Effects Of Age And Conditioning Status On Rest And Exercise Cardiac Performance
年龄和体能状态对休息和运动心脏功能的影响
基本信息
- 批准号:8931601
- 负责人:
- 金额:$ 6.47万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:
- 资助国家:美国
- 起止时间:至
- 项目状态:未结题
- 来源:
- 关键词:AbdomenAccountingAdultAerobicAgeAgingAntihypertensive AgentsBaltimoreBlood PressureBlood TestsBlood VesselsBody fatBody mass indexCardiacCardiac OutputCardiac VolumeCardiovascular DiseasesCardiovascular alterationCardiovascular systemCessation of lifeCholesterolClinicalCommunitiesConfidence IntervalsCoronaryCouplingCross-Sectional StudiesDual-Energy X-Ray AbsorptiometryEchocardiographyExerciseExercise stress testFatty acid glycerol estersFunctional disorderGenderGlomerular Filtration RateHabitsHeartHeart RateHigh Density Lipoprotein CholesterolHourIndividualLaboratoriesLeftLeft Ventricular MassLeptinLife StyleLinkLongitudinal StudiesMeasuresMediator of activation proteinMetabolic PathwayModelingMorphologyMultivariate AnalysisObesityOrganOxygenParticipantPerformancePeripheralPharmaceutical PreparationsPhysical activityPhysiologic pulsePlayPopulationPulse PressureRelaxationRestRiskRisk FactorsRoleScanningSex Hormone-Binding GlobulinSmokingStroke VolumeStructureSturnus vulgarisSurveysSymptomsSystolic PressureTechniquesTestingThickTreadmill TestsTriglyceridesVascular resistanceVenousVentricularVentricular TachycardiaVisceralVisitX-Ray Computed Tomographyadipokinesadiponectinage effectage relatedbaseblood lipidcardiovascular risk factorcohortconditioningdemographicsfasting plasma glucosefollow-uphazardhigh riskindexinginsightinterestintima mediamalemenmortalitypressureprognosticresearch clinical testingsexsubcutaneousvolunteerwhite coat hypertension
项目摘要
Effective arterial elastance (EA) is a measure of the net arterial load imposed on the heart that
integrates the effects of heart rate(HR), peripheral vascular resistance(PVR), and total arterial compliance(TAC) and is a modulator of cardiac performance. To what extent the change in EA during exercise impacts on cardiac performance and aerobic capacity is unknown. We examined EA and its relationship with cardiovascular performance in 352 healthy subjects (Chantler et al. 2012). Subjects underwent rest and exercise gated scans to measure cardiac volumes and to derive EAend-systolic pressure/stroke volume index(SV), PVRMAP/(SV*HR), and TAC(SV/pulse pressure). EA varied with exercise intensity: the EA between rest and peak exercise along with its determinants, differed among individuals and ranged from -44% to +149%, and was independent of age and sex. Individuals were separated into 3 groups based on their EAI. Individuals with the largest increase in EA(group 3;EA0.98 mmHg.m2/ml) had the smallest reduction in PVR, the greatest reduction in TAC and a similar increase in HR vs. group 1(EA<0.22 mmHg.m2/ml). Furthermore, group 3 had a reduction in end-diastolic volume, and a blunted increase in SV(80%), and cardiac output(27%), during exercise vs. group 1. Despite limitations in the Frank-Starling mechanism and cardiac function, peak aerobic capacity did not differ by group because arterial-venous oxygen difference was greater in group 3 vs. 1. Thus the change in arterial load during exercise has important effects on the Frank-Starling mechanism and cardiac performance but not on exercise capacity. These findings provide interesting insights into the dynamic cardiovascular alterations during exercise.
Another study (Marine et al. 2013) sought to determine the clinical predictors and prognostic significance of exercise-induced nonsustained ventricular tachycardia (NSVT) in a large population of asymptomatic volunteers. Subjects in the BLSA (Baltimore Longitudinal Study of Aging) free of known cardiovascular disease who completed at least 1 symptom-limited exercise treadmill test between 1977 and 2001 were included. NSVT episodes were characterized by QRS morphology, duration, and rate. Subjects underwent follow-up clinical evaluation every 2 years.
The 2,099 subjects (mean age: 52 years; 52.2% male) underwent a mean of 2.7 exercise tests, in which 79 (3.7%) developed NSVT with exercise on at least 1 test. The median duration of NSVT was 3 beats (5 beats in 84%), and the median rate was 175 beats/min. Subjects with (vs. without) NSVT were older (67 12 years vs. 51 17 years, p < 0.0001) and more likely to be male (80% vs. 51%, p < 0.0001) and to have baseline electrocardiographic abnormalities (50% vs. 17%, p < 0.0001) or ischemic ST-segment changes with exercise (20% vs. 10%, p 1/4 0.004). Over a mean follow-up of 13.5 7.7 years, 518 deaths (24.6%) occurred. After multivariable adjustment for age, sex, and coronary risk factors, exercise-induced NSVT was not significantly associated with total mortality (hazard ratio: 1.30; 95% confidence interval: 0.89 to 1.90; p 1/4 0.17). Exercise-induced NSVT occurred in nearly 4% of this asymptomatic adult cohort. This finding increased with age and was more common in men. After adjustment for clinical variables, exercise-induced NSVT did not independently increase the risk of total mortality.
It is unclear whether subcutaneous and visceral fat are differentially correlated to the decline in left ventricular (LV) diastolic function with aging. A study (Canepa et al. 2013) sought to examine the hypothesis that age-related changes in the regional fat distribution account for changes in LV diastolic function and to explore potential mediators of this association. In a cross-sectional study, we evaluated 843 participants of the Baltimore Longitudinal Study of Aging with echocardiogram, dual-energy X-ray absorptiometry (DEXA), abdominal computed tomography (CT) and blood tests performed at the same visit. LV diastolic function was assessed by parameters of LV relaxation (E/A ratio, Em and Em/Am ratio) and LV filling pressures (E/Em ratio). Total body fat was computed by DEXA, while visceral and subcutaneous fat were determined from abdominal CT. In multivariate models adjusted for demographics, cardiovascular risk factors, antihypertensive medications, physical activity and LV mass, both visceral and subcutaneous fat were associated with LV diastolic dysfunction. When both measures of adiposity were simultaneously included in the same model, only visceral fat was significantly associated with LV diastolic dysfunction. Triglycerides and sex-hormone binding globulin, but not adiponectin and leptin, were found to be significant mediators of the relationship between visceral fat and LV diastolic function, explaining 2847% of the association. Bootstrapping analyses confirmed the significance of these findings. Conclusions: Increased visceral adiposity is associated with LV diastolic dysfunction, possibly through a metabolic pathway involving blood lipids and ectopic fat accumulation rather than adipokines.
Arterial aging may link cardiovascular risk to white coat hypertension (WCH). A study (Sung et al. 2013) investigated the role of arterial aging in the white coat effect, defined as the difference between office and 24-hour ambulatory systolic blood pressures, and to compare WCH with prehypertension (PH) with respect to target organ damage and long-term cardiovascular mortality. A total of 1257 never-been-treated volunteer subjects from a community-based survey were studied. WCH and PH were defined by office and 24-hour ambulatory blood pressures. Left ventricular mass index, carotid intima-media thickness, estimated glomerular filtration rate, carotid-femoral pulse wave velocity, carotid augmentation index, amplitude of the reflection pressure wave, and 15-year cardiovascular mortality were determined. Subjects with WCH were significantly older and had greater body mass index, blood pressure values, intima-media thickness, carotid-femoral pulse wave velocity, augmentation index, amplitude of the backward pressure wave, and a lower estimated glomerular filtration rate than PH. Amplitude of the backward pressure wave was the most important independent correlate of the white coat effect in multivariate analysis (model r2=0.451; partial r2/model r2=90.5%). WCH had significantly greater cardiovascular mortality than PH (hazard ratio, 2.94; 95% confidence interval, 1.097.91), after accounting for age, sex, body mass index, smoking, fasting plasma glucose, and total cholesterol/high-density lipoprotein-cholesterol ratio. Further adjustment of the model for amplitude of the backward pressure wave eliminated the statistical significance of the WCH effect. In conclusion, the white coat effect is mainly caused by arterial aging. WCH carries higher risk for cardiovascular mortality than PH, probably via enhanced wave reflections that accompany arterial aging.
有效的动脉弹性(EA)是对心脏施加的净动脉负荷的量度
整合了心率(HR),外周血管阻力(PVR)和总动脉依从性(TAC)的影响,并且是心脏性能的调节剂。运动期间EA的变化在多大程度上影响心脏性能和有氧运动能力。我们检查了EA及其与352名健康受试者中心血管表现的关系(Chantler等,2012)。受试者进行了休息和运动封闭式扫描,以测量心脏体积,并得出Eaend-Syend-ScyStoly压力/中风体积指数(SV),PVRMAP/(SV*HR)和TAC(SV/脉冲压力)。 EA随运动强度而变化:静止和峰值运动之间的EA及其决定因素之间的差异不同,从-44%到 +149%,并且独立于年龄和性别。根据他们的EAI将个体分为3组。 EA(第3组; EA0.98 mmhg.m2/ml)增加的个体的PVR减少最小,TAC的减少最大,HR与1组相似(EA <0.22 mmhg.m2/ml)。 Furthermore, group 3 had a reduction in end-diastolic volume, and a blunted increase in SV(80%), and cardiac output(27%), during exercise vs. group 1. Despite limitations in the Frank-Starling mechanism and cardiac function, peak aerobic capacity did not differ by group because arterial-venous oxygen difference was greater in group 3 vs. 1. Thus the change in arterial load during exercise has important effects on the Frank-Starling mechanism and cardiac性能,但不具有运动能力。这些发现为运动过程中动态心血管改变提供了有趣的见解。
另一项研究(Marine等人,2013年)试图确定大量无症状志愿者中运动诱导的非维持心室心动过速(NSVT)的临床预测因子和预后意义。在1977年至2001年之间,包括了BLSA(巴尔的摩纵向研究)中没有已知的心血管疾病的受试者,这些受试者至少完成了1个症状受限的运动跑步机测试。 NSVT发作的特征是QRS形态,持续时间和速率。受试者每2年接受一次随访临床评估。
2,099名受试者(平均年龄:52岁;男性为52.2%)进行了2.7个运动测试,其中79(3.7%)在至少1个测试中进行了运动。 NSVT的中位持续时间为3次(84%的节拍5次),中位数为175次/分钟。具有(无)NSVT的受试者年龄较大(67年12岁,51年17岁,p <0.0001),更有可能是男性(80%vs. 51%,p <0.0001),并且具有基线心电图异常(50%vs.17%,P <0.0001,P <0.0001)或缺血性ST-ST-SECT sT-ST-SECT sT-ST-SEM段因锻炼而变化(20%VS. 20%Vs. 20%Vs. 10%,P.104 0.4 4. 4 0. 4 0. 4 0. 4 0. 40/p1/p 1/p 1/4 0/p1/p 1/4 0.4 4. 4. 4 0.4 4. 4. 4 0.4 4. 4. 4. 4 0.40/p。在平均随访13。5 7.7岁的情况下,发生了518例死亡(24.6%)。在对年龄,性别和冠状动脉危险因素的多变量调整后,运动引起的NSVT与总死亡率没有显着相关(危险比:1.30; 95%置信区间:0.89至1.90; p 1/4 0.17)。运动引起的NSVT发生在近4%的无症状成人队列中。这一发现随着年龄的增长而增加,在男性中更为普遍。调整了临床变量后,运动引起的NSVT并未独立增加总死亡率的风险。
目前尚不清楚皮下和内脏脂肪是否与衰老的左心室(LV)舒张功能的下降有差异性相关。一项研究(Canepa etal。2013)试图研究以下假设:区域脂肪分布中与年龄相关的变化是LV舒张功能的变化,并探索了该关联的潜在介体。在一项横断面研究中,我们评估了843名巴尔的摩纵向研究的参与者,该研究对超声心动图,双能X射线吸收仪(DEXA),腹部计算机断层扫描(CT)和血液测试和同样访问进行的血液测试的衰老研究。通过LV松弛(E/A比,EM和EM/AM比)和LV填充压力(E/EM比)评估LV舒张功能。总体脂肪是由DEXA计算的,而内脏和皮下脂肪则从腹部CT确定。在针对人口统计学调整的多元模型中,心血管危险因素,降压药,体育活动和LV质量,内脏和皮下脂肪都与LV舒张功能障碍有关。当两种肥胖度量同时包括在同一模型中时,仅内脏脂肪与LV舒张功能障碍显着相关。发现甘油三酸酯和性激素结合球蛋白,但不是脂联素和瘦素,是内脏脂肪和LV舒张功能之间关系的重要介体,解释了2847%的关联。引导分析证实了这些发现的重要性。结论:内脏肥胖的增加与LV舒张功能障碍有关,可能通过涉及血脂和异位脂肪积累而不是脂肪因子的代谢途径。
动脉衰老可能会将心血管风险与白色外套高血压(WCH)联系起来。一项研究(Sung etal。2013)研究了动脉衰老在白色外套效应中的作用,定义为在目标器官损害和长期心血管死亡率方面,将办公室和24小时的卧床收缩血压和24小时的卧床收缩压(pH)进行比较。总共研究了一项基于社区调查的1257名从未经过治疗的志愿者。 WCH和PH由办公室和24小时的门诊血压定义。左心室质量指数,颈动脉内膜厚度,估计的肾小球滤过率,颈动脉 - 股骨脉冲波速度,颈动脉增强指数,反射压力波的振幅和15年心血管死亡率。具有WCH的受试者明显年龄较大,体重指数,血压值,内膜媒体厚度,颈动脉 - 股骨脉冲波速度,增强指数,向后压力波的振幅和估计肾小球过滤率低于pH。向后压力波的振幅是多变量分析中白色外套效应最重要的独立相关性(型号R2 = 0.451;部分R2/型R2 = 90.5%)。 WCH的心血管死亡率明显高于pH(危险比,2.94; 95%置信区间,1.097.91),在考虑年龄,性别,性别,体重指数,吸烟葡萄糖和总胆固醇/高密度脂蛋白 - 胆固醇比率之后。对向后压力波的振幅进行进一步调整,消除了WCH效应的统计学意义。总之,白皮效应主要是由动脉衰老引起的。与pH相比,WCH具有更高的心血管死亡率风险,这可能是通过伴随动脉衰老的增强波反射。
项目成果
期刊论文数量(0)
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科研奖励数量(0)
会议论文数量(0)
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Edward Lakatta其他文献
Edward Lakatta的其他文献
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