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

• 批准号: 8931601
• 负责人: Edward Lakatta
• 金额: $ 6.47万
• 依托单位: NATIONAL INSTITUTE ON AGING
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/8931601
• 关键词: Abdomen; Accounting; Adult; Aerobic; Age; Aging; Antihypertensive Agents; Baltimore; Blood Pressure; Blood Tests; Blood Vessels; Body fat; Body mass index; Cardiac; Cardiac Output; Cardiac Volume; Cardiovascular Diseases; Cardiovascular alteration; Cardiovascular system; Cessation of life; Cholesterol; Clinical; Communities; Confidence Intervals; Coronary; Coupling; Cross-Sectional Studies; Dual-Energy X-Ray Absorptiometry; Echocardiography; Exercise; Exercise stress test; Fatty acid glycerol esters; Functional disorder; Gender; Glomerular Filtration Rate; Habits; Heart; Heart Rate; High Density Lipoprotein Cholesterol; Hour; Individual; Laboratories; Left; Left Ventricular Mass; Leptin; Life Style; Link; Longitudinal Studies; Measures; Mediator of activation protein; Metabolic Pathway; Modeling; Morphology; Multivariate Analysis; Obesity; Organ; Oxygen; Participant; Performance; Peripheral; Pharmaceutical Preparations; Physical activity; Physiologic pulse; Play; Population; Pulse Pressure; Relaxation; Rest; Risk; Risk Factors; Role; Scanning; Sex Hormone-Binding Globulin; Smoking; Stroke Volume; Structure; Sturnus vulgaris; Surveys; Symptoms; Systolic Pressure; Techniques; Testing; Thick; Treadmill Tests; Triglycerides; Vascular resistance; Venous; Ventricular; Ventricular Tachycardia; Visceral; Visit; X-Ray Computed Tomography; adipokines; adiponectin; age effect; age related; base; blood lipid; cardiovascular risk factor; cohort; conditioning; demographics; fasting plasma glucose; follow-up; hazard; high risk; indexing; insight; interest; intima media; male; men; mortality; pressure; prognostic; research clinical testing; sex; subcutaneous; volunteer; white coat hypertension

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.

有效动脉弹性 (EA) 是对心脏施加的净动脉负荷的衡量标准， 综合了心率 (HR)、外周血管阻力 (PVR) 和总动脉顺应性 (TAC) 的影响，是心脏性能的调节剂。运动期间 EA 的变化对心脏性能和有氧能力的影响程度尚不清楚。我们研究了 352 名健康受试者的 EA 及其与心血管功能的关系（Chantler 等人，2012 年）。受试者接受休息和运动门控扫描以测量心脏容量并得出 EA 收缩压/每搏输出量指数 (SV)、PVRMAP/(SV*HR) 和 TAC(SV/脉压)。 EA 随运动强度的变化而变化：休息和运动峰值之间的 EA 及其决定因素因个体而异，范围为 -44% 至 +149%，并且与年龄和性别无关。根据 EAI，个体被分为 3 组。与第 1 组相比，EA 增加最多的个体（第 3 组；EA0.98 mmHg.m2/ml）的 PVR 降低最小，TAC 降低最大，HR 增加类似（EA<0.22 mmHg.m2/ml）。此外，与第 1 组相比，第 3 组在运动过程中舒张末期容积减少，SV（80%）和心输出量（27%）增加减弱。尽管 Frank-Starling 机制和心脏功能存在局限性，但各组的峰值有氧能力没有差异，因为第 3 组的动静脉氧差比第 1 组更大。因此，运动期间动脉负荷的变化对 Frank-Starling 机制和心脏功能具有重要影响。 表现而不是运动能力。这些发现为运动过程中动态心血管变化提供了有趣的见解。 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发的非持续性室性心动过速 (NSVT) 的临床预测因子和预后意义。 BLSA（巴尔的摩纵向衰老研究）中没有已知心血管疾病且在 1977 年至 2001 年间完成至少 1 次症状限制运动跑步机测试的受试者被纳入研究。 NSVT 发作的特征是 QRS 形态、持续时间和发生率。受试者每两年接受一次随访临床评估。 2,099 名受试者（平均年龄：52 岁；52.2% 为男性）平均接受了 2.7 次运动测试，其中 79 名受试者（3.7%）在至少 1 次运动测试中出现 NSVT。 NSVT 的中位持续时间为 3 次（84% 为 5 次），中位频率为 175 次/分钟。患有（与不患有）NSVT 的受试者年龄较大（67±12 岁 vs. 51±17 岁，p < 0.0001），更有可能是男性（80% vs. 51%，p < 0.0001），并且有基线心电图异常（50% vs. 17%，p < 0.0001）或运动时出现缺血性 ST 段变化（20% vs. 10%）。 10%，p 1/4 0.004）。在平均 13.5±7.7 年的随访中，有 518 人死亡（24.6%）。对年龄、性别和冠状动脉危险因素进行多变量调整后，运动诱发的 NSVT 与总死亡率没有显着相关（风险比：1.30；95% 置信区间：0.89 至 1.90；p 1/4 0.17）。在该无症状成人队列中，近 4% 的人发生了运动诱发的 NSVT。这一发现随着年龄的增长而增加，并且在男性中更为常见。调整临床变量后，运动诱发的 NSVT 并不会独立增加总死亡率风险。 目前尚不清楚皮下脂肪和内脏脂肪是否与随年龄增长而导致的左心室（LV）舒张功能下降存在差异相关。一项研究（Canepa 等人，2013）试图检验这样的假设：区域脂肪分布与年龄相关的变化导致左室舒张功能的变化，并探索这种关联的潜在调节因素。在一项横断面研究中，我们对巴尔的摩纵向衰老研究的 843 名参与者进行了评估，包括超声心动图、双能 X 射线吸收测定法 (DEXA)、腹部计算机断层扫描 (CT) 和在同一次就诊时进行的血液检查。左室舒张功能通过左室舒张参数（E/A 比、Em 和 Em/Am 比）和左室充盈压（E/Em 比）进行评估。通过 DEXA 计算全身脂肪，通过腹部 CT 确定内脏和皮下脂肪。在根据人口统计、心血管危险因素、抗高血压药物、体力活动和左心室质量进行调整的多变量模型中，内脏和皮下脂肪均与左心室舒张功能障碍相关。当两个肥胖指标同时纳入同一模型时，只有内脏脂肪与左心室舒张功能障碍显着相关。甘油三酯和性激素结合球蛋白（而非脂联素和瘦素）被发现是内脏脂肪与左室舒张功能之间关系的重要调节因素，解释了 2847% 的相关性。自举分析证实了这些发现的重要性。结论：内脏肥胖增加与左心室舒张功能障碍相关，可能是通过涉及血脂和异位脂肪积累的代谢途径而不是脂肪因子。 动脉老化可能将心血管风险与白大衣高血压（WCH）联系起来。一项研究（Sung 等人，2013）调查了动脉老化在白大衣效应（定义为办公室收缩压和 24 小时动态收缩压之间的差异）中的作用，并比较了 WCH 与高血压前期 (PH) 的靶器官损伤和长期心血管死亡率。一项基于社区的调查总共对 1257 名从未接受过治疗的志愿者受试者进行了研究。 WCH 和 PH 由诊室血压和 24 小时动态血压定义。测定左心室质量指数、颈动脉内膜中层厚度、估计肾小球滤过率、颈动脉-股动脉脉搏波速度、颈动脉增强指数、反射压力波振幅和15年心血管死亡率。与 PH 患者相比，WCH 患者年龄明显较大，体重指数、血压值、内膜中层厚度、颈动脉-股动脉脉搏波速度、增强指数、反向压力波振幅更大，估计肾小球滤过率更低。在多变量分析中，后向压力波的幅度是白大衣效应最重要的独立相关性（模型r2=0.451；部分r2/模型r2=90.5%）。考虑到年龄、性别、体重指数、吸烟、空腹血糖和总胆固醇/高密度脂蛋白胆固醇比率后，WCH 的心血管死亡率显着高于 PH（风险比为 2.94；95% 置信区间为 1.097.91）。对后向压力波振幅模型的进一步调整消除了 WCH 效应的统计显着性。综上所述，白大衣效应主要是动脉老化造成的。 WCH 的心血管死亡风险比 PH 更高，这可能是由于动脉老化导致的波反射增强所致。