Peak Systolic Blood Pressure Research Articles

Meta-analysis of trimetazidine treatment for cardiomyopathy.

To explore the effect of trimetazidine (TMZ) in cardiomyopathy treatment. Literatures, related with TMZ treatment for cardiomyopathy, were retrieved between 1990 and February 2018 in the Pubmed, Embase, and Cochrane Library systems. Cardiopulmonary exercise testing [resting heart rate (RHR), peak heart rate (PHR), peak systolic blood pressure (PSBP), and resting systolic blood pressure (RSBP)] and echocardiographic results [left ventricular ejection fraction (LVEF), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), systolic wall thickening score index (SWTSI), left ventricular end-systolic diameter (LVESD), and left ventricular end-diastolic diameter (LVEDD)] were merged to detect the publication bias. Total 898 patients with cardiomyopathy were divided into two groups: TMZ-treated group (n=456) and control group (n=442). There was no difference in the improvement of cardiomyopathy between the TMZ and control group. No publication bias was shown for PHR (t= 0.9791, P=0.5067). There were significant differences in LVEF, LVESV, SWTSI, LVESD, and LVEDD between the TMZ group and the control group. TMZ-treatment significantly increased the level of LVEF (95% confidence interval (CI): 5.46–7.84, P<0.001), and reduced the level of LVESV (95% CI: −18.73 to −7.77, P<0.001), SWTSI (95% CI: −0.47 to −0.15, Z = −3.85, P=0.001), LVESD (95% CI: −1.09 to −0.08, P<0.001), and LVEDD (95% CI: −0.55 to −0.26, P=0.023). There was no publication bias except for LVEDV (t = 2.5456, P=0.0438). TMZ is effective for cardiomyopathy treatment and worth to popularize in clinic.

THE IMPACT OF EXAGGERATED BLOOD PRESSURE RESPONSE DURING TREADMILL EXERCISE TEST ON OUTCOME IN MODERATE TO SEVERE ASYMPTOMATIC AORTIC STENOSIS PATIENTS

Objective: Exaggerated blood pressure (BP) response (EBPR) during exercise predicts future hypertension and cardiovascular events in different patients groups and general population. However, the clinical and prognostic implications of EBPR during exercise treadmill test (ETT) in patients with aortic stenosis (AS) have not been tested before. <FILE IMAGE=’772_20180108164959.tif’> Design and method: We retrospectively assessed 316 patients with moderate (66%) or severe (34%) asymptomatic AS (age 65 ± 12 years) who underwent echocardiography and modified Bruce ETT at a specialist valve clinic. EBPR was defined as peak systolic BP 190mmHg or above. Results: The prevalence of EBPR was 22%. There was no difference in exercise duration, metabolic equivalents or severity of AS between patients with normal BP response and EBPR (all p = NS). Patients with EBPR were more likely to have hypertension, higher pre-test systolic BP, left ventricular (LV) ejection fraction and increased LV mass (all p < 0.05) (Table). A total of 264 events occurred during a mean follow up period of 34.9 ± 35.1 months. 234 patients reached an indication for aortic valve replacement (AVR), 75% in patients with normal BP response vs. 73% in patients with EBPR, p = NS). Among 30 (9%) deaths, 9.4% occurred in patients with normal BP response vs. 8.1% in EBPR group, p = NS). In univariate Cox regression analysis, the presence of EBPR was neither associated with all-cause mortality {HR 0.89, 95%CI 0.33–2.36, p = 0.814} nor AVR {HR 0.96, 95%CI 0.69–1.33, p = 0.785}. Conclusions: EBPR during treadmill exercise test in moderate to severe asymptomatic AS patients was strongly associated with hypertension and increased LV mass, but could not predict adverse outcomes.

Congenital heart disease in adults: Assessmentof functional capacity using cardiopulmonary exercise testing

AimThe aim of the study was to compare functional capacity in different types of congenital heart disease (CHD), as assessed by cardiopulmonary exercise testing (CPET). MethodsA retrospective analysis was performed of adult patients with CHD who had undergone CPET in a single tertiary center. Diagnoses were divided into repaired tetralogy of Fallot, transposition of the great arteries (TGA) after Senning or Mustard procedures or congenitally corrected TGA, complex defects, shunts, left heart valve disease and right ventricular outflow tract obstruction. ResultsWe analyzed 154 CPET cases. There were significant differences between groups, with the lowest peak oxygen consumption (VO2) values seen in patients with cardiac shunts (39% with Eisenmenger physiology) (17.2±7.1ml/kg/min, compared to 26.2±7.0ml/kg/min in tetralogy of Fallot patients; p<0.001), the lowest percentage of predicted peak VO2 in complex heart defects (50.1±13.0%) and the highest minute ventilation/carbon dioxide production slope in cardiac shunts (38.4±13.4). Chronotropism was impaired in patients with complex defects. Eisenmenger syndrome (n=17) was associated with the lowest peak VO2 (16.9±4.8 vs. 23.6±7.8ml/kg/min; p=0.001) and the highest minute ventilation/carbon dioxide production slope (44.8±14.7 vs. 31.0± 8.5; p=0.002). Age, cyanosis, CPET duration, peak systolic blood pressure, time to anaerobic threshold and heart rate at anaerobic threshold were predictors of the combined outcome of all-cause mortality and hospitalization for cardiac cause. ConclusionAcross the spectrum of CHD, cardiac shunts (particularly in those with Eisenmenger syndrome) and complex defects were associated with lower functional capacity and attenuated chronotropic response to exercise.

Warranty period of normal stress myocardial perfusion imaging in hypertensive patients: A parametric survival analysis

BackgroundWe evaluated the warranty period of a normal stress myocardial perfusion single-photon emission computed tomography (MPS) in hypertensive patients. Methods and ResultsA total of 471 consecutive hypertensive patients with suspected coronary artery disease and normal perfusion at stress MPS were followed for a mean of 76 ± 21 months. Endpoint events were cardiac death or nonfatal myocardial infarction. With Cox analysis, age (hazard ratio 1.1, P < .005) and stress test type (hazard ratio 2.7, P < .005) were independent predictors of events. With parametric Weibull analysis, patients ≤60 years old undergoing exercise stress test remained at low risk for the entire length of follow-up, while the highest probability of events and the major risk acceleration were observed in those > 60 years old who underwent pharmacologic stress test. In patients undergoing exercise test, peak systolic blood pressure (BP; hazard ratio 1.1, P < .005) emerged as predictor of events, and only subjects with peak systolic BP < 160 mmHg remained at low risk for the entire length of follow-up. In contrast, for patients with peak systolic BP ≥180 mmHg, the time to achieve a cumulative cardiac risk level of 3% was 18 months. ConclusionsIn hypertensive patients, the warranty period of a normal stress MPS varies according to stress type and peak systolic BP. A normal stress MPS can be considered reassuring in subjects ≤60 years old who performed exercise stress test and a peak systolic BP < 160 mmHg.

Enhanced Blood Pressure Lowering Responsiveness with Endocrine‐Sympathoinhibitory Electroacupuncture in Middle‐Aged Hypertensive Women

Our recently published study shows that 8‐week electroacupuncture (EA) at P5–6 and ST36–37 reduces blood pressure (70% responsiveness, blood pressure decrease of ≥ −6 mmHg) and sympathetic activity in a group of male and female (38–75 year) patients with mild to moderate hypertension (HTN). They were off of antihypertensive medications. Blood pressure reduction with 30‐min EA once a week treatment was observed by week 4. After 8 weeks of EA sessions, the blood pressure reduction lasted for at least a month. Here we define treatment at P5–6+ST36–37 as the sympathoinhibitory EA. Interestingly, the majority (64%) of middle‐aged women with HTN were not responsive to this treatment that reduces sympathetic activity. To this end, we formulated a targeted treatment towards middle‐aged perimenopausal hypertensive women. We hypothesized that endocrine‐sympathoinhibitory EA treatment decreases blood pressure in majority of middle‐aged perimenopausal females with mild to moderate HTN. Eleven enrolled women ages 49 to 66 year with hypertension were randomly assigned to sympathoinhibitory EA treatment (P5–6+ST36–37, n=6) or endocrine‐sympathoinhibitory EA treatment (P6+LI4+ST36+Sp6+CV3–4+LR3+KI3, n=5). Participants were not on antihypertensive medications and hormonal therapy. The enrolled patients have completed the 8‐week course of treatment. The blood pressure lowering responsiveness (≥ −6 mmHg) to endocrine‐sympathoinhibitory EA was 80% while only 33% of the subjects treated with sympathoinhibitory EA lowered their blood pressures. Peak systolic blood pressure (SBP) during 24 hours dropped from 177±7.4 to 160±5.0 mmHg (P=0.033) while averaged 24‐hour SBP dropped from 144±3.3 to 134±2.5 mmHg (P=0.036) in 5 subjects treated with endocrine‐sympathoinhibitory EA. The peak mean blood pressure (MBP) tended to decrease with P value of 0.065 in 5 subjects. On the other hand, 8‐week course of sympathoinhibitory EA treatment did not decrease SBP, MBP, peak SBP and peak MAP in 6 subjects. Thus, endocrine‐sympathoinhibitory EA in middle‐aged hypertensive women may enhance blood pressure lowering responsiveness compared with sympathoinhibitory EA treatment.Support or Funding InformationAdolf Coors FoundationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Timing of Blood Pressure Rhythms Predict Risk of Renal Injury in the Dahl Salt‐Sensitive Rats

Salt‐sensitive individuals have higher susceptibility for dysfunctional diurnal blood pressure rhythms, development of hypertension and renal injury. The aim of this study was to elucidate genetic determinants of diurnal excretion of renal injury markers and timing of systolic BP (SBP) peak and trough patterns in 4 rat models of salt‐sensitivity. We utilized male Dahl salt‐sensitive (SS) rats, NADPH oxidase p67phox knockout in SS (SS.p67phox−/−), introgression of chromosome 13 from Brown‐Norway rats into SS (SS.BN13), and introgression of 16Mbp section of BN13 (SS.BN‐(D13Rat151‐D13Rat197)) in SS (SS.Line26). Male, 12–14 week old rats (n=7–14) were maintained on normal salt (NS; 0.4% NaCl) and then fed high salt (HS; 4% NaCl) diet for 7 days (Dyets, AIN‐76A). Telemetry was used to continuously measure SBP, heart rate and locomotor activity. On NS, 24‐hr SBP was 155.9 ± 0.2 mmHg (SS), 141.6 ± 0.3 mmHg (SSp67phox−/−), 145.5 ± 0.4 mmHg (SS.BN13), and 155.2 ± 0.2 mmHg (SS.Line26). The average 24‐hr SBP in rats on high salt diet was 173.3 ± 0.5 mmHg, 152.2 ± 0.5 mmHg, 158.5 ± 0.6 mmHg, and 171.0 ± 0.6 mmHg, respectively. Eating HS did not change the timing of peak and trough SBP rhythms within each genotype. Furthermore, there were no differences in timing of peak timing of SBP across genotypes on either diet. Similarly, there was no difference in timing of trough SBP across genotypes on NS. However, HS delayed the timing of trough SBP in SS (n=14) by 5.3 hours compared to SS.p67phox−/− (n=12, p&lt;0.001) and by 2.6 hours compared to SS.BN13 rats (n=7, p=0.036). Timing of trough SBP was similar between SS.Line26 (n=12) and SS rats. Heart rate and locomotor activity were not significantly different across genotypes or diets. On HS diet, SS.p67phox−/− (n=8) had lower proteinuria and albuminuria than SS (n=14) and SS.Line26 (n=12) during the active phase (p&lt;0.0001). On HS, proteinuria, albuminuria, and nephrinuria were highest in SS.Line26 compared to SS, SS.p67phox−/−, and SS.BN13 (n=7) during active phase (p&lt;0.01). Excretion of kidney injury marker 1, KIM1, was significantly higher in SS than SS.Line26, SS.BN13, and SS.p67phox−/− (p&lt;0.005). In summary, SS and SS.Line26 rats have delays in the inactive (trough) timing of SBP, which is associated with proximal tubular injury in SS and glomerular injury in SS.Line26 rats. These findings indicate that rat chromosome 13 has a role at least in part, in the timing of SBP and risk of kidney injury in the SS rat.Support or Funding InformationAmerican Heart Association Strategically Focused Research Network ‐ Hypertension (15SFRN2390002)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effect of prolonged sleep restriction on the cardiovascular response to mental arithmetic

ObjectiveInadequate sleep is associated with an increased risk of hypertension. Exaggerated blood pressure (BP) reactivity to psychological stress is predictive of the development of hypertension. Following 24‐hours of total sleep deprivation, individuals exhibit an exaggerated BP response to mental stress (MS). The mechanisms contributing to this response and the generalizability to more prolonged exposure to restricted sleep are not clear. Thus we sought to examine the early hemodynamic response to MS in individuals before and during prolonged sleep restriction. We hypothesized the early rise in BP during MS would occur more slowly and would achieve a higher peak following 9 nights of restricted sleep when compared to control. We further hypothesized the contribution of total peripheral resistance (TPR) to the rise in BP would be greater following restricted sleep when compared to control.MethodsIndividuals completed two visits randomized to control sleep or experimental sleep restriction. Ten young (23±1 yrs) healthy, non‐obese (24±1 kg/m2) men and women (5M/5F) completed the restriction visit and seven of the same individuals (23±1 yrs; 5M/2F; 24±1 kg/m2) completed the control visit. Each visit consisted of 4 days of acclimation (9 hours of sleep per night) followed by 9 days of control (9 hours/night) or restricted (4 hours/night) sleep. For the purpose of this investigation, individuals were studied on days 2 and 13. Beat‐by‐beat heart rate (HR, electrocardiography) and BP (finger plethysmography) were measured continuously during 2 min of quiet rest followed by 5 min of mental arithmetic. Stroke volume (SV) was estimated from the pressure waveform and cardiac output (CO) and TPR were calculated. Peak change, time to peak, and rate of rise in BP were assessed during the initiation of mental stress (first 30‐s).ResultsBP increased during MS (P&lt;0.05) and the early peak BP did not differ between conditions (P=0.35–0.84). However, following prolonged experimental sleep restriction, individuals achieved peak systolic BP earlier (Time to peak: 19±4 vs 9±3 s, P=0.04) and the rate of rise in diastolic BP at the onset of MS was significantly greater (0.7± 0.3 vs 2.3±0.7 mmHg/s, P=0.01) when compared to the acclimation period. No differences in time to peak BP or rate of rise at the onset of MS were observed on the control visit (P=0.16–0.97). The peak change in SV (0.5±1.4 vs 6.3±2.1, P=0.03) and CO (1.1±0.2 vs 1.7±0.2 L/min, p=0.01) at the onset of MS were greater following prolonged sleep restriction when compared to the acclimation period. No differences in the change in SV or CO were observed on the control visit (P=0.39–0.41) and no differences in the change in TPR were observed on either visit (P=0.36–0.86).ConclusionsProlonged (9‐day) experimental sleep restriction (4 hours/night) results in a faster increase in BP in response to mental arithmetic. This rapid increase in BP at the onset of MS is achieved primarily via a greater increase in SV and CO when compared to the acclimation period. These data highlight an important role for CO in the BP response to stress in sleep restricted individuals and provide important insight into potential mechanisms which may contribute to the development of hypertension following inadequate sleep.Support or Funding InformationNIH HL130339, NIH HL114676, NIH HL114024, NIH HL083947, APS UGSRFThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Endothelial Cullin3 Mutation Causes Vascular Dysfunction, Arterial Stiffening, and Hypertension

Cullin3 (Cul3) is a critical subunit of the Cul3‐Ring‐Ligase (CRL3) ubiquitin ligase complex that targets proteins for proteasomal degradation. Mutations in CULLIN3 gene (causing in‐frame deletion of exon 9, termed Cul3Δ9) cause hypertension in humans. Evidence suggests that the hypertension in these subjects is likely to be caused by a combination of renal tubular and vascular mechanisms. We have recently shown that smooth muscle expression of Cul3Δ9 causes vascular dysfunction and elevation of blood pressure (BP) via augmented RhoA/Rho‐kinase signaling, strongly supporting a vascular role of Cul3 in BP regulation. To test the importance of endothelial Cul3 in vivo, we bred the conditionally activatable Cul3Δ9 mice with Tek‐CREERT2 mice specifically expressing tamoxifen‐inducible Cre‐recombinase in the endothelium. The resultant mice (E‐Cul3Δ9) exhibited impaired endothelial‐dependent relaxation in carotid artery (maximal relaxation in response to 30 μM acetylcholine, 69% vs 84% in littermate control mice, n=5, p&lt;0.05, two‐way ANOVA repeated measurements) and in the cerebral basilar artery (maximal relaxation in response to 100 μM acetylcholine, 41% vs 77% in littermate control mice, n=5, p&lt;0.01). No difference in smooth muscle function was observed. Moreover, E‐Cul3Δ9 mice exhibited nocturnal hypertension as determined by radiotelemetry (night time peak systolic BP, 138±3 mmHg n=7 vs 122±4 mmHg n=5, p&lt;0.01). However no difference was seen in daytime pressure. Preliminary data indicated that treatment with nitric oxide synthase (NOS) inhibitor Nω‐Nitro‐L‐arginine methyl ester markedly elevated nocturnal peak SBP in control mice (133±5 mmHg, n=3) but not in E‐Cul3Δ9 mice (143±3 mmHg, n=3), suggesting that NOS activity is low in E‐Cul3Δ9 mice. E‐Cul3Δ9 mice also exhibited arterial stiffening as indicated by elevated pulse wave velocity (3.7±0.3 m/s n=5 vs control mice 2.7±0.1 m/s n=7, p&lt;0.01). To determine the molecular mechanism of endothelial dysfunction, primary aortic endothelial cells were isolated from mice carrying the inducible Cul3Δ9 construct and Cul3Δ9 expression was robustly induced by adenovirus carrying Cre recombinase gene in vitro. Expression of Cul3Δ9 resulted in marked decreases in wild type Cul3 protein, phosphorylated eNOS, and nitric oxide production. Because protein phosphatase 2A (PP2A) is a known Cul3 substrate which negatively regulates eNOS phosphorylation, we determined whether impaired eNOS activity was attributable to PP2A. Cul3Δ9‐induced impairment of eNOS activity was rescued by a selective PP2A inhibitor Okadaic Acid (4 nM), but not by a Protein Phosphatase 1 inhibitor Tautomycetin (4 nM). These data define a novel regulatory pathway involving Cullin‐3/PP2A/phospho‐eNOS in the endothelium. Selective endothelial expression of Cul3Δ9 partially phenocopies the hypertension observed in Cul3Δ9 patients, suggesting that mutations in Cullin‐3 cause human hypertension in part through a vascular mechanism characterized by endothelial dysfunction.Support or Funding InformationDr. Jing Wu is supported by an American Heart Association Postdoctoral Fellowship (17POST33660685). This project is funded by R01 HL125603 and R01 HL131689 to Dr. Curt Sigmund.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A Cross-Sectional Study of the Prevalence of Exercise-Induced Hypertension in Childhood Following Repair of Coarctation of the Aorta

Exercise-testing may be a more tolerable method of detecting hypertension in children after coarctation repair compared to gold-standard 24-hour ambulatory blood pressure (BP) monitoring (ABPM). This study aims to determine the prevalence of exercise-induced hypertension and end-organ damage in children after coarctation repair, and the effectiveness of exercise-testing compared to 24-hour ABPM in this population. Exercise-testing (Bruce protocol), transthoracic echocardiogram, 24-hour ABPM, and pulse wave velocity were performed in 41 patients aged 8 to 18 years with previous coarctation repair. Median age at repair was 13 days. Exercise-testing data were compared to healthy paediatric controls. Hypertension was defined as BP >95th percentile on 24-hour ABPM compared to normalised data, and systolic BP (SBP) arbitrarily >200mmHg on exercise-testing. After 13±3years, 39% (14/36) were hypertensive on 24-hour ABPM and 12% (5/41) on exercise-testing. Coarctation patients had a higher peak exercise SBP and reduced endurance compared to controls (164±26mmHg vs. 148±19mmHg, p=0.003; and 13.0±1.7mins vs. 14.2±2.4mins, p=0.007; respectively). All patients with a peak exercise SBP >190mmHg were hypertensive on 24-hour ABPM. Pulse wave velocity was higher in hypertensive patients on exercise-testing and 24-hour ABPM compared to normotensive patients (p=0.004 and p=0.06; respectively). Exercise-testing may be a useful tool to detect hypertension in children and young adults after coarctation repair, particularly in those who do not tolerate 24-hour ABPM. Normative peak exercise BP data for age should be obtained to improve the accuracy of exercise-testing in detecting hypertension.

An exaggerated blood pressure response to exercise is associated with the dietary sodium, potassium, and antioxidant vitamin intake in normotensive subjects

ABSTRACTAim: This study was designed to examine the associations between an exaggerated systolic blood pressure (SBP) response to exercise and the nutrient intake in normotensive subjects.Methods: The subjects consisted of 302 normotensive subjects (64 males and 238 females; age, 48.4 ± 11.3 years) without a history of cardiovascular disease or stroke who were not taking any medications. Each subject performed a multistage graded submaximal exercise stress test using an electric bicycle ergometer, and their blood pressure was measured at rest and during the last minute of each stage. The nutrient intake was assessed using a self-administered food frequency questionnaire. An exaggerated SBP response to exercise was defined according to the criteria of the Framingham Study (peak SBP ≥210 mmHg in males, or ≥190 mmHg in females).Results: An exaggerated SBP response to exercise was observed in 85 subjects. A multiple logistic regression analysis revealed that the dietary sodium-to-potassium (Na/K) ratio (odds ratio [OR]: 5.75, 95% confidence interval [CI]: 2.37–13.75, p = 0.001) and vitamin E intake (OR: 0.67, 95% CI: 0.51–0.93, p = 0.012) were significantly associated with an exaggerated SBP response to exercise. Furthermore, the percent change in SBP during exercise was found to be significantly associated with an increase in the dietary Na/K ratio (p for trend = 0.0005) and a decrease in the vitamin E intake (p for trend = 0.018).Conclusions: These results suggest that an exaggerated SBP response to exercise was associated with the dietary sodium, potassium, and antioxidant vitamin intake in normotensive subjects.

Prognostic Role of Hypertensive Response to Exercise in Patients With Repaired Coarctation of Aorta

BackgroundThis study aimed to determine the prevalence of hypertensive response to exercise (HRE) and its association with cardiovascular adverse events (CAEs) in patients with repaired coarctation of aorta (rCOA). MethodsWe retrospectively reviewed records of adult patients with rCOA who had cardiopulmonary exercise tests (CPETs) and follow-up from 1994 to 2014 at Mayo Clinic. Patients with residual COA, defined as aortic isthmus peak velocity >2.5 m/s, were excluded. HRE was defined as peak systolic blood pressure >200 mm Hg; CAEs were defined as cardiovascular death, stroke, acute coronary syndrome, heart failure hospitalization, and left ventricular ejection fraction (LVEF) < 35%. ResultsOne hundred thirty-eight patients (82 men [59%]) underwent 213 CPETs, with follow-up of 85 ± 13 months. Age at initial COA repair was 9 ± 3 years; age at initial CPET was 40 ± 13 years. HRE occurred in 26 (19%) patients, and 24 (92%) of the patients with HRE had normal resting blood pressure. There were no differences in age, blood pressure at rest, and CPET findings between patients with HRE and those with normotensive response to exercise. There were 28 CAEs in 24 patients (17%), and HRE was an independent risk factor for CAE (hazard ratio [HR], 1.46 [1.13–2.52]; P = 0.04). ConclusionsHRE can occur even in the setting of normal blood pressure at rest, and it is a risk factor for CAE. We speculate that patients with HRE represent a high-risk group of patients who, presumably, have occult, advanced vascular dysfunction. CPET can identify these patients. The benefit of intensive antihypertension therapy needs to be confirmed.

Peak Blood Pressure Responses During Maximum Cardiopulmonary Exercise Testing

The objective of this study is to expand on previous efforts in establishing normative standards of exercising blood pressure (BP) at maximal physical exertion derived from treadmill cardiopulmonary exercise testing in the United States. Four experienced laboratories in the United States with established quality control procedures contributed data from September 1, 1986, to February 1, 2015. A total of 2917 maximal (peak respiratory exchange ratio ≥1.00) treadmill cardiopulmonary exercise testing responses from apparently healthy men and women (aged 20–79 years) without cardiovascular disease were submitted to FRIEND (Fitness Registry and the Importance of Exercise: A National Database). Percentiles of maximal systolic and diastolic BP were determined for each decade. Our results show a continued increase in peak systolic BP with age in both men and women to the sixth decade, followed by a plateau between the sixth and seventh decades. However, the trajectory of peak diastolic BP with age is different between men and women. Men showed an increase in peak systolic BP until the fifth decade, which plateaued by the seventh decade. In contrast, women showed a continued increase in peak diastolic BP across each decade. Existing reference data for exercising BP have not been updated for &gt;20 years. Normative peak exercising BP values from FRIEND can be used to provide a more current representation of maximal BP during exercise testing in the US population.

The exaggerated blood pressure response to exercise in the sub-acute phase after stroke is not affected by aerobic exercise.

The prevalence of an exaggerated exercise blood pressure (BP) response is unknown in patients with subacute stroke, and it is not known whether an aerobic exercise program modulates this response. The authors randomized 53 patients (27 women) with subacute stroke to 12weeks of twice-weekly aerobic exercise (n=29) or to usual care without scheduled physical exercise (n=24). At baseline, 66% of the patients exhibited an exaggerated exercise BP response (peak systolic BP ≥210mmHg in men and ≥190mmHg in women) during a symptom-limited ergometer exercise test. At follow-up, patients who had been randomized to the exercise program achieved higher peak work rate, but peak systolic BP remained unaltered. Among patients with a recent stroke, it was common to have an exaggerated systolic BP response during exercise. This response was not altered by participation in a 12-week program of aerobic exercise.

Systolic and Diastolic Regulation of the Cerebral Pressure-Flow Relationship Differentially Affected by Acute Sport-Related Concussion.

To determine whether acute sports-related concussion (SRC) exerts differential effects on cerebral autoregulatory properties during systole versus diastole. One hundred and thirty-six contact-sport athletes tested preseason; 14 sustained a concussion and completed follow-up testing at 72 hours, 2 weeks, and 1 month post-injury. Five minutes of repetitive squat-stand maneuvers induced blood pressure (BP) oscillations at both 0.05 and 0.10 Hz. Beat-by-beat peak-systolic and end-diastolic BP (sysBP/ diasBP) and middle cerebral artery blood velocity (sysMCAv/diasMCAv) were recorded using finger photoplethysmography and transcranial Doppler ultrasound, respectively. Relationships between sysBP-sysMCAv and diasBP-diasMCAv were quantified using transfer function analysis to estimate coherence (correlation), gain (response magnitude), and phase (response latency). Significant main effects of the cardiac cycle were observed across all outcome metrics. A significant main effect of SRC was observed for 0.10 Hz phase: systolic and diastolic phases were reduced at 72 h (21.8 ± 5.2%) and 2 weeks (22.7 ± 7.1%) compared to preseason but recovered by 1 month. Concussion significantly impaired diastolic, but not systolic, gain: 0.10 Hz diastolic gain was increased (27.2 ± 7.7%) at 2 weeks, recovering by 1 month. Impairments in autoregulatory capacity, observed for a transient period following SRC that persist beyond symptom resolution and clinical recovery, appear to be differentially affected across the cardiac cycle. Similar patterns of impairment were observed for systolic and diastolic phases (response latency); however, normalized gain (response magnitude) impairments were identified only in diastole. These findings may explain the increased cerebral vulnerability as well as exercise-induced symptom exacerbation observed post-SRC.

Factors Influencing Regional Cerebral Oxygen Saturation during One-lung Ventilation in Thoracic Surgery.

Objective To identify factors influencing regional cerebral oxygen saturation (rScO2) during one-lung ventilation (OLV) in thoracic surgery. Methods Totally 33 patients with an ASA physical status of 1-3 scheduled for elective thoracic surgery with one-lung ventilation under general anesthesia were recruited. After anesthesia was induced with propofol,fentanyl/sufentanil,and rocuronium. All patients received balanced anesthesia using sevoflurane. During OLV,volume-controlled ventilation was used with a tidal volume of 6-7 ml/kg and an inspiration:expiration ratio of 1:1.5. The ventilator frequency was adjusted with a target end-tidal carbon dioxide partial pressure (PetCO2) between 35 mmHg and 45 mmHg. During the anesthesia,patients were maintained at a pulse oxygen saturation (SpO2) of>90%,systolic blood pressure (SBP) of>90 mmHg (or reducing no more than 30% of the basic values),heart rate (HR) of>50 beat/min,and hemoglobin concentration of>90 g/L. Changes of rScO2 were monitored with FORESIGHT probes by specialized researchers. Patients were classified into low rScO2 (L-rScO2) group (n=10) or high rScO2 (H-rScO2)group(n=23) according to whether the lowest intraoperative rScO2 was under 65% or 15% lower than the baseline values. We compared gender,age,body mass index (BMI),intraoperative hemoglobin level,and the values of peak airway pressure (Ppeak),SBP,PetCO2,and SpO2 when rScO2 dropped to the lowest level between these two groups. Results Statistically higher Ppeak and lower SBP were noted in the L-rScO2 group compared with H-rScO2 group (P=0.028,P=0.046). SpO2 was lower in the L-rScO2 group compared with H-rScO2 group,but the difference was not statistically significant (P=0.421). There was also no significant difference between the two groups according to age,BMI,SpO2,PetCO2,or hemoglobin level. Ppeak appeared to be a risk factor for rScO2 reduction during OLV,as shown by unconditioned Logistic regression analysis. Conclusion During OLV in thoracic surgery,Ppeak is a risk factor for rScO2 reduction.

Myocardial Fibrosis in Competitive Triathletes Detected by Contrast-Enhanced CMR Correlates With Exercise-Induced Hypertension and Competition History

ObjectivesThis study analyzed the presence of myocardial fibrosis detected by late gadolinium-enhancement (LGE) cardiac magnetic resonance (CMR) in correlation with the performance of competitive triathletes objectified by an exercise test and individual competition history. BackgroundMyocardial fibrosis detected by LGE CMR has been reported to occur in 0% to 50% of asymptomatic athletes. However, the cause and mechanisms of myocardial fibrosis are unclear. MethodsEighty-three asymptomatic triathletes undergoing >10 training h per week (43 ± 10 years of age; 65% male) and 36 sedentary controls were studied by using LGE and extracellular volume (ECV) CMR. Parameters of physical fitness were measured by spiroergometry. Triathletes reported their lifetime competition results. ResultsLGE CMR revealed focal nonischemic myocardial fibrosis in 9 of 54 (17%) male triathletes (LGE+) but in none of the female triathletes (p < 0.05). LGE+ triathletes had higher peak exercise systolic blood pressure (213 ± 24 mm Hg) than LGE− triathletes (194 ± 26 mm Hg; p < 0.05). Furthermore, left ventricular mass index was higher in LGE+ triathletes (93 ± 7 g/m2) than in LGE− triathletes (84 ± 11 g/m2; p < 0.05). ECV in LGE− myocardium was higher in LGE+ triathletes (26.3 ± 1.8%) than in LGE− triathletes (24.4 ± 2.2%; p < 0.05). LGE+ triathletes completed longer cumulative distances in swimming and cycling races and participated more often in middle and Iron Man distances than LGE− triathletes. A cycling race distance of >1,880 km completed during competition had the highest accuracy to predict LGE, with an area under the curve value of 0.876 (p < 0.0001), resulting in high sensitivity (89%) and specificity (79%). Multivariate analysis identified peak exercise systolic blood pressure (p < 0.05) and the swimming race distance (p < 0.01) as independent predictors of LGE presence. ConclusionsMyocardial fibrosis in asymptomatic triathletes seems to be associated with exercise-induced hypertension and the race distances. There appears to be a safe upper limit, beyond which exercise may result in myocardial fibrosis.

Homocysteine, visceral adiposity-related novel cardiometabolic risk factors, and exaggerated blood pressure response to the exercise treadmill test.

Exaggerated blood pressure response to exercise is a risk factor for the development of future hypertension. In this study, we aimed to investigate the association between homocysteine, epicardial fat thickness, nonalcoholic hepatic steatosis, and exaggerated blood pressure response to exercise. We included 44 normotensive and 40 patients with exaggerated blood pressure response to exercise who have normal resting blood pressure and without a previous diagnosis of hypertension. All patients underwent treadmill exercise test and clinical, ultrasonographic, and echocardiographic evaluation. Exaggerated blood pressure response to exercise is defined as peak exercise systolic blood pressure of at least 210 mmHg in men and at least 190 mmHg in women. Homocysteine and other biochemical parameters were determined with standardized automated laboratory tests. Mean age of all participants is 47.9±8.5 years, and 36 of 84 participants were female. The frequency of diabetes mellitus in both groups was similar (P=0.250). Homeostasis model assessment index-insulin resistance had a statistically insignificant trend to be higher in a patient with exercise hypertension (P=0.058). The nonalcoholic fatty liver was more frequent in patients with exercise hypertension (13.6 vs. 47.5%, P=0.002). Epicardial fat thickness was increased in patients with exercise hypertension (5.5±1.5 vs. 7.3±1.1 mm; P=0.001). However, homocysteine levels did not significantly differ between normotensive and exercise hypertensive patients [12.3 μmol/l (5.7-16.9 μmol/l) vs. 13 μmol/l (5.9-28.3 μmol/l); P=0.883]. In our study, homocysteine levels were not associated with exaggerated blood pressure response to exercise; however, fatty liver and epicardial fat thickness as visceral adiposity-related cardiometabolic risk factors were significantly related with exaggerated blood pressure response to exercise in patients without a previous diagnosis of hypertension.

Impact of Atrial Fibrillation on Exercise Capacity and Mortality in Heart Failure With Preserved Ejection Fraction: Insights From Cardiopulmonary Stress Testing.

BackgroundAtrial fibrillation (AF) has been objectively associated with exercise intolerance in patients with heart failure with reduced ejection fraction; however, its impact in patients with heart failure with preserved ejection fraction has not been fully scrutinized.Methods and ResultsWe identified 1744 patients with heart failure and ejection fraction ≥50% referred for cardiopulmonary stress testing at the Cleveland Clinic (Cleveland, OH), 239 of whom had AF. We used inverse probability of treatment weighting to balance clinical characteristics between patients with and without AF. A weighted linear regression model, adjusted for unbalanced variables (age, sex, diagnosis, hypertension, and β‐blocker use), was used to compare metabolic stress parameters and 8‐year total mortality (social security index) between both groups. Weighted mean ejection fraction was 58±5.9% in the entire population. After adjusting for unbalanced weighted variables, patients with AF versus those without AF had lower mean peak oxygen consumption (18.5±6.2 versus 20.3±7.1 mL/kg per minute), oxygen pulse (12.4±4.3 versus 12.9±4.7 mL/beat), and circulatory power (2877±1402 versus 3351±1788 mm Hg·mL/kg per minute) (P<0.001 for all comparisons) but similar submaximal exercise capacity (oxygen consumption at anaerobic threshold, 12.0±5.1 versus 12.4±6.0mL/kg per minute; P =0.3). Both groups had similar peak heart rate, whereas mean peak systolic blood pressure was lower in the AF group (150±35 versus 160±51 mm Hg; P<0.001). Moreover, AF was associated with higher total mortality.ConclusionsIn the largest study of its kind, we demonstrate that AF is associated with peak exercise intolerance, impaired contractile reserve, and increased mortality in patients with heart failure with preserved ejection fraction. Whether AF is the primary offender in these patients or merely a bystander to worse diastolic function requires further investigation.

Arterial stiffness, sex, and age difference on hypertensive response to supine bicycle exercise.

Contributors to a hypertensive response to exercise (HTR) according to sex and age have not been fully evaluated. The authors analyzed a database of supine bicycle exercise stress echocardiography findings. HTR was defined as peak systolic blood pressure ≥210mmHg for men and ≥190mmHg for women during exercise. A total of 797 patients (306 [38%] women) were analyzed, with a mean age of 64±10years. Female sex, hypertension; higher left ventricular ejection fraction, effective arterial elastance, and pulse wave velocity; and lower total arterial compliance were significantly related to HTR. Patients with HTR had higher relative wall thickness, ratio of early diastolic mitral inflow and annular velocity, and diastolic elastance (all P≤.05). In multivariable analysis, indices of arterial stiffness such as pulse wave velocity, arterial elastance, total arterial compliance, and systemic vascular resistance were more strongly related in women, while in men, index of sympathetic activation was additionally related to HTR (all P≤.05). Female sex and lower total arterial compliance in older patients (≥65years) and higher systemic vascular resistance and left ventricular relative wall thickness in younger patients were more strongly related to HTR. In conclusion, HTR was related to arterial stiffness, sympathetic activation, and diastolic dysfunction; however, the associations were different according to sex and age, which might guide individualized therapy.

Reference values for blood pressure response to cycle ergometry in the first two decades of life: comparison with patients with a repaired coarctation of the aorta

ABSTRACTBackground: Hemodynamic responses to exercise are used as markers of diagnosis for cardiac diseases, systolic blood pressure (SBP) especially. However, the reference values for SBP in children at peak exertion level are outdated. This study aimed to establish current reference values for SBP, rate pressure product (RPP), and circulatory power (CircP).Methods: Data from children who previously underwent cardiopulmonary exercise testing were categorized as healthy (N = 184; age 12.6 ± 2.9 years), and CoA patients (N = 25; age 13.0 ± 3.2 years). With the Lambda-Mu-Sigma (LMS) method, percentile curves were made for SBP, CircP, and RPP in function of peak work rate (Wpeak). Data of CoA patients were used to validate the reference values.Results: Wpeak was the best predictor of peak SBP during exercise. The prediction equations for SBP, CircP and RPP were: (0.2853 x Wpeak) + 111.46; (10.56 x Wpeak) + 2550.2 and (61.879 x Wpeak) + 19.887, respectively. CoA patients showed significantly increased values for peak SBP (Z-score 1.063 ± 1.347).Conclusion: This study provides reference values for SBP, RPP, and CircP at peak exercise. These values can be used for objective evaluation of participants 6–18 years of age in a Dutch population.