conduction Brain vasoconstriction vessels Ang II Heart hypertrophy constriction AT1 mediated effects of Uterus contraction Angiotensin II April 2013 ghennersdorf SES FESC DGK
  • 17. Pathophysiology of Hypertension basic structure and contents of the vessel intima endothelium Contents Smooth muscle cells intima SMC SMC media Collagenes Thrombocytes Outer layer Ox-LDL NO Kinines Enzymes coagulation factors platelet activation factors thromboxane April 2013 prostacycline ghennersdorf SES FESC DGK
  • 18. Pathophysiology of Hypertension ACh Vasoconstriction Vasodilatation NE Vessel dilatation; NE endothelium intact NE ACh NE NE=Norepinephine Ach=Acetylcholine NE NE no dilatation; endothelium removed Furchgott‘s basic experiment (1980): key role of endothelium April 2013 ghennersdorf SES FESC DGK
  • 19. Pathophysiology of Hypertension platelets growth factors Endothelial dysfunction causing atherosclerosis and vasoconstriction, infarction April 2013 ghennersdorf SES FESC DGK
  • 20. Angiotensin II Actions on endothelium and NO =nitric oxide AT1 AT2 AT1 stimulation AT2 stimulation leads to: leads to: growth+ vasoconstriction differentiation vasodilatation vasoactivity NO inhibition NO Smooth muscle cell growth April 2013 ghennersdorf SES FESC DGK modified acc. to Unger T et al 1996
  • 21. Pathophysiology of Hypertension constriction vascular resistance Endothelial dysfunction causing hypertension April 2013 ghennersdorf SES FESC DGK
  • 22. Pathophysiology of Hypertension Heart rate x stroke volume x Peripheral resistance = Blood pressure n.sympathicus RAAS* Stress Genetic/Familial Vasoconstriction social ethnic familial Hereditary Endothelial salt sensitivity dysfunction *renine angiotensine aldosterone system April 2013 ghennersdorf SES FESC DGK
  • 23. Pathophysiology of Hypertension Conclusion: Conclusion: Primary Hypertension Primary Hypertension is a target disease mainly is a target disease mainly of the RAAS -- intima -- endothelium system! of the RAAS intima endothelium system! the endothelium is the major player April 2013 ghennersdorf SES FESC DGK
  • 24. Pathophysiology of Hypertension time course of hypertension development no symptoms Nonspecific Symptoms: Head ache, Palpitation, Onset,Trigger Chronic stage Exertional dyspnea target organ damage death 3 4 5 6 6+ (x10th years) accelerated course April 2013 ghennersdorf SES FESC DGK
  • 25. Pathophysiology of Hypertension Trigger example: Obesity, Hyperinsulinism, Type-2- Diabetes Hypertension Metabolic syndrome (X) April 2013 ghennersdorf SES FESC DGK
  • 26. Pathophysiology of Hypertension Heart rate x stroke volume x Peripheral resistance = Blood pressure AT2 - beta1 + (NO ) AT1 + alpha1 Norepinephrine Angiotensin II Hyperinsulinemia Sympathicus RAAS April 2013 ghennersdorf SES FESC DGK
  • 27. Pathophysiology of Hypertension April 2013 ghennersdorf SES FESC DGK
  • 28. Pathophysiology of Hypertension Target organ damage followed by arterial hypertension April 2013 ghennersdorf SES FESC DGK
  • 29. Pathophysiology of Hypertension • Target organ damage: – Brain: Stroke (ischemic, hemorrhagic) – Heart: CAD, Heart failure (mainly diastolic) – Vessels: • Peripheral arterial disease • Central arterial disease: aortic dissection, aneurysm • Renovascular disease April 2013 ghennersdorf SES FESC DGK
  • 30. Typical target organ damages following arterial hypertension CAD stroke LV hypertrophy Peripheral artery disease: necrosis, gangrene April 2013 ghennersdorf SES FESC DGK
  • 31. Pathophysiology of Hypertension Left ventricular hypertrophy Coronary Atherosclerosis Heart failure (prevalence ~50%) Main target lesions Brain: Stroke (prevalence ~20%) Wall damage Cerebral Atherosclerosis Renovascular damage April 2013 ghennersdorf SES FESC DGK
  • 32. Pathophysiology of Hypertension Left ventricular hypertrophy remodeling (w. anterior wall infarction) Heart failure April 2013 ghennersdorf SES FESC DGK
  • 33. Heart failure and hypertension Diastolic Heart failure: stiffness and relaxation disturbances u normal Early stage Late stage Ultrasound appearance of mitral flow patterns (EA relation) April 2013 ghennersdorf SES FESC DGK
  • 34. Pathophysiology of Hypertension Survival rate in relation to renal damage (by renal albuminuria) Survival rate% Alb. < median Alb. > median Median 7,52 µg/min P=0,0078 April 2013 ghennersdorf SES FESC DGK
  • 35. Pathophysiology of Hypertension Secondary Hypertension H. with primary organic cause April 2013 ghennersdorf SES FESC DGK
  • 36. Pathophysiology of Hypertension: secondary H. • Renal 5% – Parenchymal – Renovascular (0,3%) (corrected to normal by balloon treatment or surgery!) – Tumors – Little‘s disease • Endocrine – Thyroid dysfunction (1%) – Adrenal (0,3%) – Carcinoid – hormones • Aortic coarctation • Pregnancy • Neurogenic (brain tumor, lead, porphyria, sleep apnea) • Acute stress (including surgery) • iv. volume increase • Alcohol abuse Some may induce primary hypertension, so that the relationships sometimes are weak April 2013 ghennersdorf SES FESC DGK
  • 37. Pathophysiology of Hypertension Systolic Hypertension (H. of the aged w. or w/o. diastolic lowering April 2013 ghennersdorf SES FESC DGK
  • 38. Pathophysiology of Hypertension: Isolated systolic Hypertension (ISH). • Rigidity of the aorta (aged aorta) • Increased cardiac output – Aortic Valve regurgitation – AV fistula – Thyreotoxic crisis – Paget‘s disease (bone vessel fistulas) – Beriberi (Vit. B deficiency) – Hyperkinetic circulation (young, unfit) April 2013 ghennersdorf SES FESC DGK
  • 39. Definition of arterial Hypertension AH* systolic blood pressure diastolic blood pressure Normal <140 and <90 (diabetic <130 <80) mild AH 140-179 and/or 90-104 borderline AH 140-159 90-94 intermediate >=180 and/or >=105 severe AH isolated >=160 and <90 systolic AH 140-159 (ISH) April 2013 ghennersdorf SES FESC DGK *WHO 2000
  • 40. Pathophysiology of Hypertension: Systolic Hypertension. April 2013 ghennersdorf SES FESC DGK
  • 41. Pathophysiology of Hypertension: Systolic Hypertension. April 2013 ghennersdorf SES FESC DGK
  • 42. Pathophysiology of Hypertension: Systolic Hypertension (SAH). • Risk of SAH in the elderly (SHEP, SYST-EUR Trials) – Stroke 20% Reduction) – Heart failure 54% Reduction) – Death 24% These results were maintained over 5 years observation April 2013 ghennersdorf SES FESC DGK
  • 43. Pathophysiology of Hypertension: Morning Hypertension. Blood pressure Heart rate Resistance Cardiac output Renal function April 2013 ghennersdorf SES FESC DGK
  • 44. Increased cardiovascular morning risk Increased cardiovascular morning risk Morning BP rise Stroke /2h Infarction /1 h 6 pm 0:00 6 am 12 am April 2013 ghennersdorf SES FESC DGK
  • 45. Pathophysiology of Hypertension: diastolic blood pressure DBP Prognosis Stroke risk and DBP CAD risk and DBP 4,0 4,0 2,0 1,0 1,0 76 84 91 98 105 76 84 91 98 105 April 2013 ghennersdorf SES FESC DGK
  • 46. Pathophysiology of Hypertension understand Save lives and improve life quality diagnose treat control April 2013 ghennersdorf SES FESC DGK
  • 47. Cardiovascular Diseases Hypertension Management part I The End