HYPERTENSION. SOME PRELIMINARY DEFINITIONS Blood pressure (BP), sometimes referred to as arterial blood pressure, is the pressure exerted by circulating

HYPERTENSION

SOME PRELIMINARY DEFINITIONS • Blood pressure (BP), sometimes referred to as arterial blood

pressure, is the pressure exerted by circulating blood upon the walls of blood vessels, and is one of the principal vital signs.

• When used without further specification, "blood pressure" usually refers to the arterial pressure of the systemic circulation.

• During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure. The blood pressure in the circulation is principally due to the pumping action of the heart.

• Differences in mean blood pressure are responsible for blood flow from one location to another in the circulation. The rate of mean blood flow depends on the resistance to flow presented by the blood vessels.

• Mean blood pressure decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles.

SOME PRELIMINARY DEFINITIONS Mean arterial pressure

The mean arterial pressure (MAP) is a term used in medicine to describe an average blood pressure in an individual.

The mean arterial pressure (MAP) is the average over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP)

CALCULATION : 1/3 (SBP + 2 DBP)

MAP is considered to be the perfusion pressure seen by organs in the body.

It is believed that a MAP that is greater than 60 mmHg is enough to sustain the organs of the average person. MAP is normally between 70 to 110 mmHg

If the MAP falls below this number for an appreciable time, vital organs will not get enough Oxygen perfusion, and will become ischemic.

SOME PRELIMINARY DEFINITIONS Normal blood pressure•< 120/80 mmHgPre hypertension•120-129 or 80-89 mmHg

Stage 1 hypertension:• Clinic blood pressure (BP) is 140/90 mmHg or higher and• ABPM ( ambulatory blood pressure monitoring) or HBPM ( home bpm) average is 135/85 mmHg or higher.

Stage 2 hypertension: • Clinic BP 160/100 mmHg is or higher and• ABPM or HBPM daytime average is 150/95 mmHg or higher.

Severe hypertension: • Clinic systolic BP is 180 mmHg or higher or• Clinic diastolic BP is 110 mmHg or higher.

White-coat effect: • A discrepancy of more than 20/10 mmHg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis

Aims of the talk

1. To diagnose hypertension

2. To treat hypertension

•Why ?•Who ?•When ?•How ?

3. To what extend treat hypertension ?

Second part : special issues in HPT

1. Primary HPT

2. Secundary HPT

3. HPT and Diabetes Mellitus

4. HPT in Pregnancy

5. Resistant HPT

6. New insights in HPT

Case scenario 1 : MaryPresentation

38 year old, attending for routine appointment about her contraception, for which she uses a diaphragm.

Medical history

From her records you notice that Mary’s blood pressure has increased since her last check twelve months ago. She does not smoke, drinks 10-12 units of alcohol a week and has no notable medical history.

On examination

Mary’s first clinic blood pressure measurement is 158/94 mmHg. Her heart rate is 72 beats per minute and regular

You are considering a diagnosis of hypertension and therefore take another reading in Mary’s other arm. There is no notable difference between readings.

Next steps for diagnosis

Question 1.1

What would you do next?

DefinitionsNormal blood pressure•< 120/80 mmHgPre hypertension•120-129 or 80-89 mmHg

Stage 1 hypertension:• Clinic blood pressure (BP) is 140/90 mmHg or higher and• ABPM ( ambulatory blood pressure monitoring) or HBPM ( home bpm) average is 135/85 mmHg or higher.

Stage 2 hypertension: • Clinic BP 160/100 mmHg is or higher and• ABPM or HBPM daytime average is 150/95 mmHg or higher.

Severe hypertension: • Clinic systolic BP is 180 mmHg or higher or• Clinic diastolic BP is 110 mmHg or higher.

White-coat effect: • A discrepancy of more than 20/10 mmHg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis

Case scenario 1 : Mary

Answer 1.1

You would take Mary’s blood pressure a third time during the consultation.

Question 1.2

The third reading is 149/93 mmHg. You suspect hypertension – what would you do next?


Answer 1.2

Organise for Mary to receive ambulatory blood pressure monitoring (ABPM) through your GP practice. If you are responsible for setting up the monitoring device, you ensure that at least two measurements per hour are taken during Mary’s usual waking hours (for example, between 8 am and 10 pm). You would use the average value of at least 14 measurements taken during Mary’s usual waking hours to confirm a diagnosis of hypertension.

At the same time you would also carry out investigations for

1.target organ damage (such as left ventricular hypertrophy, chronic kidney disease and hypertensive retinopathy).

2.coexisting disorders

Move to the next slide for a lists of tests and further investigations

How should the Blood Pressure be Measured?

In the ClinicBy the doctor?By a nurse?By an automated device?

Outside the ClinicHome monitoring?Ambulatory monitoring?

The White Coat Effect in the Real World(Little et al, BMJ 2002; 325: 254)

• 173 hypertensive patients in 3 general practices in the UK

• Clinic (MD and RN), self-monitoring, and ABPM

• White coat effect estimated as difference between other measures of BP and daytime BP: ABPM

Physician 19/11 mmHg

Nurse 1 5/8 mmHg

Nurse 2 5/6 mmHg

Self-monitoring in clinic 10/13 mmHg

Self-monitoring at home 5/6 mmHg

24 Hour Ambulatory Monitoring

Prospective Studies Showing that Home BP Predicts CV Morbidity Better than Clinic BP

Author Year Population N Comments

Imai 1996 Population 1789 ABP & HBP predict, not CBP

Bobrie 2004 Treated 4939 HBP predicts, not CBP

Sega 2005 Population 2051 HBP predicts better than CBP

• Measurement error

• Small number of readings

• Effects of recent activities

• Expense & Inconvenience

• White coat effect

A Diagnosis of Hypertension

based exclusively on Physician readings is no longer acceptable


Answer 1.2







Answer 1.2 (continued)•test for the presence of protein in the urine by sending a urine sample for estimation of the albumin:creatinine ratio and test for haematuria using a reagent strip•take a blood sample to measure plasma glucose, electrolytes, creatinine, estimated glomerular filtration rate, serum total cholesterol and HDL cholesterol •examine the fundi for the presence of hypertensive retinopathy•arrange for a 12-lead electrocardiograph or an echocardiography to be performed

JNC 7 Recommendations for Routine Work-up of Hypertensive Patients

Routine Tests• Electrocardiogram • Urinalysis • Blood glucose, and hematocrit • Serum potassium, creatinine, or the corresponding estimated GFR,

and calcium• Lipid profile, after 9- to 12-hour fast, that includes high-density and

low-density lipoprotein cholesterol, and triglycerides

Optional tests • Measurement of urinary albumin excretion or albumin/creatinine ratio

More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved


Answer 1.2






Overlap of Four Common Conditions

Sleep Sleep Disordered Disordered BreathingBreathing

HypertensionHypertension

ObesityObesity

DiabetesDiabetesSMOKING


Answer 1.2 (continued)

You would also carry out a formal assessment of cardiovascular risk (Mary’s clinic blood pressure must be used in the calculation of cardiovascular risk) using a cardiovascular risk assessment tool, in line with Identification and assessment of CVD risk in ‘Lipid modification’ (NICE clinical guideline 67).

Additionally, you would also ascertain information about lifestyle in areas such as diet, exercise, alcohol, smoking and caffeine consumption and dietary sodium intake and offer appropriate lifestyle advice.

Record the results of all investigations and assessment in Mary’s notes.

Framingham SCORE PROCAM (Men) Reynolds (Women) Reynolds (Men)

Sample size 5345 205,178 5389 24,558 10,724

Age, range (y) 30 to 74; M:49 19 to 80; M:46 35 to 65; M:47 >45; M:52 >50; M:63

Mean follow-up (y) 12 13 10 10.2 10.8

Risk factors considered

Age, sex, total cholesterol, HDL cholesterol, smoking, systolic blood pressure, antihypertensive Medications

Age, sex, total-HDL cholesterol ratio, smoking, systolic blood pressure

Age, LDL cholesterol, HDLcholesterol, smoking, systolic blood pressure, family history, diabetes, triglycerides

Age, HbA1C (with diabetes), smoking, systolic blood pressure, total cholesterol, HDL cholesterol, hsCRP, parental history of MI at <60 y of age

Age, systolic blood pressure, total cholesterol, HDL cholesterol, smoking, hsCRP, parental history of MI at <60 y of age

Endpoints CHD (MI and CHD death)

Fatal CHD Fatal/nonfatal MI or sudden cardiac death (CHD and CVD combined)

MI, ischemic stroke, coronary revascularization, cardiovascular death (CHD and CVD combined)

MI, stroke, coronary revascularization, cardiovascular death (CHD and CVD combined)

URLs for risk calculators

http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=prof

http://www.heartscore.org/pages/welcome.aspx

http://www.chd-taskforce.com/coronary_risk_assessment.html

http://www.reynoldsriskscore.org/


Comparison of a Sample of Global Coronary and Cardiovascular Risk Scores

Note: Table 2 in full-text Guideline
















JNC 7: CVD Risk Factors

Hypertension* Cigarette smoking Obesity* (BMI >30 kg/m2) Physical inactivity Dyslipidemia* Diabetes mellitus* Microalbuminuria or estimated GFR <60 ml/min Age (older than 55 for men, 65 for women) Family history of premature CVD

(men under age 55 or women under age 65)*Components of the metabolic syndrome.


Question 1.3

You identify her dietary sodium intake is greater than recommended levels.

NICE PH25 on prevention of cardiovascular disease recommends that as part of preventing cardiovascular disease at a population level there should be a reduction in salt intake.

By 2015 an adults maximum intake of salt per day should not exceed 6g and by 2025 this should be reduced to 3g

What advice would you offer?


Answer 1.3

You would advise that healthy diet and regular exercise can reduce blood pressure.

You would also encourage her to keep her dietary sodium intake low as this can reduce blood pressure.

Dietary Approaches to Stop Hypertension (DASH)


Question 1.4

The result of Mary’s ABPM shows daytime average blood pressure of 145/92 mmHg.

What would your diagnosis and your next steps be?


Answer 1.4

This result shows that Mary has stage 1 hypertension.

If you had not already done so (answer 1.2), you would estimate cardiovascular risk and offer tests for target organ damage.

You would use the results of the cardiovascular risk assessment to discuss prognosis and healthcare options with Mary.

Continue to ascertain information about her lifestyle in order to provide tailored lifestyle advice in accordance with the guideline on areas such as diet (including sodium and caffeine intake) and exercise and alcohol consumption.

See the definitions slide for ABPM diagnosis criteria

JNC 7: Target Organ Damage

Heart• Left ventricular hypertrophy• Angina or myocardial infarction• Atrial fibrillation• Heart failure

Brain• Stroke or transient ischemic attack

Chronic kidney disease

Peripheral arterial disease Retinopathy

The Sokolow-Lyon index:S in V1 + R in V5 or V6 (whichever is larger) ≥ 35 mm (≥ 7 large squares)R in aVL ≥ 11 mm

Left axis deviation (QRS of -30° or more)

LEFT VENTRICULAR HYPERTROPHY

Retina Normal and Hypertensive Retinopathy

Normal Retina Hypertensive Retinopathy

A: HemorrhagesB: Exudates (Fatty Deposits)C: Cotton Wool Spots (Micro Strokes)

A B

C

Stage I- Arteriolar Narrowing

Arteriolar Narrowing

Stage II- AV Nicking

AV Nicking

AV Nicking

AV Nicking

Stage III- Hemorrhages (H), Cotton Wool Spots and Exudats (E)

H

E

http://www.bmii.ktu.lt:8081/unrs/eyes?trg=oneimg&nr=14&image=10

Stage IV- Stage III+Papilledema


Question 1.5

The results of the investigations for target organ damage and formal assessment of cardiovascular risk are:

• no evidence of target organ damage

• 10-year cardiovascular risk less than 20%.

Nothing abnormal was detected in the other investigations you organised.

What is your next step and what treatment and follow up would you offer?


Answer 1.5 (continued)

Mary does not have target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 20% or greater, therefore you would not offer antihypertensive drug treatment.

You would continue to provide further tailored lifestyle advice (recommendation 1.4.1 – 1.4.9) periodically in accordance with the NICE clinical guideline.

The NICE clinical guideline recommends that you would provide Mary with an annual review of care to monitor blood pressure, provide her with support and discuss her lifestyle and symptoms.

Aims of the talk

1. To diagnose hypertension

2. To treat hypertension

•Why ?•Who ?•When ?•How ?

3. To what extend treat hypertension ?

Goals of Treatment

Treating SBP and DBP to targets that are <140/90 mmHg

Patients with diabetes or renal disease, the BP goal is <130/80 mmHg

The primary focus should be on attaining the SBP goal.

To reduce cardiovascular and renal morbidity and mortality

Benefits of Treatment

Reductions in stroke incidence, averaging 35–40 percent

Reductions in MI, averaging 20–25 percent

Reductions in HF, averaging >50 percent.

Treatment guidelines (ESH/ESC 2007)

Average risk Low added risk Moderate added risk High added risk Very high added risk

ESH – ESC Guidelines Committee. J Hypertens 2007; 25: 1105–1187

Care pathway

CBPM ≥160/100 mmHg & ABPM/HBPM

≥ 150/95 mmHg

Stage 2 hypertension

Consider specialist referral

Offer antihypertensive drug treatment

Offer lifestyle interventions

If younger than 40 years

If target organ damage present or 10-year cardiovascular risk > 20%

Offer annual review of care to monitor blood pressure, provide support and discuss lifestyle, symptoms and medication

Offer patient education and interventions to support adherence to treatment

CBPM ≥140/90 mmHg & ABPM/HBPM ≥ 135/85 mmHg

Stage 1 hypertension


Question 1.6

If Mary had been eligible to receive antihypertensive drug treatment, what should you consider when prescribing antihypertensive drugs for a woman of child-bearing potential?

Normal Blood Pressure Regulation

Hydraulic equation:

Blood Pressure = Cardiac output (CO) X Resistance to passage of blood through precapillary arterioles (PVR)

Physiologically CO and PVR is maintained minute to minute by – arterioles (1) postcapillary venules (2) and Heart (3)

Kidney is the fourth site – volume of intravascular fluid

Baroreflex, humoral mechanism and renin-angiotensin- aldosterone system regulates the above 4 sites

All antihypertensives act via interfering with normal mechanisms

The Renal response

Long-term blood pressure control – by controlling blood volume

Reduction in renal pressure - intrarenal redistribution of pressure and increased absorption of salt and water

Decreased pressure in renal arterioles and sympathetic activity – renin production – angiotensin II production

Angiotensin II:

•Causes direct constriction of renal arterioles•Stimulation of aldosterone synthesis – sodium

absorption and increase in intravascular blood volume

Antihypertensive Drugs

Diuretics:

• Thiazides: Hydrochlorothiazide, chlorthalidone• High ceiling: Furosemide• K+ sparing: Spironolactone, triamterene and amiloride

MOA: Acts on Kidneys to increase excretion of Na and H2O – decrease in blood volume – decreased BP

Angiotensin-converting Enzyme (ACE) inhibitors:

• Captopril, lisinopril., enalapril, ramipril and fosinoprilMOA: Inhibit synthesis of Angiotensin II – decrease in peripheral resistance and

blood volume

Angiotensin (AT1) blockers:

• Losartan, candesartan, valsartan and telmisartanMOA: Blocks binding of Angiotensin II to its receptors

Antihypertensive Drugs

ß-adrenergic blockers:

•Non selective: Propranolol (others: nadolol, timolol, pindolol, labetolol)•Cardioselective: Metoprolol (others: atenolol, esmolol, betaxolol)

MOA: Bind to beta adrenergic receptors and blocks the activity

Calcium Channel Blockers (CCB):

•Verapamil, diltiazem, nifedipine, felodipine, amlodipine, nimodipine etc.MOA: Blocks influx of Ca++ in smooth muscle cells – relaxation of SMCs – decrease BP

ß and α – adrenergic blockers:

•Labetolol and carvedilol

α – adrenergic blockers:

•Prazosin, terazosin, doxazosin, phenoxybenzamine and phentolamineMOA: Blocking of alpha adrenergic receptors in smooth muscles - vasodilatation

Antihypertensive Drugs – Centrally acting: Clonidine, methyldopa

MOA: Act on central α2A receptors to decrease sympathetic outflow – fall in BP

K+ Channel activators:

•Diazoxide, minoxidil, pinacidil and nicorandilMOA: Leaking of K+ due to opening – hyper polarization of SMCs – relaxation of SMCs

Vasodilators:

•Arteriolar – Hydralazine (also CCBs and K+ channel activators)•Arterio-venular: Sodium Nitroprusside

Step 1 treatment: Offer people aged under 55 years step 1 antihypertensive treatment with an angiotensin-converting enzyme (ACE) inhibitor or a low-cost angiotensin-II receptor blocker (ARB). If an ACE inhibitor is prescribed and is not tolerated (for example, because of cough), offer a low-cost ARB. [new 2011]

Do not combine an ACE inhibitor with an ARB to treat hypertension. [new 2011]

Offer step 1 antihypertensive treatment with a calcium-channel blocker (CCB) to people aged over 55 years and to black people of African or Caribbean family origin of any age. If a CCB is not suitable, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic. [new 2011]

Starting treating HPT

Second part : special issues in HPT

1. Primary HPT2. Secundary HPT3. HPT and Diabetes Mellitus4. HPT in Pregnancy5. Resistant HPT6. New insights in HPT

Types of Hypertension Primary HTN: also known as essential HTN.

accounts for 95% cases of HTN.

no universally established cause known.

Secondary HTN: less common cause of HTN ( 5%).

secondary to other potentially rectifiable causes.

Primary HPT Pathogenesis — The pathogenesis of primary hypertension

(formerly called "essential" hypertension) is poorly understood. A variety of factors have been implicated, including:

Increased sympathetic neural activity, with enhanced beta-adrenergic responsiveness

Increased angiotensin II activity and mineralocorticoid excess.

Hypertension is about twice as common in subjects who have one or two hypertensive parents and multiple epidemiologic studies suggest that genetic factors account for approximately 30 percent of the variation in blood pressure in various populations

Reduced adult nephron mass may predispose to hypertension, which may be related to genetic factors, intrauterine developmental disturbance (eg, hypoxia, drugs, nutritional deficiency), and post-natal environment (eg, malnutrition, infections).

Causes of Secondary HTN Common

Intrinsic renal disease Renovascular disease Mineralocorticoid excess Sleep Breathing disorder

Uncommon Pheochromocytoma Glucocorticoid excess Coarctation of Aorta Hyper/hypothyroidism

Secondary HTN-Clues in Medical History Onset: at age < 30 yrs ( Fibromuscular dysplasia) or > 55 (atherosclerotic renal artery stenosis), sudden onset (thrombus or cholesterol embolism).

Severity: Grade II, unresponsive to treatment.

Episodic, headache and chest pain/palpitation (pheochromocytoma, thyroid dysfunction).

Morbid obesity with history of snoring and daytime sleepiness (sleep disorders)

Secondary HTN-clues on Exam Pallor, edema, other signs of renal disease.

Abdominal bruit especially with a diastolic component (renovascular)

Truncal obesity, purple striae, buffalo hump (hypercortisolism)

Secondary HTN-Clues on Routine Labs Increased creatinine, abnormal urinalysis ( renovascular and renal parenchymal disease)

Unexplained hypokalemia (hyperaldosteronism)

Impaired blood glucose ( hypercortisolism)

Impaired TFT (Hypo-/hyper- thyroidism)

Renal Parenchymal Disease Common cause of secondary HTN (2-5%) HTN is both cause and consequence of renal disease

Multifactorial cause for HTN including disturbances in Na/water balance, vasopressors/ prostaglandins imbalance

Renal disease from multiple etiologies.

Renovascular HTN Atherosclerosis 75-90% ( more common in older patients)

Fibromuscular dysplasia 10-25% (more common in young patients, especially females)

Other• Aortic/renal dissection• Takayasu’s arteritis• Thrombotic/cholesterol emboli• CVD• Post transplantation stenosis• Post radiation

Fibromuscular Dysplasia, beforeand after PTRA

Atherosclerotic RAS before and after stentSafian & Textor. NEJM 344:6;

Renovascular hypertension (RVH) Case presentation 59 yo male , no medical past history

Acute loin pain and headaches BP : 180/100,bilateral; PR 88 rr Acute renal failure:

s.creatinine: 1.13>1.75mg/ dl microhematuria

Renovascular hypertension (RVH) Risk factors:

no family history for HTN or CVD

Obesity Heavy smoker

Renovascular hypertension (RVH) Ultrasound of kidneys : symetric , normal size and shape, no uromechanical obstruction

Renovascular hypertension (RVH) One year later: non optimal blood pressure on 3 medications : 160/90 HCTZ+ACEI+BB

Renal dysfunction: s.creatinine 1.41mg/dl

New US

Renovascular hypertension (RVH) DMSA RENAL SCAN

Atherosclerotic renal artery stenosis – do we really know what to do?

Treatment decisions for management of renal artery stenosis must take into account the likelihood of:

1- Blood pressure reduction, 2- Renal preservation, 3- or Both

•RENOGRAM WITH ACE-INHIBITOR

•DUPLEX-KIDNEY US

•MR ANGIOGRAPHY

•SPIRAL CT ANGYOGRAPHY

•GOLD STANDARD: RENAL ARTERIOGRAPHY

Renin-Angiotensin System

RAS

CaptoprilCaptopril

Angiotensinogen

Angiotensin I

Angiotensin II

Aldosterone Vasoconstriction

HTN

Renin

ACE

Effect of RAS on GFR

Captopril Renal ScanMAG 3MAG 3

Renal revascularization is favored in patients who have:

1- Bilateral renal artery stenosis and a serum creatinine level 1.5 mg/dL, 2- Unilateral renal artery stenosis and fractional GFR 40%, 3- ACE inhibitor–induced renal failure,4- Hypertensive crisis, and 5- Nonischemic pulmonary edema.

Medical therapy is favored over renal revascularization in patients with:

1-Unilateral renal artery stenosis and serum creatinine level 2.5mg/dL, 2- Renal length 7 cm, 3- Proteinuria 1 g/d, 4- Severe diffuse intrarenal vascular disease, and target kidney renal resistance 80, all of which provide evidence of underlying advanced nephropathy.

Mineralocorticoid excess

Cardiovascular Events and Primary Aldosteronism

Rate of Cardiovascular Events and Cardiac Structure in Primary Aldosteronism

Primary Aldo (n=124)

Essential HTN (n=465)

Odds ratio (95% CI)

p value

Stroke (%) 12.9 3.4 4.2 (2.0-8.6) < 0.001

Myocardial infarction (%) 4.0 0.6 6.5 (1.5–27.4) < 0.005*

Atrial fibrillation 7.3 0.6 12.1 (3.2-45.2) <0.0001*

Echo LVH (%) 34 24 1.6 (1.1-2.5) < 0.01

EKG LVH (%) 32 14 2.9 (1.8-4.6) < 0.001

Milliez P et al. J Am Coll Cardiol 2005; 45(8):1243-1248

*Fisher exact test.CI = confidence interval; LVH = left ventricular hypertrophy

Case Detection

Higher prevalence: Young age of HBP onset Severe refractory HBP FH of PA or CVA <40 y/o Hypokalemia

Prevalence of Primary Aldosteronism in Hypertensive Patients

Mosso L et al. Hypertension 2003; 42(2):161-165

14 ―

12 ―

10 ―

8 ―

6 ―

4 ―

2 ―

0 ―Normal Stage 1 Stage 2 Stage 3

1.551.99

13.2

8.02

Screening for PA : ARR

Aldosterone / PRA > 30 / 1

Aldosterone >15 ng% (36% may have levels 9-16 ng%)

24 hour urine: Aldosterone > 12 mcg/day with sodium > 200 meq /day

PA : Confirmation Saline Suppression Test (>6 ng/dL)

Florinef Suppression Test ( >6ng/dL)

24 hr urine aldosterone on high salt diet >12 mcg

Subtypes of Primary Aldosteronism

May be treated surgically for cure Aldosterone-producing adenoma (APA) Primary (unilateral) adrenal hyperplasia Aldosterone-producing adrenocorticoid carcinoma

Should always be treated medically Idiopathic hyperaldosteronism (BAH) Glucocorticoid-remediable aldosteronism (FH-1)

FH-2

New insights in HPT

Renal Denervation

Renal Sympathetic Activation: Efferent NervesKidney as Recipient of Sympathetic Signals

Renal EfferentNerves

↑ Renin Release RAAS activation↑ Sodium Retention↓ Renal Blood Flow

87

HypertrophyArrhythmiaOxygen Consumption

VasoconstrictionAtherosclerosis

InsulinResistance

Renal Sympathetic Activation: Afferent NervesKidney as Origin of Central Sympathetic Drive

Renal AfferentNerves

↑ Renin Release RAAS activation↑ Sodium Retention↓ Renal Blood Flow

Sleep Disturbances

88

•Nerves arise from T10-L2•The nerves arborize around the artery and primarily lie within the adventitia

Renal Nerve Anatomy

Vessel Lumen

Media

Adventitia

Renal Nerves

8989

Renal Nerve Anatomy Allows a Catheter-Based Approach

90

• Renal artery access via standard interventional technique

• 4-6 two-minute treatments per artery

• Proprietary RF generator – Automated – Low power– Built-in safety algorithms

Spacing of e.g. 5 mm.

Symplicity HTN-2: Lancet Conclusions

Catheter-based renal denervation, done in a multicentre, randomised trial in patients with treatment-resistant essential hypertension, resulted in significant reductions in BP.

The magnitude of BP reduction can be predicted to affect the development of hypertension-related diseases and mortality

The technique was applied without major complications. This therapeutic innovation, based on the described

neural pathophysiology of essential hypertension, affirms the crucial relevance of renal nerves in the maintenance of BP in patients with hypertension.

Catheter-based renal denervation is beneficial for patients with treatment-resistant essential hypertension.

91

Symplicity HTN-2 Investigators. Lancet. 2010;376:1903-1909.

Documents

HYPERTENSION. SOME PRELIMINARY DEFINITIONS Blood pressure (BP), sometimes referred to as arterial blood pressure, is the pressure exerted by circulating