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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