正常冠状动脉造影后症状性患者运动诱导的舒张功能障碍的揭示

M. Harish Reddy, J. Maddury, A. Panda
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引用次数: 0

摘要

背景:舒张功能障碍是近一半心衰病例的原因,其血流动力学等价于心脏充盈压力升高。然而,由于它的普遍存在,它经常被诊断为偶然发现,但在许多患者中并没有建立与症状的联系。大多数高血压或左心室肥厚的患者在多普勒超声心动图上有舒张功能受损的证据,但在静息时没有任何心衰症状。然而,这些患者只有在运动时才有与舒张功能障碍相关的症状。在这项研究中,我们考虑通过超声心动图和运动来评估有原因的呼吸短促患者的左心室充盈压力,并比较已确定的舒张功能障碍患者的升高水平。方法:这是一项为期3个月的观察性前瞻性研究,在排除全身原因后,对胸痛和呼吸短促等典型症状的患者进行冠状动脉造影。如果未发现冠状动脉病变,则在冠状动脉造影期间进行有创心导管插管。患者分为两组,一组无舒张功能障碍,另一组有舒张功能障碍。同时测量静息时左室舒张末期压(LVEDP)和手握运动3分钟后左室舒张末期压并记录读数。结果:30例患者的平均年龄为55.8±7.538岁,其中男性20例。无舒张功能障碍患者静息时LVEDP均值为4.4±3.169,运动后LVEDP均值为8.40±4.169。舒张功能不全患者静息时LVEDP均值为5.30±3.948,运动后LVEDP均值为8.75±4.506。两组间配对t检验显示,运动后两组间p值均显著为0.001,提示运动后患者LVEDP显著升高。无舒张功能不全组LVEDP升高与有舒张功能不全组相当(p = 0.432)。结论:在舒张功能不全患者中,运动增加LVEDP是一个公认的事实。我们的研究增加了这样一个事实,即不明原因的呼吸短促患者在运动后可以提高LVEDP,从而揭示了潜在的舒张功能障碍。我们的研究强调了将运动作为有创性或无创性舒张功能评估的刺激试验的重要性,对于出现运动性呼吸困难的患者。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unmasking of Exercise-Induced Diastolic Dysfunction in Symptomatic Post Coronary Angiogram Patients with Normal Coronaries
Background: Diastolic dysfunction is the cause in nearly half of cases of heart failure, the hemodynamic equivalent of which is elevated cardiac filling pressures. However, owing to its ubiquity, it is often diagnosed as an incidental finding, but an association with symptoms is not established in many of the patients. Most patients with hypertension or left ventricular (LV) hypertrophy have evidence of impaired diastolic function as a finding on Doppler echocardiography, but do not have any symptoms of heart failure at rest. However, these patients do have symptoms related to diastolic dysfunction only during exercise. In this study, we have contemplated to assess invasively, left ventricular filling pressures in patients with unexplained shortness of breath with normal systolic and diastolic function on echocardiography, on exercise and compare the level of rise in patients with established diastolic dysfunction. Methods: This is an observational prospective study, done over a span of 3 months, wherein patients with typical symptoms such as chest pain and shortness of breath, after ruling out systemic causes, and were subjected to coronary angiogram. If no coronary lesion identified, patients were subjected to invasive cardiac catheterization during coronary angiogram. Patients were divided into two groups, one without diastolic dysfunction and the other with established diastolic dysfunction. Simultaneous left ventricular end diastolic pressures (LVEDP) were measured at rest and after 3-minute manual handgrip exercise and readings were noted. Results: The mean age of the population (n = 30) was 55.8 ± 7.538 and 20 were males. The mean value of LVEDP in patients with no diastolic dysfunction at resting was 4.4 ± 3.169 and after exercise was 8.40 ± 4.169. The mean value of LVEDP in patients with established diastolic dysfunction at resting was 5.30 ± 3.948 and after exercise was 8.75 ± 4.506. Paired t-test among two groups revealed a significant p-value of 0.001 after exercise among both groups, suggesting a significant increase in LVEDP in patients with exercise. Unpaired t-test comparing both groups revealed that the elevation of LVEDP in no diastolic dysfunction group was comparable with patients with diastolic dysfunction (p = 0.432). Conclusion: The increase in LVEDP with exercise is a well-established fact in patients with diastolic dysfunction. Our study adds to the fact that patients with unexplained shortness of breath can have raised LVEDP after exercise, thereby unmasking the underlying diastolic dysfunction. Our study stresses the importance of inclusion of exercise as a provocative test for the assessment of diastolic function, either invasively or non-invasively, in patients presenting with exertional dyspnea.
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