PDF(Pubmed)
Abstract：
UNASSIGNED: Increased leisure-time physical activity (LTPA) is linked with decreased mortality risk, while also with increased left ventricular mass, which may induce left ventricular hypertrophy (LVH). We investigated whether LVH modifies the association between higher LTPA and lower mortality risk in population at high cardiovascular risk.
UNASSIGNED: In a prospective national cohort, we used the left ventricular mass/body surface area (LVM/BSA) method to define LVH. Baseline LTPA was self-reported and divided into: low ( < 500 metabolic equivalent of task [MET]) min/week), moderate (500-1999 MET min/week) and high ( ≥ 2000 MET-min/week). Analyses of the dose-response relationship between LTPA and left ventricular mass were performed using restricted cubic spline regression. A multivariate adjusted Cox proportional hazards regression analysis was used to estimate hazard ratios (HRs).
UNASSIGNED: A total of 163,006 participants (55.3% females, mean [standard deviation] age, 62.4 [7.4] years) were included. During a median of 4.8 years of follow-up, 6586 (4.0%) died from all causes and 3024 (1.9%) from cardiovascular causes. Multivariate adjusted Cox proportional hazards regression analyses revealed that moderate and high LTPA were linked with less cardiovascular and all-cause mortality risk than low LTPA in the absence of LVH. In those with LVH, the association of high (0.83, 0.69-0.99) or moderate (0.72, 0.56-0.91) LTPA with cardiovascular mortality risk persisted. For all-cause mortality risk, this association was only significant in high LTPA (0.73, 0.61-0.86), while marginal in moderate LTPA (0.96, 0.84 to 1.08). Overall, the correlation patterns between LTPA and mortality risk appears distinct between those with LVH and those without LVH; the modification of LVH was not significant regarding mortality risk among the high cardiovascular risk population (all-cause: p-value for interaction = 0.074; cardiovascular cause: p-value for interaction = 0.581), except in females regarding all-cause mortality risk (p-value for interaction = 0.006).
UNASSIGNED: The association between higher LTPA and lower mortality risk was not modified by LVH in high cardiovascular risk population. However, the presence of LVH altered this association in females regarding the all-cause mortality risk.
UNASSIGNED: In a prospective national cohort, we used the left ventricular mass/body surface area (LVM/BSA) method to define LVH. Baseline LTPA was self-reported and divided into: low ( < 500 metabolic equivalent of task [MET]) min/week), moderate (500-1999 MET min/week) and high ( ≥ 2000 MET-min/week). Analyses of the dose-response relationship between LTPA and left ventricular mass were performed using restricted cubic spline regression. A multivariate adjusted Cox proportional hazards regression analysis was used to estimate hazard ratios (HRs).
UNASSIGNED: A total of 163,006 participants (55.3% females, mean [standard deviation] age, 62.4 [7.4] years) were included. During a median of 4.8 years of follow-up, 6586 (4.0%) died from all causes and 3024 (1.9%) from cardiovascular causes. Multivariate adjusted Cox proportional hazards regression analyses revealed that moderate and high LTPA were linked with less cardiovascular and all-cause mortality risk than low LTPA in the absence of LVH. In those with LVH, the association of high (0.83, 0.69-0.99) or moderate (0.72, 0.56-0.91) LTPA with cardiovascular mortality risk persisted. For all-cause mortality risk, this association was only significant in high LTPA (0.73, 0.61-0.86), while marginal in moderate LTPA (0.96, 0.84 to 1.08). Overall, the correlation patterns between LTPA and mortality risk appears distinct between those with LVH and those without LVH; the modification of LVH was not significant regarding mortality risk among the high cardiovascular risk population (all-cause: p-value for interaction = 0.074; cardiovascular cause: p-value for interaction = 0.581), except in females regarding all-cause mortality risk (p-value for interaction = 0.006).
UNASSIGNED: The association between higher LTPA and lower mortality risk was not modified by LVH in high cardiovascular risk population. However, the presence of LVH altered this association in females regarding the all-cause mortality risk.
摘要：
■增加休闲时间体力活动（LTPA）与降低死亡风险有关，虽然左心室质量也增加，这可能会导致左心室肥厚（LVH）。我们调查了在高心血管风险人群中，LVH是否改变了较高LTPA和较低死亡风险之间的关联。
■在一个前瞻性的国家队列中，我们使用左心室质量/体表面积（LVM/BSA）方法来定义LVH。基线LTPA是自我报告的，分为：低（<500代谢等效任务[MET]）分钟/周），中等（500-1999METmin/周）和高（≥2000MET-min/周）。使用限制性三次样条回归分析LTPA与左心室质量之间的剂量反应关系。使用多变量校正的Cox比例风险回归分析来估计风险比(HR)。
■共有163,006名参与者（55.3％为女性，平均[标准偏差]年龄，包括62.4[7.4]年）。在平均4.8年的随访期间，6586（4.0％）死于各种原因，3024（1.9％）死于心血管原因。多变量校正Cox比例风险回归分析显示，在没有LVH的情况下，中度和高LTPA与低LTPA相比，低LTPA与更低的心血管和全因死亡风险相关。在那些有LVH的人中，高(0.83,0.69-0.99)或中(0.72,0.56-0.91)LTPA与心血管死亡风险的相关性持续存在.对于全因死亡风险，这种关联仅在高LTPA(0.73，0.61-0.86)中显著，而在中等LTPA（0.96，0.84至1.08）中微不足道。总的来说,LVH患者和无LVH患者之间LTPA与死亡风险之间的相关模式似乎不同;LVH的改变对高心血管风险人群的死亡风险并不显著(全因:相互作用的p值=0.074;心血管原因:相互作用的p值=0.581),除了女性的全因死亡风险（相互作用的p值=0.006）。
■在高心血管风险人群中，LVH并未改变较高的LTPA和较低的死亡风险之间的关联。然而,LVH的存在改变了女性全因死亡风险的这种关联.
■在一个前瞻性的国家队列中，我们使用左心室质量/体表面积（LVM/BSA）方法来定义LVH。基线LTPA是自我报告的，分为：低（<500代谢等效任务[MET]）分钟/周），中等（500-1999METmin/周）和高（≥2000MET-min/周）。使用限制性三次样条回归分析LTPA与左心室质量之间的剂量反应关系。使用多变量校正的Cox比例风险回归分析来估计风险比(HR)。
■共有163,006名参与者（55.3％为女性，平均[标准偏差]年龄，包括62.4[7.4]年）。在平均4.8年的随访期间，6586（4.0％）死于各种原因，3024（1.9％）死于心血管原因。多变量校正Cox比例风险回归分析显示，在没有LVH的情况下，中度和高LTPA与低LTPA相比，低LTPA与更低的心血管和全因死亡风险相关。在那些有LVH的人中，高(0.83,0.69-0.99)或中(0.72,0.56-0.91)LTPA与心血管死亡风险的相关性持续存在.对于全因死亡风险，这种关联仅在高LTPA(0.73，0.61-0.86)中显著，而在中等LTPA（0.96，0.84至1.08）中微不足道。总的来说,LVH患者和无LVH患者之间LTPA与死亡风险之间的相关模式似乎不同;LVH的改变对高心血管风险人群的死亡风险并不显著(全因:相互作用的p值=0.074;心血管原因:相互作用的p值=0.581),除了女性的全因死亡风险（相互作用的p值=0.006）。
■在高心血管风险人群中，LVH并未改变较高的LTPA和较低的死亡风险之间的关联。然而,LVH的存在改变了女性全因死亡风险的这种关联.
