systemic hypertension craig a chasen md facc

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Systemic Hypertension Systemic Hypertension Craig A Chasen MD FACC Associate Professor of Medicine

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Systemic HypertensionSystemic Hypertension

Craig A Chasen MD FACCAssociate Professor of Medicine

Overview of HypertensionOverview of Hypertension

JNC VI on Prevention, Detection, Evaluation, and Rx of High Blood Pressure (1997)– 50 million hypertensive patients in the U.S.

National Health and Nutrition Examination Survey III (NHANES III) (1995)– only 21% are controlled to <140/90 mm Hg– 35% are unaware of their condition

High-normal BP is associated with an increased risk of cardiovascular disease– N Eng J Med 2001; 345: 1291-7

Joint National Committee VIJoint National Committee VI

Category Systolic BP Diastolic BP Optimal < 120 < 80 High normal 130 – 139 85 - 89 Mild HTN 140 – 159 90 - 99 Mod HTN 160 – 179 100 - 109 Severe HTN >180 > 110

MacMahon et al 1990MacMahon et al 1990

Diastolic BP increased by 5 mm Hg– 34% increase in stroke risk– 21% increase in coronary risk

Hypertension Adverse Effects:Hypertension Adverse Effects:Framingham StudyFramingham Study

Triples risk of stroke Triples risk of CHF Doubles risk of SCD Doubles risk of MI

Increases Risk of CV EventIncreases Risk of CV Event

Gender Race Age Pulse pressure

Types of Variation in BPTypes of Variation in BP

Short-term: HR and RR, autonomic NS Daytime: degree of activity Diurnal: BP fall during sleep Seasonal: cold weather increases BP

Obtaining BP MeasurementsObtaining BP Measurements

Sitting > 5 minutes Appropriate cuff size Cuff level with heart Legs uncrossed Self vs. RN vs. MD*

* Mancia et al., Hypertension 1987;9:209

False BP ElevationsFalse BP Elevations

Examinee: pain, alcohol, caffeine Equipment: leaky bulb valve, noise Examiner: expectation bias, hearing Examination: cuff uncentered, narrow or

low; elbow too low

Australian Therapeutic TrialAustralian Therapeutic Trial

Overall, 80% of the patients with mild-mod. HBP placed on placebo maintained a diastolic BP < 100 mm Hg and, during the average 3-yr follow-up, had no excess CV events.

Only 12.2% of the placebo treated patients noted a rise in diastolic BP > 110 mm Hg.

Management Committee.Lancet 1980;1:1261

Cardiovascular Consequences Cardiovascular Consequences of Hypertensionof Hypertension

Increased cardiac afterload leads to LVH Increased LV mass is associated with

elevated CV morbidity and mortality independent of other risk factors

Pts with BP > 160/95 have CAD, PVD & CVA > 3x than in normotensives

BP, Stroke & CHDBP, Stroke & CHD

In nine prospective observational studies and 420,000 patients with DBP ranging from 70 – 110 mm Hg who were followed for 6 – 25 years, the associations (with the above CV events) were “positive, continuous and apparently independent”.

MacMahon et al. Lancet 1990;335:765Kaplan’s Clinical Hypertension 2002

Hypertension Treatment and Hypertension Treatment and CV Outcomes over 5 Yrs.CV Outcomes over 5 Yrs.

Reduce BP by 15/6 mm Hg Reduce stroke by 34% Reduce CHD by 19%

Patient EvaluationPatient Evaluation

Determine type of hypertension Identify target organ damage Assess risk for early CV event

Patient History: IPatient History: I

Duration and prior Rx Pharmaceutical profile Family history Symptoms of secondary causes Target organ damage Presence of other risk factors

Patient History: IIPatient History: II

Concomitant Diseases Dietary History Sexual Function Features of Sleep Apnea Ability to modify life-style

HBP and Cardiac Risk FactorsHBP and Cardiac Risk Factors

50+Sedentary lifestyle

15Diabetes

40Obesity

25HDL-C < 40 mg/dl

40LDL-C > 140 mg/dl

35Smoking

PercentCardiac Risk Factor

Kaplan NM. Dis Mon 1992; 38:769-838

Physical Examination: IPhysical Examination: I

Accurate measure of BP, BMI Fundoscopy Carotid and thyroid abnormalities Heart sounds, rhythm, size Rales, rhonchi on lung exam

Physical Examination: IIPhysical Examination: II

Renal masses, waist circumference Aorta bruits, femoral pulses Peripheral pulses and edema Neurologic assessment, i.e. congnitive

Routine LaboratoryRoutine Laboratory

Hematocrit BMP Urinalysis Lipid profile ECG

JNC VI: BP & RxJNC VI: BP & Rx

Blood Pressure Stage (mm Hg)

Risk Group A NO RISK FACTORS

Risk Group B ONE RISK FACTOR

Risk Group C DIABETES or ORGAN DAMAGE

High-Normal BP 130-139/85-89

Lifestyle Modification

Lifestyle Modification

Medication Lifestyle Modification

Stage 1 HTN 140-159/90-99

Lifestyle Modification (up to 12 mo)

Lifestyle Modification (up to 6 mo)

Medication Lifestyle Modification

Stage 2,3 HTN ≥160/≥100

Medication Lifestyle Modification

Medication Lifestyle Modification

Medication Lifestyle Modification

Lifestyle Changes for HTNLifestyle Changes for HTN::

Reduce excess body weight Reduce dietary sodium to < 2.4 gms/day Adequate dietary intake of K, Ca and Mg Limit daily alcohol consumption Moderate aerobic exercise each day Cessation of cigarette smoking Garlic, fish oils, co-enzyme Q ???

NIH Consensus Conference on Physical NIH Consensus Conference on Physical Activity and CV Health (1995)Activity and CV Health (1995)

Review of 47 studies of exercise and HTN 70% of exercise groups decreased SBP by

an avg. of 10.5 mm Hg from 154 78% of subjects decreased DBP by an avg.

of 8.6 mm Hg from 98 Beneficial responses are 80 times more

frequent than negative responses

Hagberg, J., et.al., NIH, 1995: 69-71

Medical Therapy and Medical Therapy and Implications for Exercise TrainingImplications for Exercise Training

Pharmacologic and nonpharmocologic treatment can reduce morbidity

Some antihypertensive agents have side-effects and some worsen other risk factors

Exercise and diet improve multiple risk factors with virtually no side-effects

Exercise may reduce or eliminate the need for antihypertensive medications

Oral Contraceptives and HBPOral Contraceptives and HBP

BP rises a little in most women on OCs RR=1.5 for current users vs. never users

– 41 cases per 10,000 person-years of OC use

RR=1.1 for current users vs. previous users ERT is associated with lower BPs

Drug Therapy of Hypertension:Drug Therapy of Hypertension:CV Events ReductionCV Events Reduction

Diuretics BBs ACEIs CCBs

Randomized controlled trials

Slow BreathingSlow Breathing

Guided slow breathing to < 10 /min 15 minutes, 3-4 times per week Sustained reductions in SBP & DBP FDA approved July 2002 J Hum Hypertension 2001;15:263 Am J Hypertension 2001;14:74

Malignant Hypertension:Malignant Hypertension:Treatment ITreatment I

Loop diuretic Nitroprusside* Fenoldopam Labetolol Enalaprilat

Malignant Hypertension:Malignant Hypertension:Treatment IITreatment II

Esmolol* Hydralazine Nitroglycerin CCBs Phentolamine

Hypertension and PregnancyHypertension and Pregnancy

5% enter pregnancy with chronic HTN BP > 140/90 @ < 20 wks IUP, > 6 wks PP Drug of choice: alpha-methyldopa 10% develop gestational HTN > 20 wks PE = HTN + proteinuria (300 mg/24 hrs) Eclampsia = PE + seizures

Rx of acute, severe HBP Rx of acute, severe HBP in Pre-eclampsiain Pre-eclampsia

Hydralazine Labetolol Nifedipine Nitroprusside

Renovascular Hypertension:Renovascular Hypertension:IncidenceIncidence

Unselected hypertensives 1% Resistant to 2 drug therapy 10% Severe, rapidly progressive HBP 15% Accelerated-malignant HBP 32%*

4%*

Renovascular Hypertension:Renovascular Hypertension:Clinical Clues & TestingClinical Clues & Testing

Low suspicion No testing No clinical clues

Moderate suspicion Non-invasive Severe HBP (DBP > 120) Abdominal or flank bruit

High suspicion Angiography Severe HBP + elevated Cr Malignant HBP

Mann/Pickering. Ann Int Med 1992;117:845

Renovascular Hypertension:Renovascular Hypertension:Diagnostic TestsDiagnostic Tests

Captopril-enhanced renal scan Doppler ultrasonography Gadolinium MRA Spiral CT Angiography

EB Pedersen’s GuidelinesEB Pedersen’s Guidelines

Moderate or high index of suspicion No to mod. renal failure [Cr < 2.3]

Doppler vs. (ACEI) Renography, if ++ then Spiral CT vs. MRA, if ++ then, angiography

Severe renal impairment No doppler, no renography MRA preferred, o/w spiral CT or angiography

Renovascular Hypertension:Renovascular Hypertension:Medical TreatmentMedical Treatment

Aggressive BP control Lipid reduction therapy Antiplatelet therapy

Renovascular Hypertension:Renovascular Hypertension:TreatmentTreatment

Renal Artery Revascularization– Intolerant of medical Rx– Unresponsive to medical Rx– Progressive renal impairment

Renovascular Hypertension:Renovascular Hypertension:TreatmentTreatment

In patients with a high likelihood of success and low risk of complications, such as the majority of patients with fibromuscular hyperplasia and uncomplicated atherosclerotic RVHT, it is usually reasonable to proceed directly to revascularization.

Block/Pickering. Semin Nephrol 2000;20:474

PheochromocytomaPheochromocytoma

HBP, palpitation, sweating, HA Plasma / spot urine: metanephrines CT scan with adrenal cuts/ MRI If adrenal cuts nl : 131I–MIBG scan Phentolamine / Phenoxybenzamine

Primary AldosteronismPrimary Aldosteronism

HBP, weakness, alkalosis, hypokalemia Upright PAC/PRA ratio, if > 25, then Saline 500 cc/hr X 4 or NACl 10g/day X 3 Adrenal CT + P: 18-OH corticosterone Suppression scintiscan: NP-59 + dexameth Surgical therapy vs. spironolactone

Primary Aldosterone ExcessPrimary Aldosterone Excess

Aldosterone producing adenoma Bilateral adrenal hyperplasia Glucocorticoid-remediable

– chimeric11B-hydroxylase – aldosterone synthase gene– Glucocorticoids suppress ACTH

Adrenal carcinoma Extra-adrenal tumors

Corticosteroid induced HBPCorticosteroid induced HBP

Obesity, purple striae, osteopenia, DM Must r/o depression, alcoholism 1 mg dexamethasone (dexa) overnight

plasma suppression test Low dose dexa suppression test (urinary);

24-hr urinary free cortisol; plus sleeping midnight plasma cortisol test

Localization of Cortisol Localization of Cortisol ExcessExcess

Localization Pituitary Adrenal Ectopic CTH Corticotropin normal/high Low High CRH Response No response No response Dexa 8 mg Suppression No supp. No suppression Adrenal CT Nl/enlarged Tumor Nl/enlarged Pituitary CT Tumor Normal Normal Inferior petrosal Central/periph No central/peri

sinus sampling gradient gradient

Secondary HypertensionSecondary Hypertension

Hormonal: thyroid, hyperpara, acromegaly Neurologic: brain tumors, quadriplegia Acute physical stress: burns, resp distress Increased volume: EryP Rx, SIADH, PRV Chemical agents: cyclosporine, tacrolimus Sleep apnea

Reasons for Decline in CHD Reasons for Decline in CHD deaths from 1980-1990deaths from 1980-1990

43% from improved Rxs (i.e. CABG) 29% from secondary prevention (i.e. BP) 25% from primary prevention (i.e. BP)

Hunink et al JAMA1997;277:535

Exaggerated BP Response Exaggerated BP Response to Exerciseto Exercise

Among normotensive men who had an exercise test between 1971-1982, those who developed HTN in 1986 were 2.4 times more likely to have had an exaggerated BP response to exercise

Exaggerated BP Response Exaggerated BP Response to Exerciseto Exercise

Exaggerated BP was change from rest in SBP >60 mm Hg at 6 METs; SBP > 70 mm Hg at 8 METs; DBP > 10 mm Hg at any workload.

CARDIA study: subjects with exaggerated exercise BP were 1.7 times more likely to develop HTN 5 years later

J Clin Epidemiol 51 (1): 1998

Sleep, BP and CV EventsSleep, BP and CV Events

Inverted Dippers Non-dippers Excessive Dippers Dippers

Treatment of Orthostatic Treatment of Orthostatic HypotensionHypotension

Avoid overtreatment of BP Slow rising from chair/bed Supportive panty hose Avoid dehydration Volume expanders Sympathomimetics

NHANES III, phase 2NHANES III, phase 2HypertensionHypertension

Awareness 68.4% Treated 53.6% Controlled 27.4%

Acute BP Response to ExerciseAcute BP Response to Exercise