Tascanov Mustafa Begenc
Department of Cardiology, Harran University Faculty of Medicine, Sanliurfa, Turkey.
Comb Chem High Throughput Screen. 2019;22(1):69-75. doi: 10.2174/1386207322666190306143317.
Tissue fibrosis increases in the structure of the atrial tissue of atrial fibrillation patients. Prolidase enzyme regulates collagen synthesis. There may be an association between electrocardiography (ECG) findings and prolidase activity.
This study investigated the association between atrial conduction time and prolidase activity, a collagen synthesis enzyme, and P-wave dispersion (PWD) in patients with Paroxysmal Atrial Fibrillation (PAF).
Exclusion criteria included the age of <18 years, heart failure, diabetes, hypertension, hyperlipidemia, malignancy, cerebrovascular disease, chronic respiratory distress, osteoporosis, rheumatoid arthritis, renal disease, cirrhosis, and other types of arrhythmia. Patients diagnosed with PAF within 48 hours were considered to have a definite diagnosis. PWD was calculated using a 12-lead ECG, and inter- and intraatrial electromechanical delay (EMD) was assessed using tissue Doppler imaging and conventional echocardiography. Serum prolidase levels were measured in both groups.
A total of 43 patients with PAF (20 female, 23 male; mean age, 46.8 ± 5.7 years) and 42 healthy volunteers (21 female, 21 male; mean age, 43.9 ± 5.1 years) were included in the study. Inter- and intraatrial EMD, PWD, minimum P-wave (Pmin), and maximum P-wave (Pmax) measurements were significantly higher (39.7 ± 2.7, 35.7 ± 2.3, p < 0.001; 13.2 ± 2.6, 8.5 ± 1.9, p < 0.001; 47.1 ± 11, 24.1 ± 7.1, p < 0.001; 69.8 ± 8.8, 66.7 ± 10.2, p < 0.130; 114.8 ± 13, 93.6 ± 8.6, p < 0.001, respectively) and serum prolidase levels were significantly lower in patients with PAF compared to healthy controls (3.96 ± 1.2, 8.5 ± 3.56, p < 0.001). In patients with PAF, correlation analysis showed a negative correlation between prolidase levels and intra- and interatrial EMD, PWD, and Pmax (r = -0.41, p < 0.05; r = -0.54, p < 0.05; r = -0.62, p < 0.05; r = -0.49, p < 0.05, respectively). Interatrial EMD showed a significant positive correlation with intraatrial EMD, Pmax, and PWD in patients with PAF (r = 0.90, p < 0.05; r = 0.574, p < 0.05; r = 0.43, p < 0.05, respectively). Additionally, the level of high-sensitivity C-reactive protein (hs-CRP) was significantly higher in patients with PAF (6.6 ± 8, 1.8 ± 1.6, p < 0.001).
The decreased plasma prolidase activity in patients with PAF may explain the irregularity of the collagen metabolism of different extracellular components and may indicate the onset of atrial remodeling. Changes in PWD, interatrial EMD, and serum prolidase level may predict PAF before diagnosis.
心房颤动患者心房组织结构中的组织纤维化增加。脯氨酰肽酶调节胶原蛋白合成。心电图（ECG）结果与脯氨酰肽酶活性之间可能存在关联。
本研究调查阵发性心房颤动（PAF）患者的心房传导时间与脯氨酰肽酶活性（一种胶原蛋白合成酶）及P波离散度（PWD）之间的关联。
排除标准包括年龄<18岁、心力衰竭、糖尿病、高血压、高脂血症、恶性肿瘤、脑血管疾病、慢性呼吸窘迫、骨质疏松、类风湿关节炎、肾脏疾病、肝硬化及其他类型的心律失常。48小时内确诊为PAF的患者被视为明确诊断。使用12导联心电图计算PWD，使用组织多普勒成像和传统超声心动图评估心房内和心房间的机电延迟（EMD）。两组均测量血清脯氨酰肽酶水平。
本研究共纳入43例PAF患者（20例女性，23例男性；平均年龄46.8±5.7岁）和42名健康志愿者（21例女性，21例男性；平均年龄43.9±5.1岁）。PAF患者的心房内和心房间EMD、PWD、最小P波（Pmin）和最大P波（Pmax）测量值显著更高（分别为39.7±2.7、35.7±2.3，p<0.001；13.2±2.6、8.5±1.9，p<0.001；47.1±11、24.1±7.1，p<0.001；69.8±8.8、66.7±10.2，p<0.130；114.8±13、93.6±8.6，p<0.001），且与健康对照组相比，PAF患者的血清脯氨酰肽酶水平显著更低（3.96±1.2、8.5±3.56，p<0.001）。在PAF患者中，相关性分析显示脯氨酰肽酶水平与心房内和心房间EMD、PWD及Pmax呈负相关（r分别为-0.41，p<0.05；r=-0.54，p<0.05；r=-0.62，p<0.05；r=-0.49，p<0.05）。PAF患者的心房间EMD与心房内EMD、Pmax及PWD呈显著正相关（r分别为0.90，p<0.05；r=0.574，p<0.05；r=0.43，p<0.05）。此外，PAF患者的高敏C反应蛋白（hs-CRP）水平显著更高（6.6±8、1.8±1.6，p<0.001）。
PAF患者血浆脯氨酰肽酶活性降低可能解释不同细胞外成分胶原蛋白代谢的异常，并可能提示心房重构的开始。PWD、心房间EMD和血清脯氨酰肽酶水平的变化可能在诊断前预测PAF。
