Article Index
Current Consensus
Systemic Arterial Hypertension (SAH) is not just a high number on the sphygmomanometer. It is a complex multifactorial syndrome characterized by low-grade inflammation, endothelial dysfunction, vascular remodeling, and neuro-hormonal dysregulation, requiring a therapeutic approach that targets not only pressure reduction but also end-organ protection.
1. Introduction and Global Impact
Systemic Arterial Hypertension (SAH) remains the leading modifiable risk factor for global cardiovascular morbidity and mortality. It is estimated to affect more than 1.28 billion adults worldwide, with an alarming prevalence in low- and middle-income countries.
Known as "the silent killer," SAH often progresses asymptomatically until the manifestation of catastrophic events such as Stroke, Acute Myocardial Infarction (AMI), Heart Failure, and Chronic Kidney Disease. The most recent guidelines (SBC, AHA/ACC, ESC/ESH) emphasize the need for early diagnosis and rigorous control to mitigate residual risk.
2. Hemodynamic Pathophysiology
Blood pressure is the product of Cardiac Output (CO) and Peripheral Vascular Resistance (PVR). Sustained BP elevation results from an imbalance in complex regulatory systems:
2.1 Renin-Angiotensin-Aldosterone System (RAAS)
Inappropriate activation of the RAAS is central to the genesis of SAH. Angiotensin II promotes potent vasoconstriction and stimulates aldosterone secretion, which increases renal sodium and water reabsorption, elevating blood volume. Chronically, angiotensin II induces myocardial fibrosis and vascular hypertrophy.
2.2 Endothelial Dysfunction
Healthy endothelium regulates vascular tone through the balance between vasodilators (Nitric Oxide - NO) and vasoconstrictors (Endothelin-1). In SAH, oxidative stress reduces NO bioavailability, resulting in a pro-constrictor, pro-inflammatory, and pro-thrombotic state.
3. Precision Diagnosis
Diagnosis should not be based on a single isolated measurement, except in cases of hypertensive emergency. BP variability requires robust confirmation methods.
| Method | Definition | Clinical Advantages | Main Indication |
|---|---|---|---|
| Office BP | Standardized measurement in a clinical setting. | Universal screening and basic follow-up. | Initial screening. |
| 24h ABPM | Ambulatory Blood Pressure Monitoring. | Evaluates nocturnal dipping and pressure load. | Suspected masked or white-coat hypertension. |
| HBPM | Home Blood Pressure Monitoring. | Multi-day protocol (e.g., 3 days, morning and evening). | Therapeutic adjustment and patient engagement. |
4. Classification and Therapeutic Goals
Although there are slight variations between American (AHA) and Brazilian/European (SBC/ESC) guidelines, the general consensus for classification in adults (>18 years) follows the pattern below:
- Optimal: < 120/80 mmHg
- Pre-Hypertension (Elevated): 130-139 / 85-89 mmHg
- Stage 1 Hypertension: 140-159 / 90-99 mmHg
- Stage 2 Hypertension: ≥ 160 / 100 mmHg
- Hypertensive Crisis: > 180/120 mmHg (Urgency vs Emergency depends on end-organ damage).
5. Non-Pharmacological Management (Lifestyle Changes)
Lifestyle Modifications (LSM) are the cornerstone of treatment and should be prescribed for all patients. In Stage 1 with low cardiovascular risk, they may be the sole initial therapy for 3-6 months.
- DASH Diet: Rich in fruits, vegetables, whole grains, and low-fat dairy; low in saturated fat. Proven reduction of 8-14 mmHg in SBP.
- Sodium Restriction: Limit to < 2g sodium/day (< 5g table salt).
- Weight Control: Maintain BMI < 25 kg/m². Weight loss is the most effective single intervention.
- Physical Activity: Moderate aerobic exercise (150 min/week) complemented by dynamic resistance training.
6. Pharmacotherapy Algorithm
For most patients, monotherapy is insufficient. Combined therapy from the start is recommended for greater efficacy and adherence, preferably in a single pill.
First-Line Classes (ABCD)
A - RAAS Blockers: ACEi (e.g., Enalapril, Ramipril) or ARB (e.g., Losartan, Valsartan). *Never combine ACEi + ARB.*
B - Beta-Blockers: Indicated in specific situations (HF, post-MI, rate control). Not first-line for uncomplicated primary hypertension.
C - Calcium Channel Blockers (CCB): Dihydropyridines (e.g., Amlodipine). Excellent for the elderly and reducing arterial stiffness.
D - Thiazide Diuretics: (e.g., Hydrochlorothiazide, Chlorthalidone, Indapamide). Potentiate the effect of other antihypertensives.
Stepped Strategy
- Step 1: ACEi or ARB + CCB (or Thiazide).
- Step 2: ACEi or ARB + CCB + Thiazide (Full Dose).
- Step 3 (Resistant Hypertension): Add Spironolactone (mineralocorticoid antagonist).
7. Resistant and Secondary Hypertension
Resistant Hypertension is defined as BP not controlled despite the use of 3 drugs at optimized doses (including a diuretic), or BP controlled with the use of 4 or more drugs. In these cases, it is imperative to investigate secondary causes (Obstructive Sleep Apnea, Primary Aldosteronism, Renal Artery Stenosis) and evaluate poor therapeutic adherence (pseudo-resistance).
8. Conclusion
Contemporary management of hypertension requires a paradigm shift: from treatment focused solely on numbers to an approach based on global cardiovascular risk. Integrating precise monitoring (ABPM/HBPM), early combination therapy, and patient engagement in lifestyle changes is key to reducing the devastating burden of this pathology.