1. The document discusses hypertension in young adults, including definitions of different types of elevated blood pressure (e.g. hypertensive urgency, emergency), risk factors, clinical presentation, causes (primary vs. secondary), evaluation approach, and ambulatory blood pressure monitoring. 2. Most young adults with hypertension have primary/essential hypertension with no identifiable cause, though secondary hypertension can occur in about 10% of cases. Evaluation aims to confirm the diagnosis, assess cardiovascular risk, detect target organ damage, and identify secondary causes. 3. Ambulatory blood pressure monitoring provides blood pressure readings outside the office and can help identify white coat hypertension or masked hypertension, which have implications for risk stratification and treatment.

1. Prof. G. Subramanian Dr. Chandan
Kumar
MD,DM,FIAE,FISC,FCSI,FMMC

2. Persistent elevation of office blood pressure >140/90 mmHg
based on the evidence from RCTs that in patients with these
BP values treatment-induced BP reductions are beneficial
European Heart Journal (2013) 34, 2165

3.  Hypertensive urgency: Blood pressure ≥180/120 mm Hg in
the absence of progressive target organ dysfunction
 Hypertensive emergency: persistent ≥180/120 mmHg
associated with impending or progressive organ dysfunction, such
as major neurological changes, hypertensive encephalopathy,
stroke, acute LVF, acute pulmonary edema, aortic dissection,
renal failure, or eclampsia
 Malignant hypertension: is a syndrome a/w an abrupt
increase of BP with ischemic organ dysfunction (retina, kidney,
heart or brain) in a patient with underlying hypertension or related
to the sudden onset of hypertension in a previously normotensive
individual
 Accelerated hypertension: recent significant increase of
baseline BP a/w target organ damage (vascular damage) seen as
presence of retinal flame shaped hemorrhage or exudate
without papilledema National Heart Foundation Hypertension Guideline – 2016

4. Risk factors for hypertension in young
1. Yan LL, Liu K, Matthews KA, et al. Psychosocial factors and risk of hypertension. The Coronary Artery Risk Development
in Young Adults (CARDIA) study. JAMA 2003;290(16):2138–2148.
2. Manolio TA, Burke GL, Savage PJ, et al. Exercise blood pressure response and 5-year risk of elevated blood pressure in a
cohort of young adults: the CARDIA Study. Am J Hypertens. 1994;7:234–241.
• Physical inactivity
• Family history
• Diabetes
• Obesity
• Tobacco products & alcohol
• Drugs- Amphetamine, Cocaine
• Psychosocial risk factors, higher time urgency, impatience,
and hostility in young adults aged 18– 30 year1
• In one study, 20-35 year age group, having exaggerated
response to exercise towards SBP & DBP 2

5. • The prevalence of hypertension (age adjusted) among US adults
≥ 18 years of age is estimated to be 28.6%, based on National
Health and Nutrition Examination Survey (NHANES) data1
• Among adolescents and young adults (18 – 39 years old) the
incidence is >10%2
• Worryingly, there has been a startling increase, with the
prevalence approximately doubling in this age group within a
decade3
Epidemiology:
(18-39 year age group)
1. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics—2014 update. A report from the American Heart
Association. Circulation. 2014;129: e28–e292.
2. Shisana O, Labadarios D, Rehle T, et al. South African National Health and Nutrition Examination Survey (SANHANES-1): 2014.
Cape Town: HSRC Press, 2014.
3. Bradshaw D, Steyn K, Levitt N, Nojilana B. Non-communicable Diseases: A Race Against Time. Cape Town: Medical Research
Council South Africa, 2011.

6. Clinical presentation of hypertension
• Most young patients are asymptomatic and diagnosed
during screening or when presenting with an unrelated
condition
• May present with symptom of raised blood pressure is
Headache i.e., “Hypertensive headache” occurs in the
morning and is localized to the occipital region generally
occurs only in patients with severe hypertension
• A minority present with a hypertensive emergency ( heart
failure, renal failure or malignant hypertension etc.)

7. Primary hypertension
• Primary hypertension (also called essential hypertension)
has no specific cause,genetic and environmental factors
play an important role1
• More than 90% (85-95%) of young people with hypertension
have primary hypertension2,3
• It is often associated with a family history of hypertension and
frequently accompanied by obesity or the metabolic syndrome
• Novel mechanisms implicated in the pathogenesis include:
• Low birth weight (Barker-Brenner hypothesis)
1. Weber M, Schiffrin E, White W, et al. Clinical Practice Guidelines for the Management of Hypertension in the Community. A Statement by the
American Society of Hypertension and the International Society of Hypertension. J Hypertens 2014;32(1):3-15.
2. Assadi F. The growing epidemic of hypertension among children and adolescents: A challenging road ahead. Pediatr Cardiol 2012;33(7):1013-1020.
[http://dx.doi.org/10.1007/s00246-012-0333-5]
3. Flynn JT. Hypertension in children. In: Kaplan N, ed. Kaplan’s Clinical Hypertension. 9th ed. Philadelphia: Lippincott Williams and Wilkins,
2006.

8. Secondary Hypertension
• Secondary hypertension is a type of hypertension with
an underlying identifiable and potentially correctable
cause
• Hypertension due to underlying etiology affects
approximately 10% of young hypertensives1
• The probability of secondary hypertension is inversely
proportional to the age of the patient (i.e. higher in a
school-going child, but lower in a young adult)1
• Secondary hypertension is curable with appropriate
treatment
1. Assadi F. The growing epidemic of hypertension among children and adolescents: A challenging road ahead. Pediatr Cardiol 2012;33(7):1013-
1020. [http://dx.doi.org/10.1007/s00246-012-0333-5]

9. General Approach to the Patient
 Proper history including patient’s diet, habits & family history
 Physical examination
 Investigation: Oriented towards
 To detect risk factors
 To detect etiology of hypertension
 To detect target organ damage
The majority(>90%) of young patients will have primary
hypertension, while only a minority (<10%) will have secondary
hypertension. it is not recommended an extensive workup for
all newly diagnosed young hypertensives, as has been the
practice in the past.
 Management
S Afr Med J 2016;106(1):36-38. DOI:10.7196/SAMJ.2016.v106i1.10329

10. Initial evaluation for hypertension accomplishes following
goals:
① Accurate measurement of blood
pressure/confirmation
① Assessment of the patient’s overall cardiovascular
risk
② Detection of target organ disease
③ Detection of secondary forms of hypertension
Evaluation of the patient:

11. Retinal photographs showing the stages of hypertension retinopathy. A, Mild diffuse arteriolar narrowing. B,
Arterial-venous nicking. C, Hemorrhages and exudates. D, Papilledema. (From Grosso A, Veglio F, Porta M, et
al: Hypertensive retinopathy revisited: some answers, more questions. Br J Ophthalmol 89:1646, 2005.)

12. Technique for Office Blood Pressure Measurement
1. The patient should be resting comfortably for 5 minutes in the
seated position with back support with no talking and patients’s
legs should not be crossed
1. Choose a cuff of bladder size matched to the size of the arm with
bladder width ≈40% & length 80–100% of arm circumference
2. Place the lower edge of cuff 3 cm above elbow crease and
bladder centered over brachial artery
3. Increase the pressure rapidly 30 mmHg above the level of
extinguished radial pulse
4. Cuff deflation rate must be of 2 mmHg per beat for accurate
systolic & diastolic estimation
European Society of Hypertension guidelines for the management of high blood pressure in children and adolescents
2016
①Accurate measurement of blood pressure

13. White coat hypertension:
 Which encompasses subjects with office systolic/diastolic
blood pressure readings of ≥140/90 mm Hg and a 24-hour
blood pressure <130/80 mm Hg
 White-coat hypertension occurs in 15% - 30% of subjects
with an elevated office blood pressure
• O’Brien E, Parati G, Stergiou G, et al; on behalf of the European Society of Hypertension Working Group on Blood
Pressure Monitoring. European Society of Hypertension position paper on ambulatory blood pressure monitoring. J
Hypertens. 2013;31:1731–1767

14. When to suspect white coat hypertension
(1) If office blood pressure is ≥140/90 mm Hg on ≥3 separate
office visits
(2) If ≥2 blood pressure readings taken outside the office are
<140/90 mm Hg
(3) If no evidence of hypertensive target organ damage
• Staessen JA, Asmar R, DeBuyzere M, Imai Y, Parati G, Shimada K, Stergiou G, Redón J,Verdecchia P; Participants of the
2001 Consensus Conference on Ambulatory Blood Pressure Monitoring. Task Force II: blood pressure measurement and
cardiovascular outcome. Blood Press Monit. 2001;6:355–370

15. Masked hypertension:
• If office blood pressure lesser than out-of-office blood
pressure
• This may be due to sympathetic over-activity in daily life
caused by job or stress, tobacco abuse, or other adrenergic
stimulation
• It may affect >10% of patients and clearly increases
cardiovascular risk, despite normal office blood pressure
readings Courtesy Dr. R.G. Victor, Cedars-Sinai Medical Center, Los Angeles.

16. • It involves measuring blood pressure (BP) at
regular intervals (usually every 20–30 min.)
over a 24 hour period while patients undergo
normal daily activities, including sleep
• The portable monitor is worn on a belt
connected to a standard cuff on the upper
arm and uses an oscillometric technique to
detect systolic, diastolic and mean BP with
heart rate
Australian Family Physician Vol. 40, No. 11,November 2011 877-880
Ambulatory blood pressure monitoring (ABPM):

17. Indications of ABPM :
• Suspected white-coat hypertension (including in pregnancy)
• Suspected masked hypertension
• Suspected nocturnal hypertension or no night time
reduction/dipping in BP
• Hypertension despite appropriate treatment
• Suspected episodic hypertension
Australian Family Physician Vol. 40, No. 11, november 2011 877-880

18. ABPM can also be used in :
• Titrating antihypertensive therapy
• Borderline hypertension
• Hypertension detected early in pregnancy
• Syncope or other symptoms suggesting orthostatic
hypotension, that may not be demonstrated in the clinic
Australian Family Physician Vol. 40, No. 11, November 2011 877-880

19. Canadian Journal of Cardiology 2015 31, 549-568DOI: (10.1016/j.cjca.2015.02.0

20.  Cardiovascular risk increases dramatically with hypertensive target
organ damage and with additional cardiovascular risk factors
②Assessment of the overall cardiovascular risk
• Mancia G, De Backer G, Dominiczak A, et al: 2007 guidelines for the management of arterial hypertension: the Task Force for the
Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology
(ESC). Eur Heart J 28:1462, 2007.
 Lowering SBP by 10–12 mmHg and DBP by 5–6 mmHg decease in relative risk
by 35–40% for stroke and 12–16% for CHD within 5 years

21. ③Detection of target organ disease
A. Heart:
 This is because of structural and functional adaptations may result into
LVH, CHF, coronary artery disease
 Early detection and aggressive control of HTN may reverse LVH and
reduces CVD risk
 CHF may be due to Systolic as well as diastolic dysfunction(≈33%) or
both
 Diastolic dysfunction may be assessed by:-
• Electrocardiography
• Echocardiography
• Angiography

22. ECG changes in hypertension:
 Features of chronic hypertension:-
• Sign of LVH due to systolic overload
• Left axis deviation
 Earliest features of left ventricular overload:-
• T-wave in lead V1 taller than T-wave in V6
• U-wave become inverted in left oriented leads
• Frontal plane of QRS-T angle begins to increase and exceeds
45°
• Evidence of left atrial abnormality
• Increase in VAT in left oriented leads

23. B. Brain:
Stroke:
 Hypertension accounts for 50% of strokes*
 In hypertensive persons, 80 - 85% of strokes are ischemic
(thrombotic or embolic) and 15 - 20% are hemorrhagic(ICH,SAH)
Hypertensive encephalopathy:
 Occurs due to failure of cerebral blood flow autoregulation i.e.,
malignant hypertension resulting into vasodilation & hyper-
perfusion
 May present as Severe headache, Nausea/Vomiting, focal
neurological signs, altered mental status. May progress into
coma, seizure and death

24. C. Kidney:
• Renal risk occurs more in black than white
• Renal compromise is more related to raised systolic blood pressure
Raised systolic pressure
Hypertension related vascular
injury on preglomerular arterioles
Direct damage to glomerular capillaries
due to hyperperfusion
Ischemic changes in glomeruli
& post-glomerular structure
Glomerular injury
Autoregulation failure & GFR
Glomerulosclerosis Tubular ischemia & atrophy

25.  Malignant hypertension may cause:-
• Fibrinoid necrosis of afferent arteriole
• Focal necrosis of glomerular tuft, if involve glomerulus
 Micro(Urinary albumin/creatinine ratio 30-300 mg/g) &
macroalbuminuria (>300 mg/g) are early markers of renal injury
 Gross pathologic change of small, scarred kidneys (Hypertensive
nephrosclerosis)

26. D. Perpheral vessels:
 Atherosclerotic changes occurs in vessels due to long standing
hypertension
 Risk is overwhelming if there is:-
• Aortic dissection (distal > proximal)
• Abdominal aortic aneurysm
• Peripheral arterial disease
 Ankle brachial index i.e., ratio of SBP of ankle to brachial, is useful
approach to asymptomatic patient or with intermittent claudication
 ABI <0.9 diagnostic to PAD & a/w >50% stenosis to at least one
major limb vessels

27. ④ Detection of secondary forms of hypertension
Features of secondary Hypertension
 Poor response to therapy (resistant hypertension)
 Worsening of control in previously stable hypertensive patient
 SBP > 180 mm Hg or DBP >110 mm Hg
 Onset of hypertension in persons younger than age 30 or older
than age 55
 Significant hypertensive target organ damage
 Lack of family history of hypertension

28. Causes of secondary Hypertension
• Renal/Renovascular :
Renal parenchymal disease
Renal artery stenosis
Fibromuscular dysplasia
• Vascular:
Coarctaction of aorta
• Endocrinological:
Thyroid associated
Cortisole excess associated
Mineralocorticoid excess associated
Catecholamine associated
• Drugs
• Obstructive Sleep Apnea Syndrome
• Lifestyle – Diet / Nutrition

29. 1. Omura M, Saito J, Yamaguchi K, Kakuta Y, Nishikawa T. Prospective study on the prevalence of secondary hypertension
among hypertensive patients visiting a general outpatient clinic in Japan. Hypertens Res. 2004;27(3):193-202.
2. Haas DC, Foster GL, Nieto FJ, et al. Age-dependent associations between sleep-disordered breathing and hypertension:
importance of discriminating between systolic/diastolic hypertension and isolated systolic hypertension in the Sleep Heart
Health Study. Circulation. 2005;111(5):614-621.

30. Renal & renovascular hypertension
 Most common causes in young:
 Renal parenchymal disease(acute/chronic)
 Fibromuscular dysplasia
 Takayasu’s artritis
 Renin-Secreting Tumors

31. History:
 Abrupt onset of hypertension <30 years or >50 years of age
 Severe or resistant hypertension (≥3 drugs)
 Symptoms of atherosclerotic disease elsewhere
 Negative family history of hypertension
 Smoker
 Worsening renal function after renin-angiotensin inhibition
i.e., increase in S. creatinine level by ≥30%
 Recurrent “flash” pulmonary edema
Approach to renal/renovascular hypertension

32. Physical Examination Findings:
• Abdominal bruits
• Other bruits
• Advanced fundal changes
Laboratory Findings:
• Raised serum creatinine level
• Low serum K+ & Na+ level
• Raised plasma renin level
• Proteinuria, usually moderate
• Secondary aldosteronism
• USG-Unilateral small (atrophic) kidney size
Approach to renal/renovascular hypertension

33. Special tests for renovascular hypertension:
• Renal vein renin ratio (>1.5affacted/contralateral)
• Captopril enhanced radioisotope renal scan
• Doppler sonography
• Magnetic resonance angiography
• CT- angiography (for those with normal renal function)
Hypertension Canada CHEP Guidelines for the Management of Hypertension 2016
Approach to renal/renovascular hypertension

34. Renal CT angiogram with 3D reconstruction
Severe prox. atherosclerotic
stenosis of the Rt. renal artery and
mild stenosis of the left renal artery
Classic “string-of-beads” lesion of
fibromuscular dysplasia

35. Fibromuscular Dysplasia, before and after PTRA

36. Mineralocorticoid-Induced Hypertension
Primary aldosteronism:
 Aldosterone-producing adenoma
 Unilateral/Bilateral adrenal hyperplasia
 Glucocorticoid-remediable aldosteronism
Cortisol Excess:
 Cushing syndrome
Deoxycorticosterone Excess:
 Deoxycorticosterone-secreting tumors
 Congenital adrenal hyperplasia
• 11β-Hydroxylase deficiency
• 17α-Hydroxylase deficiency

37. Screening for hyperaldosteronism:
 Serum K+ and HCO3
- & serum Na+ and Mg2+
 Plasma aldosteron/plasma renin activity
 Oral salt loading suppression test
 Adrenal vein sampling
Hyperaldosteron induced hypertension
Clinical feature:
Hypertensive patients with spontaneous hypokalemia (K+ <3.5
mmol/L) or marked diuretic-induced hypokalemia (K+ <3.0 mmol/L)

38. Cortisole excess hypertension
Clinical feature:
• Suspected in hypertensive patients with truncal obesity, wide
purple striae, thin skin, muscle weakness, and osteoporosis (80%)
• If left untreated, it can cause marked LVH and congestive heart
failure
• The secretion of mineralocorticoids can increase along with
cortisol, which itself is a potent activator of the mineralocorticoid
receptor
Screening:
 Measurement of free cortisol in a 24-hour urine sample
 Dexamethasone suppression test
 Determination of late-night salivary cortisol

39. Deoxycorticosteron excess hypertension
• If hypertension with
pseudohermaphroditism/virilisation/musculinization
Screening for hyperaldosteronism:
 Serum K+ and HCO3
- & serum Na+
 Plasma aldosteron/plasma renin activity

41. Catecholamine related hypertension
 Patients with hypertension(paroxysmal) and multiple
symptoms suggestive of catecholamine excess (e.g.,
Headaches, palpitations, sweating, panic attacks and pallor)
 Sudden paroxysms used to occur in :
• Stress: anesthesia, angiography, parturition
• Pharmacologic provocation: Histamine, Nicotine,
Caffeine, ß-blockers, TCA,MAO inhibitors
• Manipulation of tumors: abdominal palpation, urination

42. Screening :
 Serum Metanephrine testing highest sensitivity (96%) lower
specificity (85%)
 24 Hr Urinary metanephrin/Normetanephrin
sensitivity(87.5%),sp(99.7%)
 localization of Pheochromocytomas or Paragangliomas
• Magnetic resonance imaging
• Computed tomography (if MRI unavailable)
• I131 Metaiodobenzylguanidine (MIBG) scintigraphy

43. Vascular causes of hypertension
 Most common cause of hypertension is coarctation of aorta in children
and ≈8 times more common in boys
 Typically diagnosed around 5 years age with the onset of HTN or a
cardiac murmur, rarely, mild cases of coarctation have occurred in adults
 Discrepancies between bilateral brachial, or brachial and femoral blood
pressures
Screening & diagnosis:
 Chest radiography:-
In younger patients, may be nonspecific, in adults the classic
“three”sign or rib notching may be evident
 Barium swallow:-
Show “Reverse 3” sign
 Transthoracic echocardiography
 Magnetic resonance imaging

44. Red arrows - rib notching caused by the dilated intercostal arteries
Yellow arrow - the aortic knob,
Blue arrow - the actual coarctation and
Green arrow -the post-stenotic dilation of the descending aorta

45. Hormone related hypertension
 Half of patients with various hormonal disturbances have
hypertension:
• Hypothyroidism
• Hyperparathyroidism
• Acromegaly
• Hypercalcemia
 Thyroid hormone affects cardiac output and systemic vascular
resistance, which in turn affect BP
• Hypothyroidism can cause an elevation in DBP
• Hyperthyroidism may cause isolated elevation of SBP(wide
P.P.)

46. Treatment of hypertension in young
A. Non pharmacological:
Lifestyle changes:
• Weight reduction and diet modification
 Eliminating refined carbohydrate, reducing saturated fat
intake
 Salt intake must be reduced, Avoidance of junk food
 Fresh fruit and vegetables in the diet should be
encouraged
• Exercise programme or joining an organised sports programme
• Alcohol use needs to be moderated and tobacco product use
discontinued
Falkner B, Daniels S. Summary of the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in
Children and Adolescents. Hypertension 2004;44(4):387-388.

48. B. Pharmacological:
Considered in the following situations:-
 Severe hypertension
 After failure of lifestyle therapy
 Patients with target-organ damage
 Secondary causes of hypertension

50.  First to identify the actual hypertensive patients
 Take proper history for symptoms, life style, habits and family
history & other risk factor
 Complete physical examination from head to toe and order to run
basic lab tests
 Extensive workup in all newly diagnosed young hypertensive in
search of sec. cause not recommended always*
 If no evidence of sec. hypertension start early treatment, non-
pharmacological/pharmacological otherwise treat the cause
 Maintain target blood pressure <140/90 mmHg
 Council for treatment adherence
* S Afr Med J 2016;106(1):36-38. DOI:10.7196/SAMJ.2016.v106i1.10329