Sections

Hypertension

Workup

Approach Considerations

In general, the evaluation of hypertension primarily involves accurately measuring the patient’s blood pressure, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies.^{[5, 6]}A 12-lead electrocardiogram should also be obtained. These steps can help determine the following^{[5, 6, 7]}:

Presence of end-organ disease
Possible causes of hypertension
Cardiovascular risk factors
Baseline values for judging biochemical effects of therapy

In an analysis of 4388 patients enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study, a prediction model based on Framingham Heart Study criteria was better than prehypertension at identifying young adults who went on to develop new hypertension in the following 25 years. The c index for incident hypertension was 0.84 using the Framingham prediction model and 0.71 using prehypertension.^{[64, 65]}

Criteria used in the CARDIA prediction model included age, sex, body mass index (BMI), smoking, systolic blood pressure (BP), and parental history of hypertension. Prehypertension was defined as systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg.

Pulse wave velocity appears to have the potential to predict the progression of BP and development of hypertension in young adults (age 30-45 years).^[66]

Initial workup

Initial laboratory tests may include urinalysis; fasting blood glucose or A1c; hematocrit; serum sodium, potassium, creatinine (estimated or measured glomerular filtration rate [GFR]), and calcium; and lipid profile following a 9- to 12-hour fast (total cholesterol, high-density lipoprotein [HDL] cholesterol, low-density lipoprotein [LDL] cholesterol, and triglycerides). An increase in cardiovascular risk is associated with a decreased GFR level and with albuminuria.^[5]

Assessment of suspected secondary causes

Other studies may be obtained on the basis of clinical findings or in individuals with suspected secondary hypertension and/or evidence of target-organ disease, such as complete blood count (CBC), chest radiograph, uric acid, and urine microalbumin.^[5]Table 2, below, summarizes the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) screening tests for specific identifiable causes of hypertension.

Table 2. Identifiable Hypertension and Screening Tests (Open Table in a new window)

Condition	Screening Test
Chronic kidney disease	Estimated glomerular filtration rate
Coarctation of the aorta	Computed tomography angiography
Cushing syndrome; other states of glucocorticoid excess (eg, chronic steroid therapy	Dexamethasone suppression test
Drug-induced/drug-related hypertension^*	Drug screening
Pheochromocytoma	24-hour urinary metanephrine and normetanephrine
Primary aldosteronism, other states of mineralocorticoid excess	Plasma aldosterone to renin activity ratio (ARR). If abnormal, refer for further evaluation such as saline infusion to determine if aldosterone levels can be suppressed, 24-hour urinary aldosterone level, and specific mineralocorticoid tests
Renovascular hypertension	Doppler flow ultrasonography, magnetic resonance angiography, computed tomography angiography
Sleep apnea	Sleep study with oxygen saturation (screening would also include the Epworth Sleepiness Scale [ESS])
Thyroid/parathyroid disease	Thyroid stimulating hormone level, serum parathyroid hormone level
Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52.^[5] ^* Some examples of agents that induce hypertension include nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors; illicit drugs; sympathomimetic agents; oral contraceptive or adrenal steroid hormones; cyclosporine and tacrolimus; licorice; erythropoietin; and certain over-the-counter dietary supplements and medicines, such as ephedra, ma huang, and bitter orange. Drug-related causes of hypertension may be due to nonadherence, inadequate doses, and inappropriate combinations.

Microalbuminuria is an early indication of diabetic nephropathy and is also a marker for a higher risk of cardiovascular morbidity and mortality. Recommendations suggest that individuals with type I diabetes should be screened for microalbuminuria. Usefulness of this screening in hypertensive patients without diabetes has not been established.^[12]

Measurement of the ratio of aldosterone to plasma renin activity (PRA) is performed to detect evidence of primary hyperaldosteronism. A ratio of more than 20-30 is suggestive of this condition. Most antihypertensive medications can falsely raise or lower this ratio; thus, an appropriate washout period is necessary to obtain an accurate aldosterone-renin ratio.

As mentioned above, less than half of patients with PA have hypokalemia. However, an underlying secondary cause of hyperaldosteronism should be strongly suspected in patients with unprovoked hypokalemia or who exhibit an exaggerated hypokalemic response to a thiazide. It is important to note that aldosterone levels can be falsely low in the presence of hypokalemia. Hypokalemia and metabolic alkalosis are relatively late manifestations of primary hyperaldosteronism. A 24-hour urine specimen should be collected for sodium and potassium measurement. If the urine sodium level is more than 100 mmol/L and urine potassium is less than 30 mmol/L, hyperaldosteronism is unlikely.

If urinary potassium exceeds 30 mmol/L, the patient should have plasma renin activity measured. If the PRA is high, the likely cause is estrogen therapy, renovascular hypertension, malignant hypertension, or salt-wasting renal disease (or blockade of the renin-angiotensin system—the far more common reason). In the presence of low PRA, the serum aldosterone level can be measured (aldosterone and renin should be measured together; separate measurements will lead to inaccuracy). A low aldosterone level indicates licorice ingestion or other mineralocorticoid ingestion. A high aldosterone level indicates primary hyperaldosteronism. A computed tomography scan may identify the presence of an adenoma. In the absence of CT scan findings, differentiating hyperplastic hyperaldosteronism from adenoma is often difficult.

Determination of a sensitive thyroid-stimulating hormone (TSH) level excludes hypothyroidism or hyperthyroidism as a cause of hypertension.

If pheochromocytoma is suspected, urinary catecholamines and fractionated metanephrines are the tests of choice. Plasma fractionated metanephrines have specificity, but their sensitivity is too low for screening purposes. Urinary vanillylmandelic acid (VMA) is no longer recommended because of its poor sensitivity and specificity.

Evaluation of hypertensive emergencies

Electrolytes, blood urea nitrogen (BUN), and creatinine levels are used to identify renal impairment. A complete blood cell (CBC) count and smear help exclude microangiopathic anemia. Dipstick urinalysis can be used to detect hematuria or proteinuria (renal impairment), and microscopic urinalysis can be used to detect red blood cells (RBCs) or RBC casts (renal impairment). Optional studies include a toxicology screen, pregnancy test, and endocrine testing.

Radiologic Studies

If the patient’s history suggests renal artery stenosis and if a corrective procedure is considered, further noninvasive radiologic investigations (eg, computed tomographic angiography [CTA], magnetic resonance angiography [MRA]) or invasive renal angiography can be performed.^{[5, 6, 67]}Concern over the risk of nephrogenic systemic fibrosis (NSF) due to gadolinium has reduced the use of MRA, particularly in patients with chronic kidney disease who have a glomerular filtration rate lower than 30 mL/min. This is a rare, debilitating, life-threatening disorder associated with gadolinium. CT or invasive angiography carries the risk of dye nephropathy.

For more information on NSF and contrast-induced nephropathy, see the US Food and Drug Administration (FDA) Web page Information on Gadolinium-Based Contrast Agents^[68]and the American College of Radiology’s (ACR) Manual on Contrast Media (version 7).

Digital subtraction angiography

Digital subtraction angiography (DSA) with arterial injection of radiocontrast dye is the criterion standard for the evaluation of renal and pulmonary causes of hypertension, but this modality carries the risk of dye nephropathy and atheroemboli in patients with diabetes or chronic kidney disease. Captopril radionuclide scanning imaging technique does not give anatomic detail and is less often used, but this study can provide important information regarding the functionality of renal artery stenosis in the absence of advanced chronic kidney disease.

Echocardiography

The main indication for echocardiography is evaluation for end-organ damage in a patient with borderline-high blood pressure (BP). Therefore, the presence of left ventricular hypertrophy (LVH) despite normal or borderline-high BP measurements requires antihypertensive therapy. Echocardiography may detect left atrial dilatation, LVH, and diastolic or systolic left ventricular dysfunction more frequently than electrocardiography. In addition, a stress echocardiogram can provide prognostic information in patients with hypertension and coronary artery disease (CAD).^[69]

Treatment & Management

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Media Gallery

Hypertension. Anteroposterior x-ray from a 28-year old woman who presented with congestive heart failure secondary to her chronic hypertension, or high blood pressure. The enlarged cardiac silhouette on this image is due to congestive heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs, known as pulmonary congestion.
Hypertension. Electrocardiogram (ECG) from a 47-year-old man with a long-standing history of uncontrolled hypertension. This image shows left atrial enlargement and left ventricular hypertrophy.
Hypertension. Electrocardiogram (ECG) from a 46-year-old man with long-standing hypertension. This ECG shows left atrial abnormality and left ventricular hypertrophy with strain.
Hypertension. Hypertrophied cardiac myocytes with enlarged "box car" nuclei.
Hypertension. Age-adjusted trends in hypertension and controlled hypertension among adults aged 18 and over: United States, 1999–2016. Courtesy of the Centers for Disease Control and Prevention (CDC), National Center for Health Statistics (NCHS).
Hypertension. Prevalence of hypertension among adults aged 18 and over, by sex and age: United States, 2015–2016. Courtesy of the Centers for Disease Control and Prevention (CDC), National Center for Health Statistics (NCHS).

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Table 2. NHIS/NCHS Age-Adjusted Prevalence Estimates in Individuals Aged 18 Years and Older in 2015.

Race/Ethnic Group	Have Hypertension, %	Have Heart Disease, %	Have Coronary Heart Disease, %	Have Had a Stroke, %
White only	23.8	11.3	5.6	2.4
Black/African American	34.4	9.5	5.4	3.7
Hispanic/Latino	23.0	8.2	5.1	2.4
Asian	20.6	7.1	3.7	1.4
American Indian/Alaska Native	28.4	13.7	9.3	2.2 (this number is considered unreliable)
Source: Summary health statistics: National Health Interview Survey, 2015. Available at: https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2015_SHS_Table_A-1.pdf. Accessed: November 14, 2016. NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey.

Table 2. Identifiable Hypertension and Screening Tests

Condition	Screening Test
Chronic kidney disease	Estimated glomerular filtration rate
Coarctation of the aorta	Computed tomography angiography
Cushing syndrome; other states of glucocorticoid excess (eg, chronic steroid therapy	Dexamethasone suppression test
Drug-induced/drug-related hypertension^*	Drug screening
Pheochromocytoma	24-hour urinary metanephrine and normetanephrine
Primary aldosteronism, other states of mineralocorticoid excess	Plasma aldosterone to renin activity ratio (ARR). If abnormal, refer for further evaluation such as saline infusion to determine if aldosterone levels can be suppressed, 24-hour urinary aldosterone level, and specific mineralocorticoid tests
Renovascular hypertension	Doppler flow ultrasonography, magnetic resonance angiography, computed tomography angiography
Sleep apnea	Sleep study with oxygen saturation (screening would also include the Epworth Sleepiness Scale [ESS])
Thyroid/parathyroid disease	Thyroid stimulating hormone level, serum parathyroid hormone level
Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52.^[5] ^* Some examples of agents that induce hypertension include nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors; illicit drugs; sympathomimetic agents; oral contraceptive or adrenal steroid hormones; cyclosporine and tacrolimus; licorice; erythropoietin; and certain over-the-counter dietary supplements and medicines, such as ephedra, ma huang, and bitter orange. Drug-related causes of hypertension may be due to nonadherence, inadequate doses, and inappropriate combinations.

Table 3. Hypertensive Disorders in Pregnancy

Classification	Characteristics
Chronic hypertension	Prepregnancy or before 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg that persists >12 weeks postpartum
Preeclampsia	After 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg with proteinuria (>300 mg/24 h) Can progress to eclampsia More common in nulliparous women, multiple gestation, women with hypertension =4 years, family history of preeclampsia, previous hypertension in pregnancy, and renal disease
Chronic hypertension with superimposed preeclampsia	New-onset proteinuria after 20 weeks in hypertensive woman In a woman with hypertension and proteinuria before 20 weeks’ gestation Sudden 2- to 3-fold increase in proteinuria Sudden increase in BP Thrombocytopenia Elevated AST or ALT levels
Gestational hypertension	Temporary diagnosis Hypertension without proteinuria after 20 weeks’ gestation May be a preproteinuric phase of preeclampsia or a recurrence of chronic hypertension that abated in mid-pregnancy May lead to preeclampsia Severe cases may cause higher rates of premature delivery and growth retardation relative to mild preeclampsia
Transient hypertension	Diagnosis made retrospectively BP returns to normal by 12 weeks’ postpartum May recur in subsequent pregnancies Predictive of future primary hypertension
ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; DBP = diastolic BP; SBP = systolic BP. Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52.^[5]

Table 4. Guidelines for Blood Pressure Screening in Adults

Issuing Organization	Year	Screening Populations	Screening Measurement	Screening Interval
European Society of Cardiology/ European Society of Hypertension (ESC/ESH)^[9]	2018	All adults	Office measurement	At regular intervals on the basis of the blood pressure level: Healthy people with optimal office blood pressure (< 120/80 mm Hg): Every 5 years; remeasure if seen sooner. Patients with normal blood pressure (120-129/80-84 mm Hg): Minimum of every 3 years. Patients with high-normal blood pressure (130–139/85–89 mm Hg): Annually.
US Preventive Services Task Force (USPSTF)^[127]	2015	Adults ≥18 years without known hypertension	Measurements outside of the clinical setting should be obtained for diagnostic confirmation before starting treatment. No evidence was found for a single gold standard protocol for HBPM or ABPM. However, both may be used in conjunction with proper office measurement to make a diagnosis and guide management and treatment options.	Annually for adults age ≥40 and those at increased risk for high blood pressure including those who have high-normal blood pressure (130–139/85–89 mm Hg), are overweight or obese, or are African American. Adults ages ≥18 to < 40 years with normal blood pressure (≤130/85mm Hg) with no known risk factors should be screened every 3-5 years
Seventh Report of the Prevention, Detection, Evaluation, and Treatment of the Joint National Committee on High Blood Pressure (JNC 7)^[5]	2003	Adults ages ≥18 years	Diagnosis based on average of 2 or more seated blood pressure readings on each of two or more office visits	At least once every 2 years in adults with blood pressure less than 120/80 mm Hg and every year in those with levels of 120–139/80–89 mm Hg.
American College of Obstetricians and Gynecologists (ACOG)^[128]	2013	All females ages ≥13 years	Office measurement	Annually as part of routine well-woman care
Department of Veterans Affairs/Department of Defense (VA/DoD)^[129]	2014	All adults	Office measurement; Diagnosis based on 2 readings at 2 separate visits; For patients where diagnosis remains uncertain, home blood pressure monitoring (2-3 times a day for 7 days) or 24 hour ambulatory monitoring to confirm diagnosis	Periodic, preferably annually, at time of routine preventative care or health assessment;
European Society of Hypertension /European Society of Cardiology (ESH/ESC)^[126]	2013	All adults	Office measurement; Diagnosis based on at least 2 readings at 2 separate visits; Consider home blood pressure monitoring or 24 hour ambulatory monitoring to confirm diagnosis	At time of routine preventative care or health assessment

Table 5. Target Blood Pressure Recommendations

Issuing Organization	Year	Population	Target Blood Pressure
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7)^[5]	2003	All adults except those with diabetes or chronic kidney disease Adults with diabetes or chronic kidney disease	< 140/90 mm Hg < 130/80 mm Hg
Eighth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8)^[88]	2014	Adults age < 60 years and those >18 with diabetes or chronic kidney disease Adults age ≥60 years	< 140/90 mm Hg < 150/90 mm Hg
European Society of Hypertension/European Society of Cardiology (ESH/ECS)^[126]	2013	All adults except those with diabetes Adults with diabetes	140-150 mm Hg systolic; consider < 140 mm Hg if the patient is fit and healthy; for ages ≥80 years, the patient's mental capacity and physical heath should also be considered if targeting to < 140 mm Hg < 85 mm Hg diastolic BP
American Heart Association/American College of Cardiology/American Society of Hypertension (AHA/ACC/ASH)^[130]	2015	Adults ages >80 years Adults with CAD, except as noted below Adults with MI, stroke, TIA, carotid artery disease, peripheral artery disease or abdominal aortic aneurysm	< 150/90 mm Hg < 140/90 mm Hg < 130/80 mm Hg
American Heart Association/American College of Cardiology (ACC)/Centers for Disease Control and Prevention (AHA/ACC/CDC)^[131]	2014	All adults	< 140/90 mm Hg
American College of Cardiology/American Heart Association (ACC/AHA)^[1]	2017	All adults	< 130/80 mm Hg
American Society of Hypertension/International Society of Hypertension (ASH/ISH)^[132]	2014	Adults ages 18-79 years Adults ages ≥80 years	< 140/90 mm Hg; < 130/80 mm Hg BP target may be considered in younger adults < 150/90 mm Hg
Department of Veterans Affairs/Department of Defense (VA/DoD)^[129]	2014	All adults Adults with diabetes	< 150/90 mm Hg < 150/85 mm Hg
American Diabetes Association (ADA)^[71]	2016	Adults with diabetes	< 140/90 mm Hg; < 130/80 mm Hg target may be appropriate in younger adults
American Diabetes Association (ADA)^[83]	2017	Adults with diabetes	< 140/90 mm Hg; < 130/80 mm Hg target may be appropriate for those at high risk of cardiovascular disease (if achievable without undue treatment burden)
CAD = coronary artery disease; MI = myocardial infarction; TIA = transient ischemic attack.

Table 6. American Society of Hypertension/International Society of Hypertension Treatment Recommendations

Patients Without Other Major Medical Condition	First-line Drugs	Added 2^nd Drug (if needed to reach BP target)	Added 3^rd Drug (if needed to reach BP target)
African ancestry	CCB or thiazide diuretic	ARB or ACEI	Combination of CCB plus ACEI or ARB plus thiazide diuretic
White and other non-African ancestry ages < 60 years	ARB or ACEI	CCB or thiazide diuretic	Combination of CCB plus ACEI or ARB plus thiazide diuretic
White and other non-African ancestry ages ≥60 years	CCB or thiazide diuretic; ARB or ACEI also effective	ARB or ACEI; CCB or thiazide diuretic if ARB or ACEI used first	Combination of CCB plus ACEI or ARB plus thiazide diuretic
Major medical condition
Diabetes (white and other non-African ancestry)	ARB or ACEI	CCB or thiazide diuretic	Alternative 2^nd drug (CCB or thiazide diuretic)
Diabetes (African ancestry)	CCB or thiazide diuretic	ARB or ACEI	Alternative 1^st drug (CCB or thiazide diuretic)
Chronic kidney disease	ARB or ACEI	CCB or thiazide diuretic	Alternative 2^nd drug (CCB or thiazide diuretic)
Coronary artery disease	Beta-blocker plus ARB or ACEI	CCB or thiazide diuretic	Alternative 2^nd drug (CCB or thiazide diuretic)
Stroke	ACEI or ARB	CCB or thiazide diuretic	Alternative 2^nd drug (CCB or thiazide diuretic)
Symptomatic heart failure	Beta-blocker plus ARB or ACEI plus diuretic plus spironolactone regardless of BP; CCB can be added if needed for BP control
ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; BP = blood pressure; CCB = calcium channel blocker.

Table 7. JNC 7 Classification of Hypertensive Disorders in Pregnancy

Classification	Characteristics
Chronic hypertension	SBP ≥140 mm Hg or DBP ≥90 mm Hg, present pre-pregnancy or before 20 weeks’ gestation and persisting >12 weeks postpartum
Preeclampsia	SBP ≥140 mm Hg or DBP ≥90 mm Hg with proteinuria (>300 mg/24 h) that develops >20 weeks’ gestation; Can progress to eclampsia More common in nulliparous women, multiple gestation, women with hypertension ≥4 years, family history of preeclampsia, previous hypertension in pregnancy, and renal disease
Chronic hypertension with superimposed preeclampsia	New-onset proteinuria after 20 weeks’ gestation in a hypertensive woman or In a woman with hypertension and proteinuria before 20 weeks’ gestation: • Sudden 2- to 3-fold increase in proteinuria • Sudden increase in BP • Thrombocytopenia • Elevated AST or ALT levels
Gestational hypertension	Temporary diagnosis Hypertension without proteinuria after 20 weeks’ gestation May be a preproteinuric phase of preeclampsia or a recurrence of chronic hypertension that abated in mid-pregnancy May lead to preeclampsia Severe cases may cause higher rates of premature delivery and growth retardation relative to mild preeclampsia
Transient hypertension	Diagnosis made retrospectively BP returns to normal by 12 weeks postpartum May recur in subsequent pregnancies Predictive of future primary hypertension
ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; DBP = diastolic BP; SBP = systolic BP

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Author

Matthew R Alexander, MD, PhD Assistant Professor of Medicine, Department of Medicine, Division of Clinical Pharmacology, Division of Cardiovascular Medicine, Vanderbilt University School of Medicine; Assistant Professor of Molecular Physiology and Biophysics, Vanderbilt University

Matthew R Alexander, MD, PhD is a member of the following medical societies: American Association of Immunologists, American Heart Association, American Physiological Society, Federation of Clinical Immunology Societies, Vanderbilt Institute for Infection, Immunology, and Inflammation

Disclosure: Nothing to disclose.

Coauthor(s)

Meena S Madhur, MD, PhD, FACC, FAHA Associate Professor with Tenure, Division Chief of Clinical Pharmacology, Department of Medicine, Division of Clinical Pharmacology and Division of Cardiology, Adjunct Associate Professor of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine; Adjunct Associate Professor of Medicine, Vanderbilt University School of Medicine

Meena S Madhur, MD, PhD, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American Heart Association, American Physiological Society, American Society for Clinical Investigation

Disclosure: Nothing to disclose.

David G Harrison, MD Betty and Jack Bailey Professor of Medicine and Pharmacology, Director of Clinical Pharmacology, Vanderbilt University School of Medicine

David G Harrison, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Physiological Society, American Society for Clinical Investigation, Association of American Physicians, Central Society for Clinical and Translational Research, American Federation for Clinical Research, Society for Vascular Medicine

Disclosure: Nothing to disclose.

Albert W Dreisbach, MD Associate Professor of Medicine, Division of Nephrology, University of Mississippi Medical Center

Disclosure: Nothing to disclose.

Kamran Riaz, MD Clinical Assistant Professor, Department of Internal Medicine, Section of Cardiology, Wright State University, Boonshoft School of Medicine

Kamran Riaz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Society of Echocardiography, Ohio State Medical Association, Royal College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH Professor of Medicine, Director of CME Programs, Team Leader, Root Cause Analysis, Tulane University Heart and Vascular Institute; Director of In-Patient Cardiology, Tulane Service, University Hospital; Visiting Physician, Medical Center of Louisiana at New Orleans; Faculty, Pennington Biomedical Research Institute, Louisiana State University; Professor, Tulane University School of Medicine

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Acknowledgements

George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation