Clinical implications of combined glucose intolerance in treatment-naïve hypertensive patients.

BACKGROUND: This study is the first study to evaluate clinical significance of combined glucose intolerance (CGI) in treatment-naïve hypertensive patients. METHODS: We compared the results of demographic, anthropometric, clinical, laboratory examinations, echocardiography, arterial stiffness, central blood pressure (BP) and ambulatory BP monitoring (ABPM) between the groups according to fasting blood sugar (FBS), postprandial 2 hour blood glucose (PP2) and gender in treatment-naïve hypertensive patients. A total of 376 concecutively-eligible patients were categorized as follows: (1) normal glucose tolerance (NGT); FBS<100 mg/dL and PP2 < 140 (2) isolated glucose intolerance (IGI); 100≤FBS<126 or 140≤PP2 < 200, but not both 100≤FBS<126 and 140≤PP2 < 200 (3) CGI; both 100≤FBS<126 and 140≤PP2 < 200. RESULTS: Males were divided into NGT (n = 58, 33.1%), IGI (n = 88, 50.3%), CGI (n = 29, 16.6%) and females were divided into NGT (n = 59, 43.1%), IGI (n = 48, 35%), CGI (n = 30, 21.9%). In males multivariate analyses revealed that mitral average E/Ea (IGI vs CGI, p = 0.022), brachial-ankle pulse wave velocity baPWV(Rt.) (IGI vs CGI, p = 0.026), baPWV(Lt.) (IGI vs CGI, p = 0.018), office systolic BP (SBP) (NGT vs. CGI, p = 0.005; IGI vs. CGI, p = 0.001), office diastolic BP (DBP) (NGT vs. CGI, p = 0.034; IGI vs. CGI, p = 0.019), night-time SBP (NGT vs. CGI, p = 0.049; IGI vs. CGI, p = 0.018) were significantly higher in the CGI group than in the NGT or IGI group. However, there were no significant differences between the female groups. CONCLUSIONS: Treatment-naïve hypertensive males with CGI revealed subclinical diastolic dysfunction, arterial stiffness, and BPs.

A randomized comparison study assessing the impact of cilostazol on the heart rate and arrhythmias by 24-hour ambulatory holter electrocardiographic monitoring after drug-eluting stent implantation for coronary artery disease.

AIMS: Cilostazol may have a positive chronotropic or pro-arrhythmic effect. However, there have been no randomized trials to confirm these effects. METHODS: This randomized prospective trial compared dual (DAT, aspirin and clopidogrel, n=114) versus triple antiplatelet therapy (TAT, DAT plus cilostazol, n=113) at baseline and after six months in patients receiving intracoronary drug-eluting stents (DES). The primary endpoint was the 24-hour heart rate (24h-HR) at six months determined using 24h-Holter ECG monitoring. The secondary endpoints were the 24h-HR ≥70 bpm, 24h-HR increase ≥5 bpm and the counts or presence of arrhythmias. RESULTS: At six months after DES implantation, the 24h-HR (73 [68-83] vs. 68 [62-75] bpm, p＜0.001), presence of a 24h-HR ≥70 bpm (71.4 vs. 47.1%, p＜0.001) and presence of a 24h-HR increase ≥5 bpm (44.8 vs. 24.5%, p=0.002) were significantly higher for the TAT group than for the DAT group. A multivariate analysis showed that the use of cilostazol (OR: 3.10, p=0.035) and a baseline 24h-HR ＜70 bpm (OR: 4.60, p＜0.001) were strong predictors of a 24h-HR increase ≥5 bpm. However, there were no significant intergroup differences in arrhythmias. CONCLUSIONS: Cilostazol appears to result in an increase in the 24h-HR after DES implantation. Therefore, some caution should be exercised regarding the use of cilostazol in patients with tachycardia, when planning DES implantation.

Left ventricular diastolic dyssynchrony in patients with treatment-naive hypertension and the effects of antihypertensive therapy.

AIMS: The presence of left ventricular diastolic dyssynchrony is well known to be a frequent and important manifestation in heart failure. We investigated diastolic dyssynchrony in patients with treatment-naive hypertension, compared with normal controls; the determinants of the presence of diastolic dyssynchrony by performing comprehensive studies including laboratory, arterial stiffness, central blood pressure (BP), ambulatory BP monitoring (ABPM), and transthoracic echocardiography (TTE) evaluations; the effects of 6-month antihypertensive therapy on diastolic dyssynchrony; and the predictors associated with the change of diastolic dyssynchrony after medical therapy. METHODS: A total of 325 treatment-naive hypertensive patients and 172 normal controls were prospectively enrolled. Hypertensive patients were followed up at 6 months after medical therapy, and were assessed by serial TTE (at baseline and 6-month follow-up visit) and clinical evaluations. The time-to-peak myocardial early diastolic velocity (Te) of the 12 left ventricular segments was measured with reference to the QRS complex. The standard deviation (SD) of Te of all 12 left ventricular segments (Te-SD12) and the maximal difference in Te between any two of the 12 left ventricular segments (Te-Max) were calculated. A Te-SD12 at least 34 or Te-Max at least 113 ms was regarded as indicating the presence of diastolic dyssynchrony. RESULTS: Diastolic dyssynchrony was more prevalent in treatment-naive hypertensive patients, compared with normal controls (15.4 versus 7.0%, P = 0.007). Male sex [odds ratio (OR), 9.36 (1.93-45.41)], magnesium [OR per 1 SD, 2.54 (1.32-4.90)], night-time heart rate [HR; OR per 1 SD, 2.44 (1.18-5.05)], and mitral E/A [OR per 1 SD, 0.13 (0.04-0.45)] were independent determinants for the diastolic dyssynchrony in hypertensive patients. A 6-month follow-up, echocardiography was performed in 74 of 275 patients without diastolic dyssynchrony (group 1) and 26 of 50 patients with diastolic dyssynchrony (group 2). Diastolic dyssynchrony (Te-SD12, Δ = -8.3 ms; Te-Max, Δ = -27.6 ms; prevalence, Δ = -42.3%; all P < 0.05) improved in group 2, whereas it did not in group 1. Baseline daytime HR (P = 0.008) and magnesium levels (P = 0.029) and changes of the midwall fractional shortening (P = 0.026), mitral E/A (P = 0.003), mean annulus Ea (P = 0.003), mean annulus Ea/Aa (P = 0.020), and mitral peak E (P = 0.042) were independent predictors for changes of Te-SD12. CONCLUSION: Diastolic dyssynchrony is not rare in treatment-naive hypertensive patients. Male sex, magnesium levels, night-time HR, and mitral E/A are independent determinants for the impaired diastolic dyssynchrony. Antihypertensive therapy reduces both the severity and prevalence of diastolic dyssynchrony in patients with impaired diastolic dyssynchrony. Daytime HR, magnesium levels, and indications of systolic or diastolic dysfunction are independent predictors for improvements in diastolic dyssynchrony. Thus, magnesium levels, HR, and diastolic dysfunction seem to have important implications for diastolic dyssynchrony in hypertensive patients, whereas left ventricular hypertrophy, office BPs, arterial stiffness, central BPs, and ABPM parameters do not.

A high normal thyroid-stimulating hormone is associated with arterial stiffness, central systolic blood pressure, and 24-hour systolic blood pressure in males with treatment-naïve hypertension and euthyroid.

BACKGROUND: We compared the results of laboratory examinations, echocardiography, arterial stiffness, central blood pressure (BP) and ambulatory BP monitoring (ABPM) between treatment-naïve patients with low normal thyroid-stimulating hormone (TSH) and those with high normal TSH levels. METHODS: A total of 285 consecutively-eligible patients with both treatment-naïve hypertension and euthyroid were divided into two groups: those with low-normal TSH (0.40-1.99 µIU/mL, group 1) and high-normal TSH (2.00-4.50 µIU/mL, group 2) and compared according to group and gender. RESULTS: Males were divided into group 1 (n = 113, 68.9%) and group 2 (n = 51, 31.1%) and females were divided into group 1 (n = 71, 58.7%) and group 2 (n = 50, 41.3%). Multivariate analyses revealed that the augmentation index (71.0 [adjusted mean] ± 1.7 [standard error] vs. 78.8 ± 2.5%, P = 0.045), central systolic BP (SBP) (143.3 ± 2.1 vs. 153.0 ± 3.2 mmHg, P = 0.013), systemic vascular resistance (SVR, 21.4 ± 0.6 vs. 23.9 ± 0.9 mmHg/L/min, P = 0.027), SBP during daytime (144.1 ± 1.4 vs. 151.6 ± 2.1 mmHg, P=0.004) and nighttime (130.4 ± 1.6 vs. 138.5 ± 2.5 mmHg, P=0.008), and nighttime pulse pressure (PP, 47.2 ± 0.9 vs. 51.7 ± 1.4 mmHg, P = 0.010) were significantly higher while cardiac output (5.4 ± 0.1 vs. 4.8 ± 0.2L/min, P = 0.043) and PP amplification (1.02 ± 0.02 vs. 0.94 ± 0.03, P = 0.039) were significantly lower in the male group 2 than in the male group 1. However, there were no significant differences between the two groups in females. CONCLUSIONS: Treatment-naïve hypertensive males with high normal TSH and euthyroid showed higher arterial stiffness, central SBP, SVR, and SBP in ABPM and lower cardiac output and PP amplification as compared to the the low normal TSH group, but not females.

The associations of epicardial adipose tissue with coronary artery disease and coronary atherosclerosis.

Epicardial adipose tissue (EAT) is presumed to play an important role in the development of coronary artery disease (CAD). The purpose of our study was to examine the influence of EAT volume measured by cardiac CT on the severity and presence of CAD. A total of 209 subjects (114 normal subjects and 95 patients with CAD) underwent cardiac and abdominal computed tomography (CT) scan before diagnostic coronary angiography. Pixels with a threshold range of -190 to -30 Hounsfield units were identified as EAT. CAGE ≥ 20, CAGE ≥ 50, and modified Gensini index were used to define the extent and severity of CAD. While there was no significant difference in BMI and WC between the two groups, the mean EAT volume was higher in the CAD group than in the normal subjects (102.4 ± 41.87 cm(3) versus 125.36 ± 47.64 cm(3), P < 0.001). EAT was significantly associated with CAGE ≥ 20, CAGE ≥ 50, and Gensini score by linear regression analyses after adjusting for age, gender, smoking, and alcohol use. The severity of CAD increased linearly with each tertile increase in EAT volume (P for trend < 0.05). Similarly, the coronary artery calcium (CAC) score was also increased with each increase in EAT tertile (P = 0.002). In multivariate logistic regression models, EAT and VAT were significantly associated with the presence of CAD and CAC in age, gender, smoking, alcohol use, and BMI adjusted models. In conclusion, EAT volume measured by CT is associated with the presence and severity of CAD. EAT may give important information for risk evaluation in CAD.

Epicardial adipose tissue: relationship between measurement location and metabolic syndrome.

Epicardial adipose tissue (EAT) is a contributing factor of metabolic syndrome (MS) and coronary artery disease (CAD). However, it is still unclear which measurement location of EAT area best reflects its cardiometabolic risk. The purpose of our study was to investigate the distribution of EAT and its relationship to the total EAT volume and MS. To assess volume and cross-sectional areas of EAT, coronary CT angiography were obtained in 256 asymptomatic subjects. The EAT areas within the threshold range of -190 to -30 Hounsfield units were measured at six representative slices. Correlations between single slice EAT areas and total EAT volumes were high across all measurement locations (correlation coefficient r > 0.80). The receiver-operator characteristic curves demonstrated EAT area at left main coronary artery (LMCA) was well discriminative for MS (AUC 0.82, p < 0.001) and CAD (AUC 0.76, p < 0.001). EAT areas across all measurement locations were significantly increased linearly with increasing number of MS components. EAT areas were significantly associated with MS at all measurement locations; the highest odds ratio (OR) between EAT area and MS was at the LMCA level (OR 5.86, p < 0.001). The OR between EAT area and coronary artery calcium was also significant in LMCA locations (OR 1.56, p = 0.042). We demonstrated that the single-slice EAT area measurement is a simple and reliable method compared with time-consuming volumetric measurements. The EAT area at LMCA level was the best single slice representing the risk of metabolic syndrome and coronary atherosclerosis.

Independent determinants for presence and degree of left ventricular systolic dyssynchrony in treatment-naive patients with hypertension.

OBJECTIVE: Prevalence of left ventricular systolic dyssynchrony (LVSD) is over 40% in treatment-naive patients with hypertension and it improves after chronic antihypertensive treatment. These findings might support the hypothesis that blood pressure (BP), BP-derived parameters, central BP, or arterial stiffness would contribute to LVSD. Therefore, we aimed to investigate possible factors associated with LVSD in treatment-naive patients with hypertension. METHODS: The study groups consisted of 266 treatment-naive hypertensive patients who underwent anthropometric, clinical, laboratory, echocardiographic, arterial stiffness, central blood pressure, and 24-h ambulatory blood pressure monitoring evaluations. Echocardiographic measurement was recorded as follows: peak systolic velocity (Sa, subclinical left ventricular systolic function), peak early diastolic and late diastolic velocity at the mitral annulus (Ea and Aa, respectively), mitral E/Ea ratio (subclinical left ventricular diastolic function), standard deviation of time from ECG Q to systolic peak velocity of 12 left ventricular segments (Ts-SD12), and maximal difference between peak systolic velocities of any 2 of the 12 segments (Ts-Max). A Ts-SD12 at least 33 or Ts-Max at least 100 ms was regarded as presence of LVSD. RESULTS: Patients were divided into those without LVSD (group 1, n = 151, 56.8%) and those with LVSD (group 2, n = 115, 43.2%). Group 2 had higher E/Ea and high-density lipoprotein and lower Sa and triglyceride than group 1. On multivariate analysis, Sa was independently and inversely associated with the presence of LVSD [odds ratio (OR) 0.67, 95% confidence interval (CI) 0.48-0.93, P = 0.018]. The linear relationship between variables and degree of LVSD showed that serum potassium levels, E/Ea, and Sa remained significant after multivariate analysis (potassium, ß = 0.199, P = 0.006; E/Ea, ß = 0.211, P = 0.017; Sa, ß = -0.301, P < 0.001 in Ts-SD12 and potassium, ß=0.187, P = 0.010; E/Ea, ß = 0.234, P = 0.008; Sa, ß = -0.322, P < 0.001 in Ts-Max, respectively). CONCLUSION: Subclinical left ventricular systolic function is independently associated with both the presence and degree of LVSD in treatment-naive hypertensive patients. Subclinical left ventricular diastolic function and serum potassium levels are independently associated with the degree of LVSD. However, arterial stiffness and BP parameters are not determinants.

Metabolically obese status with normal weight is associated with both the prevalence and severity of angiographic coronary artery disease.

OBJECTIVE: We evaluated prevalence and severity of angiographic coronary artery disease (CAD) according to groups by metabolically obese (MO) and/or weight status. MATERIAL/METHODS: Normal weight was defined as body mass index (BMI, kg/m²)<25 and obesity was defined as BMI≥25. The MO was determined using the National Cholesterol Education Program-Adult Treatment Panel III classification with Korean-specific cutoffs for abdominal obesity. Therefore, a total of 856 subjects were categorized as follows: (1) metabolically healthy and normal weight (MHNW); (2) metabolically obese but normal weight (MONW); (3) metabolically healthy but obese (MHO); and (4) metabolically abnormally obese (MAO). The presence of obstructive lesion≥50% of coronary artery was considered as an angiographic CAD and the Gensini scoring system was used for the severity. RESULTS: MONW or MO showed a higher prevalence of CAD than MHNW or non-MO after adjustment for age and sex, respectively (MONW, odds ratio [OR]=1.69, 95% confidence interval [CI]: 1.13-2.51 and MO, OR=1.44, 95% CI: 1.09-1.91). In subjects without diabetes mellitus (DM), MONW or MO showed a marginally higher prevalence of CAD (MONW, OR=1.58, 95% CI: 0.96-2.61 and MO, OR=1.41, 95% CI: 0.96-2.08). MONW was independently associated with a higher severity of angiographic CAD than MHNW after age, sex, glomerular filtration rate, smoking status, high sensitive C-reactive protein, and use of anti-platelet and anti-angina drugs (ß=0.118, P=0.005). And MO was associated with a higher severity of angiographic CAD than non-MO after adjustment for age and sex (ß=0.077, P=0.024). The above associations were also consistent in subjects without DM (MONW, ß=0.147, P=0.003 and MO, ß=0.129, P=0.005). CONCLUSIONS: MONW or MO is associated with both the prevalence and severity of angiographic CAD after adjustment for age and sex and MONW is independently associated with the severity of angiographic CAD irrespective of DM. Therefore, subjects with MO but normal weight (MONW) should be carefully examined for angiographic CAD.

Comparison of the efficacy between hydrochlorothiazide and chlorthalidone on central aortic pressure when added on to candesartan in treatment-naïve patients of hypertension.

Thiazide-type diuretics are the most commonly used blood pressure (BP)-lowering drug for patients with uncomplicated hypertension. However, it has remained unclear whether hydrochlorothiazide (HCTZ) or chlorthalidone (CTD) shows better improvement in central aortic pressure. We conducted an open-label, randomized, prospective cross-over study with an 8-week active treatment (HCTZ of 25 mg with candesartan of 8 mg or CTD of 12.5 mg with candesartan of 8 mg) with a 4-week washout period (only candesartan during this period). Twenty-eight treatment-naïve patients of hypertension were enrolled (mean age: 50±9 years, male: 44.4%). Central aortic pressure, pulse wave velocity (PWV), augmentation index (AIx) and other BP-derived parameters were measured. After 8 weeks of active treatment, there was no significant difference in changes of central aortic pressure between HCTZ and CTD treatments (Δ=-14±8 vs. -16±7 mm Hg, P=0.645). However, CTD treatment showed a significant reduction in PWV compared with baseline (1321±194 vs. 1439±190 cm s(-1), P=0.007) and HCTZ treatment (Δ=-118±82 vs. Δ=5±72 cm s(-1), P=0.033), whereas HCTZ treatment showed a marginal, but not a significant reduction in AIx compared with baseline. In conclusion, CTD of 12.5 mg is as potent as HCTZ of 25 mg, when combined with candesartan of 8 mg, in lowering central aortic pressure. In addition, CTD treatment resulted in a significant reduction of PWV.

A case of left ventricular noncompaction accompanying fasciculo-ventricular accessory pathway and atrial flutter.

Left ventricular hypertrabeculation/noncompaction (LVHT) is an uncommon type of genetic cardiomyopathy characterized by trabeculations and recesses within the ventricular myocardium. LVHT is associated with diastolic or systolic dysfunction, thromboembolic complications, and arrhythmias, including atrial fibrillation, ventricular arrhythmias, atrioventricular block and Wolff-Parkinson-White syndrome. Herein, we describe a patient who presented with heart failure and wide-complex tachycardia. Echocardiography showed LVHT accompanied with severe mitral regurgitation. The electrophysiologic study revealed a fasciculo-ventricular accessory pathway and atrial flutter (AFL). The AFL was successfully treated with catheter ablation.

Impact of antihypertensive treatment on left ventricular systolic dyssynchrony in treatment-naïve hypertensive patients.

Dyssynchrony is common in asymptomatic patients with hypertension. We sought to investigate the impact of antihypertensive treatment on dyssynchrony in patients with hypertension. A total of sixty patients who had uncomplicated hypertension that had never been treated (treatment-naïve hypertensive patients) underwent echocardiographic evaluations of left ventricular (LV) dyssynchrony at baseline and after a 6-month treatment with antihypertensive drugs. The measured parameters were as follows: (1) the s.d. of 12 LV-segment time-to-peak systolic velocities (Ts-SD12), and (2) the maximal difference between peak systolic velocities of any 2 of the 12 segments (Ts-Max). Patients with Ts-SD12 ≥ 33 ms or Ts-Max ≥ 100 ms were regarded as having LV systolic dyssynchrony. Patients with systolic dyssynchrony (group 1, n = 29) and without systolic dyssynchrony (group 2, n = 31) were compared. Among the patients in group 1, antihypertensive treatment significantly improved LV systolic dyssynchrony (ΔTs-SD12, -13.1 ms; P<0.001 and ΔTs-Max, -34.0 ms; P = 0.003), whereas it did not demonstrate additional benefit among group 2 patients. The change in LV systolic dyssynchrony was significantly associated with changes in the mean annulus E' velocity, mean annulus S' velocity and mean annulus E'/A' ratio, but not with changes in blood pressure and LV mass index. It is likely that chronic antihypertensive treatment could reverse the LV systolic dyssynchrony and simultaneously improve subclinical systolic and diastolic function in patients with hypertension and LV systolic dyssynchrony.

Randomized comparison of the efficacy and safety of zotarolimus-eluting stents vs. sirolimus-eluting stents for percutaneous coronary intervention in chronic total occlusion--CAtholic Total Occlusion Study (CATOS) trial.

BACKGROUND: Limited data are available regarding the direct comparison of angiographic and clinical outcomes after percutaneous coronary intervention (PCI) with drug-eluting stents (DESs) for chronic total occlusion (CTO). METHODS AND RESULTS: A prospective, randomized, multicenter trial was conducted to evaluate the non-inferiority of a zotarolimus-eluting stent (ZES; Endeavor Sprint®, n=80) to a sirolimus-eluting stent (SES; Cypher®, n=80) in patients with CTO lesion with a reference vessel diameter ≥ 2.5mm. The primary endpoint was in-segment binary restenosis rate at 9-month angiographic follow-up. Key secondary endpoints included target vessel failure (TVF; including cardiac death, myocardial infarction, and target vessel revascularization) and Academic Research Consortium-defined definite/probable stent thrombosis (ST) within 12 months. The ZES was non-inferior to the SES with respect to the primary endpoint, which occurred in 14.1% (95% confidence interval [CI]: 6.0-22.2) and in 13.7% (95%CI: 5.8-21.6) of patients, respectively (non-inferiority margin, 15.0%; P for non-inferiority <0.001). There were no significant between-group differences in the rate of TVF (10.0% vs. 17.5%; P=0.168) nor in the rate of ST (0.0% vs. 1.3%; P=0.316) during the 12-month clinical follow-up. CONCLUSIONS: The effectiveness and safety of ZES are similar to those of SES and therefore it is a good treatment option in patients undergoing PCI for CTO with DESs.

Optimal antithrombotic strategy in patients with atrial fibrillation after coronary stent implantation.

BACKGROUND AND OBJECTIVES: Little evidence is available on the optimal antithrombotic therapy following percutaneous coronary intervention (PCI) in patients with atrial fibrillation (AF). We investigated the outcomes of antithrombotic treatment strategies in AF patients who underwent PCI. SUBJECTS AND METHODS: Three hundred sixty-two patients (68.0% men, mean age: 68.3±7.8 years) with AF and who had undergone PCI with stent implantation between 2005 and 2007 were enrolled. The clinical, demographic and procedural characteristics were reviewed and the stroke risk factors as well as antithrombotic regimens were analyzed. RESULTS: THE ACCOMPANYING COMORBIDITIES WERE AS FOLLOWS: hypertension (59.4%), diabetes (37.3%) and congestive heart failure (16.6%). The average number of stroke risk factors was 1.6. At the time of discharge after PCI, warfarin was prescribed for 84 patients (23.2%). Cilostazol was used in addition to dual antiplatelet therapy in 35% of the patients who did not receive warfarin. The mean follow-up period was 615±385 days. The incidences of major adverse cardiac events (MACE), stroke and major bleeding were 11.3%, 3.6% and 4.1%, respectively. By Kaplan-Meier survival analysis, warfarin treatment was not associated with a lower risk of MACE (p=0.886), but it was associated with an increased risk of major bleeding (p=0.002). CONCLUSION: Oral anticoagulation therapy after PCI may increase hemorrhagic events in Korean AF patients.

Systolic synchrony is impaired in nonleft ventricular hypertrophy of never-treated hypertensive patients.

OBJECTIVE: The objective of the current study was to confirm the degrees of dyssynchrony in patients with nonleft ventricular hypertrophy (LVH) and never-treated hypertension compared with normal controls or patients with LVH and never-treated hypertension. METHODS AND RESULTS: We enrolled 200 consecutive never-treated hypertensive patients and 104 age-matched and sex-matched normal controls. The following parameters were evaluated by echocardiography comprising conventional Doppler, tissue Doppler imaging, and strain imaging: global dyssynchrony; systolic dyssynchrony (longitudinal); diastolic dyssynchrony; and contractile diastolic dyssynchrony. Systolic dyssynchrony in the LVH group with hypertension was more aggravated than in normal controls (P < 0.001). In addition, global, diastolic, and contractile diastolic dyssynchrony in the LVH group with hypertension were more aggravated than in the non-LVH group with hypertension (all P < 0.001), but systolic dyssynchrony was not different between the two groups. All of the above associations remained significant after adjustment for confounding factors. CONCLUSION: Systolic synchrony was impaired in patients with non-LVH and never-treated hypertension to a similar degree in the LVH group with never-treated hypertension.

Computed tomographic analysis of the esophagus, left atrium, and pulmonary veins: implications for catheter ablation of atrial fibrillation.

PURPOSE: The aim of this study was to investigate the anatomic relationship around the left atrium (LA) and to provide clinical information to help avoid the risk of an atrio-esophageal fistula during atrial fibrillation (AF) ablation. METHODS: The multidetector spiral computed tomography images of 77 male patients (mean age, 54 ± 9 years) with drug-refractory AF and 37 male control subjects (mean age, 50 ± 11 years) were analyzed. We measured the following variables: (1) distance between the ostia of the pulmonary veins (PVs) and the ipsilateral esophageal border, (2) presence of a pericardial fat pad around each PV, and (3) contact width/length and presence of a fat pad between the LA and the esophagus. RESULTS: The distance between the esophagus and the ostia of right superior PV, right inferior PV (RIPV), left superior PV, and left inferior PV (LIPV) was 27.2 ± 9.4 mm, 22.9 ± 10.3 mm, 2.7 ± 9.4 mm, and 7.1 ± 8.8 mm, respectively. A fat pad between the esophagus and the superior PV was present in more than 90% of the subjects in both groups. However, the fat pad around inferior PV was present less frequently in the patients than in the control group (p = 0.011, RIPV; p < 0.001, LIPV). The average length of the LA-esophagus contact in the patients and the control group subjects was 26.2 ± 10.4 and 18.5 ± 5.1 mm, respectively (p < 0.001). CONCLUSION: Caution should be exercised when ablating the LIPV because the esophagus is located in close proximity to the left-sided PV and most of the inferior PVs in patients with AF are not covered with fat pads.

Rapidly Progressive Cardiac Manifestation of Behçet's Disease Involving Conduction System and Aortic Valve.

Cardiac conduction system impairment is a rare clinical manifestation of Behçet's disease. We report a patient who showed 1st degree atrioventricular block at first presentation, and showed aggravated finding of 3rd degree atrioventricular block on five months later. His cardiac manifestation finally developed to acute severe aortic regurgitation on six months later from his first cardiac manifestation. We observed this rapid progression during 6 months and successfully improved symptom and disease severity of the patient with treatment targeting Behçet's disease.

Prognosis of heart failure patients with reduced and preserved ejection fraction and coexistent chronic obstructive pulmonary disease.

AIMS: The long-term prognosis of patients with heart failure with preserved left ventricular ejection fraction (HFPEF) and coexistent chronic obstructive pulmonary disease (COPD) has not been previously investigated. The primary aim of this study was to determine whether the long-term prognosis of HFPEF patients with COPD differs from that of heart failure patients with reduced left ventricular ejection fraction (HFREF) and COPD. The secondary aim was to identify independent predictors of event-free survival in patients with HF and COPD. METHODS AND RESULTS: We investigated 184 patients with coexistent HF and COPD. Heart failure with preserved left ventricular ejection fraction was present in 98 cases (53%) and HFREF in the remaining 86 cases (47%). Mean follow-up time was 731±369 days. Cardiovascular/pulmonary hospitalization or mortality occurred in 71 patients (39%). No significant difference was observed between the two study groups in terms of event-free survival (P=0.457), but event-free survival was found to be independently associated with New York Heart Association (NYHA) class [III vs. I, hazard ratio (HR) 2.92, 95% confidence interval (CI) 1.09-7.82], Global initiative for chronic Obstructive Lung Disease (GOLD) stage (III vs. I, HR 3.20, 95% CI 1.33-7.68), systemic hypertension (SHT; HR 2.99, 95% CI 1.41-6.33), and pulmonary hypertension (PH; HR 4.35, 95% CI 1.95-9.68). CONCLUSION: In HF patients with coexisting COPD, cardiovascular and pulmonary event-free survival of HFPEF was found to be similar to that of HFREF over 3 years follow-up. Furthermore, severe NYHA class, severe GOLD stage, SHT, and PH were found to be independent predictors of event-free survival.