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Biomedical subjects

M Bilge

Publications and source records attributed to M Bilge.

30 records · Page 2Linked to original sources
PubMed2000

Right atrial appendage function in patients with chronic nonvalvular atrial fibrillation.

To assess right atrial appendage (RAA) flow and its possible relationship to left atrial appendage (LAA) flow in chronic nonvalvular atrial fibrillation (AF), transesophageal echocardiography (TEE) was performed in 26 patients with chronic nonvalvular AF (group I). For the purpose of comparison, an additional group of 27 patients with chronic valvular AF due to mitral stenosis (group II) was analyzed. The clinically estimated duration of AF in group I was significantly longer than that of group II (8.7+/-3.4 versus 2.7+/-1.1 years). Although right atrial size and RAA maximal area were larger in group I than those in group II, left atrial size was larger in group II than that in group I. Group II had larger LAA maximal areas than group I, but this difference did not reach statistical significance. The two groups were not different with respect to the RAA or LAA emptying velocities. Significant correlations were observed between echocardiographic parameters of the two atria in patients with nonvalvular AF (r range, 0.4 to 0.7). In contrast, in patients with valvular AF, no correlation was observed between the echocardiographic parameters of the two atria (appendage emptying velocity, r = 0.38, p = 0.051; atrial size, r = -0.03, p = 0.89; maximal appendage area, r = 0.07, p = 0.75, respectively). There were no significant differences in the presence of right and left atrial spontaneous echo contrast and thrombus between the groups. All of the right and left atrial thrombi were confined to their respective appendages and were found in the atria with spontaneous echo contrast. Both RAA and LAA thrombi were present in one patient. In conclusion, our findings suggest that AF could affect both atria equally in nonvalvular AF, in contrast to valvular AF. Therefore, the assessment of RAA function as well as LAA may be important in patients with chronic nonvalvular AF.

Aged↗
PubMed2000

The effect of autonomic nervous system activity on exaggerated blood pressure response to exercise: evaluation by heart rate variability.

OBJECTIVE: We investigated the effect of autonomic nervous system activity on exaggerated systolic blood pressure (SBP) response to exercise in healthy subjects using heart rate variability (HRV) analysis. METHOD AND RESULTS: We studied 53 healthy volunteer subjects with exercise treadmill test according to the Bruce protocol. Time domain and frequency domain of HRV were measured for each 5-minute segment before (rest) and after exercise (recovery) and during the total exercise period. The mean change in SBP (delta SBP) was 39 +/- 18 mm Hg. The delta SBP above the value of mean (> or = 40 mm Hg) was defined as an exaggerated delta SBP. According to the delta SBP, subjects were classified into two groups. Group I consisted of 32 patients who showed a normal delta SBP, group II consisted of 21 patients who showed exaggerated delta SBP. There were no significant differences in baseline clinical characteristics and exercise duration between the two groups. There were no significant differences in the mean RR intervals, SDNN (standard deviation of all RR intervals), RMSSD (the square root of the mean of the sum of the squares of differences between adjacent RR intervals), and HF (high-frequency power, 0.15 to 0.40 Hz) at rest between the two groups. However, LF (low-frequency power, 0.04 to 0.15 Hz) and LF/HF ratio at rest were significantly higher at rest in group II than in group I. There were no significant differences in the mean RR intervals and HF at exercise between the groups. However, SDNN and RMSSD were significantly lower, LF and the LF/HF ratio were significantly higher at exercise in group II than in group I. No differences in these parameters were observed at recovery between the two groups. CONCLUSIONS: The sympathetic activity was higher at rest and during the total exercise period, parasympathetic activity was lower during the total exercise period in healthy subjects with exaggerated SBP response to exercise than in those with normal SBP response.

Adult↗
PubMed2000

Effects of cigarette smoking on the circadian rhythm of heart rate variability.

BACKGROUND: The effects of cigarette smoking on the circadian rhythm of heart rate variability (HRV) are not known. METHODS: We studied the effects of cigarette smoking on the circadian rhythm of HRV in 24 smoking and 21 non-smoking healthy subjects. Twenty-four hour ambulatory electrocardiograms were recorded and time domain parameters of HRV (SDNN [standard deviation of all R-R intervals], SDANN [standard deviation of the averages of R-R intervals in all 5-minute segments of the entire recording], RMSSD [the square root of the mean of the sum of the squares of differences between adjacent R-R intervals]) were determined for the entire 24-hour period and for each 3-hour period. RESULTS: In total, SDNN and SDANN were significantly lower in smokers than non-smokers (116 +/- 26 vs 136 +/- 27, p < 0.05 for SDNN, 109 +/- 25 vs 121 +/- 24, p < 0.05 for SDANN). However, there were no statistical differences between smokers and non-smokers in heart rate (81 +/- 9 vs 76 +/- 10, p > 0.05) and RMSSD (32 +/- 12 vs 37 +/- 18, p > 0.05). These HRV parameters showed a circadian variation: they increased at night and decreased during the day in both groups. The parameters were lower in smokers than non-smokers during daytime (especially, between 8-14 hours). However, no differences were detected during night-time. CONCLUSIONS: Time domain parameters of HRV (SDNN, SDANN and RMSSD) in both smoking and non-smoking healthy subjects have a circadian rhythm. SDNN and SDANN were lower in smokers than non-smokers during daytime.

Adult↗
PubMed1999

Evaluation of right atrial appendage blood flow by transesophageal echocardiography in subjects with a normal heart.

Right atrial appendage (RAA) blood flow pattern was analyzed in 42 normal subjects-without cardiovascular disease (aged 30 to 48 years, mean 40 +/- 6) who underwent transesophageal echocardiography. RAA flow pattern was demonstrated to be bi-, tri- or quadriphasic and heart rate dependent (p < 0.01) in this study. In 15 subjects (36%), a biphasic pattern was observed. A triphasic pattern was observed in 12 subjects (28%). Fifteen subjects (36%) had a quadriphasic pattern. In these subjects, we observed a pattern consisting of two diastolic forward flow waves, each followed by a backward flow wave. Mean heart rates among subjects with bi-, tri- and quadriphasic patterns were 110 +/- 6, 91 +/- 4 and 72 +/- 13 beats/min, respectively. In the triphasic pattern, the onset of superior vena cava diastolic forward flow began 18 +/- 4 ms after the onset of tricuspid E wave, whereas the first diastolic forward flow wave in the RAA began 40 +/- 7 ms after onset of the tricuspid E wave. A similar relation was also noted in the quadriphasic pattern. This sequence was constant and independent of heart rate (p < 0.05), suggesting a temporal relation between right ventricular relaxation and the first diastolic forward flow wave in the RAA. In normal subjects, the RAA flow pattern is heart rate dependent and three distinct flow patterns can be differentiated. Right ventricular relaxation appears to induce both the superior vena cava diastolic forward flow wave and the first diastolic forward flow wave of the RAA. These results can be used for comparison with patterns found in disease states.

Adult↗
PubMed1999

Relation of plasma lipoprotein(a) with myocardial viability and left ventricular performance in survivors of myocardial infarction.

Previous studies have reported that high serum lipoprotein(a) levels may be responsible for total occlusion of the infarct-related artery via inhibition of intrinsic fibrinolysis during acute myocardial infarction. We evaluated whether this would result in a greater extent of myocardial necrosis and impaired left ventricular function in patients with high lipoprotein(a) levels. Sixty-eight patients with prior myocardial infarction, who were not receiving thrombolytic therapy underwent coronary angiography and stress-redistribution-reinjection Tl-201 scintigraphy. Antegrade TIMI flow in the infarct-related artery was lower (1.54 +/- 1.14 vs 2.15 +/- 1.05; p = 0.03) and the collateral index was higher (1.3 +/- 1.0 vs 0.8 +/- 0.9; p = 0.07) in patients with high lipoprotein(a) levels (> 30 mg/dl) compared to those with low lipoprotein(a) levels (< or = 30 mg/dl). Regional wall motion score index was lower (0.8 +/- 0.8 vs 1.4 +/- 0.5; p = 0.008) and global ejection fraction was higher (46 +/- 10% vs 40 +/- 11%; p = 0.03) in patients with low lipoprotein(a) levels. On SPECT images, the number of non-viable defects was higher in patients with high lipoprotein(a) levels (4.0 +/- 2.5 vs 1.9 +/- 1.3; p = 0.0002), whereas the number of viable defects was higher in those with low lipoprotein(a) levels (2.5 +/- 1.8 vs 1.5 +/- 1.3; p = 0.02). We conclude that high lipoprotein(a) levels may prolong the occlusion of infarct-related artery during acute myocardial infarction and lead to a greater extent of myocardial necrosis and impaired left ventricular function.

Adult↗
PubMed1999

Recurrent pulmonary emboli and thrombus attached to a permanently implanted pacemaker wire in pregnancy.

We present a case of pacer wire thrombus and recurrent pulmonary emboli in pregnancy associated with a permanent pacemaker. Transthoracic echocardiography demonstrated a thrombus attached to the pacer wire at the point where it crossed the tricuspid valve. After the uncomplicated vaginal delivery, thrombolytic therapy was given. This thrombus persisted despite thrombolytic therapy. Consequently, the patient was referred for cardiac surgery. The suspected cause was confirmed during the surgery.

Adult↗
PubMed1999

The effects of halothane and sevoflurane on QT dispersion.

QT dispersion is defined as the difference between QT (max) and QT (min) in the 12-lead surface ECG. It has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with arrhythmic events than in those without them. The aim of this study was to examine the effects of halothane and sevoflurane on QT and QTc dispersion during inhalational induction of anaesthesia. The effects on QT and QTc dispersion of halothane and sevoflurane have been investigated during induction of anaesthesia. Forty-six ASA (American Society of Anaesthesiologists) physical status I-II patients, aged 16-50 years, undergoing general anaesthesia were randomly allocated to receive either halothane or sevoflurane. The mean baseline values for QT and QTc dispersion were not significantly different between the two groups (P > 0.05). QT dispersion was increased with halothane compared with baseline values (50 +/- 16 ms vs. 29 +/- 9 ms, P < 0.01) and after sevoflurane compared with baseline (48 +/- 15 vs. 33 +/- 8 ms, P < 0.01). Also, QTc dispersion was increased with halothane compared with baseline values (48 +/- 13 ms vs. 31 +/- 9 ms, P < 0.001) and after sevoflurane compared with baseline (50 +/- 14 vs. 40 +/- 11 ms, P < 0.01). The QTc interval did not change by both sevoflurane (443 +/- 7 vs. 431 +/- 21 ms, P > 0.05) and halothane (419 +/- 33 vs. 431 +/- 19 ms, P > 0.05) compared with baseline. Both halothane and sevoflurane cause myocardial repolarisation abnormalities in man in terms of increased QTc dispersion. This may be relevant in the aetiology of arrhythmias in patients during anaesthesia with halothane or sevoflurane.

Adolescent↗
PubMed1998

The effect of electroconvulsive therapy on QT dispersion.

Electroconvulsive therapy (ECT) is used frequently in psychiatric practice and various electrocardiographic (ECG) changes have been described during ECT. QT dispersion (defined as maximal QT interval minus minimal QT interval) as assessed on the surface electrocardiogram has been demonstrated to reflect regional inhomogeneity of ventricular repolarization. The aim of this study is to examine the effect of electroconvulsive therapy on QT dispersion. We studied 27 patients (age range 24-42 y, mean age 34 y, 11 men) without heart disease who were treated with ECT. Structural heart disease was eliminated with routine clinical examination and laboratory tests, echocardiography, and exercise treadmill test. QT interval and corrected QT (QTc) dispersion was measured on a 12-lead ECG before and just after ECT. QTc dispersion increased from 28.9 +/- 7.4 ms at baseline to 81.4 +/- 12.8 ms after the procedure (P < 0.0001). This result demonstrated that QTc dispersion increased significantly during ECT. This finding may explain that increased inhomogeneity of ventricular repolarization is associated with enhanced vulnerability to arrhythmias during ECT.

Adult↗