M. Kozák, IKK, FN Brno HYPERTENSION HT THERAPY - HISTORY • life regime • gymnastics • eating moderation • salt reducing • nonsmoking • analgetics • physical th. • liquor drenaige • iodids • rhodanid • Ca • NTG ETIOLOGY CHF - Framingham st. 1950 -70 0 10 20 30 40 50 60 70 %pacientů ICHS Hypertenze Dilatační KMP Vady chlopní ETIOLOGY CHF - European data 1990 - 2000 BP MEASUREMENT - HOLTER • diagnostic - hypertension • epizodic HT • white-coat syndrome • autonomic dysfunction • therapeutical effect • hypotension ? INDICATIONS Dipping versus non-dipping Ambulatory blood pressure monitoring 24 hours HT IMPACTS BP VALUES ACC/AHA 2018 X RAY CORRELATION ECG CORRELATION • McPhie - SVmax + RVmax over 40 mm • Sokolov/Lyon - SV1 + RV5,6 over 35 mm ETIOLOGY • essential HT(primary, idiopathic) • secondary HT (10%) • renal (acute, chronic dissease) • renovascular • endocrine (hyperA, hyperK, feochromocytom, acromegaly, hyperparathyreozis) • neurogenic (Tu, injuries) • coarctation ao • sleeping apnoe • iatrogenic (contraceptives, steroids, cocain, liquorice) ETIOLOGY MORBUS CUSHING FUNDUSCOPIC CORRELATION Arteriosclerotic and hypertensive retinopathy HT IMPACTS 1. Hypertensive  Left ventricular hypertrophy  Heart failure  Intracerebral bleeding, ischemic stroke  Renal insuficiency (Na retention, MAU, CKD)  Hypertonic retinopathy  Hypertonic crisis with encephalopathy  Aneurysma dissecans 2. Atherosclerotic  CAD (AP, IM, SCD)  CVD (stroke, TIA, aneurysm, vascular malf.)  Aortic aneurysm  PAD, CLTI – chron. limb threateing, CLI – critical HYPERTENSION + METABOLIC SYNDROM •Reaven´s sy (1996) : hypertension in pt with obesity, hyperglycemia (insulin resistance) ATP III (Adult Treatment Panel) 2001 - 3 or more from: • obezity • TG • HDL • hypertension • hyperglycemia 0.12 0.10 0.08 0.06 0.04 0.02 0 0 ProportionofPatients Time (years) Placebo Ramipril The HOPE and HOPE-TOO Investigators. Circulation 2005; 112:1339-46. Main HOPE Trial Ends In-trial Period RR: 0.69 (95% CI, 0.56-0.85) p=0.0006 1 2 3 4 5 6 7 DEVELOPMENT OF DM 1 2 3 4 5 6 0 500 1,000 1,500 0 IncidenceofStroke(%) Days of follow-up Placebo Ramipril Bosch J, et al. BMJ 2002; 324(7339):699-702. RR: 0.68 (95% CI, 0.56-0.84) p<0.0002 INCIDENCE OF STROKE 0.5 1.0 2.0 Composite CV mortality/morbidity Cardiovascular mortality Non-fatal MI Non-fatal stroke Hospitalization for unstable angina Coronary revascularization procedure Resuscitated sudden death Risk Ratio (95%) Favors CCB / ACEI Favors ACEI / HCTZ 0.80 (0.72–0.90) 0.81 (0.62-1.06) 0.81 (0.63-1.05) 0.87 (0.67-1.13) 0.74 (0.49-1.11) 0.85 (0.74-0.99) 1.75 (0.73-4.17) ACCOMPLISH - Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension Jamerson K et al. A Engl J Med 2008;359:2417-28  Estimation of risk of fatal CV events (SCORE)  Subclinical organ damage (SOP)  Clinical organ damage (POP) PROGNOSTIC FACTORS HT  Risk prediction of fatal CV events  Based on 12 overall population studies 205 178 pts; 2,7 mil. person/years follow-up  Cholesterol level /HDL cholesterol  Projected risk multiplied 2x for male DM pts, multiplied 4x for female DM pts  High risk ≥ 5%  SCORECARD SCORE  LV hypertrophy EKG: Sokolow-Lyons  38 mm Cornell  2 440 mm x ms ECHO: LVMI  125, F  110 g/m2  USG thickening of the arteriol wall (thickening of the carotid wall  0,9 mm or plaque)  Moderate elevation serum creatinine level M 115-133, F 107-124 mol/l  Lowering GF bellow 60ml/min  Microalbuminuria 30 – 300 mg/24h ratio albumin/creatinine M  2,5 F  3,5 mg/mmol SOP – SUBCLINICAL ORGAN DAMAGE  CVD: ischemic stroke, cerebral bleeding; TIA  Structural heart disease: CAD post MI, AP, revascularization, CHF  Renal disease: diabetic nefropathy renal function decrease S creatinine: M  133, F  124 mol/l proteinuria:  300 mg/24 h  PAD, CLTI, CLI  Advanced retinopathy: hemorrhage or exsudate, papilledema POP – CLINICAL ORGAN DAMAGE ANTIHYPERTENSIVE DRUGS ANTIHYPERTENSIVE DRUGS ANTIHYPERTENSIVE DRUGS ANTIHYPERTENSIVE DRUGS • 2-3x higher prevalence of HT in DM population • comparable total risk of HT + DM and HT +MI populations • CV risk estimation male 2x, female 4x higher with DM • treated HT - positive effect to macroangiopathy HYPERTENSION + DM Nonpharmacological therapy  intake Na, weight Target BP < 130/80 mmHg RAS blockade – ACEI, ARB prefered Almoust combined therapy MAU is indication for RAS blockator Intervention of all risk factors HYPERTENSION + DM ANTIHYPERTENSIVE DRUGS /STROKE • benefit for pts with normal BP and hypertension • profit without consideration to type of stroke • sex and age • time interval from stroke • we prefer monotherapy ACEI/ARB • CAB better in older pts (PATS, PROGRESS, EUROPA, Syst-Eur, EWPHE, MRC, SHEP…) Cumulativeevent rate HR (95% CI): 0.80 (0.72, 0.90) 20% Risk Reduction Time to 1st CV morbidity/mortality (days) p = 0 ACEI / HCTZ CCB / ACEI 650 526 .0002 ACCOMPLISH - Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension 11.000 hypertonics with CV risk or CKD. - amlodipin 10, benazepril 40 mg Jamerson K et al. A Engl J Med 2008;359:2417-28 ASCOT Anglo-Scandinavian Cardiac Outcomes Trial - 19.257 pts. hypertension + 3 risk factors - 5year follow-up CKD CKD CKD HT - TREATMENT SIDE EFFECTS ACEI + CAB • cough • peripheral edema, palpitations • flush ACEI + diuretic • cough • obstipation, dryness in mouth nauzea, pain in epigastrium, anorexie • K depletion • Na depletion, hypovolemia • hyperglycemia, hyeruricemia