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Prevalence and clinical features of atrial fibrillation in diabetic neuropathy: a cross-sectional, observational study/Diyabetik noropatide atriyal fibrilasyonun prevalansi ve klinik ozellikleri: kesitsel, gozlemsel bir calisma.

Abstract

Objective: This cross-sectional, observational study investigated prevalence and clinical features of atrial fibrillation (AF) in diabetic patient groups with or without autonomic neuropathy.

Methods: One hundred and fourteen consecutive patients with pharmacologically treated type-II diabetes mellitus were enrolled for this study in our institution between January 2010 and December 2010. All patients underwent 12-lead electrocardiography on the day of enrollment for AF detection. All diabetic patients underwent neurologic examination for the presence of diabetic autonomic neuropathy (DAN). Following clinical evaluation, sympathetic skin responses (SSR) and RR interval variability (RRIV) analysis were used for the detection of autonomic neurologic involvement. Patients were divided into two groups according to presence (Group 1) or absence (Group 2) of DAN. Patient groups with or without DAN were compared for AF occurrence. Continuous and categorical data were compared with independent samples t- test and Chi-square statistical tests respectively.

Results: Atrial fibrillation prevalence was 24% (n=29) in study population. Diabetic autonomic neuropathy was diagnosed in 47 (39%) patients. Basal characteristics of patients with or without DAN were comparable except glycosylated hemoglobin A ([HbA.sub.1c]) levels. [HbA.sub.1c] levels were found significantly higher in patients with DAN. Atrial fibrillation was diagnosed in 14 patients in Group 1 and in 15 patients in Group 2. Significantly increased AF prevalence (31.9% vs. 20.8%, p=0.014, in groups with and without DAN respectively) was observed in patient group with diabetic autonomic neuropathy.

Conclusion: The results of this study demonstrated an increased prevalence of AF in patients with diabetic autonomic neuropathy compared with non-neuropathic, diabetic patients. Further investigation of this relation with prospective studies is needed to demonstrate a causal relationship between diabetic autonomic neuropathy and AF.

Key words: Atrial fibrillation, diabetes mellitus, prevalence, autonomic neuropathy

OZET

Amac: Bu kesitsel ve gozlemsel calismada, tip-2 diyabetes mellituslu olgularda, diyabetik noropatisi olan ve olmayan hasta gruplarinda atriyal fibrilasyon (AF) prevalansi ve klinik ozellikler arastirilmistir.

Yontemler: Bu calismaya Ocak 2010 ile Aralik 2010 tarihleri arasinda kardiyoloji polikliniginde gorulen, farmakolojik tedavi altindaki tip-2 diyabetli 114 hasta alindi. Atriyal fibrilasyonun tespiti icin calismaya alinma gununde tum olgulara 12 derivasyonlu elektrokardiyografi cekildi. Diyabetik otonomik noropati varliginin tespiti icin olgular norolojik muayeneye alindi. Otonomik noropati tanisi icin klinik degerlendirmeyi takiben, gerekli olgularda elektromiyografik olarak sempatik deri yanitlari ve RR interval degiskenligi incelendi. Hastalar diyabetik otonomik noropatinin varligi (Grup 1) ve yokluguna (Grup 2) gore iki gruba ayrildi. Diyabetik noropatisi olan ve olmayan hasta gruplari karsilastirildi. Surekli ve kategorik verilerin karsilastirilmasi icin sirasi ile bagimsiz orneklem t- testi ve Ki-kare istatistiksel testleri kullanildi.

Bulgular: Calisma grubunda AF sikligi %24 (n:29) olarak tespit edildi. Diyabetik otonomik noropati 47 (%39) olguda saptandi. Diyabetik otonomik noropatisi olan ve olmayan hasta gruplarinin bazal ozellikleri [HbA.sub.1c] seviyeleri disinda benzerdi. [HbA.sub.1c] seviyeleri noropatisi olan grupta anlamli derecede yuksek bulundu. Atriyal fibrilasyon 1. Grupta 14 olguda ve 2. Grupta 15 olguda mevcuttu. Diyabetik otonomik noropatili hasta grubunda, noropatisi olmayan hasta grubu ile karsilastirildiginda anlamli derecede artmis AF prevalansi gozlendi (sirasi ile %31.9 ve %20.8, p=0.014).

Sonuc: Diyabetes mellitusu olan hastalarda, otonomik noropati ile artmis atriyal fibrilasyon prevalansi arasinda anlamli bir iliski vardir. Otonomik noropati ve AF arasinda nedensellik iliskisini gostermek iCin prospektif Calismalara da ihtiyaC vardir. (Anadolu Kardiyol Derg 2012; 12:646-51)

Anahtar kelimeler: Atriyal fibrilasyon, diyabetes mellitus, prevalans, otonomik noropati

Introduction

Atrial fibrillation (AF) is the most common, clinically significant cardiac arrhythmia. This arrhythmia affects 1-2% of the population, and this figure is likely to increase in the next 50 years (1, 2). AF is associated with increased rates of death, thromboembolic events, heart failure, and hospitalizations, decreased quality of life, reduced exercise capacity, and left ventricular (LV) dysfunction. It is a potent risk factor for ischemic stroke. AF confers a 5-fold risk of stroke, and 20% of all strokes are attributed to this arrhythmia (2,3).

Aging, valvular heart disease and left ventricular dysfunction have been shown to be important risk factors for the development of AF (3-5). However, atrial fibrillation is a multifactorial disease. It has been shown that, diabetes is also associated with increased risk of AF (6). The influence of autonomic neuropathy on the development of AF in patients with diabetes was not studied previously except the studies of Kanorski et al. (7) and Bissinger et al. (8). Autonomic nerve activity plays an important role in cardiac cellular electrophysiology and in the pathogenesis of AF (9). Kanorski et al. (7) compared patient groups of with and without diabetic autonomic neuropathy (DAN) and found augmentation of adrenergic influences on the heart and comparatively higher anti-recurrence efficacy of sotalol among patients with DAN. In the study of Bissinger et al. (8) recurrence of paroxysmal AF was higher in patient group with DAN compared to patient group without DAN. These studies evaluated only recurrence rates of paroxysmal AF and/or efficacy of beta-blocker treatment on these recurrence rates in patients with DAN. In contrast, our study did not try to find recurrence rate of AF or efficacy of anti-adrenergic treatment on these recurrence rates.

We investigated prevalence and clinical features of AF (mostly non-paroxysmal) in patients with diabetic neuropathy.

Methods

Study design

This study has a cross-sectional, observational design.

Study population

One hundred and fourteen consecutive patients with pharmacologically treated type II diabetes mellitus were enrolled for this cross-sectional study in our institution between January 2010-and December 2010. Eligible patients were between 18-80 years old. Current study excluded patients with known coronary and/or valvular heart disease. On the screening period, patients were evaluated with echocardiography and patients with systolic left ventricular dysfunction (ejection fraction <50%) and pulmonary hypertension were also excluded. Renal dysfunction, pulmonary disease, and thyroid dysfunction were other exclusion criteria. Patients with more than mild alcohol consumption were not included. Current study also excluded patients with infectious and active inflammatory diseases. Approval of local Ethics committee and patients' consent were obtained.

Study protocol

All patients underwent 12- lead electrocardiography (ECG) on the day of enrollment for the detection and documentation of presence of AF (paroxysmal, persistent or permanent). Standard 12-lead ECG was recorded at 25 mm/s (1 mV/cm calibration). In our study, AF was defined as replacement of sinus P waves by rapid oscillations or fibrillatory waves that varied in size, shape, and timing and were associated with an irregular ventricular response when atrioventricular conduction was intact. ECGs were read by a cardiologist blinded to the other study data. Patients were evaluated for the presence of DAN at neurology department after enrollment. Neurologist who performed the neurological evaluation was not blinded to the results of cardiological evaluation because of methodology of RR interval variability. Patients' data were reviewed and baseline demographic, clinical, echocardiographic, and laboratory data were obtained from patients' charts.

Neurologic evaluation

All diabetic patients underwent neurologic examination for the presence of DAN after enrollment. Following clinical evaluation, in patients with clinical signs and symptoms of autonomic neuropathy, sympathetic skin responses (SSR) and RR interval variability (RRIV) analysis were used for detection of diabetic autonomic involvement. Methodology of RRIV makes it inapplicable in patients with AF So that, in patients with AF only SSR was used for evaluation of DAN. Detailed descriptions of methodologies of SSR and RRIV analysis were given elsewhere (10). Briefly, SSR was performed in a dark room, while the patient was lying in the supine position. Surface electrodes were used for recording and stimulation. A single rectangular electrical stimulus of 0.1 ms duration and 300 mV intensity was delivered at irregular time intervals to opposite extremity. Four responses were recorded from right hand and foot. Absence of response is considered abnormal for SSR (11). Again, in a dark room, RRIV was measured while the patient was lying in the supine position. Surface recording electrodes were placed on the dorsum of each hand. Fifty traces were recorded at rest and twenty traces during forced deep breathing. When the percentage of RRIV was lower than 95% confidence limits of normal, RRIV was considered as abnormal (12). Patients were considered as having diabetic autonomic neuropathy in the presence of at least one abnormal electrophysiological test in addition to relevant clinical findings. These clinical findings were orthostatic hypotension, urinary symptoms such as urgency, incontinence, GI tract manifestations such as nausea, bloating, diarrhea or constipation, sweating abnormalities, and erectile dysfunction. Medelec Sapphire 4ME electromyography machine (Medelec Ltd, Surrey, United Kingdom) was used for the recording of SSR and RRIV.

Statistical analysis

Statistical analysis was performed with SPSS version 13.0 software (Chicago, IL, USA). Continuous data are expressed as mean [+ or -] standard deviation. Categorical data are expressed as number (percentage). Normally distributed continuous data were compared with independent samples t- test and categorical data were compared with Chi-square statistics.

Results

Baseline characteristics of patient population are presented in Table 1. Mean age of patients was 61.2 [+ or -] 8.7 years. Study population was mostly women, hypertensive, and overweight. AF prevalence was found as 24% (n=29) in this study cohort with type II diabetes mellitus.

Autonomic neuropathy was diagnosed in 47 (39%) patients. Clinical manifestations of DAN were as following: orthostatic hypotension in 8 (17%), urinary symptoms such as urgency, incontinence in 14 (29%), gastrointestinal tract manifestations such as nausea, bloating, diarrhea or constipation in 22 (46%), sweating abnormalities in 4 (8%), erectile dysfunction in 3 (6%) patients. Patients were divided into two groups according to presence (Group 1) or absence of (Group 2) DAN.

Comparison of patients in both groups did not reveal any significant difference in terms of clinical, biochemical and echocardiographic parameters except [HbA.sub.1c] levels (Table 2). [HbA.sub.1c] levels was found significantly higher in patients with DAN. Concomitant medications were also found comparable in both groups (Table 3).

Atrial fibrillation was diagnosed in 14 patients in Group 1 (31.9%) and in 15 patients in Group 2 (20.8%). There was a significant difference between groups for AF prevalence (Fig. 1, p=0.014).

We also compared patient groups with and without AF Left atrial diameter was found significantly larger in AF group. History of CVA was also prevalent in patient group with AF (Table 4). Concomitant treatment regimens in patient groups with and without AF were evaluated finally. Only antiplatelet and beta-blocker treatments were significantly higher in patient group with AF (Table 5).

Discussion

In a diabetic cohort, the results of this study demonstrated an increased prevalence of AF in patients with diabetic autonomic neuropathy compared with non-neuropathic patients.

Risk factors for AF development are increased age, hypertension, male gender, smoking, thyrotoxicosis, diabetes, obesity, stroke, left ventricular hypertrophy, left atrial enlargement, valvular disease, coronary heart disease, and congestive heart failure (13). Prior studies examining risk of AF in relation to diabetes or impaired glucose metabolism have yielded conflicting results. The role of diabetes as a risk factor for AF is shown firstly, in the Framingham Heart Study. Diabetes was the sole cardiovascular risk factor to be predictive of AF after controlling for age and other predisposing conditions in addition to hypertension in this study (13). In contrast, many studies did not observe an association between diabetes and AF (14-16). Only one study observed an association in women but not men [adjusted OR 1.26 (1.08 1.46) for women and 1.09 (0.96-1.24) for men], (17). However, primary focus of these studies was not diabetes-AF relationship and in most of these prior studies, results were not adjusted for known risk factors such as body mass index (BMI) or age. Contrarily, several prospective studies, reported ORs in the range of 1.4 to 1.6 for AF development in diabetic population (18-20). In a recent study, diabetes was associated with higher risk of developing AF, and risk was higher with longer duration of treated diabetes and worse glycemic control (21).

The discrepant findings of these studies may reflect methodological differences including sample size, leading to low power in some studies, as well as the definition and method of diagnosing diabetes and AF Another reason for conflicting results of prior studies might be presence of different subgroups in diabetic population with different AF prevalence. Only one study has examined the potential role of diabetes duration and or glycemic control on AF development (6). In this population-based case-control study people receiving pharmacologic treatment for diabetes had 40% higher risk of developing AF than people without diabetes. Results of this study also demonstrated that AF risk was higher with longer duration of treated diabetes, and there was a suggestion of higher risk with worse glycemic control. The risk of AF was increased 3% for each additional year they were treated for diabetes, a surrogate marker for diabetes duration, and was doubled among patients with [HbA.sub.1c] levels >9% compared with people without diabetes.

At present, not much is known about why people with diabetes are at an increased risk for AF Increased incidence of hypertension, coronary artery disease, diastolic dysfunction, and increased risk of sleep apnea are some of proposed mechanisms for this connection (21, 22). Lastly, elevated C-reactive protein (CRP) is known to be a marker of inflammation and increased CRP levels have been described in people with type 2 diabetes (23). Elevated plasma CRP is robustly associated with increased risk of AF (24). So that increased CRP levels may be responsible for diabetes-AF connection.

Autonomic nerve activity and autonomic balance play an important role in cardiac cellular electrophysiology and in the pathogenesis of AF (9). The pro-arrhythmic effect of autonomic imbalance has been shown in experimental models of AF It has been possible to observe that both sympathetic and vagal activations were capable of reducing atrial refractoriness and therefore to favor reentry. The effect on atrial refractoriness was noticed during either an increase of atrial cycle length secondary to vagal activation or during a shortening of atrial cycle length secondary to sympathetic activation (25). In the past, a few clinical studies were made in order to verify the existence of a link between AF episodes and autonomous nervous system (26, 27). The influence of autonomic neuropathy on the development of AF in patients with diabetes was not studied previously except the studies of Kanorski et al. (7) and Bissinger et al. (8). According to the results of study of Kanorski et al. (7) comparison of patient groups of with and without DAN revealed augmentation of adrenergic influences on the heart and comparatively higher anti-recurrence efficacy of sotalol among patients with diabetic autonomic neuropathy. In the study of Bissinger et al. (8) recurrence of paroxysmal AF was higher in patient group with DAN compared to patient group without DAN (p<0.01). The results also showed that the presence of diabetic autonomic neuropathy caused a significant increase in P-wave duration and dispersion, which might be responsible for the recurrence of AF (8). This study evaluated only recurrence rate of paroxysmal AF. So that we hypothesized that diabetic subgroups with or without DAN might have different AF prevalence. Unlike many prior studies, our primary focus was on the diabetic autonomic neuropathy-AF relationship, beyond the known other associations. To our knowledge, this study is the first to examine risk of AF in relation to diabetic autonomic neuropathy. AF prevalence was found as 24% (n: 29) in this study cohort with Type II diabetes mellitus. This prevalence figure is higher than previously reported AF prevalence rates in diabetic population (17). Almost all patients also had hypertension in this study. This additional comorbidity might have increased prevalence rates of AF We observed significantly increased prevalence of AF in diabetic autonomic neuropathy group compared to non-neuropathic patients with diabetes mellitus. These findings support a relation between DAN and AF. The result of this pilot study should be interpreted cautiously. Further investigation of this relation with prospective studies is needed to demonstrate a causal relationship between diabetic autonomic neuropathy and AF Ourfinding of higher [HbA.sub.1c] levels in patients with diabetic autonomic neuropathy is a well known association and has been reported previously (28).

Study limitations

Based on our study method, we might have detected more likely non-paroxysmal AF forms than paroxysmal AF in the study population. Current cross-sectional study mostly identified patients with permanent or persistent AF and detected nonparoxysmal AF prevalence figures in this cohort. Probably, most patients with paroxysmal AF (PAF) could not be included in AF group of the study. If diabetes conveys increased risk of PAF and these cases were classified as not having AF, real prevalence figures might be higher than our figures. Previous documentation of AF with 12-lead ECG, rhythm strip or ECG Holter recording may be used to identify paroxysmal forms of AF with a retrospective study design. Future studies with prospective design may also confirm incidence rates in addition to AF prevalence. Almost all patients in both groups were hypertensive in this study. As a result, findings of this study cannot be applied to diabetic patients without hypertension. Study population was chosen from outpatient cardiology clinic. So that AF prevalence rates might be affected by a selection bias. To reduce the effect of selection bias, we excluded patients with known cardiovascular diseases. Enrollment of diabetic patients out of cardiology department may result in lower AF prevalence rate. Smoking and presence of left ventricular hypertrophy may exert an arrhythmic effect. Absence of these data is another limitation. Lastly, sample size of current study is relatively small and further studies on larger cohort of patients are required.

Conclusion

We observed significantly increased prevalence of AF in diabetic autonomic neuropathy group compared with non-neuropathic patients with diabetes mellitus. These findings support a relation between diabetic autonomic neuropathy and AF This study is the first to show increased risk of AF in relation to autonomic neuropathy in patient population with treated diabetes mellitus. Further investigation of this relation with prospective studies is needed to demonstrate a causal relationship and independent contribution of diabetic autonomic neuropathy to increased prevalence of AF

Conflict of interest: None declared.

Authorship contributions. Concept--M.Y., S.B., I.G.K.Y.; Design M.Y., S.B., T.K.I.; Supervision--M.Y., S.B., T.K.I.; Resource--M.Y., T.K.I., N.R; Materials - I.G.K.Y., E.A., N.P; Data collection&/or Processing T.K.I., I.G.K.Y.; Analysis &/or interpretation--T.K.I., I.G.K.Y.; Literature search--I.G.K.Y., T.K.I., N.R; Writing--S.B., E.A., T.K.I.; Critical review --S.B., E.A., N.R, M.Y., T.K.I, I.G.K.Y.; Other-E.A, N.P

References

(1.) Stewart S, Hart CL, Hole DJ, McMurray JJ. Population prevalence, incidence and predictors of atrial fibrillation in the Renfrew/Paisley study. Heart 2001; 86: 516-21.

(2.) Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 2001; 285: 2370-5.

(3.) Kannel WB, Abbott RD, Savage DD, McNamara PM. Epidemiologic features of chronic atrial fibrillation: the Framingham study. N Engl J Med 1982; 306: 1018-22.

(4.) Onundarson PT, Thorgeirsson G, Jonmundsson E, Sigfusson N, Hardarson T. Chronic atrial fibrillation-epidemiologic features and 14 -year follow-up: a case control study. Eur Heart J 1987; 8: 521-7.

(5.) Alpert JS, Petersen P Godtfredsen J. Atrial fibrillation: natural history, complications and management. Annu Rev Med 1988; 39: 41-52.

(6.) Dublin S, Glazer NL, Smith NL, Psaty BM, Lumley T, Wiggins KL, et al. Diabetes mellitus, glycemic control, and risk of atrial fibrillation. J Gen Intern Med 2010; 25: 853-8.

(7.) Kanorski SG, Kanorskaia luS. Atrial fibrillation in patients with type 2 diabetes mellitus: specific features of development and antirecurrence therapy. Kardiologiia 2010; 50:31-7.

(8.) Bissinger A, Grycewicz T, Grabowicz W, Lubinski A. The effect of diabetic autonomic neuropathy on P-wave duration, dispersion and atrial fibrillation. Arch Med Sci 2011; 7: 806-12.

(9.) Chen PS, Tan AY. Autonomic nerve activity and atrial fibrillation. Heart Rhythm 2007; 4: 61-4.

(10.) Recommendations for the practice of clinical neurophysiology: guidelines of the International Federation of Clinical Neurophysiology. Electroencephalogr Clin Neurophysiol 1999; 52: 1-304.

(11.) Oh SJ. Clinical electromyography: nerve conduction studies. 3rd ed. Philadelphia: Lippincott Williams and Wilkins; 2003.

(12.) Shahani BT, Day TJ, Cros D, Khalil N, Kneebone CS. RR interval variation and sympathetic skin response in the assessment of autonomic function in the peripheral neuropathy. Arch Neurol 1990; 47: 659-64.

(13.) Kannel WB, Wolf PA, Benjamin EJ, Levy D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population based-estimates. Am J Cardiol 1998; 82: 2-9.

(14.) Zhou Z, Hu D. An epidemiological study on the prevalence of atrial fibrillation in the Chinese population of mainland China. J Epidemiol 2008; 18:109-16.

(15.) Smith JG, Platonov PG, Hedblad B, Engstrom G, Melander 0. Atrial fibrillation in the Malmo Diet and Cancer study: a study of occurrence, risk factors and diagnostic validity. Eur J Epidemiol 2010; 25: 95-102.

(16.) Ostgren CJ, Merlo J, Rastam L, Lindblad U. Atrial fibrillation and its association with type 2 diabetes and hypertension in Swedish community. Diabetes Obes Metabol 2004; 6: 367-74.

(17.) Nichols GA, Reinier K, Chugh SS. Independent contribution of diabetes to increased prevalence and incidence of atrial fibrillation. Diabetes Care 2009; 32:1851-6.

(18.) Aksnes TA, Schmieder RE, Kjeldsen SE, Ghani S, Hua TA, Julius S. Impact of new-onset diabetes mellitus on development of atrial fibrillation and heart failure in high risk hypertension (from the VALUE trial). Am J Cardiol 2008; 101: 634-8.

(19.) Benjamin EJ, Levy D, Vaziri SM, D'Agostino RB, Belanger AJ, Wolf PA. Independent risk factors in atrial fibrillation in a populationbased cohort. The Framingham Heart Study. JAMA 1994; 271: 840-4.

(20.) Watanabe H, Tanabe N, Watanabe T, Darbar D, Roden DM, Sasaki S, et al. Metabolic syndrome and risk of development of atrial fibrillation: the Niigata preventive medicine study. Circulation 2008; 117:1255-60.

(21.) Garni AS, Pressman G, Caples SM, Kanagala R, Gard JJ, Davison DE, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation 2004; 110: 364-7.

(22.) Healey JS, Connolly SJ. Atrial Fibrillation: hypertension as a causative agent, risk factor for complications, and potential therapeutic Target. Am J Cardiol 2003; 91: 9-14.

(23.) Pradhan A, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001; 286: 327-34.

(24.) Marott SC, Nordestgaard BG, Zacho J, Friberg J, Jensen GB, Tybjaerg-Hansen A, et al. Does elevated C-reactive protein increase atrial fibrillation risk? A Mendelian randomization of 47,000 individuals from the general population. J Am Coll Cardiol 2010; 56: 789-95.

(25.) Shimizu W, Tsuchioka Y, Karakawa S, Nagata K, Mukai J, Yamagata T et al. Differential effect of pharmacological autonomic blockade on some electrophysiological properties of the human ventricle and atrium. Br Heart J 1994; 71: 34-7.

(26.) Lok NS, Lau CR Abnormal vasovagal reaction, autonomic function and heart rate variability in patients with paroxysmal atrial fibrillation. Pacing Clin Electrophysiol 1998; 21: 386-95.

(27.) Lombardi F, Tarricone D, Tundo F, Colombo F, Belletti S, Fiorentini C. Autonomic nervous system and paroxysmal atrial fibrillation: a study based on the analysis of RR interval changes before, during and after paroxysmal atrial fibrillation. Eur Heart J 2004; 25:1242-8.

(28.) Chang CW, Chuang LM. Correlation of [HbA.sub.1c] concentration and single-fiber EMG findings in diabetic neuropathy. Electromyogr Clin Neurophysiol 1996; 36: 425-32.

Idil Gokcen Kocagra Yagiz, Serdar Bayata, Murat Yesil, Tulay Kurt incesu *, Erdinc Arikan, Nursen Postaci

Clinics of Cardiology and * Neurology, Ataturk Education and Research Hospital, Izmir-Turkey

Address for Correspondence/Yazisma Adresi: Dr. Serdar Bayata, Ataturk Egitim ve Arastirma Hastanesi, 1. Kardiyoloji Klinigi, izmir- Turkiye

Phone: +90 232 464 97 97 Fax: +90 232 244 91 15 E-mail: sbayata@hotmail.com

Accepted Date/Kabul Tarihi: 21.05.2012 Available Online Date/Cevrimici Yayin Tarihi: 11.09.2012

doi: 10.5152/akd.2012.216
Table 1. Baseline characteristics of patient population

Patients, n 114
Mean age, years 61.2 [+ or -] 8.7
Women, n (%) 70 (61)
Age of diabetes, year 9.1 [+ or -] 7.2
Hyperlipidemia, n (%) 83 (72)
Hypertension, n (%) 102 (89)
Hb[A.sub.1c], mg/dL 8.2 [+ or -] 1.9
Left atrium, mm 39.6 [+ or -] 5.8
LV ejection fraction, % 61.1 [+ or -] 5.1
BMI, kg/[m.sup.2] 27.5 [+ or -] 4.4
Previous CVA, n (%) 10 (8)

Continuous data are expressed as mean [+ or -] SD. Categorical data
are expressed as n (%) BMI--body mass index, CVA--cerebrovascular
accident, Hb[A.sub.lc]--glycosylated hemoglobin A, LV--left ventricule

Table 2. Clinical, biochemical, and echocardiographic characteristics
of patients with and without diabetic autonomic neuropathy

Variables Group 1 Group 2 * p
 (n = 47) (n = 67)
 Pts with DAN Pts w/o DAN

Mean age, years 62.1 [+ or -] 8.5 60.5 [+ or -] 8.8 NS
Women, n (%) 29 (59) 41 (61) NS
Diabetes age, year 9.3 [+ or -] 6.9 8.9 [+ or -] 7.3 NS
Hyperlipidemia, n (%) 34 (72) 49 (73) NS
Left atrium, mm 38.9 [+ or -] 5.5 40.0 [+ or -] 5.9 NS
Ejection fraction, % 60.8 [+ or -] 4.9 61.3 [+ or -] 5.2 NS
BMI, kg/[m.sup.2] 27.1 [+ or -] 4.2 27.7 [+ or -] 4.5 NS
HbAlc, mg/dL 8.8 [+ or -] 2.4 7.7+1.5 0.002
Hypertension, n (%) 41 (87) 61 (91) NS
Previous CVA, n (%) 4 (8) 6 (8) NS

Continuous data are expressed as mean [+ or -] SD. Categorical data
are expressed as n (%).

* Chi-square test and independent samples t-test

BMI--body mass index, CVA--cerebrovascular accident, DAN--diabetic
autonomic neuropathy, Hb[A.sub.1c]--glycosylated hemoglobin A,
NS--not significant, pts--patients, W/O--without

Table 3. Concomitant treatment regimens in patient groups

Medications Group 1 Group 2 * p
 (n = 47) (n = 67)
 Pts with DAN Pts w/o DAN

Antiplatelet 38 (80) 55 (82) NS
Statin 24 (51) 32 (47) NS
Insulin 5 (10) 7 (10) NS
ACEI/ARB 33 (70) 52 (77) NS
Betablocker 18 (38) 24 (35) NS
Metformin 29 (61) 43 (64) NS

Categorical data are expressed as n (%)

* Chi-square test

ACEI--angiotensin converting enzyme inhibitor, ARB--angiotensin
receptor blocker, DAN--diabetic autonomic neuropathy, NS--not
significant, pts--patients, W/O-without

Table 4. Clinical, biochemical, and echocardiographic characteristics
of patients with and without atrial fibrillation

Variables Pts with atrial Pts w/o atrial * p
 fibrillation fibrillation
 (n = 29) (n = 85)

Mean age, years 60.1 [+ or -] 7.8 61.5 [+ or -] 9.2 NS
Women, n (%) 18 (62) 52 (61) NS
Diabetes age, year 9.3 [+ or -] 6.9 9.0 [+ or -] 7.3 NS
Hyperlipidemia, n (%) 20 (68) 63 (74) NS
Left atrium, mm 42.4 [+ or -] 6.5 38.6 [+ or -] 5.3 0.01
Ejection fraction, % 60 5 [+ or -] 5.3 61.3 [+ or -] 5.0 NS
BMI, kg/[m.sup.2] 26.8 [+ or -] 4.5 27.7 [+ or -] 4.4 NS
Hb[A.sub.1c], mg/dL 7.7 [+ or -] 2.2 8.3 [+ or -] 1.8 NS
Hypertension, n (%) 24 (82) 78 (91) NS
Previous CVA, n (%) 6 (20) 4 (4) 0.02

Continuous data are expressed as meantSD. Categorical data are
expressed as n (%).

* Chi-square test and independent samples t-test

BMI--body mass index, CVA--cerebrovascular accident, Hb[A.sub.1c]--
glycosylated hemoglobin A, NS-not significant, pts--patients,
W/O--without

Table 5. Concomitant treatment regimens in patient groups
with or without atrial fibrillation

Medications Pts with AF Pts w/o AF * p
 (n = 29) (n = 85)

Antiplatelet 28 (96) 65 (76) 0.04
Statin 16 (55) 40 (47) NS
Insulin 3 (10) 9 (10) NS
ACEI/ARB 21 (72) 64 (75) NS
Beta-blocker 16 (55) 26 (30) 0.03
Metformin 17 (58) 55 (64) NS

Categorical data are expressed as n (%).

* Chi-square test

ACEI--angiotensin converting enzyme inhibitor, AF--atrial
fibrillation, ARB--angiotensin receptor blocker, NS--not significant,
pts--patients, W/0--without

Figure 1. Atrial fibrillation prevalence in patient groups
with or without diabetic autonomic neuropathy

 AF PREVALENCE

 P=0.014

PTS WITH NEUROPATHY 31
PTS W/O NEUROPATHY 20

AF--atrial fibriallation, pts--patients, w/o--without

Note: Table made from bar.
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Title Annotation:Original Investigation/Ozgun Arastirma
Author:Yagiz, Idil Gokcen Kocagra; Bayata, Serdar; Yesil, Murat; Incesu, Tulay Kurt; Arikan, Erdinc; Postac
Publication:The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)
Article Type:Clinical report
Date:Dec 1, 2012
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