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1 Hypertension The Importance of Hypertension Prevalence data The first killer Silent killer Masked killer Financial burden Preventable Treatable Definition of Blood Pressure The pressure exerted by blood against the artery through which it flows Blood pressure = cardiac output X systemic vascular resistance CO X SVR = BP 4 Hypertension is defined as: the level of blood pressure linked with a doubled increased long-term risk for adverse events OR The level of blood pressure at which the benefits of action (i.e. therapeutic intervention) exceed those of inaction.” Evans and Rose Brit Med Bull 1971;27:37-42 5 6 7 Definitions of hypertension by office and out-of-office blood pressure levels 8 What clinical guidelines are used to categorize HTN? The Joint Committee on Prevention, Evaluation, and Treatment of High Blood Pressure (JNC 8) guidelines provide the most current guidelines 9 11 Prevalence >65 million Americans have hypertension (HTN) Of those diagnosed with HTN < 50% have their blood pressure under control Lack of treatment leads to serious complications 12 High Prevalence of Hypertension Worldwide Prevalence of hypertension (%) 60 55 38 40 38 47 49 Spain Finland 42 28 20 0 USA Italy Sweden England Adults aged 35–64 y (data are age- and sex-adjusted), except* (adults aged ≥ 30 y) Hypertension defined as BP 140/90 mmHg or on treatment 13 49 Wolf-Maier et al. JAMA. 2003;289:23632369; Sekikawa, Hayakawa. J Hum Hypertens. 2004; 2004;18:911–912. Japan* Germany Prevalence of Hypertension 14 Awareness, Treatment and Control of Hypertension is Rather Low Worldwide Proportion of patients in the population (%) Country Aware Treated Controlled* Japan 16.0 – 4.1 England 35.8 24.8 10.0 Germany 36.5 26.1 7.8 Spain 38.9 26.8 5.0 Sweden 48.0 26.2 5.5 Italy 51.8 32.0 9.0 USA 69.3 52.5 28.6 * BP < 140/90 mmHg 15 Wolf-Maier et al. Hypertension. 2004;43:10–17; Sekikawa, Hayakawa. J Hum Hypertens. 2004;18:911–912. 15 BP Control Rates Trends in awareness, treatment, and control of high blood pressure in adults ages 18–74 National Health and Nutrition Examination Survey, Percent Awareness Treatment Control II 1976–80 51 II (Phase 1) 1988–91 73 II (Phase 2) 1991–94 68 1999–2000 70 31 10 55 29 54 27 59 34 16 Awareness, Treatment and Control of Blood Pressure 1976-2000 (NHANES) 80 70 60 50 Awareness Treatment Control 40 30 20 10 0 1976-1980 1988-1991 1991-1994 1999-2000 17 18 19 Benefits of Lowering BP Average Percent Reduction Stroke incidence 35–40% Myocardial infarction 20–25% Heart failure 50% 20 Risk of CV Mortality Doubles With Each 20/10 mmHg BP Increase • Meta-analysis of 61 prospective, observational studies • 1 million adults aged 40–69 y with BP > 115/75 mmHg • 12.7 million person-years Fold increase in relative CV risk 10 8-fold 8 6 4-fold 4 2 2-fold 1-fold 0 115/75 135/85 155/95 SBP/DBP (mmHg) 175/105 21 Each 2 mmHg Decrease in SBP Reduces CV Risk by 7–10% • Meta-analysis of 61 prospective, observational studies • 1 million adults aged 40–69 y with BP > 115/75 mmHg • 12.7 million person-years 2 mmHg decrease in mean SBP 22 Lewington et al. Lancet. 2002;360:1903–1913. 7% reduction in risk of IHD and other vascular disease mortality 10% reduction in risk of stroke mortality 22 23 Factors contribute to the development of primary HTN 1. 2. 3. Sympathetic nervous system hyperactivity Renin-angiotensin-aldosterone system hyperactivity Endothelial dysfunction 24 25 Types of HTN? Primary • ?? ‘essential’idiopathic • Most common type found in 90-95% of those with HTN • Cause not well understood • Salt sensitive • RAAS dependent Secondary • Caused by some other medical problem or condition: • • • • • • High-dose estrogen Renal artery stenosis Pregnancy (PET) Cushing’s syndrome pheochromocytoma Others? 26 27 ABPM ? Renin level ?? 28 What are the Symptoms? Symptoms may or may not be present • • • • • • • • Dizziness (unsteadiness) Early morning headache activity tolerance Malaise, fatigue Blurring of vision Spontaneous nosebleed Palpitations, angina, dyspnea Early signs/symptoms are often missed 29 30 31 32 BP measurement Physical assessment • Height & weight • Blood pressure Measuring BP accurately: • No smoking or caffeine 30 minutes before • Rest for 5 minutes prior to BP • Apply cuff to bare arm • Proper size cuff applied 1 inch above brachial artery • Inflate cuff to 30 mmHg above initial radial pulse check If BP elevated, wait 2 minutes, recheck • Check BP in other arm 33 BP Measurement Techniques Method Brief Description In-office Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm. 140/90 Ambulatory BP monitoring Indicated for evaluation of “whitecoat” HTN. Absence of 10–20% BP decrease during sleep may indicate increased CVD risk. 130/80 Self-measurement Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN. 135/85 34 35 36 37 38 White Coat and Ambulatory BP monitoring ABPM 39 40 41 Key Messages For persons over age 50, SBP is a more important than DBP as CVD risk factor, likewise wide pulse pressure Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10 mmHg throughout the BP range. Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN. Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be considered prehypertensive who require health-promoting lifestyle modifications to prevent CVD. 42 Key Messages (Continued) Thiazide-type diuretics should be initial drug therapy for most, either alone or combined with other drug classes. Certain high-risk conditions are compelling indications for other drug classes. Most patients will require two or more antihypertensive drugs to achieve goal BP. If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic. 43 Key Messages (Continued) The most effective therapy prescribed by the careful clinician will control HTN only if patients are motivated. Motivation improves when patients have positive experiences with, and trust in, the clinician. Empathy builds trust and is a potent motivator. The responsible physician’s judgment remains paramount. 44 Complications of HTN The higher the BP and the longer an individual has hypertension, the higher the risk of complications which include: • • • • • Hypertensive heart disease Cerebrovascular disease Peripheral vascular disease Kidney disease Retinal damage 45 46 47 Complications of Hypertension Heart • resistance workload left ventricular hypertrophy • CAD, angina, MI • Heart failure 48 Complications of Hypertension Brain • Atherosclerosis, stroke 49 Complications of Hypertension Peripheral vascular disease • Aortic aneurysm or dissection Retinal damage • damage to blood vessels of the eye Kidney disease • vessels less elastic decreased perfusion renal failure 50 Acute Complications Hypertensive Crisis: Severe and abrupt elevation of BP Diastolic over 120mm hg High Mortality Sx: papilledema, progressive renal failure, encephalopathy Most common cause is untreated hypertension Goal: slowly decrease BP 51 Classifications Hypertensive Crisis Hypertensive crisis is categorized by the degree of organ damage Hypertensive emergency: BP is severely elevated and there is evidence of target organ damage Hypertensive urgency: BP is elevated but there is no evidence of target organ damage • Especially brain 52 GOAL: Reduce Complications JNC 8 guidelines recommend a target BP of less than 140/90 Except elderly above 60 150/90 Patients with renal disease or diabetes need BP less than 140/90 53 What Reduces Risk of Complications? REDUCING MODIFIABLE RISK FACTORS IS A KEY INTERVENTION Goal = Patient teaching to reduce risk factors Drug therapy is initiated if lifestyle changes are not effective to control BP 54 Management of Hypertension Depends on risk group Lifestyle modifications Drug therapy is initiated if lifestyle modifications do not achieve goal Add or change drugs if goal not achieved 55 Lifestyle Modification Lose excess weight Cut back on salt Exercise regularly Cease alcohol intake Adopt the DASH eating plan to decrease cholesterol intake STOP smoking 56 DASH Diet http://www.nhlbi.nih.gov/health/publi c/heart/hbp/dash/ Dietary Approaches to Stop Hypertension = DASH • A diet rich in fruits, vegetables and lowfat dairy products with reduced fat content • Limits sodium intake to 2.4 g/day 57 Non-pharmacologic Management of Hypertension Weight management • DASH Low sodium-low fat diet Smoking cessation Restrict alcohol and caffeine Regular aerobic exercise Stress management • bio-feedback, relaxation, yoga, Tai Chi 58 59 Drug Therapy for HTN Diuretics • Flush excess water and sodium from the body • Thiazide diuretics • Loop diuretics: furosemide (Lasix) • Potassium sparing: Aldactone Beta adrenergic blockers Three classes: • Cardioselective • Non-selective • Combined alphabeta-blockers 60 The Majority of Hypertensive Patients Need Combination Therapy to Achieve BP Goals Trial (SBP achieved) ASCOT-BPLA (137 mmHg) ALLHAT (138 mmHg) IDNT (138 mmHg) RENAAL (141 mmHg) UKPDS (144 mmHg) ABCD (132 mmHg) MDRD (132 mmHg) HOT (138 mmHg) AASK (128 mmHg) 1 61 Bakris et al. Am J Med. 2004;116(5A):30S–38S; Dahlöf et al. Lancet. 2005;366:895–906. 2 3 4 Average number of antihypertensive medications Pharmacologic Management of Hypertension Alpha-adrenergic blockers • Suppress nerve impulses to blood vessels, which allows blood to pass more easily so BP goes ↓ • prazosin (Minipress) Calcium channel blockers • decrease the influx of Ca++ into muscle cells • Act on vascular smooth muscles (primary arteries) to decrease spasm and promote vasodilation • Amlodipine (Norvasc); felodipine (Plendil) 62 Pharmacologic Management of Hypertension Angiotensin converting enzyme (ACE) inhibitors • Decrease effect of RAA system: Capoten, Lisinopril • Diabetes mellitus w/proteinuria, heart failure Angiotensin II receptor blockers (ARB) • Prevent action of angiotensin II and produce vasodilation • losartan (Cozaar) 63 Pharmacologic Management of Hypertension Vasodilators • Direct arterial vasodilation • Sodium nitroprusside (Nipride) • Often used in hypertensive crisis Alpha-receptor agonists • Clonidine • Acts on central nervous system • Lowers peripheral vascular resistance 64 Why don’t some patients respond to therapy? Non-adherence to therapy • Patients don’t take their HTN meds → complications!!! • Cost, inadequate teaching, side effects, inconvenient dosing Drug related causes Other conditions Secondary hypertension Volume overload 65 Causes of Resistant Hypertension Improper BP measurement Excess sodium intake Inadequate diuretic therapy Medication • Inadequate doses • Drug actions and interactions (e.g., nonsteroidal anti-inflammatory drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives) • Over-the-counter (OTC) drugs and herbal supplements Excess alcohol intake Identifiable causes of HTN 66 Summary Key Points Two types of HTN: primary & secondary Inadequate BP control leads to serious complications including STROKE Key point: risk factor modification Treatment focuses on lifestyle management and drug therapy JNC 7 provides the most current treatment guidelines for hypertension 67 Identifiable Causes of Hypertension Sleep apnea Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushing’s syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease 68 Pheochromocytoma 0.01-0.1% of HTN population • Found in 0.5% of those screened M=F 3rd to 5th decades of life Rare, investigate only if clinically suspicion: • • • • • Signs or Symptoms Severe HTN, HTN crisis Refractory HTN (> 3 drugs) HTN present @ age < 20 or > 50 ? Adrenal lesion found on imaging (ex. Incidentaloma) 69 Pheo: Signs & Symptoms The five P’s: • • • • • Pressure (HTN) Pain (Headache) Perspiration Palpitation Pallor 90% 80% 71% 64% 42% • Paroxysms (the sixth P!) The Classical Triad: • Pain (Headache), Perspiration, Palpitations • Lack of all 3 virtually excluded diagnosis of pheo in a series of > 21,0000 patients 70 Pheo: Paroxysms, ‘Spells’ 10-60 min duration Frequency: daily to monthly Spontaneous Precipitated: • Diagnostic procedures, I.A. Contrast (I.V. is OK) • Drugs (opiods, unopposed -blockade, anesthesia induction, histamine, ACTH, glucagon, metoclopramide) • Strenuous exercise, movement that increases intra-abdo pressure (lifting, straining) • Micturition (bladder paraganlgioma) 71 Pheo: ‘Rule of 10’ 10% extra-adrenal (closer to 15%) 10% occur in children 10% familial (closer to 20%) 10% bilateral or multiple (more if familial) 10% recur (more if extra-adrenal) 10% malignant 10% discovered incidentally 72 Plasma Metanephrines Not postural dependent: can draw normally Secreted continuously by pheo SEN 99% SPEC 89% False Positive: acetaminophen Assay not widely available yet 73 Localization: Imaging CT abdomen • Adrenal pheo SEN 93-100% • Extra-adrenal pheo SEN 90% MRI • > SEN than CT for extra-adrenal pheo MIBG Scan • SEN 77-90% SPEC 95-100% 74 75 Renovascular Hypertension 76 77 Endocrine Hypertension Catecholamine producing tumours Mineralocorticoid hypertension Renin-dependent hypertension Hyperthyroidism and hypothyroidism Acromegaly Hyperparathyroidism 78 Typical clinical scenarios Difficult hypertension with hypokalaemia, on polypharmacy- referred to endocrinologist for exclusion of 2ary hypertension Coincidentaloma of adrenal with hypertension, on polypharmacy Which drugs are permissible, and after how much delay should there be before investigation? 79 80 Mineralocorticoid hypertension- in whom should it be suspected? Diagnosis should be suspected in patient with hypertension, spontaneous hypokalaemia (<3.5mmol/l), and alkalosis. Severe hypokalaemia (<3.0) on diuretics Investigate patient hypertension refractory to conventional therapy, or adrenal coincidentaloma Recent onset of hypertension Normokalaemia present in >35% patients on low salt diet 81 Clinical features of hyperaldosteronism Mild to severe hypertension Sodium retention + intravascular vol exp mineralocorticoid escape Resetting of osmostat (thirst provoked at higher [Na+]) K+ loss (kaliuresis) +/- low serum K+ (unprovoked: rule out diuretics, laxatives, vomiting, herbal supplements) Suppression of renin generation (rule out drugs,excessive dietary sodium intake) Polyuria, nocturia,fatigue,cramps, Mg++↓ Exclude liquorice abuse / carbenoxolone therapy NB minor mineralocorticoids DOC, compound B 82 Imaging in 1ary hyperaldosteronism High resolution CT scanning with thin (2-3mm) slices Bilateral adrenal venous catheter (measure cortisol, adrenaline + aldosterone) remains gold standard – operator dependent: right adrenal notoriously difficult to cannulate. Give iv ACTH (2μg/min) during sampling to magnify difference between tumour and non-tumorous side Non-tumorous side PAC = peripheral value because of suppressed PRA 83 Glucocorticoid remediable hyperaldosteronism GRA (FH1) Due to aberrant expression of chimeric gene formed by unequal recombination of promoter and initial parts of CYP11B1 and section of CYP11B2 with aldosterone synthase activity Aldosterone under ACTH control Autosomal dominant: FH of early onset BP↑ with CVA ,K+↓ High levels of 18-hydroxy and 18-oxocortisol Rx : chronic administration of low dose GC, spironolactone, or amiloride 84 Liddle syndrome Familial BP↑, unprovoked K+↓, PRA↓, and undetectable PAC Autosomal dominant, caused by constitutive activation of distal renal epithelial sodium channel (β,γ C-terminal subunit mutations prevent trafficking of channel) Treated by amiloride 85 Liddle's – low renin, low aldo Licorice and SAME -- low renin, low aldo Renal artery stenosis and renin-secreting tumors -- high renin, high aldo Adrenal hyperfunction -- low renin, high aldo 86 Renin Aldo Liddle low low Licorice low low RAS high high Conn’s low high 87 Renin-AngiotesninAldosterone System A drop in BP or blood volume causes kidneys to secrete renin, a precursor to angiotensin I Angiotensin-converting enzyme turns angiotensin I into angiotensin II, a potent vasoconstrictor Stimulates adrenal glands to release aldosterone This prompts the kidneys to retain sodium and water The increased volume and vasoconstriction raise BP 88 89 90