Journal of Hypertension最新文献

Background and aim: Some studies have suggested a negative correlation between obesity and peripheral arterial disease (PAD), a phenomenon known as the obesity paradox. Some have suggested that this phenomenon occurs due to the inability of the body mass index (BMI), a commonly used indicator of obesity, to differentiate between lean body mass (LBM) and fat mass (FM). We attempted to investigate the relationship between LBM and FM in relation to PAD events, respectively.

Methods and results: This post hoc analysis was conducted using data from the Systolic Blood Pressure Intervention Trial (SPRINT), and we employed Cox proportional hazards regression to investigate the relationship of LBM and FM with incident PAD. After an average follow-up of 3.7 years for 9285 participants, the study found that 5989 were male and 3296 were female. A total of 172 had an outcome event. We found a significant negative correlation between FMI and PAD events [hazard ratio (HR) 0.70, 95% confidence interval (CI) 0.56-0.86], while there was a significant positive correlation between LBMI and PAD events (HR 1.56, 95% CI 1.19-2.05). A restricted cubic spline analysis also confirmed this relationship, and it was consistent across the different subgroups.

Conclusions: In hypertensive patients, higher FM may be associated with a lower risk of PAD events, whereas higher LBM may be related to a higher risk of PAD events. The obesity paradox in PAD events may not be attributed to BMI's inability to distinguish between LBM and FM.

Objective: Baroreflex activation therapy (BAT) is a treatment option for resistant hypertension. However, data from randomized trials are scarce, especially regarding long-term efficacy.

Methods: This exploratory, prospective, randomized, two-center study investigated the impact of BAT deactivation and reactivation on office and home blood pressure (BP) in patients with resistant hypertension scheduled for BAT device replacement after multiannual treatment. Patients were randomized 8 weeks before device replacement: group one was deactivated from week -8 to -4 and reactivated from week -4 until surgery, group two remained activated from week -8 to -4 and was deactivated from week -4 until surgery. Patients were not aware of assignment. BP values were monitored during outpatient visits by a blinded physician and by telemetric home measurements. Statistical analysis using paired, two-tailed t-tests was considered significant at a P value less than 0.05.

Results: Sixteen patients with BAT for 50 months in median (IQR: 38-77 months) were included in the study. Office BP was significantly lower under active BAT compared to preimplantation values (146 ± 27 vs. 172 ± 21 mmHg systolic, P < 0.01). Home BP with deactivated device was 5 ± 7 mmHg higher than during active BAT (P < 0.05), office BP after 4 weeks of deactivation was 8 ± 14 mmHg higher (P = 0.06) than at baseline. Two patients met the predefined termination criteria and were reactivated immediately. In total, nine patients (60%) were classified as BAT responders based on at least 5 mmHg BP increase or early reactivation.

Conclusion: Deactivation of BAT increased home BP significantly, even after multiannual therapy, supporting a moderate BP-lowering effect of BAT in the long-term.

Optimal blood pressure (BP) targets for type 2 diabetes remain controversial. Although intensive BP control reduces cardiovascular risk in the general population, its net benefit in diabetes is uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials comparing intensive BP control (target < 130/80 mmHg or achieved systolic <130 mmHg) with routine control in adults with type 2 diabetes. Databases (PubMed, Embase, Cochrane CENTRAL) were searched through November 2024; two reviewers independently extracted data and assessed bias. Random-effects meta-analysis estimated pooled relative risks (RRs) with 95% confidence intervals (CIs), and trial sequential analysis (TSA) assessed robustness. Eleven trials comprising 24,308 participants met inclusion criteria. Intensive BP control reduced stroke (RR: 0.64; 95% CI: 0.51-0.81) and major cardiovascular events (RR: 0.86; 95% CI: 0.72-1.03) with no significant differences in mortality or heart-failure hospitalization. TSA confirmed firm evidence for stroke reduction, mortality and heart failure results remained inconclusive.

Background and aims: The magnesium depletion score (MDS) estimates magnesium deficiency risk by integrating dietary intake and physiological losses. This study evaluated the association between MDS and arterial stiffness in a rural Mediterranean population.

Methods: We analyzed data from 2048 participants (49.2% men, 50.8% women) in the Brisighella Heart Study. MDS and arterial stiffness parameters - augmentation index (AIx) and carotid-femoral pulse wave velocity (cfPWV) - were assessed using validated methods. Multiple regression models adjusted for age and mean arterial pressure included sex, smoking, physical activity, BMI, heart rate, fasting glucose, low-density lipoprotein cholesterol (LDL-C), triglycerides, serum uric acid, estimated glomerular filtration rate (eGFR), and MDS.

Results: An MDS at least 2 was observed in 51.6% of participants, more often in men (P < 0.001). Higher MDS was significantly associated with increased AIx and cfPWV in both sexes (P < 0.001). MDS remained an independent predictor of AIx (β = 0.087, P = 0.011) and cfPWV (β = 0.131, P = 0.013) after adjustment.

Conclusion: Higher MDS values correlate with greater arterial stiffness, suggesting that magnesium imbalance may negatively affect vascular health.

Objectives: This study investigated whether lowering the home blood pressure (BP) threshold for the diagnosis of hypertension from 135/85 to 130/80 mmHg enhances diagnostic accuracy when assessed against ambulatory BP monitoring (ABPM).

Methods: A total of 646 untreated participants (mean age 52 ± 10  years; 310 men) with valid 3-day office BP, 7-day home BP, and 24-h ABPM data and preserved renal function were included. Hypertension phenotypes were classified as normotension, white-coat, masked, and sustained hypertension according to office BP and ABPM criteria.

Results: Lowering the home BP threshold increased sensitivity from 72.3 to 89.5% but reduced specificity from 81.8 to 69.1%, thereby improving overall diagnostic accuracy from 73.1 to 87.8% and the kappa coefficient from 0.238 to 0.247. At the conventional threshold of 135/85 mmHg, 63.2% of masked and 15.1% of sustained hypertension were misclassified as normotension, whereas these rates declined to 30.3 and 3.4%, respectively, at the 130/80 mmHg threshold. Individuals with home BP between 130/80 and 134/84 mmHg showed intermediate office and ambulatory BP values, with a high prevalence of masked (32.9%) and sustained hypertension (11.7%). Within this subgroup, isolated nighttime and daytime-nighttime hypertension were identified in 35.7 and 13.5% of participants, respectively.

Conclusion: The conventional home BP threshold of 135/85 mmHg may fail to identify a considerable proportion of masked, sustained, and nighttime hypertension. Lowering the threshold to 130/80 mmHg, or designating 130/80-134/84 mmHg as a diagnostic 'gray zone' warranting ABPM confirmation, may improve diagnostic precision and facilitate earlier detection of hypertension in clinical practice.

Background: Although the invasive measurement of intra-arterial pressure is considered the gold standard, it is not feasible for routine clinical practice. This study aimed to investigate the prognostic value of invasively measured aortic pulse pressure (aPP) in patients undergoing invasive coronary angiography (ICA).

Methods: A total of 1110 patients who underwent ICA (mean age 65 years, 35.5% female) were prospectively enrolled. Just before ICA, aortic pressures were measured using a pigtail catheter positioned 3 cm above the aortic valve. Major adverse cardiovascular events (MACE), a composite of cardiac death, nonfatal acute myocardial infarction, coronary revascularization, and ischemic stroke, were assessed during clinical follow-up after ICA.

Results: During a median follow-up of 6.3 years (interquartile range, 2.8-8.9 years), there were 153 cases of MACE (13.8%). Patients with MACE had a higher aPP compared to those without MACE (83.0 ± 25.3 vs. 62.9 ± 18.1 mmHg; P < 0.001). Kaplan-Meier survival analysis demonstrated that a higher aPP (≥78 mmHg) was associated with an increased risk of MACE (log-rank P < 0.001). Multiple Cox regression analysis revealed that an increase in aPP by 10 mmHg was significantly associated with a higher risk of MACE, even after adjusting for potential confounders (hazard ratio, 1.68; 95% confidence interval, 1.49-1.82; P < 0.001).

Conclusion: Invasively measured aPP is a strong and independent predictor of long-term cardiovascular outcomes in patients undergoing ICA. aPP could be a valuable addition to current risk assessment tools in this high-risk population.

Introduction: Treatment-resistant hypertension (TRH) is defined as uncontrolled blood pressure despite the use of ≥3 antihypertensive medications at maximum tolerated doses. It is associated with increased risks of cardiovascular events, kidney disease, and mortality. White-coat hypertension, nonadherence, and inappropriate drug combinations overestimate its prevalence. The exact cause of TRH remains unclear, though obesity, obstructive sleep apnoea, and sympathetic overactivity may contribute. This study aimed to better understand the factors associated with true TRH.

Methods: Adult patients with treated hypertension without confirmed secondary causes from the West Midlands Hypertension Centre, UK were recruited for comprehensive evaluation. Patients underwent thorough clinical assessment, including tests for endothelial function, body composition, arterial stiffness, sleep study, and inflammation and endothelial biomarkers; comparing true TRH with non-TRH patients.

Results: Of 141 patients, 60 (43%) had true TRH after excluding whitecoat effect, secondary hypertension and medication nonadherence. The TRH patients were significantly older, had a longer duration of hypertension, and more frequently had diabetes. They had higher rates of left ventricular hypertrophy, higher extracellular water, lower eGFR, and higher urine albumin. They also had higher cardiac biomarkers, (serum NT-proBNP and hs-troponin), inflammatory markers (serum free light chains), aldosterone:renin ratio, and serum Endothelin-1. There was no difference between the groups in adjusted arterial stiffness, reactive hyperaemia or overnight pulse oximetry. Multivariate analysis identified only NT-proBNP as a significant factor associated with TRH (P = 0.027).

Conclusion: The FACT-RHY study provides valuable insights into the possible pathophysiological mechanisms of TRH. These results emphasize the need for further research into the mechanisms underlying TRH and potential management strategies.

Objective: The relation between classical orthostatic hypotension (cOH) and supine hypertension is largely unknown. We investigated the relative contributions of heart rate (HR), stroke volume (SV) and total peripheral resistance (TPR) to supine and upright blood pressure (BP).

Methods: In this retrospective study, tilt tests were divided in four groups: 19 normotensive and 61 hypertensive controls, 50 cOH patients with SH (cOH/SH+) and 30 without (cOH/SH-). Hypertension was defined as supine SBP at least 140 mmHg. We used linear regression to relate cOH severity to supine SBP, and the logratio method to analyse relative contributions of HR, SV and TPR. P values less than 0.003 were considered significant.

Results: High supine SBP was associated with high TPR in patients and controls. Orthostatic SBP decrease in cOH was larger in those with higher supine SBP. The main parameter explaining this effect was a high supine TPR that did not increase after tilt in cOH/SH+ compared to cOH/SH- (logratio difference, P  < 0.002). SV logratio decreased more in cOH/SH- than in cOH/SH+ ( P  < 0.003), and HR logratio contributed similarly to orthostatic SBP in both cOH groups ( P  = 0.028).

Conclusion: While high supine TPR explained SH, a failure to further increase upright TPR explained the orthostatic SBP fall in patients. Autonomic failure can explain the SBP fall but not directly the high supine TPR that causes SH. We assume that slow-acting humoral vasoconstrictors are triggered in the upright position and continue to act after tilting back, causing high TPR and SH.

Obstructive sleep apnea (OSA) is a common disorder in the general population and individuals with hypertension. We reviewed the literature on the prevalence of OSA in hypertension and hypertension subgroups. The current literature shows a high prevalence of OSA in patients with nocturnal and resistant hypertension, up to more than 90% in patients with refractory hypertension. The prevalence of OSA in patients with primary aldosteronism is greater than 45%. We also conducted an Italian national survey to assess the diagnostic approach to OSA in centers associated with European and Italian Societies of Hypertension. The median rate of OSA diagnosis was 10 patients/year, with a higher rate in Excellence Centers. The most common criterion for OSA screening was the combination of hypertension, snoring, and daytime somnolence (90%), followed by hypertension and a nondipping profile (55%). Resistant hypertension was considered a criterion by only 23% of the specialists.

Background: Renal denervation (RDN) has been approved in Europe and the United States and is recommended by the ESH and ESC hypertension guidelines as a therapeutic option for patients with resistant or uncontrolled hypertension. The aim of this study was to evaluate the long-term outcomes of radiofrequency (RF) RDN in a cohort of patients treated at an ESH center of excellence, with a mean follow-up of 8  years, and to review current evidence on the durability and safety of the procedure.

Methods: From a pool of patients with uncontrolled hypertension who had previously undergone RF RDN, we included those with a follow-up longer than 3  years ( n  = 97). Baseline and follow-up data were collected for each patient, including office blood pressure (OBP), ambulatory blood pressure (ABP), use of antihypertensive medication, and markers of renal function. A propensity-matched control group of patients with resistant hypertension managed conservatively (without RDN) was selected for comparison. All-cause mortality and nonfatal cardiovascular events were recorded. Additionally, we conducted a systematic review and meta-analysis of studies reporting RDN outcomes with follow-up periods exceeding 3 years.

Results: A total of 76 patients (mean age 61.4 ± 10.5 years, 25% female) had follow-up data over a mean of 8.3 ± 3.4 years. OBP decreased significantly from baseline by 21.8 ± 16.9 mmHg systolic and 13.1 ± 9.6 mmHg diastolic ( P  < 0.001 for both). In 41 patients with ABP data, systolic ABP decreased by 19.4 ± 13.1 mmHg and diastolic ABP by 12.7 ± 10.0 mmHg ( P  < 0.001 for both). The number of prescribed antihypertensive medications was reduced by 0.54 ± 1.2 ( P  < 0.01). By the end of follow-up, 9 of the 97 RDN patients (9.3%) had died, compared with 5 of 44 control patients (11.4%) over a mean follow-up of 8.1 ± 2.3 years. Twelve patients were lost to follow-up. Estimated glomerular filtration rate declined significantly in the RDN group from 83.0 ± 14.4 to 75.5 ± 19.2 mL/min/1.73 m 2 ( P  < 0.001). A meta-analysis of eight studies, including ours, with a mean follow-up of 8.7 years, showed a reduction in 24-h systolic ABP of -15.7 mmHg [95% confidence interval (CI): -18.4 to -13.0] and diastolic ABP of -9.2 mmHg (95% CI: -10.5 to -7.9), consistent with our findings. No major adverse events were reported.

Conclusion: RDN is a safe procedure that provides durable antihypertensive effects lasting for at least 8 years.