- Email: [email protected]
Silent ischemia normalized for coronary collateral function in patients with and without diabetes mellitus
Letters to the Editor
In conclusion, there is a high incidence of congestive heart failure mainly due to post rheumatic valvulopathies in young patients in our centre. A national program for fight against rheumatic fever and complications is of great urgency in our country. The compensation treatment of congestive heart failure is challenging in our milieu, characterized by poor compliance and financial limitation. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [5]. Special thanks to the Tertiairy Sisters of Saint Francis for their devotion in the management of the cardiac centre.
319
References [1] Mayosi BM. Contemporary trends in the epidemiology and management of cardiomyopathy and pericarditis in sub-Saharan Africa. Heart 2007;93:1176–83. [2] Bardgett HP, Dixon M, Beeching NJ. Increase in hospital mortality from noncommunicable disease and HIV-related conditions in Bulawayo, Zimbabwe, between 1992 and 2000. Trop Doct 2006;36:129–31. [3] Kingue S, Dzudie A, Menanga A, et al. A new look at adult chronic heart failure in Africa in the age of the Doppler echocardiography: experience of the medicine department at Yaounde General Hospital. Ann Cardiol Angeiol (Paris) 2005;54:276–83. [4] Ladipo GO. Congestive cardiac failure in elderly Nigerians: a prospective clinical study. Trop Geogr Med 1981;33:257–62. [5] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.12.067
Silent ischemia normalized for coronary collateral function in patients with and without diabetes mellitus Rainer Zbinden a, Ursula Wenger b, Pascal Meier b, Steffen Gloekler b, Stephan Windecker b, Bernhard Meier b, Christian Seiler b,⁎ a b
Triemlispital, CH-8000 Zurich, Switzerland University Hospital Bern, CH-3010 Bern, Switzerland
a r t i c l e
i n f o
Article history: Received 8 December 2010 Accepted 13 December 2010 Available online 6 January 2011 Keywords: Diabetes mellitus Silent ischemia Coronary collateral flow
Silent myocardial ischemia (SMI) is a term used to describe myocardial ischemia without chest pain, but in the presence of other evidence of ischemia [1]. After an MI, between 20 and 30% of patients present with SMI [2]. Seiler et al. [3] showed in a study using a 1-min coronary balloon occlusion that only 27% of patients with sufficient collateral flow (i.e. collateral relative to normal coronary flow, CFI≥ 0.25) had chest pain during vascular occlusion compared to 88% of the patients with insufficient collateral flow (collateral flow index, CFI, <0.25) irrespective of diabetic status. This indicates that coronary collateral flow is an important determinant of chest pain when using the vascular occlusion model. Regarding the prognostic impact of SMI, the data is controversial [4,5]. The purpose of the present study was to assess the prevalence and impact of SMI under specific consideration of coronary collateral function in patients with and without DM. Four-hundred and fifty two patients (354 (78%) men, mean age 64 +/− 9 years) referred for diagnostic coronary angiography were included in the study. One⁎ Corresponding author. University Hospital Bern, 3010 Bern, Switzerland. Tel.: +41 31 632 21 11. E-mail address: [email protected] (C. Seiler).
hundred and thirteen had DM type II and 339 patients served as the non-diabetic control group. Each diabetic patient was matched with 3 non-diabetic control patients for collateral flow index (CFI, see below), age and gender. All patients underwent left heart catheterization for diagnostic purposes. Either a 0.014 inch pressure-sensor tipped guidewire (n= 307), a Doppler guidewire (n = 75), or both (n = 70) were used during coronary balloon occlusion to assess the CFI. CFI (no units) is calculated as coronary occlusive pressure minus central venous pressure divided by aortic pressure minus central venous pressure when using the pressure wire or flow velocity during balloon occlusion divided by flow velocity during resting conditions using the Doppler guidewire. CFI correlates well with absolute collateral flow during balloon occlusion [6] During the 1-min coronary balloon occlusion patients were asked to report chest pain, and an intracoronary ECG was recorded. SMI was defined as significant ST-segment elevation in the intracoronary ECG (>0.1 mV) in the absence of chest pain. The diabetic and non-diabetic groups were matched for gender, age and CFI (Table 1). 359 patients had significant ST-segment changes in the i.c. ECG (78% diabetics vs. 80% non-diabetics; p = 0.64) during the 1-min coronary balloon occlusion. CFI was significantly higher in patients without i.c. ECG changes than in patients with i.c. ECG changes (0.33± 0.15 vs. 0.17 ± 0.08; p = <0.0001) (irrespective of diabetic status). 77 (17%) patients had silent ischemia (i.e. i.c. ECG changes without any symptoms): 22% diabetic vs. 15% non-diabetic patients (p= 0.10) (Fig. 1). Diabetic patients with a diagnosis of diabetic neuropathy were more likely to suffer from SMI (62% vs. 38%; p =0.05) as were diabetic patients with higher fasting blood glucose (10.0±3.6 vs. 8.5±3.0; p =0.03). There was a strong association between the patient's symptoms and the occurrence of silent ischemia during balloon occlusion. Only 58% of the patients with silent ischemia during balloon occlusion had typical anginal symptoms before admission compared to 88% of the patients with symptomatic ischemia (p<0.0001).
320
Letters to the Editor
Table 1 Patient characteristics.
Men Age (years) BMIa(kg/m2) Mean blood pressure (mm Hg) Heart rate (beats/min) Ejection fraction (%) History of previous MI† LVEDP‡ (mm Hg) Cardiovascular risk factors Hypertension Smoking Dyslipidemia Family history of CAD§ Antianginal medication Betablocker Nitrates Calcium antagonists Blood chemistry Total cholesterol (mmol/l) HDL cholesterol (mmol/l) LDL cholesterol (mmol/l) Triglycerides (mmol/l) Fasting glucose (mmol/l) HbA1c (%) Hemodynamic characteristics Ejection fraction (%) Target vessel (LADb/LCX††/RCA‡‡) Number of vessels diseased Percent diameter stenosis (%) Collateral flow index (no unit)
Diabetics (n = 113)
Non-diabetics (n = 339)
88 (78%) 64 ± 9 28.4 ± 3.6 94.4 ± 15.0 72 ± 12 63 ± 11 54 (48%) 12.8 ± 6.4
266 (78%) 64 ± 10 26.9 ± 4.0 94.1 ± 15.1 70 ± 12 65 ± 11 119 (35%) 12.3 ± 5.9
0.90 0.68 0.0004 0.88 0.14 0.16 0.007 0.47
85 26 93 33
189 101 251 133
0.0003 0.18 0.13 0.05
(75%) (23%) (82%) (29%)
(56%) (30%) (74%) (39%)
61 (54%) 43 (38%) 28 (25%)
209 (62%) 116 (34%) 59 (17%)
5.3 ± 1.1 1.2 ± 0.4 3.3 ± 1.2 2.2 ± 1.6 8.8 ± 3.2 7.2 ± 1.7 (n = 76)
5.4 ± 1.2 1.3 ± 0.3 3.3 ± 1.2 1.9 ± 1.7 6.0 ± 1.2 5.5 ± 0.6 (n = 49)
63 ± 11 41%/28%/31% 1.8 ± 0.8 72.5 ± 23.8 0.20 ± 0.12
65 ± 11 50%/26%/24% 1.6 ± 0.9 63.1 ± 32.2 0.20 ± 0.12
p value
0.15 0.46 0.09 0.29 0.0001 0.99 0.15 < 0.0001 < 0.0001
0.16 0.47 0.11 0.005 0.99
a
Body mass index, Myocardial infarction. Left ventricular enddiastolic pressure. § Coronary artery disease. b Left anterior descending coronary artery. †† Left circumflex coronary artery. ‡‡ Right coronary artery. † ‡
Follow-up was completed in 445 patients (98%). During a mean follow-up of 60 ± 34 months, there were 56 deaths in total (9 (11.7%) in the SMI group vs. 47 (12.5%) in the non-SMI group; p = 0.82). Non-
Fig. 1. 78% of diabetic and 80% of non-diabetic patients had ST-segment changes in the intracoronary (i.c.) ECG, indicating that 22% of the diabetic and 20% of the non-diabetic patients had enough collateral flow to avoid signs of ischemia during the 1-min balloon inflation (i.e. no ST segment changes in the i.c. ECG). 22% of diabetic and 15% of non-diabetic patients had silent ischemia during the 1-min balloon occlusion (i.e. ST-segment changes in the i.c. ECG but no chest pain).
Fig. 2. Kaplan–Meier curve for the combined endpoint of death or non-fatal myocardial infarction in all patients (diabetic and non-diabetic) comparing patients with and without silent ischemia. There is no difference regarding the combined endpoint in patients with vs. patients without silent ischemia.
fatal MI occurred in 4 patients ((5.2%) in the SMI group vs. 11 (2.9%) in the non-SMI group; p = 0.31). SMI had no influence on the occurrence of death/non-fatal MI neither in the whole group nor in the diabetic subgroup (Figs. 2 and 3). The only independent predictors of death/non-fatal MI in the multivariate analysis were calculated creatinine clearance (using the Cockroft formula) (HR 0.95–0.98; p < 0.0001) and left ventricular ejection fraction (HR 0.95–0.99; p = 0.003). First observations of a higher prevalence of SMI in diabetics date back to the early 1960s, when Bradley and Partaminan [7] found that 33 of 77 diabetic patients who died of acute myocardial infarction had evidence of at least one healed infarction that was not related to the patient's clinical history. A series of studies on SMI in diabetics followed [8–12], and showed controversial results mainly because of lack of control for important cofactors and different methods/ diagnostic tests to assess SMI. Very few studies have used the coronary balloon occlusion model during PCI to explore the phenomenon of SMI [13]. In our study, clinical symptoms correlated well with the occurrence of SMI using the balloon occlusion model and diabetic and non-diabetic patients were matched for important cofactors. There was a significant difference in the frequency of SMI between patients with and without diagnosis of diabetic neuropathy, and there was a significant difference in fasting blood glucose concentration between diabetic patients with and without SMI. This suggests that a poor blood sugar control leading to diabetic neuropathy is associated with the occurrence of SMI (this is in accordance with previous findings [14]).
Fig. 3. Kaplan–Meier curve for the combined endpoint of death or non-fatal myocardial infarction in diabetic patients only comparing patients with and without silent ischemia. There is no difference regarding the combined endpoint in diabetic patients with vs. patients without silent ischemia.
Letters to the Editor
Patients with SMI had significantly lower left ventricular ejection fraction compared to patients without SMI. This is in accordance with previous work of an association of Q-wave MI and SMI [13]. The prognostic impact of SMI regarding major cardiovascular events is controversial [5,10]. Our data did not show any differences regarding death or non-fatal MI in patients with SMI compared to patients without SMI (irrespective of diabetic status). The principal finding of this study is that there is no difference in the prevalence of SMI between diabetic and non-diabetic patients using the balloon occlusion model when important cofactors like coronary collateral flow, age and gender are considered. There seems to be a trend towards more SMI in diabetic patients with diabetic neuropathy and/or poor blood sugar control. Regardless of diabetic status, silent myocardial ischemia has no influence on the combined endpoint of mortality and/or non-fatal MI. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [15]. References [1] Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction. An update on the Framingham study. N Engl J Med 1984;311 (18):1144–7. [2] Cohn PF. Current concepts. The role of noninvasive cardiac testing after an uncomplicated myocardial infarction. N Engl J Med 1983;309(2):90–3. [3] Seiler C, Fleisch M, Garachemani A, Meier B. Coronary collateral quantitation in patients with coronary artery disease using intravascular flow velocity or pressure measurements. J Am Coll Cardiol 1998;32(5):1272–9.
321
[4] Weiner DA, Ryan TJ, Parsons L, et al. Significance of silent myocardial ischemia during exercise testing in patients with diabetes mellitus: a report from the Coronary Artery Surgery Study (CASS) Registry. Am J Cardiol 1991;68(8):729–34. [5] Biagini E, Schinkel AF, Bax JJ, et al. Long term outcome in patients with silent versus symptomatic ischaemia during dobutamine stress echocardiography. Heart 2005;91(6):737–42. [6] Vogel R, Zbinden R, Indermühle A, Windecker S, Meier B, Seiler C. Collateral-flow measurements in humans by myocardial contrast echocardiography: validation of coronary pressure-derived collateral-flow assessment. Eur Heart J 2006 Jan;27 (2):157–65. [7] Bradley RF, Partamian JO. Coronary heart disease in the diabetic patient. Med Clin North Am 1965;49:1093–104. [8] Nesto RW, Phillips RT, Kett KG, et al. Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: assessment by exercise thallium scintigraphy. Ann Intern Med 1988;108(2):170–5. [9] Chiariello M, Indolfi C, Cotecchia MR, Sifola C, Romano M, Condorelli M. Asymptomatic transient ST changes during ambulatory ECG monitoring in diabetic patients. Am Heart J 1985;110(3):529–34. [10] Weiner DA, Ryan TJ, Parsons L, et al. Significance of silent myocardial ischemia during exercise testing in patients with diabetes mellitus: a report from the Coronary Artery Surgery Study (CASS) Registry. Am J Cardiol 1991;68(8):729–34. [11] Chipkin SR, Frid D, Alpert JS, Baker SP, Dalen JE, Aronin N. Frequency of painless myocardial ischemia during exercise tolerance testing in patients with and without diabetes mellitus. Am J Cardiol 1987;59(1):61–5. [12] Smith JW, Buckels LJ, Carlson K, Marcus FI. Clinical characteristics and results of noninvasive tests in 60 diabetic patients after acute myocardial infarction. Am J Med 1983;75(2):217–24. [13] Titus BG, Sherman CT. Asymptomatic myocardial ischemia during percutaneous transluminal coronary angioplasty and importance of prior Q-wave infarction and diabetes mellitus. Am J Cardiol 1991;68(8):735–9. [14] Ambepityia G, Kopelman PG, Ingram D, Swash M, Mills PG, Timmis AD. Exertional myocardial ischemia in diabetes: a quantitative analysis of anginal perceptual threshold and the influence of autonomic function. J Am Coll Cardiol 1990;15 (1):72–7. [15] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.12.069
The rate-corrected QT interval calculated from 24-hour Holter recordings may serve as a significant arrhythmia risk stratifier in heart failure patients Petros Arsenos a,⁎, Konstantinos A. Gatzoulis a, Polychronis Dilaveris a, Theodoros Gialernios a, Skevos Sideris b, George Lazaros a, Stephanos Archontakis a, Dimitrios Tsiachris a, Efstathios Kartsagoulis c, Christodoulos Stefanadis a a b c
First Department of Cardiology, Medical School, National & Kapodistrian University of Athens, Greece Department of Cardiology, Hippokration Hospital, Athens, Greece Department of Cardiology, Thriasio General Hospital, Elefsina, Greece
a r t i c l e
i n f o
Article history: Received 17 November 2010 Accepted 21 December 2010 Available online 15 January 2011 Keywords: Holter QTc Heart failure CABG Repolarization prolongation Sudden cardiac death Risk stratification
⁎ Corresponding author. Chalkidos Athinon 12, Avlonas Attikis, 190 11, Greece. Tel./ fax: +30 2295042807. E-mail address: [email protected] (P. Arsenos).
To examine the ability of repolarization markers: QT, QTc, QTa/RR, QTe/RR to serve as predictors of life-threatening arrhythmias in heart failure (HF) patients [1], we screened non-invasively a cohort of 221 patients presenting with left ventricular ejection fraction (LVEF) <50%. All patients gave informed consent and the study was approved by our institution's Ethics Committee. All patients underwent 12 lead ECG, ECHO, Signal Averaged ECG (SAECG) and 24-h Holter (HM). Patients with nonsustained ventricular tachycardia (NSVT) were further risk stratified by EPS. The patients with clinical or inducible on EPS ventricular tachycardia and/or ventricular fibrillation (VT/VF) received an ICD. The study population was divided in the high risk group including 62 patients (20 with history of clinical VT/VF and 42 with inducible VT/VF on EPS) and in the low risk group including the rest 159 arrhythmia-free patients. Each participant underwent a 12lead ECG at 25 mm/s (MAC 5000, GE Marquette Medical, Milwaukee, USA). The following intervals were measured in lead II: RR , QRS, QT and QTc (correction with Bazett's formula: QTc = QT/√RR.) A SAECG (MAC 5000 GE Medical, Milwaukee, USA) was performed. The conventional as well the modified criteria [2] were applied for the
In conclusion, there is a high incidence of congestive heart failure mainly due to post rheumatic valvulopathies in young patients in our centre. A national program for fight against rheumatic fever and complications is of great urgency in our country. The compensation treatment of congestive heart failure is challenging in our milieu, characterized by poor compliance and financial limitation. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [5]. Special thanks to the Tertiairy Sisters of Saint Francis for their devotion in the management of the cardiac centre.
319
References [1] Mayosi BM. Contemporary trends in the epidemiology and management of cardiomyopathy and pericarditis in sub-Saharan Africa. Heart 2007;93:1176–83. [2] Bardgett HP, Dixon M, Beeching NJ. Increase in hospital mortality from noncommunicable disease and HIV-related conditions in Bulawayo, Zimbabwe, between 1992 and 2000. Trop Doct 2006;36:129–31. [3] Kingue S, Dzudie A, Menanga A, et al. A new look at adult chronic heart failure in Africa in the age of the Doppler echocardiography: experience of the medicine department at Yaounde General Hospital. Ann Cardiol Angeiol (Paris) 2005;54:276–83. [4] Ladipo GO. Congestive cardiac failure in elderly Nigerians: a prospective clinical study. Trop Geogr Med 1981;33:257–62. [5] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.12.067
Silent ischemia normalized for coronary collateral function in patients with and without diabetes mellitus Rainer Zbinden a, Ursula Wenger b, Pascal Meier b, Steffen Gloekler b, Stephan Windecker b, Bernhard Meier b, Christian Seiler b,⁎ a b
Triemlispital, CH-8000 Zurich, Switzerland University Hospital Bern, CH-3010 Bern, Switzerland
a r t i c l e
i n f o
Article history: Received 8 December 2010 Accepted 13 December 2010 Available online 6 January 2011 Keywords: Diabetes mellitus Silent ischemia Coronary collateral flow
Silent myocardial ischemia (SMI) is a term used to describe myocardial ischemia without chest pain, but in the presence of other evidence of ischemia [1]. After an MI, between 20 and 30% of patients present with SMI [2]. Seiler et al. [3] showed in a study using a 1-min coronary balloon occlusion that only 27% of patients with sufficient collateral flow (i.e. collateral relative to normal coronary flow, CFI≥ 0.25) had chest pain during vascular occlusion compared to 88% of the patients with insufficient collateral flow (collateral flow index, CFI, <0.25) irrespective of diabetic status. This indicates that coronary collateral flow is an important determinant of chest pain when using the vascular occlusion model. Regarding the prognostic impact of SMI, the data is controversial [4,5]. The purpose of the present study was to assess the prevalence and impact of SMI under specific consideration of coronary collateral function in patients with and without DM. Four-hundred and fifty two patients (354 (78%) men, mean age 64 +/− 9 years) referred for diagnostic coronary angiography were included in the study. One⁎ Corresponding author. University Hospital Bern, 3010 Bern, Switzerland. Tel.: +41 31 632 21 11. E-mail address: [email protected] (C. Seiler).
hundred and thirteen had DM type II and 339 patients served as the non-diabetic control group. Each diabetic patient was matched with 3 non-diabetic control patients for collateral flow index (CFI, see below), age and gender. All patients underwent left heart catheterization for diagnostic purposes. Either a 0.014 inch pressure-sensor tipped guidewire (n= 307), a Doppler guidewire (n = 75), or both (n = 70) were used during coronary balloon occlusion to assess the CFI. CFI (no units) is calculated as coronary occlusive pressure minus central venous pressure divided by aortic pressure minus central venous pressure when using the pressure wire or flow velocity during balloon occlusion divided by flow velocity during resting conditions using the Doppler guidewire. CFI correlates well with absolute collateral flow during balloon occlusion [6] During the 1-min coronary balloon occlusion patients were asked to report chest pain, and an intracoronary ECG was recorded. SMI was defined as significant ST-segment elevation in the intracoronary ECG (>0.1 mV) in the absence of chest pain. The diabetic and non-diabetic groups were matched for gender, age and CFI (Table 1). 359 patients had significant ST-segment changes in the i.c. ECG (78% diabetics vs. 80% non-diabetics; p = 0.64) during the 1-min coronary balloon occlusion. CFI was significantly higher in patients without i.c. ECG changes than in patients with i.c. ECG changes (0.33± 0.15 vs. 0.17 ± 0.08; p = <0.0001) (irrespective of diabetic status). 77 (17%) patients had silent ischemia (i.e. i.c. ECG changes without any symptoms): 22% diabetic vs. 15% non-diabetic patients (p= 0.10) (Fig. 1). Diabetic patients with a diagnosis of diabetic neuropathy were more likely to suffer from SMI (62% vs. 38%; p =0.05) as were diabetic patients with higher fasting blood glucose (10.0±3.6 vs. 8.5±3.0; p =0.03). There was a strong association between the patient's symptoms and the occurrence of silent ischemia during balloon occlusion. Only 58% of the patients with silent ischemia during balloon occlusion had typical anginal symptoms before admission compared to 88% of the patients with symptomatic ischemia (p<0.0001).
320
Letters to the Editor
Table 1 Patient characteristics.
Men Age (years) BMIa(kg/m2) Mean blood pressure (mm Hg) Heart rate (beats/min) Ejection fraction (%) History of previous MI† LVEDP‡ (mm Hg) Cardiovascular risk factors Hypertension Smoking Dyslipidemia Family history of CAD§ Antianginal medication Betablocker Nitrates Calcium antagonists Blood chemistry Total cholesterol (mmol/l) HDL cholesterol (mmol/l) LDL cholesterol (mmol/l) Triglycerides (mmol/l) Fasting glucose (mmol/l) HbA1c (%) Hemodynamic characteristics Ejection fraction (%) Target vessel (LADb/LCX††/RCA‡‡) Number of vessels diseased Percent diameter stenosis (%) Collateral flow index (no unit)
Diabetics (n = 113)
Non-diabetics (n = 339)
88 (78%) 64 ± 9 28.4 ± 3.6 94.4 ± 15.0 72 ± 12 63 ± 11 54 (48%) 12.8 ± 6.4
266 (78%) 64 ± 10 26.9 ± 4.0 94.1 ± 15.1 70 ± 12 65 ± 11 119 (35%) 12.3 ± 5.9
0.90 0.68 0.0004 0.88 0.14 0.16 0.007 0.47
85 26 93 33
189 101 251 133
0.0003 0.18 0.13 0.05
(75%) (23%) (82%) (29%)
(56%) (30%) (74%) (39%)
61 (54%) 43 (38%) 28 (25%)
209 (62%) 116 (34%) 59 (17%)
5.3 ± 1.1 1.2 ± 0.4 3.3 ± 1.2 2.2 ± 1.6 8.8 ± 3.2 7.2 ± 1.7 (n = 76)
5.4 ± 1.2 1.3 ± 0.3 3.3 ± 1.2 1.9 ± 1.7 6.0 ± 1.2 5.5 ± 0.6 (n = 49)
63 ± 11 41%/28%/31% 1.8 ± 0.8 72.5 ± 23.8 0.20 ± 0.12
65 ± 11 50%/26%/24% 1.6 ± 0.9 63.1 ± 32.2 0.20 ± 0.12
p value
0.15 0.46 0.09 0.29 0.0001 0.99 0.15 < 0.0001 < 0.0001
0.16 0.47 0.11 0.005 0.99
a
Body mass index, Myocardial infarction. Left ventricular enddiastolic pressure. § Coronary artery disease. b Left anterior descending coronary artery. †† Left circumflex coronary artery. ‡‡ Right coronary artery. † ‡
Follow-up was completed in 445 patients (98%). During a mean follow-up of 60 ± 34 months, there were 56 deaths in total (9 (11.7%) in the SMI group vs. 47 (12.5%) in the non-SMI group; p = 0.82). Non-
Fig. 1. 78% of diabetic and 80% of non-diabetic patients had ST-segment changes in the intracoronary (i.c.) ECG, indicating that 22% of the diabetic and 20% of the non-diabetic patients had enough collateral flow to avoid signs of ischemia during the 1-min balloon inflation (i.e. no ST segment changes in the i.c. ECG). 22% of diabetic and 15% of non-diabetic patients had silent ischemia during the 1-min balloon occlusion (i.e. ST-segment changes in the i.c. ECG but no chest pain).
Fig. 2. Kaplan–Meier curve for the combined endpoint of death or non-fatal myocardial infarction in all patients (diabetic and non-diabetic) comparing patients with and without silent ischemia. There is no difference regarding the combined endpoint in patients with vs. patients without silent ischemia.
fatal MI occurred in 4 patients ((5.2%) in the SMI group vs. 11 (2.9%) in the non-SMI group; p = 0.31). SMI had no influence on the occurrence of death/non-fatal MI neither in the whole group nor in the diabetic subgroup (Figs. 2 and 3). The only independent predictors of death/non-fatal MI in the multivariate analysis were calculated creatinine clearance (using the Cockroft formula) (HR 0.95–0.98; p < 0.0001) and left ventricular ejection fraction (HR 0.95–0.99; p = 0.003). First observations of a higher prevalence of SMI in diabetics date back to the early 1960s, when Bradley and Partaminan [7] found that 33 of 77 diabetic patients who died of acute myocardial infarction had evidence of at least one healed infarction that was not related to the patient's clinical history. A series of studies on SMI in diabetics followed [8–12], and showed controversial results mainly because of lack of control for important cofactors and different methods/ diagnostic tests to assess SMI. Very few studies have used the coronary balloon occlusion model during PCI to explore the phenomenon of SMI [13]. In our study, clinical symptoms correlated well with the occurrence of SMI using the balloon occlusion model and diabetic and non-diabetic patients were matched for important cofactors. There was a significant difference in the frequency of SMI between patients with and without diagnosis of diabetic neuropathy, and there was a significant difference in fasting blood glucose concentration between diabetic patients with and without SMI. This suggests that a poor blood sugar control leading to diabetic neuropathy is associated with the occurrence of SMI (this is in accordance with previous findings [14]).
Fig. 3. Kaplan–Meier curve for the combined endpoint of death or non-fatal myocardial infarction in diabetic patients only comparing patients with and without silent ischemia. There is no difference regarding the combined endpoint in diabetic patients with vs. patients without silent ischemia.
Letters to the Editor
Patients with SMI had significantly lower left ventricular ejection fraction compared to patients without SMI. This is in accordance with previous work of an association of Q-wave MI and SMI [13]. The prognostic impact of SMI regarding major cardiovascular events is controversial [5,10]. Our data did not show any differences regarding death or non-fatal MI in patients with SMI compared to patients without SMI (irrespective of diabetic status). The principal finding of this study is that there is no difference in the prevalence of SMI between diabetic and non-diabetic patients using the balloon occlusion model when important cofactors like coronary collateral flow, age and gender are considered. There seems to be a trend towards more SMI in diabetic patients with diabetic neuropathy and/or poor blood sugar control. Regardless of diabetic status, silent myocardial ischemia has no influence on the combined endpoint of mortality and/or non-fatal MI. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [15]. References [1] Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction. An update on the Framingham study. N Engl J Med 1984;311 (18):1144–7. [2] Cohn PF. Current concepts. The role of noninvasive cardiac testing after an uncomplicated myocardial infarction. N Engl J Med 1983;309(2):90–3. [3] Seiler C, Fleisch M, Garachemani A, Meier B. Coronary collateral quantitation in patients with coronary artery disease using intravascular flow velocity or pressure measurements. J Am Coll Cardiol 1998;32(5):1272–9.
321
[4] Weiner DA, Ryan TJ, Parsons L, et al. Significance of silent myocardial ischemia during exercise testing in patients with diabetes mellitus: a report from the Coronary Artery Surgery Study (CASS) Registry. Am J Cardiol 1991;68(8):729–34. [5] Biagini E, Schinkel AF, Bax JJ, et al. Long term outcome in patients with silent versus symptomatic ischaemia during dobutamine stress echocardiography. Heart 2005;91(6):737–42. [6] Vogel R, Zbinden R, Indermühle A, Windecker S, Meier B, Seiler C. Collateral-flow measurements in humans by myocardial contrast echocardiography: validation of coronary pressure-derived collateral-flow assessment. Eur Heart J 2006 Jan;27 (2):157–65. [7] Bradley RF, Partamian JO. Coronary heart disease in the diabetic patient. Med Clin North Am 1965;49:1093–104. [8] Nesto RW, Phillips RT, Kett KG, et al. Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: assessment by exercise thallium scintigraphy. Ann Intern Med 1988;108(2):170–5. [9] Chiariello M, Indolfi C, Cotecchia MR, Sifola C, Romano M, Condorelli M. Asymptomatic transient ST changes during ambulatory ECG monitoring in diabetic patients. Am Heart J 1985;110(3):529–34. [10] Weiner DA, Ryan TJ, Parsons L, et al. Significance of silent myocardial ischemia during exercise testing in patients with diabetes mellitus: a report from the Coronary Artery Surgery Study (CASS) Registry. Am J Cardiol 1991;68(8):729–34. [11] Chipkin SR, Frid D, Alpert JS, Baker SP, Dalen JE, Aronin N. Frequency of painless myocardial ischemia during exercise tolerance testing in patients with and without diabetes mellitus. Am J Cardiol 1987;59(1):61–5. [12] Smith JW, Buckels LJ, Carlson K, Marcus FI. Clinical characteristics and results of noninvasive tests in 60 diabetic patients after acute myocardial infarction. Am J Med 1983;75(2):217–24. [13] Titus BG, Sherman CT. Asymptomatic myocardial ischemia during percutaneous transluminal coronary angioplasty and importance of prior Q-wave infarction and diabetes mellitus. Am J Cardiol 1991;68(8):735–9. [14] Ambepityia G, Kopelman PG, Ingram D, Swash M, Mills PG, Timmis AD. Exertional myocardial ischemia in diabetes: a quantitative analysis of anginal perceptual threshold and the influence of autonomic function. J Am Coll Cardiol 1990;15 (1):72–7. [15] Shewan LG, Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
0167-5273/$ – see front matter © 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2010.12.069
The rate-corrected QT interval calculated from 24-hour Holter recordings may serve as a significant arrhythmia risk stratifier in heart failure patients Petros Arsenos a,⁎, Konstantinos A. Gatzoulis a, Polychronis Dilaveris a, Theodoros Gialernios a, Skevos Sideris b, George Lazaros a, Stephanos Archontakis a, Dimitrios Tsiachris a, Efstathios Kartsagoulis c, Christodoulos Stefanadis a a b c
First Department of Cardiology, Medical School, National & Kapodistrian University of Athens, Greece Department of Cardiology, Hippokration Hospital, Athens, Greece Department of Cardiology, Thriasio General Hospital, Elefsina, Greece
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Article history: Received 17 November 2010 Accepted 21 December 2010 Available online 15 January 2011 Keywords: Holter QTc Heart failure CABG Repolarization prolongation Sudden cardiac death Risk stratification
⁎ Corresponding author. Chalkidos Athinon 12, Avlonas Attikis, 190 11, Greece. Tel./ fax: +30 2295042807. E-mail address: [email protected] (P. Arsenos).
To examine the ability of repolarization markers: QT, QTc, QTa/RR, QTe/RR to serve as predictors of life-threatening arrhythmias in heart failure (HF) patients [1], we screened non-invasively a cohort of 221 patients presenting with left ventricular ejection fraction (LVEF) <50%. All patients gave informed consent and the study was approved by our institution's Ethics Committee. All patients underwent 12 lead ECG, ECHO, Signal Averaged ECG (SAECG) and 24-h Holter (HM). Patients with nonsustained ventricular tachycardia (NSVT) were further risk stratified by EPS. The patients with clinical or inducible on EPS ventricular tachycardia and/or ventricular fibrillation (VT/VF) received an ICD. The study population was divided in the high risk group including 62 patients (20 with history of clinical VT/VF and 42 with inducible VT/VF on EPS) and in the low risk group including the rest 159 arrhythmia-free patients. Each participant underwent a 12lead ECG at 25 mm/s (MAC 5000, GE Marquette Medical, Milwaukee, USA). The following intervals were measured in lead II: RR , QRS, QT and QTc (correction with Bazett's formula: QTc = QT/√RR.) A SAECG (MAC 5000 GE Medical, Milwaukee, USA) was performed. The conventional as well the modified criteria [2] were applied for the