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INTRODUCTION: The formation and collapse of vapor-filled bubbles near a mechanical heart valve is called cavitation. Microbubbles can be detected in vivo by doppler ultrasonography (USG) as HITS (high intensity transient signals) in cranial circulation. We investigated the relationship between exercise induced heart rate increase and HITS formation in cranial circulation. MATERIAL AND METHODS: Thirty-nine mechanical heart valve implanted (8 aortic valve replacement (AVR) + mitral valve replacement (MVR), 9 AVR, 22 MVR) patients aged 18-80 years old were included in our study. Microbubbles were counted in the left ventricular cavity via transthoracic echocardiography at rest per cardiac cycle. Afterwards transcranial Doppler USG was performed and HITS were counted in each patient's middle cerebral artery at 5 min duration. Subsequently an exercise test according to the Bruce protocol was performed. After achieving maximal heart rate, microbubbles in the left ventricle and HITS were counted again. RESULTS: Microbubbles in the left ventricle and transcranial HITS increased after exercise significantly compared to resting values (15.79 ±10.91 microbubbles/beat vs. 26.51 ±18.00 microbubbles/beat, p < 0.001; 6.13 ±8.07 HITS/5 min vs. 13.15 ±15.87 HITS/5 min, p = 0.001). There was a significant correlation between microbubbles and HITS counts after peak exercise (r = 0.55, p < 0.001). CONCLUSIONS: In our study, we found that the microbubbles were increasing as the heart rate increased and more HITS were propelled to the cerebral circulation. As previously shown, HITS can alter cognitive functions. Therefore heart rate control is essential in mechanical heart valve patients to protect neurocognitive functions.

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BACKGROUND: Atrial electromechanical delay (EMD) parameters predict the development of atrial fibrillation. We investigated the effect of telmisartan treatment on atrial EMD parameters in patients with newly diagnosed essential hypertension. METHODS: Thirty-six patients with essential hypertension were treated with telmisartan (80 mg/day) for 6 months. Baseline electrocardiographic P-wave measurements and echocardiographic atrial EMD parameters were compared with the 6-month follow-up. RESULTS: Pmax and Pd were significantly decreased (108.4 ± 6.1 vs 93.9 ± 6.2 milliseconds, 33.4 ± 8.6 vs 19.5 ± 7.0 milliseconds, respectively, P = .0001 for each) after 6-month telmisartan therapy. The atrial EMD parameters were decreased from baseline (mitral EMD, 68.9 ± 4.9 vs 53.8 ± 4.9 milliseconds; septum EMD, 51.6 ± 7.1 vs 42.6 ± 7. milliseconds1; tricuspid EMD, 48 ± 6.9 vs 39 ± 6.9 milliseconds; interatrial EMD, 20.9 ± 5.5 vs 14.8 ± 5.7 milliseconds; P = .0001 for each parameter). The reduction of interatrial EMD was correlated with the reduction in systolic BP nighttime and the increase in mitral E wave velocity/mitral A wave velocity ratio. CONCLUSION: Telmisartan decreased the atrial EMD parameters in patients with newly diagnosed essential hypertension.

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BACKGROUND: Acute alcohol consumption can cause atrial fibrillation in patients with, and without, heart disease. Increased atrial electromechanical delay (EMD) has been associated with atrial fibrillation. We evaluated the atrial conduction properties by tissue Doppler imaging (TDI) echocardiography in healthy men following acute alcohol intake. METHODS: Thirty healthy male volunteers were included in this study. Baseline ECG, heart rate, blood pressure, and TDI echocardiographic findings were compared to readings taken one hour after drinking six 12-oz cans of beer (76.8 g of ethanol). RESULTS: Although the blood pressure and heart rate remained similar before and one hour after alcohol intake, Pmax and Pd values were significantly prolonged (114.2 ± 10.4 vs 100.8 ± 10.6, p = 0.002; 50.6 ± 9.6 vs 34.5 ± 8.8, p < 0.0001). Interatrial EMD was significantly increased after drinking alcohol compared to the baseline (19.8 ± 9.2 vs 14.0 ± 5.5 ms, p < 0.0002). CONCLUSIONS: Acute moderate alcohol intake was associated with an increased interatrial EMD obtained by TDI echocardiography. This finding may help explain how these patients express increased susceptibility to atrial fibrillation.

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BACKGROUND: Carotid intima-media thickness (CIMT) is a potential indicator of subclinical atherosclerosis in patients with metabolic syndrome (MetS). Epicardial fat thickness (EFT) is suggested as a new cardiometabolic risk factor. We investigated the association between EFT and CIMT in patients with MetS. METHODS: Forty patients with MetS were compared with 40 age- and sex-matched subjects without MetS in terms of echocardiographic EFT, CIMT, anthropometric measurements, and metabolic profile in this cross-sectional study. RESULTS: The waist circumference, total and LDL-cholesterol, fasting glucose, triglycerides, systolics and diastolic blood pressure levels, hs-CRP, and homeostasis model assessment index for insulin resistance (HOMA-IR) were significantly increased in patients with MetS. The EFT and CIMT were also increased significantly in patients with MetS compared to controls (7.2 ± 2 mm vs. 5.7 ± 1.9 mm; P = 0.001, 0.74 ± 0.1 mm vs. 0.59 ± 0.1 mm; P < 0.01, respectively). Echocardiographic EFT was the only independent predictor of CIMT in the multivariate analysis (standardized ß coefficient = 0.74, P < 0.001). CONCLUSION: EFT is associated with increased CIMT in patients with MetS.

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BACKGROUND: Coronary artery ectasia (CAE) is associated with increased sympathetic activity, plasma levels of inflammatory markers, and oxidative stress. These factors can also cause arrhythmias such as atrial fibrillation. Atrial conduction abnormalities in patients with CAE have not been investigated in terms of atrial electromechanical delay obtained by tissue Doppler echocardiography. METHODS: Ninety patients with pure CAE (n = 30), nonobstructive coronary artery disease (NO-CAD) (n = 30), and angiographically normal coronary arteries "controls" (n = 30) were compared in terms of electrocardiographic P-wave measurements, echocardiographic atrial electromechanical coupling (AEC) parameters, and interatrial conduction delay. RESULTS: The mean left atrium diameter in the CAE group was similar to the NO-CAD group but significantly greater than the control group (3.62 ± 0.28 vs 3.46 ± 0.32 vs 3.41 ± 0.31 cm, P = 0.021). P maximum and P-wave dispersion were significantly increased in the CAE group compared to the NOCAD group and the control group (108.6 ± 6.6 vs 97.9 ± 6.6 vs 93.5 ± 6.2, P = 0.0001; 34.4 ± 7.6 vs 23.2 ± 7.8 vs 19.4 ± 7.7 ms, P < 0.0001). Mitral AEC, septal AEC, and tricuspid AEC were significantly higher in the CAE group than the NO-CAD group and the control group (68 ± 4.5 vs 57 ± 4.5 vs 53 ± 4.6 ms, P < 0.0001; 50.7 ± 7 vs 42.7 ± 7 vs 41.7 ± 7.2 ms, P = 0.0001; 47 ± 6.7 vs 39.1 ± 6.7 vs 38.1 ± 6.6 ms, P < 0.0001). Interatrial conduction delay was significantly increased in the CAE group compared to the NO-CAD group and the control group (21 ± 5.5 vs 17.8 ± 5.6 vs 15 ± 5.6 ms, P < 0.0001).The correlation analysis demonstrated that the interatrial conduction delay and P-wave dispersion (Pd) were positively correlated with number of ectatic segments (ESN) (r = 0.41, P = 0.024 vs r = 0.49, P = 0.006). Stepwise multiple linear regression analysis revealed that the ESN was the only independent determinants of interatrial conduction delay (P = 0.024). CONCLUSION: Pd and interatrial conduction delay are prolonged in patients with CAE compared to NO-CAD patients and the healthy controls.

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