平板运动试验QTc频率适应性变化诊断冠心病的初步探讨
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摘要
目的:评价平板运动试验QTc间期频率适应性变化对冠心病及早期冠状动脉病变的诊断价值。方法:选择我院先后行平板运动试验和冠状动脉造影的148例患者,根据冠状动脉造影结果,以频率适应性QTc间期(RAQTc)延长(≥420ms)为阳性判定标准,进行回顾性病例对照研究。结果:①运动状态下,CAG阳性和CAG阴性两组的QT间期变化不同;②RAQTc延长诊断冠心病的敏感性、特异性、准确性、阳性预测值,均高于ST段改变标准;③两指标(RAQTc延长和ST段改变)联用可提高冠心病诊断的准确性;④经Spearman秩相关分析显示,RAQTc与冠状动脉病变程度呈正相关,有统计学显著差异;⑤与无冠状动脉病变组比较,冠状动脉病变<50%组的RAQTc变化无统计学差异。结论:平板运动试验中RAQTc延长可作为诊断冠心病的一个参考指标。早期冠状动脉病变患者运动中QTc间期的频率适应性尚可,RAQTc无明显延长。
Objective: To evaluate the diagnostic value of the change of QTc interval rate adaptation for detecting coronary artery disease and coronary artery lesion early in patients. Methods: Treadmill exercise test was conducted in 148 patients with undergoing coronary angiography. Based on coronary angiography results and heart rate adaptative QTc prolongation(≥420ms) as a positive criteria,the retrospective case-control study was performed. Results:①During Treadmill exercise test,the changes of QT interval of positive CAG and negative CAG groups are different;②Heart rate adaptation of QTc prolongation is higher sensitivity,specificity,accuracy, positive predictive value than those of abnormal ST-segment for detecting coronary artery disease;③The combination of abnormal ST-segment and heart rate adaptation of QTc prolongation diagnoses CAD more accurately;④There is a positive relationship between RAQTc and CAL by Spearman rank correlation analysis;⑤The RAQTc intervals of 0% coronary artery lesion and coronary artery lesion<50% are no statistical differences.Conclusion: Heart rate adaptation of QTc prolongation may be a useful index for diagnosing coronary artery disease.During treadmill exercise test ,the rate adaptation of QTc interval may be well in coronary artery lesion early prtients,whose QTc interval are not prolongative.
Objective: To evaluate the diagnostic value of the change of QTc interval rate adaptation for detecting coronary artery disease and coronary artery lesion early in patients. Methods: Treadmill exercise test was conducted in 148 patients with undergoing coronary angiography. Based on coronary angiography results and heart rate adaptative QTc prolongation(≥420ms) as a positive criteria,the retrospective case-control study was performed. Results:①During Treadmill exercise test,the changes of QT interval of positive CAG and negative CAG groups are different;②Heart rate adaptation of QTc prolongation is higher sensitivity,specificity,accuracy, positive predictive value than those of abnormal ST-segment for detecting coronary artery disease;③The combination of abnormal ST-segment and heart rate adaptation of QTc prolongation diagnoses CAD more accurately;④There is a positive relationship between RAQTc and CAL by Spearman rank correlation analysis;⑤The RAQTc intervals of 0% coronary artery lesion and coronary artery lesion<50% are no statistical differences.Conclusion: Heart rate adaptation of QTc prolongation may be a useful index for diagnosing coronary artery disease.During treadmill exercise test ,the rate adaptation of QTc interval may be well in coronary artery lesion early prtients,whose QTc interval are not prolongative.
引文
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[4] Arab D, Valeti V, Schunemann HJ, et al. Usefulness of the QTc interval in predicting myocardial ischemia in patients undergoing exercise stress testing[J].Am J Cardiol, 2000, 85: 764–766.
[5] Stoletniy LN, Pai RG. Value of QT Dispersion in the Interpretation of Exercise Stress Test in Women[J]. Circulation, 1997, 96:904-910.
[6] Robbins J, Nelson JC, Rautaharju PM, et al. The association between the length of the QT interval and mortality in the cardiovascular health study[J]. Am J Med, 2003, 115:689-694.
[7] Kenigsberg DN, Khanal S, Kowalski M, et al. Prolongation of the QTc interval is seen uniformly during early transmural ischemia[J]. J Am Coll Cardiol, 2007, 49:1299-1305.
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[9] Chiang CE, Roden DM. The long QT syndromes:genetic basis and clinical imlication[J]. J Am Coll Cardiol, 2000, 36:1-12.
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[19] Nash MP, Panfilov AV. Electromechanical model of excitable tissue to study reentrant cardiac arrhythmias[J]. Prog Biophys Mol Biol, 2004, 85:501–522.
[20]单其俊,沈建华.获得性长QT综合征[J].中国心脏起搏与心电生理杂志, 2008, 22:103-110.
[21] Roden DM. Taking the“idio”out of“idiosyncratic”: predictingTorsades de Pointes[J]. PACE, 1998, 21:1029-1037.
[22] Aiba T, Shmiizu W, Inagaki M. Cellular and ionic mechanism for Drug-induced long QT syndrome and effectiveness of verapamil[J]. J Am Coll Cardiol, 2005, 45:300-315.
[23] Burashnikov A, Antzelevitch C. Prominent IKs in ep icardium and endocardium contributes to development of transmural dispersion of repolarization but protects against development of early afterdepolarizations[J]. J Cardiovasc Electrophysiol, 2002, 13:172-178.
[24] Antzelevitch C. Arrhythmogenic mechanisms of QT prolonging drugs:Is QT p rolongation really the p roblem[J]? J Electrocardiol, 2004, 37:15-20.
[25] Shivkumar K, Deutsch NA, Lamp ST, et al. Mechanism of hypoxic K loss in rabbit ventricle[J]. J Clin Invest, 1997, 100:1782-1788.
[26] Zipes DP, Miyaki T. The autonomic nervous system and the heart: basis for understanding interactions and effects on arrhythmias development[J]. Cardiac Electrophysiology, 1990, 18: 312–330.
[27] Kang YJ. Cardiac hypertrophy:a risk factor for QT-prolongation and cardiac suddendeath[J]. Toxicol Pathol, 2006, 34:58-65.
[28] Domenighetti AA, Boixel C, Cefai D, et al. Chronic angiotensin II stmiulation in the heart produces an acquired long QT syndrome associated with IK1 potassium current downregulation[J]. J Mol Cell Cardiol, 2007, 42:63-70.
[29] Hoshino K, Ogawa K, H ishitani T, et al. Effect of slow coronary flow on electrocardiographic parameters reflecting ventricular heterogeneity[J]. Angiology, 2007, 58: 289-294.
[30] Kuller LH, Shemanski L, Psaty BM, et al. Subclinical disease as an independent risk factor for cardiovascular disease[J].Circulation, 995, 92:720–726.
[31] Festa A, D'Agostino R, Rautaharju P, et al. Is QT Interval a Marker of Subclinical Atherosclerosis in Nondiabetic Subjects[J]? Stroke, 1999, 30:1566-1571.
[1]陆再英. T波电交替[J].中华心血管病杂志, 2002, 30:199-200.
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[7] Antzelevitch C , Belardinelli L.The Role of Sodium Channel Current in modulating Transmural Dispersion of Repolarization and Arrhythmogenesis [J]. J Cardiovasc Electrophysiol, 2006, 17:79-85.
[8] Garfinkel A, Kim YH, Voroshilovsky O, et al. Preventing ventricular fibrillation by flattening cardiac restitution[J]. Proc Natl Acad Sci USA , 2000, 97:6061-6066.
[9] Nash MP, Bradley CP, Sutton PM, et al. Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study[J]. Experimental Physiology, 2005, 91: 339-354.
[10] Nash MP , Bradley CP, Sutton PM.Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study[J]. Experimental Physiology, 2006, 39-354.
[11] Nash MP, Panfilov AV. Electromechanical model of excitable tissue to study reentrant cardiac arrhythmias[J]. Prog Biophys Mol Biol, 2004, 85:501-522.
[12] Franz MR, Swerdlow CD, Liem LB, et al. Cycle length dependence of human action potential duration in vivo.Effects of single extrastimuli,sudden sustained rate acceleration and deceleration, and different steady-state frequencies[J]. J Clin Invest 1988, 82:972-979.
[13] Narayan SM. T-Wave Alternans and the Susceptibility to Ventricular Arrhythmias[J]. JACC , 2006, 47:261-281.
[14] Banville I, Gray RA. Effect of action potential duration and conduction velocity restitution and their spatial dispersion on alternans and the stability of arrhythmias[J].JCardiovasc Electrophysiol , 2002, 13:1141-1149.
[15] Gehi AK, Stein RH, Metz LD, et al. Microvolt T-wave alternans for risk stratification of ventricular tachyarrythmic events: a meta-analysis [J]. J Am Coll Cardiol, 2005, 46:75-82.
[16] Franz M. The electrical restitution curve revisited: steep or flat slope-which is better[J]? J Cardiovasc Electrophysiol, 2003, 14:140-147.
[17] Lewis T. Notes upon alternation of the heart[J]. QJ Med, 1910, 4:141-146.
[18] Shimizu W, Antzelevitch C. Cellular and ionic basis for T-wave alternans under long-QT conditions[J]. Circulation, 1999, 99:1499-1502.
[19] Tanno K. Microvolt T-wave alternans as a predictor of ventricular tachyarrhythmias[J]. Circulation, 2004, 109:1854-1860.
[20] Morita H, Zipes DP. Wave alternans in an in vitro canine tissue model of Brugada syndrome[J]. Am Physiol Heart Circ Physiol, 2006, 291:421-429.
[21] Pruvot EJ, Katra RP, Rosenbaum DR, et al . Role of calcium cycling versus restitution in the mechanism of repolarizati on alternans[J].Circ Res, 2004, 94: 1083-1087.
[22] Walker ML, Wan XP, Kirsch GE, et al. Hysteresis effect implicates calcium cycling as a mechanism of repolarization alternans[J]. Circulation, 2003, 108:2704-2710.
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[36] Shivkumar K, Deutsch NA, Lamp ST, et al. Mechanism of hypoxic K loss in rabbit ventricle[J].J Clin Invest, 1997, 100:1782-1788.
[37] Kenigsberg DN, Khanal S, Kowalski M, et al. Prolongation of the QTc interval is seen uniformly during early transmural ischemia[J]. J Am Coll Cardiol, 2007, 49:1299-1305.
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[2]陈颧珠主编.实用内科学[M].第12版,北京:人民卫生出版社, 2005:1467-1468.
[3]张开滋,罗昭林,肖传实,等.简明心脏负荷试验图解[M].湖南:湖南科学技术出版社.2005:1-6.
[4] Arab D, Valeti V, Schunemann HJ, et al. Usefulness of the QTc interval in predicting myocardial ischemia in patients undergoing exercise stress testing[J].Am J Cardiol, 2000, 85: 764–766.
[5] Stoletniy LN, Pai RG. Value of QT Dispersion in the Interpretation of Exercise Stress Test in Women[J]. Circulation, 1997, 96:904-910.
[6] Robbins J, Nelson JC, Rautaharju PM, et al. The association between the length of the QT interval and mortality in the cardiovascular health study[J]. Am J Med, 2003, 115:689-694.
[7] Kenigsberg DN, Khanal S, Kowalski M, et al. Prolongation of the QTc interval is seen uniformly during early transmural ischemia[J]. J Am Coll Cardiol, 2007, 49:1299-1305.
[8] Mclaughlin NB, Campbell RW. Murray comparision of automatic QT measeurement techniques in the normal 12 lead electrocardiogram[J]. BrHeart, 1995, 74:84-89.
[9] Chiang CE, Roden DM. The long QT syndromes:genetic basis and clinical imlication[J]. J Am Coll Cardiol, 2000, 36:1-12.
[10] Dekker JM, Schouten EG, Klootwijk P, et al. Association between QT interval and coronary heart disease in middle-aged and elderly men [J]. Circulation, 1994, 90:779-785.
[11] Gianrossi R, Detrano R, Mulvihill D, et al. Exercise-induced ST depression diagnosisi of cornary artery disease.A meta-analysis[J]. Circulation, 1989, 80:87-89.
[12] Puddu PE, Bourassa MG. Prediction of sudden death from QTc interval prolongation in patients with chronic ischemic heart disease[J]. J Electrocardiol. 1986, 19:203–211.
[13] Nilsson G, Hedberg P, Jonasson T, et al. QTc interval and survival in 75-year-old men and women from the general population[J]. Europace, 2006, 8:233-240.
[14] Antzelevitch C , Belardinelli L. The Role of Sodium Channel Current in modulating Transmural Dispersion of Repolarization and Arrhythmogenesis[J]. J Cardiovasc Electrophysiol, 2006, 17:79-85.
[15] Antzelevitch C . Ionic, molecular, and cellular bases of QT-interval prolongation and torsade de pointes[J]. Europace, 2007, 9:4-15.
[16] Garfinkel A, Kim YH, Voroshilovsky O, et al. Preventing ventricular fibrillation by flattening cardiac restitution[J]. Proc Natl Acad Sci USA , 2000, 97:6061–6066.
[17] Nash MP, Bradley CP, Sutton PM, et al. Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study[J]. Experimental Physiology, 2005, 91: 339-354.
[18] Nash MP, Bradley CP, Sutton PM. Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study[J]. Experimental Physiology, 2006, 9:352-354.
[19] Nash MP, Panfilov AV. Electromechanical model of excitable tissue to study reentrant cardiac arrhythmias[J]. Prog Biophys Mol Biol, 2004, 85:501–522.
[20]单其俊,沈建华.获得性长QT综合征[J].中国心脏起搏与心电生理杂志, 2008, 22:103-110.
[21] Roden DM. Taking the“idio”out of“idiosyncratic”: predictingTorsades de Pointes[J]. PACE, 1998, 21:1029-1037.
[22] Aiba T, Shmiizu W, Inagaki M. Cellular and ionic mechanism for Drug-induced long QT syndrome and effectiveness of verapamil[J]. J Am Coll Cardiol, 2005, 45:300-315.
[23] Burashnikov A, Antzelevitch C. Prominent IKs in ep icardium and endocardium contributes to development of transmural dispersion of repolarization but protects against development of early afterdepolarizations[J]. J Cardiovasc Electrophysiol, 2002, 13:172-178.
[24] Antzelevitch C. Arrhythmogenic mechanisms of QT prolonging drugs:Is QT p rolongation really the p roblem[J]? J Electrocardiol, 2004, 37:15-20.
[25] Shivkumar K, Deutsch NA, Lamp ST, et al. Mechanism of hypoxic K loss in rabbit ventricle[J]. J Clin Invest, 1997, 100:1782-1788.
[26] Zipes DP, Miyaki T. The autonomic nervous system and the heart: basis for understanding interactions and effects on arrhythmias development[J]. Cardiac Electrophysiology, 1990, 18: 312–330.
[27] Kang YJ. Cardiac hypertrophy:a risk factor for QT-prolongation and cardiac suddendeath[J]. Toxicol Pathol, 2006, 34:58-65.
[28] Domenighetti AA, Boixel C, Cefai D, et al. Chronic angiotensin II stmiulation in the heart produces an acquired long QT syndrome associated with IK1 potassium current downregulation[J]. J Mol Cell Cardiol, 2007, 42:63-70.
[29] Hoshino K, Ogawa K, H ishitani T, et al. Effect of slow coronary flow on electrocardiographic parameters reflecting ventricular heterogeneity[J]. Angiology, 2007, 58: 289-294.
[30] Kuller LH, Shemanski L, Psaty BM, et al. Subclinical disease as an independent risk factor for cardiovascular disease[J].Circulation, 995, 92:720–726.
[31] Festa A, D'Agostino R, Rautaharju P, et al. Is QT Interval a Marker of Subclinical Atherosclerosis in Nondiabetic Subjects[J]? Stroke, 1999, 30:1566-1571.
[1]陆再英. T波电交替[J].中华心血管病杂志, 2002, 30:199-200.
[2] Priori SG, Zip DP. Sudden Cardiac Death:a handbook for clinical practice[J]. J Cardiovasc Electrophysiol, 2006, 4:89-100.
[3]何秉贤.心脏性猝死心电学检测的进展[J] .心电学杂志, 2002, 21:75-76.
[4]郭继鸿.猝死高危预警的新指标:缺血性J波[J].中国心脏起搏与心电生理杂志, 2008, 22:6-10.
[5] Antzelevich C, Sicouri S, Litovsky SH, et al. Heterogeneity within the ventricular wall:eletrocardiology and pharmacology of epicardial, endocardial and M cell[J]. Cir Res, 1991, 69:1427-1430.
[6] Yamada KA, Kanter EM, Green KG, Saffitz JE. Transmural distribution of connexins in rodent hearts[J]. J Cardiovasc Electrophysiol, 2004, 15:710-715.
[7] Antzelevitch C , Belardinelli L.The Role of Sodium Channel Current in modulating Transmural Dispersion of Repolarization and Arrhythmogenesis [J]. J Cardiovasc Electrophysiol, 2006, 17:79-85.
[8] Garfinkel A, Kim YH, Voroshilovsky O, et al. Preventing ventricular fibrillation by flattening cardiac restitution[J]. Proc Natl Acad Sci USA , 2000, 97:6061-6066.
[9] Nash MP, Bradley CP, Sutton PM, et al. Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study[J]. Experimental Physiology, 2005, 91: 339-354.
[10] Nash MP , Bradley CP, Sutton PM.Whole heart action potential duration restitution properties in cardiac patients: a combined clinical and modelling study[J]. Experimental Physiology, 2006, 39-354.
[11] Nash MP, Panfilov AV. Electromechanical model of excitable tissue to study reentrant cardiac arrhythmias[J]. Prog Biophys Mol Biol, 2004, 85:501-522.
[12] Franz MR, Swerdlow CD, Liem LB, et al. Cycle length dependence of human action potential duration in vivo.Effects of single extrastimuli,sudden sustained rate acceleration and deceleration, and different steady-state frequencies[J]. J Clin Invest 1988, 82:972-979.
[13] Narayan SM. T-Wave Alternans and the Susceptibility to Ventricular Arrhythmias[J]. JACC , 2006, 47:261-281.
[14] Banville I, Gray RA. Effect of action potential duration and conduction velocity restitution and their spatial dispersion on alternans and the stability of arrhythmias[J].JCardiovasc Electrophysiol , 2002, 13:1141-1149.
[15] Gehi AK, Stein RH, Metz LD, et al. Microvolt T-wave alternans for risk stratification of ventricular tachyarrythmic events: a meta-analysis [J]. J Am Coll Cardiol, 2005, 46:75-82.
[16] Franz M. The electrical restitution curve revisited: steep or flat slope-which is better[J]? J Cardiovasc Electrophysiol, 2003, 14:140-147.
[17] Lewis T. Notes upon alternation of the heart[J]. QJ Med, 1910, 4:141-146.
[18] Shimizu W, Antzelevitch C. Cellular and ionic basis for T-wave alternans under long-QT conditions[J]. Circulation, 1999, 99:1499-1502.
[19] Tanno K. Microvolt T-wave alternans as a predictor of ventricular tachyarrhythmias[J]. Circulation, 2004, 109:1854-1860.
[20] Morita H, Zipes DP. Wave alternans in an in vitro canine tissue model of Brugada syndrome[J]. Am Physiol Heart Circ Physiol, 2006, 291:421-429.
[21] Pruvot EJ, Katra RP, Rosenbaum DR, et al . Role of calcium cycling versus restitution in the mechanism of repolarizati on alternans[J].Circ Res, 2004, 94: 1083-1087.
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