Evaluation of Hypertension
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  • 1 Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Learning Objectives

  1. Describe the indications for and distinctions between different methods of blood pressure measurement, including clinic blood pressure measurement, ambulatory blood pressure monitoring, and self-monitoring of blood pressure at home
  2. Identify which patients should be evaluated for masked hypertension, white coat hypertension, and nocturnal hypertension and the prognostic importance of these blood pressure patterns
  3. Explain the importance of using validated blood pressure monitors in and out of the office
  4. Identify which patients should be evaluated for secondary causes of hypertension, including renovascular disease, aldosterone excess, and catecholamine-secreting tumors
  5. Discuss the appropriate screening tests in patients with suspected secondary causes of hypertension
  6. State the optimal management of patients with secondary hypertension

Screening to Make a Diagnosis of Hypertension

Appropriate measurement of BP is extremely important when diagnosing hypertension (1). Recent hypertension guidelines recommend lower BP thresholds for the diagnosis of hypertension (24), necessitating accurate assessment of BP to avoid misdiagnosis, overtreatment, and undertreatment. With the obsolescence of mercury sphygmomanometers, BP measurements can be performed using manual aneroid manometers with auscultation of Korotkoff sounds or using automated (i.e., oscillometric) BP monitors. Automated devices have the potential to decrease human error and facilitate out-of-office BP measurement, but require validation. Clinic, or in-office, BP measurements are often poorly correlated with out-of-office BP measurements. Growing evidence supports the use of out-of-office BP monitoring for the diagnosis, monitoring, and management of hypertension. Consequently, international guidelines now recommend broader adoption of out-of-office BP monitoring for the initial diagnosis and longitudinal monitoring of hypertension (24).

Measurement Technique

Ensuring the accuracy of BPs is critical to the appropriate diagnosis of hypertension in and out of the office (1). Appropriate BP measurement technique for in-office measurements and when educating patients on performing self-monitoring of BP (SMBP) is often overlooked, owing to space and time constraints in routine practice. Additionally, the quality of initial training and retraining of healthcare professionals on correct BP measurement technique is highly variable and often inadequate (5). Both in-office and SMBP should occur after the patient rests for 3 to 5 minutes, in a quiet room, in the seated position, with feet flat on the floor, back supported, arm supported and at the level of the heart, correct cuff size, against a bare arm, with an empty bladder, and with no caffeine or cigarette smoking 30 minutes before the measurement (6). Of note, an examination table often does not provide sufficient leg, back, and arm support to facilitate accurate BP measurement. For educating patients on SMBP, infographics reviewing the necessary steps for accurate BP measurement can be extremely helpful and are freely available (7,8).

Blood pressures often decline with each successive measurement, and treatment recommendations are based on trial data using the average of two to three office readings (1,2). Thus, two to three successive BP measurements should be performed approximately 1 minute apart for both in-office (when feasible) and SMBP measurements. Patients should also be assessed for interarm differences in blood pressure during at least one BP assessment. If there is consistently a ≥10 mmHg difference in systolic or diastolic BP between arms, the arm with the higher BP reading should be used for guiding diagnosis and treatment of hypertension (1).

Device Selection and Accuracy of Different Devices

Owing to the wide elimination of mercury devices over concerns of toxicity risk, aneroid manometers are now used to perform most manual BP measurements in the clinic. Aneroid manometers are prone to miscalibration over time and require reassessment every 6 to 12 months by qualified clinical engineering staff (which is not always available) to ensure accuracy (9). Automated in-office, home, and ambulatory monitors are somewhat less prone to miscalibration, but require population-wide and individual-level validation (10). These devices apply proprietary algorithms to calculate the systolic and diastolic BPs, which can be affected by differences in vascular characteristics across patient populations and by arrhythmias. Most countries, including the United States, do not have stringent requirements for device validation prior to permitting devices to be marketed to the public, and fewer than 15% of commercially available BP measurement devices have a published validation study (11). Validated device listings are maintained by Hypertension Canada (12), the British and Irish Hypertension Society (13), the International Society of Hypertension (14), and other international hypertension societies. The American Medical Association has a rigorous, peer-reviewed, validated device listing for devices readily available in the United States (10) at https://www.validatebp.org.

Wrist and finger BP devices are currently not recommended because of frequently poor performance in validation studies (10), with a few exceptions. Kuwabara et al. (15) and Saito et al. (16) evaluated the accuracy of a total of four automated wrist BP devices that did fulfil the rigorous American National Standards Institute/Association for the Advancement of Medical Instrumentation/International Organization of Standardization validation criteria; these devices must be strictly held with the arm supported and the wrist at the level of the heart in order to provide an accurate BP measurement.

Methods of Measuring Blood Pressure

In-Office Blood Pressure Measurement

In most patients, BP is routinely assessed in the clinic setting using a manual aneroid sphygmomanometer or an automated blood pressure monitor. Accordingly, clinic BPs are often used to diagnose hypertension and for the titration of antihypertensive medications. Following the initial clinic visit with a new provider, there can be a substantial fall in the systolic and diastolic BP with each subsequent clinic visit (17). Thus, patients with mild to moderate elevations in BP should not be diagnosed with hypertension based on an initial office reading. Furthermore, many confounding factors can influence the quality of BPs obtained in the clinic setting, including inadequate time to perform multiple high quality BP measurements and inadequate training and retraining of clinical staff on correct methods of BP measurement. In a systematic review of 328 studies, Kallioinen et al. (6) identified 29 factors that can potentially impact the accuracy of BP measurements; individual factors impacted systolic BP by as much as −24 to +33 mmHg, and diastolic BP by as much as −14 to 23 mmHg. Another study by Rakotz et al. (5) evaluated the adequacy of BP measurement skills in medical students who reported having received prior training in BP measurement. Out of 159 students from medical schools in 37 states, only one student was proficient in all 11 steps required to demonstrate proficiency, and the mean number of properly performed steps was four.

Automated office BP measurement (AOBP) uses a fully automated oscillometric BP monitor to measure multiple consecutive BP readings with a single activation. AOBP may overcome the white coat effect (i.e., isolated office hypertension) because it is more closely correlated to research-quality BPs and daytime ambulatory BP readings than routine in-office BP measurements. In a systematic review and meta-analysis of 31 studies, Roerecke et al. (18) found that routine office systolic BP readings were, on average, 14.5 mmHg (95% confidence interval [95% CI], 11.8 to 17.2 mmHg) higher than AOBP readings, whereas there was only a 0.3 mmHg (95% CI, −1.1 to 1.7) difference between daytime ambulatory BP monitoring (ABPM) and AOBP readings (though with a very high level of heterogeneity across studies; I2 = 90%). Evidence suggests that it may be reasonable to perform AOBP in either the presence or the absence of a clinician. In a post-hoc analysis of the Systolic Blood Pressure Intervention Trial (SPRINT), study centers were surveyed about whether AOBP measurements were attended or unattended by staff during the trial, given that the protocol did not specify a preferred approach (19). AOBP attendance status was not associated with any difference in achieved BP levels at the majority of follow-up visits nor with cardiovascular risk reduction from intensive BP control (interaction P-value 0.88). AOBP yields more accurate BP readings than typical in-office measurements, largely because of the ability to program a rest period and to obtain multiple successive readings. However, AOBP is not a sufficient substitute for out-of-office BP measurement.

Out-of-Office Blood Pressure Measurement

We agree with the recommendations of the American College of Cardiology/American Heart Association (ACC/AHA) and other expert consensus groups to use out-of-office BP monitoring for the diagnosis of hypertension (2,3). Out-of-office BP is more closely linked to long-term cardiovascular and renal outcomes than in-office BP monitoring (20). Out-of-office BP monitoring is particularly useful for evaluating individuals with potential discrepancies between BP readings performed out of the office and BP readings performed in the clinic (i.e., white coat and masked hypertension). Out-of-office BP measurement can be performed using 24-hour or 48-hour ABPM and SMBP at home. Noteworthy distinctions between these two modalities are described in Table 1. Kiosk-based BP monitoring is becoming increasingly available as an alternative method of out-of-office BP monitoring. We do not currently recommend kiosk-based measurements because of the several barriers to accurate measurement using this method, including ambient noise, lack of sufficient rest time, and lack of published validation studies for most of these devices.

In most patients, out-of-office blood pressure monitoring with a validated device should be used to supplement clinic blood pressure measurements.

Table 1.

Distinctions between out-of-office methods for blood pressure measurement

Measurement characteristicsAmbulatory blood pressure monitoringSelf-monitoring of blood pressure
Recommended indications• Confirmation of initial diagnosis of hypertension• Confirmation of initial diagnosis of hypertension
• Diagnosis and monitoring of white coat, masked, and apparently resistant hypertension• Diagnosis and monitoring of white coat, masked, and apparently resistant hypertension
• Diagnosis and monitoring of nocturnal nondipping• Longitudinal, repeated blood pressure monitoring and medication titration
Measurement frequency• Every 15–30 minutes during the daytime• At least two measurements, 1 minute apart, in the morning upon awakening and in the evening before bed
• Every 30–60 minutes during the nighttime
Setting• During routine daily activities• During daytime only
• During sleep• Following a 3- to 5-minute rest
• Quiet room
• Sitting
Activation• Preprogrammed, fully automated device• Semiautomated device
• Activated by clinician with initial reading• Activated by patient with each measurement
Reading ascertainment• Patient is blinded to readings• Patient is able to see the readings
• Results are downloaded and interpreted by the provider at the end of the measurement period• Results are transferred by the patient to the provider, with potential for error
Access• Often only available in certain practices• Widely available commercially
• High cost to providers for initial purchase of devices and software• Relatively low cost, but must be purchased by patients
Measurement quality• Reliable readings, strongly associated with cardiac prognosis• Potentially unreliable readings, depend upon patient technique
• Highly reproducible readings
Tolerability• Often perceived as intrusive of daily activities and sleep• Often perceived as highly tolerable

Ambulatory Blood Pressure Monitoring

ABPM is currently recommended by the ACC/AHA for the initial diagnosis of hypertension in most patients with a clinic blood pressure ≥120/70 mmHg (2). Owing to its distinctively strong association with adverse cardiovascular outcomes, ABPM is considered to be the reference standard for BP measurement (1). ABPM measures BPs over a 24-hour to 48-hour period using a fully automated device. The BP measurements are programmed to occur at fixed intervals, often every 15 to 30 minutes during the daytime and every 30 to 60 minutes during the nighttime. Thus, ABPM captures BPs during routine daily activities and during sleep.

Elevated 24-hour ABPM is strongly associated with cardiovascular events and mortality. For example, in an international cohort study of 11,135 adults who underwent 24-hour ABPM, every 20 mmHg increase in 24-hour systolic BP was associated with a 40% increased risk of major cardiovascular events (hazard ratio [HR], 1.40; 95% CI, 1.31 to 1.50) after adjustment for clinic BP (21).

ABPM is subject to higher patient-level and provider-level burden compared with SMBP (22). ABPM requires patients to present to clinic for two visits spaced closely together for placement and return of the ABPM device. Ideally, ABPM should be performed on a “typical” day for a patient to be generalizable to their usual daily activities. Accounting for these factors and the high frequency of daytime and nighttime measurements, ABPM can be perceived as intrusive (22). In routine clinical settings, it is challenging to repeat ABPM in most patients within close succession because of poor tolerability, inconvenience, and potentially cost. Additionally, ABPM is associated with a relatively high initial expense to providers because of the cost of the devices and the required software for their use.

Among individuals with chronic kidney disease (CKD), elevated 24-hour ABPM is associated with poorer kidney function, higher degree of proteinuria, and greater prevalence of left ventricular hypertrophy (LVH) at the time of ABPM assessment (23,24). ABPM is also highly prognostic of adverse cardiovascular events among individuals with CKD and ESRD. For example, in 610 participants of the AASK Cohort Study, Ku et al. (25) demonstrated a U-shaped association between the magnitude of the difference between systolic BP measured in the office and by ABPM with regard to mortality risk (i.e., individuals with much higher or lower in-office readings compared with their ABPM readings had much higher risk than those who had concordant in-office and ABPM readings).

Self-Monitoring of Blood Pressure at Home

SMBP typically occurs using a semiautomated device that patients activate themselves to measure their BPs at home. SMBP engages patients directly in the diagnosis and management of their own hypertension, and can provide the opportunity for improved BP control among those patients who already have a diagnosis of hypertension (26). For the diagnosis of hypertension, SMBP should ideally be measured twice in the morning and twice in the evening before going to sleep for 5 to 7 consecutive days (1). In contrast to ABPM, SMBP measurements occur exclusively while awake and at rest. Additionally, SMBP requires patient education on appropriate BP measurement practices, such as correct body position and premeasurement rest time. Despite this requirement, there are fewer perceived patient-level and provider-level barriers to performing SMBP compared with ABPM (22). In part because of its greater tolerability and minimal intrusiveness, SMBP demonstrates greater within-individual consistency of BP patterns than ABPM and in-office BP measurement when performed repeatedly over time. This was demonstrated in a study of 1049 individuals with untreated hypertension who underwent both 24-hour ABPM and 7 days of SMBP (27). A total of 135 participants underwent repeated 24-hour ABPM and SMBP within 1 month of the initial measurements. The repeated SMBP measurements showed less within-individual variation (coefficient of variation = 5%) than the 24-hour ABPM measurements (coefficient of variation = 11%).

SMBP improves upon in-office BP measurement by eliminating the white coat effect (i.e., isolated office hypertension) and identifying masked hypertension (i.e., normal office BPs and elevated BPs outside of the office) (28). However, SMBP is not as consistently linked to cardiovascular prognosis as ABPM. Some evidence suggests comparable cardiovascular risks identified with BP patterns in studies that used ABPM compared with studies that used SMBP (28,29). However, this is not consistent across studies. For example, Kang et al. (30) evaluated 573 patients who performed ABPM and SMBP within the same 30-day period and found that SMBP had a 47% to 74% sensitivity of identifying daytime ABPM BP patterns. Similarly, Anstey et al. (31) demonstrated up to 70% discordance between SMBP and daytime ABPM in identifying BP profiles such as masked hypertension and sustained uncontrolled hypertension. The prognostic significance of discordant SMBP and ABPM values is not well understood, and it may be related to the differences in environments and approach between SMBP and ABPM. Thus, there is inadequate evidence to support using SMBP and ABPM interchangeably for the diagnosis of hypertension (32).

The renal and cardiac prognostic significance of SMBP among individuals with CKD is not well established. In a study of 217 veterans who underwent concurrent 24-hour ABPM and SMBP, Agarwal et al. (33) found that higher BPs obtained by SMBP were associated with an increased risk of ESRD but not with a composite endpoint of myocardial infarction, stroke, and death. In contrast, higher BPs obtained by 24-hour ABPM were associated with myocardial infarction, stroke, and death.

Blood Pressure Patterns Determined Using Out-of-Office Blood Pressure Monitoring

Masked and Masked Uncontrolled Hypertension

In individuals not yet on antihypertensive therapy, normal BP in the office with elevated BP out of the office is known as masked hypertension (Figure 1). In those who are already on antihypertensive therapy, this phenomenon is called masked uncontrolled hypertension. Both masked hypertension and masked uncontrolled hypertension are associated with an increased risk of adverse cardiovascular outcomes that is comparable in magnitude to that of sustained hypertension (i.e., elevated BP both in and out of the office). In a meta-analysis of 11 studies including over 30,000 patients who underwent ABPM or SMBP, Pierdomenico et al. (29) found that masked uncontrolled hypertension was associated with an 80% increased risk of major adverse cardiovascular events and all-cause mortality compared with controlled hypertension (HR, 1.80; 95% CI, 1.57 to 2.06). Masked hypertension seems to be most highly prevalent among men, individuals with self-reported black race, those with CKD, and those with obstructive sleep apnea (34).

Figure 1.
Figure 1.

Patterns of BP based on concordance and discordance of in-office and daytime out-of-office BP. Because guidelines change periodically, rather than specify a threshold number for diagnosing hypertension, the axes are labeled in the middle with “BP threshold.” The reader should substitute currently recommended thresholds for diagnosing hypertension in, or out, of the office using current societal norms.

Citation: Nephrology Self-Assessment Program nephsap 19, 1; 10.1681/nsap.2020.19.1.2

Based on an analysis of data from the National Health and Nutrition Examination Survey, Booth et al. (35) determined that over one-third of adults who are not yet being treated with antihypertensive therapy and over half of adults who are on antihypertensive therapy are recommended by the ACC/AHA guidelines to be assessed for masked hypertension with out-of-office BP monitoring. Specifically, the ACC/AHA guidelines recommend that patients not yet on antihypertensive therapy should undergo screening for masked hypertension using ABPM or SMBP if they have clinic BP readings that are ≤10 mmHg below their threshold for hypertension diagnosis or if they have labile clinic BPs (24). Patients who are on antihypertensive therapy who have normal clinic blood BPs are recommended to undergo screening for masked uncontrolled hypertension if they are at elevated cardiovascular risk (e.g., 10-year risk of atherosclerotic cardiovascular disease >10%) or if they have evidence of target organ damage. We recommend using ABPM for initially screening for masked hypertension in most patients, if feasible and available, given its greater association with adverse outcomes and the ability to assess nocturnal BP. Given the high cardiovascular risk of masked hypertension (2), we agree with current guidelines recommending initiation of antihypertensive therapy in individuals who have masked hypertension, using out-of-office BP monitoring to guide therapy.

White Coat Hypertension and White Coat Effect

In individuals not yet on antihypertensive therapy, elevated BP in the office with normal daytime BP out of the office is termed white coat hypertension. In those who are already on antihypertensive therapy, this finding is labeled white coat uncontrolled hypertension or white coat effect. White coat hypertension is most highly prevalent among children, older adults, women, and individuals with apparent treatment-resistant hypertension (34). In a systematic review and meta-analysis of 27 studies including over 25,000 participants, we found that untreated white coat hypertension was associated with an increased risk of adverse cardiovascular outcomes compared with normotension (HR, 1.36; 95% CI, 1.03 to 2.00) (36) that was substantially lower in magnitude than the cardiovascular risk observed in individuals with sustained hypertension (HR, 2.31; 95% CI 1.91 to 3.15) (37). White coat effect was not associated an increased risk of adverse outcomes compared with controlled hypertension (HR, 1.12; 95% CI, 0.91 to 1.39) (36). Individuals with white coat hypertension had a threefold to fourfold increased risk of transition to sustained hypertension (26,37). We concluded that there is no evidence to support the initiation of antihypertensive treatment in individuals with white coat hypertension. The missed transition from white coat hypertension to sustained hypertension likely contributes to the elevated cardiovascular risk observed in these individuals. Thus, ongoing out-of-office monitoring is recommended in all patients with white coat hypertension.

Blood Pressure Variability

Short-term BP variability determined by 24-hour ABPM can be a normal physiologic response to changes in position, activity, time of day, and stressors. Elevated short-term BP variability can be representative of factors such as poor exercise tolerance, endothelial dysfunction, elevated humoral activity, and elevated sympathetic activity (38). Elevated long-term BP variability, as determined by SMBP or repeated in-office measurements, can be a result of factors such as medication nonadherence, arterial stiffness, and aging (38). Both elevated short-term and long-term BP variability are associated with increased risk of major adverse cardiovascular events and mortality (39,40). Individuals with CKD and ESRD are particularly vulnerable to elevated short-term and long-term BP variability (23) and have a greater risk of adverse effects associated with elevated BP variability compared with the general population (41).

Nocturnal Blood Pressure

Nocturnal BP is typically assessed using ABPM. However, newer SMBP devices are able to perform a limited number of preprogrammed nocturnal BP measurements (42). Elevated nocturnal BPs and the absence of a 10% decline in BP while sleeping (known as nocturnal nondipping) are common in individuals with CKD, obesity, and obstructive sleep apnea (23,43,44). Nondipping is strongly and independently associated with an increased risk of major adverse cardiovascular events after accounting for daytime and 24-hour systolic BP (44,45). Whereas some evidence suggests that nocturnal dosing of at least one antihypertensive medication can improve nondipping and reduce the risk of adverse cardiovascular events (46), additional studies are needed to corroborate these findings.

The Future of Blood Pressure Measurement

Several novel BP measurement technologies are under development that will become available to consumers in the next several years. A clinically validated watch-type BP monitor recently became available (15). This device is intended for SMBP and has a small wrist cuff that expands during measurement. Validated cuffless devices are not yet available, although several are undergoing evaluation for possible clinical use. Most cuffless devices use photoplethysmography and pulse transit time to indirectly calculate BP based on blood flow in capillaries at the surface of the skin or based on arterial stiffness (4749). At this time, devices using these technologies require extremely frequent recalibration with a reference BP device or are otherwise not validated across broad populations of patients, making them inadequately reliable for clinical use (50).

SMBP using telemonitoring in conjunction with feedback and guidance on medication titration from providers improves BP control in individuals with hypertension. In a systematic review and meta-analysis of individual patient data from 25 trials, Tucker et al. (51) found that SMBP was associated with a mean 3.2 mmHg (95% CI, −4.9 to −1.6 mmHg) decline in clinic BP compared with usual care at 12 months. The greatest improvement in clinic BP was observed in those trials that combined SMBP with intensive cointervention (such as medication titration by clinicians, patient education, or lifestyle counseling), which demonstrated a mean systolic BP reduction of 6.1 mmHg (95% CI, −9.0 to −3.2 mmHg). Nonetheless, in a randomized controlled trial that randomized 1182 participants to SMBP, SMBP with telemonitoring, or usual care, McManus et al. (52) found that SMBP with (−4.7 mmHg; 95% CI, −7.0 to −2.4) or without (−3.5 mmHg; 95% CI, −5.8 to −1.2) telemonitoring to guide titration of antihypertensive medications was associated with similarly reduced BP in contrast to usual care. Increasing use of SMBP will be facilitated by greater ease of remote transmission of BP data to the electronic health record and the ability to upload BP data directly to the cloud using mobile health technology (53,54). The adoption of these technologies will benefit from careful education of patients regarding privacy risks and, most importantly, the need for correct measurement technique and use of validated BP devices.

Evaluation for Secondary Hypertension

Identification of some secondary causes of BP elevation can result in a cure if they are amenable to specific treatment. An example is the presence of a unilateral adrenal adenoma with autonomous aldosterone secretion in which adrenalectomy may be curative of the elevated BP (55). Second, especially when a surgical cure is unlikely, identification of secondary hypertension can help identify targeted therapy addressing the mechanism of BP elevation. An example is identification of sleep-disordered breathing. Using continuous positive airway pressure and addressing weight loss in these patients helps improve daytime vigilance and are useful adjuncts to BP medications (56).

The patient history is invaluable here. Table 2 describes the role of the history in five examples of possible forms of secondary hypertension. In many cases the onset of high BP is a relatively symptomless event, earning high BP the label of the “silent killer” (57). The history is geared toward identifying elements that suggest that the elevation in BP in this patient is out of the ordinary. Here “ordinary” is loosely defined as a person 30 to 60 years of age, often with a family history of high BP in parents and siblings, frequently overweight or obese, who breathes well and is not encumbered with chest or leg discomfort with usual degrees of activity. Persons of a minority group, particularly those who self-identify with African descent, are more likely to have high BP (2).

Table 2.

Examples of history questions pursuing selected secondary forms of hypertension

Secondary hypertension typeQuestions to askReferences
Primary aldosterone excessDo you have a family history of severe hypertension, stroke at an early age, and aldosterone excess (glucocorticoid remediable aldosteronism)? Do you have muscle cramps or weakness, fatigue, nocturia/polyuria, or headaches (generic symptoms of aldosterone excess)?For glucocorticoid remediable aldosteronism (93)
For generic aldosterone excess (59)
Parenchymal kidney diseaseDo you have a family history of kidney disease? Have you been told you have blood or protein in your urine? Have you been told your kidney function is impaired?(94)
Sleep disordered breathing/sleep apneaDo you know if, or have you been told that, you snore loudly? Do you wake up at night, or from naps, snorting or gasping for breath? Have you been told you seemed to stop breathing or were struggling for breath during sleep or naps?(95)
Renovascular diseaseDid the elevation of blood pressure seem to have a sudden onset? Do you smoke? Have you had any circulatory trouble like discomfort in the legs when walking? Have you had a history of stroke, transient ischemic attack, or heart attack?(96)
Medication-relatedHave you needed to use prescription or over-the-counter pain medicines like ibuprofen or naproxen? Are you taking prescription or over-the-counter medication for asthma, allergies, or a cough/cold preparation? Have you purchased medication through the internet to boost energy or wellbeing? Have you used, or are you using, drugs purchased for recreational purposes like cocaine?(62)

When the history identifies unexpected findings in the respiratory, cardiac, vascular, neurologic, or urogenital system, especially coupled with an age out of the range specified above, consideration of a secondary form of hypertension is reasonable.

It is critical to take a careful medical history to identify patients who may benefit from diagnosis and treatment of secondary causes of hypertension.

Common secondary causes of hypertension include primary aldosteronism, renovascular disease, CKD, obstructive sleep apnea, and drug-induced or alcohol-induced hypertension. Less common causes include pheochromocytoma and paraganglioma, Cushing’s syndrome, hypothyroidism and hyperthyroidism, aortic coarctation, and hyperparathyroidism. Below we discuss recent publications in screening for secondary hypertension

Primary Aldosteronism

Recent studies, editorials, and consensus guidelines support frequent screening for primary aldosteronism in a hypertensive population. The rationale for more frequent screening is that patients with primary aldosteronism are at higher cardiovascular risk compared with those with essential hypertension, and the risk is reduced by specific treatment. A meta-analysis of observational studies including 3838 patients with primary aldosteronism and 9284 patients with essential hypertension suggested that patients with primary aldosteronism had an increased risk for development of stroke, coronary artery disease, atrial fibrillation, heart failure, diabetes, metabolic syndrome and LVH (with odds ratios of 2.58, 1.77, 3.52, 2.05 1.33, 1.53, and 2.29, respectively) (58).

The 2017 ACC/AHA guidelines recommend screening for primary aldosteronism in all patients with resistant hypertension and in all patients who have hypertension that is co-existent with hypokalemia (either spontaneous or diuretic induced) or an incidentally discovered adrenal mass or family history of early-onset hypertension or stroke under the age of 40 (2).

In a Scientific Statement published in 2018, the AHA defined resistant hypertension as blood pressure above goal with three or more optimally-dosed antihypertensive agents including a diuretic, or above goal with at least four antihypertensive agents (59). Blood pressure measurement, and diagnosis and treatment goals should be consistent with recent clinical practice guidelines, and white coat effect and non-adherence should be excluded. The Endocrine Society Clinical Practice guidelines additionally recommend screening patients who have hypertension coexistent with sleep apnea, and all hypertensive first-degree relatives of individuals with known primary aldosteronism (55). Data published subsequent to these guidelines suggest that hypertension coexistent with unexplained atrial fibrillation may also provide an indication for screening. Primary aldosteronism is a risk factor for atrial fibrillation, as was noted in the meta-analysis cited above (58).

Even among patients with resistant hypertension, screening for primary aldosteronism may be underused. A recent study of 4660 adults with resistant hypertension demonstrated that only 2% of individuals were screened for primary aldosteronism (60).

Renovascular Disease

The ACC/AHA guidelines suggest screening for renovascular disease among patients with early-onset hypertension (particularly women who are at risk for fibromuscular dysplasia ), with a history of flash pulmonary edema, or if physical examination reveals abdominal or other bruits (2). Consistent with prior recommendations, the ACC/AHA suggested renal duplex doppler ultrasound, magnetic resonance angiography (MRA) or computed tomography (CT) for diagnosis with selective intra-arterial angiography as a confirmatory test. This group did not distinguish between evaluation for atherosclerotic renovascular disease and fibromuscular dysplasia.

In 2019 an international consensus guideline on the diagnosis and management of fibromuscular dysplasia was published by the European Society of Hypertension and the Society for Vascular Medicine (61). This guideline identified the following clinical signs of renal artery fibromuscular dysplasia: onset of hypertension <30 years; accelerated, malignant hypertension (BP >180/110 mmHg); drug resistance; unilateral small kidney without causative urologic abnormality; abdominal bruit in the absence of atherosclerotic risk factors; suspected renal artery dissection; presence of fibromuscular dysplasia in another artery. The consensus group recommended CT angiography (CTA) for the initial screening test but noted that MRA could be used if CTA was contraindicated. This recommendation was based on the belief that compared with MRA, CTA provided better spatial resolution and allowed discrimination from atherosclerotic renovascular disease. This consensus group specifically recommended that duplex ultrasound be used only in centers with extensive expertise in this imaging modality. Catheter-based angiography with measurement of a pressure gradient is the criterion standard for diagnosis and is the only modality that allows determination of the clinical significance of lesions observed with either CTA or MRA.

Obstructive Sleep Apnea

A history of gasping during sleep, episodes of nonbreathing reported by a significant other, and daytime somnolence are clues to the presence of sleep apnea. Although sleep apnea is debated as a true cardiovascular risk factor, it is nonetheless worth pursuing a positive history of sleep-disordered breathing symptoms with a sleep evaluation because treatment often improves the daytime performance of patients with moderate to severe sleep apnea. The ACC/AHA guidelines suggest screening for obstructive sleep apnea among patients with resistant hypertension and a history of snoring, fitful sleep, breathing pauses during sleep, or daytime sleepiness (2).

Renal Parenchymal Disease

CKD is a common cause of hypertension and is suggested by increases in serum creatinine, coupled with urinary findings like hematuria or proteinuria.

Drug-Induced or Alcohol-Induced Hypertension

A thorough drug exposure history is essential because several illicit, prescription, and over-the-counter medications may elevate the blood pressure (6264).

Focused Evaluation

The physical examination focuses on the circulation and the abdomen. The circulation aspects are evident when pulses are delayed, reduced, or absent in the femoral and pedal circulation consistent with coarctation of the aorta (65), or the more generalized atherosclerosis noted with long-term cigarette use (66). The presence of carotid, abdominal, or epigastric bruits also points to generalized atherosclerosis and may be a clue to underlying renovascular disease (67). The (rare) presence of bilaterally palpable kidneys is consistent with polycystic kidney disease, the most common form of hereditary kidney disease in adults (68).

Laboratory evaluation should include hemoglobin or hematocrit, electrolytes, creatinine, glucose, a fasting lipid panel, and urinalysis (2). Elevation in blood hematocrit suggests increased viscosity, which can elevate BP (69). Reductions in serum potassium, especially coupled with an elevation in the serum bicarbonate level and a modest elevation in serum sodium, suggest that aldosterone excess is present (70).

Specific additional laboratory testing is guided by the history and examination results. In some cases, a search for catecholamine excess by measurement of plasma metanephrines is recommended when the history suggests sweating, headaches, and palpitations and the physical findings show increases in heart rate or BP during attacks of feeling unwell in these patients (71). Suspicion of parathyroid excess from, for example, an elevation in a random serum calcium level, or the unexpected finding of significant osteopenia on an X-ray image, should prompt measurement of parathyroid hormone level (72). Young age and a unilateral epigastric bruit prompt the consideration of plasma renin activity, which is typically elevated in unilateral renovascular diseases such as fibromuscular dysplasia (73).

Genetic testing may be performed once secondary causes are identified. Genetic testing is typically done post hoc after confirmatory testing or tissue is obtained. Genetic tests have been developed for pheochromocytomas and paragangliomas (71). There is genetic testing for polycystic kidney disease and for a growing number of somatic mutations noted in adenomatous adrenal tissue that influence the stimuli to aldosterone release through various sensing mechanisms and channels (74). In general, genetic testing is still nascent as a technology to apply to all newly diagnosed hypertensive individuals because the individual genetic mutations identified to date typically explain only a small fraction of the BP elevation in populations tested so far (75).

Three examples are provided here using the principles described previously in identifying patients with secondary causes of hypertension. In the first example, a 28-year-old man was found to have a BP of 158/102 mmHg on repeated examinations. He had no significant family history of hypertension, nor was there any medication use (prescription or over the counter) at the time of his evaluation for hypertension. His examination results were unremarkable, with a body mass index of 23.8 kg/m2, normal pulses, and no bruits. His routine laboratory studies disclosed a potassium level of 3.1 mEq/L with a serum bicarbonate of 29 mEq/L and a serum sodium of 141 mEq/L. He was initially treated with potassium supplementation and an amlodipine/angiotensin receptor blocker combination. Patients who have hypertension in the setting of spontaneous or diuretic-induced hypokalemia should be evaluated for primary aldosteronism.

After the potassium normalized, plasma renin activity was <0.01 ng A1-mL/hr (normal range 2–4 ng A1-mL/hr). His serum aldosterone was 44 ng/dL (normal range 3–16 ng/dL]. A CT scan with adrenal cuts showed a 3-cm right adrenal adenoma with a Hounsfield unit of 9, and >75% washout of contrast material. The Hounsfield unit is a calculation of radiodensity used by radiologists when evaluating some CT scans, like those of the adrenal gland (76). A Hounsfield unit of <10 for a mass in the adrenal gland is typically considered reflective of an adrenal cortex adenoma (i.e., tissue containing more lipid than water). For evaluating washout, a dedicated adrenal CT protocol consists of a noncontrast scan, followed by a contrast-enhanced scan following a delay of 60 to 90 seconds, and finishing with a delayed scan at 15 minutes. For estimating washout of contrast material, the region of interest needs to focus on the side with the lesion. The radiologist will estimate the enhancement washout, and values of at least 60% are consistent with an adenoma of the adrenal cortex (77). In the case presented here, adrenal vein sampling was performed following intravenous synthetic cosyntropin and showed the following values in the blood sampled at the sites shown (Table 3).

Table 3.

Adrenal vein sampling results

SiteAldosterone (ng/dL)Cortisol (µg/dL)Aldosterone/cortisol (ratio)Selectivity index (AV cortisol)/(IVC cortisol)
Right adrenal vein24943786.69.9
Left adrenal vein4915280.913.9
Inferior vena cava5138

Interpreting these values requires several steps. The first step is to assure a low likelihood of dilution of adrenal vein blood with inferior vena cava (IVC) blood, using the selectivity index. The IVC sample is obtained below the kidney veins so that it is not enriched with adrenal vein effluent. A selectivity index >5.1 (determined as a simple ratio of the cortisol in the adrenal vein [AV] divided by the cortisol in the IVC) indicates a good likelihood of relatively undiluted AV sample (55). Next the aldosterone value in the AV is divided by the cortisol value in the same AV (ignoring the units of measurement). This generates the A/C ratio for each adrenal vein, and the lateralization index is calculated as the A/C value on the side suspected as the source of autonomous aldosterone production divided by the A/C value on the opposite side. In the example shown, the lateralization index = (6.6)/(0.9), yielding a value of 7.3, above the typical threshold of 4.1 considered a positive indication of lateralization (55). Used with permission from reference 55 (Funder JW, Carey RM, Mantero F, Murad MH, Reincke M, Shibata H, et al.: The management of primary aldosteronism: Case detection, diagnosis, and treatment: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 101: 1889–1916, 2016).

He underwent a laparoscopic right adrenalectomy. His potassium remained normal off potassium supplements, and his BP fell to 116/66 mmHg off antihypertensive treatment. In this case, the history and physical examination were not helpful, but insight into the secondary nature of the elevated BP was gained through routine screening laboratory values demonstrating the hypokalemia.

In the second example, a 20-year-old woman entered the hospital for an elective tonsillectomy. Upon induction her BP soared from 112/70 mmHg to 210/136 mmHg on the operating table. Her heart rate increased from 71 beats/minute to 134 beats/minute. The operative procedure was aborted, and the heart rate and BP returned to prior levels after 2 hours. A more detailed history revealed headaches and some palpitations that occurred in episodic fashion and were thought to be migraines. Paroxysmal hypertension in the setting of a history suggesting catecholamine excess raises the possibility of pheochromocytoma or paraganglioma.

A 24-hour urine for metanephrines, and a plasma level of metanephrine confirmed marked elevation. Magnetic resonance imaging of the abdomen showed a large mass at the aortic bifurcation (organ of Zuckerkandl) and two tumors on the lower side of the liver. These were identified as neuroendocrine tumors by an 123I-meta-iodo-benzyl-guanidine scan. She was treated preoperatively with phentolamine (an α-blocking drug) and methyltyrosine (a tyrosine hydroxylase inhibitor) and underwent removal of the organ of Zuckerkandl tumor and resection of the two masses under the liver. All three tissues were identified as paragangliomas histologically. Genetic testing showed her to have the succinate dehydrogenase isoform B mutation, which was also identified in one parent. She has no children. She is currently managed with carvedilol and monitored for new or recurrent tumor. In this case, the rise in BP during anesthesia induction prompted a more thorough history, which revealed symptoms of possible catecholamine excess. The physical finding of elevated heart rate and blood pressure that returned to normotensive levels after a secretory episode was a further clue to a disorder of catecholamine excess, confirmed by high levels of urinary metanephrine excretion and plasma metanephrine concentrations.

In a third example a 24-year-old woman was referred from gynecology for hypertension about 6 months after starting an oral contraceptive agent. Despite discontinuation of the agent, her BP persisted at values of 154/106 mmHg. Her father had died in a motor vehicle accident, her mother was alive and normotensive. She had no medication use. Her physical examination revealed a right upper quadrant bruit in the abdomen and showed otherwise negative results. Her young age (<30 years) and the abdominal bruit suggested renovascular disease, particularly fibromuscular dysplasia.

The results of screening laboratory studies were negative. Her BP was managed by amlodipine and nebivolol. A CT angiogram showed a “string-of-beads” appearance in the mid and distal portions of the right kidney artery. A kidney angiogram confirmed these findings and found a 22 mmHg systolic pressure gradient across the area of narrowing. After several transluminal angioplasty treatments there was a good cosmetic appearance to the right kidney artery and a 4 mmHg pressure gradient across the treated area. Nebivolol and amlodipine were both discontinued. She had a BP of 126/76 mmHg off medications. In this case the sudden onset of elevated BP, coupled with young age and an uninformative family history in concert with the physical finding of a right upper quadrant bruit, were clues to a possible renovascular source for her elevated blood pressure.

Assessment for Cardiovascular Risk Factors

It is important to assess for additional cardiovascular risk factors when evaluating a hypertensive patient. First, hypertensive patients frequently have comorbid findings. Common coexistent cardiovascular risk factors include overweight/obesity, diabetes mellitus, dyslipidemias, cigarette use, low levels of physical activity, and an unhealthy diet (2). Second, some BP medications may have adverse effects on non–BP-related cardiovascular risk factors (78). Diuretics and β-blockers may alter the lipid profile or raise the blood sugar level (79,80). β-blockers may also reduce physical activity with an associated small weight gain, and reduce concentrations of high-density lipoprotein cholesterol concentrations (81). In addition, the treatment of elevated BP is intended to reduce the likelihood of a cardiovascular event, and it makes intuitive sense to ensure that the treatment regimen for any hypertensive patient is undertaken in view of the additional cardiovascular risk factors.

The history is again useful here. A review of medication use can disclose agents specifically tailored to comorbidities like diabetes (for example, metformin use) and dyslipidemia (for example, statin use). A dietary history can disclose a predilection for high-salt-content, lipid-enriched foods, particularly when the patient eats few or no meals at home. When overweight/obesity is evident, noting the timing of weight gain may help. Recent weight gains may have pushed prior prehypertensive BPs above threshold values for the diagnosis of hypertension, and the likelihood of successful BP control may be higher if the trend can be reversed in the motivated patient. Altering lifelong overweight/obesity is a more challenging treatment goal and will usually require a team-based approach with good nutritional support, often lacking in many practice settings.

Smoking, whether firsthand or secondhand exposure, is an important risk factor to address for both cardiovascular prevention and reduction in cancer risk when efforts to quit or avoid secondhand smoke are successful. Increasingly, many people have smart technologies that record the number of steps taken per day. Although this is only one aspect of physical activity, it is a useful one, and often patients know their average “steps/day.” Current AHA recommendations are to work up 10,000 steps/day (82). The average adult American achieves about 4800 steps/day (83).

The physical examination begins with height and weight, to calculate the patient’s body mass index. A body mass index is >27.4 kg/m2 confirms the presence of overweight/obesity. An examination of the fundi is recommended in the initial examination of all hypertensive patients. The fundi may disclose the presence of diabetic retinopathy, and more commonly the fundi frequently show grade 1 or 2 Keith-Wagener-Barker changes (84) consistent with the presence of hypertension and atherosclerosis. The eyes may also show a white ring in a segment of the iris (arcus senilis) or completely encircling the iris (anulus senilis). These findings, and yellow-orange raised plaques on the skin, often in the periorbital area, known as xanthelasma, reflect underlying dyslipidemia. The presence of vascular bruits supports the potential presence of dyslipidemia and/or cigarette exposure.

The laboratory investigation may show elevations in glucose or creatinine in the chemistry panel, confirming the presence of diabetes or kidney disease. The urinalysis may show blood or proteinuria, pointing to the possibility of renal parenchymal diseases. The lipid profile may reveal, or confirm known, dyslipidemia.

The electrocardiogram may show the presence of LVH, or the occurrence of pathologic Q waves indicating prior cardiac damage. The latter may be a further clue to the presence of dyslipidemia, diabetes, and cigarette exposure.

The presence of target organ damage increases the likelihood of further adverse target organ outcomes. When treating elevated BP for secondary prevention, i.e., when a patient has already experienced target organ damage, the benefits of treatment are even more evident in that the numbers needed to treat to prevent another cardiovascular outcome are lower than the numbers needed in those without prior damage (85). This lesson was first learned in the Hypertension Detection and Follow-Up Program, which allowed the recruitment of hypertensive patients with existing target organ damage (86), a bold and unusual move at a time (c. 1970–1980) when hypertension trials typically excluded the elderly (>75 years), patients with diabetes, patients with CKD, and patients with known cardiovascular diseases. Specific query should be made for prior heart attack or coronary artery disease, heart failure, stroke or transient ischemic attack, kidney disease, and peripheral arterial disease. Some patients will have a history of prior radiologic or surgical interventions. In addition, known LVH by an echocardiogram or cardiac magnetic resonance imaging is an essential element in the history (87).

The physical examination may disclose motor and sensory findings from a prior stroke. Patients with cardiac involvement may have gallop rhythms (S3 or S4), lateral displacement of the apical cardiac impulse, and potentially signs of pulmonary congestion (rales). Pulses may be reduced or absent in the lower extremities. Bruits in the carotid arteries, abdomen, and femoral regions are clues to advanced atherosclerosis (8890). Surgical scars over major vessels or in the sternum support prior vascular surgeries.

Laboratory data may reveal elevated creatinine consistent with parenchymal kidney disease, and reduced hemoglobin/hematocrit is consistent with this as well. Again, the electrocardiogram may show the presence of LVH, or the occurrence of pathologic Q waves reflecting prior cardiac damage.

Summary

Equipped with a good history, physical examination results, and standard and selected laboratory and imaging data, a reasonably thorough evaluation of a newly diagnosed hypertensive patient is accomplished, and insight gained into potential therapies (medication and lifestyle) to prefer or avoid. Additional reviews and guidelines detailing the value of the history, physical examination, laboratory, and imaging data are available (24,91,92).

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    Patterns of BP based on concordance and discordance of in-office and daytime out-of-office BP. Because guidelines change periodically, rather than specify a threshold number for diagnosing hypertension, the axes are labeled in the middle with “BP threshold.” The reader should substitute currently recommended thresholds for diagnosing hypertension in, or out, of the office using current societal norms.

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