Diastolic Dysfunction in Patients with Chronic Obstructive Pulmonary Disease: A Meta-Analysis of Case Controlled Studies.

Angelina Zhyvotovska, Denis Yusupov, Haroon Kamran, Tarik Al-Bermani, Rishard Abdul, Samir Kumar, Nikita Mogar, Angeleque Hartt, Louis Salciccioli, Samy I McFarlane
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引用次数: 8

Abstract

Background: Chronic obstructive pulmonary disease (COPD) and left ventricular diastolic dysfunction (LVDD) are major causes of morbidity and mortality and have overlapping symptomatology including cough and dyspnea. Whether COPD is a risk factor for LVDD remains largely unclear.The objective of this meta-analysis was to determine if the prevalence of the LVDD as determined by echocardiographic parameters is increased in COPD patients.

Methods: We used a time-and-language-restricted search strategy resulting in identification of 4,912 studies of which 15 studies met our apriori inclusion criteria; 4,897 were excluded, such duplicates, foreign language articles were excluded. We performed a meta-analysis of standard echo parameters on the fifteen case control studies related to diastolic dysfunction. The meta-analysis was performed using Review Manager, version 5.3 (Cochrane Collaboration).

Results: A total of 15 studies with 1,403 subjects were included. There were no differences in left ventricular ejection fraction between COPD and non-COPD population. Patients with COPD had prolonged isovolumetric relaxation time (IVRT) (mean difference 20.84 [95% CI 12.21, 29.47]; P< 0.00001), lower E/A ratio (mean difference - 0.24 [95% CI -0.34, 00.14]; P < 0.00001), higher transmitral A wave peak velocity (Apv) (mean difference 11.71 [95% CI 4.80, 18.62]; P< 0.00001), higher E/e' ratio (mean difference 1.88 [95% CI 1.23, 2.53]; P< 0.00001), lower mitral E wave peak velocity (Epv) (mean difference -8.74 [95% CI -13.63, -3.85]; P< 0.0005), prolonged deceleration time (DT) (mean difference 50.24 [95% CI 15.60, 84,89]; P< 0.004), a higher right ventricular end diastolic diameter (RVEDD) (mean difference 8.02 [95% CI 3.45, 12.60]; P< 0.0006) compared to controls. COPD patients had a higher pulmonary arterial pressure (mean difference 10.52 [95% CI 3.98, 17.05]; P< 0.002). Differences in septal e' velocity (mean difference -2.69 [95% CI -6.07, 0.69]; P< 0.12) and in lateral e' velocity (mean difference -2.84 [95% CI 5.91, 0.24]; P< 0.07) trended towards significance but did not meet our cutoff for statistical significance (p < 0.05).

Conclusions: Patients with COPD are more likely to have LVDD as established by echocardiographic parameters. Our findings are likely explainable, in part, by factors such as lung hyperinflation, chronic hypoxia, hypercapnia, systemic inflammation, increased arterial stiffness, subendocardial ischemia, as well as ventricular interdependence; all of which might contribute to the pathogenesis of diastolic dysfunction. Further research is needed to elucidate the pathophysiologic mechanisms of increased LVDD in the COPD population with the potential impact on developing effective therapeutic interventions for these serious disorders.

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慢性阻塞性肺疾病患者的舒张功能障碍:病例对照研究的荟萃分析
背景:慢性阻塞性肺疾病(COPD)和左心室舒张功能障碍(LVDD)是发病率和死亡率的主要原因,并且具有咳嗽和呼吸困难等重叠症状。COPD是否是LVDD的危险因素仍不清楚。本荟萃分析的目的是确定超声心动图参数确定的慢性阻塞性肺病患者LVDD的患病率是否增加。方法:我们使用时间和语言受限的搜索策略,最终确定了4,912项研究,其中15项研究符合我们的先验纳入标准;排除4897篇重复、外文文章。我们对15例与舒张功能障碍相关的病例对照研究进行了标准回声参数的荟萃分析。meta分析使用Review Manager版本5.3 (Cochrane Collaboration)进行。结果:共纳入15项研究,1403名受试者。COPD与非COPD人群左心室射血分数无差异。COPD患者的等容松弛时间(IVRT)延长(平均差20.84 [95% CI 12.21, 29.47];P< 0.00001),较低的E/A比(平均差- 0.24 [95% CI -0.34, 00.14];P < 0.00001),更高的透射A波峰速度(Apv)(平均差值11.71 [95% CI 4.80, 18.62];P< 0.00001),较高的E/ E比值(平均差1.88 [95% CI 1.23, 2.53];P< 0.00001),较低的二尖瓣E波峰值速度(Epv)(平均差为-8.74 [95% CI -13.63, -3.85];P< 0.0005),减速时间延长(DT)(平均差异50.24 [95% CI 15.60, 84,89];P< 0.004),右心室舒张末期直径(RVEDD)较高(平均差异8.02 [95% CI 3.45, 12.60];P< 0.0006)。COPD患者肺动脉压较高(平均差10.52 [95% CI 3.98, 17.05];P < 0.002)。间隔流速差异(平均差-2.69 [95% CI -6.07, 0.69];P< 0.12)和横向速度(平均差-2.84 [95% CI 5.91, 0.24];P< 0.07)趋于显著,但未达到我们的统计显著性截止值(P< 0.05)。结论:超声心动图参数表明,COPD患者更容易发生LVDD。我们的研究结果可以部分解释为肺过度膨胀、慢性缺氧、高碳酸血症、全身炎症、动脉僵硬度增加、心内膜下缺血以及心室相互依赖等因素;这些都可能与舒张功能障碍的发病机制有关。需要进一步的研究来阐明慢性阻塞性肺病人群LVDD增加的病理生理机制,并对开发有效的治疗干预措施产生潜在影响。
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