Department of Cardiology, Rajender Institute of Medical Sciences, Ranchi, India.
Department of Cardiology, GIPMER, New Delhi, India.
Clin Exp Rheumatol. 2022 May;40(4):714-719. doi: 10.55563/clinexprheumatol/53koap. Epub 2022 Apr 1.
To determine the factors (clinical, biochemical, angiographic, and echocardiographic) which predict left ventricular (LV) dysfunction in Takayasu's arteritis (TAK). TAK causes inflammation of the aorta and its large branches. Systemic hypertension, aortic valvular disease, and coronary artery involvement are probable contributors to LV dysfunction in some patients. In other patients, inflammation and resulting myocarditis play an essential role. However, the prevalence and relative contribution of such predictors of LV dysfunction in TAK patients is unknown.
We enrolled 87 patients with angiographically confirmed TAK in the study after proper informed consent. A complete clinical, biochemical, and echocardiographic evaluation of all the cases was done. We defined LV systolic dysfunction as an ejection fraction below 50% and diastolic dysfunction by ASE 2016 criteria into grades I, II, and III.
We evaluated 87 consecutive angiographically proven TAK patients. The incidence of LV systolic and diastolic dysfunction in our study was 19.5% (17/87) and 100% (87/87), respectively. All the patients with LV dysfunction (n=17, 100%) had an ITAS 2010 score of more than two suggestive of active disease. In 15 (88%) out of 17 patients with LV systolic dysfunction, we could identify a significant haemodynamic cause of LV dysfunction (untreated hypertension HTN, descending thoracic or abdominal aorta stenosis, renal artery stenosis, coronary stenosis, significant valvular regurgitation). In the rest 2 cases, no important haemodynamic factor was present, and here LV dysfunction was probably because of myocarditis and its sequalae.
This study represents the largest cohort of TAK patients to estimate LV systolic and diastolic dysfunction. We have found LV systolic and diastolic dysfunction multifactorial, with hemodynamic and inflammatory factors contributing to its pathophysiology.
确定预测大动脉炎(TAK)患者左心室(LV)功能障碍的因素(临床、生化、血管造影和超声心动图)。TAK 会引起主动脉及其大分支的炎症。在一些患者中,高血压、主动脉瓣疾病和冠状动脉受累可能是 LV 功能障碍的原因。在其他患者中,炎症和由此导致的心肌炎则起着至关重要的作用。然而,TAK 患者 LV 功能障碍的这些预测因素的流行程度和相对贡献尚不清楚。
在获得适当的知情同意后,我们将 87 例经血管造影证实的 TAK 患者纳入研究。对所有病例进行全面的临床、生化和超声心动图评估。我们将射血分数低于 50%定义为 LV 收缩功能障碍,根据 ASE 2016 标准将舒张功能障碍分为 I、II 和 III 级。
我们评估了 87 例连续的经血管造影证实的 TAK 患者。本研究中 LV 收缩和舒张功能障碍的发生率分别为 19.5%(17/87)和 100%(87/87)。所有 LV 功能障碍患者(n=17,100%)的 ITAS 2010 评分均大于 2,提示存在活动期疾病。在 17 例 LV 收缩功能障碍患者中(88%),我们可以确定 LV 功能障碍的一个重要血流动力学原因(未经治疗的高血压 HTN、降主动脉或腹主动脉狭窄、肾动脉狭窄、冠状动脉狭窄、明显的瓣膜反流)。在其余 2 例中,没有明显的血流动力学因素存在,在这里 LV 功能障碍可能是由于心肌炎及其后遗症所致。
本研究代表了迄今为止对 TAK 患者进行 LV 收缩和舒张功能障碍评估的最大队列研究。我们发现 LV 收缩和舒张功能障碍是多因素的,血流动力学和炎症因素共同导致其病理生理学改变。