Exercise-induced Hypertension Research Articles

Exercise-induced arterial hypertension - an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes?

Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. EIAH might be related to the “cardiac fatigue” caused by endurance training. The goal of this study was to examine whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman-triathletes. Methods: We used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was the participation in at least one middle or long distance triathlon. Results : When comparing triathletes with LVM <220g  and athletes with LVM >220g there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2± 21.5 mmHg vs. 198.8 ±22.3 mmHg, p=0.037). The spiroergometric results were: maximum oxygen uptake (relative VO 2 max) 57.3 ±7.5ml/min/kg vs . 59.8±9.5ml/min/kg (p=ns). Cut-point analysis for the relationship of BP >170 mmHg at the aerobic threshold and the probability of LVM >220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM >220g increased with higher BP during exercise (OR: 1.027, 95% CI 1.002-1.052, p= 0.034) or with higher training volume (OR: 1.23, 95% CI 1.04 -1.47, p = 0.019). Echocardiography showed predominantly concentric remodelling, followed by concentric hypertrophy. Conclusion : Significant left ventricular hypertrophy with LVM >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. The endurance athletes with EIAH may require a therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue.

Effect of atorvastatin on exercise tolerance in patients with diastolic dysfunction and exercise-induced hypertension

To investigate the effect of atorvastatin on exercise tolerance in patients with diastolic dysfunction and exercise-induced hypertension. A randomized, double-blind, placebo-controlled prospective study was performed. Sixty patients with diastolic dysfunction (mitral flow velocity E/A <1) and exercise-induced hypertension (SBP>200 mm Hg) treated with atorvastatin (20 mg q.d) or placebo for 1 year. Cardiopulmonary exercise test and exercise blood pressure measurement were performed. Plasma B-natriuretic peptide (BNP) concentration at rest and at peak exercise, plasma high sensitive-C reaction protein (hs-CRP) and endothelin (ET) concentration were determined at baseline and after treatment. After treatment by atorvastatin, the resting SBP, pulse pressure, the peak exercise SBP and BNP were significantly decreased; and the exercise time, metabolic equivalent, maximal oxygen uptake and anaerobic threshold were increased. All of these parameters had significant differences with baseline levels (P<0.05) and the rest pulse pressure, the peak exercise SBP and BNP, and the exercise time had significant differences compared with placebo treatment (P<0.05). Plasma concentrations of hs-CRP and ET were markedly reduced by atorvastatin treatment compared with baseline and placebo (P<0.05). No difference in above parameters was found before and after placebo treatment (P>0.05). In patients with diastolic dysfunction at rest and exercise-induced hypertension, atorvastatin can effectively reduce plasma hs-CRP and ET level, lower blood pressure and peak exercise SBP, decrease peak exercise plasma BNP concentration, and ultimately improve exercise tolerance.

EComment. Late complications after aortic coarctation repair

We have read the article by O'Sullivan et al. and we would like to add a comment on the complications of this pathological entity [1]. Aortic coarctation (AC) carries an incidence of 4 per 10 000 live births (5-8% of all congenital heart disease) and it can occur in association with patent ductus arteriosus, ventricular septal defect, bicuspid aortic valve (present in nearly two-thirds of patients with coarctation), concomitant hypoplastic aortic arch as well as parachute mitral valve stenosis, circle of Willis cerebral aneurysms and other congenital heart diseases (transposition of the great vessels, Taussig-Bing anomaly, hypoplastic left heart syndrome etc). Finally, AC is the commonest cardiac anomaly present in females with Turner syndrome [2, 3]. More importantly, the mean survival without treatment is 35 years and the vast majority of patients (90%) die before their 50s [2]. The choice of treatment has to be decided by a multi disciplinary team meeting with relevant specialists (Recommendation Class I, Level of Evidence C) [3]. Despite successful outcomes of its surgical treatment, late survival is compromised. For patients who are operated at a mean age of 16 years, the 10-, 20- and 30-year survival rates are 91%, 84% and 72% respectively [2]. Late complications can be subdivided into 8 categories namely: (i) re-coarctation, (ii) aortic aneurysm formation/aortic dissection, (iii) related to coexisting bicuspid aortic valve, (iv) endocarditis, (v) premature coronary atherosclerosis, (vi) strokes secondary to cerebrovascular aneurysms, (vii) systemic hypertension, and (viii) aortobronchial or aorto-oesophageal fistulas [2]. Re-coarctation is usually treated with primary balloon angioplasty with or without stent or surgical intervention. The probability of re-coarctation after surgery may be as high as 44% in neonates and 11% in older children, while adults carry a much lower risk (0-9%) [2]. About 9% of surgically-treated patients can develop aneurysms or pseudoaneurysms while those treated with balloon dilatation carry a much higher risk (20%) [2]. Those with coexisting bicuspid aortic valves are at an additional risk of developing aortic root dilatation [2]. Endocarditis can occur at the site of repair or at the coexisting bicuspid aortic valve and antibiotic prophylaxis is recommended subsequently according to the American Heart Association Guidelines [2, 3]. Premature atherosclerosis is usually the commonest cause of late death (25-37% of cases), leading to an increased risk of myocardial infarction and sudden death [2]. Circle of Willis aneurysms are present in 3-5% of patients and may cause cerebral haemorrhages even in normotensive individuals [2]. Systemic hypertension is found in 20-40% of patients followed-up 10 to 20 years after treatment and it represents a big challenge for the screening of either pregnant women or those with exercise-induced hypertension [2]. Aortobronchial fistulas are a rare though lethal complication and they can be safely managed with TEVAR [1, 2, 4]. All patients with treated AC should have lifelong close follow-up (at least yearly - Recommendation Class I, Level of Evidence C), magnetic imaging resonance/computed tomography should be repeated at intervals of 5 years at least (depending on anatomic findings) and management of blood pressure (Recommendation Class I, Level of Evidence B) and other risk factors should be applied [1, 3].

Long-term follow-up after aortic coarctation repair: The unsolved issue of exercise-induced hypertension

IntroductionDespite successful repair of aortic coarctation (AC), systemic hypertension (HTN) can persist in a significant percentage of patients. Exercise-induced HTN is also common in these patients, although its clinical significance is still unclear. In this study we aimed to assess the prevalence of exercise-induced HTN in adult patients with repaired AC. MethodsWe retrospectively reviewed the clinical records of patients aged >18 years with repaired AC followed at an adult congenital heart disease outpatient clinic in a tertiary care center. Demographic and clinical data including age at intervention, blood pressure (BP) at rest and on exercise, transthoracic echocardiogram (TTE) and treadmill exercise test results were evaluated. Exercise-induced HTN was defined as peak systolic BP ≥210 mmHg for men and ≥190 mmHg for women. ResultsWe analyzed 65 patients (40 [61.5%] male; mean age at follow-up 30±8 years). Median age at AC repair was 7 years (P25-P75: 4-20) and mean follow-up was 20±7 years. Only one patient had diabetes and 10 (15.4%) had dyslipidemia. The majority of patients had controlled BP at rest and only nine (18%) were under antihypertensive medication. Forty-nine patients performed a treadmill exercise test. The mean duration of exercise was 10.7±3.1 minutes and mean peak heart rate was 166±18 beats per minute. Eleven (22%) patients had a hypertensive response, among whom only three (33%) had uncontrolled BP at rest. In our study treatment with angiotensin-converting enzyme inhibitors (ACEI) (OR 4.0 [95% CI 1.9–18.1]) and the peak instantaneous gradient in the descending aorta by TTE (OR 8.2 [95% CI 1.8–37.0]) were predictors of a hypertensive response with exercise. Age at surgery and type of AC repair were not associated with a hypertensive response on exercise. ConclusionsIn this study we found a significant prevalence of exercise-induced HTN in adult patients after successful AC repair despite adequate BP control at rest. Exercise-induced HTN was significantly related to higher peak gradient in the descending aorta and treatment with ACEI. These results highlight the complexity of the adult AC population and show that, even after a good surgical result, several patients remain at high cardiovascular risk and require long-term follow-up.

Long-term follow-up after aortic coarctation repair: The unsolved issue of exercise-induced hypertension

IntroductionDespite successful repair of aortic coarctation (AC), systemic hypertension (HTN) can persist in a significant percentage of patients. Exercise-induced HTN is also common in these patients, although its clinical significance is still unclear. In this study we aimed to assess the prevalence of exercise-induced HTN in adult patients with repaired AC. MethodsWe retrospectively reviewed the clinical records of patients aged >18 years with repaired AC followed at an adult congenital heart disease outpatient clinic in a tertiary care center. Demographic and clinical data including age at intervention, blood pressure (BP) at rest and on exercise, transthoracic echocardiogram (TTE) and treadmill exercise test results were evaluated. Exercise-induced HTN was defined as peak systolic BP ≥210 mmHg for men and ≥190 mmHg for women. ResultsWe analyzed 65 patients (40 [61.5%] male; mean age at follow-up 30±8 years). Median age at AC repair was 7 years (P25-P75: 4-20) and mean follow-up was 20±7 years. Only one patient had diabetes and 10 (15.4%) had dyslipidemia. The majority of patients had controlled BP at rest and only nine (18%) were under antihypertensive medication. Forty-nine patients performed a treadmill exercise test. The mean duration of exercise was 10.7±3.1 minutes and mean peak heart rate was 166±18 beats per minute. Eleven (22%) patients had a hypertensive response, among whom only three (33%) had uncontrolled BP at rest. In our study treatment with angiotensin-converting enzyme inhibitors (ACEI) (OR 4.0 [95% CI 1.9–18.1]) and the peak instantaneous gradient in the descending aorta by TTE (OR 8.2 [95% CI 1.8–37.0]) were predictors of a hypertensive response with exercise. Age at surgery and type of AC repair were not associated with a hypertensive response on exercise. ConclusionsIn this study we found a significant prevalence of exercise-induced HTN in adult patients after successful AC repair despite adequate BP control at rest. Exercise-induced HTN was significantly related to higher peak gradient in the descending aorta and treatment with ACEI. These results highlight the complexity of the adult AC population and show that, even after a good surgical result, several patients remain at high cardiovascular risk and require long-term follow-up.

Exercise-induced exaggerated blood pressure response in men with the metabolic syndrome

Abnormalities in the autonomic nervous system in the presence of insulin resistance may be involved in the pathophysiology of obesity-associated hypertension. We evaluated the association between exercise-induced exaggerated blood pressure (BP) response [exercise-induced hypertension (EIH)] and heart rate variability (HRV) and insulin resistance in men with metabolic syndrome (MetS). Ninety-eight resting normotensive men with MetS underwent a maximal symptom-limited treadmill test. BP was measured after a 5-min rest (anticipatory BP) every 3 min during exercise and during the recovery period. EIH was defined as maximum systolic BP of 220 mmHg or higher and/or maximum diastolic BP of 100 mmHg or higher. Insulin resistance was estimated using HOMA-IR. Each participant underwent a 3-h oral glucose tolerance test (OGTT). HRV was derived from a 24-h Holter. About half of the participants (52%) presented EIH. Resting BPs at baseline were 125 ± 10/83 ± 7 mmHg in participants with EIH and 120 ± 9/80 ± 6 mmHg (P = 0.01) in the group with normal BP response to exercise. OGTT glucose levels were higher in the group with EIH (all P < 0.04) as well as HOMA-IR compared with participants with normal BP response to exercise (P = 0.03). In terms of HRV, 24-h standard deviation of the RR intervals (SDNN) was lower in participants with EIH (P = 0.04) as well as 24-h daytime and night-time high frequency and low frequency (P < 0.05). Normotensive men with MetS but with EIH have greater insulin resistance as well as lower HRV parasympathetic and sympathetic indices. These features may be involved in the pathophysiology of EIH.

Effect of a Prolonged Endurance Marathon on Vascular Endothelial and Inflammation Markers in Runners with Exercise-Induced Hypertension

The aim of this study was to observe the changes in endothelial and inflammatory markers in middle-aged male runners with exercise-induced hypertension (EIH) at baseline and at 100-km, 200-km, and 308-km checkpoints during a prolonged endurance ultramarathon. Among a total of 62 ultramarathon volunteers, 8 with systolic blood pressure higher than 210 mm Hg and 8 with normal systolic blood pressure were selected for this study. The subjects were designated to EIH and control (CON) groups. Blood was collected for the analysis of soluble vascular cell adhesion molecule-1, soluble E-selectin, leukocytes, creatine kinase, and high-sensitivity C-reactive protein. Soluble vascular cell adhesion molecule-1 showed a significantly greater increase in the EIH group than in the CON group at 100 km and 200 km. Soluble E-selectin also showed a significantly greater increase in the EIH group than in the CON group at 100 km. Leukocytes significantly increased in the EIH group than in the CON group at 308 km. Creatine kinase and high-sensitivity C-reactive protein showed no group differences. Leukocytes, creatine kinase, and high-sensitivity C-reactive protein showed delayed-onset increases in both groups. Increased exercise intensity may stimulate greater endothelial responses independent of the inflammatory markers in EIH. The loss of a protective effect may be greater in those with EIH than in CONs. Acknowledging and prescribing proper exercise intensity may be critical in preventing possible vascular-related complications in runners with EIH.

Effects of Marathon Running on Cardiac Markers and Endothelin-1 in EIH Athletes

The aim of the present study was to determine the changes in cardiac makers and endothelin-1 (ET-1) in marathoners with exercise induced hypertension compared to normotensive controls before and after running a marathon. Among a total of 70 volunteers, 10 marathoners with systolic blood pressure (SBP) greater than 210 mmHg during a treadmill exercise stress test were selected as an exercise-induced hypertension group (EIH) and 10 marathoners with normal SBP were selected as a control group (CON). Blood was collected from all volunteers 2 h before and immediately after a marathon: creatinine kinase (CK), CK-MB, cardiac tropoin-I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and endothelin-1(ET-1). Cardiac markers, CK, CK-MB, and CK-MB/CK ratio significantly increased in both EIH and CON; significance was not observed between the groups. Significant increases were not observed in high sensitive-C reactive protein (hs-CRP) after the race nor between the groups. Significant increases in cTnI and NT-proBNP were observed after the race in both groups. In addition, EIH showed greater increase than CON after the race. In conclusion, increased vascular tone in EIH during a marathon increased blood pressure and myocardial burden which in turn increased myocardial cell membrane permeability to further increase myocardial tension to the point of cTnI release.

Exercise-Induced Hypertension: Not Quite Ready for Prime Time

Metabolic Syndrome and Related DisordersVol. 11, No. 1 EditorialExercise-Induced Hypertension: Not Quite Ready for Prime TimeDavid SiegelDavid SiegelMedical Service, Department of Veterans Affairs, Northern California Health Care System, Mather, California.Department of Medicine, School of Medicine, University of California, Davis, Sacramento, California.Search for more papers by this authorPublished Online:23 Jan 2013https://doi.org/10.1089/met.2013.1502AboutSectionsView articleView Full TextPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetails Volume 11Issue 1Feb 2013 InformationCopyright 2013, Mary Ann Liebert, Inc.To cite this article:David Siegel.Exercise-Induced Hypertension: Not Quite Ready for Prime Time.Metabolic Syndrome and Related Disorders.Feb 2013.1-3.http://doi.org/10.1089/met.2013.1502Published in Volume: 11 Issue 1: January 23, 2013PDF download

Exercise-Induced Hypertension, Cardiovascular Events, and Mortality in Patients Undergoing Exercise Stress Testing: A Systematic Review and Meta-Analysis

The prognostic relevance of a hypertensive response to exercise (HRE) is ill-defined in individuals undergoing exercise stress testing. The study described here was intended to provide a systematic review and meta-analysis of published literature to determine the value of exercise-related blood pressure (BP) (independent of office BP) for predicting cardiovascular (CV) events and mortality. Online databases were searched for published longitudinal studies reporting exercise-related BP and CV events and mortality rates. We identified for review 12 longitudinal studies with a total of 46,314 individuals without significant coronary artery disease, with total CV event and mortality rates recorded over a mean follow-up of 15.2±4.0 years. After adjustment for age, office BP, and CV risk factors, an HRE at moderate exercise intensity carried a 36% greater rate of CV events and mortality (95% CI, 1.02-1.83, P = 0.039) than that of subjects without an HRE. Additionally, each 10mm Hg increase in systolic BP during exercise at moderate intensity was accompanied by a 4% increase in CV events and mortality, independent of office BP, age, or CV risk factors (95% CI, 1.01-1.07, P = 0.02). Systolic BP at maximal workload was not significantly associated with the outcome of an increased rate of CV, whether analyzed as a categorical (HR=1.49, 95% CI, 0.90-2.46, P = 0.12) or a continuous (HR=1.01, 95% CI, 0.98-1.04, P = 0.53) variable. An HRE at moderate exercise intensity during exercise stress testing is an independent risk factor for CV events and mortality. This highlights the need to determine underlying pathophysiological mechanisms of exercise-induced hypertension.

Exercise-induced hypertension among healthy firefighters—a comparison between two different definitions

Different studies have yielded conflicting results regarding the association of hypertensive response to exercise and cardiovascular morbidity. We compared two different definitions of exaggerated hypertensive response to exercise and their association with cardio-respiratory fitness in a population of healthy firefighters. We examined blood pressure response to exercise in 720 normotensive male career firefighters. Fitness was measured as peak metabolic equivalent tasks (METs) achieved during maximal exercise treadmill tests. Abnormal hypertensive response was defined either as systolic blood pressure ≥ 200 mm Hg; or alternatively, as responses falling in the upper tertile of blood pressure change from rest to exertion, divided by the maximal workload achieved. Using the simple definition of a 200 mm Hg cutoff at peak exercise less fit individuals (METs ≤12) were protected from an exaggerated hypertensive response (OR 0.45, 95%CI 0.30–0.67). However, using the definition of exercise-induced hypertension that corrects for maximal workload, less fit firefighters had almost twice the risk (OR 1.8, 95%CI 1.3–2.47). Blood pressure change corrected for maximal workload is better correlated with cardiorespiratory fitness. Systolic blood pressure elevation during peak exercise likely represents an adaptive response, whereas elevation out of proportion to the maximal workload may indicate insufficient vasodilation and a maladaptive response. Prospective studies are needed to best define exaggerated blood pressure response to exercise.

Exercise-Induced Hypertension in Men with Metabolic Syndrome: Anthropometric, Metabolic, and Hemodynamic Features

Metabolic syndrome is associated with increased cardiac morbidity. The aim of this study was to evaluate exercise-induced hypertension (EIH) in men with metabolic syndrome and to explore potential associations with anthropometric and metabolic variables. A total of 179 normotensive men with metabolic syndrome underwent a maximal symptom-limited treadmill test. Blood pressure was measured at 5-min rest prior to exercise testing (anticipatory blood pressure), at every 3 min during the exercise, and during the recovery period. EIH was defined as maximum systolic blood pressure (SBP) ≥220 mmHg and/or maximum diastolic blood pressure (DBP) ≥100 mmHg. Of the 179 men, 87 (47%) presented EIH. Resting blood pressure values at baseline were 127±10/83±6 mmHg in EIH and 119±9/80±6 mmHg (P=0.01 for both) in normal blood pressure responders to exercise. Anticipatory SBP and DPS were higher in the group with EIH (P=0.001). Subjects with EIH presented higher waist circumference (WC) (P<0.01), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein B (ApoB) levels as well as insulin resistance (all P<0.05). Abdominal subcutaneous adipose tissue and total body fat mass were comparable between groups. Subjects with EIH had higher abdominal visceral adipose tissue (P<0.001). The best predictors of EIH were resting SBP and abdominal obesity. Each increment of 5 cm in WC was associated with an odds ratio of 1.30 (1.20-1.68) for EIH. About half of our subjects with metabolic syndrome showed EIH. These men are characterized by a worsened metabolic profile. Our data suggest that a treadmill exercise test may be helpful to identify a potentially higher risk metabolic syndrome subset of subjects.

Predictors of exaggerated exercise-induced systolic blood pressures in young patients after coarctation repair

In normotensive subjects, an exaggerated blood pressure response to exercise is associated with the development of resting hypertension. We sought to determine the prevalence of elevated blood pressures during exercise in post-operative coarctation patients with normal resting blood pressure, and investigate associations with exercise-induced hypertension in this population. A total of 38 patients were enrolled after end-to-end anastomosis repair and resting normotension. All patients underwent anthropometric and blood pressure measurements, echocardiographic evaluation of function, arterial stiffness assessment by pulse wave velocity, and a graded exercise test. An abnormal response was defined as a maximum systolic blood pressure greater than the 95th percentile of published normal values. Correlation analyses and stepwise regression analyses were performed. The mean age was 12.7 years, including 79% male patients. The mean resting systolic blood pressure was 111.3 millimetres of mercury and the mean exercise systolic blood pressure was 178.1 millimetres of mercury. The prevalence of a systolic blood pressure greater than the 95th percentile was 16.7%. In multivariate analysis, the exercise systolic blood pressure index was associated with body mass index, age, aortic valve annulus, shortening fraction, and pulse wave velocity (R2 equal to 0.79, p equal to 0.0009). Estimates of ventricular filling and indexed left ventricular mass were elevated. There is a risk of elevated systolic blood pressure during exercise in normotensive patients after coarctation repair. Resting blood pressures are useful but not sufficient. Echocardiography demonstrated abnormalities suggestive of a chronic cardiac burden despite resting normotension. Regular imaging may be necessary to improve long-term outcomes. New paradigms for the continued follow-up of these patients are necessary.

Comparison of Exercise-Induced Hypertension in Low Birth Weight and Normal Birth Weight Young Black Adults in Zimbabwe

The objective of the study was to compare blood pressure changes during exercise between low and normal birth weight young Black adults. Eighty medical students in their first and second year who had neonatal clinic cards as proof of birth weight were included in the study. Resting blood pressures and heart rates were recorded. Participants then underwent a multistage 9-minute exercise stress test while blood pressure responses were recorded at 3-minute intervals. The study was conducted in the Department of Physiology, University of Zimbabwe, College of Health Sciences, Harare, Zimbabwe. Of the 80 subjects recruited, 34 had low birth weight (LBW), 26 of these were female and 8 were male. The proportion of LBW individuals, 62% (n = 21), who developed exercise-induced hypertension (EIH) was significantly higher (p < 0.05) than the proportion of those with normal birth weight (NBW), 32% (n = 11). In addition to LBW being significantly associated with EIH (χ2 test p < 0.05, odds ratio 7.5) compared with NBW, the LBW group had a significantly higher (p < 0.05) and exaggerated systolic and diastolic response in stages I and II of the exercise protocol compared with the NBW group. LBW was associated with EIH in these young Black adults.

Cardiorespiratory Screening in Elite Endurance Sports Athletes: The Quebec Study

Background: Cardiorespiratory disorders are common in athletes. However, these conditions are often underdiagnosed, which potentially results in impaired performance and increased health risks. The aim of this study was to evaluate, in a research setting, the prevalence of cardiorespiratory disorders in athletes in order to determine the potential value of a screening program. Methods: One hundred thirty-three athletes were studied. Each subject underwent a physical examination. A eucapnic voluntary hyperventilation (EVH) test and a methacholine inhalation test were performed to confirm the diagnosis of asthma. A cardiovascular evaluation was also performed, including maximal exercise test with electrocardiogram, 24-hour ambulatory blood pressure monitoring, 24-hour Holter monitoring, and blood sampling. Results: Seventy-four (56%) athletes had airway hyperresponsiveness to EVH or the methacholine inhalation test. Among those with airway hyperresponsiveness, 45 (61%) athletes were only hyperresponsive to EVH, and 10 (14%) were only hyperresponsive to the methacholine inhalation test (using the criteria of a PC20 ≤ 4 mg/mL). Thirty-two (24%) athletes had a known diagnosis of asthma, while 34 (26%) athletes received a new asthma diagnosis. Ninety-seven (73%) athletes were sensitized to common airborne allergens. Forty-seven (35%) athletes completed the cardiovascular evaluation. Three (6%) and 7 (15%) athletes had a previous or new diagnosis of cardiovascular disease, respectively. Resting systemic hypertension was documented in 2 (4%) athletes and exaggerated blood pressure response to exercise was found in 12 (26%) athletes. Conclusion: This cardiorespiratory screening data set in athletes showed a high prevalence of exercise-induced asthma and exercise hypertension, which in many cases were not previously diagnosed.

Comparison of Exercise-Induced Hypertension in Low Birth Weight and Normal Birth Weight Young Black Adults in Zimbabwe

Comparison of Exercise-Induced Hypertension in Low Birth Weight and Normal Birth Weight Young Black Adults in Zimbabwe

Cardiac Markers of EIH Athletes in Ultramarathon

This study aimed to investigate effects of a 100-km ultramarathon on cardiac markers of exercise-induced-hypertensive marathoners. 10 marathoners with exercise-induced hypertension and 10 normal marathoners participated in the study. Their blood samples were collected before starting, at 50 km, and after finishing the course (100 km). Creatinine kinase was more significantly increased in the exercise-induced-hypertensive group than in the normal group at 100 km (P<0.05). N-terminal pro-brain nutriuretic peptide was significantly increased in the exercise-induced-hypertensive group at 50 km and 10 km (P<0.05) which was significant being doubled compared to the normal group (P<0.05). Exercise-induced-hypertensive marathoners showed a significant triple-increase in C-Reactive protein at 100 km (P<0.05). In conclusion, although the exercise-induced-hypertensive runners did not have myocardial damage during the 100 km ultramarathon, they had higher myocardial stress and more damage in active muscles due to a bloodstream disability.

Hemodynamic Modeling of Surgically Repaired Coarctation of the Aorta

PURPOSE: Late morbidity of surgically repaired coarctation of the aorta includes early cardiovascular and cerebrovascular disease, shortened life expectancy, abnormal vasomodulator response, hypertension and exercise-induced hypertension in the absence of recurrent coarctation. Observational studies have linked patterns of arch remodeling (Gothic, Crenel, and Romanesque) to late morbidity, with Gothic arches having the highest incidence. We evaluated flow in native and surgically repaired aortic arches to correlate respective hemodynamic indices with incidence of late morbidity. METHODS: Three dimensional reconstructions of each remodeled arch were created from an anatomic stack of magnetic resonance (MR) images. A structured mesh core with a boundary layer was generated. Computational fluid dynamic (CFD) analysis was performed assuming peak flow conditions with a uniform velocity profile and unsteady turbulent flow. Wall shear stress (WSS), pressure and velocity data were extracted. RESULTS: The region of maximum WSS was located in the mid-transverse arch for the Crenel, Romanesque and Native arches. Peak WSS was located in the isthmus of the Gothic model. Variations in descending aorta flow patterns were also observed among the models. CONCLUSION: The location of peak WSS is a primary difference among the models tested, and may have clinical relevance. Specifically, the Gothic arch had a unique location of peak WSS with flow disorganization in the descending aorta. Our results suggest that varied patterns and locations of WSS resulting from abnormal arch remodeling may exhibit a primary effect on clinical vascular dysfunction.

Usefulness of Exercise-Induced Hypertension as Predictor of Chronic Hypertension in Adults After Operative Therapy for Aortic Isthmic Coarctation in Childhood

Chronic hypertension is a major concern in adults who have undergone resection of coarctation of the aorta (CoA) in childhood. In otherwise healthy subjects, exercise-induced hypertension is prognostic for chronic hypertension; however, the prognostic value in patients with CoA remains unknown. The aim of the present study was to evaluate the predictive value of exercise-induced hypertension for chronic hypertension in these patients. In the present prospective follow-up study, 74 patients with CoA (58% men, age 30.9 ± 9.5 years) underwent ambulatory blood pressure (BP) monitoring and exercise testing twice from 2001 to 2009 with a follow-up period of 6.3 ± 0.8 years. Hypertension was defined as a mean systolic BP ≥140 mm Hg and/or mean diastolic BP ≥90 mm Hg or the need for antihypertensive treatment. Exercise-induced hypertension was defined as a mean systolic BP of <140 mm Hg and peak exercise systolic BP of ≥200 mm Hg. At baseline, 27 patients (36%) were hypertensive, 11 (15%) had exercise-induced hypertension, and 36 (49%) were normotensive. At follow-up, all 27 hypertensive patients remained hypertensive. Of the 11 with exercise-induced hypertension, 7 (64%) had developed chronic hypertension, and 4 (36%) continued to have exercise-induced hypertension. Of the 36 normotensive patients, 7 (19%) had developed hypertension, 12 (33%) had developed exercise-induced hypertension, and 17 (47%) remained normotensive. On multivariate analysis, baseline maximum exercise systolic BP was independently associated with the mean systolic BP at follow-up (β = 0.13, p = 0.005). In conclusion, the maximum exercise systolic BP was a predictor for chronic hypertension in patients with CoA. These findings demonstrate the clinical importance of exercise-induced hypertension and warrant additional study into the long-term consequences of exercise-induced hypertension and the potential beneficial role of early antihypertensive treatment in adult patients after CoA repair with exercise-induced hypertension.

Effects Of Aerobic Exercise On Cardiopulmonary Functions In Exercise-induced Hypertension

Effects Of Aerobic Exercise On Cardiopulmonary Functions In Exercise-induced Hypertension