Moro O. Salifu, MD, MBA, MPH, MACP Professor & Chair Department of Medicine Chief, Division of Nephrology SUNY Downstate Medical Center, Brooklyn, NY

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1 Moro O. Salifu, MD, MBA, MPH, MACP Professor & Chair Department of Medicine Chief, Division of Nephrology SUNY Downstate Medical Center, Brooklyn, NY

2 Outline Overview Definition/considerations Causes of secondary hypertension Conclusion Disclosures: None

3 Disclosures: None

4 CDC/NHNS, National Health and Nutrition Examination Survey, Available at Accessed 8/24/14.

5 Source: Cutler JA, Sorlie PD, Wolz, M, Thorn T, Fields LE, Rocella, E J. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between and Hypertension 2008; 52:

6 Chobanian AV et al. JAMA 2003;289:

7 Chobanian AV et al. JAMA 2003;289:

8 Chobanian AV et al. JAMA 2003;289:

9 In patients <60 years of age, start medications at blood pressure of >140/90mm Hg and treat to goal of <140/90mm Hg In patients >60 years of age, start medications at blood pressure of >150/90mm Hg and treat to goal of <150/90mm Hg In all adult patients with diabetes or chronic kidney disease, start medications at blood pressure of >140/90mm Hg and treat to goal of <140/90mm Hg James PA et al. JAMA 2014;311:

11 For the non-black population (including diabetes), initial antihypertensive treatment may include a thiazide, ACEI, ARB, or CCB For the black population (including diabetes), initial antihypertensive treatment should include a thiazide or CCB For all patients with CKD, initial (or add-on) therapy for hypertension should include an ACEI or ARB James PA et al. JAMA 2014;311:

12 African-American patients are at; High risk for CV events Less responsive to drugs that act on the renin-angiotensinaldosterone system ACEI, ARB, BB Subgroup analysis of black patients in ALLHAT showed; Less BP reduction with lisinopril than amlodipine Risk of stroke was significantly higher with lisinopril than with amlodipine (RR 1.51, 95% CI ) Lisinopril less effective than chlorthalidone in preventing heart failure, stroke, and combined CHD The ALLHAT Collaborative Research Group. JAMA 2002;288:

13 Non-black (no DM or CKD) Black (no DM or CKD) Diabetes JNC-7 JNC-8 ASH/ISH ESC/ESH CHEP Thiazide Thiazide ACEI, ARB, CCB, BB, thiazide Thiazide, ACEI, ARB, CCB Thiazide, CCB CCB, thiazide <60:ACEI, ARB >60:CCB, thiazide Thiazide, CCB ACEI, ARB, CCB, thiazide Thiazide, ACEI, ARB, CCB, BB Thiazide, ACEI, ARB, CCB, BB ACEI, ARB Thiazide, ACEI, ARB (BB if <60) Thiazide, ARB (BB if <60) ACEI, ARB, CCB, thiazide CKD ACEI, ARB ACEI, ARB ACEI, ARB ACEI, ARB ACEI, ARB Adapted from Salvo M et al. Ann Pharmacother 2014;48:

14 Over 8,000 patients were randomized to Standard treatment goal, SBP 140 mmhg OR Intensive treatment goal, SBP 120 mmhg The SPRINT Research Group A Randomized Trial of Intensive versus Standard Blood-Pressure Control N Engl J Med. DOI: /NEJMoa

15 There was no significant difference between Standard and Intensive treatment goals in African Americans *p=0.34, after Hommel adjustment for multiple comparisons The SPRINT Research Group A Randomized Trial of Intensive versus Standard Blood-Pressure Control N Engl J Med. DOI: /NEJMoa

16 DASH trial found that the original DASH diet especially the diet rich in fruits and vegetables, and low fat dairy products, was very effective at lowering blood pressure in minorities, mostly African Americans Sacks FM, et al, for the DASH Study Group. NEJM 2001:344, 3-10

17 Blood pressure remaining above goal in spite of concurrent use of 3 antihypertensive agents of different classes. Ideally, 1 of the 3 agents should be a diuretic & all agents should be prescribed at optimal dose amounts.

18 Use of diuretic recommended but not required before diagnosing resistant hypertension. Doses should be optimal but not necessarily maximal before diagnosing resistant hypertension. Controlled resistant hypertension: high blood pressure controlled but with use of 4 of more agents should be considered resistant.

19 National Health and Nutrition Examination Survey (NHANES) Essential HTN 53% were controlled to <140/90 mm Hg. CKD, only 37% were controlled to <130/80 mm Hg Diabetic 25% of diabetic participants were controlled to <130/85 mm Hg. Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) 27% of participants were on 3 or more medications Hajjar I, Kotchen TA. JAMA 2003; 2Peralta CA et al. Hypertension 2005; 3Cushman WC et al. Clin Hypertens.

20 Older age Obesity Excessive dietary salt ingestion Chronic kidney disease Diabetes Left ventricular hypertrophy African American race Female gender Residence in Southeastern United States

21 Obesity or overweight High salt diet Physical inactivity Ingestion of low-fiber, high-fat diet Heavy alcohol ingestion Poor adherence with prescribed medications Inaccurate blood pressure measurement White coat hypertension

22 Non-Narcotic Analgesics NSAIDS, COX-2 inhibitors Sympathomimetic agents Decongestants, diet pills, cocaine Stimulants Methylphenidate, amphetamines Other Alcohol, Oral contraceptives, Cyclosporine, erythropoietin, Natural licorice, Herbal compounds

24 Resistant Hypertension: Approach. BP indicates blood pressure; CKD, chronic kidney disease; DBP, diastolic blood pressure; egfr, estimated glomerular filtration rate; NSAIDs, nonsteroidal antiinflammatory drugs; and SBP, systolic blood pressure. Adapted with permission from Calhoun et al.

25 Screening for Secondary Hypertension General principles: New onset HTN if <30 or >50 years of age HTN refractory to medical Rx (>3-4 meds) Specific clinical/lab features typical for dz i.e., hypokalemia, metabolic alkalosis, epigastric bruits, differential BP in arms, episodic HTN/flushing/palp, etc

26 Causes of Secondary HTN Common Intrinsic Renal Disease Renovascular Dz Mineralocorticoid excess/ aldosteronism? Sleep Breathing d/o Uncommon Pheochromocytoma Glucocorticoid excess/ Cushing s dz Coarctation of Aorta Hyper/hypothyroidism

27 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, depletion or antagonism of vasodepressors/ prostaglandins, pressor effects on TPR Renal disease from multiple etiol, treat underlying disease, dialysis/ transplant if necessary

28 Renovascular HTN Incidence 1-30% Etiology Atherosclerosis 75-90% Fibromuscular dysplasia 10-25% Other Aortic/renal dissection Takayasu s arteritis Thrombotic/cholesterol emboli CVD Post transplantation stenosis Post radiation

29 Interrelation among Renal-Artery Stenosis, Hypertension, and Chronic Renal Failure. Safian RD, Textor SC. N Engl J Med 2001;344:

30 Renovascular HTN - Pathophysiology Elevated Ang II Unilateral RAS: Contralateral kidney responds with diuresis/ Na, H2O excretion which can return plasma volume to normal. ACEI not contraindicated Bilateral RAS or solitary kidney RAS: leads to rapid volume expansion and ultimate decline in renin secretion. ACEI contraindicated

31 Renovascular HTN - Clinical History onset HTN age <30 or >55 Sudden onset uncontrolled HTN in previously well controlled pt Accelerated/malignant HTN Intermittent pulm edema (flush pulmonary edema) with nl LV fxn PE/Lab Epigastric bruit, particularly systolic/diastolic Azotemia induced by ACEI Unilateral small kidney

32 Renovascular HTN - diagnosis Physical findings (bruit) Duplex U/S Captopril renography Magnetic Resonance Angiography Renal Angiography

33 RAS screening/diagnostics Duplex U/S Captopril Renography MRA Bruit Angiography Sens Spec Cost 90-95% 83-91% 88-95% 39-65% Gold std 60-90% 87-93% 95% 90-99% Gold std $117 $968 $572? -? Limitation/Etc Operator dependent, 10-20% Meds, accuracy reduced in pt with renal insufficiency, lacks anatomical info; good predictor of BP response False positive artifact resp, peristalsis, tortuous vessels; cost Insensitive, severe stenosis may be silent Invasive, nephrotoxicity, little value in predicting BP response

34 Angiographic Appearance of the Two Most Common Forms of RAS Safian RD, Textor SC. N Engl J Med 2001;344:

35 Renovascular HTN Medical Rx Aggressive risk fx modification (lipid, tobacco, etc) ACEI/ARB safe in unilateral RAS Ultrasound ablation of renal sympathetic nerves

36 Primary Aldosteronism (Conn's Syndrome) Prevalence.5-2.0% (5-12% in referral centers) Etiology Adrenal adenoma Other: bilat adrenal hyperplasia, glucocorticoid suppressible hyperaldo, adrenal carcinoma Clinical: May be asymptomatic; headache, muscle cramps, polyuria Retinopathy, edema uncommon Hypokalemia (K normal in 40%), metabolic alkalosis, high-nl Na

37 Primary Aldosteronism- Dx Aldosterone / Plasma Renin Activity ratio Early am after ambulation ~10-15 min Ratio >20-25 with PRA <1 and Aldo >15 should prompt further testing, endo referral Confirmatory/physiologic testing Withold BP meds 2wks High serum aldo after IV saline (1.25L x 2hr) load followed by low PRA after salt restricted diet (40mg/d) or diuretic (lasix up to 120mg) serum aldo <8.5 ng/dl after IV saline rules out primary aldosteronism Imaging CT, scintography: If no mass consider adrenal hyperplasia

38 Primary Aldosteronism - Treatment Surgical removal of adrenal tumor, can be done laparoscopically Pretreatment for 3-4 wks with spironolactone minimizes postoperative hypoaldosteronism and restores K to normal levels Response of BP to spironolactone treatment is predictor of surgical outcome

39 Obstructive Sleep Apnea 30-80% of pts with essential HTN have OSA and 50% of pts with OSA have HTN 1 Prospective studies show link between OSA (apneic-hyponeic index) and development of HTN independent of other risk factors Clinical Daytime somnolescence, am headaches, snoring or witnessed apneic episodes Dx Sleep studies Rx wt loss, CPAP, surgical (UPPP) 1 Silverberg, et al.curr Opinion Nephrol Hyperten 1998:7; Peppard, et al. NEJM 2000:342:

40 OSA BP improvement with Rx Pankow, et al. NEJM 343:

41 Pheochromocytoma Rare cause of HTN (.1-1.0%) Tumor containing chromaffin cells which secrete catecholamines Young-middle age with female predominance Clinical Intermittent HTN, palpitations, sweating, anxiety spells May be provoked by triggers such as tyraminecontaining foods (beer,cheese,wine), pain, trauma, drugs (clonidine, TCA, opiates)

42 Pheochromocytoma - Screen Best detected during or immediately after episodes Plasma free metanephrine >.66nmol/L 24hr urine metanephrine (>3.7nmol/d) Sensitivity 99% 89% Specificity 77% (95%) 93% (96%) 24 urine VMA 64% 95% Lenders, et al. JAMA 2002 Mar 20;287(11):

43 Pheochromocytoma - Diagnosis Imaging for localization of tumor Sens Spec PPV NPV (MIBG) scintigraphy 78% 100% 100% 87% CT 98% 70% 69% 98% MRI 100% 67% 83% 100% Akpunonu, et al. Dis Month.October 1996, p688

44 Pheochromocytoma - treatment Surgical removal of tumor Anesthesia- avoid benzo, barbiturates or demerol which can trigger catechol release Caution with BB can cause unopposed alpha stimulation/pheo crisis BP control with peripheral alpha blockers (phentolamine, phenoxybenzamine, and prazosin)

45 Cushing s syndrome/ hypercortisolism Rare cause of secondary HTN (.1-.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

46 Cushings syndrome

47 Cushings syndrome - dx Screen: 24 Hr Urine free cortisol >90ug/day is 100% sens and 98% spec Confirm Low dose dexamethasone suppression test 1mg dexameth. midnight, measure am plasma cortisol (>100nmol is +) Other tests include dexa/crh suppresion test IPSS (inferior petrosal sinus sampling) Imaging CT/MRI head (pit) chest (ectopic ACTH tumor)

48 Cushings syndrome - Rx Pituitary adenoma Transphenoidal resection Pituitary irradiation Bromocriptine, octreotide Adrenal tumors adrenalectomy Removal of ACTH tumor

49 Coarctation of Aorta Congenital defect, male>female Clinical Differential systolic BP arms vs legs (=DBP) DBP between arms if stricture is proximal to subclavian vein Brickner, et al. NEJM 2000;342:

50 Thyroid Disease Hyperthyroidsm 33% of thyrotoxic pt develop HTN Usually obvious signs of thyrotoxicosis Dx: TSH, Free T4/3, thyroid RAIU Rx: radioactive ablation, propanolol Hypothyroidsm 25% hypothyroid pt develop HTN Mechanism mediated by local control, as basal metabolism falls so does accumulation of local metabolites; relative vasoconstriction ensues

51 Summary General principles: New onset HTN if <30 or >50 years of age HTN refractory to medical Rx (>3-4 meds) Specific clinical/lab features typical for disease i.e., hypokalemia, metabolic alkalosis, epigastric bruits, differential BP in arms and legs, episodic HTN/flushing/palp, etc

52 Conclusions Remember clinical/diagnostic features of common forms of resistant/secondary HTN Important to appropriately screen patient suspected of having potentially correctable causes of HTN Understand limitations of screening/treatment (atherosclerotic RAS) Treat to Target MOS

53 Contact Information Moro O. Salifu, MD, MBA, MPH, MACP Department of Medicine SUNY Downstate Medical Center Phone - (718) Moro.Salifu@downstate.edu

Hypertension. Omar Obeidat, MD FACC Interventional Cardiology

Hypertension. Omar Obeidat, MD FACC Interventional Cardiology Hypertension Omar Obeidat, MD FACC Interventional Cardiology Hypertension Definition Hypertension is sustained elevation of BP Systolic blood pressure ³ 140 mm Hg Diastolic blood pressure ³ 90 mm Hg Factors