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THE YOUNG HYPERTENSIVE Brian Rayner, Division of Hypertension, University of Cape Town CHILD OF OUR TIMES POWER OF ADVERTISING SUPER SIZE ME!!!! Neck and waist MYTHS ABOUT YOUNG HPT • Hypertension is adult disease • Attributed to secondary causes • It is unrelated to adult HT • TOD is uncommon • The overall impact is small • Up to 10% of adolescents have HT, much higher than autism and epilepsy • The common diagnosis is EH • Multiple studies show tracking into adulthood • 30% have evidence of TOD • Significant impact on hospitalisation Adapted Samuels J, Hypertension 2012 PREVALENCE • Steadily rising since 1979 when it considered rare • About 25% of referrals to GSH Hypertension clinic are “young hypertensives” • Strongly linked to obesity and low birth weight (reduced nephron number or Barker-Brenner hypothesis) • Childhood BP predicts TOD, hypertension and mortality in adulthood • Genetics – family history of hypertension but also stroke, diabetes, IHD, etc Kaplan N, 2006, Gray L et al JACC 2011 Scope of Problem Deaths attributable to high blood pressure in males, South Africa 2000 7000 6000 5000 4000 3000 2000 1000 0 30 - 44 45 - 49 Stroke Hypertensive disease 60 - 69 Ischaemic heart disease 70 - 79 other cardiovascular Prevalence of Hypertension in SA men Bradshaw et al MRC and CDiA 2011 Norman et al. 2007 BOD at the MRC 80+ Prevalence of BP categories according to age Prevalence, awareness and control according to age Survival analysis for progression to hypertension during young adulthood. Amir Tirosh et al. Hypertension. 2010;56:203-209 Copyright © American Heart Association, Inc. All rights reserved. CLASSIFICATION • In infants and children use blood pressure charts based on BP percentile charts • Persistently > 95th centile = hypertension, < 90th normotension • In adolescents over 15 years use adult values for diagnosis • BP levels must be confirmed by multiple readings and preferably by ambulatory BP monitoring to exclude white coating (NICE guidelines) Pathogenesis (uric acid) • HT is associated with uric acid, but attributed to diuretics, ↓ kidney fx, and IR/MS syndrome • ↑ UA predicts future HT even in absence of MS • Present in 90% of adolescents with EHT • Experimentally ↑ UA in rats induces HT and microvascular disease in the kidney • Allopurinol and probenicid ↓ BP in children with EHT and ↑ UA compared to placebo Feig D, et al. JAMA 2008 Estimated probability of BP) reaching pre-HTN and HTN Cohort n =1111 Mean age 10.2 years Semi-annual height, weight and BP over mean 4.5 years Copyright © American Heart Association Tu W et al. Hypertension 2011;58:818-824 Estimated levels of serum leptin concentration (A) and heart rate (B) at different BMI percentiles Tu W et al. Hypertension 2011;58:818-824 Copyright © American Heart Association Figure 2. Sleep BP values according to the degree of overweight and tertiles of HOMA index. Lurbe E et al. Hypertension 2008;51:635-641 Copyright © American Heart Association Relationship between sleep BP and fasting insulin (top) and HOMA index (bottom). Lurbe E et al. Hypertension 2008;51:635-641 Copyright © American Heart Association CONSEQUENCES OF HT • 18,881 male students with mean age of 18.3 years (Harvard Alumni Health Study) • Height, weight, BP, BMI, and physical activity assessed at university entry between 1914 – 1952, and followed to death or until 1998 • Each SD in SBP mortality ↑by 5%, CV mortality by 8-9%, and even more pronounced for CHD Gray L, JACC, 2011 CHD MORTALITY HR 2 1.8 1.6 1.4 1.2 1 0.8 0.6 Normal pre HT HT Stage 1 Ht Stage2 Gray L, JACC, 2011 GSH Preliminary Data • Retrospective cohort • 84 patients as of 04/05/2016 Demographics • • • • Ages: 14-30 years (mean 22years) Sex: 55% female 22% obese; overweight 21%; 53% normal BMI Substances: – 28% are active cigarette smokers; 10% ex-smokers – 5% active drug users usually TIK • Family history: – 66% had at least one relative with HTN; – 32% had a family history of DM Clinical • 68% had any TOD – i.e. LVH and/or retinopathy and/or nephropathy – (57% had ECG-LVH; 32% had retinopathy, 32% had nephropathy) – no cases of cerebrovascular, coronary or peripheral vascular disease Labs • Renal function: – 32% had microalbuminuria – Only 1 patient with GFR < 60 (this patient had previous malignant hpt) – Creatinine range 40 – 185 μmol/L • Echo done only in 15% (one-fifth of these with echoLVH) • Only 38% had KUB sonars – 83% of scans done were normal • Genetic: – 92% had were normal for ENaC R563Q mutation – 8% were homo-/ heterozygous for R563Q CAUSES Infants School-Age Adolescents Primary <1 15-30 85-95 Secondary 99 70-85 5-15 Renal 20 60-70 Renovascular 25 5-10 Endocrine 1 3-5 Coarctation 35 10-20 Reflux 0 5-10 Neoplastic 4 1-5 Miscellaneous 20 1-5 Flynn J. In: Kaplan’s clinical Hypertension, 9th Ed Diagnoses • Essential Hypertension 75% • Secondary hypertension – – – – Renovascular hypertension 9.7% (half of them = Takayasu) Renal parenchymal disease 4% Endocrine-related 1.3% ( one case of primary hyperaldosteronism) Other: 4% (one case Gordon’s syndrome, one case of contraceptive-assoc. HTN, one case of malignant HT) • Prehypertension 3.9% Overview • To diagnosis hypertension • To assess the impact of hypertension on target organs and complications • To estimate the patient’s overall risk profile for the development of premature CV disease • To determine if there are underlying secondary causes • TO GUIDE FURTHER INVESTIGATION AND TREATMENT History • Duration and prior treatment of the hypertension including adverse effects of drugs • Family history of hypertension, diabetes, kidney disease and premature CV disease • The use of agents that interfere with hypertension • Presence of other risk factors like obesity, diabetes, dyslipidaemia, and smoking, or established CV, cerebrovascular or kidney disease • Lifestyle and dietary history • Sexual function • Symptoms of secondary causes e.g. sleep apnoea, PAD or phaeochromocytoma • Symptoms of complications of hypertension – heart failure, IHD, etc • The ability to understand hypertension and comply with therapy. DRUG INDUCED • • • • • • • • • • • Oral Contraceptives NSAIDs Tik, cocaine, Khat Sympathomimetics Excess alcohol Licorice Steroids Cyclosporin Erythropoetin Herbal remedies Other Examination • accurate measurement of BP and interpretation • measurement of the waist circumference, height and weight, and calculation of the BMI • assessment of heart rate, character of pulse and rhythm • Examination of the fundi, heart, abdomen and lungs with reference to renal/abdominal masses, pulses, radiofemoral delay, bruits over the major arteries, presence of oedema, jugular venous pressure, character of the apex and any added heart sounds or murmurs • Neurological assessment should include assessment of cognition • Features of a secondary cause e.g. Cushing’s syndrome, Turner’s MALIGNANT HYPERTENSION MODIFIED KEITH-WAGNER CLASSIFICATION • I – mild narrowing of retinal vessels • II – moderate to marked narrowing with light reflex and AV nipping • III – haemorrhages and exudates • IV – papilloedema + III LEFT VENTRICULAR HYPERTROPHY S4, pressure overloaded Apex beat ECG Echo Weight 3 kg down, But abd. circumference 113 cm ↑ by 9 cm in 12 months IDENTIFIABLE CAUSES OF HYPERTENSION • Sleep apnoea • Drug induced or related (OC, NSAIDs, Tik, cocaine, excess alcohol, etc) • Chronic kidney disease (dipsticks, creatinine, ultrasound) • Primary aldosteronism (K+, ARR ratio) • Renovascular (CT angio, captopril renogram) • Turner’s, neurofibromatosis, • Cushing’s syndrome (24 hour urine for cortisol) • Phaeochromocytoma (24 hr nma) • Coarctation (r-f delay, echo) • Thyroid or parathyroid disease SIGNIFICANCE OF AN ELEVATED BP • Raised blood pressure with TOD/Complications is by definition serious and requires treatment • In the absence of TOD/Complications repeat measurements on separate occasions unless severe (> 180/110 mmHg) • If in doubt, home blood pressure monitoring or 24 hour ABPM Mandatory Investigations Investigation TOD Secondary cause Risk stratification Dipsticks urine Yes, usually ≤1+ protein in 2+ or more proteinuria Yes hypertensive and/or haematuria nephrosclerosis suggests kidney disease ECG LVH (see ECG criteria) No Yes creatinine Yes Yes Yes K+ No Low K+ may suggest No primary aldosteronism Fasting glucose No no yes Fasting lipogram or cholesterol No no yes Urine albumin/creatinine ratio* Yes Yes, if markedly elevated Yes * Mandatory in diabetics aVL > 11 LA+ = diastolic dysfunction Cornel – (S in V3 + R in aVL + 6 in females) x QRS duration > 2440 aVL > 11 >=35 – Sokolow-Lyon) ESC/ESH/SAHS Harbinger of death Albuminuria • mandatory in diabetics, first voided morning urine specimen • < 3mg – normal • 3-30 microalbuminuria • > 30 macro-albuminuria • spot urines tend to overestimate ratio (2X) • Trace albumin on dipsticks usually represents microalbuminuria * * Suggest subdivision to 3a (45-59) and 3b (30-44) SPECIAL INVESTIGATIONS • Clinical suspicious based on history, examination, and basic investigations • resistant hypertension • severe hypertension in a lean young adult without family history and obesity • all hypertensives < 18 years of age Condition Clinical context Screening tests Kidney disease Renal artery stenosis Screen all hypertensives Bruits, discrepant pulses in older vasculopath or young female Dipsticks, renal ultrasound Ultrasound kidneys, captopril renogram, CT angiography Phaeochromocytoma Sweating, palpations, headaches, labile BP, weight loss (rare if symptoms absent) 24 hour nor-meta-adrenaline Primary aldosteronism Resistant hypertension or low K+ Low K+, aldosterone renin ratio (ratio > 70, and aldosterone > 500 pmol/L highly suggestive) Partial Liddle’s Sleep apnoea Resistant hypertension Snoring, day time somnolence, obesity R563Q mutation Refer Thyroid disease Symptoms of hypo- or hyperthyroidism TSH Parathyroid disease Cushing’s syndrome Rare Rapid weight gain, features of Cushing’s Ca, PTH 24 hour urine cortisol Coarctation of the aorta Young hypertensive with radiofemoral delay Chest radiograph PROBABILITY OF CHD EVENT IN MALES WITH MILD HYPERTENSION 40 35 30 10 year % 25 probability of event 20 Average risk 15 10 NNT ranges from about 5 100 to 12 events prevented 0 for CHD BP 150-160 For stroke 50 to 6 events TC 6.2-6.77 HDL 0.85-0.89 Diabetes Smoker ECH-LVH + + + + + + + + + + + + + + + + + + + + + RISK STRATIFICATIONS MAJOR RISK FACTORS. Levels of systolic and diastolic BP. Smoking. Dyslipidaemia: o total cholesterol > 5.1 mmol/L, OR o LDL > 3 mmol/L, OR o HDL men <1 and women <1.2 mmol/L. Diabetes mellitus. Men > 55 years. Women > 65 years. Family history of early onset of CVD: o Men aged <55 years; o Women aged <65 years. Waist circumference- abdominal obesity: o Men ≥ 102 cm; o Women ≥ 88 cm. o The exceptions are South Asians and Chinese: Men: >90 cm and Women: >80 cm. TOD LVH: based on ECG o Sokolow-Lyons >35mm o R in aVL > 11 mm o Cornel > 2440 (mm.ms) Microalbuminuria: albumin creatine ratio 3-30 mg/mmol preferably spot morning urine and eGFR > 60ml/min Complications Coronary heart disease Heart failure o Chronic kidney disease: macroalbuminuria > 30mg/mmol o OR eGFR < 60ml/min Stroke or TIA Peripheral arterial disease Advanced retinopathy: o haemorrhages OR; o exudates; o papilloedema. SAHS 2012 CONCLUSIONS • • • • • • Ideally a careful history and examination Accurate measurement of BP Mandatory measurements and investigations Assess TOD and complications Stratify risk Treatment and investigation is based on this evaluation INITIATION OF TREATMENT • • • • • Symptomatic or severe HT Secondary HT HT with TOD HT associated with type I or II diabetes Persistent HT despite non-pharmacological measures Flynn J. In: Kaplan’s clinical Hypertension, 9th Ed DRUG TREATMENT • • • • Diuretics (urate, predisposition to T2DM) ACE/ARB CCB Beta blocker (weight gain, poor exercise tolerance, predisposition to T2DM) 4th Report on the Diagnosis Evaluation, and treatment of high BP in children and adolescents. Hypertens 2004 CONCLUSIONS • • • • • HT in children and adolescents is increasingly prevalent It is closely linked to obesity and positive FH Childhood BP tracks adult BP It is linked to increased mortality in adulthood In adolescents the majority of patients have primary HT, but careful search for secondary causes must be undertaken by history and examination, and basic investigations • Treatment should focus on lifestyle and in more severe cases drug therapy