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OBJECTIVE: Heart rate turbulence (HRT) indicates the impairment of cardiac autonomic function. With the literature containing insufficient information on HRT in stable coronary artery disease (CAD), this study aimed to investigate the role of HRT in patients with stable CAD. METHODS: The study included 58 patients (mean age: 58.9 ± 10.0 years; 25 male) with documented CAD and demonstrating ventricular premature complexes on Holter monitoring, and a control group of 52 patients (mean age: 55.9 ± 9.3 years; 36 male) with no history of CAD and demonstrating ventricular premature complexes. HRT parameters such as turbulence onset (TO) and slope (TS) were analyzed. Angiographic Gensini score were used to evaluate CAD severity. RESULTS: There was a significant difference in HRT parameters between the 2 groups. TO: 0.47 ± 1.52% vs. -1.61 ± 2.0% (p=0.001) and TS: 4.7 ± 3.0 vs. 6.4 ± 3.7 ms/RR (p=0.009) in patients with CAD and control group respectively. Given also that TO ≥ 0% and TS ≤ 2.5 ms/ RR values are considered abnormal, there was significant difference between the two groups; TO abnormal: 27 patients (46.6%) vs. 7 patients (13.5%), p=0.001, and TS abnormal: 15 patients (25.9%) vs. 4 patients (7.7%), (p=0.004) in CAD patients and control group respectively. A positive correlation was detected between TO and Gensini score (r=0.282, p=0.001) and a negative correlation detected between TS and Gensini score (r=-0.287, p=0.001). CONCLUSION: The study demonstrated that HRT variables are impaired in patients with stable CAD when compared to those in the control group, and that these variables also correlate with severity of CAD.

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OBJECTIVE: P- wave dispersion (PD) is an indicator of inhomogeneous and discontinuous propagation of sinus impulses. In the present study we aimed to investigate the PD and its association with the severity of the disease. in patients with stable coronary artery disease. METHODS: We prospectively analyzed 60 subjects with coronary artery disease (CAD) and 25 subjects with nor-mal coronary angiograms (control group). The maximum and minimum P-wave duration and PD were measured from the 12-lead surface electrocardiograms. The CAD severity was assessed by the severity score (Gensini score) and the number of vessels involved (vessel score). RESULTS: P max was longer in CAD group compared with the control group (p<0.001). PD was greater in the CAD group, compared with the control group (p<0.001). However, P min did not differ between the two groups. In bi-variate correlation, increased PD was correlated with presence of diabetes mellitus (r=0.316, p=0.014), smoking (r=0.348, p=0.006), left ventricular ejection fraction (r=-0.372, p=0.003), vessel score (r=0.848, p=0.001), and Gensini score (r=0.825, p=0.001). Multiple linear regression analysis showed that PD was independently associ¬ated with vessel score ((3=0.139, p=0.002) and Gensini score ((3=0.132, p=0.007). CONCLUSION: PD was greater in patients with CAD than in controls and it was associated with CAD severity.

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Left ventricular outflow tract pseudoaneurysm is a rare but a potentially lethal complication, mainly after aortic root endocarditis or surgery. Usually, it originates from a dehiscence in the mitral-aortic intervalvular fibrosa and arises posteriorly to the aortic root. We report a rare case of a patient with cardiac tamponade due to left ventricular pseudoaneurysm after aortic valve replacement. The subsequent surgical resection was performed successfully.

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We present an interesting case of 'pseudo' atrial fibrillation which was further diagnosed as atrial standstill with irregular junctional ectopic rhythm during electrophysiologic study. A 56-year-old woman presented to a health facility with symptoms of palpitation, lightheadedness, and shortness of breath. Upon detection of irregular rhythm with narrow QRS complexes and no visible P waves on the electrocardiogram, newly developed atrial fibrillation was considered and a direct current cardioversion was performed, during which cardiac asystole developed necessitating cardiopulmonary resuscitation. The patient was then transferred to our institution. Echocardiographic examination showed biatrial dilatation, normal left ventricular systolic function, marked left ventricular hypertrophy, severe aortic stenosis, moderate mitral regurgitation, and severe tricuspid regurgitation. The electrocardiogram showed an irregular rhythm with narrow QRS complexes without any fibrillatory f waves and 24-hour Holter monitoring revealed three episodes of ventricular asystole lasting for more than 3.5 seconds. During the electrophysiologic study, no electrical activity was observed at the high and low levels of the right atrial lateral free wall and septal wall. The final diagnosis was established as atrial standstill and irregular junctional ectopic rhythm. The patient refused aortic valve replacement and died due to progression of the underlying disease one year following permanent pacemaker implantation..

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BACKGROUND: Evaluation of repolarization during sequentional biventricular pacing. METHODS: Patients with biventricular devices, and left ventricular leads placed to the basal part of lateral left ventricular wall were enrolled. QRS, QTc, JTc, and corrected Tpeak-Tend intervals were compared during sequentional biventricular, left ventricular, and right ventricular pacing. RESULTS: Five patients with nonischemic and five with ischemic cardiomyopathy due to anterior myocardial infarction were enrolled. No correlation was observed between values of repolarization among patients. The optimal values of repolarization were significantly different from values of echocardiographically guided hemodynamic optimization. Two patients with biventricular pacing-induced ventricular fibrillation were successfully treated by reprogramming of V-V delay according to interventricular delay resulting in shorter Tpeak-Tend interval, although delayed effect of amiodarone in one of these patients cannot be ruled out. CONCLUSIONS: Patients with biventricular devices may be prone to development of ventricular arrhythmias depending on programmed V-V interval. We suggest that optimization of repolarization may be performed in patients with biventricular pacemakers in the absence of backup ICD and those with frequent episodes of ventricular tachyarrhythmias, although this finding deserves further study.

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BACKGROUND: In this study we evaluate wide QRS complexes observed during pharmacologic termination of supraventricular tachycardias. METHODS: Patients with supraventricular tachycardia, undergoing electrophysiologic study were enrolled. 12 mg of adenosine or 10 mg of verapamil were administered during tachycardia, under continuous monitoring of intaracardiac and surface electrocardiograms. Electrocardiographic features of ventricular ectopy were noted. RESULTS: Seventy-four patients were enrolled. 48 patients were randomized to adenosine and 26 to verapamil. Five different appearance patterns of ventricular ectopy were observed during termination of tachycardias. All wide QRS complexes were of ventricular origin and all of them were observed during the termination of tachycardia. Adenosine more frequently resulted in appearance of ventricular beats (15.4% vs 41.7%, P = 0.003), and this was more frequently observed in patients with atrioventricular nodal reentrant tachycardia. Patients with ventricular beats were younger than those without, in both, verapamil (47.5 +/- 15.6 vs 65.0 +/- 8.8 years, P = 0.04) and adenosine (40.9 +/- 13.8 vs 49.7 +/- 16.8, P = 0.03) groups. Left bundle branch block (LBBB)/superior axis morphology was most frequent morphology in adenosine group (55%). Two of 4 patients in verapamil group displayed LBBB/inferior axis QRS morphology and another 2 patients displayed LBBB/superior axis morphology. CONCLUSIONS: Noncatheter induced, five different appearance patterns and four distinct morphologies of ventricular origin were observed. Most of them do not directly terminate tachycardia, but are associated with its termination and are not observed in ongoing tachycardia.

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AIMS: Although cases of acute mad honey intoxication have been reported earlier, chronic mad honey intoxication (CMHI) syndrome has not been described and we address this issue only in this study. METHODS AND RESULTS: We prospectively evaluated the history of non-commercial honey intake in all patients referred to our institution for investigation of slow heart rate or atrioventricular (AV) conduction abnormalities. Between April 2008 and December 2008, 173 patients were referred to our institution for assessment of sinus bradycardia and various degrees of AV block and/or permanent pacemaker implantation. All patients were questioned about history of honey intake. Detailed evaluation revealed a history of daily honey intake for a long period of time in five of the patients (2.8%). This non-commercial honey was made by different amateur beekeepers in eastern Back Sea region of Turkey. Discontinuation of honey intake resulted in prompt normalization of conduction and significant symptomatic improvement. None of the patients were admitted to hospital and all were asymptomatic during 3 months follow-up. Holter monitoring for 24-h revealed no abnormality at first and third month. CONCLUSIONS: This is the first report of CMHI. This issue should be suggested during assessment of patients with unexpected conduction abnormalities, because abandonment of honey intake results in prompt symptomatic and electrocardiographic improvement.

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