Abnormal Blood Pressure Response Research Articles

P990Assessment of clinical risk factors for all-cause mortality among hypertrophic cardiomyopathy patients with ICDs

Abstract Introduction According to the literature, the annual mortality rate of hypertrophic cardiomyopathy (HCM) patients is estimated to 1–2%. Sudden cardiac death (SCD), heart failure and thromboembolism are the main causes of death among this population. Patients at high risk for SCD, identified using HCM risk score, are qualified for ICD implantation. Unfortunately for clinicians, there is no validated model or statistical tool for assessment of the risk of mortality within the HCM patients with ICDs. Purpose The aim of this study was to determine the main risk factors of all- cause mortality in HCM patients with ICDs. Methods The long-term follow-up of group of 104 consecutive patients with HCM, who had the ICD implanted between 1996 and 2006 in tertiary reference clinical unit was performed. Twenty patients who died during observation were the subject of the current analysis. ICD was implanted for primary (n=16) and secondary (n=4) prevention of SCD within this subpopulation. Analysis were performed for mentioned below potential risk factors: age at the time of implantation, syncopes, family history of SCD, atrial fibrillation/supraventricular tachycardia, decreased left ventricular ejection fraction (LVEF), non-sustained ventricular tachycardia (nsVT), maximum left ventricular wall thickness, abnormal exercise blood pressure response, left ventricular outflow tract obstruction. Results The average time of survival since ICD implantation was 8,5±4,6 years. Decreased LVEF (Wald chi2 4,57; p=0,033), secondary prevention (Wald chi2 8,57; p=0,003), family history of SCD (Wald chi2 4,93; p=0,026) and episodes of nsVT (Wald chi2 3,49; p=0,062) are the clinical risk factors that significantly affect the time of survival. The probability of death, expressed as Hazard Ratio, was 27-fold higher in secondary prevention group (HR=27,18), almost 10-fold higher in patients with positive family history of SCD (HR=9,74) and 3,7-fold higher when nsVT was detected. The cause of death was established in 16/20 patients. In 15 cases, these were deaths from cardiovascular causes: end-stage heart failure (8), complications of heart transplantation or circulatory support (4), SCD (1) and other cardiovascular (2). Conclusion Secondary prevention, positive family history of SCD, nsVT and decreased LVEF seem to be the most significant risk factors associated with all- cause mortality in HCM patients with ICDs. Despite the ICD implantation, subpopulation studied had poor prognosis with high incidence of progression to end-stage heart failure. Further studies to create validated model for assessment of death risk in long-term observation of patients with HCM after ICD implantation are required.

A practical guide to active stand testing and analysis using continuous beat-to-beat non-invasive blood pressure monitoring.

The average adult stands approximately 50-60 times per day. Cardiovascular responses evoked during the first 3min of active standing provide a simple means to clinically assess short-term neural and cardiovascular function across the lifespan. Clinically, this response is used to identify the haemodynamic correlates of patient symptoms and attributable causes of (pre-)syncope, and to detect autonomic dysfunction, variants of orthostatic hypotension, postural orthostatic tachycardia syndrome and orthostatic hypertension. This paper provides a set of experience/expertise-based recommendations detailing current state-of-the-art measurement and analysis approaches for the active stand test, focusing on beat-to-beat BP technologies. This information is targeted at those interested in performing and interpreting the active stand test to current international standards. This paper presents a practical step-by-step guide on (1) how to perform active stand measurements using beat-to-beat continuous blood pressure measurement technologies, (2) how to conduct an analysis of the active stand response and (3) how to identify the spectrum of abnormal blood pressure and heart rate responses which are of clinical interest. Impairments in neurocardiovascular control are an attributable cause of falls and syncope across the lifespan. The simple active stand test provides the clinician with a powerful tool for assessing individuals at risk of such common disorders. However, its simplicity belies the complexity of its interpretation. Care must therefore be taken in administering and interpreting the test in order to maximise its clinical benefit and minimise its misinterpretation.

Risk factors for lethal arrhythmic events in children and adolescents with hypertrophic cardiomyopathy and an implantable defibrillator: An international multicenter study

Predictors of risk of lethal arrhythmic events (LAE) is poorly understood and may differ from adults in children with hypertrophic cardiomyopathy (HCM). The purpose of this study was to determine predictors of LAE in children with HCM. A retrospective data collection was performed on 446 children and teenagers 20 years and younger (290 [65%] male; mean age 10.1 ± 5.7 years) with idiopathic HCM from 35 centers. Patients were classified as group 1 (HCM with LAE) if having a secondary prevention implantable cardioverter-defibrillator (ICD) or primary prevention ICD with appropriate interventions or group 2 (HCM without LAE) if having a primary prevention ICD without appropriate interventions. There were 152 children (34%) in group 1 and 294 (66%) in group 2. Risk factors for group 1 by univariate analysis wereseptal thickness, posterior left ventricular (LV) wall thickness, lower LV outflow gradient, and Q wave > 3 mm in inferior electrocardiographic leads. Factors not associated with LAE were family history of SCD, abnormal blood pressure response to exercise, and ventricular tachycardia on ambulatory electrocardiographic monitoring. Risk factors for SCD by multivariate analysis were age at ICD placement (hazard ratio [HR] 0.9; P = .0025), LV posterior wall thickness z score (HR 1.02; P < .005), and LV outflow gradient < 30 mm Hg (HR 2.0; P < .006). LV posterior wall thickness z score ≥ 5 was associated with LAE. Risk factors for LAE appear different in children compared to adults. Conventional adult risk factors were not significant in children. Further prospective studies are needed to improve risk stratification for LAE in children with HCM.

Rapid early rise in heart rate on treadmill exercise in patients with asymptomatic moderate or severe aortic stenosis: a new prognostic marker?

ObjectiveTo examine the clinical significance and prognostic value of an early rapid rise in heart rate (RR-HR) in asymptomatic patients with moderate or severe aortic stenosis (AS).MethodsWe retrospectively assessed the...

Role of Myocardial Fibrosis in Hypertrophic Cardiomyopathy: A Systematic Review and Updated Meta-Analysis of Risk Markers for Sudden Death.

BackgroundHypertrophic cardiomyopathy (HCM) is associated with sudden death (SD). Myocardial fibrosis is reportedly correlated with SD.ObjectiveWe performed a systematic review with meta-analysis, updating the risk markers (RMs) in HCM emphasizing myocardial fibrosis.MethodsWe reviewed HCM studies that addressed severe arrhythmic outcomes and the certain RMs: SD family history, severe ventricular hypertrophy, unexplained syncope, non-sustained ventricular tachycardia (NSVT) on 24-hour Holter monitoring, abnormal blood pressure response to exercise (ABPRE), myocardial fibrosis and left ventricular outflow tract obstruction (LVOTO) in the MEDLINE, LILACS, and SciELO databases. We used relative risks (RRs) as an effect measure and random models for the analysis. The level of significance was set at p < 0.05.ResultsTwenty-one studies were selected (14,901 patients aged 45 ± 16 years; men, 62.8%). Myocardial fibrosis was the major RISK MARKER (RR, 3.43; 95% CI, 1.95-6.03). The other RMs, except for LVOTO, were also predictors: SD family history (RR, 1.75; 95% CI, 1.39-2.20), severe ventricular hypertrophy (RR, 1.86; 95% CI, 1.26-2.74), unexplained syncope (RR, 2.27; 95% CI, 1.69-3.07), NSVT (RR, 2.79; 95% CI, 2.29-3.41), and ABPRE (RR, 1.53; 95% CI, 1.12-2.08).ConclusionsWe confirmed the association of myocardial fibrosis and other RMs with severe arrhythmic outcomes in HCM and emphasize the need for new prediction models in managing these patients.

Exercise Treadmill Testing in Moderate or Severe Aortic Stenosis: The Left Ventricular Correlates of an Exaggerated Blood Pressure Rise.

BackgroundExaggerated blood pressure response during exercise predicts future hypertension and cardiovascular events in general population and different patients groups. However, its clinical and prognostic implications in patients with aortic stenosis have not been previously evaluated.Methods and ResultsWe retrospectively studied 301 patients with moderate to severe asymptomatic aortic stenosis (aged 65±12 years) who underwent echocardiography and a modified Bruce exercise treadmill test. An exaggerated blood pressure response was defined as peak systolic blood pressure ≥190 mm Hg. An abnormal blood pressure response (either blunted or exaggerated) was found in 58% of patients and abnormal left ventricular geometry in 82%. There was no difference in the rates of abnormal blood pressure responses between patients with moderate and severe aortic stenosis ([exaggerated blood pressure response: 21% versus 22%, P=0.876] and [blunted blood pressure response: 35% versus 40%, P=0.647]). Patients with exaggerated blood pressure response (21%) were more likely to be older, have hypertension, higher pretest systolic blood pressure, left ventricular ejection fraction and mass, and increased arterial stiffness (all P<0.05). In a multivariate logistic regression analysis, an exaggerated blood pressure response was associated with higher pulse pressure/stroke volume index (odds ratio 2.45, 95% confidence interval 1.02–6.00, P=0.037) and left ventricular mass (odds ratio 2.04, 95% confidence interval 1.23–3.38, P=0.012) independent of age, hypertension, aortic annulus and left atrium diameter, and left ventricular ejection fraction.ConclusionsIn those with aortic stenosis, exaggerated blood pressure was strongly related to higher resting blood pressure values, left ventricular mass, and increased arterial stiffness independent of hypertension.

Abstract 17066: Indications for Implantable Cardioverter-Defibrillator Placement in Pediatric Patients With Hypertrophic Cardiomyopathy

Background: Sudden cardiac death (SCD) is the most common cause of death in children and adolescents with hypertrophic cardiomyopathy (HCM). Implantable cardio-defibrillators (ICD) are highly effective in preventing SCD, however, indications for ICD placement in the young is mainly guided from the adult experience. Methods: We conducted a retrospective single institution study of all children with HCM who had an ICD implanted from July 1999 through February 2016. Results: Thirty-three patients were identified. The mean age at ICD placement was 12.3±3 years with a mean follow up of 3.6±2.5 years. The mean maximal septal wall thickness Z score was 9.3± 2.9 and mean peak LV outflow tract gradient 17±12 mmHg. The median number of indications for ICD placement per patient was 3 (21%, 52%, 15% and 12% of the patients had 2, 3, 4 and 5 indications respectively). The most common indications were: severe HCM (Z-score ≥ + 6) (84%), abnormal blood pressure response to exercise (51%) and late gadolinium enhancement (LGE) (27%). Using the European Society of Cardiology HCM SCD risk calculator, the 5-year SCD risk was highest when the indication was ventricular tachycardia (VT). However, no patient with VT received ICD therapy (shock or anti tachycardia pacing (ATP)) during the study period. Fifteen patients received ICD therapy; 73% appropriately (73% a shock, 9% ATP and 18% both). Inappropriate shocks were delivered to 67% of the patients. One patient had slow rate VT (below the therapy zone) and one patient had ventricular fibrillation that did not elicit ICD therapy and required external defibrillation. The incidence rate ratios for appropriate ICD therapy were higher when the indication for the ICD placement was LGE (3.69), severe HCM (2.3) or compound heterozygosity (1.2) p &lt;0.05. The majority of patients (&gt;95%) were alive and free of transplant at 1 and 5 years after ICD placement. Conclusions: The risk stratification and selection of patients for ICD placement in the pediatric population is challenging. LGE, severe HCM and compound heterozygosity are associated with higher rate of appropriate ICD therapy. Optimal functioning of the ICD device in children and adolescents is difficult. The overall immediate survival and freedom from transplant is excellent.

Exercise hemodynamics in hypertrophic cardiomyopathy identify risk of incident heart failure but not ventricular arrhythmias or sudden cardiac death

ObjectiveTo determine whether abnormal blood pressure response (ABPR), with or without left ventricular outflow tract obstruction (LVOTO), is associated with adverse heart failure and arrhythmia outcomes in hypertrophic cardiomyopathy (HCM). MethodsA retrospective, single-center analysis was performed for adult HCM patients who underwent exercise stress testing. ResultsOf 589 patients included in the study, 192 (33%) demonstrated ABPR. A similar proportion of patients with ABPR had LVOTO compared to those without ABPR (56% vs 63%, p = 0.11). Patients with ABPR demonstrated lower percent predicted VO2 and METs achieved than those with LVOTO (16.9 ± 6.8 vs 21.6 ± 7.9, p = 0.002 and 5.3 ± 2.4 vs 7.4 ± 3.1, p < 0.001). In a subgroup of 17 patients with LVOTO and ABPR who subsequently underwent successful myectomy, 5 (30%) demonstrated persistent ABPR. 23 patients (3.8%) experienced sudden cardiac death or ventricular arrhythmias, which were not associated with ABPR, regardless of age group. In multivariable analysis, syncope (p = 0.04), left ventricular hypertrophy (p = 0.02) and left atrial diameter (p = 0.006) were significantly associated with the composite outcome of sudden death or severe ventricular arrhythmia, whereas ABPR was not (p = 0.38). In contrast, ABPR was associated with subsequent heart failure hospitalization (p = 0.002), regardless of presence or absence of LVOTO (p = 0.04, p = 0.02). ConclusionsABPR is associated with reduced functional capacity in HCM regardless of the presence of LVOTO but is not associated with adverse arrhythmia outcomes. Patients with ABPR have a higher incidence of subsequent heart failure hospitalization.

Autonomic function test in progressive lacunar infarction.

Neurological progression is a major problem in managing the patients with acute lacunar infarction. The purpose of this was to investigate whether autonomic dysfunction is associated with neurological progression in patients with acute lacunar infarction. The study comprised 60 patients with acute lacunar infarction. All enrolled subjects underwent autonomic function tests including the 30° head-up tilt test, Valsalva test, heart rate response to deep breathing, and sympathetic skin response. The primary endpoint is the neurological progression, and the secondary endpoint is the 3-month outcome. Increased initial National Institute of Health stroke scale (NIHSS), decreased time to admission from onset, decreased rise of heart rate in the 30° head-up tilt test, abnormal blood pressure response in the Valsalva test, and decreased rise of systolic blood pressure in stage IV of the Valsalva test are associated with neurological progression of acute lacunar infarction; an abnormal blood pressure response in the Valsalva test is significant in logistic regression analysis of neurological progression. Advanced age, increased initial NIHSS and modified Rankin scale, decreased expiration/inspiration ratio of heart rate to deep breathing, decreased rise of systolic blood pressure in stage IV of the Valsalva test, and neurological progression were associated with an unfavorable 3-month outcome; neurological progression was significant in logistic regression analysis of 3-month outcome. An abnormal blood pressure change in the Valsalva test is associated with neurological progression in patients with acute lacunar infarction, and neurological progression can induce an unfavorable 3-month outcome.

Rest and Stress Longitudinal Systolic Left Ventricular Mechanics in Hypertrophic Cardiomyopathy: Implications for Prognostication

Exercise intolerance is the most common symptom in hypertrophic cardiomyopathy (HCM). We examined whether inability to augment myocardial mechanics during exercise would influence functional performance and clinical outcomes in HCM. Ninety-five HCM patients (32 nonobstructive, 32 labile-obstructive, 31 obstructive) and 26 controls of similar age and gender distribution were recruited prospectively. They underwent rest and treadmill stress strain echocardiography, and 61 of them underwent magnetic resonance imaging. Mechanical reserve (MRES) was defined as percent change in systolic strain rate (SR) immediately postexercise. Global strain and SR were significantly lower in HCM patients at rest (strain: nonobstructive, -15.6±3.0; labile-obstructive, -15.9±3.0; obstructive, -13.8±2.9; control, -17.7%±2.1%, P<.001; SR: nonobstructive, -0.92±0.20; labile-obstructive, -0.94±0.17; obstructive, -0.85±0.18; control, -1.04±0.14s-1, P=.002); and immediately postexercise (strain: nonobstructive, -15.6±3.0; labile-obstructive, -17.6±3.6; obstructive, -15.6±3.6; control, -19.2±3.1%; P=.001; SR: nonobstructive, -1.41±0.37; labile-obstructive, -1.64±0.38; obstructive, -1.32±0.29; control, -1.82±0.29s-1, P<.001). MRES was lower in nonobstructive and obstructive compared with labile-obstructive and controls (51%±29%, 54%±31%, 78%±38%, 77%±30%, P=.001, respectively). Postexercise SR and MRES were associated with exercise capacity (r=0.47 and 0.42, P<.001 both, respectively). When adjusted for age, gender, body mass index, E/e', and resting peak instantaneous systolic gradient, postexercise SR best predicted exercise capacity (r=0.74, P=.003). Postexercise SR was correlated with extent of late gadolinium enhancement (r=0.34, P=.03). By Cox regression, exercise SR and MRES predicted ventricular tachycardia/ventricular fibrillation (VT/VF) even after adjustment for age, gender, family history of sudden cardiac death, septum≥3cm and abnormal blood pressure response (P=.04 and P=.046, respectively). Nonobstructive and obstructive patients have reduced MRES compared with labile-obstructive and controls. Postexercise SR correlates with LGE and exercise capacity. Exercise SR and MRES predict VT/VF.

Blood Pressure Response to Exercise and Cardiovascular Disease.

This review aimed to provide a clinical update on exercise blood pressure (BP) and its relationship to cardiovascular disease (CVD), outlining key determinants of abnormal exercise BP responses. We also highlight current evidence gaps that need addressing in order to optimise the relevance of exercise BP as clinical CVD risk factor. Abnormal exercise BP manifests as either exercise hypotension (low BP response) or as exaggerated exercise BP (high BP response). Exercise hypotension is an established sign of existing and likely severe CVD, but exaggerated exercise BP also carries elevated CVD risk due to its association with sub-clinical hypertension. Although exaggerated exercise BP is related to heightened CVD risk at any exercise intensity, recent data suggest that the BP response to submaximal intensity exercise holds greater prognostic and clinical significance than BP achieved at peak/maximal intensity exercise. Cardiorespiratory fitness is a strong modifier of the exercise BP response, and should be taken into consideration when assessing the association with CVD. Both exercise hypotension and exaggerated exercise BP serve as markers that should prompt evaluation for potential underlying CVD. However, the clinical utility of these markers is currently inhibited by the lack of consensus informing the definitions and thresholds for abnormalities in exercise BP.

O50-1 - Abnormal Blood Pressure Response to Exercise and Exercise Tolerance in Patients with Stable Heart Failure

Background: Abnormal blood pressure (BP) response to exercise is often observed and reported to be associated with adverse cardiac events in patients with coronary artery disease. Reduced exercise tolerance is an independent predictor of adverse cardiac events in patient with heart failure (HF), but few data are available regarding the relation between exercise tolerance and abnormal BP response to exercise. Method: A total of 81 patients with stable HF underwent a symptom-limited cardiopulmonary exercise test. BP was noninvasively measured at an interval of one minute, and considered abnormal when exercise-induced increases in systolic BP were less than 25 mmHg. Exercise tolerance was evaluated with peak oxygen uptake (peak VO2). Result: The peak VO2 was 18.3 ± 4.8 ml/kg/min in all the patients. Abnormal BP response to exercise was observed in 29 patients (36%). There were no significant differences in resting BP and heart rate between the two groups. The peak VO2 was significantly lower in patients with abnormal BP response (15.9 ± 3.7 ml/kg/min) than in patients without abnormal BP response (19.7 ± 4.8 ml/kg/min, P < .05). Conclusions: Abnormal BP response to exercise was associated with reduced exercise tolerance in patients with stable HF. Further study is warranted to examine whether abnormal BP response is associated with adverse cardiac events in patients with stable HF.

Comparison of two European models estimating risk of ­sudden cardiac death in hypertrophic cardiomyopathy

Objective Hypertrophic cardiomyopathy (HCM) is associated with a risk of sudden cardiac death (SCD). Several models have been developed to estimate SCD risk and guide preventive therapy. The comparison of the previous 2003 with novel 2014 SCD risk models have never been studied. MethodsOver a year we included 103 consecutive HCM patients without previous cardiac arrest and/or ICD implanted (65% males; aged 53.3 ± 13.9 years; mean EF 62.3 ± 18%). The SCD risk was calculated for each patient.Results Based on the 2003 model, patients had following scores: 0 points -15 (15%) patients, 1-28 (27%), 2-34 (33%), 3-18 (17%), ≥ 4-8 (8%). According to the 2014 model 83 (80%) had low risk, 12 (12%) intermediate risk, and only 8 (8%) high risk. Patients who had an intermediate or high risk in the 2003 model but a low risk in 2014 model were the oldest, experienced less frequently syncope and nsVT, but had more often abnormal blood pressure response to exercise and an intermediate LVOT gradient in comparison to the patients who had consistently low or high risk in both models.Conclusions Calculation of SCD risk using two models provides completely different risk estimates and consequently different guidance on SCD primary prevention. According to the 2003 model up to 85% of patients have indications for ICD, whereas based on the 2014 risk model only 20% of the patients had non-negligible SCD risk and are candidates for ICD therapy. SCD risk markers, used in the 2003 and 2014 models, have various discriminating power.

Risk factors for sudden cardiac death in childhood hypertrophic cardiomyopathy: A systematic review and meta-analysis.

Aims To perform a systematic literature review and meta-analysis of clinical risk factors for sudden cardiac death (SCD) in childhood hypertrophic cardiomyopathy. Methods Medline and PubMed databases were searched for original articles published in English from 1963 through to December 2015 that included patients under 18 years of age with a primary or secondary end-point of either SCD or SCD-equivalent events (aborted cardiac arrest or appropriate implantable cardioverter-defibrillator discharge) or cardiovascular death (CVD). Results Twenty-five studies (3394 patients) met the inclusion criteria. We identified four conventional major risk factors that were evaluated in at least four studies and that we found to be statistically associated with an increased risk of death in at least two studies: previous adverse cardiac event (pooled hazard ratio [HR] 5.4, 95% confidence interval [CI] 3.67-7.95, p < 0.001); non-sustained ventricular tachycardia (pooled HR 2.13, 95% CI 1.21-3.74, p = 0.009); unexplained syncope (pooled HR 1.89, 95% CI 0.69-5.16, p = 0.22); and extreme left ventricular hypertrophy (pooled HR 1.80, 95% CI 0.75-4.32, p = 0.19). Left atrial diameter did not meet the major risk factor criteria; however, this is likely to be an additional significant risk factor. 'Minor' risk factors included a family history of SCD, gender, age, symptoms, electrocardiogram changes, abnormal blood pressure response to exercise and left ventricular outflow tract obstruction. Conclusions A lack of well-designed, large, population-based studies in childhood hypertrophic cardiomyopathy means that the evidence base for individual risk factors is not robust. We have identified four clinical parameters that are likely to be associated with increased risk of SCD, SCD-equivalent events or CVD. Multi-centre prospective studies are needed in order to further determine the relevance of these factors in predicting SCD in childhood hypertrophic cardiomyopathy and to identify novel risk markers. Condensed abstract A systematic review and meta-analysis of clinical risk factors predicting sudden cardiac death in childhood hypertrophic cardiomyopathy was performed, identifying four 'major' factors: previous adverse cardiac event; non-sustained ventricular tachycardia; syncope; and extreme left ventricular hypertrophy. Well-designed multi-centre studies are required in the future in order to confirm these findings.

Frequency, Predictors, and Implications of Abnormal Blood Pressure Responses During Dobutamine Stress Echocardiography.

It is not known whether abnormal blood pressure (BP) responses during dobutamine stress echocardiography (DSE) are associated with abnormal test results, nor if such results indicate obstructive coronary artery disease (CAD). We sought to define the frequency of abnormal BP responses during DSE and their impact on accuracy of test results. We studied 21 949 patients who underwent DSE at Mayo Clinic, Rochester, MN, grouped by peak systolic BP achieved during the test. We also analyzed a subgroup who underwent coronary angiography within 30 days after positive DSE. The positive predictive value of DSE was calculated for each BP group. Patients with hypertensive response (n=1905; 9%) were more likely to have positive DSE than those with normal (n=19 770; 90%) or hypotensive (n=274; 1%) BP responses (32% versus 21% versus 23%, respectively; P<0.0001). Angiography, performed in 1126 patients, showed obstructive CAD (≥50% stenosis) in 814 patients and severe CAD (≥70% stenosis) in 708 patients. Positive predictive value of DSE was similar for patients who had hypertensive and normal BP responses (69% versus 73%; P=0.3), considering 50% stenosis cut point. The proportion of severe CAD (≥70% stenosis) was lower in patients who had hypertensive response compared with those who had normal BP response (54% versus 65%; P=0.005). Patients with hypertensive response during DSE are more likely to have stress-induced myocardial ischemia compared with those with normal or hypotensive BP responses but are not more likely to have false-positive DSE results. They are, however, less likely to have higher grade or multivessel CAD.

Blood pressure dynamics during exercise rehabilitation in heart failure patients.

Background Patients suffering from heart failure (HF) may demonstrate an abnormal blood pressure response to exercise (ABPRE), which may revert to a normal one following medical treatment. It is assumed that this change correlates positively with prognosis and functional aspects. The aim of this study was to characterize patients with ABPRE and assess ABPRE normalization and the correlation with clinical and functional outcomes. Methods In the study, 651 patients with HF who underwent cardiac rehabilitation (CR) were examined. Patients who presented an ABPRE during stress testing were identified and divided into those who corrected their initial ABPRE following CR and those who did not. Results Pre-rehabilitation ABPRE was present in 27% of patients, 68% of whom normalized their ABPRE following CR. Two parameters were independently predictive of failure to normalize the blood pressure response: female gender (odds ratio (OR) 3.5; 95% confidence interval (CI) 1.4-9.0) and decreased systolic function (OR 3.2; 95% CI 1.0-9.4). Patients with hypertrophic cardiomyopathy demonstrated higher rates of ABPRE normalization than patients with other causes of HF (93% vs. 62%, respectively, P = 0.03). The research population exhibited an average improvement in exercise capacity (4.7 to 6.4 metabolic equivalents (METS), P < .001), ejection fraction (35.4% to 37.7%, P < .001) and percentage of patients with New York Heart Association (NYHA) class 3-4 (50% to 43.4%, P = .123). The group who normalized their ABPRE exhibited greater improvement. Conclusions Amongst a population of patients suffering from HF, an ABPRE was normalized following CR in two thirds of patients. Female gender and a reduced systolic function independently predicted the failure to correct the ABPRE, while patients with hypertrophic cardiomyopathy demonstrated exceptionally high rates of normalization.

High sucrose intake during gestation increases angiotensin II type 1 receptor-mediated vascular contractility associated with epigenetic alterations in aged offspring rats

Accruing evidence have confirmed that the fetal programming in response to adverse environmental in utero factors plays essential roles in the pathogenesis of hypertension in later life. High sugar intake has been accepted worldwide in everyday life diet and becomes the critical public health issue. Our previous studies indicated that intake of high sucrose (HS) during pregnancy could change the vascular reactivity and dipsogenic behavior closely associated with abnormal renin-angiotensin system (RAS), to increase the risk of hypertension in adult offspring. In the present study, we tested the hypothesis that maternal HS intake in pregnancy may further deteriorate the Ang II-induced cardiovascular responses in the aged offspring. HS intake was provided to pregnant rats throughout the gestation. Blood pressure (BP) in conscious state and vascular contractility in vitro were measured in 22-month-old aged offspring rats. In addition, mRNA and protein expressions and epigenetic changes of Ang II type 1 receptor (AT1R) gene in blood vessels were determined with the methods of real-time RT-PCR, Western blotting, and Chromatin Immunoprecipitation Assay (CHIP). Results showed that, in the aged offspring, maternal HS intake during gestation would cause the elevation of basal BP which could be diminished by losartan. Although the circulatory Ang II was not changed, levels of local Ang II were significantly increased in blood vessels. In addition, prenatal HS exposure would significantly enhance the AT1R-mediated vasoconstrictions in both aorta and mesenteric arteries of the aged offspring. Moreover, in the aged offspring of prenatal HS exposure, mRNA and protein expressions of AT1R gene in both large and small blood vessels were significantly increased, which should be closely associated with the changes of epigenetic mechanisms such as histone modifications. Collectively, we proposed that maternal HS intake during gestation would cause abnormal BP responses mediated via the enhancement of vascular RAS, together with the increased expression of AT1R gene related to the its epigenetic changes, which would actually lead to the overt phenotype of hypertension in the aged offspring.

Safety profile and utility of treadmill exercise in patients with high-gradient hypertrophic cardiomyopathy

Exercise echocardiography in the evaluation of hypertrophic cardiomyopathy (HCM) provides valuable information for risk stratification, selection of optimal treatment, and prognostication. However, HCM patients with left ventricular outflow tract gradients ≥30mm Hg are often excluded from exercise testing because of safety considerations. We examined the safety and utility of exercise testing in patients with high-gradient HCM. We evaluated clinical characteristics, hemodynamics, and imaging variables in 499 consecutive patients with HCM who performed 959 exercise tests. Patients were divided based on peak left ventricular outflow tract gradients using a 30-mm Hg threshold into the following: obstructive (n=152), labile-obstructive (n=178), and nonobstructive (n=169) groups. There were no deaths during exercise testing. We noted 20 complications (2.1% of tests) including 3 serious ventricular arrhythmias (0.3% of tests). There was no difference in complication rate between groups. Patients with obstructive HCM had a higher frequency of abnormal blood pressure response (obstructive: 53% vs labile: obstructive: 41% and nonobstructive: 37%; P=.008). Obstructive patients also displayed a lower work capacity (obstructive: 8.4±3.4 vs labile obstructive: 10.9±4.2 and nonobstructive: 10.2±4.0, metabolic equivalent; P<.001). Exercise testing provided incremental information regarding sudden cardiac death risk in 19% of patients with high-gradient HCM, and we found a poor correlation between patient-reported functional class and work capacity. Our results suggest that exercise testing in HCM is safe, and serious adverse events are rare. Although numbers are limited, exercise testing in high-gradient HCM appears to confer no significant additional safety hazard in our selected cohort and could potentially provide valuable information.

Abnormal blood pressure response to exercise in badminton athletes

Summary Purpose This study aimed to examine blood pressure changes in response to exercise and to identify blood pressure abnormalities in collegiate male and female athletes. Material and methods Sixteen collegiate badminton players 16–22 years of age and with 3–8 years of badminton experience participated in the study. Participants’ blood pressure was recorded before and after a multistage fitness test. Results Following exercise, blood pressure significantly increased; mean maximum systolic blood pressure (SBPmax) and SBP delta (the difference between post- and pre-exercise SBP) were 100 mmHg, an abnormal blood pressure response to exercise. Conclusion The findings support the notion that blood pressure response to exercise may be an important diagnostic parameter in normotensive athletes at risk of developing hypertension and/or cardiovascular diseases. Monitoring athletes’ exercise blood pressure by coaches, trainers, or sports scientists thus constitutes an important part of athletes’ fitness evaluation.

Stratification du risque de la mort subite dans la cardiomyopathie hypertrophique en 2016

Patients with hypertrophic cardiomyopathy (HCM) are at an increased risk of death from many causes and sudden cardiac death is one of them. The study of the sudden cardiac death of patients with HCM has allowed the identification of risk factors and among them major risk factor are: family history of sudden cardiac death, the occurrence of syncope/dizziness, the existence of non-sustained ventricular tachycardia an abnormal blood pressure response during stress test, presence of severe left ventricular hypertrophy≥30mm. Risk stratification for sudden cardiac death is essential, for symptomatic or asymptomatic HCM patients. Two approaches are possible: the classical approach or risk stratification methods with major risk factors and the new approach using the risk-calculator recommended by the ESC. Both methods are not in opposition but complementary. The risk stratification in hypertrophic cardiomyopathy should be still improved to be sure that only the most high-risk patients receive an implantable cardiac defibrillator.