Reduction In Systolic Blood Pressure Levels Research Articles

The Effect of Tirzepatide on Weight, Lipid Metabolism and Blood Pressure in Overweight/Obese Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.

To explore the effects of Tirzepatide (TZP), a new hypoglycemic drug, on weight, blood lipids and blood pressure in overweight/obese patients with type 2 diabetes mellitus (T2DM). Relevant studies investigating the influence of TZP therapy on weight, lipid profiles and blood pressure in overweight/obese T2DM patients were selected from the PubMed, Embase, Web of Science and Cochrane databases from establishment until November 2022. A systematic review and meta-analysis were conducted to evaluate the effect of TZP on weight, blood lipids and blood pressure in overweight/obese patients with T2DM. Eight randomized controlled trials (RCTs), comprising 7491 patients with T2DM, were included in the meta-analysis. Results showed that compared with the glucagon-like peptide-1 receptor agonist (GLP-1RA), insulin, and placebo groups, body weight, triglycerides (TG), very low-density lipoprotein cholesterol (VLDL-C), total cholesterol (TC), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), and glycosylated hemoglobin (HbA1c) levels were significantly decreased in the TZP-treated groups, while high-density lipoprotein cholesterol (HDL-C) levels increased. With the gradual increase of TZP doses, the proportions of T2DM patients with weight loss >5% gradually increased. The 10 mg and 15 mg TZP doses had a stronger effect on the levels of TG, VLDL-C, and HDL-C. Moreover, the reduction in SBP levels in the 15 mg TZP-treated group was more pronounced than those in the 10 mg and 5 mg TZP-treated groups [MD=-2.07, 95% CI (-2.52, -1.63) and MD=-3.14, 95% CI (-4.42, -1.87)]. Compared with GLP-1RA, insulin, and placebo groups, the proportions of patients with HbA1c<7% in 10mg and 15mg TZP-treated groups were significantly higher than in the 5mg TZP-treated group [OR=1.53, 95% CI (1.25, 1.8)], OR=1.7, 95% CI (1.15, 2.50)].There was no significant difference regarding the risk of adverse reactions.

Use of the Cardiovascular Polypill in Secondary Prevention of Cerebrovascular Disease: A Real-Life Tertiary Hospital Cohort Study of 104 Patients

Background: The use of the cardiovascular polypill, a fixed-dose combination treatment, is conceived to improve adherence. However, randomized controlled trials (RCTs) may overestimate it. Studies focusing on cerebrovascular disease and real-life efficacy compared with conventional treatment are lacking. Methods: This is a retrospective, hospital-based cohort study of acute ischaemic stroke patients who were prescribed a polypill (aspirin 100 mg, atorvastatin 20/40 mg, ramipril 2.5/5/10 mg) versus conventional treatment (aspirin 100 mg and other blood pressure/lipid-lowering agents) in secondary prevention (2017–2018). Clinical records were reviewed 90 days after discharge for stroke recurrence, vascular risk factor control, and safety. Adherence was assessed using the adapted Morisky-Green scale. Results: A total of 104 patients were included (61% male; mean age 69.7 ± 13.9 years); 54 were treated with the polypill and 50 with conventional treatment. No baseline differences in clinical or demographic variables were detected. No recurrences were registered in the polypill group, compared to 1 recurrence in the conventional treatment group. A significant reduction of systolic blood pressure (SBP) was achieved in the polypill group (12.1 mm Hg) compared to the conventional treatment group (6.8 mm Hg) (p = 0.002). No significant differences were detected regarding the goal of LDL cholesterol ≤70 mg/dL (41 vs. 44%). The adverse events were mild and their frequency was similar in the two groups (9 vs. 2%, ns). Adherence was similarly good in the two groups (93 vs. 88%, ns). Polypill group adherence was similar to that reported in a previous meta-analysis of RCTs (93 vs. 84%, ns). Conclusion: In our experience, the cardiovascular polypill achieved a higher reduction in SBP levels and was well tolerated. Adherence was similar to that found in the previous literature, which is remarkable given the real-life setting of our study.

The Effects of Coenzyme Q10 Supplementation on Blood Pressures Among Patients with Metabolic Diseases: A Systematic Review and Meta-analysis of Randomized Controlled Trials.

Although several trials have assessed the effect of coenzyme Q10 (CoQ10) supplementation on blood pressures among patients with metabolic diseases, findings are controversial. This review of randomized controlled trials (RCTs) was performed to summarize the evidence on the effects of CoQ10 supplementation on blood pressures among patients with metabolic diseases. Randomized-controlled trials (RCTs) published in PubMed, EMBASE, Web of Science and Cochrane Library databases up to 10 August 2017 were searched. Two review authors independently assessed study eligibility, extracted data, and evaluated risk of bias of included studies. Heterogeneity was measured with a Q-test and with I2 statistics. Data were pooled by using the fix or random-effect model based on the heterogeneity test results and expressed as standardized mean difference (SMD) with 95% confidence interval (CI). A total of seventeen randomized controlled trials (684 participants) were included. Results showed that CoQ10 supplementation significantly decreased systolic blood pressure (SBP) (SMD -0.30; 95% CI -0.52, -0.08). However, CoQ10 supplementation decreased diastolic blood pressure (DBP), but this was not statistically significant (SMD -0.08; 95% CI -0.46, 0.29). CoQ10 supplementation may result in reduction in SBP levels, but did not affect DBP levels among patients with metabolic diseases. Additional prospective studies regarding the effect of CoQ10 supplementation on blood pressure in patients with metabolic diseases are necessary.

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Objective: Cardiovascular disease is the principal cause of death worldwide. Although the dose-response relationship between stress and hypertension is well established, there is a paucity of non-pharmaceutical intervention programs. The purpose of this study was to investigate the effectiveness of a stress management and lifestyle change program on blood pressure (BP) control and psychosocial wellbeing. Design and method: This was a quasi-experimental design with a waitlist control group in Attica, Greece, which was funded from EPANAD 2007–2013 (N = 553, 50% women and mean age 52.4 ± 8.46 years). The study comprised of an 8-week stress management and lifestyle change program including weekly sessions of stress management, dietary counseling, physical exercise and psychoeducation. Pre- and post- intervention BP measurements and psychosocial wellbeing factors were assessed. Results: Post-intervention there was a statistically significant reduction in systolic BP levels (mean: 126.05 vs 129.37, p < 0.001, intervention (IG) and control (CG) group, respectively). A 35.7% of the IG receded BP category vs. 17.5% of the CG (p < 0.001). After controlling for gender, age, educational level and BP cutoffs, we found significant improvements in stress, anxiety, self-esteem, spirituality, body weight, hours of sleep and in the subscales of the Healthy Lifestyle and Personal Control Questionnaire. Concerning the sub-categories of chance and powerful others in the health locus of control scale, improvements were recorded for the individuals of tertiary education. Conclusions: This non-pharmaceutical stress management and lifestyle change program resulted in significant benefits for regulation of BP, as well as for body weight, lifestyle and the psychosocial wellbeing of the participants. Future non-pharmaceutical programs are strongly encouraged both for the clinical and the community settings.

Renin-angiotensin system blockade and exercise-induced increase in aortic stiffness.

In physiological conditions, the cushioning function of central conduit arteries transforms the cyclic high-flow and pressure oscillations in the ascending aorta into continuous and low-pressure blood flow at the level of microcirculation. Aging and elevated blood pressure (BP) induces structural and functional changes in arterial wall viscoelastic properties, resulting in arterial stiffening. The latter is reflected in progressive impairment of the cushioning function of central arteries and is typically associated with the development of isolated systolic hypertension and left ventricular hypertrophy. Importantly, prospective cohort studies have demonstrated that arterial hardening represents a strong and independent predictor of all-cause and cardiovascular mortality in various diseased populations, including patients with essential hypertension. Current guidelines on the management of arterial hypertension recommend regular physical activity as a major nonpharmacologic treatment approach towards BP lowering and cardiovascular risk reduction. In contrast, several lines of evidence from clinical studies suggest that acute high-intensity exercise can transiently elevate the risk of fatal and nonfatal cardiovascular events, mainly in prediposed individuals with substrate of structural cardiovascular disease. The mechanistic background of this deleterious impact of acute exercise on the cardiovascular system remains largely unclear. Activation of the sympathetic nervous system, aggravation of oxidative stress, platelet activation, impaired coagulation and fibrinolysis, and acute deterioration of large artery elasticity represent some of the mechanisms that have been proposed to be involved. It has to be noted that the type, frequency, duration, and intensity of physical exercise, play an important role in the exercise-induced alterations on the cardiovascular system. In this regard, previous clinical studies that investigated the effects of acute exercise on arterial elasticity, provide variable results. Some studies have shown high-intensity exercise to be associated with an acute increase in stiffness of central conduit arteries in healthy individuals. In other clinical studies, maximal aerobic exercise was found not to acutely affect large artery elasticity in young healthy patients. In contrast to the above, other investigators observed a sustained and prolonged improvement in compliance of peripheral muscular-type arteries and no change in elasticity of central conduit arteries after submaximal acute exercise in healthy patients. In this issue of The Journal of Clinical Hypertension, Gkaliagkousi and coworkers add important information to our knowledge, in this area, by reporting the results of a clinical study that explored acute changes in aortic stiffness after a high-intensity aerobic exercise test: (1) in untreated hypertensive compared with normotensive individuals, and (2) in hypertensive patients after 3 months of treatment with the angiotensin receptor blocker (ARB), valsartan. The study included 25 young patients with never-treated, newly diagnosed, stage I hypertension and 15 ageand sexmatched healthy volunteers. The investigators performed a careful workup of patients prior to study enrollment, excluding patients with secondary causes of hypertension and patients with white-coat or masked hypertension by performing 24-hour ambulatory BP monitoring. Arterial stiffness was assessed by measuring carotid to femoral pulse wave velocity (cf-PWV) with the use of the Sphygmocor device (AtCor Medical, West Ryde, Australia) at maximal exercise and at 10, 30, and 60 minutes after the completion of a treadmill exercise test. At baseline exercise test, significant elevations in systolic BP were noted at maximal exercise in both, hypertensive patients and healthy controls, which returned to pre-exercise levels after 10 and 30 minutes of recovery, respectively. In contrast, diastolic BP was not significantly different during acute high-intensity exercise, in both study groups. With regards to exercised-induced changes in aortic stiffness, cf-PWV was significantly elevated at maximal exercise in the group of hypertensive patients but not in the group of healthy controls. Of importance, despite the post-exercise reduction in systolic BP levels, the increase in cf-PWV persisted, even after 30 minutes of recovery in hypertensive patients. As expected, systolic BP and cf-PWV levels at all 5 timepoints of the baseline exercise test were significantly higher in hypertensive patients than in controls. After completion of the baseline test, 15 hypertensive participants who had indications to receive BP-lowering therapy according to guidelines were included in a subsequent interventional phase of the study to receive treatment with valsartan 160 mg daily for 3 months. Valsartan treatment resulted in significant reductions in both office and ambulatory BP and all treated hypertensive patients achieved adequate BP control at study Address for correspondence: Pantelis E. Zebekakis, MD, PhD, Section of Nephrology and Hypertension, 1st Department of Medicine, AHEPA University Hospital, St. Kiriakidi 1, GR54636, Thessaloniki, Greece E-mail: pzebeka@med.auth.gr

Abstract 204: Blood Pressure Reduction And Stroke Recurrence: The Progress Trial

Background: A recent observational analysis of a large-scale randomized controlled trial identified a “J-curve” phenomenon such that low and high blood pressure (BP) levels are associated with increased risks of recurrent stroke among patients with recent ischemic stroke. The objective of the present analysis was to determine whether larger reduction in BP associated with treatment increases the risks of recurrent stroke among patients with cerebrovascular disease. Methods: This is a subsidiary analysis of the PROGRESS trial, a randomized, placebo-controlled trial that established the beneficial effects of BP lowering in secondary prevention of stroke. A total of 6105 patients with prior stroke or transient ischemic attack were randomly assigned to either active treatment (perindopril ± indapamide) or matching placebo(s). There were no BP criteria for entry. BP was measured at every visit and groups of participants defined by reduction in systolic BP (SBP) from baseline (&lt;0, 0-9, 10-19 and ≧20 mm Hg) were used for these analyses. Outcomes of the present analyses were recurrent hemorrhagic and ischemic stroke. Results: During a mean follow-up of 3.9 years, 111 hemorrhagic stroke and 565 ischemic stroke events were observed. There were clear inverse associations between SBP reduction and the risk of hemorrhagic stroke even after adjustment for age, sex, region, baseline SBP, diabetes, current smoking and randomized treatment: adjusted annual incidence rates were 0.08%, 0.06%, 0.05% and 0.03% for participant groups defined by reduction in SBP levels of &lt;0, 0-9, 10-19 and ≧20 mm Hg, respectively. The lowest risks of hemorrhagic stroke were observed among patients who achieved ≧20 mm Hg reduction in SBP associated with treatment. Annual incidence of ischemic stroke was 2.19%, 1.74%, 1.73% and 1.72% for the same participant groups. Compared with patients who did not achieve any SBP reduction, the decreases in the risk of ischemic stroke were similar in the groups achieving SBP reductions of 0-9, 10-19 and ≧20 mm Hg. Conclusions: The present analysis provided no evidence of increase in recurrent stroke associated with larger reduction in SBP produced by BP lowering treatment among patients with cerebrovascular disease.

Cardiopulmonary and arterial baroreflex-mediated control of forearm vasomotor tone is impaired after acute stroke.

Elevated blood pressure (BP) levels are well recognized after acute stroke and are associated with increased BP variability. The underlying mechanisms producing such changes are unclear but may include abnormalities of baroreceptor-mediated control of heart rate and vasomotor tone. Lower body negative pressure (LBNP) can be used to assess the integrity of "low-pressure" cardiopulmonary and "high-pressure" arterial baroreceptor-derived responses by inducing nonhypotensive and hypotensive stimuli. Cardiovascular responses, including BP, heart rate, forearm blood flow, and forearm vascular resistance, to nonhypotensive and hypotensive LBNP were assessed in 13 consecutive stroke patients. Patients were studied within 72 hours of stroke (acute) and again at 10 to 14 days (subacute) and were compared with 13 control subjects individually matched for age, sex, and BP. At an LBNP of -10 mm Hg, BP was unchanged in all groups, but a significant increase in forearm vascular resistance occurred only in the control group (11 U [interquartile range, 7 to 15]; P < .05) compared with stroke patients in the acute (9 U [3 to 14]; P = NS) or subacute phases (7 U [2 to 12]; P = NS). After LBNP at -40 mm Hg, the reductions in systolic BP levels were similar in all groups (control: -9 mm Hg [-16 to -3]; acute stroke: -9 mm Hg [-22 to 3]; subacute stroke: -7 mm Hg [-35 to 20]), as was the associated increase in heart rate (control: 8 bpm ([4 to 11]; acute stroke: 6 bpm ([1 to 12]; subacute stroke: 9 bpm [2 to 19]). However, forearm vascular resistance increased significantly only in control subjects (20 U [9 to 30]; P < .01). The present study has identified abnormal vasomotor responses to LBNP after acute stroke, with an increase in FVR only being observed in control subjects in response to nonhypotensive and similar hypotensive levels of LBNP. In acute stroke patients, the stimulus of hypotensive LBNP appears to be compensated by an increase in cardiac output since there appears to be no increase in peripheral vascular resistance, unlike the changes seen in control subjects. However, the exact mechanisms for these changes are still unclear and are the subject of further study.

Comparison of Relaxation Techniques, Routine Blood Pressure Measurements, and Self-Learning Packages in Hypertension Control

Background.Even though the effectiveness of meditation and relaxation skills is controversial in blood pressure control, extensive field studies are limited. A national study targeting 50 communities randomly selected from northern Taiwan was conducted to test and compare the effectiveness of hypertension control incorporating three strategies.Methods.Five hundred ninety hypertensives identified from 3,128 adults at a screening survey among the 50 communities were invited to participate in the study and were randomly assigned to three treatment modalities, (a) relaxation techniques training at home, (b) routine blood pressure measurement by a health professional, and (c) reading self-learning packages, or to a control group.Results.After a 2-month intervention period, the three treatment groups showed a significant reduction in systolic blood pressure levels compared with the control group (11.O mm Hg for group 1, 9.2 mm Hg for group 2, and 5.1 mm Hg for group 3). The relax-ation group had the most significant reduction insystolic blood pressure levels, followed by the rou-tine blood pressure monitoring group and the self-learning group. However, the effect of relaxation training at home was not significantly greater than routine blood pressure measurement by a health professional.