Baseline Pulse Pressure Research Articles

Baseline pulse pressure predicts 30-day mortality in patients with acute myocardial infarction: lessons from GUSTO-V

Baseline pulse pressure predicts 30-day mortality in patients with acute myocardial infarction: lessons from GUSTO-V

Reduction of systolic blood pressure and pulse pressure with olmesartan medoxomil

At all levels of systolic blood pressure (SBP), an increase in pulse pressure (PP) is a significant independent predictor of cardiovascular disease among individuals ≥50 years of age. In this analysis, the newest angiotensin II receptor blocker, olmesartan medoxomil, was evaluated for its ability to reduce both SBP and PP among subjects with mild-to-moderate hypertension. Data from 7 multicenter, randomized, double-blind, placebo-controlled, 6- to 12-week efficacy trials of olmesartan medoxomil, given in dosages of 2.5 to 80 mg once daily, were analyzed among 2 separate groups: 1) the entire cohort (n=2693); and 2) a cohort of subjects with a wide baseline PP >55 mm Hg (n=1413). The changes from baseline in mean seated SBP and PP at the primary study time point were assessed at the 20 mg and 40 mg dosages of olmesartan medoxomil vs placebo for the total study population and for the wide PP cohort. All statistical comparisons used model-adjusted (least-squares) mean values. In the entire cohort, mean seated SBP/diastolic blood pressure (DBP) at baseline was 159/104 mm Hg (PP of 55.2 mm Hg) in the placebo group (n=548), and 162/104 mm Hg (PP of 57.8 mm Hg) and 160/104 mm Hg (PP of 56.5 mm Hg) in the 20 mg (n=436) and 40 mg (n=195) groups, respectively. Among the wide PP subjects, mean baseline SBP/DBP was 170/104 mm Hg (PP of 65.4 mm Hg) in the placebo group (n=268), and 172/105 mm Hg (PP of 67.4 mm Hg) and 170/104 mm Hg (PP of 65.5 mm Hg) in the 20 mg (n=239) and 40 mg (n=103) groups, respectively. In the total population, dosages of 20 mg and 40 mg olmesartan medoxomil reduced SBP/DBP by 15.1/12.2 mm Hg and 17.6/13.1 mm Hg, respectively (P<0.001, both doses vs placebo). Pulse pressure was reduced by 2.8 mm Hg and 4.3 mm Hg with 20 mg and 40 mg olmesartan medoxomil, respectively, compared with 1.2 mm Hg in the placebo group (P<0.001, both doses vs placebo). Among the wide PP subjects, olmesartan medoxomil at 20 mg and 40 mg reduced SBP/DBP by 17.7/10.8 mm Hg and 22.0/12.9 mm Hg, and PP by 7.4 mm Hg and 8.8 mm Hg, respectively. Pulse pressure was reduced by 2.8 mm Hg with placebo (P<0.001 for SBP, DBP, and PP, both doses of olmesartan medoxomil vs placebo). Olmesartan medoxomil at 20 mg and 40 mg daily significantly reduces SBP and PP among hypertensive individuals. This effect is even more pronounced for patients with a pre-existing wide PP >55 mm Hg.

Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study.

Although hypertension is a principal precursor of congestive heart failure (CHF), the separate relations of systolic, diastolic, and pulse pressure with risk for heart failure have not been fully elucidated. To examine the value of blood pressure predictors of heart failure. Community-based inception cohort study. Framingham, Massachusetts. 2040 free-living Framingham Heart Study participants (mean age, 61 years [range, 50 to 79 years]). The association of baseline systolic, diastolic, and pulse pressure with risk for incident CHF was examined in 894 men and 1146 women. Framingham Heart Study participants free of CHF at the baseline examination (performed from 1968 to 1973) were monitored for up to 24 years (mean, 17.4 years) for new-onset heart failure. Cox proportional hazards models were used to adjust for age, sex, smoking, left ventricular hypertrophy, body mass index, diabetes mellitus, high-density lipoprotein cholesterol level, and heart rate; hazard ratios and 95% CIs for blood pressure variables were estimated. CHF developed in 234 participants (11.8%) during the follow-up period. All three blood pressure components were related to the risk for CHF, but the relation was strongest for systolic and pulse pressure. A 1-SD (20 mm Hg) increment in systolic pressure conferred a 56% increased risk for CHF (hazard ratio, 1.56 [95% CI, 1.37 to 1.77]); similarly, a 1-SD (16 mm Hg) increment in pulse pressure conferred a 55% increased risk for CHF (hazard ratio, 1.55 [CI, 1.37 to 1.75]). These associations were unrelated to age, duration of follow-up, and initiation of treatment for hypertension during follow-up; they were also observed in patients with systolic hypertension (systolic blood pressure > or = 140 mm Hg) at the baseline examination (hazard ratio, 1.41 [CI, 1.18 to 1.69] for pulse pressure and 1.42 [CI, 1.14 to 1.76] for systolic pressure). Although each component of blood pressure was associated with risk for CHF, pulse and systolic pressure conferred greater risk than diastolic pressure. Increased pulse pressure may help identify hypertensive patients at high risk for overt CHF who are candidates for aggressive blood pressure control.

Angiotensin II type 1 receptor polymorphisms in the cardiovascular health study: relation to blood pressure, ethnicity, and cardiovascular events

Background The angiotensin II type 1 receptor A1166C polymorphism has been associated with increased risks of hypertension and myocardial infarction in several small studies. We examined the association between this polymorphism and new-onset hypertension, blood pressure (BP) control, and incident cardiovascular events in a large population-based cohort of older adults. Methods Eight hundred self-identified African Americans and 1371 randomly selected white participants in the Cardiovascular Health Study were genotyped. The median duration of follow-up was 8.1 years. Results The A1166C polymorphism was not associated with new-onset hypertension, with BP control, or with incident cardiovascular events in the overall population. In white participants, the CC genotype was associated with higher baseline systolic BP and pulse pressure, compared to the AC or AA genotype. In whites with treated hypertension at baseline, compared to the AA genotype, the CC genotype was associated with increased risks of incident congestive heart failure (hazard ratio = 2.5, 95% confidence interval [CI] 1.3–4.9) and incident ischemic stroke (hazard ratio = 2.6, 95% CI 1.1–6.0). These associations were not observed among white participants without treated hypertension, but the interaction of genotype with treated hypertension on ischemic stroke and heart failure was only marginally significant. Conclusions On the whole, in this large cohort of older adults, the A1166C polymorphism was not associated with BP control or incident cardiovascular events. The subgroup findings in treated hypertensives need to be confirmed in additional studies.

Predictors of one year blood pressure control and treatment resistance in the value trial

The Valsartan Antihypertensive Long-Term Use Evaluation (VALUE) Trial is testing the hypothesis that for the same level of BP control, the AT1-receptor blocker valsartan reduces serious cardiac events by 15% compared to the CCB amlodipine. VALUE is a double-blind, randomized, in 31 countries, prospective trial of 15314 previously treated (92%) or untreated hypertensives, 42.4% women, mean age 67.2 yrs, BMI 28.6 kg/m2, coronary heart disease (CHD) in 45.8%, high cholesterol in 32.9%, type-2 diabetes mellitus (DM) in 31.7% and 24.0% smokers. The primary endpoint is expected in 1450 pts. in 2-3 yrs. The aim of this analysis is to identify predictors of 1-year BP control and resistance to treatment in the VALUE population. BP decreased from 154.7/87.6 at randomization to 141.3/80.9 mmHg at 12 months and control rate <140/90 mmHg improved from 21.4 to 54.6%. Responsive (n=4328) achieved goal BP on monotherapy and resistant (n=1091) remained >160 and/or >100 mmHg at the highest drug titration step (step 5). Characteristics are shown in the accompanying table. The odds of being controlled were up 23% in pts. with controlled SBP at baseline, decreased by 3% per mmHg rise in baseline pulse pressure (PP) and 2% per year of age, were 23% less in DM, 25% higher in USA, 85% higher in Asians, 25% higher in CHD and 34% higher in smokers. In the “best” model, pts. not in USA (RR 1.58, p<0.0001), Oriental (RR 0.49, p<0.0004) and PP (3% per mmHg rise, RR 1.03, p<0.0001) predicted resistance. Thus, overall the 1-year blood pressure control in VALUE is comparable to the best previously reported in large hypertension outcome trials. Geographical origin and pulse pressure at baseline most strongly predicted resistance to drug therapy.

Cross-sectional and 4-year longitudinal associations between brachial pulse pressure and common carotid intima-media thickness in a general population. The EVA study.

The cross-sectional and 4-year longitudinal associations between brachial pulse pressure (PP) and ultrasound measurements of common carotid intima-media thickness (CCA-IMT) were assessed. A population of 957 volunteers aged 59 to 71 years was recruited from the electoral rolls of the city of Nantes (western France) and reexamined 4 years later. Longitudinal changes in PP and CCA-IMT were computed as the difference between 4-year follow-up and baseline values. Baseline CCA-IMT and PP were positively associated in both age- and sex-adjusted analysis (partial correlation coefficient=0.20, P<0.001) and in multivariate analysis adjusted for traditional cardiovascular risk factors and mean blood pressure (partial correlation coefficient=0.18, P<0.001). In longitudinal analysis, baseline PP was associated with the change in 4-year CCA-IMT (partial correlation coefficient=0.11, P<0.001), and baseline CCA-IMT was a predictor of the 4-year change in PP (partial correlation coefficient=0.10, 0.001<P<0.01). No association between mean blood pressure and CCA-IMT was observed once PP was taken into account, in either cross-sectional or longitudinal analyses (partial correlation coefficients ranged from 0.00 to 0.03). Similar patterns of results were observed in hypertensive, nonhypertensive, and antihypertensive-treated and -nontreated subjects. This longitudinal study of a large population of relatively aged subjects suggests that elevated levels of PP are associated with the progression of CCA-IMT, and increased CCA-IMT is associated with PP widening. The nature of these relationships and whether atherosclerosis progression over time is involved or not in these associations merit further investigations.

Independent prognostic information provided by sphygmomanometrically determined pulse pressure and mean arterial pressure in patients with left ventricular dysfunction

OBJECTIVESThe purpose of this study was to evaluate the relationship of baseline pulse pressure and mean arterial pressure to mortality in patients with left ventricular dysfunction.BACKGROUNDIncreased conduit vessel stiffness increases pulse pressure and pulsatile load, potentially contributing to adverse outcomes in patients with left ventricular dysfunction.METHODSPulse and mean arterial pressure were analyzed for their effect on mortality, adjusting for other modifiers of risk, using Cox proportional hazards regression analysis of data collected from 6,781 patients randomized into the Studies of Left Ventricular Dysfunction trials.RESULTSPulse and mean arterial pressure were related positively to each other, age, ejection fraction and prevalence of diabetes and hypertension and inversely to prior myocardial infarction and beta-adrenergic blocking agent use. Higher pulse pressure was associated with increased prevalence of female gender, greater calcium channel blocking agent, digoxin and diuretic use, lower heart rate and a higher rate of reported smoking history. Higher mean arterial pressure was associated with higher heart rate, lower calcium channel blocker and digoxin use and lower New York Heart Association functional class. Over a 61-month follow-up 1,582 deaths (1,397 cardiovascular) occurred. In a multivariate analysis adjusting for the above covariates and treatment assignment, higher pulse pressure remained an independent predictor of total and cardiovascular mortality (total mortality relative risk, 1.05 per 10 mm Hg increment; 95% confidence interval, 1.01 to 1.10; p = 0.02). Mean arterial pressure was inversely related to total and cardiovascular mortality (total mortality relative risk, 0.89; 95% confidence interval, 0.85 to 0.94; p <0.0001).CONCLUSIONSOne noninvasive blood pressure measurement provides two independent prognostic factors for survival. Increased conduit vessel stiffness, as assessed by pulse pressure, may contribute to increased mortality in patients with left ventricular dysfunction, independent of mean arterial pressure.

Effect of ouabain on pressor responsiveness in normal man

To assess the effects of ouabain on pressor and vasoactive hormone responsiveness, 10 healthy volunteers were pretreated with ouabain (0.5 mg i.v. 42 and 18 h before study) or placebo before pressor challenge with angiotensin II (ANG II; 2, 4, and 8 ng.kg-1.min-1 for 30 min/dose) and norepinephrine (NE; 5, 15, and 45 ng.kg-1.min-1 for 15 min/dose). There were no differences at baseline between the two study days regarding mean arterial pressure (MAP) or heart rate. Baseline pulse pressure, however, was significantly greater after ouabain (47 +/- 3 vs. 41 +/- 1 mmHg; P < 0.05). The mean maximum increments in MAP during ANG II and NE infusions were 17.5 +/- 1.1 and 10.5 +/- 1.3 (SE) mmHg, respectively, after ouabain and 19.2 +/- 1.3 and 10.4 +/- 1.5 mmHg after placebo (not significant). The mean heart rate was lower during both infusion periods on the ouabain study day compared with control (P < 0.05). Baseline plasma levels of ANG II, aldosterone, plasma renin activity, atrial and brain natriuretic peptide, guanosine 3',5'-cyclic monophosphate, NE, and epinephrine and achieved levels during the two infusions were similar on the two study days. We conclude that short-term ouabain administration does not alter pressor responsiveness or plasma levels of vasoactive hormones in healthy volunteers.

Hypoxemia and hemodynamic changes during the hypercarbia stimulation test

The hypercarbia stimulation test is a valuable technique to document the absence of brainstem responsiveness to elevated levels of carbon dioxide (P co 2); however, its application has been limited by concern that hypoxemia may induce cardiovascular instability. We investigated hemodynamic and oxygen (P o 2) changes in 19 patients: group 1 (17 patients) had no spontaneous ventilations at P co 2 values ranging from 37–129 torr; group 2 (2 patients) had spontaneous ventilations at < 38 torr. Group 1 was separated into 2 subgroups: A (10 patients) with P o 2 > 153 torr and B (7 patients) with P o 2 < 80 torr. Hemodynamic changes (> 10% variation in baseline pulse and blood pressure) occurred in 9 of 10 patients in group 1A and all patients in Group 1B. Mean differences in pulse and blood pressure changes between these groups were not significant; therefore, pulse and blood pressure changes are not predictive of hypoxemia and hypercarbia is not necessary to induce spontaneous ventilation in patients with intact medullary function.

Isolated systolic hypertension in 14 communities.

In the Hypertension Detection and Follow-up Program, 158,906 individuals from 14 communities around the United States had their blood pressure measured in their homes in 1972-1973. Of the total population screened, 2.4% had isolated systolic hypertension (systolic blood pressure greater than or equal to 160 mmHg and diastolic blood pressure less than 90 mmHg). Isolated systolic hypertension was present for 0.5% of those aged 30-39 years and 6.8% among those aged 60-69 years. The prevalence in blacks and women was greater than the prevalences in both whites and men. The prevalence among those taking antihypertensive medications at the time of screening was 6.1%, and 1.9% among those not on antihypertensive medications. From the individuals with "normal" diastolic blood pressure on the single home measurement (less than 90 mmHg), a random sample of 5,032 individuals were followed for mortality for eight years. Prevalence of isolated systolic hypertension was similar in this sample to that in the total. Among those not on antihypertensive medications, 8-year life table all-cause mortality rates adjusted for age, race, and sex were 17.6% for those with systolic blood pressure greater than or equal to 160 mmHg and 7.7% for those with systolic blood pressure greater than 160 mmHg. Among this population, all of whom had a diastolic blood pressure less than 90 mmHg, a multiple logistic analysis adjusting for baseline treatment status, age, race, sex, education, smoking, weight, pulse, physical activity, and systolic blood pressure revealed that each millimeter increase in systolic blood pressure was associated with approximately a 1% increase in mortality over the eight years of follow-up (p less than 0.05). Isolated systolic hypertension is both relatively common and a significant risk factor for subsequent mortality.

Diagnosis of hydrocephalus by CSF pulse-wave analysis: A clinical study

Pulsatility of the cerebrospinal fluid (CSF) is augmented in hydrocephalus. Analysis of pulsatility, including the CSF waveform, may be a more valid criterion for the diagnosis of hydrocephalus than mean CSF pressure. To test this possibility, CSF pressures were measured in 118 patients with presumed hydrocephalus. The pressure measurements included baseline mean pressure and pulse pressure, responses to jugular compression, and CSF wave analysis (amplitude and peak latency). Four groups of pressure recordings were identified and matched with four clinical groups: normal, arrested hydrocephalus, communicating hydrocephalus, and aqueduct stenosis hydrocephalus. The CSF pulse pressure and systolic slope form were highly reliable in the diagnosis of hydrocephalus, whereas mean CSF pressure was not reliable.