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

Morning rise in blood pressure (morning surge; MS) has been shown to be associated with the occurrence of myocardial ischemic events and stroke. This study aimed to elucidate the incidence and the mechanism of MS in hypertensive patients (HT). We monitored ambulatory blood pressure (BP) and physical activity in 68 untreated HTs using TM2421 (A & D Co. Ltd.) and ACTIVETRACER (GMS Ltd.) for detection of MS. MS was defined as a rise in BP > 50 mmHg (90% tile of 35 normotensives) during early morning (4:00 to 9:00 A.M.) compared with the lowest basal BP at night. MS was seen in 41 patients (52.6%) and was classified into two groups; MS1: BP rose steeply after waking up (27 patients) and MS2: BP started to rise gradually during sleep (14 patients). The mean age of MS1 was significantly higher than that of MS2 (72 vs. 62 years, p < 0.01). BP reached its basal value earlier in MS2 than in MS1 at night though the basal BP values were comparable between the two groups. Mean 24-hour BP and physical activity were similar between the two groups, though significantly higher incidence of cases with a correlation between SBP and activity was seen in MS1. In conclusion, there are two types of MS, the mechanisms of which may differ. MS occurring immediately after waking up was more common in older HTs, and possibly was related to augmented arousal response in BP, while MS beginning gradually during sleep was more common in younger HTs and was characterized by reaching basal BP earlier at night.
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PMID:[The relation between blood pressure variation and daily physical activity in early morning surge in blood pressure]. 830 55

Seated recovery [at 5, 15, 20, 40, and 60 min (R5,15,20,40,60)] body temperature (T) and blood pressure were examined after 45 min of cycling exercise (54 +/- 5% maximal O2 uptake) in 12 normotensive males to study the relationship between postexercise thermal and hemodynamic responses. Data were analyzed with a repeated-measures analysis of variance. Systolic (SBP, R15,20,40; P < 0.01) and mean arterial (MAP, R15,20; P < 0.05) blood pressures were significantly lower, but diastolic blood pressure (DBP) was unchanged. Heart rate (R5,15,20, P < 0.001) was above that measured at rest. Decreases in mean skin T (Tsk, R15,20,60; P < 0.01) and increases in core T (Tc, R5,15,20; P < 0.01) were found. Significant negative correlations averaging -0.68 (R15,20,40) and -0.69 (R15,20,40) were demonstrated for Tsk and SBP and MAP, respectively. Increases in thigh Tsk (R5,15,20; P < 0.00001) and decreases in calf (R15,20,40,60; P < 0.00001) and chest (Tchest, R5,15,20,40; P < 0.00001) Tsk were found. Significant negative correlations averaging -0.67 (R5,15,20,40) and -0.71 (R20,40,60) were demonstrated for Tchest and SBP and MAP, respectively. Inverse relationships between various regional Ts and blood pressure and the increased R Tc suggest a vasodilatory response in the visceral organs and/or lower limbs leading to a pooling of blood and transient decreases in blood pressure by a reduced venous return, although not affecting stroke volume and cardiac output.
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PMID:Blood pressure, hemodynamic, and thermal responses after cycling exercise. 837 70

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

Despite methodological differences in the limited number of studies reviewed, it appears that cardiovascular responses at rest and during exercise in the cold differ between patients with CAD and healthy subjects (Figures 1 and 2). This difference remains, even when attempting to control for investigation time and conditions. Typical exercise time reported for patients with CAD exercising in the cold is 4 to 8 minutes, where HR and SBP are generally the same or higher. Data corresponding to a similar time frame (5-15 minutes) in healthy subjects show HR to be lower or no different, whereas SBP was similar in both studies. Logically, healthy subject's RPP values would be similar or lower in the cold, which may be a teleological development to conserve myocardial oxygen uptake in the face of elevated sympathetic stimulation during cold exposure. The lower HR would offset the cold-induced hypertension and also help to preserve cardiac output. In healthy subjects, cardiac output is similar in the cold despite a higher stroke volume (SV) due to the lower HR. However, the similar cardiac output reported by Epstein and colleagues in patients with CAD, both at rest and during exercise at 15 degrees C, was obtained by increases in SV and HR. A blunted peripheral vasoconstriction response in older subjects could lead to reduced central blood volume with a corresponding decrease in venous return and SV. An inability to maintain an appropriate SV in the cold by patients with CAD may be responsible for the elevated HR to maintain cardiac output. However, in healthy subjects, SV appears to have a triphasic response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A review of heart rate and blood pressure responses in the cold in healthy subjects and coronary artery disease patients. 852 83

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

Our purpose was to compare baseline hemodynamic parameters of mild and severe preeclampsia. Patients admitted to the Medical University Labor and Delivery Unit with the diagnosis of preeclampsia who had not received prior antihypertensive or magnesium sulfate therapy were recruited for noninvasive hemodynamic monitoring with thoracic electrical bioimpedance. After stabilization in the lateral recumbent position, hemodynamic monitoring was begun. Baseline hemodynamic parameters, mean arterial pressure (MAP), heart rate (HR), systemic vascular resistance index (SVRI), cardiac index (CI), and stroke index (SI) were recorded. Stroke systemic vascular resistance index (SSVRI), the resistance imposed by vasculature on each beat of the heart, was calculated for each patient by multiplying SVRI by HR. For statistical analysis, unpaired Student's t-tests (two-tailed) were utilized (P < 0.01). Forty-one preeclamptic patients (20 mild, 21 severe) were enrolled. Mean gestational age of severe patients was 32.2 +/- 4.0 and of mild patients was 37.0 +/- 3.5. MAP, SBP, diastolic blood pressure, HR, and SSVRI were higher in the severe group. SVRI, CI, cardiac output, and SI did not differ significantly between groups. Severe preclampsia appears to be a more intensely vasoconstricted state than mild preeclampsia. Although CI is inversely proportional to SVRI, increased HR in severe preeclampsia prevents this expected decrease in cardiac output.
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PMID:Hemodynamic comparison of mild and severe preeclampsia: concept of stroke systemic vascular resistance index. 893 Jul 98

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


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