Effect of previous statin use on the incidence of sustained ventricular tachycardia and ventricular fibrillation in patients presenting with acute coronary syndrome/Akut koroner sendromlu hastalarda onceden statin kullaniminin surekli ventrikuler tasikardi ve ventrikuler fibrilasyon gelisimi uzerine etkisi.
Objective: Recent studies suggest that statins have anti-arrhythmic effects. The aim of this study was to evaluate the effects of statins on sustained ventricular tachycardia or ventricular fibrillation (S-VT or VF) in patients presenting with acute coronary syndrome (ACS).
Methods: The population of this study consisted of consecutive patients admitted to coronary care unit. It was an observational case-controlled retrospective analysis performed on prospective cohort. From a total of 1000 patients presenting with ACS, 241 were on and 759 were not on statin. Patient demographics, clinical characteristics and previous medical treatment including statins were recorded. A S-VT or VF episode during hospitalization was accepted as endpoint. Multiple logistic regression model was performed which considered the occurrence of S-VT or VF as the response variable.
Results: Sustained VT or VF occurred in 3.3% of patients in statin group and in 9% of patients in non-statin group. Univariate positive predictors of S-VT or VF were ST elevation myocardial infarction as clinical presentation, smoking and thrombolysis; univariate negative predictors of S-VT or VF were ejection fraction, use of acetylsalicylic acid before hospitalization, use of statin before hospitalization, initiation of clopidogrel at the hospital and normal coronary arteries. In the multiple logistic regression analysis, the only independent predictor of S-VT or VF was ejection fraction (OR 0.96; 95% CI 0.93 to 0.99; p=0.005).
Conclusion: Our results indicate that, although the incidence of S-VT/VF was significantly lower in patients with ACS and previous statin use; statin use is not an independent predictor of the occurrence of S-VT or VF in patients presenting with ACS.
Key words: Statins, acute coronary syndrome, ventricular arrhythmia, logistic regression analysis
Amac: Statinlerin antiaritmik etkileri son yillardaki calismalarda gosterilmistir. Bu calismada, akut koroner sendromu (AKS) olan hastalarda onceden statin kullanimmm surekli ventrikuler tasikardi ve ventrikuler fibrilasyon (S-VT ve VF) olusmasi uzerine olan etkisi degerlendirildi.
Yontemler: Akut koroner sendrom (AKS) tamsi ile muracaat eden hastalar calismaya dahil edildi. Prospektif kohortta gozlemsel vaka kontrollu retrospektif analiz yapildi. Toplam 1000 hastanin arasinda 241 hasta statin kullanmakta iken, 759 hasta statin kullanmamaktaydi. Hastalarin demografik, klinik ozellikleri ve kullanmakta olduklari ilaclar (statin dahil) kaydedildi. Hastanede kalis suresince, surekli VT ve VF epizodu olusmasi sonlanim noktasi olarak kabul edildi. Coklu regresyon analizinde S-VT ve VF uzerine etkili faktorler degerlendirildi.
Bulgular: Statin kullanan hastalarin %3.3' unde statin kullanmayan hastalarin %9'unda S-VT ve VF epizodu saptandi. Klinik taninin ST elevasyonlu miyokart enfarktusu olmasi, sigara icimi, trombolitik tedavi yapilmis olmasi, S-VT ve VF olusmasi icin pozitif tek degiskenli gostergeleri olarak tespit edilirken, onceden asetil salisilik asit ve statin kullanimi, hastanede klopidogrel baslanmasi, ejeksiyon fraksiyonu ve normal koroner arterler surekli S-VT ve VF olusmasi icin negatif tek degiskenli gostergeleri olarak bulundu. Cok degiskenli lojistik regresyon analizinde surekli S-VT ve VF olusmasinda, ejeksiyon fraksiyonunun tek bagimsiz belirtec oldugu tespit edildi (OR 0.96; %95 guven araligi 0.93-0.99; p=0.005).
Sonuc: Akut koroner sendromlu hastalarda, statin alan hastalar S-VT/VF sikligi anlamli olarak daha dusuk olsa da; statin kullanimi S-VT ve VF olusumu icin bagimsiz bir belirtec degildir.
(Anadolu Kardiyol Derg 2017 1:22-8)
Anahtar kelimeler: Statinler, akut koroner sendrom, ventrikiiler aritmi, lojistik regresyon analizi
Sudden cardiac death is the most frequent cause of death in industrialized countries (1, 2). The most common cause of sudden cardiac death is coronary artery disease (CAD) and the most common arrhythmias causing sudden cardiac death are ventricular tachycardia (VT) and ventricular fibrillation (VF) (2). Previous trials have suggested that statins may decrease the incidence of sudden cardiac death in patients with CAD (3-5). This beneficial effect of statins could partly be explained with their antiarrhythmic properties (6, 7).
However, conflicting results have been obtained about the effects of statins on ventricular arrhythmias (3, 4, 6, 8-21).
The aim of the present study was to examine the effect of previous statin use on the occurrence of sustained VT (S-VT) or VF in patients presenting with acute coronary syndrome (ACS).
The population of this study consisted of 1000 consecutive patients admitted to Coronary Care Unit between January 2004 and July 2007. It was an observational case-controlled retrospective analysis performed on prospective cohort. Calculation of the number of patients needed was based on the assumption of 5% and 10% rate of S-VT or VF in statin and non-statin groups, respectively. With an alpha level of 0.05 anda power of 0.80 it was necessary to include 474 patients in each group (total 948 patients).
Exclusion criteria included hyperthyroidism, moderate to severe rheumatic valvular disease, sepsis, documented previous S-VT and/or VF, patients taking antiarrhythmic drugs for other arrhythmias such as atrial fibrillation, accelerated idioventricular rhythm and polymorphic VT. Among the screened 1020 patients, 20 were excluded due to hyperthyroidism (n=7), moderate to severe rheumatic valvular disease (n=4), accelerated idioventricular rhythm (n=8) or sepsis (n=1).
Among the statin users, 154 were on atorvastatin, 27 on fluvastatin, 10 on pravastatin, 9 on rosuvastatin and 41 on simvastatin. The mean time between initiation of statin and index ACS was 258 [+ or -] 256 days. All ACS patients (ST elevation or non-ST elevation myocardial infarction and unstable angina) were included.
Acute myocardial infarction was diagnosed based on the presence of chest pain and/or electrocardiographic changes suggestive of infarction or ischemia, associated with the increased level of cardiac enzymes to at least twice the upper limit of the normal value. Unstable angina was diagnosed based on the presence of ischemic symptoms that were new, accelerated or occurred at rest, and dynamic ST changes other than ST elevation, but without elevation of cardiac enzymes.
A transthoracic echocardiogram was recorded in each patient (22). Modified Simpson method was used for measuring ejection fraction (23). All the patients were treated according to the latest published guidelines and clinical practice. No primary percutaneous coronary intervention is performed in our centre. Therefore, thrombolytic treatment was used as reperfusion therapy.
Follow-up for ventricular tachycardia or ventricular fibrillation
Patients were followed prospectively with continuous electrocardiogram (ECG) monitoring during coronary care unit stay and with ECG taken twice daily in the wards for the occurrence of VF or monomorphic S-VT, which was defined as sustained ventricular tachycardia (the rate >120/min) lasting >30 seconds or requiring intervention. A S-VT or VF episode during hospitalization was accepted as endpoint. Multiple logistic regression model was performed which considered the occurrence of S-VT or VF as the response variable. The mean duration of the stay in the coronary care unit was 2 days and the mean duration of entire hospitalization was 5 days.
All the analyses were performed using SPSS 9.0 (SPSS Inc., Chicago, IL, USA). Continuous variables were expressed as mean [+ or -] SD and categorical variables were presented as percentages. Categorical variables were compared with Chi-square test. Continuous variables were compared with unpaired Student t-test.
Predictors of S-VT or VF were determined by multiple logistic regression analysis. Strength of association between variables and occurrence of S-VT or VF was represented by odds ratios (ORs) and their accompanying 95% confidence intervals (CIs). Demographic or clinical characteristics and procedural profile shown in Tables 1 and 2 were evaluated in a univariate analysis, and those with p<0.15 (gender, use of statin and use of acetyl salicylic acid before hospitalization, gender, ST-elevation myocardial infarction as clinical presentation, ejection fraction, smoking, diabetes mellitus, thrombolysis, initiation of clopidogrel in the hospital and normal coronary arteries) were then entered into a multiple logistic regression analysis. The identification of the predictors was based on a forward stepwise selection method. Normality of distribution was checked with Kolmogorov-Smirnov test and non-parametric test was required for the comparison of required energy for the convertion of VT into sinus rhythm. A p value of <0.05 (2-tailed) was considered significant.
From a total of 1000 patients, 241 were on and 759 were not on statin treatment. Male gender and thrombolytic treatment were more frequent in non-statin group compared with statin group (both p<0.05). Diabetes mellitus, hypertension, previous percutaneous coronary intervention (PCI), previous coronary bypass graft (CABG), beta-blocker, angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) and acetyl salicylic acid use before hospitalization and clopidogrel prescription at index hospitalization were more frequently encountered in statin group compared with non-statin group (all p<0.05). Ejection fraction was higher, total cholesterol and low-density lipoprotein cholesterol levels were lower in statin group compared with non-statin group (all p<0.05). Unstable angina/ non-ST elevation myocardial infarction was more frequent in statin group and ST-elevation myocardial infarction was more frequent in non-statin group (p<0.05 for both) compared with statin group. Other demographic or clinical variables were similar in the both groups (all p>0.05, Tables 1, 2).
Ventricular tachycardia or ventricular fibrillation
Sixty-eight patients in non-statin group (9%) and 8 patients in statin group (3.3%) had developed S-VT or VF (Table 3, p=0.003). All VF cases were successfully converted into sinus rhythm with defibrillation. The methods and required energy to convert VT into sinus rhythm, occurrence of S-VT or VF in different clinical presentations and their occurrence within or beyond 48 h of presentation were similar in the both groups (Table 3, both p>0.05).
Comparison of patients with and without S-VT or VF during hospitalization (Table 4)
Smoking, thrombolytic treatment and ST-elevation myocardial infarction were more frequent and ejection fraction was lower in patients with S-VT or VF compared to those without S-VT or VF (p<0.05 for all). Clopidogrel prescription at index hospitalization, unstable angina/non-ST elevation myocardial infarction and normal coronary arteries at angiography were more frequently encountered in patients without arrhythmia compared to those with S-VT or VF (p<0.05 for all). Other demographic or clinical variables were similar in the both groups (all p>0.05).
Predictors of ventricular tachycardia/ventricular fibrillation (Table 5)
Univariate positive predictors of S-VT or VF were ST elevation myocardial infarction as clinical presentation (OR 3.39; 95% CI 1.90 to 6.05; p<0.0001), smoking (OR 1.79; 95% CI 1.09 to 2.94; p=0.02) and thrombolysis (OR 1.89; 95% CI 1.41 to 2.52; p<0.001); univariate negative predictors of S-VT or VF were ejection fraction (OR 0.94; 95% CI 0.92 to 0.97; p<0.0001), use of acetylsalicylic acid before hospitalization (OR 0.61; 95% CI 0.38 to 0.99; p=0.046), use of statin before hospitalization (OR 0.34; 95% CI 0.17 to 0.74; p=0.006), initiation of clopidogrel at the hospital (OR 0.29; 95% CI 0.17 to 0.48; p<0.001) and normal coronary arteries (OR 0.25; 95% CI 0.08 to 0.80; p=0.02). In the stepwise logistics regression analysis, the only independent predictor of S-VT or VF was ejection fraction (OR 0.96; 95% CI 0.93 to 0.99; p=0.005).
Our results indicate that statin use is not an independent predictor of the occurrence of S-VT or VF in patients presenting with ACS.
Coronary artery disease and ventricular arrhythmias
Both chronic CAD and ACS may cause sudden cardiac death mostly due to ventricular arrhythmias (24-26). Most commonly chronic CAD causes reentrant arrhythmias and ACS causes non-reentrant arrhythmias (1, 2, 24-26).
Statins, coronary artery disease and ventricular arrhythmias
Statin use was associated with a reduced probability of ventricular arrhythmias in patients with CAD and implantable cardioverter defibrillator implants (6, 8, 12-15), in patients with non-ischemic cardiomyopathy (12), and in patients who underwent revascularization procedures (11). Their use has also been associated with lower rate of mortality (13, 16, 27, 28), which could partly be explained by reduced rate of ventricular arrhythmias. On the other hand, statins have been found to be ineffective in preventing ventricular arrhythmias in patients with highrisk hypertension (4), resuscitated cardiac arrest in diabetic patients (29), or in patients with chronic CAD (3, 18-20). With respect to ACS, there are four positive (9, 10, 17, 30) and one negative previous studies (21) evaluating the effects of statins on ventricular arrhythmias. Statin administration following an acute myocardial infarction was associated with low incidence of VT/VF (9,17) and late potentials (17) and withdrawal of statins after presentation of a non-ST-segment elevation myocardial infarction was associated with higher rates of ventricular arrhythmias (10). Lorenz et al. (30) have shown that under statin therapy, non-sustained VT occurring after acute ST-elevation myocardial infarction is not associated with an adverse longterm prognosis, however; in patients not on statin treatment, the occurrence of non-sustained VT is associated with marked increase in 1-year mortality. On the other hand, MIRACL study (21) indicated that atorvastatin did not decrease the incidence of resuscitated cardiac arrest in patients with unstable angina and non-Q wave myocardial infarction. Present study is in agreement with MIRACL study and indicates that previous statin use is not associated with the occurrence of VT/VF Endpoint was resuscitated cardiac arrest in MIRACL study; however, it was sustained VT or VF in our study.
Present study is different from those four positive studies with some respects: Kayikcioglu et al. (17) prospectively evaluated the effects of a specific statin at a specific dose. However, we evaluated different statins with different doses in an observational fashion. Although other three positive studies were observational (9,10, 30), they were very large and only patients with ST-elevation or non-ST elevation myocardial infarction were included. Patients with unstable angina were included only in our study. Not all the statins may show the same effects on ventricular arrhythmias and they may show different effects in patients with unstable angina and myocardial infarction with respect to ventricular arrhythmias. These differences and low incidence of ventricular arrhythmias (for example, incidence of ventricular arrhythmia was 3.3% vs 9% in statin and non-statin groups in the present study, however it was 26% vs 63% in the study of KayikciogTu et al., 17) may explain the negative result in the present study as opposed to previous studies (9,10, 17, 30). In theory, statins may be more effective in modulating scar related changes in chronic CAD and as in the present study, may be less effective in ACS where electrical instability is the principal mechanism (24-26). Cardioprotective agent use such as acetyl salicylic acid, beta-blockers, angiotensin converting enzyme inhibitors or angiotensin receptor blockers before hospitalization and clopidogrel use after hospitalization was lower in non-statin group, while thrombolytic use was lower and ejection fraction was higher in statin group. These medications and ejection fraction may change the probability of the occurrence of ventricular arrhythmias making it inconclusive for statin alone reducing the arrhythmias.
Potential mechanisms of action of statins on ventricular arrhythmias
Potential mechanisms of action of statins on ventricular arrhythmias include improvement of endothelial function, reduction of oxidative stress and modulation the autonomic nervous system and also their anti-ischemic, anti-inflammatory and direct anti-arrhythmic effects (2, 31).
There are major differences in the patient groups with and without statins such as diabetes mellitus, hypertension, clinical presentation, prior therapies and ejection fraction, which are the limitations inherent to an observational study. Since it was not a randomized, double-blind clinical trial, other unmeasured potential factors, which are predictors of ventricular arrhythmias might also be distributed unequally between two groups and might affect the results. Although sustained VT usually causes symptoms, some patients may have suffered asymptomatic episodes. Since the ECG recording on the wards was performed only twice a day, some cases may have been missed. We did not measure C- reactive protein, which is used as an indicator of the tissue inflammation. The indiscriminate inclusion of patients with a large spectrum of doses and molecules of statins is an important drawback. Many patients with ACS and ventricular arrhythmias die suddenly and do not reach the hospital. However, mortality data is lacking and the study group was selected among survived patients. One of the limitations of our study is that we calculated the sample size with the assumption of equal sized groups; however, it is appeared that percentage of patients with acute coronary syndrome with previous statin use comprised only about 25% of patents. Although, we were able to demonstrate the significant difference in the incidence of VT/VF between patients with and without statin therapy before admission, further studies on the predictive value of statin use on larger number of patients should be performed.
Our results indicate that, although the incidence of S-VT/VF was significantly lower in patients with ACS and previous statin use; statin use is not an independent predictor of the occurrence of S-VT or VF in patients presenting with ACS.
Conflict of interest: None declared.
Accepted Date/Kabul Tarihi: 14.05.2010 Available Online Date/Cevrimici Yayin Tarihi: 24.12.2010
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The study results were partly presented at the 4th Annual Congress on Update in Cardiology and Cardiovascular Surgery, 28 November-2 December, 2008, Antalya, Turkey
Mehmet Ozaydin, Yasin Turker , Dogan Erdogan, Mustafa Karabacak, Ercan Varol, Abdullah Dogan, Zehra Kucuktepe, Atilla Icli
Department of Cardiology, Faculty of Medicine, Suleyman Demirel University, Isparta  Gulkent State Hospital, Isparta, Turkey
Address for Correspondence/Yazisma Adresi: Dr. Mehmet Ozaydin, Department of Cardiology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey Phone: +90 246 232 45 10 E-mail: firstname.lastname@example.org
Table 1. Comparison of heart rate turbulence parameters between patient and control groups Non-statin Statin Variables (n=759) (n=241) Age, years 62 [+ or -] 12 61 [+ or -] 11 Male gender, n(%) 597 (78.7) 158 (65.6) Smoking, n(%) 423 (55.7) 120 (49.8) Diabetes mellitus, n(%) 159 (20.9) 77 (32) Hypertension, n(%) 377 (49.7) 173 (71.8) Ejection fraction, % 41 [+ or -] 11 46 [+ or -] 13 (20-70) (20-75) Clinical presentation, n(%) Unstable AP/Non ST-elevation MI 369 (48.6) 180 (74.7) ST-elevation MI 390(51.4) 61 (25.3) Paroxysmal atrial 49 (6.5) 20 (8.3) fibrillation, n(%) Previous PCI, n(%) 12 (1.6) 16 (6.6) Previous CABG, n(%) 21 (2.8) 18 (7.5) Previous MI, n(%) 5 (0.7) 1 (0.4) PAD, n(%) 8 (1.1) 6 (2.5) Chronic renal failure, n(%) 4 (0.5) 1 (1.7) Cerebrovascular accident, n(%) 11 (1.4) -- NYHA class II heart failure, n(%) 45 (5.9) 14 (5.8) Prior therapies at index hospitalization, n(%) B-blocker 137 (18.1) 127 (52.7) ACEI or ARB 170 (22.4) 121 (50.2) Acetyl salicylic acid 281 (37) 198 (82.2) Clopidogrel 28 (3.6) 23 (9.5) Spironolactone 28 (3.6) 14 (5.8) Prescribed therapies after index event, n(%) B-blocker 740 (97.5) 236 (97.9) ACEI or ARB 603 (79.4) 203 (84.2) Acetyl salicylic acid 750 (98.8) 237 (98.3) Heparin 759 (100) 241 (100) Clopidogrel 379 (49.9) 183 (75.9) Thrombolysis 295 (38.8) 48 (19.9) Streptokinase 190 33 T-pa 105 15 Total cholesterol, mg/dl 186 [+ or -] 41 172 [+ or -] 46 LDL cholesterol, mg/dl 111 [+ or -] 49 94 [+ or -] 41 HDL cholesterol, mg/dl 39 [+ or -] 10 40 [+ or -] 9 Triglyceride, mg/dl 147 [+ or -] 68 147 [+ or -] 65 Variables p * Age, years 0.89 Male gender, n(%) <0.0001 Smoking, n(%) 0.11 Diabetes mellitus, n(%) 0.001 Hypertension, n(%) <0.0001 Ejection fraction, % <0.0001 Clinical presentation, n(%) Unstable AP/Non ST-elevation MI <0.0001 ST-elevation MI Paroxysmal atrial 0.31 fibrillation, n(%) Previous PCI, n(%) <0.0001 Previous CABG, n(%) 0.002 Previous MI, n(%) 1 PAD, n(%) 0.11 Chronic renal failure, n(%) 0.1 Cerebrovascular accident, n(%) 0.07 NYHA class II heart failure, n(%) 1 Prior therapies at index hospitalization, n(%) B-blocker <0.0001 ACEI or ARB <0.0001 Acetyl salicylic acid <0.0001 Clopidogrel 0.53 Spironolactone 0.19 Prescribed therapies after index event, n(%) B-blocker 0.81 ACEI or ARB 0.11 Acetyl salicylic acid 0.52 Heparin 1 Clopidogrel <0.0001 Thrombolysis <0.0001 Streptokinase T-pa Total cholesterol, mg/dl 0.03 LDL cholesterol, mg/dl 0.005 HDL cholesterol, mg/dl 0.6 Triglyceride, mg/dl 0.9 Data are presented as mean [+ or -] SD (range) or numbers (percentages) * Chi-square and unpaired Student's t test ACEI--angiotensin-converting enzyme inhibitor, AP--angina pectoris, ARB--angiotensin receptor blocker, CABG--coronary artery bypass surgery, HDL--high-density lipoprotein, LDL--low-density lipoprotein, MI--myocardial infarction, PAD--peripheral artery disease, PCI--percutaneous coronary intervention, T-pa--tissue plasminogen activator Table 2. Coronary angiography profile Non-statin Statin Variables (n=759) (n=241) p * Coronary angiography, n 673 224 -- Normal coronary arteries, n(%) 126 (18.7) 32 (14.3) 0.15 Diseased vessel, n(%) Single-vessel 175 (32) 72 (37.5) Multi-vessel 372 (68) 120 (62.5) 0.18 Data are presented as numbers (percentages) * Chi-square test Table 3. Follow-up findings Variables Non-statin Statin (n=759) (n=241) S-VT or VF yes, n (%) 68 8.00 Methods used to convert VT intosinus, n (%) Spontaneous 14(1.8) 1(0.4) Pharmacological 5(0.7) 3(1.2) Lidocaine 3(0.4 1(0.4) Amiodarone 2(0.3) 2(0.8) Electrical cardioversion 34(4.5) 4(1.7) Required energy, J 249 [+ or -] 98 192 [+ or -] 106 Occurrence of S-VT or VF, n (%) In patients with USAP 13(4.3) 2(1.4) In patients with NSTEMI 3(4.1) 2(4.7) In patients with STEMI 52(13.3) 4(6.5) Within 48 h of presentation 59(7.8) 7(2.9) After 48 h of presentation 8(1.1) 1(0.4) Variables p * S-VT or VF yes, n (%) 0.003 Methods used to convert VT intosinus, n (%) Spontaneous Pharmacological Lidocaine 0.08 Amiodarone Electrical cardioversion Required energy, J 0.42 Occurrence of S-VT or VF, n (%) In patients with USAP 0.16 In patients with NSTEMI 1 In patients with STEMI 0.2 Within 48 h of presentation 1 After 48 h of presentation 1 Data are presented as mean [+ or -] SD or numbers (percentages) * Chi-square and Mann-Whitney U test NSTEMI--non-ST-elevation myocardial infarction, STEMI--ST-elevation myocardial infarction, USAP--unstable angina pectoris, VF--ventricular fibrillation, VT--ventricular tachycardia Table 4. Comparison of patients with and without VT/VF during hospitalization Variables Without VT/VF (n=924) Age, years 61 [+ or -] 11 Male gender, n (%) 691 (74.8) Smoking, n (%) 492 (53.2) Diabetes mellitus, n (%) 224 (24.2) Hypertension, n (%) 502 (54.3) Ejection fraction, % 43 [+ or -] 12(20-75) Clinical presentation, n (%) Unstable AP/Non 529 (57.3) ST-elevation Ml ST-elevation Ml 395 (42.7) NYHA Class II Heart 51 (5.5) failure, n (%) Previous PCI, n (%) 24 (2.6) Previous CABG, n (%) 37 (4) Previous Ml, n (%) 6 (0.6) Peripheral artery 12 (1.3) disease, n (%) Chronic renal failure, n (%) 8 (0.9) Cerebrovascular accident, n (%) 8 (0.9) Prior therapies at index hospitalization, n (%) B-blocker 244 (26.4) ACEI or ARB 272 (29.4) Acetyl salicylic acid 451 (48.8) Clopidogrel 48 (5.2) Spironolactone 37 (4) Prescribed therapies after index event, n (%) B-blocker 901 (97.5) ACEI or ARB 737 (79.8) Acetyl salicylic acid 913 (98.8) Heparin 924 (100) Clopidogrel 540 (58.4) Thrombolysis 299 (32.4) Total cholesterol 184 [+ or -] 42 LDL cholesterol 109 [+ or -] 50 HDL cholesterol 40 [+ or -] 10 Triglyceride 145 [+ or -] 65 Coronary angiography, n (%) 840 (90.9) Normal coronary arteries, n (%) 155 (16.8) Diseased vessel, n (%) Single-vessel 231 (25) Multi-vessel 454 (49.1) Variables With VT/VF P * (n=76) Age, years 62 [+ or -] 12 0.42 Male gender, n (%) 64 (84.2) 0.07 Smoking, n (%) 51 (67.1) 0.02 Diabetes mellitus, n (%) 12 (15.8) 0.12 Hypertension, n (%) 46 (60.5) 0.3 Ejection fraction, % 36 [+ or -] 10 (20-60) <0.0001 Clinical presentation, n (%) Unstable AP/Non 20 (26.3) <0.0001 ST-elevation Ml ST-elevation Ml 56 (73.7) NYHA Class II Heart 8 (10.5) 0.8 failure, n (%) Previous PCI, n (%) 4 (5.3) 0.15 Previous CABG, n (%) 2 (2.6) 0.76 Previous Ml, n (%) 0 1 Peripheral artery 2 (2.6) 0.28 disease, n (%) Chronic renal failure, n (%) 0 1 Cerebrovascular accident, n (%) 3 (3.9) 0.45 Prior therapies at index hospitalization, n (%) B-blocker 20 (26.3) 1 ACEI or ARB 19 (25) 0.51 Acetyl salicylic acid 28 (36.8) 0.055 Clopidogrel 3 (3.9) 1 Spironolactone 5 (6.5) 0.24 Prescribed therapies after index event, n (%) B-blocker 75 (98.7) 1 ACEI or ARB 69 (90.8) 0.22 Acetyl salicylic acid 74 (97.4) 0.25 Heparin 76 (100) 1 Clopidogrel 22 (28.9) <0.0001 Thrombolysis 43 (56.6) <0.0001 Total cholesterol 183 [+ or -] 46 0.83 LDL cholesterol 106 [+ or -] 40 0.52 HDL cholesterol 38 [+ or -] 10 0.27 Triglyceride 158 [+ or -] 83 0.28 Coronary angiography, n (%) 57 (75) Normal coronary arteries, n (%) 3 (3.9) 0.01 Diseased vessel, n (%) Single-vessel 16 (21.1) 0.65 Multi-vessel 38 (50) Data are presented as mean [+ or -] SD (range) or numbers (percentages) * Chi-square test and unpaired Studentt-test ACEI--angiotensin-converting enzyme inhibitor, AP--angina pectoris, ARB--angiotensin receptor blocker, CABG--coronary artery bypass surgery, HDL--high-density lipoprotein, LDL--low-density lipoprotein, Ml--myocardial infarction, PAD--peripheral artery disease, PCI--percutaneous coronary intervention, VF--ventricular fibrillation, VT--ventricular tachycardia Table 5. Predictors of S-VT or VF Variables P OR 95% CI Positive univariate predictors Smoking 0.02 1.79 1.09 to 2.94 ST-elevation MI <0.0001 3.39 1.90 to 6.05 Thrombolysis <0.0001 1.89 1.41 to 2.52 Negative univariate predictors Ejection fraction <0.0001 0.94 0.92 to 0.97 Previous acetyl salicylic acid use 0.046 0.61 0.38 to 0.99 Previous statin use 0.006 0.35 0.17 to 0.74 Normal coronary arteries 0.02 0.25 0.08 to 0.80 Prescription of clopidogrel <0.0001 0.29 0.17 to 0.48 at the hospital Multivariate predictors Ejection fraction 0.005 0.96 0.93 to 0.99 Logistic regression analysis MI--myocardial infarction, S-VT--sustained ventricular tachycardia, VF--ventricular fibrillation
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|Title Annotation:||Original Investigation/Ozgun Arastirma|
|Author:||Ozaydin, Mehmet; Turker, Yasin; Erdogan, Dogan; Karabacak, Mustafa; Varol, Ercan; Dogan, Abdullah; K|
|Publication:||The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)|
|Date:||Feb 1, 2011|
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