- Email: [email protected]
Effects of cardiac rehabilitation and exercise training on indexes of dispersion of ventricular repolarization in patients after acute myocardial infarction
Effects of Cardiac Rehabilitation and Exercise Training on Indexes of Dispersion of Ventricular Repolarization in Patients After Acute Myocardial Infarction Thomachan Kalapura, MD, Carl J. Lavie, MD, Waseem Jaffrani, Vijay Chilakamarri, MD, and Richard V. Milani, MD We studied 50 consecutive patients with relatively preserved systolic function (ejection fraction >40%, mean 53 ⴞ 11%) after acute myocardial infarction, and assessed indexes of dispersion of ventricular repolarization before and after a formal, phase II cardiac rehabilitation and exercise training program. After cardiac rehabilitation, statistically significant reductions occurred in QT dispersion, JT dispersion, and in the heart rate corrected indexes. These benefits add to the proven benefits of formal cardiac rehabilitation and exercise training programs and may reduce the subsequent risks of malignant ventricular arrhythmias and sudden cardiac death. 䊚2003 by Excerpta Medica, Inc. (Am J Cardiol 2003;92:292–294)
fter acute myocardial infarction (AMI), patients have a high incidence of malignant ventricular arA rhythmias and sudden cardiac death (SCD). Studies have suggested that a standard 12-lead surface electrocardiogram (ECG) can provide prognostic information, particularly when related to ventricular repolarization dispersion. The heterogeneity of ventricular repolarization dispersion, as measured by calculating the QT dispersion (QTd), which is the difference between maximum and minimum QT intervals on a 12-lead surface ECG, has been shown to be a marker of myocardial electrical instability and may predict SCD.1 JT dispersion (JTd) has also been shown to be a very good predictor of SCD in patients with AMI.2 Pooled data from randomized clinical trials of cardiac rehabilitation have demonstrated 20% to 25% reductions in major cardiovascular events, including coronary artery disease mortality and total mortality.3,4 We have previously demonstrated the benefits of aerobic exercise training on ventricular repolarization indexes in patients with heart failure with severely reduced systolic function.5 Indexes of dispersion of ventricular repolarization have not been fully assessed before and after cardiac rehabilitation and exercise training programs in patients after AMI. •••
We evaluated the effects of monitored cardiac rehabilitation and aerobic exercise training (12 weeks, 36 sessions) on ventricular repolarization indexes in 50 conFrom the Department of Cardiology, Ochsner Clinic Foundation, New Orleans, Louisiana. Dr. Lavie’s address is: Department of Cardiology, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, Lousiana 70121. E-mail: [email protected]. Manuscript received February 11, 2003; revised manuscript received and accepted April 17, 2003.
292
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 August 1, 2003
MD,
secutive post-AMI patients referred for cardiac rehabilitation (ejection fraction ⬎40%, mean 53 ⫾ 11). Standard 12-lead ECGs were obtained at the beginning and end of the exercise training program. The QT and JT intervals were measured manually. QTd and JTd were calculated by subtracting the shortest from the longest QT and JT intervals, respectively, and rate corrected using Bazett’s formula (QTc-d, JTc-d). Entry criteria included the following: (1) absence of clinical congestive heart failure and echocardiographic evidence of ejection fraction of ⬎40%; (2) absence of active ischemia as revealed by a clinical examination or by exercise testing at enrollment; (3) a stable medical regimen for ⱖ2 weeks before starting exercise training and during the entire training period; (4) absence of any recent coronary revascularization procedure (⬍3 months); and (5) no history of AMI in the 8 weeks before enrollment. Exclusion criteria included the following: (1) class IA or III antiarrhythmic medications; (2) inability to complete the exercise training program; (3) absence of sinus rhythm at entry or completion of training; (4) complete right or left bundle branch block; and (5) presence of electrolyte abnormalities. All patients completed 12-week (36 exercise sessions), phase II cardiac rehabilitation and exercise training programs as described elsewhere.6 – 8 Each session consisted of approximately 10 minutes of warm-up exercises, including stretching and calisthenics, followed by 30 to 40 minutes of continuous upright aerobic and dynamic exercises (various combinations of walking, bicycling, jogging, rowing, and so forth), light isometric exercises (hand weights), and approximately 10 minutes of cool-down stretching and calisthenics. Exercise intensity was prescribed individually so that patients’ heart rates were approximately 70% to 85% of the maximum heart rate. In addition to the supervised exercise sessions, approximately 1 to 3 times per week of exercise outside the formal program was encouraged. Before entering the program, patients underwent symptom-limited exercise testing, which usually consisted of using a ramping treadmill protocol. Breathto-breath on-line gas analysis was performed using a metabolic cart (MedGraphics CPX/day; Medical Graphics Corporation; St. Paul, Minnesota), with incremental data collected every 15 seconds. Maximal oxygen consumption, anaerobic threshold, and METs were determined on the basis of established criteria. After the outpatients’ cardiac rehabilitation exercise training programs, patients underwent protocols similar to the preprogram exercise assessment. Standard 12-lead surface ECGs were recorded at the 0002-9149/03/$–see front matter doi:10.1016/S0002-9149(03)00628-3
exclusion criteria were included in the analysis. All patients were on a stable medical regimen of aspirin,  blockers, and angiotensin-converting en% Change p Value zyme inhibitors; most were on statins. 14 ⬍0.01 No changes were made to the dosage ⫺29 ⬍0.01 of these medications during the train⫺31 ⬍0.01 ing period. ⫺27 ⬍0.02 As demonstrated in Table 1, there ⫺27 ⬍0.01 was a statistically significant increase in the measured METs after the training period. There were no significant changes in weight, percent body fat, or body mass indexes. Regarding QTd, QTc-d, JTd, and JTc-d, there were statistically significant decreases in all intervals after completion of the cardiac rehabilitation and exercise training program. The greatest decrease (Figure 1) was in the corrected QTd (⫺31%). These improvements did not significantly correlate with other characteristics (e.g., gender, exercise capacity, age, and left ventricular ejection fraction) in either univariable or multivariable analyses.
TABLE 1 Effects of Formal Cardiac Rehabilitation (Rehab) and Exercise Training Programs on Exercise Capacity and Indexes of Ventricular Repolarization Dispersion in Patients After AMI (n ⫽ 50) Parameter
Pre-Rehab
Exercise capacity (METs) QTd (ms) QTd heart rate corrected (ms) JTd (ms) JTd heart rate corrected (ms)
4.9 48 51 45 48
All values expressed as mean ⫾ SD.
⫾ ⫾ ⫾ ⫾ ⫾
1.9 37 36 30 28
Post-Rehab 5.6 34 35 33 35
⫾ ⫾ ⫾ ⫾ ⫾
2.1 15 16 19 20
FIGURE 1. Effects of cardiac rehabilitation and exercise training on QTc-d and JTc-d (n ⴝ 50).
beginning of the study at a paper speed of 25 m/s and an amplifier gain of 10 mm/mV. All ECGs were examined by 1 observer who was blinded to clinical status and follow-up results. Measurements of QT, JT, and RR intervals were performed manually. The QT interval was measured from the beginning of the QRS complex to the end of the T wave at the level of the TP isoelectric baseline. Biphasic T waves were measured to the time of their final return to the TP isoelectric baseline. If U waves were present, the QT interval was measured from the beginning of the QRS complex to the nadir of the curve between the T and U waves. The JT interval was measured from the end of the QRS complex, which was defined as the point at which the QRS complex returned to the TP isoelectric baseline (J point), to the end of the T wave at the level of the TP isoelectric baseline. Extrasystolic and post-extrasystolic cycles were excluded from the measurement. If the end of the T wave could not be reliably determined, or if the T waves were isoelectric or of very low amplitude, QT or JT interval measurements were not made, and these electrocardiographic leads were excluded from the analysis. To obtain reasonably standardized sets of electrocardiographic leads, a lower limit of ⱖ8 technically adequate measurable leads per ECG was set for inclusion into the study. Heart rate corrected QT (QTc) and JT intervals (JTc) were calculated using Bazett’s formula (QTc ⫽ QT/ RR).9 The ventricular repolarization dispersions were determined by calculating the difference between maximum and minimum QT or JT intervals on each ECG, which were termed QTd, heart rate corrected QTd (QTcd), JTd, and heart rate corrected JTd (JTc-d). ECGs were recorded at the initiation and completion of the training program. Fifty consecutive patients (mean age 58 years; 38 men, 12 women; ejection fraction 53 ⫾ 11%) who were referred for cardiac rehabilitation and did not meet the
•••
Post-AMI patients are at increased risk of SCD due to malignant ventricular arrhythmias. In our study, in a group of patients who survived AMI, the indexes of dispersion of ventricular repolarization, which serve as a marker of SCD, significantly improved after a formal cardiac rehabilitation and exercise training program. The precise mechanism behind the increases in the homogeneity of ventricular repolarization dispersion remains elusive. The duration of action potential is primarily responsible for the time span of the repolarization. If the prolongation of the action potential were homogenous, it would not necessarily produce an arrhythmogenic milieu.10 However, variations in the duration of the action potential would create a ventricular repolarization dispersion that could be arrhythmogenic.11 Regional differences in the density of the potassium currents have been demonstrated in failing and ischemic human hearts; this could explain the nonhomogeneity of ventricular repolarization dispersion seen in these patients.12,13 Influences of the autonomic nervous system on QT dispersion are well known.13 Aerobic exercise training restores heart rate variability, increases vagal tone, and reduces sympathetic tone in patients after AMI,14 and we have previously reported marked benefits in autonomic regulation following formal cardiac rehabilitation.15,16 These beneficial effects on the autonomic nervous system could be partially responsible for the improvements in the indexes of ventricular repolarization dispersion and decreased risk of SCD.17 Measurements of QTd may provide an advantage over those of heart rate variability in clinical settings. A limitation in using heart rate variability as an index of the effect of the autonomic nervous system on the ventricle is that it is indirect, reflecting changes in the RR interval by way of reflex mechanisms mediated by the sinus node. The QT interval is an index of repolarization dispersion that is directly influenced by myocardial health and autonomic nervous system activity. Therefore, variability of the QT interval should predict cardiac BRIEF REPORTS
293
risk more directly and accurately than variability of the RR interval does.11 Our study adds to the evidence of the beneficial effects of formal cardiac rehabilitation and exercise training in patients with coronary artery disease. Measurements of QTd and JTd on a surface ECG is a noninvasive technique that seems to reflect the risk of malignant ventricular dysrhythmias and SCD. Although marked improvements were noted in indexes of repolarization dispersion in this group of relatively low-risk patients, large-scale prospective trials are needed to validate these findings and to determine whether these improvements translate into significant reductions in major cardiac events, and, particularly, the incidence of SCD. 1. Barr CS, Naas A, Freeman M, Lang CC, Struthers AD. QT dispersion and
sudden unexpected death in chronic heart failure. Lancet 1994;343:327–329. 2. Amlie JP. QT dispersion and sudden cardiac death. Eur Heart J 1996;18:189 –190. 3. Oldridge NB, Guyatt GH, Fischer ME, Rimm AA. Cardiac rehabilitation after
myocardial infarction: combined experience of randomized clinical trials. JAMA 1988;260:945–950. 4. O’Connor GT, Buring JE, Yusuf S, Goldhaber SZ, Olmstead EM, Paffenbarger RS Jr, Hennekens CH. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation 1989;80:234 –244. 5. Ali A, Mehra MR, Malik FS, Lavie CJ, Bass D, Milani RV. Effects of aerobic exercise training on indices of ventricular repolarization in patients with chronic heart failure. Chest 1999;116:83–87.
6. Milani RV, Lavie CJ. Disparate effects of outpatient cardiac and pulmonary rehabilitation programs upon work efficiency and peak aerobic capacity in patients with coronary disease or severe obstructive pulmonary disease. J Cardiopulm Rehabil 1998;18:17–22. 7. Lavie CJ, Milani RV. Effects of cardiac rehabilitation, exercise training and weight reduction on exercise capacity, coronary risk factors, behavioral characteristics and quality of life in obese patients with coronary artery disease. Am J Cardiol 1997;79:397–401. 8. Lavie CJ, Milani RV. Effects of cardiac rehabilitation programs on exercise capacity, coronary risk factors, behavioral characteristics, and quality of life in a large elderly cohort. Am J Cardiol 1995;76:177–179. 9. Bazett HC. An analysis of the time relations of electrocardiograms. Heart 1920;7:353–367. 10. Scamps F, Mayoux E, Charlemagne D, Vassort G. Calcium current in single cells isolated from normal and hypertrophied rat heart: effects of beta adrenergic stimulation. Circ Res 1990;67:199 –208. 11. Tomaselli GF, Beuckelmann DJ, Calkins HG, Berger RD, Kessler PD, Lawrence JH, Kass D, Feldman AM, Marban E. Sudden cardiac death in heart failure: the role of abnormal repolarization. Circulation 1994;90:2534 –2539. 12. Wettwer E, Amos GJ, Posival H, Ravens U. Transient outward current in human ventricular myocytes of subepicardial and subendocardial origin. Circ Res 1994;75:473–482. 13. Uemura S, Fujimoto S, Tomoda Y, Matsukura Y, Yamamoto H, Hashimoto T, Dohi K. Influence of autonomic blockade on QT dispersion in man. J Am Coll Cardiol 1997;29(suppl):34A. 14. Tavazzi L, Mortara A. Exercise training and the autonomic nervous system in chronic heart failure. Eur Heart J 1995;16:1308 –1310. 15. Lavie CJ, Milani RV. Autonomic tone and benefits of cardiac rehabilitation programs. Mayo Clin Proc 2002;77:398 –399. 16. Lucini D, Milani RV, Costantino G, Lavie CJ, Porta A, Pagani M. Effects of cardiac rehabilitation and exercise training on autonomic regulation in patients with coronary artery disease. Am Heart J 2002;143:977–983. 17. Curtis BM, O’Keefe JH. Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight. Mayo Clin Proc 2002;77:45–54.
Degrees of Severe Stenoses in Sigma-Shaped Versus C-Shaped Right Coronary Arteries Danny Dvir,
MD,
Ran Kornowski, MD, Jacob Gurevich, Dan Aravot, MD
The right coronary artery (RCA) appears either C-shaped or sigma-shaped during standard angiography. The purpose of the present investigation was to assess whether C-shaped RCAs are associated with more atherosclerotic disease than sigma-shaped RCAs. The study sample comprised 120 consecutive patients who underwent coronary catheterization and multivariate analysis was conducted using several systemic risk factors for atherosclerosis. The proportion of sigmashaped RCAs found in a group whose angiograms showed little or no obstruction (70%) was significantly higher than that found in the group with significant obstruction (33%, p <0.001). In conclusion, a C-shaped RCA is associated with atherosclerosis. 䊚2003 by Excerpta Medica, Inc. (Am J Cardiol 2003;92:294 –298) From the Department of Cardiothoracic Surgery, Carmel Medical Center, affiliated with the Rapparort Faculty of Medicine, Technion, Haifa; and the Cardiac Catheterization Unit, Rabin Medical Center, affiliated with the Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel. Dr. Aravot’s address is: Department of Cardiothoracic Surgery, Carmel Medical Center, 7 Michal Street, Haifa, 34362, Israel. E-mail: [email protected]. Manuscript received January 29, 2003; revised manuscript received and accepted April 21, 2003.
294
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 August 1, 2003
MD,
Boris Orlov,
MD,
and
therosclerosis, although associated with systemic risk factors such as hypertension, smoking, hyperA lipidemia, and diabetes mellitus, is mostly a focal disease, highly influenced by the hemodynamic forces inside the vessels,1– 4 which, in turn, are influenced by the local vascular geometry. Several researchers have suggested that certain geometric features, or “geometric risk factors,” may predispose the vasculature to atherogenesis in their vicinity through their effect on the local flow field.5– 8 Recent biomechanical studies in models of the right coronary artery (RCA) have reported that C-shaped RCAs are predisposed to atherosclerosis in their proximal-middle region.9,10 However, these studies did not examine flow patterns in RCAs with a different morphology, such as sigma-shaped RCAs, which have a bend in the middle region and, therefore, a different flow pattern. In a previous study, we found an association between short RCA length and atherosclerotic plaques.11 The present investigation determines if C-shaped RCAs have a greater association with atherosclerosis than sigma-shaped RCAs. •••
The study sample consisted of 120 consecutive patients who underwent cardiac catheterization in our center and were found to have either no significant RCA obstruction (⬍30% of the vessel diameter, group 0002-9149/03/$–see front matter doi:10.1016/S0002-9149(03)00629-5
fter acute myocardial infarction (AMI), patients have a high incidence of malignant ventricular arA rhythmias and sudden cardiac death (SCD). Studies have suggested that a standard 12-lead surface electrocardiogram (ECG) can provide prognostic information, particularly when related to ventricular repolarization dispersion. The heterogeneity of ventricular repolarization dispersion, as measured by calculating the QT dispersion (QTd), which is the difference between maximum and minimum QT intervals on a 12-lead surface ECG, has been shown to be a marker of myocardial electrical instability and may predict SCD.1 JT dispersion (JTd) has also been shown to be a very good predictor of SCD in patients with AMI.2 Pooled data from randomized clinical trials of cardiac rehabilitation have demonstrated 20% to 25% reductions in major cardiovascular events, including coronary artery disease mortality and total mortality.3,4 We have previously demonstrated the benefits of aerobic exercise training on ventricular repolarization indexes in patients with heart failure with severely reduced systolic function.5 Indexes of dispersion of ventricular repolarization have not been fully assessed before and after cardiac rehabilitation and exercise training programs in patients after AMI. •••
We evaluated the effects of monitored cardiac rehabilitation and aerobic exercise training (12 weeks, 36 sessions) on ventricular repolarization indexes in 50 conFrom the Department of Cardiology, Ochsner Clinic Foundation, New Orleans, Louisiana. Dr. Lavie’s address is: Department of Cardiology, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, Lousiana 70121. E-mail: [email protected]. Manuscript received February 11, 2003; revised manuscript received and accepted April 17, 2003.
292
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 August 1, 2003
MD,
secutive post-AMI patients referred for cardiac rehabilitation (ejection fraction ⬎40%, mean 53 ⫾ 11). Standard 12-lead ECGs were obtained at the beginning and end of the exercise training program. The QT and JT intervals were measured manually. QTd and JTd were calculated by subtracting the shortest from the longest QT and JT intervals, respectively, and rate corrected using Bazett’s formula (QTc-d, JTc-d). Entry criteria included the following: (1) absence of clinical congestive heart failure and echocardiographic evidence of ejection fraction of ⬎40%; (2) absence of active ischemia as revealed by a clinical examination or by exercise testing at enrollment; (3) a stable medical regimen for ⱖ2 weeks before starting exercise training and during the entire training period; (4) absence of any recent coronary revascularization procedure (⬍3 months); and (5) no history of AMI in the 8 weeks before enrollment. Exclusion criteria included the following: (1) class IA or III antiarrhythmic medications; (2) inability to complete the exercise training program; (3) absence of sinus rhythm at entry or completion of training; (4) complete right or left bundle branch block; and (5) presence of electrolyte abnormalities. All patients completed 12-week (36 exercise sessions), phase II cardiac rehabilitation and exercise training programs as described elsewhere.6 – 8 Each session consisted of approximately 10 minutes of warm-up exercises, including stretching and calisthenics, followed by 30 to 40 minutes of continuous upright aerobic and dynamic exercises (various combinations of walking, bicycling, jogging, rowing, and so forth), light isometric exercises (hand weights), and approximately 10 minutes of cool-down stretching and calisthenics. Exercise intensity was prescribed individually so that patients’ heart rates were approximately 70% to 85% of the maximum heart rate. In addition to the supervised exercise sessions, approximately 1 to 3 times per week of exercise outside the formal program was encouraged. Before entering the program, patients underwent symptom-limited exercise testing, which usually consisted of using a ramping treadmill protocol. Breathto-breath on-line gas analysis was performed using a metabolic cart (MedGraphics CPX/day; Medical Graphics Corporation; St. Paul, Minnesota), with incremental data collected every 15 seconds. Maximal oxygen consumption, anaerobic threshold, and METs were determined on the basis of established criteria. After the outpatients’ cardiac rehabilitation exercise training programs, patients underwent protocols similar to the preprogram exercise assessment. Standard 12-lead surface ECGs were recorded at the 0002-9149/03/$–see front matter doi:10.1016/S0002-9149(03)00628-3
exclusion criteria were included in the analysis. All patients were on a stable medical regimen of aspirin,  blockers, and angiotensin-converting en% Change p Value zyme inhibitors; most were on statins. 14 ⬍0.01 No changes were made to the dosage ⫺29 ⬍0.01 of these medications during the train⫺31 ⬍0.01 ing period. ⫺27 ⬍0.02 As demonstrated in Table 1, there ⫺27 ⬍0.01 was a statistically significant increase in the measured METs after the training period. There were no significant changes in weight, percent body fat, or body mass indexes. Regarding QTd, QTc-d, JTd, and JTc-d, there were statistically significant decreases in all intervals after completion of the cardiac rehabilitation and exercise training program. The greatest decrease (Figure 1) was in the corrected QTd (⫺31%). These improvements did not significantly correlate with other characteristics (e.g., gender, exercise capacity, age, and left ventricular ejection fraction) in either univariable or multivariable analyses.
TABLE 1 Effects of Formal Cardiac Rehabilitation (Rehab) and Exercise Training Programs on Exercise Capacity and Indexes of Ventricular Repolarization Dispersion in Patients After AMI (n ⫽ 50) Parameter
Pre-Rehab
Exercise capacity (METs) QTd (ms) QTd heart rate corrected (ms) JTd (ms) JTd heart rate corrected (ms)
4.9 48 51 45 48
All values expressed as mean ⫾ SD.
⫾ ⫾ ⫾ ⫾ ⫾
1.9 37 36 30 28
Post-Rehab 5.6 34 35 33 35
⫾ ⫾ ⫾ ⫾ ⫾
2.1 15 16 19 20
FIGURE 1. Effects of cardiac rehabilitation and exercise training on QTc-d and JTc-d (n ⴝ 50).
beginning of the study at a paper speed of 25 m/s and an amplifier gain of 10 mm/mV. All ECGs were examined by 1 observer who was blinded to clinical status and follow-up results. Measurements of QT, JT, and RR intervals were performed manually. The QT interval was measured from the beginning of the QRS complex to the end of the T wave at the level of the TP isoelectric baseline. Biphasic T waves were measured to the time of their final return to the TP isoelectric baseline. If U waves were present, the QT interval was measured from the beginning of the QRS complex to the nadir of the curve between the T and U waves. The JT interval was measured from the end of the QRS complex, which was defined as the point at which the QRS complex returned to the TP isoelectric baseline (J point), to the end of the T wave at the level of the TP isoelectric baseline. Extrasystolic and post-extrasystolic cycles were excluded from the measurement. If the end of the T wave could not be reliably determined, or if the T waves were isoelectric or of very low amplitude, QT or JT interval measurements were not made, and these electrocardiographic leads were excluded from the analysis. To obtain reasonably standardized sets of electrocardiographic leads, a lower limit of ⱖ8 technically adequate measurable leads per ECG was set for inclusion into the study. Heart rate corrected QT (QTc) and JT intervals (JTc) were calculated using Bazett’s formula (QTc ⫽ QT/ RR).9 The ventricular repolarization dispersions were determined by calculating the difference between maximum and minimum QT or JT intervals on each ECG, which were termed QTd, heart rate corrected QTd (QTcd), JTd, and heart rate corrected JTd (JTc-d). ECGs were recorded at the initiation and completion of the training program. Fifty consecutive patients (mean age 58 years; 38 men, 12 women; ejection fraction 53 ⫾ 11%) who were referred for cardiac rehabilitation and did not meet the
•••
Post-AMI patients are at increased risk of SCD due to malignant ventricular arrhythmias. In our study, in a group of patients who survived AMI, the indexes of dispersion of ventricular repolarization, which serve as a marker of SCD, significantly improved after a formal cardiac rehabilitation and exercise training program. The precise mechanism behind the increases in the homogeneity of ventricular repolarization dispersion remains elusive. The duration of action potential is primarily responsible for the time span of the repolarization. If the prolongation of the action potential were homogenous, it would not necessarily produce an arrhythmogenic milieu.10 However, variations in the duration of the action potential would create a ventricular repolarization dispersion that could be arrhythmogenic.11 Regional differences in the density of the potassium currents have been demonstrated in failing and ischemic human hearts; this could explain the nonhomogeneity of ventricular repolarization dispersion seen in these patients.12,13 Influences of the autonomic nervous system on QT dispersion are well known.13 Aerobic exercise training restores heart rate variability, increases vagal tone, and reduces sympathetic tone in patients after AMI,14 and we have previously reported marked benefits in autonomic regulation following formal cardiac rehabilitation.15,16 These beneficial effects on the autonomic nervous system could be partially responsible for the improvements in the indexes of ventricular repolarization dispersion and decreased risk of SCD.17 Measurements of QTd may provide an advantage over those of heart rate variability in clinical settings. A limitation in using heart rate variability as an index of the effect of the autonomic nervous system on the ventricle is that it is indirect, reflecting changes in the RR interval by way of reflex mechanisms mediated by the sinus node. The QT interval is an index of repolarization dispersion that is directly influenced by myocardial health and autonomic nervous system activity. Therefore, variability of the QT interval should predict cardiac BRIEF REPORTS
293
risk more directly and accurately than variability of the RR interval does.11 Our study adds to the evidence of the beneficial effects of formal cardiac rehabilitation and exercise training in patients with coronary artery disease. Measurements of QTd and JTd on a surface ECG is a noninvasive technique that seems to reflect the risk of malignant ventricular dysrhythmias and SCD. Although marked improvements were noted in indexes of repolarization dispersion in this group of relatively low-risk patients, large-scale prospective trials are needed to validate these findings and to determine whether these improvements translate into significant reductions in major cardiac events, and, particularly, the incidence of SCD. 1. Barr CS, Naas A, Freeman M, Lang CC, Struthers AD. QT dispersion and
sudden unexpected death in chronic heart failure. Lancet 1994;343:327–329. 2. Amlie JP. QT dispersion and sudden cardiac death. Eur Heart J 1996;18:189 –190. 3. Oldridge NB, Guyatt GH, Fischer ME, Rimm AA. Cardiac rehabilitation after
myocardial infarction: combined experience of randomized clinical trials. JAMA 1988;260:945–950. 4. O’Connor GT, Buring JE, Yusuf S, Goldhaber SZ, Olmstead EM, Paffenbarger RS Jr, Hennekens CH. An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation 1989;80:234 –244. 5. Ali A, Mehra MR, Malik FS, Lavie CJ, Bass D, Milani RV. Effects of aerobic exercise training on indices of ventricular repolarization in patients with chronic heart failure. Chest 1999;116:83–87.
6. Milani RV, Lavie CJ. Disparate effects of outpatient cardiac and pulmonary rehabilitation programs upon work efficiency and peak aerobic capacity in patients with coronary disease or severe obstructive pulmonary disease. J Cardiopulm Rehabil 1998;18:17–22. 7. Lavie CJ, Milani RV. Effects of cardiac rehabilitation, exercise training and weight reduction on exercise capacity, coronary risk factors, behavioral characteristics and quality of life in obese patients with coronary artery disease. Am J Cardiol 1997;79:397–401. 8. Lavie CJ, Milani RV. Effects of cardiac rehabilitation programs on exercise capacity, coronary risk factors, behavioral characteristics, and quality of life in a large elderly cohort. Am J Cardiol 1995;76:177–179. 9. Bazett HC. An analysis of the time relations of electrocardiograms. Heart 1920;7:353–367. 10. Scamps F, Mayoux E, Charlemagne D, Vassort G. Calcium current in single cells isolated from normal and hypertrophied rat heart: effects of beta adrenergic stimulation. Circ Res 1990;67:199 –208. 11. Tomaselli GF, Beuckelmann DJ, Calkins HG, Berger RD, Kessler PD, Lawrence JH, Kass D, Feldman AM, Marban E. Sudden cardiac death in heart failure: the role of abnormal repolarization. Circulation 1994;90:2534 –2539. 12. Wettwer E, Amos GJ, Posival H, Ravens U. Transient outward current in human ventricular myocytes of subepicardial and subendocardial origin. Circ Res 1994;75:473–482. 13. Uemura S, Fujimoto S, Tomoda Y, Matsukura Y, Yamamoto H, Hashimoto T, Dohi K. Influence of autonomic blockade on QT dispersion in man. J Am Coll Cardiol 1997;29(suppl):34A. 14. Tavazzi L, Mortara A. Exercise training and the autonomic nervous system in chronic heart failure. Eur Heart J 1995;16:1308 –1310. 15. Lavie CJ, Milani RV. Autonomic tone and benefits of cardiac rehabilitation programs. Mayo Clin Proc 2002;77:398 –399. 16. Lucini D, Milani RV, Costantino G, Lavie CJ, Porta A, Pagani M. Effects of cardiac rehabilitation and exercise training on autonomic regulation in patients with coronary artery disease. Am Heart J 2002;143:977–983. 17. Curtis BM, O’Keefe JH. Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight. Mayo Clin Proc 2002;77:45–54.
Degrees of Severe Stenoses in Sigma-Shaped Versus C-Shaped Right Coronary Arteries Danny Dvir,
MD,
Ran Kornowski, MD, Jacob Gurevich, Dan Aravot, MD
The right coronary artery (RCA) appears either C-shaped or sigma-shaped during standard angiography. The purpose of the present investigation was to assess whether C-shaped RCAs are associated with more atherosclerotic disease than sigma-shaped RCAs. The study sample comprised 120 consecutive patients who underwent coronary catheterization and multivariate analysis was conducted using several systemic risk factors for atherosclerosis. The proportion of sigmashaped RCAs found in a group whose angiograms showed little or no obstruction (70%) was significantly higher than that found in the group with significant obstruction (33%, p <0.001). In conclusion, a C-shaped RCA is associated with atherosclerosis. 䊚2003 by Excerpta Medica, Inc. (Am J Cardiol 2003;92:294 –298) From the Department of Cardiothoracic Surgery, Carmel Medical Center, affiliated with the Rapparort Faculty of Medicine, Technion, Haifa; and the Cardiac Catheterization Unit, Rabin Medical Center, affiliated with the Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel. Dr. Aravot’s address is: Department of Cardiothoracic Surgery, Carmel Medical Center, 7 Michal Street, Haifa, 34362, Israel. E-mail: [email protected]. Manuscript received January 29, 2003; revised manuscript received and accepted April 21, 2003.
294
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 August 1, 2003
MD,
Boris Orlov,
MD,
and
therosclerosis, although associated with systemic risk factors such as hypertension, smoking, hyperA lipidemia, and diabetes mellitus, is mostly a focal disease, highly influenced by the hemodynamic forces inside the vessels,1– 4 which, in turn, are influenced by the local vascular geometry. Several researchers have suggested that certain geometric features, or “geometric risk factors,” may predispose the vasculature to atherogenesis in their vicinity through their effect on the local flow field.5– 8 Recent biomechanical studies in models of the right coronary artery (RCA) have reported that C-shaped RCAs are predisposed to atherosclerosis in their proximal-middle region.9,10 However, these studies did not examine flow patterns in RCAs with a different morphology, such as sigma-shaped RCAs, which have a bend in the middle region and, therefore, a different flow pattern. In a previous study, we found an association between short RCA length and atherosclerotic plaques.11 The present investigation determines if C-shaped RCAs have a greater association with atherosclerosis than sigma-shaped RCAs. •••
The study sample consisted of 120 consecutive patients who underwent cardiac catheterization in our center and were found to have either no significant RCA obstruction (⬍30% of the vessel diameter, group 0002-9149/03/$–see front matter doi:10.1016/S0002-9149(03)00629-5