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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The National High Blood Pressure Education Program (NHBPEP) was launched 20 years ago based on data from population studies and clinical trials that showed high blood pressure (HBP) was a major unsolved--but soluble--mass public health problem. The present review summarizes recent data from US prospective population studies on blood pressure--systolic (SBP), diastolic (DBP)--and cardiovascular risk. The outcome variables include blood pressure-related risks, primarily incidence and mortality from coronary heart disease, stroke, other and all cardiovascular diseases (CVD); also cardiac abnormalities (roentgenographic, electrocardiographic, echocardiographic); also, all-cause mortality and life expectancy. Data accrued during the past 20 years confirm that SBP and DBP have continuous, graded, strong, independent, etiologically significant relationships to the outcome variables. These relationships are documented for young, middle-aged, and older men and for middle-aged and older women of varying socioeconomic backgrounds and ethnicity. Among persons aged 35 years or more, most have SBP/DBP above optimal (< 120/< 80 mm Hg); hence, they are at increased CVD risk, ie, the blood pressure problem involves most of the population, not only the substantial minority with clinical HBP. For middle-aged and older persons, SBP relates even more strongly to risk than DBP; at every DBP level, higher SBP results in greater CVD risk and curtailment of life expectancy. A great potential exists for improved health and increased longevity through control of the blood pressure problem. Its realization requires a strategy combining population wide and high-risk approaches, the former to prevent rise of blood pressure with age and to achieve primary prevention of HBP by nutritional-hygienic means; the latter to enhance detection, treatment, and control of HBP. The newly expanded goals of the NHBPEP, aimed at implementing this broader strategy for the solution of the blood pressure problem, merit active support from physicians and all health professionals.
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PMID:Blood pressure, systolic and diastolic, and cardiovascular risks. US population data. 843 23

Although the central cardiovascular adjustments to exercise in the heat have been identified, little is known about the post-exercise hemodynamics during recovery from exercise and heat stress. This study examined heart rate (HR), stroke index (SI), cardiac index (CI), systemic vascular resistance (SVR), systolic (SBP) and diastolic (DBP) blood pressure in 8 males during 15 min of passive seated recovery preceded by 30 min of cycle ergometry (60% VO2max) on two separate occasions: under control (C) and heat stress (HS) conditions. During both recovery conditions, SI significantly declined (p < 0.05) to below pre-exercise values. No differences were observed between groups with respect to SI. The decrease in recovery HR was slower (p < 0.05) in HS than C. The greater elevation in HR during HS accounted for the relative increase in CI above that observed prior to exercise. The estimated SVR measured immediately following exercise in both groups was lower (p < 0.05) than pre-exercise values. By 5 min of C recovery, SVR returned to baseline values but remained significantly depressed (p < 0.05) for the entire HS condition. These results indicate that the pressor responses were attenuated during HS; however, CI was maintained above pre-exercise levels due to higher HR responses compensating for the reduction in SI. Stimulation of the baroreceptor reflex and increased myocardial contractility could possibly explain the maintenance of output at a time when preload and afterload were reduced.
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PMID:Cardiovascular responses during recovery from exercise and thermal stress. 844 4

1. Impedance cardiography is a well-established noninvasive method to assess within-subject changes of cardiovascular function. We compared the standard approach (ZCG) which requires tedious signal analysis with an automated approach (TEB: NCCOM 3) with its own specific equipment, algorithms and equations in order to assess agreement of the method-specific measurements and calculations. 2. Ten healthy men were studied on two occasions with either ZCG or TEB, at rest and at the end of 5 min i.v.-infusions with 1 microgram min-1 isoprenaline and 100 micrograms min-1 phenylephrine. 3. There was good agreement for the method-independent changes (HR, SBP/DBP), but there were large differences for method-specific measurements: dZ/dtmax [TEB-ZCG] = -0.68, CI: -0.83 to -0.53 ohm s-1, PEP [TEB-ZCG] = -22.1, CI: -35.0 to -9.2 ms and QS2c [TEB-ZCG] = -16.5, CI: -32.4 to -0.6 ms and for the calculated stroke volume SV [TEB-ZCG] = 30.3, CI: 15.5 to 45.2 ml. The responses of dZ/dtmax and SV to isoprenaline and phenylephrine, although qualitatively similar, reached no quantitative agreement either. A substantial disagreement was evident for the STI responses to isoprenaline where TEB failed to detect the expected reduction of VETc and thus grossly underestimated the shortening of QS2c. 4. It is concluded that TEB-measurements and -calculations did not agree with standard ZCG, that the methods, albeit related, cannot be considered as interchangeable and that suspicion is justified that TEB might yield erroneous results under specific circumstances.
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PMID:Disagreement between standard transthoracic impedance cardiography and the automated transthoracic electrical bioimpedance method in estimating the cardiovascular responses to phenylephrine and isoprenaline in healthy man. 848 14

Genetic influences in cerebrovascular disease (CVD) may act either independently or by predisposing to, or modulating, the effect of risk factors such as hypertension. Factors involved in the pathogenesis of atherosclerosis, thrombosis and vasoconstriction are important in CVD. The angiotensinogen gene has recently been linked with essential hypertension in affected sibships and a particular polymorphism in exon 2 of the angiotensinogen gene, a threonine to methionine substitution at position 235 (M235T), has been associated with pre-eclampsia and hypertension. In this study we examined the relation of M235T polymorphism to cerebrovascular disease and carotid atheroma in 100 consecutive Caucasian patients with internal carotid artery territory ischaemia (TIA or stroke), presenting to a carotid ultrasound service. Forty five age-matched controls (mostly patients' spouses) were also studied. Hypertension was defined as current treatment with anti-hypertensive agents, or SBP > 160 mm Hg or DBP > 95 mm Hg. Twelve of 100 cases (12%) and eight of 45 controls (12%) were homozygous for the T235 allele. T:M allele ratios were 0.34:0.66 in cases and 0.34:0.66 in controls. There was no relation between the polymorphism and either internal carotid stenosis or common carotid artery intima-media thickness. In the cases, mean percentage internal carotid artery stenosis was TT 18.3 (SD 18.7)%, MT 38.0 (27.1)% and MM 36.8 (30.2)%. Mean intima-media thickness was TT 0.87 (0.18) mm, MT 0.95 (0.34) mm and MM 0.88 (0.23) mm. There was no relation between the polymorphism and hypertension (TT 11 of 100 cases, six of 45 controls).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of association between angiotensinogen polymorphism (M235T) and cerebrovascular disease and carotid atheroma. 852 90

An overview of the 17 completed randomised trials of antihypertensive treatment demonstrates that a 5-6 mm Hg reduction in DBP reduced stroke risk by 38% (SD 4) and CHD risk by 16% (SD 4). These results indicate that a few years' treatment with diuretic- or beta-blocker-based therapy produces most or all of the long-term stroke avoidance and much of the long-term CHD avoidance that would be predicted from observational epidemiological studies, given the blood pressure reductions that were achieved in the trials. The relative risk reductions were similar in trials of older and younger patients, although the absolute reduction in events was more than twice as great in the trials in older patients. From these results it can be estimated that in fully compliant patients at similar risk of vascular disease to those included in the trials, antihypertensive treatment for 5 years would prevent one major vascular event among every 20 older patients and one major vascular event among every 60 younger patients. Obviously the benefits of treatment will be greater among those at higher risk than the patients included in the previous trials. The greatest benefits are likely to be achieved in those with a history of vascular disease since their risk of future events is particularly high. Among such patients it is possible that blood pressure reduction will confer worthwhile benefits in those without hypertension, as well as those with hypertension. It is also possible that the benefits of treatment will be determined by the size of the blood pressure reduction and by the choice of the anti-hypertensive agent. However, each of these possibilities requires confirmation in large scale randomised controlled trials.
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PMID:Blood pressure lowering for the primary and secondary prevention of coronary and cerebrovascular disease. 857 Oct 98

Post-stroke Antihypertensive Treatment Study (PATS) was a randomized, double-blind and placebo-controlled trial, which aimed at determining whether antihypertensive treatment could reduce the risk of fatal and nonfatal stroke incidence in patients with a history of stroke or transient ischemic attack (TIA). 5,665 patients were randomized by a sealed envelope system. Systolic blood pressure (SBP) ranged from 80 to 280 mm Hg and diastolic (DBP) from 50 to 150 mmHg. The average SBP was 154 mmHg and average DBP 93 mmHg. The mean age was 60 years. Among the patients, women accounted for 28%. In 71% the latest stroke was ischemic. Average follow-up approximated to 2 years. The three-year average SBP was 149 mmHg for the placebo group and 144 mmHg for the indapamide treatment group, and the three-year DBP was 89 mmHg and 87 mmHg respectively. The three-year first incidence of fatal and nonfatal stroke was 12.3 per 100 patients placebo treatment and 9.4 per 100 with indapamide. The relative risk by proportional hazards regression analysis was 0.71 (P = 0.0009). For deaths from all causes, the relative risk was 0.91. (P > 0.05). The findings of this trial indicate that in patients with a history of stroke or TIA, blood pressure reduction of 5/2 mmHg with 2.5 mg indapamide reduced the first incidence of fatal and nonfatal stroke by 29%, with three-year absolute benefit of 29 events per 1000 participants.
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PMID:Post-stroke antihypertensive treatment study. A preliminary result. 857 41

A sample of 861 Roman children, aged 7 to 14 years, was investigated in order to evaluate the association between some cardiovascular risk factors such as high systolic (SBP) and diastolic (DBP) blood pressure levels, body mass index (BMI), arm fat area (AFA) and a history of diabetes, stroke, angina pectoris, myocardial infarction, hypertension and overweight in their parents. The sample investigated was subdivided into three subgroups, based on whether the children had just one parent, both parents or no parent with a positive history. For all the variables considered, the highest values were found in the group of children with a positive history for both parents and the lowest ones in children with a negative history for both parents. The analysis of significance, based on the mean values for the three groups, revealed statistically significant differences for SBP, DBP, BMI and AFA between the group of children with a positive history for both parents and that of children with a negative history for both parents. Significant differences also emerged for DBP, BMI and AFA between the mean values of children positive for one parent and those negative for both parents and for BMI and AFA between the means of children positive for one parent and those positive for both parents. The odds ratio of high systolic and/or diastolic BP, BMI and AFA levels was consistently higher in children with one or two parents with a positive history compared to children with both parents with a negative history, and even higher considering only children with both parents with a positive history vs children with both parents with a negative history.
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PMID:Family history of cardiovascular diseases and risk factors in children. 887 39

The aim of this multicenter study was to evaluate the efficacy and tolerability of manidipine hydrochloride, a new calcium-antagonist of the dihydropyridine group, in the long-term treatment of mild to moderate hypertension. After a 2-week run-in period on placebo, 183 patients, 98 males and 85 females, with mean age of 53.8 years, sitting DBP > or = 95 and < or = 115 mmHg and SBP < or = 210 mmHg, were given manidipine 10 mg once daily. Two weeks later, patients whose DBP was > or = 90 mmHg or with a reduction in DBP < 10 mmHg were administered with manidipine 20 mg once daily. Follow-up visits were performed at 6, 10, 14, 26, 38 and 52 weeks after starting manidipine treatment. All BP (by mercury sphygmomanometer, Korotkoff I and V) and heart rate (HR) measures were made 24 h after dosing. Adverse events and laboratory data were recorded. Particular attention was paid to the collection of possible major cardiovascular (angina pectoris, myocardial infarction) and cerebrovascular (IRA, stroke) events, observed during the treatment period. One-hundred-and-fifty-one patients completed the study (79 on a 10 mg dose and 72 on a 20 mg dose), whereas 32 dropped out (11 lost to follow-up, 11 insufficient therapeutic response, 7 ADRs, 3 other causes). Significant reductions of BP values were achieved during the manidipine 10 mg treatment period. Analysis of covariance between doses confirmed a more potent hypotensive effect of manidipine 20 mg as compared to 10 mg on sitting DBP and mean BP and on standing SBP, especially in patients with moderate hypertension. At the end of 1 year of treatment the success rates (defined as sitting DBP > or = 90 mmHg or a reduction of > or = 10 mmHg vs baseline) were similar in the two groups (manidipine 10 mg: 96.1%; manidipine 20 mg: 94.5%). No clinically relevant change in HR was observed. Overall, 28 patients (17 in the manidipine 20 mg and 11 in the manidipine 10 mg treated group) complained of adverse events, the most common being ankle oedema (4.9%), headache (3.8%), palpitation (2.7%) and flushing (2.2%). Neither cardiovascular nor cerebrovascular events or other serious adverse event were reported. In conclusion, a significant and constant reduction of BP values was observed with long-term treatment with manidipine. The reduction in BP was dose-related especially in patients suffering from moderate hypertension. Adverse events were mild and relatively more frequent with the higher manidipine dosage.
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PMID:Efficacy and tolerability of manidipine hydrochloride in the long-term treatment of mild-moderate hypertension. Manidipine Efficacy in Long-Term Treatment Group. 897 89

The cardiovascular responses to various inodilatory interventions were investigated noninvasively in healthy man by monitoring heart rate (HR), blood pressure (SBP/DBP, according to Korotkoff I and IV criteria), systolic time intervals (PEP, VET and QS2) and impedance cardiographic estimates of stroke volume (SV) and cardiac output (CO). The following inodilatory interventions were evaluated and compared: the i.v. infusion of adrenaline (1 microgram/min), the i.v. infusion of isoprenaline (1 microgram/min) with and without pretreatment with 100 mg talinolol (a beta 1-selective beta-adrenoceptor antagonist), the p.o. administration of 1200 mg celiprolol (a beta 1-adrenoceptor antagonist with ancillary beta-adrenergic agonistic properties at the chosen dose level), the p.o. administration of 0.4 mg bimakalim (a K+ channel activator without direct cardiac effect) with and without pretreatment with 5 mg bisoprolol and the p.o. administration of the PDE-III inhibitors meribendan and isomazole. The extent of the inodilatory rise of HR, shortening of PEP, rise of SV and CO relative to the associated reduction of the calculated total peripheral resistance (TPR) proved a powerful tool to differentiate inodilatory properties: adrenaline, isoprenaline after beta 1-selective beta-adrenoceptor blockade and celiprolol led to similar ancillary adrenaline-like cardiovascular changes relative to the vasodilatation; bimakalim led to similar associated changes except for a relatively larger rise in HR, which could be blocked by bisoprolol; isoprenaline induced clearly larger associated changes, for which HR, VET, and QS2c were particularly sensitive; meribendan and isomazole resulted in the largest ancillary changes, characterized by a critical shortening of the ejection time VET, so that the rise of CO was almost exclusively defined by the rise of HR. These differences could be detected and differentiated sufficiently and adequately by HR, SV, CO, TPR, PEP, and VET. There seems little value in using more assumptive variables such as HR-corrected VETc and QS2c, the Weissler index and the impedance cardiographic Heather index.
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PMID:Differentiation of inodilatory responses by non-invasive measures of cardiovascular performance in healthy man. 899 46

The effect of atenolol and reserpine on incidence of strokes, coronary heart disease (CHD), cardiovascular disease (CVD), and mortality was assessed in 4736 persons aged 60 years and older with isolated systolic hypertension. Participants were randomized to either chlorthalidone (2371), with step-up to atenolol, or reserpine if needed, or placebo (2365). The average baseline SBP/DBP was 170/77 mm Hg. In the active treatment group, step 1, dose 1 was chlorthalidone, 12.5 mg/day; dose 2 was 25 mg/day. For step 2, dose 1 was atenolol 25 mg/day (or reserpine 0.05 mg/day if atenolol was contraindicated); dose 2 was 50 mg/day (reserpine, 0.10 mg/day). During 4.5 years average follow-up, 32% (757) of the active treatment group were on atenolol, with an average exposure of two years and 8% (193) were on reserpine with an average exposure of 1.7 years. Overall there were 96 strokes, 140 CHD events and 289 CVD events among the 2365 active group participants. Using time-dependent lifetable regression with adjustment for several variables, the addition of either atenolol or reserpine to chlorthalidone did not substantially alter the risk ratios for chlorthalidone alone. The relative risk for CHD events for atenolol versus no atenolol was 1.04 (95% confidence interval: 0.58, 1.86) and for reserpine versus no reserpine was 0.93 (95% confidence interval: 0.29, 2.96). The relative risk for atenolol were 0.84 (95% confidence interval: 0.54, 1.30) for death, 1.34 (95% confidence interval: 0.80, 2.28) for stroke, and 1.07 (95% confidence interval: 0.71, 1.61) for CVD. For reserpine, the corresponding relative risks and confidence intervals were 0.65 (0.26, 1.59) for death, 0.27 (0.04, 2.26) for stroke, and 0.55 (0.20, 1.49) for CVD. Thus, the beneficial effects in several outcomes in Systolic Hypertension in the Elderly Program (SHEP) were due to the treatment regimen of lowering blood pressure based on low-dose chlorthalidone (plus atenolol or reserpine as required to meet blood pressure criteria). Additional (independent) benefits attributable to atenolol or to reserpine were not identified. However, a greater number of patients might have been necessary to adequately evaluate potential differential effects of these drugs, especially for reserpine.
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PMID:Effect of atenolol and reserpine on selected events in the systolic hypertension in the elderly program (SHEP). 899 47


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