Hypertension Diagnosis, Staging, and Evidence‑Based Management

Diagnostic Thresholds and Staging

The American College of Cardiology/American Heart Association (ACC/AHA) defines hypertension as systolic ≥ 130 mmHg or diastolic ≥ 80 mmHg, whereas the World Health Organization (WHO) retains the traditional threshold of ≥ 140/90 mmHg, creating an international divergence in diagnostic criteria. [@1][@2]
Stage 1 hypertension (ACC/AHA): systolic 130–139 mmHg or diastolic 80–89 mmHg. [@1]
Stage 2 hypertension (both ACC/AHA and WHO): systolic ≥ 140 mmHg or diastolic ≥ 90 mmHg. [@1][@2]
Diagnosis requires the average of ≥ 2 readings on ≥ 2 separate occasions, confirmed with out‑of‑office (home or 24‑h ambulatory) monitoring to exclude white‑coat hypertension. [@1]

In adults with confirmed hypertension and either established atherosclerotic cardiovascular disease (ASCVD) or a 10‑year ASCVD risk ≥ 10 % (calculated with ACC/AHA pooled‑cohort equations), the target is < 130/80 mmHg. [@1]
General adult population < 65 years: target < 130/80 mmHg. [@1]
Non‑institutionalized adults ≥ 65 years: aim for systolic < 130 mmHg if tolerated. [@1]
Patients with diabetes mellitus: target < 130/80 mmHg. [@1]
Patients with chronic kidney disease (CKD): target < 130/80 mmHg. [@1]
Patients with stable ischemic heart disease: target < 130/80 mmHg. [@1]
WHO recommendation for patients without comorbidities: target < 140/90 mmHg. [@2]

Stage 1 hypertension (130–139/80–89 mmHg): start antihypertensive medication when the patient has established ASCVD or a 10‑year ASCVD risk ≥ 10 %. [@1]
Stage 2 hypertension (≥ 140/90 mmHg): initiate lifestyle measures and pharmacologic therapy simultaneously; do not delay treatment beyond 3 months. [@2]

The ACC/AHA and WHO endorse four first‑line classes: thiazide or thiazide‑like diuretics, ACE inhibitors, angiotensin‑receptor blockers (ARBs), and long‑acting dihydropyridine calcium‑channel blockers (CCBs). [@1][@2]
In non‑Black patients without compelling indications, thiazide diuretics (especially chlorthalidone) are considered optimal first‑line agents, supported by outcome trials involving > 50 000 participants. [@1]
In Black patients without heart failure or CKD, initiate therapy with a thiazide diuretic or a CCB; ACE inhibitors and ARBs are 30–36 % less effective for stroke prevention in this population due to lower renin activity. [@1]
For patients with diabetes mellitus, an ACE inhibitor or ARB is preferred as initial therapy to protect renal function, particularly when albuminuria is present. [@1]
For patients with CKD (stage 3 + or albuminuria), an ACE inhibitor or ARB is first‑line to slow eGFR decline and reduce proteinuria. [@1]
Post‑myocardial infarction or stable ischemic heart disease: combine a β‑blocker with an ACE inhibitor or ARB as foundational therapy. [@1]
Heart failure with reduced ejection fraction: use a three‑drug regimen (ACE inhibitor or ARB + β‑blocker + diuretic). [@1]

Stage 1 hypertension: begin with single‑agent monotherapy and titrate upward before adding a second agent from a different class. [@1]
Stage 2 hypertension: start with a two‑drug combination from different first‑line classes, preferably as a single‑pill formulation to improve adherence. [@1][@2]
Preferred two‑drug combinations:
Single‑pill combinations markedly improve medication adherence and persistence. [@1][@2]

β‑blockers should not be used as first‑line therapy in uncomplicated hypertension, especially in patients > 60 years, because they are ≈ 36 % less effective than CCBs and ≈ 30 % less effective than thiazides for stroke prevention. [@1]
Dual renin‑angiotensin system blockade (ACE inhibitor + ARB or addition of a direct renin inhibitor) is prohibited due to increased risk of hyperkalemia and acute kidney injury without added cardiovascular benefit. [@1]

After initiating or adjusting antihypertensive therapy, review patients monthly until the BP target is achieved, then every 3–5 months for maintenance. [@1][@2]
Out‑of‑office BP monitoring (home or ambulatory) is essential to assess treatment response, detect white‑coat effect, and identify masked uncontrolled hypertension. [@1]