7^th Brazilian Guideline of Arterial Hypertension: Chapter 3 - Clinical and Complementary Assessment

Clinical history and objectives

The major objectives of clinical and laboratory assessment are shown in Chart 1. Meeting those goals allows the correct AH diagnosis and prognosis, enabling choosing the better therapy for the patient.

Chart 1
Objectives of clinical and laboratory assessment

Confirmation of AH diagnosis by use of BP measurement

Identification of CVRF

Search for TOD, both subclinically and clinically manifested

Search for other associated diseases

Stratification of global CV risk

Assessment of evidence for suspected secondary AH

Clinical assessment

Clinical history

Complete clinical history with questions about time since AH diagnosis, course and previous treatment should be obtained. Information on the family history is essential to increase the chance of an accurate diagnosis of primary AH.¹ (GR: I; LE: B). The patient should be asked about specific RF for CVD, comorbidities, socioeconomic aspects and lifestyle,² in addition to previous and current use of medications or other substances that can interfere with BP measurement and/or AH treatment. Similarly, evidence of a secondary cause of AH should be investigated.

Physical examination

Blood pressure should be measured with proper technique (Chapter 2). Anthropometric data, such as weight, height [for body mass index (BMI) calculation], abdominal circumference (AC) and heart rate (HR), should be recorded. The normal values of AC and BMI are those recommended by the International Diabetes Federation (IDF) in 2006, and can vary according to ethnicity.^3,4 (GR: IIa; LE: C).

Assessment (Chart 2) should comprise palpation and auscultation of the heart, carotid arteries and pulses, ankle-brachial index (ABI) measurement and retinal exam.

Chart 2
Clinical assessment

Physical Examination
BP measurement in both arms
Weight, height, BMI and HR
Abdominal circumference
Signs of TOD
Brain: motor or sensorial deficits
Retina: lesions on retinal exam
Arteries: pulse absence, asymmetry or reduction, skin lesions and murmurs
Heart: apical beat displaced, presence of S3 or S4, murmurs, arrhythmias, peripheral edema, pulmonary rales
Suggestive signs of secondary causes*
Cushingoid characteristics
Abdominal palpation: enlarged kidneys (polycystic kidney)
Abdominal or thoracic murmurs (renovascular, coarctation of the aorta, disease of the aorta or its branches)
Decreased femoral pulses (coarctation of the aorta, disease of the aorta or its branches)
Difference of BP between arms (coarctation of the aorta and subclavian stenosis)

• ^*
  For further information, see Chapter 12.

To calculate ABI, measure SBP in the arm and ankle, in both sides. An arm SBP/ankle SBP ratio greater than 0.90 is defined as normal, while PAD is defined as mild, if that ratio is 0.71-0.90, moderate, if 0.41-0.70, and severe, if 0.00-0.40.

Basic laboratory investigation, assessment of subclinical and clinical target-organ damage

Complementary assessment is aimed at detecting subclinical or clinical TOD to better stratify CV risk. To stratify global CV risk, the classical RF (Chart 3), as well as the new ones identified, should be considered, although they have not been incorporated to the clinical scores of risk stratification.^4,5

Chart 3
Additional cardiovascular risk factors

Age (men > 55 years, women > 65 years)

Smoking habit

Dyslipidemias: triglycerides > 150 mg/dL; LDL-C > 100 mg/dL; HDL-C < 40 mg/dL

DM

Family history of premature CVD: men < 55 years, women < 65 years

Of the new RF, the following stand out: fasting glycemia between 100 mg/dL and 125 mg/dL, abnormal glycated hemoglobin (HbA1c), abdominal obesity (metabolic syndrome - MS), PP (SBP-DBP) > 65 mm Hg in the elderly,⁵ history of preeclampsia, and family history of AH (for borderline hypertensive patients).

The laboratory assessment shown in Chart 4 should be part of the initial routine of all hypertensive patients.⁴

Chart 4
Routine tests for hypertensive patients

Urinalysis (GR: I; LE: C)

Serum potassium (GR: I; LE: C)

Fasting glycemia (GR: I; LE: C) and HbA1c (GR: I; LE: C)

Estimated glomerular filtration rate (GR: I; LE: B)

Serum creatinine (GR: I; LE: B)

Total cholesterol, HDL-C and serum triglycerides (GR: I; LE: C)*

Serum uric acid (GR: I; LE: C)

Conventional electrocardiogram (GR: I; LE: B)

• ^*
  LDL-C is calculated by use of the formula: LDL-C = total cholesterol - (HDL-C + triglycerides/5) (when triglycerides < 400 mg/dL).

The Cockroft-Gault formula is used to calculate creatinine clearance:⁶ CrCl (mL/min) = [140 - age] x weight (kg) /serum creatinine (mg/dL) x 72 for men; for women, multiply the result by 0.85.

To estimate glomerular filtration rate (GFR) use the CKD-EPI equation.⁷ The interpretation of the GFR values to classify CKD (stages) is performed according to the National Kidney Foundation (NKF).⁷

The CKD-EPI equation⁸ used to estimate GFR is available at: www.nefrocalc.net

• GFR (mL/min/1.73m²:

• Stage 1: ≥ 90 = normal or high;

• Stage 2: 60-89 = mildly decreased;

• Stage 3a: 45-59 = mildly to moderately decreased;

• Stage 3b: 30-44 = moderately to severely decreased;

• Stage 4: 15-29 = severely decreased;

• Stage 5: < 15 = end-stage kidney disease (KDIGO).

Certain clinical situations, discussed in Chart 5, require more detailed complementary tests.

Chart 5
Tests recommended for certain populations

Test/assessment	Recommended population and indication
Chest X ray	Follow-up of patients with clinical suspicion of cardiac (GR: IIa; LE: C) and/or pulmonary impairment. Assessment of hypertensive individuals with aorta impairment when echocardiogram is not available.9
Echocardiogram More sensitive than ECG to diagnose LVH. Important in the assessment of the geometrical forms of left atrial hypertrophy and size, analysis of systolic and diastolic function. Consider LVH when left ventricular mass corrected for body surface is equal to or greater than 116 g/m2 for men and 96 g/m2 for women.10	Evidence of LVH on ECG or patients with clinical suspicion of HF (GR: I; LE: C).
Albuminuria Predicts fatal and non-fatal CV events. Normal values < 30 mg/24h (GR: I; LE: C).7,11 *	Diabetic hypertensive patients, with MS or at least two RF.
Carotid US The carotid IMT and/or identification of plaques predict the occurrence of stroke and MI independently of other CVRF. IMT values > 0.9 mm, as well as the presence of atherosclerotic plaques, have been considered abnormal (GR: IIa; LE: B).12	Carotid murmur, CbVD signs or atherosclerotic disease in other sites.
Renal US or with Doppler	Patients with abdominal masses or abdominal murmur (GR: IIa; LE: B).13
HbA1c	- When fasting glycemia > 99 mg/dL - Family history of type 2 DM or previous diagnosis of type 2 DM and obesity (GR: IIa; LE: B).14
Exercise test	- Suspicion of stable CAD, DM or family antecedent of CAD in patients with controlled BP (GR: IIa; LE: C).15
ABPM/HBPM	- According to the conventional indication of those methods (GR: IIa; LE: B).
PWV “Standard” for assessing arterial stiffness. Values greater than 12 m/s are abnormal (GR: IIa; LE: B).16	- Intermediate-to-high-risk hypertensive patients.
MRI of the brain: to detect silent infarctions and micro hemorrhages (GR: IIa; LE: C).17	- Patients with cognitive disorders and dementia.

• LVH: left ventricular hypertrophy; CV: cardiovascular; RF: risk factor; US: ultrasonography; IMT: intima-media thickness; MS: metabolic syndrome; MI: myocardial infarction; CVRF: cardiovascular risk factor; CbVD: cerebrovascular disease; HbA1c: glycated hemoglobin; DM: diabetes mellitus; CAD: coronary arterial disease; ABPM: ambulatory blood pressure monitoring; HBPM: home blood pressure monitoring; PWV: pulse wave velocity; MRI: magnetic resonance imaging.
• ^*
  Next figure shows the current classification and nomenclature for albuminuria and GFR according to KDIGO, 2012.⁷

Figure 1
Prognosis of CKD according to the category of GFR and albuminuria. Green: low risk; yellow: moderately increased risk; orange: high risk; red: extremely high risk.

References

• ¹
  Murabito JM, Nam BH, D'Agostino RB Sr, Lloyd-Jones DM, O'Donnell CJ, Wilson PW. Accuracy of offspring reports of parental cardiovascular disease history: the Framingham Offspring Study. Ann Intern Med. 2004;140(6):434-40.
• ²
  International Diabetes Federation. (IDF). The IDF consensus worldwide definition of the metabolic syndrome. [Internet]. [Cited in 2016 May 15]. Available from: http://www.idf.org/webdata/docs/MetSyndrome_FINAL.pdf
  » http://www.idf.org/webdata/docs/MetSyndrome_FINAL.pdf
• ³
  Simão AF, Precoma DB, Andrade JP, Correa FH, Saraiva JF, Oliveira GM, et al; Sociedade Brasileira de Cardiologia. [I Brazilian Guidelines for cardiovascular prevention]. Arq Bras Cardiol. 2013;101(6 Suppl 2):1-63. Erratum in: Arq Bras Cardiol. 2014;102(4):415.
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  Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M, et al; Task Force Members. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) J Hypertens. 2013;31(7):1281-357.
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  D'Agostino RB Sr, Vasan RS, Pencina MJ, Wolf PA, Cobain M, Massaro JM, et al. General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation. 2008;117(6):743-53.
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  Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron. 1976;16(1):31-41.
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  Kidney Disease Improvement Global Outcomes (KDIGO). KDIGO 2012 Clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1-150.
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  Matsushita K, Mahmodi BK, Woodward M, Emberson JR, Jafar TH, Jee SH, et al; Chronic Kidney Disease Prognosis Consortium. Comparison of risk prediction using the CKD-EPI equation and the MDRD study equation for estimated glomerular filtration rate. JAMA. 2012;307(18):1941-51.
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  Rayner BL, Goodman H, Opie LH. The Chest Radiograph. A useful investigationin the evaluation of hypertensive patients. Am J Hypertens. 2004;17(6):507-10.
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  Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellika PA, et al; Chamber Quantification Writing Group; American Society of Echocardiography's Guidelines and Standards Committee; European Association of Echocardiography. Recommendations for chamber quantifications. A report from the American Society of Echocardiography's Guidelines and Standards Committee and the chamber quantifications writing group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18(12):1440-63.
• ¹¹
  Tsioufis C, Kokkinos P, Macmanus C, Thomopoulos C, Faselis C, Doumas M, et al. Left ventricular hypertrophy as a determinant of renal outcome in patients with high cardiovascular risk. J Hypertens. 2010;28(11):2299-308.
• ¹²
  Nambi V, Chambless L, Folsom AR, He M, Hu Y, Mosley T, et al. Carotid intima-media thickness and presence or absence of plaque improves prediction of coronary heart disease risk: the ARIC (Atherosclerosis Risk In Communities) study. J Am Coll Cardiol. 2010;55(15):1600-7.
• ¹³
  Vasbinder GB, Nelemans PJ, Kessels AG, Kroon AA, de Leeuw PW, van Engelshoven JM. Diagnostic tests for renal artery stenosis in patients suspected of having renovascular hypertension: a meta-analysis. Ann Intern Med. 2001;135(6):401-11.
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  Selvin E, Steffes MW, Zhu H, Matsushita K, Wagenknecht L, Pankow J, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med. 2010; 362(9):800-11.
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  Chin D, Battistoni A, Tocci G, Passerini J, Parati G, Volpe M. Non-invasive diagnostic testing for coronary artery disease in the hypertensive patient: potential advantages of a risk estimation-based algorithm. Am J Hypertens. 2012;25(12):1226-35.
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  Safar ME, Levy BI, Struijker-Boudier H. Current perspectives on arterial stiffness and pulse pressure in hypertension and cardiovascular diseases. Circulation. 2003;107(22):2864-9.
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  de Leeuw FE, de Groot JC, Oudkerk M, Witteman JC, Hofman A, van Gijn J, et al. Hypertension and cerebral white matter lesions in a prospective cohort study. Brain. 2002;125(Pt 4):765-72.

Publication Dates

• Publication in this collection
  Sept 2016