section name header

Info


A. Definitions

  1. Blood Pressure (BP) Categories have been definied; all in mm Hg sitting at rest
  2. Optimal BP: Systolic (SBP) <120 and Diastolic (DBP) <80
  3. Normal BP: Systolic <130 and Diastolic <85 normal
  4. High Normal BP: Systolic 130-139 OR Diastolic 85-89
  5. HTN defined as Systolic Blood Pressure (SBP) >140mm and/or Diastolic BP >90mm
  6. Categories of HTN
    1. Mild (Stage I): SBP 140-159 OR DBP 90-99
    2. Moderate (Stage II): SBP 160-179 OR DBP 100-109
    3. Severe (Stage III): SBP >179 OR DBP >109
  7. Isolated systolic HTN (>140mm) is fairly common in elderly and should be treated [12]
  8. Resistant or Refractory HTN [4]
    1. In patients adhering to at least 3 antihyperensive agents including a diuretic at full doses:
    2. BP >140/90 OR
    3. BP >130/80 in diabetes OR
    4. BP >130/80 in renal disease (creatinine >1.5mg/dL or >300m protein/24 hour urine)
    5. Increased risk of target organ damage
    6. Resistant systolic HTN is more common in persons >60 years than in younger persons
  9. HTN in children is defined based on normal BP for age and height
  10. Main complications of HTN are heart disease, stroke, renal failure [3]

B. Epidemilogy [1,2,3]

  1. About 50 million cases of HTN in USA in 2002 [2]
  2. Main concern is link between HTN and cardiovascular disease (CVD)
    1. Even high normal BP is associated with 1.6X (men) and 2.5X (women) risk for CVD [75]
    2. Risks associated with elevated BP is dependent on age and comorbid conditions, and likely has a threshold component [6]
    3. Most cases of uncontrolled HTN in USA are isolated systolic HTN in older adults who have good contact with physicians [74]
    4. Systolic blood pressure (SBP) is better predictor of risk CVD than diastolic BP (DBP), particularly in those >50 years old
  3. Reducing BP reduces all forms of CVD
  4. Presence of HTN is of particular concern in setting of other common CVD risks:
    1. Smoking
    2. Dyslipidemia
    3. Diabetes mellitus
    4. Age >60
    5. Men OR post-menopausal women
    6. Family history of CVD: women <65 year or men <55 year
  5. Persons with blood pressure >135/80 mm or being treated for HTN should be screened for type 2 diabetes [29,86]

C. Causes [7]

  1. Idiopathic
    1. Genetic predisposition is clear, with familial tracking (see below)
    2. Increased renal sodium retention and potassium losses associated with "Western" diet [19]
    3. Sodium intake >100nmol/day associated with increased HTN risk, SBP 4mm elevation [19]
    4. Renal Abnormalitiies (see below)
    5. Basal total body nitric oxide production is reduced in patients with essential HTN [69]
    6. BP increases with age
    7. Systemic inflammation (elevated CRP level) associated with increased risk of developing HTN in women [10]
    8. High normal aldosterone in non-HTN patients is 1.6X risk factor for developing HTN [35]
    9. Primary hyperaldosteronism occurs in 11% of patients with resistant HTN [21]
    10. Nonpregnant women who consumed >1000µg/day total folate had a 45% reduced risk of developing HTN than those who consumed <200µg/day [14]
    11. Soybean protein supplements lead to reduction in both SBP and DBP [15]
  2. Physiological Dysregulation in HTN
    1. Activation of sympathetic nervous system
    2. Hyperactivity of renin-angiogensin (AT)-aldosterone system [35]
    3. Apparent mineralocorticoid excess in absence of mutations may be quite common
    4. Abnormal renal handling of sodium (retention) and potassium (losses) in setting of "high- salt" Western diet [19]
    5. Renal endothelial damage is also likely a major contributor to systemic HTN
    6. Increased vascular stiffness - collagen overproduction
    7. Elevation of reactive oxygen species (ROS)
    8. All of these defects contribute to endothelial dysfunction
    9. Hyperlipidemia and diabetes mellitus exacerbate endothelial damage
  3. Subclinical Renal Dysfunction
    1. Prior to increases in creatinine, BUN, and/or development of microalbuminuria
    2. Reduced nephron numbers associated with increased risk for HTN in white persons [81]
    3. Elevated serum cystatin C associated with increased incident HTN across ethnic groups [13]
  4. Acute and Chronic Renal Insufficiency
    1. Elevated renin and AT2
    2. Volume overload
    3. Reduced nitric oxide production [69]
    4. Nephrosclerosis from secondary causes leads to HTN and renal insufficiency
    5. Removal of atrophic kidney can improve BP without compromising renal function [24]
    6. Renovascular HNT (see below) [80]
    7. Living kidney donors have ~5mm Hg BP increase above age matched controls at 5-10 years [25]
  5. Insulin Resistance Syndromes
    1. HTN rarely exists alone (<20% of cases)
    2. Often found with obesity, hyperglycemia, hypercholesterolemia
    3. This complex is often due to insulin resistance
    4. These syndromes are also called "metabolic syndrome"
  6. Obesity
    1. Obesity itself is a 3-6 fold risk factor for HTN [61]
    2. Weight loss reduces risk for HTN and for Type II diabetes
    3. Weight loss reduces blood pressure in both men and women [67]
    4. Loss of 10 pounds sustained for >6 months reduced HTN risk 65% [67]
  7. Thyroid Anomalies [68]
    1. Hyperthyroidism - mainly systolic HTN
    2. Hypothyroidism - mainly diastolic HTN
  8. Hypercalcemia
    1. Most commonly with Primary Hyperparathyroidism
    2. Other causes of hypercalcemia
  9. Other Endocrine Dysfunction [4]
    1. Cushing's Syndrome
    2. Hyperaldosteronism (Conn's Syndrome)
    3. Pheochromocytoma [70]
    4. All of these conditions involve overproduction of insulin counter-regulatory hormones
  10. Drugs
    1. Stimulants - ß-agonists, cocaine, amphetamines.
    2. Pseudoephedrine does not increase blood pressure in hypertensive patients
    3. Thyroid Replacement
    4. NSAIDs - can antagonize antihypertensive medicines, mild increase in blood pressures
  11. Sleep-Related Breathing Disorders [60,62,63]
    1. Sleep apnea (most common) and related syndromes
    2. Odds ratio for HTN with presence of any sleep related breathing disorder 1.4-6.6X
    3. Increasing Respiratory Disturbance Index (RDI) increases risk of HTN
  12. Genetic Anomalies
    1. Abnormalities in angiotensinogen gene regulation may be involved
    2. Genome wide mapping suggests locus on chromosome 6q and other loci [84]
    3. T594M mutationin ß-subunit of Na channel are 1associated with HTN in black women
    4. T594M mutation likely causes resistance of Na channel to down regulation by PK-C
    5. Other mutations of Na channel cause Liddle syndrome, associated with resistant HTN
    6. Mutations in G protein ß3-subunit linked to HTN
    7. Mutations in 17alpha or 11ß-hydroxylase genes
  13. HTN in Children
    1. Essential HTN is very unusual in persons <11 years old
    2. Search for a secondary cause should be undertaken in all children with HTN
    3. Renal disease and coarctation of the aorta are the most common causes in children
    4. Adrenal disease is not uncommon

D. Renovascular Hypertension [22,80]

  1. Types of Renal Artery Stenosis [80]
    1. Atherosclerotic Disease
    2. Fibromuscular Dysplasia
    3. Hypoperfusion of kidney leads to elevated renin and AT2
    4. Renin-AT-aldosterone increase ROS leading to vascular (enbdothelial) dysfunction
  2. Moderate to High Index of Suspicion
    1. Severe HTN (Diastolic >120)
    2. Refractory Hypertension (high doses of 2 or more medications)
    3. Progressive renal insufficiency
    4. Rapid normalization of blood pressure, or rapid increase in creatinine, by ACE-I
    5. ACE-I may provoke acute renal failure [23]
    6. Hypertension with asymmetric renal size
  3. Non-Invasive Tests
    1. Magnetic resonance angiography (MRA) and computed tomographic (CT) angiography preferred in patients with possible RAS and hypertension [73]
    2. Captopril trial (simplest test; high suspicion if excellent BP response)
    3. Captopril - Renin Test (captopril will cause an increase in renin level)
    4. Captopril renin test has ~90% positive and negative predictive values
    5. MRA and CT angiography are superior to captopril-renal scans [73]
    6. Plasma Renin - only 50-80% sensitive; no longer recommended for screening
    7. Duplex ultrasound is 98% specific and 98% sensitive for renal artery stenosis
  4. DTPA Renogram with ACE-I
    1. Patient is given 12.5-25mg of captopril one hour before second DTPA scan
    2. DTPA renal (flow) scan is carried out prior to captopril then 1 hour after it
    3. Affected kidney will show much decreased perfusion following captopril
    4. Sensitivity ~90%, Specificity ~95%
  5. Invasive Testing
    1. Intravenous pyelogram (IVP) - poor sensitivity, specificity
    2. Arteriography - gold standard but relatively high risk of renal failure
    3. Has largely been replaced with CT angiography or MRA
  6. Treatment
    1. ACE-I must be used very cautiously in patients with true renovascular HTN
    2. Surgical Correction
    3. Angioplasty - particularly for resistant HTN with renal atherosclerosis
    4. Dialysis when needed
  7. Angioplasty Results
    1. Fibromuscular Dysplasia: 91% dilated; 57% cured, 35% improved, 8% failed
    2. Atheroscerotic Disease: 91% dilated; 35% cured, 49% improved, 16% failed
    3. Balloon angioplasty is as or more effective than drugs alone for treating HTN associated with renal artery stenosis [61,82]
    4. Balloon angioplasty may prevent reduce renal dysfunction compared with drug therapy alone [61] though this is not clear [82]

E. Less Common Causes of Hypertension

  1. True Hyperaldosteronism
    1. Accounts for 5-10% of cases of therapy-resistant hypertension
    2. Causes: Adenomas 65%, Bilateral Hyperplasia ~34%, Adrenal Carcinoma <1%
    3. Typically with low serum potassium, high urinary potassium, metabolic alkalosis
    4. Baseline aldosterone level may be misleading depending on volume status
    5. Diagnosis by baseline level versus level following iv saline infusion (hypervolemic)
    6. Aldosterone level should decrease significantly with volume infusion
    7. Once diagnosis is made, search for location of lesion (CT or MRI)
  2. Pheochromocytoma [70]
    1. Typically presents as paroxysms of (intermittent) symptoms (intermittant)
    2. Includes HTN, headaches, diaphoresis, palpitations, hot flashes
    3. HTN in pheochromocytoma: 65% sustained, 25% paroxysmal, 4% pregnancy
    4. Majority of patients are <40 years old
    5. Surgical resection is usually required
  3. Scleroderma Renal Crisis
    1. Acute onset of very high blood pressure in patients with scleroderma
    2. Most of these patients have the progressive systemic sclerosis type
    3. Accompanied (? caused) by very high renin state
    4. BP control with ACE-I and/or CCB appears to reduce renal damage
    5. Schizocytic RBCs often seen in these patients during crisis
    6. May progress to renal failure and become dialysis dependent
    7. Creatinine >3.0mg/dL usually predicts irreversible renal failure
    8. Begin ACE inhibitors (or calcium blockers) prior to creatinine reaching 3.0 mg/dL
  4. Genetic Mutations [26]
    1. Mutations in epithelial sodium channel subunits can lead to HTN
    2. Systolic blood pressure correlated with specific mutaoins in ß and gamma subunits
    3. Therefore, regulation of sodium clearly has some role in BP regulation

F. Complications

  1. Cardiac
    1. Overall, HTN increases risk of CVD >2-3 fold [2]
    2. Myocardial Ischemia and Infarction (MI)
    3. Microvascular dysfunction and silent ischemia
    4. Left Ventricular Hypertrophy (LVH)
    5. LVH is an HTN risk factor for CVD, atrial fibrillation (AFib), heart failure [16,17]
    6. Levels of Brain Natriuretic Peptide (BNP) correlate with degree of LVH in HTN patients [64]
    7. Elevated levels of BNP early in HTN may predict patients at risk for developing LVH
    8. Reduction of LVH during anti-HTN therapy is independently associated with improved cardiovascular (CV) outcomes [8,9], reduced AFib [16], reduced heart failure [17]
    9. Congestive Heart Failure (CHF)
  2. Vascular Disease
    1. Aneurysm and dissection
    2. Peripheral Arterial (Vascular) Disease (PAD)
    3. May contribute to atherosclerosis
  3. Cerebral
    1. Ischemia: thrombosis, hemorrhage
    2. Cerebrovascular disease
  4. Renal [18]
    1. HTN associated with a ~2 fold increase in risk of renal failure (ESRD)
    2. About 30% of ESRD is related to HTN which causes nephrosclerosis [20]
    3. Renal hemorrhage / thrombosis
    4. Reduction of BP to ~125/80 reduces progression of renal insufficiency [18]
    5. ACE inhibitors (ACE-I) reduce progression of HTN-associated renal dysfunction
    6. ACE-I preferred over amlodopine for HTN-patients with or without proteinuria [71]
    7. ACI-I should be used in renal insufficiency and even slightly elevated BP
    8. Cautious use of ACE-I in patients with renovascular HTN
  5. Optic: blindness due to hemorrhage
  6. Relationship of BP level to complications is non-linear and dependent on other factors [6]

G. Evaluation [4]

  1. Basic Studies
    1. History and physical focused on all cardiovascular parameters
    2. Urinalysis - microalbuminuria
    3. Blood chemistry - renal function, blood glucose, lipids, uric acid
    4. Electrocardiography (ECG)
  2. Studies for Resistant or Difficult to Treat HTN
    1. Repeat mesurement of or ambulatory BP
    2. Echocardiography
    3. Consider secondary causes of HTN as above, and perform specific tests

H. Treatment Overview

  1. Multiple drugs are often needed for adequate control of BP [4]
  2. Aerobic exercise reduces systolic (~4 mm Hg) and diastolic (~2.5 mm Hg) BP [77]
  3. Efficacy of HTN Treatment [1]
    1. Reduction in diastolic BP 2mm: 6-9% reduction in CHD, 15% reduction in stroke
    2. Reduction in diastolic BP 5-6mm: 16-25% reduction in CHD, ~38% reduction in stroke
    3. Reduction in diastolic BP 7.5mm: 21-29% reduction in CHD, ~46% reduction in stroke
    4. Overall vascular death rates are reduced ~23% by treating HTN
    5. All first line antihypertensive agents reduce CVD and overall risks [30,31]
    6. Captopril was as effective as diuretics or ß-blockers in reducing mortality [30]
    7. About 45% of patients presently have controlled HTN, and >85% are now diagnosed
    8. In elderly with HTN, treatment with chlorthalidone reduced CHF risk by ~50%
    9. Treatment of systolic HTN in elderly reduces incidence of dementia [32]
    10. Treatment of systolic HTN with BP>160mm in elderly reduces complications [56]
    11. Diltiazem, ß-blockers and diuretics had similar effects on overall vascular mortility [65]
    12. Hormone replacement therapy (HRT) reduces rise of BP with age in women [72]
  4. Treatment Goals
    1. Aggressive therapy, often with >1 agent, required for adequate control of BP [4]
    2. Current recommendation for target BP is <130/85 in most persons
    3. In elderly, treat systolic BP >140mm, as tolerated, to systolic 125-140mm [11]
    4. In patients with diabetes or existing renal disease, goal BP should be lower
    5. Goal diastolic BP to <85 in non-diabetics and ~80 mmHg in diabetics recommended [33]
    6. Reductions in BP in this range lead to ~30% reduction in mortality [33]
    7. Reduction of diastolic BP below 75mm Hg may lead to increased cardiac events [33]
    8. Normalization of BP is particularly critical in patients with diabetes
    9. Nonpharmacologic means should be tried first, but medications usually required
    10. More than 1 pharmacologic agent usually required to meet treatment goals [2]
  5. Nonpharmacologic Therapy [1,76]
    1. Weight loss reduces HTN [38,39] and likely reduces mortality
    2. Aerobic exercise reduces systolic (~4 mm Hg) and diastolic (~2.5 mm Hg) BP [77]
    3. Exercise improves glucose tolerance, lipid profiles, and clearly improves quality of life
    4. Increase in dietary potassium reduced need for hypertensive medications [40]
    5. Dietary changes to high K+ diet included 3-6 portions of fruits / vegetables per day
    6. In black patients with HTN on low potassium diets, addition of 80mmol/day of potassium supplements reduced SBP ~7mm and DBP ~2.5mm [41]
    7. Recommended that patients with HTN increase potassium intake [40]
    8. Non-pharmacologic therapy for mild HTN improved quality of life [42]
    9. NSAIDs are associated with elevation of BP and should be tapered when possible [43]
    10. Combined diet, weight loss, exercise, moderate alcohol reduce BP and HTN incidence [76]
    11. Moderate alcohol consumption in men with HTN reduces MI risk, but not mortality or overall cardiovascular risk [85]
  6. Sodium Restriction [44]
    1. Reducing sodium consumption reduces blood pressure slightly [38,39]
    2. However, reduced sodium intake activates compensatory mechanisms
    3. Reduced sodium stimulates renin and aldosterone production (which raise BP)
    4. Reducing sodium intake in patients on ACE inhibitors or ATII blockers may be helpful
    5. Reduced sodium also raises serum noradrenaline and cholesterol levels
    6. Overall, reduction of sodium intake in patients with HTN may be mildly beneficial
  7. Medication Compliance
    1. Complianc often poor due to side effects of medications
    2. Also due to relative lack of symptoms in patients with uncontrolled HTN
    3. Compliance problems may explain apparently poor "efficacy" of agents in one study [34]
    4. ACE inhibitors may have better compliance than ß-blockers [30]
  8. Diuretics Usually First Line [12]
    1. Low-dose diuretics wer most effective first line therapy for preventing CVD mortality, morbidity, particularly in older persons and black ethnic group [3,5]
    2. High dose diuretics may increase risk of sudden cardiac death [36]
    3. Likely due to diuretic induced hypokalemia and hypomagnesemia
    4. Diuretics may also worsen lipid profiles
    5. ß-blockers and high dose diuretics did not reduce overall mortality or heart disease [37]
    6. Thiazides and ß-blockers show excellent reduction in stroke risk, however [37]
    7. Chlorthalidone use in elderly with HTN and MI reduced CHF risk ~80%
    8. With diuretics, potassium, magnesium and thiamine levels should be monitored
    9. Also consider obtaining lipid levels, systolic left ventricular function, glucose levels
  9. Treatment with atorvastatin (Lipitor®) in patients with HTN and average or low cholesterol levels reduces stroke and cardiovascular events ~30% [83]

I. Evaluation of Antihypertensive Agents

  1. Efficacy in Treatment of Hypertension in Men (TOHMS) [45]
    1. Diastolic BP 95-109 at beginning of trial
    2. Randomized to Placebo, HCTZ, Atenolol, Captopril, Clonidine, Diltiazem CD, Prazosin
    3. Diltiazem had highest rate of success (~60% control of BP overall)
    4. Diltizem showed best control in younger and older blacks; poor control in younger whites
    5. Atenolol had best control for older whites (68%)
    6. Captopril (an ACE-I) had best control for younger whites
    7. Diastolic BP controlled best overall with Diltiazem > Clonidine ~ Atenolol
    8. Systolic BP controlled best overall with Clonidine ~ HCTZ > Diltiazem ~ Atenolol
    9. Clonidine and prazosin had highest rates of drug intolerance
  2. Treatment of Mild Hypertension Study (TOMHS) [42]
    1. Men and women with BP 45-69 yrs old with diastolic BP < 100
    2. Agents: acebutolol, amlodipine, chlorthalidone, doxazosin, enalapril
    3. No significant differences between different agents in terms of dropout
    4. Major non-fatal cardiovascular events decreased from 7.3% to 5.1% in 4 years
    5. Total non-fatal major events decreased from 16.2 to 11% with treatment
    6. Quality of life improved with both non-pharmacologic and pharmacologic therapies
  3. HTN in Elderly [12,46,47]
    1. Meta-analysis >15,000 patients at least 60 years old showed 12% mortality reduction [46]
    2. In various studies, stroke mortality is reduced reduction 25-36%
    3. Coronary artery disease (CAD) related mortality decreases 25%
    4. In patients >75 years old, efficacy is less pronounced in some studies
    5. Risk for death was 21% higher in elderly persons with SBP>160mm compared to SBP <160mm [47]
    6. Diastolic BP was not related to mortality rates [47]
    7. After 3 years of followup, there was no "J" or "U" shaped effect on mortality [39,47]
    8. SHEP and STOP trials showed that low dose diuretics are effective and safe [48,49]
    9. SHEP data review show that chlorthalidone (12.5-25mg/d) ± atenolol (50mg/d) reduced cardiovascular events, all cause mortality, in type II diabetics and nondiabetics [50]
    10. SHEP data show that chlorthalidone therapy reduces risk of CHF by 50-80%
    11. SHEP data also show that chlorthalidone ± other drugs reduces risk of renal decline [51]
    12. ß-blockers appear to be less effective for BP reductions in elderly patients [52]
    13. No apparent overall mortality benefit of treatment in >80 year patients, though non- fatal events were reduced including overall stroke rates [53]
    14. STOP-2 trial showed equivalent efficacy of older and newer antihypertensive agents in preventing CVD and overall death [31]
  4. Elderly White Women with HTN [54]
    1. Compared atenolol (50-100mg/d), enalapril (5-20mg/d) and isradipine (1.25-5mg bid)
    2. Added HCTZ as needed to attain target blood pressure
    3. HCTZ had greatest BP reducing effect on enalapril, mainly by lowering systolic BP
    4. All agents had similar effects on BP, with goals achieved in 70-80% of patients
    5. 26% of patients on enalapril developed cough
    6. Atenolol lowers HDL cholesterol, raises triglycerides, lowers heart rate [55]
    7. Israpidipine caused peripheral edema in ~15% of patients
  5. MIDAS Trial [56]
    1. Comparison of rate of progression of atherosclerosis in patients HTN on therapy
    2. Patients randomized to isradipine or hydrochlorothiazide (HCTZ) for 3 years
    3. No change in progression of atheroscerolosis (by angiography) in each group
    4. Increased rate of major vascular events in patients on isradipine versus HCTZ
    5. Caution in using CCB given this information
  6. HTN and Insulin Resistance
    1. ß-blockers and diuretics may exacerbate insulin resistance, poor glucose control
    2. These agents cause hyperinsulinemia even in previously non-diabetic persons
    3. ß-adrenergic blockers may increase risk of developing DM, but thiazides do not [59]
    4. Hyperinsulinemia is associated with poor lipid profiles and increased atherosclerosis
    5. In contrast, alpha-blockers and ACE-I reduce insulin resistance
    6. These agents, along with calcium blockers, also improve cholesterol profiles
    7. Excellent control of HTN in DM is as or more important than glucose control [57]
    8. ACE-I, with second line CCB, may be used in DM with HTN [59]
  7. LIFE Trial (Losartan Intervention for Endpoint Reduction) [78,79]
    1. 9193 persons 55-80 years with essential HTN and LVH (± diabetes)
    2. Evaluation for cardiovascular endpoints and death for >4 years
    3. Begin at losartan 50mg qd or atenolol 50mg qd and escalate
    4. HCTZ diuretic may be added
    5. Losartan had 10% reduction in cardiac death and 25% reduction in stroke versus atenolol
    6. Losartan was better tolerated than atenolol

J. Pharamacologic Agent Overview [1,2,27]

  1. Comorbid conditions are of greatest importance when selecting an (initial) agent (see below)
  2. Recommended First Line (most patients)
    1. Low-Dose Diuretics (usually thiazides; electrolyte monitoring required)
    2. ß-adrenergic blockers - mainly with CAD
    3. ACE-I or ARB recommended in younger persons (more active renin-angiotensin systems)
  3. Alternative First Line
    1. ACE-I - first line in all diabetic patients and in patients with LVH, younger persons
    2. Angiotensin II receptor blocker (ARB) are generally better tolerated than ACE-I
    3. Long acting CCB reduce overall vascular mortality similar to other agents [65,66]
  4. Hydralazine usually used only in heart failure when ACE-I or AT2RB are not tolerated
  5. Nitrates are generally poor BP medications
  6. Other agents
    1. Alpha2-adrenergic agonists (such as clonidine) - generally 3rd line
    2. Alpha1-adrenergic antagonists may increase cardiovascular events and are 4th line
  7. Plasma Renin Profiles may help predict responses to classes of agents [28]
    1. Diltiazem and clonidine responses were independent of renin profile
    2. Hydrochlorothiazide (HCTZ) and prazosin were best in low to medium renin patients
    3. Captopril was best for medium and high-renin profiles

K. Use of Antihypertensives in Patients with Comorbid ConditionsTable: Antihypertensive Agents and Comorbid Conditions
Group:Thiazidesß-BlockersACE-IARBCCBa1-Blockera2-Agonist
Diabetes----*+++++/-+--
Hyperlipidemia±+/-±+--+++
CHF±+/-*+++++--++
LVH--+++++++++----
Bradycardia+--+++++/-+--
Post-MI--+++++++---+--
Elderly++++/-++++++/---
Blacks±+/-+/-+++++
Young++++++++++
*Carvidolol improves glucose and lipid control in diabetics [57]
However, standard ß-adrenergic blockers increase risk of diabetes and hypoglycemia [59]

Resources

calcMean Arterial Pressure (MAP)

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