Hypertension trials update

Abstract

Hypertension is one of the most prevalent cardiovascular diseases and its treatment requires multimodal therapeutic approaches. This review aims to provide a summary and update on relevant evidence in hypertension research published in 2019/2020. These include trials dealing with the prognostic effect of systolic and diastolic blood pressure values, the association between hypertension and valve disease, reproducibility of masked and white-coat hypertension, and the prognostic importance of ambulatory and night-time blood pressure measurements. Treatment of hypertension focusing on elderly patients but also the potential cancer risk of thiazide diuretics, the valsartan recall, chronotherapy, and device-based hypertension therapy are discussed.

Fig. 1. The effect of systolic and diastolic blood pressure on cardiovascular outcomes.

The relationship between systolic blood pressure (solid line) and diastolic blood pressure (dashed line) z scores and the risk of the composite outcome among participants with systolic blood pressure > 133 mmHg or diastolic blood pressure > 78 mmHg are shown [3].

Fig. 2. Prevalence of systolic blood pressure ≥130 or ≥140 mmHg depending on age.

Systolic blood pressure measurements indicating hypertension (systolic blood pressure ≥ 130 mmHg or ≥140 mmHg) increased as a function of age [3].

Fig. 3. The effect of systolic blood pressure on aortic valve diseases.

Shown are hazard ratios for aortic stenosis (a) and aortic regurgitation (b) by categories of systolic blood pressure. Hazard ratios (HR) and 95% confidence intervals (CI) are displayed using floating absolute risk. Square sizes are inversely proportional to standard error and horizontal lines depict 95% confidence intervals. Models are adjusted for age, sex, body mass index, smoking, year of initial blood pressure measurement, total cholesterol, LDL, HDL, and practice-level index of multiple deprivation [6].

Fig. 4. Association between systolic blood pressure increment and valvular heart disease outcomes.

The figure shows an increase in the odds ratio per 20 mmHg increment in systolic blood pressure. Circles show point estimation and vertical lines represent 95% CIs. Odds ratio indicates hazard ratio in observational cohort studies and odds ratio in mendelian randomization estimation. Data collected from observation analyses and genetic studies [7].

Fig. 5. Incidence of mortality and cardiovascular outcomes, adjusted for gender, age, nighttime and 24-h BP.

Shown is the incidence of mortality, adjusted for sex, age and 24-h systolic blood pressure (A), cardiovascular outcomes, adjusted for sex, age and 24-h systolic blood pressure (B), total mortality, adjusted for sex, age and night-time systolic blood pressure (C) and cardiovascular outcomes, adjusted for sex, age and night-time systolic blood pressure (D) over follow-up in years based on systolic dipping ratio [8].

Fig. 6. Prevalence of different hypertensive phenotypes over the 4-year follow-up period.

Masked uncontrolled hypertension (MUCH), white-coat uncontrolled hypertension (WUCH), controlled hypertension, and uncontrolled hypertension are shown as % values during the 4 years of antihypertensive treatment in the European Lacidipine Study on Atherosclerosis trial [10].

Fig. 7. Proportion of patients diagnosed with masked or white coat hypertension during the 4-year follow-up period.

The percentage of these patients decreases over time, which indicates a limited reproducibility by frequently blood pressure measurements [10].

Fig. 8. Primary and stratified analyses of participants.

Forest-plot summarizing the primary analysis and the stratified analyses for blood pressure values <140/90 or >140/90 mmHg [14].

Fig. 9. Treatment strategy for uncomplicated hypertension.

ACEi angiotensin-converting enzyme inhibitor, ARB angiotensin receptor blocker, CCB calcium channel blocker [2].

Fig. 10. Prescribing behavior after the Valsartan recall in Canada.

Most patients (74%) were switched to a different ARB (not 357 valsartan). No alternative antihypertensive drug was prescribed in 11% of the patients [24].

Fig. 11. Time to discontinuation of spironolactone in patients with and without patiromer.

The proportion of patients who did not have to discontinue spironolactone was higher in patients receiving patiromer compared with those receibing a placebo [27].

Fig. 12. Automated, unobserved systolic blood pressure.

Patiromer enables the administration of spironolactone in more patients. However, the use of patiromer in addition with spironolactone was not associated with a significant reduction of blood pressure after 12 weeks [27].

Fig. 13. Survival of the two groups.

Kaplan–Meier curve for the combined endpoint (cardiovascular death, myocardial infarction, coronary revascularization, heart failure and stroke) comparing treatment upon awakening and at night-time [28].

Fig. 14. Primary and secondary endpoint after renal denervation.

Posterior distribution of between-group differences in (a) primary efficacy endpoint (24-h systolic blood pressure) and (b) secondary effectiveness endpoint (office systolic blood pressure). BCI Bayesian 95% credible interval, SBP systolic blood pressure [35].