Hipertensão Arterial Secundária

8/11/2019 Hipertensão Arterial Secundária

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Hypertension Rounds:

Secondary HypertensionOscar H. Cingolani, MD

Co-Director Hypertension Center

Assistant Professor of Medicine.Division of Cardiology

Johns Hopkins University Hospital

ocingol1@jhmi.edu

Disclosures: None

Objectives:

• Present a hypertension patient and discuss

assessment, evaluation and treatment.

• Identify situations where secondary forms of

hypertension should be suspected.

• Discuss appropriate tests.

Hypertension Rounds

• 42 year-old gentleman with recurrent “nervous

heart episodes” characterized by tremors,

sweating, raising HR and headaches.

• Blood pressure as high as 210/140 mmHg.

• Episodes last between 10 minutes and 1 hr.

Patient quite tired after these episodes.• Lost 10 Kg over the last 2 years.

Hypertension Rounds

• These spells started 3 years before, and they

were getting worse and more frequent.

• On one occasion, he was taken to a local ER,

propranolol was given and his BP rose from

170/100 to 220/120 mm Hg.

Case Presentation.

• How many of you think this is secondary

hypertension?

• How many of you think this is a

Pheochromocytoma?

• How many think this is another form of secondary

hypertension?

- Onset before 20 or suddently after 50 years of age.

- Level of BP > 180/110 mmHg.

- Organ damage

Funduscopic grade 2 or higher

Serum creatinine >1.5 mg/100ml

Cardiomegaly or LVH

- Unprovoked hypokalemia

- Abdominal bruit- Variable pressures with tachycardia, sweating, tremor.

- Poor response to therapy that is usually effective.

According to European and US guidelines, these are situations

when secondary forms of hypertension should be considered.

When to suspect secondary hypertension.

Evaluation:

• Assess lifestyle and identify cardiovascular risk factors.

• Assess the presence or absence of target organ

damage.

• Search for identifiable causes of hypertension.

According to current guidelines, these three main aspects should be kept inmind when evaluating a patient with hypertension. The search for anidentifiable cause of hypertension should be based on history and physicalexamination first, to avoid unnecessary testing. The chances of an elderlypatient with family history of hypertension to have a secondary form of highblood pressure is less likely than a young woman with marked elevations in

her BP, no family history and an audible abdominal bruit.

Primary Aldosterosim is now considered the most common identifiable form of

hypertension, being underdiagnosed in the general clinical practice.

Other less likely causes, such as renal vascular disease, Cushing’s or pheochromocytoma

should be always suspected, not because they are frequent, but because theconsequences are quite relevant.

Other identifiable causes of high blood pressure are sleep apnea1, ethanol

consumption2, and chronic use of NSAIDs3.

1) Konecny T, Kara T, Somers VK. Hypertension. 2014 Feb;63(2):203-9. Steinhorst AP et

al. Sleep Breath. 2013 Oct 3.

2) O'Keefe JH, Bhatti SK, Bajwa A, Dinicolantonio JJ, Lavie CJ. Mayo Clin Proc. 2014

Mar;89(3):382-393

3) Di Gennaro FP, Cingolani OH, Abbate AF, Toblli JE, Vilches A. Medicina (B Aires).

2004;64(4):301-5.

Target Organ Damage in Hypertension

• Assessment of target organ damage (TOD)

should always take place in evaluatinghypertensive patients. The presence of TODindicates more severe and or sustainedhypertension. On contrary, in patients with

white coat hypertension, TOD is usually notpresent.

• Fundoscopic eye exam is key in the initialassessment, since it gives us the opportunityto look at the vessels directly.

LVH: ECG

ECG revealing marked LVH. When LVH is

disproportionately for the degree of hypertension,

primary ALDO or other forms of hypertension should

be suspected.

LVH: echocardiography

Tanabe A et al: Left ventricular hypertrophy is more prominent in patients withprimary aldosteronism than in patients with other types of secondary

hypertension. Hypertens Res 1997; 20:85-90.

Echocardiography (long parasternal view) image from a hypertensive patient revealing left ventricular

hypertrophy (LVH). Note the thick LV walls and dilated left atrium (LA). When LVH is out of proportion

tothe level of BP, primary aldosteronsm should be suspected, among other secondary causes ofhypertension.

Primary Aldo and renal cysts

Torres V.E., Young Jr. W.F., Offord K.P., Hattery R.R.: Association of hypokalemia,

aldosteronism, and renal cysts. N Engl J Med 1990; 322:345-351.

Primary aldosteronism might be associated with deep-seated renal cysts in 60% of cases.

A history or finding consistent with renal cysts should raise suspicious of primary also in

patients with resistant hypertension, specially if hypokalemia is present.

Primary Aldosteronism: prevalence.

It is now recognized that primary ALDo is probably the most common cause of secondary

hypertension.

Primary Aldosteronism: Pathophysiology.

Pathophysiology of primary aldosteronism, explaining symptoms.

Primary Aldosteronism

• Aldosterone-producing adenoma (APA)— 35% of cases.

• Bilateral idiopathic hyperplasia (IHA)— 60% of cases.

• Primary (unilateral) adrenal hyperplasia— 2% of cases.

• Aldosterone-producing adrenocortical carcinoma—<1% of cases.

• Familial hyperaldosteronism (FH)

• Glucocorticoid-remediable aldosteronism (FH type I) —<1% of

cases• FH type II (APA or IHA) —<2% of cases

• Ectopic aldosterone-producing adenoma or carcinoma—<0.1% of

Primary Aldosteronism

• In the first 262 cases of primary aldosteronism diagnosed at

the Mayo Clinic (1957-1986), the highest blood pressure (BP)was 260/155 mm Hg; mean (±SD) was 184/112 ± 28/16 mmHg. Patients with APA tend to have higher BPs than those withIHA.

• Hypokalemia leads to muscle weakness and cramping,headaches, palpitations, polydipsia, polyuria, nocturia.

• Periodic paralysis is a very rare presentation in whites, but it isnot an infrequent in patients of Asian descent.

• Another rare presentation can be tetany associated with adecrease in ionized calcium and marked hypokalemic alkalosis.

Young Jr. W.F., Klee G.G.: Primary aldosteronism. Diagnostic evaluation. Endocrinol Metab Clin North

Am 1988; 17:367-395.

Propossed algorithm to evaluate for primary Aldo.

Primary Aldosteronism: diagnosis

• Saline suppression test.

• Captopril suppression.

Response to spironolactone.• Adrenal venous sampling.

• Imaging.

Suggested methods to confirm diagnosis of primary aldosteronism.

Spironolactone seems to drop BP substantially in patients with resistant

hypertension, when added as a 4th agent.

Could we be missing undiagnosed primary Aldo in these patients?

Renovascular HTN

• Incidence 1-30%• Etiology

– Atherosclerosis 75-90%

– Fibromuscular dysplasia 10-25%

– Other• Aortic/renal dissection

• Takayasu’s arteritis

• Thrombotic/cholesterol emboli.

• Post transplantation stenosis.• Post radiation.

Different etiologies of renal artery stenosis. It is quite important to suspect fibromuscular

dysplasia in young women with elevated BP, since early diagnosis and treatment can

dramatically change the course of this disease.

RAS screening/diagnostics

Sens Spec Cost Limitation/Etc

Duplex U/S90-95%

60-90%

$200Operator dependent.

CaptoprilRenography

83-91%

87-93% $1000

Meds, accuracy reduced in ptwith renal insufficiency, lacksanatomical info; goodpredictor of BP response

MRA88-95%

95% $500False positive artifact resp,peristalsis, tortuous vessels;cost

Bruit39-65%

90-99%

-Insensitive, severe stenosismay be silent

AngiographyGoldstd

Goldstd

?Invasive, nephrotoxicity, littlevalue in predicting BPresponse

MRA unilateral and bilateral RAS. Currently, MRA and Duplex are the non-invasive

tests more commonly used in many centers.

Fibromuscular Dysplasia, before

and after PTRAAtherosclerotic RAS before and after stent

Safian & Textor. NEJM. 2001 Feb 8;344(6):431-42.

Angiography is still considered the gold standard,

although its major disadvantages are invasiveness

and contrast nephrotoxicity.

St ti d di l th f th l ti l t

Stenting and medical therapy for atherosclerotic renal-artery

stenosis.

Cooper CJ et al. N Engl J Med 2014;370:13-22.

CORAL study. Kaplan – Meier Curves for the Primary Outcome. Survival curves are truncated

at 5 years owing to instability of the curves because few participants remained in the study after

5 years.

Indications for Revascularization

Resistant hypertension.

Deteriorating renal function.

Critical stenosis (or stenosis with worsening function

of a solitary kidney).

Fibromuscular dysplasia

Associated heart failure ("flash" pulmonary edema”)

Cushing’s syndrome/ hypercortisolism

• Rare cause of secondary HTN (0.1- 0.6%)

• Etiology: pituitary microadenoma, iatrogenic (steroid

use), ectopic ACTH, adrenal adenoma

• Clinical

– Sudden weight gain,truncal obesity, moon facies,

abdominal striae, DM/glucose intolerance, HTN,

prox muscle weakness, skin atrophy,

hirsutism/acne

Cushing’s syndrome

Coarctation of Aorta

Brickner, et al. NEJM 2000;342:256-263

Coarctation of the aorta should always be suspected in young adults with hypertension (upper

extremities), specially if it is associated with proggresive weakness of lower extremities. Typical findings

include the presence of a bruit (mid scapular or subclavicular), pulsatile intercostal arteries (with notching

of the inferior aspect of the ribs in the chest X-ray, together with a “3 sign”).

Coarctation of Aorta

• Congenital defect, male > female

• Clinical

– Differential systolic BP arms vs legs.

– May have differential BP in arms if defect is prox to L

subclavian artery. – Diminished/absent femoral arterial pulses.

– Often asymptomatic

– Associated with Turner’s, bicuspid AV.

• If uncorrected 67% will develop LV failure by age 40 and 75%will die by age 50.

• Surgical Rx, long term survival better if corrected early.

The Relationship between Obstructive Sleep

Apnea and Hypertension

• The odds of having

hypertension is 37% greater

in persons with obstructive

sleep apnea.

• The odds of having

hypertension is 46% greater

in those who spend greater

percentage of sleep timebelow 90% oxygen

saturation.

Nieto, F. J. et al. JAMA 2000;283:1829-1836

Ch i 24 h ABPM ft 2 k f th

Norman, D. et al. Hypertension 2006;47:840-845

Change in 24-hour ABPM after 2 weeks of therapywith CPAP

Norman et al, as well as many others have shown that OSA patients’ BP responds to CPAP.

Pheochromocytoma

• Uncommon tumors composed of chromaffin cells

which synthesize and release catecholamines.

• Surgically correctable forms of hypertension.

0.1% to 0.3% of hypertensive patients have anunderlying pheochromocytoma.

Clinical Features

• Hypertension: often severe, occasionally malignant,and may be resistant to treatment with standardantihypertensive drugs.

• Paroxysms or Crisis: frequent or sporadic, occurringat intervals as long as weeks or months. With time,the paroxysms usually increase in frequency,duration, and severity.

Other Distinctive Clinical Features

• Increased metabolic rate, such as profuse sweating

and mild to moderate weight loss.

• Sinus tachycardia, sinus bradycardia,supraventricular arrhythmias, and ventricular

premature contractions have all been noted.

• Angina and acute myocardial infarction.

Diagnosis

• The diagnosis is established by the demonstration of

increased production of catecholamines or

catecholamine metabolites.

• The diagnosis can usually be made by the analysis of

a single 24-h urine sample, provided the patient is

hypertensive or symptomatic at the time of

collection.

Ph h t

Pheochromocytoma

Pheochromocytomas are usually seen on imaging studies when they are symptomatic.

Back to our patient: outside studies.

• ECG: Normal sinus rythm/sinus tachycardia.

• Labs: All in the normal range.

• Stress echo, abdominal and thoracic CT

(contrast), and full body MRI were normal.

• Thyroid hormones, plasma epinephrine and

norepinephrine, serum Aldo and plasma Renin

all normal.

• Renal Duplex unremarkable.

Back to our patient: physical exam

• HR= 64/min, BP (4 limbs) = 126/72. No ortho.

• Normal physical exam (fundoscopic evaluation)

• Uppon abdominal exam, he became tachycardic,

diaphoretic and BP rose to 190/102 mmHg.• HR and BP returned to normal after 15 min.

• Plasma metanephrine levels were slightlyelevated at 80 pg/mL (normal < 57 pg/mL) withnormal normetanephrine values andchromogranin-A.

Hypertension Rounds

• How many of you think this is secondary

hypertension?

• How many of you think this is a Pheo?

How many think this is another form ofsecondary hypertension?

Abdomen CT and MIBG scan

Cingolani OH et al . Circulation. 2014. Mar 4;129(9).

Although CT scan revealed normal adrenal glands, a Iodine-131-metaiodobenzylguanidine

(MIBG) radioisotope scan was strikingly positive for isotope uptake from the left adrenal

gland, therefore the gland was succesfully removed laparoscopically after alpha and beta

blocking treatment was instituted.

Adrenal Medullary Hyperplasia

Cingolani OH et al . Circulation. 2014. Mar 4;129(9)

Normal adrenal gland Primary adrenal medullary hyperplasia

Adrenal Medullary Hyperplasia

Uncommon condition that can clinically mimicpheochromocytoma.

• Most commonly, the condition is associated with

multiple endocrine neoplasia (MEN) syndromes.

• It might antecede the formation of Pheo.

• It might recur in the contralateral gland.

• Responds to alpha and beta blockade.

Kurihara K, Mizuseki K, Kondo T, Ohoka H, Mannami M, Kawai K. Adrenal medullary

hyperplasia. Hyperplasia-pheochromocytoma sequence. Acta Pathol Jpn. 1990;40:683-686

Thank You!

Oscar H. Cingolani, MD

ocingol1@jhmi.edu

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