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Among patients with chronic HTN, structural and functional changes in the heart can lead to the development of HF. BP management not only prevents asymptomatic HTN-mediated organ damage that can cause HF but can also prevent further disease progression. The intensive control of BP is recommended for patients with HTN who are at risk of HF; however, the optimal range within which BP should be controlled and the benefits of intensive BP control in patients with established HF remain unclear. Future randomized clinical trials are warranted to understand the complex association between BP and patients’ prognoses in the context of HF management.

Blood pressure and heart failure prevention

Two issues arise regarding HF when treating HTN. The first is strictly controlling high BP to prevent structural remodeling and the development of HF. The presence of a J-curve association between BP and CV outcomes have been long debated, but evidence has been controversial. The current consensus is that strict control is mostly beneficial for hypertensive patients with low CV risk, while the risk of CV outcome increases in patients with high risk for coronary heart disease.. Recently, the findings from the Systolic Blood Pressure Intervention Trial (SPRINT), which assessed the role of intensive HTN treatment on a composite outcome that included HF, showed that a target SBP < 120 mmHg was associated with a 38% relative risk reduction in HF. BP lowering in patients with ventricular hypertrophy can delay further remodeling and reduce the incidence of HF. The LV hypertrophy induced by HTN is not unidirectional, and a regression of LV mass has been observed after the pharmacological treatment of elevated Bp]. Improvements in LV hypertrophy have also been associated with reduced risks of CV events, including CV death, myocardial infarction, and stroke .

Identifying patients at an increased risk of developing hypertensive HF is important to enable attentive monitoring and begin timely treatment. LA enlargement in the absence of mitral valve disease could be a marker of diastolic dysfunction; this has been demonstrated by the correlation between the LA volume and the natriuretic peptide levels in asymptomatic patients with preserved systolic function . Biomarkers such as uric acid, metalloproteinases, and natriuretic peptides, may also predict the development of HF in patients with HTN . Patients with HTN and a high clinical risk of HF should be screened regularly for diastolic dysfunction or LV hypertrophy to prevent progression to advanced disease.

HTN treatment relies on many classes of drugs, including angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs), beta-blockers, calcium channel blockers (CCBs), and diuretics. A meta-analysis of randomized clinical trials that analyzed HF as an outcome showed significant reductions in the new-onset HF rates in association with all of these classes of drug, except for ARBs, which may have been a consequence of the small number trials reviewed. The findings from head-to-head comparisons of the different drug classes have shown that CCBs seem to be inferior at preventing HF compared with ACE inhibitors/ARBs, beta-blockers, and diuretics; however, the inferiority of the CCBs was largely attributable to differences in the use of concomitant drugs [59]. Thiazide-like diuretics, which are widely used to treat HTN, but are not frequently used in patients with HF, also reduced the new-onset HF rate compared with placebo [60], which suggests that reducing the BP itself is probably the most important factor in HF prevention. Indeed, for every 10mmHg reduction in SBP, the HF rate declines by 12%. Currently, no specific class of drugs is recommended for the prevention of HF in patients with HTN, and patients should be treated according to the guidelines.

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