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Background: While arterial stiffening is a known risk factor for cardiovascular diseases, it remains unclear whether there is an early vascular aging (EVA) in patients who have experienced acute ischemic stroke (AIS). This systematic review and meta-analysis aims to investigate whether patients with AIS exhibit EVA through pulse wave velocity (PWV) measurements shortly after the stroke onset, shedding light on the relationship between arterial stiffness, hypertension, and stroke., Methods: Thirteen case-control studies were included, comparing PWV measurements between AIS patients and non-AIS individuals. A meta-analysis was performed to compare PWV levels, age, blood pressure, and the prevalence of different cardiovascular risk factors among 1711 AIS patients and 1551 controls., Results: Despite AIS patients showing higher PWV compared to controls (mean difference: 1.72 m/s, 95 % CI: 1.05-2.38, p < 0.001; I 2 = 88.3 %), their age did not significantly differ (95 % CI: -0.47-0.94, p = 0.519; I 2 = 0 %), suggesting EVA in AIS patients. Moreover, AIS patients exhibited elevated systolic and diastolic blood pressure and had higher odds of smoking, hypertension, diabetes, and male gender compared to controls., Conclusions: This study's findings underscore the presence of EVA in AIS patients, evident through increased PWV measurements shortly after stroke onset. Notably, smoking, hypertension, and diabetes mellitus emerge as substantial factors contributing to accelerated arterial stiffness within this population., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: The association between blood pressure (BP) levels and BP variability (BPV) following acute ischaemic stroke (AIS) and outcome remains controversial., Aims: To investigate the predictive value of systolic BP (SBP) and diastolic BP (DBP) and BPV measured using 24-h ambulatory blood pressure monitoring (ABPM) methods during AIS regarding outcome., Methods: A total of 228 AIS patients (175 without prior disability) underwent ABPM every 20 min within 48 h from onset using an automated oscillometric device (TM 2430, A&D Company Ltd) during day time (7:00-22:59) and night time (23:00-6:59). Risk factors, stroke subtypes, clinical and laboratory findings were recorded. Mean BP parameters and several BPV indices were calculated. End-points were death and unfavourable functional outcome (disability/death) at 3 months., Results: A total of 61 (26.7%) patients eventually died. Multivariate logistic regression analysis revealed that only mean night-time DBP (hazard ratio (HR): 1.04; 95% confidence interval (CI): 1.00-1.07) was an independent prognostic factor of death. Of the 175 patients without prior disability, 79 (45.1%) finally met the end-point of unfavourable functional outcome. Mean 24-h SBP (HR: 1.03; 95% CI: 1.00-1.05), day-time SBP (HR: 1.02; 95% CI: 1.00-1.05) and night-time SBP (HR: 1.03; 95% CI: 1.01-1.05), SBP nocturnal decline (HR: 0.93; 95% CI: 0.88-0.99), mean 24-h DBP (HR: 1.08; 95% CI: 1.03-1.13), day-time DBP (HR: 1.07; 95% CI: 1.03-1.12) and night-time DBP (HR: 1.06; 95% CI: 1.02-1.10) were independent prognostic factors of an unfavourable functional outcome., Conclusions: In contrast with BPV indices, ABPM-derived BP levels and lower or absence of BP nocturnal decline in the acute phase are prognostic factors of outcome in AIS patients., (© 2022 Royal Australasian College of Physicians.)

Objective: The purpose of this study was to investigate the association of blood pressure (BP) time-in-target range (TTR) derived from 24-h ambulatory BP monitoring (ABPM) during the acute phase of ischemic stroke (AIS), with the severity of stroke and its predictive value for the 3 months outcome., Methods: A total of 228 AIS patients (prospective multicenter follow-up study) underwent ABPM every 20 min within 48 h from stroke onset using an automated oscillometric device. Clinical and laboratory findings were recorded. Mean BP parameters, BP variability and TTR for SBP (90-140 mmHg), DBP (60-90 mmHg), and mean arterial pressure (MAP) were calculated. Endpoints were death and disability/death at 3 months., Results: A total of 14 942 BP measurements were recorded (∼66 per AIS patient) within 72 h of stroke onset. Patient's 24-h TTR was 34.7 ± 29.9, 64.3 ± 24.2, and 55.3 ± 29.4% for SBP, DBP and MAP, respectively. In patients without prior hypertension, TTR was lower as stroke severity increased for both DBP (P = 0.031) and MAP (P = 0.016). In 175 patients without prior disability, increase in TTR of DBP and MAP associated significantly with a decreased risk of disability/death (hazard ratio 0.96, 95% CI 0.95-0.99, P = 0.007 and hazard ratio 0.97, 95% CI 0.96-0.99, P = 0.007). TTR of SBP in 130-180 mmHg and 110-160 mmHg ranges seems to be related with mortality and disability outcomes, respectively., Conclusion: TTR can be included for a more detailed description of BP course, according to stroke severity, and for the evaluation of BP predictive role, in addition to mean BP values, derived from ABPM during the acute phase of AIS., Clinical Trial Registrationurl: http://www.clinicaltrials.gov. Unique identifier: NCT01915862., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

The effect of antihypertensive drugs on lipoprotein subfraction profile is still under investigation. In this study the effects of fixed combination of valsartan with either amlodipine (V-A) or hydrochlorothiazide (V-H) on low-density-lipoprotein (LDL) and high-density-lipoprotein (HDL) subfraction profile of patients with stage 2 or 3 hypertension were assessed. A total of 60 drug-naive patients were randomized to either V-A (160/5 mg, n=30) or V-H (160/12.5 mg, n=30). At baseline as well as 16 weeks post-treatment analysis of the LDL and HDL subfraction profile was conducted by using LDL Lipoprint System. Both V-A and V-H effectively reduced blood pressure (BP) to similar levels. An increase in the cholesterol concentration of small-dense LDL subfractions (by 18.2%, P<0.05) was observed in the V-H group, whereas this parameter remained unchanged in the V-A group. Therefore, mean LDL particle size was decreased in the V-H group (from 267 ± 5 to 266 ± 5Å, P<0.05). HDL-Cholesterol (HDL-C) levels were reduced by 4.7% (P<0.05) in the V-H group, mirrored by a reduction in the cholesterol mass of small and intermediate HDL particles. In conclusion, despite similar reductions in BP, V-H combination may adversely affect serum lipids as well as LDL and HDL subfraction profile as compared with V-A.

Antihypertensive pharmacologic treatment may be associated with diverse disturbances of electrolyte homeostasis. These drug-induced disorders are relatively common, typically including hyponatraemia, hypokalaemia, hyperkalaemia, hypomagnesaemia, hypophosphataemia and hypercalcaemia. Diuretics, beta-blockers, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are particularly likely to cause these complications. Recognised risk factors include high-dosage regimens (especially diuretics), old age, diabetes and impairment of renal function. Strategies to prevent these adverse drug reactions involve careful consideration of risk factors and clinical and laboratory evaluation in the course of treatment.

Hypertension (HT) is highly prevalent in rheumatoid arthritis (RA). Serum uric acid (SUA) has been associated with HT in the general population. The mutual exclusion of gout and RA, and the systemic inflammatory component of RA may alter this association in this patient population. We explored a potential association between SUA levels and HT in RA and evaluated whether this association is independent of HT risk factors, RA characteristics and relevant drugs. A total of 400 consecutive RA patients were assessed. SUA and complete biochemical profile were measured. Demographic, HT-related factors, RA characteristics and drugs were assessed as potential covariates. Results were analysed using binary logistic models to test the independence of the association between SUA and HT. SUA levels were higher in hypertensive compared to normotensive RA patients (5.44+/-1.6 mg dl(-1) (323.57+/-95.17 micromol l(-1)) vs 4.56+/-1.1 mg dl(-1) (271.23+/-65.43 micromol l(-1)), P<0.001). When adjusted for HT risk factors, renal function, RA characteristics, non-steroidal anti-inflammatory drugs, oral prednisolone, cyclosporine, leflunomide and low-dose aspirin, the odds of being a hypertensive RA patient per 1 mg dl(-1)(59.48 micromol l(-1)) SUA increase were significantly increased: OR=1.59 (95% CI: 1.21-2.1, P=0.001). This was also significant for the subgroup of patients who were not on diuretics (OR=1.5, 95% CI: 1.1-2.05; P=0.011). This cross-sectional study suggests that SUA levels are independently associated with HT in RA patients. Prospective longitudinal studies are needed to confirm and further explore the causes and implications of this association.

Objectives: Rheumatoid arthritis (RA) associates with excessive cardiovascular morbidity and mortality. Hypertension (HT) contributes significantly to the development of cardiovascular disease (CVD). Little is known about the factors that influence blood pressure (BP) in patients with RA. In this study, we assessed the prevalence of HT in a secondary care cohort of RA patients, and aimed to identify factors associated with its presence and inadequate control., Methods: A total of 400 consecutive RA patients were studied. HT was defined as systolic BP >/=140 mmHg and/or diastolic BP >/=90 mmHg or current use of antihypertensive drugs. The association of HT with several demographic and RA-related factors, comorbidities and drugs was evaluated using logistic regression., Results: HT was present in 282 (70.5%) patients. Of those, 171 (60.6%) received anti-hypertensive therapy, but 111 (39.4%) remained undiagnosed. Of those treated, only 37/171 (21.8%) were optimally controlled. Multivariable logistic regression revealed age (OR = 1.054, CI: 1.02 to 1.07, P = 0.001), body mass index [BMI (OR = 1.06, CI: 1.003-1.121, P = 0.038)] and prednisolone use (OR = 2.39, CI: 1.02-5.6, P = 0.045) to be independently associated with the presence of HT. BMI (OR = 1.11, CI: 1.02-1.21, P = 0.002) and the presence of CVD (OR = 4.01, CI: 1.27-12.69, P = 0.018) associated with uncontrolled HT., Conclusions: HT is highly prevalent in RA, under-diagnosed particularly in the young, and under-treated particularly in old RA patients with CVD. RA patients receiving steroids should be specifically targeted for screening and treatment; those with any cardiovascular comorbidity may require particularly aggressive monitoring and treatment strategies.

Objective: To record the prevalence of overweight, obesity and hypertension in primary schoolchildren living in one of the poorest regions in Europe and furthermore to identify certain behavioural, lifestyle and physiological parameters associated with body mass index (BMI) and blood pressure (BP)., Design: Cross-sectional study., Setting: Nineteen primary schools within the county of Ioannina, Greece., Subjects and Methods: Demographic, dietary and physical activity data as well as anthropometrical, BP and cardiorespiratory fitness measurements were obtained from a representative sample of 312 school children (153 boys and 159 girls) attending 5th grade. Inclusion of subjects in the study was voluntary. One-way analysis of variance and multiple linear regression analysis were mainly applied for the evaluation of the tested hypotheses., Results: The prevalence of overweight and obesity was 29.4 and 11.8% for boys and 39.0 and 7.5% for girls. The prevalence of systolic and diastolic hypertension was 28.1 and 7.8% for boys and 26.4 and 17.0% for girls. Furthermore, BMI and BP (systolic and diastolic) were positively related to frequency of fast food meals (rho: + 0.28, P = 0.033, rho: + 1.09, P = 0.03 and rho: +0.86, P = 0.014, respectively) but negatively to leisure time physical activity (rho: -5.55, P = 0.005, rho: -3.32 x 10(-2), P < 0.001 and rho: -2.08 x 10(-2), P < 0.001, respectively)., Conclusions: The current study revealed an increased prevalence of overweight, obesity and hypertension among schoolchildren in Ioannina, indicating the need for early preventive measures in one of the less privileged regions of Europe.

The assessment of global cardiovascular risk is an essential step in the management of atherosclerotic disease prevention. Among the risk factors to be addressed are hypertension and hyperlipidaemia; these commonly coexist. A neutral or lipid-friendly antihypertensive agent is probably useful in the presence of lipid abnormalities. Similarly, statins have been shown to decrease cardiovascular risk in hypertensive patients. There is also experimental and clinical evidence that statins have blood pressure (BP)-lowering effects. In this review, we discuss the beneficial effects of statins on BP, and provide an overview of the underlying pathophysiology. We also consider the evidence justifying the use of statins in the management of hypertensive patients.

Objective: A number of adverse metabolic effects are associated with indapamide administration, including an increase in serum uric acid levels. It has been reported that losartan can significantly decrease serum uric acid levels. However, there are no data on the effects of combination therapy of losartan with indapamide on uric acid metabolism., Methods: We studied 20 hypertensive patients in whom serum metabolic parameters, including uric acid levels in serum and urine, were studied before and after eight weeks of indapamide administration (2.5 mg once daily) as well as eight weeks after combination treatment with indapamide (2.5 mg once daily)and losartan (50 mg/day)., Results: Indapamide evoked a significant decrease in systolic and diastolic blood pressure from a mean value of 157 +/- 12 mmHg/96 +/- 10 mmHg to a mean value of 139 +/- 14 mmHg/92 +/- 5 mmHg (p<0.01 for both comparisons). However, a significant increase in serum uric acid levels was noticed after indapamide administration (from a mean value of 4.9 +/- 1.6 mg/dl to a mean value of 5.9 +/- 1.2 mg/dl, p<0.01), associated with a decrease in the fractional excretion of uric acid(from a mean value of 9 +/- 5% to a mean value of 7 +/- 5.5%, p<0.05). The addition of losartan caused a further decrease in blood pressure from a mean value of 139 +/- 14 mmHg/92 +/- 5 mmHg to a mean value of 120 +/- 15 mmHg/84 +/- 4 mmHg (p<0.01 for both comparisons). This was followed by a significant decrease in serum uric acid levels to 5 +/- 1.1 mg/dl(p<0.01) due to a substantial increase in fractional urate excretion (from 7 +/- 5.5 to 8.7 +/- 6%, p<0.05)., Conclusion: The addition of losartan could offset the hyperuricaemic effect of indapamide administration.

A number of studies have shown that hyperuricaemia is associated with an increased incidence of coronary heart disease. It has been proposed that the elevated serum uric acid levels are linked to other risk factors, such as hypertension, dyslipidaemia and diabetes. Hyperuricaemia is commonly encountered in patients with essential hypertension and is considered as a risk factor for morbidity and mortality associated with hypertension. In addition, lipid abnormalities (mainly hypertriglyceridaemia) are also found more frequently in hypertensive patients than in normotensives. There is evidence that the angiotensin II receptor antagonist, losartan, increases urate excretion by reducing reabsorption of urate in the renal proximal tubule. It is also known that fibric acid derivatives (fibrates) have several beneficial actions in addition to their lipid-lowering capacity. Fenofibrate administration is associated with a uric acid lowering effect. In this respect, we present two patients with hypertension and dyslipidaemia together with elevated serum uric acid levels. We also discuss (in the format of questions and answers) the pathophysiological mechanisms underlying the association of serum uric acid with cardiovascular disease, and we review the relevant literature to justify an evidence-based decision to choose an antihypetensive agent (losartan) or a lipid-lowering drug (fenofibrate) with an additional hypouricaemic effect.

Hypertension is another predictor of erectile dysfunction (ED). This is further evidence supporting a link between the pathogenesis of atherosclerotic disease and ED. In one study (TOMHS) involving hypertensive patients, the incidence of ED was 14.4%. The drugs used to treat hypertension may cause ED. However, there is little trial-based evidence to indicate which drugs are more likely to cause this side effect. In general, thiazide diuretics and beta-blockers seem to cause ED more often. In contrast, the alpha-blocker, doxazosin, has not been associated with an increased incidence of ED as a side effect. Doxazosin also improves urinary flow in patients with benign prostatic hyperplasia (BPH). This condition is common in elderly men as is hypertension and ED. Therefore, doxazosin may present a special advantage among this group of patients. This alpha-blocker would also be a good choice in patients with impaired glucose tolerance/diabetes because it improves insulin sensitivity. Moreover, ED and hypertension are more prevalent among diabetics. On a more speculative note, doxazosin may potentiate the therapeutic impact of specific treatments for ED.