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Importance: High visit-to-visit blood pressure variability (BPV) in late life may reflect increased dementia risk better than mean systolic blood pressure (SBP). Evidence from midlife to late life could be crucial to understanding this association., Objective: To determine whether visit-to-visit BPV at different ages was differentially associated with lifetime incident dementia risk in community-dwelling individuals., Design, Setting, and Participants: This cohort study analyzed data from the Adult Changes in Thought (ACT) study, an ongoing population-based prospective cohort study in the US. Participants were 65 years or older at enrollment, community-dwelling, and without dementia. The study focused on a subset of deceased participants with brain autopsy data and whose midlife to late-life blood pressure data were obtained from Kaiser Permanente Washington medical archives and collected as part of the postmortem brain donation program. In the ACT study, participants underwent biennial medical assessments, including cognitive screening. Data were collected from 1994 (ACT study enrollment) through November 2019 (data set freeze). Data analysis was performed between March 2020 and September 2023., Exposures: Visit-by-visit BPV at ages 60, 70, 80, and 90 years, calculated using the coefficient of variation of year-by-year SBP measurements over the preceding 10 years., Main Outcomes and Measures: All-cause dementia, which was adjudicated by a multidisciplinary outcome adjudication committee., Results: A total of 820 participants (mean [SD] age at enrollment, 77.0 [6.7] years) were analyzed and included 476 females (58.0%). A mean (SD) of 28.4 (8.4) yearly SBP measurements were available over 31.5 (9.0) years. The mean (SD) follow-up time was 32.2 (9.1) years in 27 885 person-years from midlife to death. Of the participants, 372 (45.4%) developed dementia. The number of participants who were alive without dementia and had available data for analysis ranged from 280 of those aged 90 years to 702 of those aged 70 years. Higher BPV was not associated with higher lifetime dementia risk at age 60, 70, or 80 years. At age 90 years, BPV was associated with 35% higher dementia risk (hazard ratio [HR], 1.35; 95% CI, 1.02-1.79). Meta-regression of HRs calculated separately for each age (60-90 years) indicated that associations of high BPV with higher dementia risk were present only at older ages, whereas the association of SBP with dementia gradually shifted direction linearly from being incrementally to inversely associated with older ages., Conclusions and Relevance: In this cohort study, high BPV indicated increased lifetime dementia risk in late life but not in midlife. This result suggests that high BPV may indicate increased dementia risk in older age but might be less viable as a midlife dementia prevention target.

Objectives: To systematically review and synthesize the evidence on differential associations between antihypertensive medication (AHM) classes and the risk of incident dementia., Design: Systematic review and random effects frequentist network meta-analysis. Embase, MEDLINE, and the Cochrane library were searched from origin to December 2019., Setting and Participants: Randomized controlled trials (RCTs) and prospective cohort studies that compared associations of different AHM classes with incident all-cause dementia and/or Alzheimer's disease over at least 1 year of follow-up., Measures: All cause dementia and/or Alzheimer's disease., Results: Fifteen observational studies and 7 RCTs were included. Data on AHM classes were available for 649,790 participants and dementia occurred in 19,600 (3.02%). Network meta-analysis showed that in observational studies, treatment with either calcium channel blockers (CCBs) or angiotensin II receptor blockers (ARBs) was associated with lower dementia risks than treatment with other antihypertensives: CCBs vs angiotensin converting enzyme inhibitors (ACE inhibitors) (HR=0.84, 95% CI 0.74-0.95), beta blockers (HR=0.83, 95% CI 0.73-0.95) and diuretics (HR=0.89, 95% CI 0.78-1.01) and ARBs vs ACE inhibitors (HR=0.88, 95% CI 0.81-0.97), beta blockers (HR=0.87, 95% CI 0.77-0.99), and diuretics (HR=0.93, 95% CI 0.83-1.05). There were insufficient RCTs to create a robust network based on randomized data alone., Conclusions and Implications: Recommending CCBs or ARBs as preferred first-line antihypertensive treatment may significantly reduce the risk of dementia. If corroborated in a randomized setting, these findings reflect a low-cost and scalable opportunity to reduce dementia incidence worldwide., (Copyright © 2020 AMDA – The Society for Post-Acute and Long-Term Care Medicine. Published by Elsevier Inc. All rights reserved.)

Objectives: This investigation was undertaken to compare diabetic and non-diabetic hypertensive patients with a first acute non-ST segment elevation myocardial infarction (NSTEMI) and to assess the impact of clinical and laboratory parameters on the occurrence of in-hospital complications., Methods: The study population comprised 112 consecutive male hypertensive patients with their first NSTEMI, who were divided into two groups according to the presence of type 2 diabetes mellitus. All patients underwent echocardiography and 24-h electrocardiographic (ECG) and blood pressure monitoring within 48 h from admission., Results: Diabetic hypertensive patients had significantly higher mean daytime, night-time, 24-h systolic blood pressure and heart rate and hypertensive peaks (P < 0.01), more episodes of asymptomatic ST segment depression (P < 0.05), which were also more severe and prolonged (P < 0.01), and more episodes of non-sustained ventricular tachycardia (P = 0.01). Diabetic patients showed a greater left ventricular mass index (LVMI) and a lower left ventricular ejection fraction (LVEF) (P < 0.01). In-hospital adverse clinical events were more frequent in diabetic hypertensives compared to non-diabetics (40.3% versus 18.1%, P = 0.01). In particular, heart failure occurred during hospitalization in 33.3% versus 14.5% (P = 0.02). The difference in transient cerebral ischaemic attacks did not reach statistical significance (7.0% versus 1.8%, P = 0.18). Multivariate Cox proportional hazards analysis showed that the only independent predictors for the occurrence of in-hospital adverse clinical events in diabetic patients were: 24-h systolic blood pressure variability [relative risk (RR) = 1.013, 95% confidence interval (CI) = 1.001-1.025, P = 0.03]; mean 24-h heart rate (RR = 7.05, 95% CI = 1.35-35.9, P = 0.02) and the LVMI (RR = 1.9, 95% CI = 1.121-3.785, P = 0.02)., Conclusions: This study indicates that in-hospital complications, including heart failure and transient cerebral ischaemia, occur frequently during the acute phase of a first NSTEMI in patients with both diabetes and hypertension. The coexistence of diabetes and hypertension doubles the risk of complications with respect to hypertension alone. In addition, adverse events may appear despite an initial uncomplicated clinical presentation, which can be predicted by the early assessment of heart rate and blood pressure behaviour and by the echocardiographic assessment of left ventricular mass.

Background: Increased sympathetic drive to the heart might contribute to the development and progression of myocardial damage in hypertensive patients (HTs). This study assessed the possible presence of abnormalities in myocardial uptake of (123)I-metaiodobenzylguanidine (MIBG), a marker of sympathetic activity, in HTs with left ventricular hypertrophy (LVH)., Methods: Eleven HTs with LVH and 10 matched normotensive controls underwent clinical and laboratory examination, as well as LVH determination by echocardiography. The presence of myocardial ischemia was ruled out by exercise stress testing. Global and regional myocardial uptake of (123)I-MIBG was determined in both groups using planar and single proton emission tomography scintigraphy. In addition, thallium-201 (Tl-201) myocardial scintigraphy was performed in HTs. The heart/mediastinum (H/M) ratio on planar (123)I-MIBG images at different time points was compared between HTs and controls. Moreover, regional cardiac uptake of (123)I-MIBG was compared between groups and, within the HTs group, with regional Tl-201 uptake., Results: At all study times, the H/M ratio was lower in HTs than in controls (all p <0.05). A significant reduction in (123)I-MIBG uptake in the mid-inferolateral and mid-inferior segments was observed in HTs compared to controls. Also, a significant reduction in (123)I-MIBG uptake compared to Tl-210 uptake was observed in non-septal segments of HTs., Conclusions: Cardiac abnormalities in global and regional uptake of (123)I-MIBG, as well as impaired (123)I-MIBG compared to Tl-201 uptake, are present in HTs with LVH. Given the effect of sympathetic nervous system on the heart, these abnormalities might play a role in hypertension-related cardiac damage.

In order to define cardiac hypertensive involvement a group of 25 consecutive elderly male hypertensive outpatients and 25 age-matched male normotensive controls underwent full non-invasive assessment of cardiac status by resting 12-lead electrocardiography, Doppler-echocardiographic examination and simultaneous ambulatory blood pressure and electrocardiographic monitorings. Elderly hypertensives showed a higher prevalence of electrocardiographic left ventricular hypertrophy, an increased echocardiographic left ventricular mass, an impaired left ventricular filling pattern and more frequent ventricular arrhythmias when compared with normotensive controls. In elderly patients, left ventricular mass was found to be correlated with 24-hour ambulatory blood pressure (r = 0.47, p < 0.01) and 24-hour ambulatory blood pressure variability (r = 0.52, p < 0.01), while ventricular arrhythmias were correlated with left ventricular mass (r = 0.52, p < 0.01), the Doppler synthetic index of diastolic function E/A ratio (r = -0.56, p < 0.01) and both 24-hour systolic (r = 0.54, p < 0.01) and diastolic (r = 0.59, p < 0.01) ambulatory blood-pressure variabilities. These data suggest that hypertension induces in elderly patients an impairment of cardiac structure and function comparable with that already shown in younger hypertensives. Therefore, the assessment of hypertensive target-organ damage currently employed in younger subjects should be also considered in elderly hypertensives, at least when no other relevant medical disease is present.

[123I]MIBG has been proposed as a suitable tracer of the adrenergic system of the heart. The aims of this study was to investigate the adrenergic functional status of the heart in hypertensive patients with left ventricular hypertrophy (LVH), and to evaluate the distribution of neuroadrenergic terminals in patients with left ventricular aneurysms (LVA) presenting complex arrhythmias. We studied 21 patients (4 normals, 11 with LVH and hypertension, and 6 with previous myocardial infarction, LVA and complex arrhythmias) who underwent series of [123I]MIBG planar scans (from 0.5 to 24 hours p.i.) and SPECT scans using both [123I]MIBG and 201Tl. Data quantification was performed by calculating the heart/mediastinum ratio (planar scan) and the percent uptake in 5 myocardial regions (SPECT scan). No significant differences between normals and hypertensive patients were found either in the heart/mediastinum ratio or in the regional distribution of [123I]MIBG and 201Tl. In hypertensive patients the uptake of [123I]MIBG was significantly higher than that of 201Tl in the septal wall while in the lateral and inferior walls it was significantly lower. In patients with anteroapical myocardial infarction (MI), the size of the [123I]MIBG defect was slightly smaller than the 201Tl defect; moreover a constant, severe [123I]MIBG defect was observed in the inferior walls whereas 201Tl uptake was normal. We conclude that while in hypertensive patients adrenergic innervation seems to be slightly impaired as compared to myocardial perfusion, in patients with MI a large area of functional or anatomical denervation may be detected despite the preserved perfusion and viability; this mismatch may be the trigger of complex arrhythmias.

Plasma viscosity, fibrinogen, haematocrit and beta-thromboglobulin were assessed on venous blood samples taken within 24 hours of admission from 20 consecutive male hypertensive patients with unstable angina and 20 male hypertensive patients with stable angina, matched for clinical variables. Besides, all patients underwent automated indirect blood pressure monitoring for 24 hours, starting just after hospitalization. Despite similar average 24-hour, day-time and night-time systolic and diastolic blood pressure, hypertensive patients with unstable angina showed an increased variability of 24-hour (p <0.01) and day-time (p < 0.05) systolic and disatolic blood pressure, together with higher values of all haemorhelogical parameters (plasma viscosity, fibrinogen and haematocrit) (p < 0.01) and beta-thrombogobulin (p< 0.05), when compared with hypertensive patients with stable angina. Moreover, significant correlations between plasma viscosity and 24-hour systolic (r = 0.42, p < 0.01) and diastolic (r = 0.39, p < 0.05) blood pressure variability were shown in hypertensive patients with unstable angina. Besides, in the same patients, the haematocrit was positively correlated with 24-hour systolic blood pressure variability (r = 0.37, P < 0.05). Our data further support the relevance of rheological determinants, platelet activation and haemodynamic factors in the genesis of the high risk condition of unstable angina.

In order to assess left ventricular structure and diastolic function, 50 hypertensive male subjects, 25 with and 25 without a history of alcohol abuse, and 20 normotensive male controls underwent Doppler echocardiographic examination followed by ambulatory blood pressure monitoring for 24 hours. Left ventricular mass was significantly higher in alcoholic hypertensives in relation to non-alcoholic hypertensives (p < 0.05) and normotensive controls (p < 0.001). Moreover, Doppler parameters expressing left ventricular filling pattern were significantly worse in alcoholic than in non-alcoholic hypertensives (p < 0.01). Clinic and ambulatory blood pressure were similar in alcoholic and non-alcoholic hypertensives, while mean day-time heart rate was significantly higher in alcoholics (p < 0.01). Collected data suggest that non-hemodynamic factors are probably involved in the development of cardiovascular abnormalities in hypertensive alcoholics, and that echocardiography should be employed for risk-profile definition in alcohol-associated hypertension.

Thirty-five asymptomatic diabetic patients with non insulin-dependent diabetes and mild moderate essential hypertension (18 males and 17 females, mean age 60 +/- 6 years) underwent echocardiographic examination, followed by simultaneous ambulatory blood pressure and electrocardiographic monitorings. Three hundred and sixteen significant episodes of asymptomatic ST segment depression (at least 1 mm 80 msec after the J point, lasting more than 1 min) were recorded in 21 patients (60%) with a total duration of 5637 minutes. Patients with asymptomatic episodes of ST segment depression had significantly higher values of total cholesterol (p < 0.05), LDL cholesterol (p < 0.05), Glycosylated hemoglobin (p < 0.001), left ventricular mass index (p < 0.02), mean 24-hour systolic and diastolic ambulatory blood pressure (p < 0.001), systolic (p < 0.02) and diastolic (p < 0.01) ambulatory blood pressure variability and hypertensive peaks (p < 0.05), with respect to the rest of the study population. The number of ST segment depression episodes was significantly related to total cholesterol levels (r = 0.40, p < 0.05), LDL cholesterol levels (r = 0.36, p < 0.05) glycosylated hemoglobin levels (r = 0.50, p < 0.01), left ventricular mass index (r = 0.48, p < 0.01), ambulatory systolic (r = 0.43, p < 0.01) and diastolic (r = 0.51, p < 0.01) blood pressure variability and hypertensive peaks (r = 0.50, p < 0.01). Our data suggest that haemodynamic and metabolic factors could have a relevant role in high prevalence of SMI in asymptomatic diabetic patients with EH. The evidence of SMI in these patients warrants further diagnostic work-up and prognostic assessment.

Seventy-eight men with borderline hypertension according to the World Health Organization criteria underwent echocardiographic examination, followed by simultaneous ambulatory blood pressure and electrocardiographic monitorings for 24 h. The prevalence of echocardiographic left ventricular hypertrophy was 16.6% (13/78). Borderline hypertensives with left ventricular hypertrophy had more supraventricular (P less than .001) and ventricular ectopic beats (P less than .001) than normotensive controls and borderline hypertensives without cardiac involvement. Furthermore, ventricular ectopic activity was significantly related to left ventricular mass (r = 0.58, P less than .05) in borderline hypertensives showing echocardiographic evidence of left ventricular hypertrophy. Our findings suggest that noninvasive assessment of target organ status, including echocardiography, should be employed to optimize risk stratification in borderline hypertension.

In order to assess the prevalence of target organ damage 78 men with borderline hypertension, according to the World Health Organization criteria, and 67 normotensive controls underwent echocardiographic, electrocardiographic and fundoscopic examination, followed by ambulatory blood pressure monitoring for 24 hours. Echocardiographic left ventricular hypertrophy was found in 13 borderline hypertensive subjects (16.6%), while no electrocardiographic or fundoscopic abnormalities could be detected. Our data suggest that noninvasive assessment of cardiovascular status, including echocardiography, allows recognition of a subset of borderline subjects with an increased risk for subsequent cardiac morbid events, thereby improving prognostic stratification.

The above study was intended to assess the efficacy of nicardipine in mild to moderate essential arterial hypertension and to check whether there are medium term changes in kidney function and urinary excretion of electrolytes in the course of nicardipine treatment. Twenty patients with mild to moderate essential arterial hypertension were treated daily with 40-80 mg doses of slow-release nicardipine after a wash-out period. Systolic and diastolic blood pressure was measured with traditional sphygmomanometer on entry and after 4, 8, and 12 weeks' treatment. Also, on entry and at conclusion of the study, the following parameters were measured: plasma renin activity, creatinine clearance, 24-hour urinary excretion of Na, K, Ca, and aldosterone. Nicardipine treatment was well tolerated and no significant changes of heart rate, creatinine clearance and urinary excretion of Na, K, Ca and aldosterone were observed after 12 weeks' treatment. The efficacy of nicardipine for the management of mild to moderate hypertension was thus confirmed. The absence of a natriuretic effect after 12 weeks' treatment goes to show that any diuretic action of the drug is irrelevant to its therapeutic effect which appears to be due mainly to its vasodilatory action.

BackgroundCurrently available treatment options for Parkinson's disease are symptomatic and do not alter the course of the disease. Recent studies have raised the possibility that cardiovascular risk management may slow the progression of the disease.ObjectivesWe estimated the effect of baseline cardiovascular risk factors on the progression of Parkinson's disease, using measures for PD-specific motor signs and cognitive functions.MethodsWe used data from 424 de novo Parkinson's disease patients and 199 age-matched controls from the observational, multicenter Parkinson's Progression Markers Initiative (PPMI) study, which included follow-up of up to 9 years. The primary outcome was the severity of PD-specific motor signs, assessed with the MDS-UPDRS part III in the “OFF”-state. The secondary outcome was cognitive function, measured with the Montreal Cognitive Assessment, Symbol Digit Modalities Test, and Letter-Number Sequencing task. Exposures of interest were diabetes mellitus, hypertension, body mass index, cardiovascular event history and hypercholesterolemia, and a modified Framingham risk score, measured at baseline. The effect of each of these exposures on disease progression was modeled using linear mixed models, including adjustment for identified confounders. A secondary analysis on the Tracking Parkinson's cohort including 1,841 patients was performed to validate our findings in an independent patient cohort.ResultsMean age was 61.4 years, and the average follow-up was 5.5 years. We found no statistically significant effect of any individual cardiovascular risk factor on the MDS-UPDRS part III progression (all 95% confidence intervals (CIs) included zero), with one exception: in the PD group, the estimated effect of a one-point increase in body mass index was 0.059 points on the MDS-UPDRS part III per year (95% CI: 0.017 to 0.102). We found no evidence for an effect of any of the exposures on the rate of change in cognitive functioning in the PD group. Similar results were observed for the Tracking Parkinson's cohort (all 95% CIs overlapped with PPMI), but the 95% CI of the effect of body mass index on the MDS-UPDRS part III progression included zero.ConclusionsBased on this analysis of two large cohorts of de novo PD patients, we found no evidence to support clinically relevant effects of cardiovascular risk factors on the clinical progression of Parkinson's disease.

Background: Currently available treatment options for Parkinson's disease are symptomatic and do not alter the course of the disease. Recent studies have raised the possibility that cardiovascular risk management may slow the progression of the disease. Objectives: We estimated the effect of baseline cardiovascular risk factors on the progression of Parkinson's disease, using measures for PD-specific motor signs and cognitive functions. Methods: We used data from 424 de novo Parkinson's disease patients and 199 age-matched controls from the observational, multicenter Parkinson's Progression Markers Initiative (PPMI) study, which included follow-up of up to 9 years. The primary outcome was the severity of PD-specific motor signs, assessed with the MDS-UPDRS part III in the "OFF"-state. The secondary outcome was cognitive function, measured with the Montreal Cognitive Assessment, Symbol Digit Modalities Test, and Letter-Number Sequencing task. Exposures of interest were diabetes mellitus, hypertension, body mass index, cardiovascular event history and hypercholesterolemia, and a modified Framingham risk score, measured at baseline. The effect of each of these exposures on disease progression was modeled using linear mixed models, including adjustment for identified confounders. A secondary analysis on the Tracking Parkinson's cohort including 1,841 patients was performed to validate our findings in an independent patient cohort. Results: Mean age was 61.4 years, and the average follow-up was 5.5 years. We found no statistically significant effect of any individual cardiovascular risk factor on the MDS-UPDRS part III progression (all 95% confidence intervals (CIs) included zero), with one exception: in the PD group, the estimated effect of a one-point increase in body mass index was 0.059 points on the MDS-UPDRS part III per year (95% CI: 0.017 to 0.102). We found no evidence for an effect of any of the exposures on the rate of change in cognitive functioning in the PD group. Similar results were observed for the Tracking Parkinson's cohort (all 95% CIs overlapped with PPMI), but the 95% CI of the effect of body mass index on the MDS-UPDRS part III progression included zero. Conclusions: Based on this analysis of two large cohorts of de novo PD patients, we found no evidence to support clinically relevant effects of cardiovascular risk factors on the clinical progression of Parkinson's disease. [ABSTRACT FROM AUTHOR]