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Disclosure: There is no potential conflict of interest to declare.
Original Article
Epicardial adipose tissue assessed by cardiac magnetic resonance imaging in patients with heart failure due to dilated cardiomyopathy†
Version of Record online: 16 APR 2013
DOI: 10.1002/oby.20149
Copyright © 2012 The Obesity Society
Volume 21, Issue 3, pages E253–E261, March 2013
Additional Information
How to Cite
Doesch, C., Streitner, F., Bellm, S., Suselbeck, T., Haghi, D., Heggemann, F., Schoenberg, S. O., Michaely, H., Borggrefe, M. and Papavassiliu, T. (2013), Epicardial adipose tissue assessed by cardiac magnetic resonance imaging in patients with heart failure due to dilated cardiomyopathy. Obesity, 21: E253–E261. doi: 10.1002/oby.20149
- †
Publication History
- Issue online: 16 APR 2013
- Version of Record online: 16 APR 2013
- Accepted manuscript online: 6 NOV 2012 08:16AM EST
- Manuscript Accepted: 10 OCT 2012
- Manuscript Revised: 30 AUG 2012
- Manuscript Received: 31 OCT 2011
- Abstract
- Article
- References
- Cited By
We sought to investigate the association of the EAT with CMR parameters of ventricular remodelling and left ventricular (LV) dysfunction in patients with non-ischemic dilated cardiomyopathy (DCM).
Design and Methods:
One hundred and fifty subjects (112 consecutive patients with DCM and 48 healthy controls) underwent CMR examination. Function, volumes, dimensions, the LV remodelling index (LVRI), the presence of late gadolinium enhancement (LGE) and the amount of EAT were assessed.
Compared to healthy controls, patients with DCM revealed a significantly reduced indexed EAT mass (31.7 ± 5.6 g/m2 vs 24.0 ± 7.5 g/m2, p<0.0001). There was no difference in the EAT mass between DCM patients with moderate and severe LV dysfunction (23.5 ± 9.8 g/m2 vs 24.2 ± 6.6 g/m2, P = 0.7). Linear regression analysis in DCM patients showed that with increasing LV end-diastolic mass index (LV-EDMI) (r = 0.417, P < 0.0001), increasing LV end-diastolic volume index (r = 0.251, P = 0.01) and increasing LV end-diastolic diameter (r = 0.220, P = 0.02), there was also a significantly increased amount of EAT mass. However, there was no correlation between the EAT and the LV ejection fraction (r = 0.0085, P = 0.37), right ventricular ejection fraction (r = 0.049, P = 0.6), LVRI (r = 0.116, P = 0.2) and the extent of LGE % (r = 0.189, P = 0.1). Among the healthy controls, the amount of EAT only correlated with increasing age (r = 0.461, P = 0.001), BMI (r = 0.426, P = 0.003) and LV-EDMI (r = 0.346, P = 0.02).
In patients with DCM the amount of EAT is decreased compared to healthy controls irrespective of LV function impairment. However, an increase in LV mass and volumes is associated with a significantly increase in EAT in patients with DCM.
Non-ischemic dilated cardiomyopathy (DCM) is characterized by left ventricular (LV) dilatation and a progressive impairment of cardiac contractility (1). Activation of macrophages and fibroblasts (2) as well as inflammatory processes seem to play an important role in the propagation of a diffuse interstitial and perivascular fibrosis (3) that is supposed to lead to cardiac remodeling in these patients.
Epicardial adipose tissue (EAT) is a metabolically active tissue, secreting several adipokines with pro- and anti-inflammatory properties (4–6). So far, the role of EAT has been studied mainly in the development of coronary artery disease (CAD) (7, 8). Additionally, recent studies showed decreased amounts of EAT in patients with congestive heart failure irrespective of the underlying cause (9–11). Furthermore, in consecutive patients undergoing cardiac computed tomography to rule out significant coronary artery stenosis, analysis of epicardial fat volume revealed a stepwise decrease in patients with moderate to severe LV dysfunction compared to controls (11). However, to date, there are scarce data about the role of EAT in the development of heart failure in patients with DCM. Therefore, the aim of our study was to investigate the association of the EAT amount with the severity of the LV dysfunction and parameters of ventricular remodeling using CMR.
Study population
One hundred twelve consecutive patients with DCM (87 males and 25 females; mean age 59.4±13.9 years) who were referred to our hospital between January 2007 and December 2010 were recruited. The cardiac magnetic resonance imaging (CMR) study was performed in these patients as part of the clinical evaluation for patients with known or suspected cardiomyopathy at our institution. In patients with chronic renal failure and an estimated glomerular filtration rate (GFR) <30 ml/min/1.73m2, the CMR protocol was performed without the administration of a contrast agent. The diagnosis of DCM was made according to the World Health Organization/International Society and Federation of Cardiology criteria (12). Patients had to exhibit a depressed LV systolic function, that is, LV ejection fraction (LVF) < 50% on a non-CMR study in the absence of significant CAD defined as coronary artery stenoses ≥ 50% or a history of coronary revascularization or previous myocardial infarction. Patients with valvular heart disease, hypertensive heart disease, or congenital abnormalities were also not included. None of the patients showed signs or symptoms of ongoing myocarditis. Patients with a normal LVF on CMR > 55% were excluded.
Forty-eight age- and sex-matched healthy subjects served as controls and satisfied the following criteria: normal physical examination, normal blood pressure (systolic blood pressure <130 mm Hg and diastolic blood pressure <85 mm Hg), normal ECG findings, no history of chest pain or dyspnea, no diabetes, no hyperlipidemia, and normal 2D echocardiography and Doppler examination. None of the subjects was on medication. Any potential subjects with evidence of heart disease, hypertension, or other systemic disorders were excluded from the study.
All patients and volunteers underwent CMR examination with identical protocols. Informed consent for the CMR protocol was obtained from all subjects, and the study was approved by the local ethics commission.
Image acquisition
All studies were performed using a 1.5 Tesla whole-body imaging system (Magnetom Avanto, Siemens Healthcare Sector, Erlangen, Germany). A dedicated six-element, phased-array cardiac coil was used. Images were acquired during repeated end-expiratory breath-holds. Scout images (coronal, sagittal, and axial planes) were obtained for planning of the final double-oblique long-axis and short-axis views. To evaluate functional parameters, electrocardiogram-gated cine images were then acquired using a segmented steady-state free precession [fast imaging with steady-state precession (true-FISP)] sequence (time to echo/time of repetition 1.6/3.2 ms, temporal resolution 35 ms, in-plane spatial resolution 1.4×1.8 mm, slice thickness 8 mm, and interslice gap 2 mm). Seven to twelve short-axis views covering the whole left and right ventricle were obtained. For the assessment of the EAT, we used a dark blood prepared T1-weighted multislice turbo spin-echo pulse sequence with a water suppression prepulse to obtain a transversal four-chamber view and short-axis images in the same orientations used for the cine short-axis images. Imaging parameters were as follows: time of repetition = 800 ms, time to echo = 24 ms, slice thickness = 6 mm, interslice gap = 2 mm, and field of view = 30-34 cm.
Late gadolinium enhancement
Late gadolinium enhancement (LGE) images in the same orientation as the cine images were acquired 10 min after the intravenous administration of a gadolinium-based contrast agent (Magnevist, Bayer-Schering Pharma AG, Berlin, Germany), using an inversion recovery Turbo FLASH 2D sequence: field of view 300-340 mm, TR 9.56 ms, TE 4.38 ms, flip angle 25°; matrix, 166 × 256, and slice thickness 6 mm. Inversion time was individually adjusted to optimally null myocardial signal (200-360 ms). In all patients, imaging was repeated for each short-axis image in two separate phase-encoding directions to exclude artifacts.
Image analysis and determination of ventricular parameters
Image analysis and quantitative analysis were performed offline using the dedicated software (ARGUS, Siemens). Each study was examined for abnormalities in the morphology of the right and left ventricle. End-diastolic (EDV) and end-systolic volumes (ESV) and LV mass were analyzed with the serial short-axis true-FISP cine loops, using manual segmentation. Stroke volumes and LV and right ventricular (RV) ejection fractions were calculated. Additionally, LV and RV diameters were measured.
For the LV ejection fraction (LVF), the most basal section was the section that at end diastole and end systole still showed a wall thickness that was compatible with the LV myocardium and that extended over at least 50% of the myocardial circumference. At end systole, the most basal section could also show a part of the LV outflow tract or the mitral valve leaflets. The most basal section could differ by one section position between end diastole and end systole (13). For the right ventricle (RV), volumes below the pulmonary valve were included. From the inflow tract, RV volumes were excluded if the surrounding muscle was thin and not trabeculated, suggestive of right atrium (14).
Additionally, the LV remodeling index (LVRI) was calculated as the ratio of LV mass (LV-EDM) to LV volume (LV-EDV) (15).
Relative wall thickness (RWT) was calculated as follows: [2 × LV posterior wall thickness/LV end-diastolic diameter (LV-EDD)] (16). A value 0.45 was defined as abnormal. An LV-EDMI >71.5 g/m2 for men and >66.6 g/m2 for women were used to define the presence of LV hypertrophy (14). According to the values of LV-EDMI and RWT, the patients were categorized into four geometric patterns: normal (normal LV-EDMI and normal RWT), concentric remodeling (normal LV-EDMI and increased RWT), eccentric LV hypertrophy (LVH) (increased LV-EDMI and normal RWT), and concentric LVH (increased LV-EDMI and increased RWT) (17).
Volumetric assessment of the absolute mass of EAT
EAT is located between the outer wall of the myocardium and the visceral layer of pericardium. Therefore, we draw one line along the myocardial border and a second one at the visceral layer of the pericardium, subtending the area of EAT between these lines (18). For EAT mass determination, the area subtended by the manual tracings was determined on consecutive end-diastolic short-axis slice beginning with the most basal slice at the level of the mitral valve and moving apically through the stack until the most inferior margin of EAT was traced (18). Total EAT volume was obtained after the data summation of all slices (EAT volume = ∑ [EAT area × (slice thickness + interslice gap) using the modified Simpson's rule (19). To obtain EAT mass, the EAT volume was multiplied by the specific weight of fat (0.92 g/cm3). The observer was blinded to patient details.
Presence of LGE
The presence of LGE was assessed visually by two independent experienced readers blinded to all patient details. LGE was only considered to be present if it was also present in the same slice after swapping phase encoding, thus excluding artifacts. Patients were divided into those with enhancement (LGE+) and those without (LGE−). The pattern of LGE was characterized as mid-wall, subendocardial extending to epicardial surface, patchy foci, epicardial, or diffuse (20, 21). For quantification of fibrosis, LGE was defined as areas with a signal intensity > 2 standard deviations (SD) above mean signal intensity of remote myocardium in the same short-axis slice (22). Areas were measured by manual planimetry and expressed as percentage of the myocardial area using the VPT tool (Siemens Healthcare Systems Erlangen, Germany).
Statistical analysis
Body mass index (BMI) was calculated by the common formula: BMI (kg/m2) = weight (kg)/height (m)2. Body surface area (BSA) was assessed by a variation of the DuBois and DuBois formula: BSA (m2) = [weight (kg)0.425 × height (cm)0.725] × 0.007184 (23). The Kolmogorow-Smirnow test was used to test for normality. The data are presented as mean ± SD for normally distributed quantitative variables and n (%) for qualitative variables. Data that are not normally distributed are given as medians and interquartile ranges. Continuous variables between two groups were analyzed by the unpaired, two-tailed student's t-test. The Mann-Whitney U test (Chi-square test) was applied for nonparametric data. A P-value <0.05 was considered statistically significant. Univariate linear regression analysis was performed to correlate the indexed EAT mass with CMR parameters in patients with DCM and in healthy controls. A multiple regression analysis adjusted for age and BMI was performed among patients with DCM to identify independent correlates of EAT.
Analysis was performed using the SPSS statistical software (version 14.0, SPSS, Chicago, Illinois).
Patient characteristics
Patients' baseline demographic and clinical characteristics are summarized in Table 1. Our patient cohort consisted of 112 patients with DCM [thereof 87 men (78%)] with a mean ± SD age of 59.4 ± 13.9 years and 48 sex- and age-matched healthy controls. There were no significant differences, regarding body weight, BSA, and BMI between patients with DCM and healthy controls. The majority of DCM patients with moderate LV dysfunction had no or only mild symptoms NYHA (New York Heart Association) class I/II 15/28 (54%), whereas 71/84 (85%) with severe dysfunction were in NYHA class III/IV. In adherence with current treatment guidelines, DCM patients with LVF ≤ 35% received significantly more ACE/ARB, diuretics, and digoxin than those with LVF >35% due to standard heart failure treatment (Table 1).
|Patients with DCM
|LVF >35% (n = 28)
|LVF ≤35% (n = 84)
|All patients with DCM (n = 112)
|Healthy controls n = 48
|Age (years)
|57.2 ± 13.4
|60.1 ± 14.0
|59.4 ± 13.9
|60.9 ± 9.8
|Male sex, n (%)
|22 (79)
|65 (77)
|87 (78)
|37 (77)
|Body weight (kg)
|82.4 ± 15.2
|82.5 ± 17.1
|82.5 ± 16.6
|81.9 ± 14.5
|BSA (m2)
|2.0 ± 0.2
|2.0 ± 0.2
|2.0 ± 0.2
|2.0 ± 0.2
|BMI (kg/m2)
|26.6 ± 4.6
|27.3 ± 4.8
|27.2 ± 4.7
|27.3 ± 6.0
|Systolic BP (mm Hg)
|111.5 ± 9.3
|108.0 ± 14.3
|108.9 ± 13.2
|124.0 ± 6.0
|Diastolic BP (mm Hg)
|74.6 ± 5.8
|71.9 ± 7.1
|72.6 ± 6.9
|80.9 ± 8.0
|Heart rate (beats/min)
|83.9 ± 9.7
|78.1 ± 17.9
|79.6 ± 16.3
|70.2 ± 11.4
|Atrial fibrillation, n (%)
|8 (29)
|28 (33)
|36 (32)
|Hypertension, n (%)
|13 (46)
|41 (49)
|54 (48)
|Diabetes, n (%)
|2 (7)
|27 (32)
|29 (32)
|Smoking, n (%)
|2 (7)
|18 (21)
|20 (18)
|Family history of DCM, n (%)
|3 (11)
|5 (6)
|8 (7)
|Time since diagnosis (years)
|2.4 ± 3.4
|4.6 ± 3.3
|4.0 ± 3.4
|NYHA functional class, n (%)
|11 (39)
|2 (2)
|13 (12)
|48 (100)
|4 (14)
|11 (13)
|15 (13)
|13 (46)
|38 (45)
|51 (46)
|33 (39)
|33 (29)
|ACEI /ATII, n (%)
|11 (39)
|69 (82)
|80 (71)
|Beta blockers, n (%)
|5 (18)
|11 (13)
|16 (14)
|Spironolactone, n (%)
|3 (11)
|24 (29)
|97 (87)
|Diuretics, n (%)
|8 (20)
|69 (82)
|77 (69)
|Angicoagulation, n (%)
|13 (46)
|56 (67)
|69 (62)
|Digoxine, n (%)
|2 (7)
|28 (33)
|30 (27)
|Amiodarone, n (%)
|2 (7)
|2 (2)
|4 (4)
|Statins, n (%)
|14 (50)
|51 (61)
|65 (58)
CMR parameters
Table 2 summarizes the CMR characteristics of all DCM patients and healthy controls. In 35 patients, no LGE study was performed due to chronic renal failure GFR < 30 ml/min/1.73 m2 (n = 20), patient's refusal of contrast agent administration (n = 8), and discontinuation of CMR examination due to dyspnea before performance of the LGE study (n = 7). Among the 77 DCM patients with a LGE study, LGE was present in 24/77 (31%) with the following regional patterns: septal midwall 13/24 (54%), subendocardial extending to the epicardial surface 3/24 (12.5%), patchy foci 7/24 (29.3%), epicardial 1/24 (4.2%), and diffuse 0/24. Among patients with LGE, the median extent of fibrosis was 8.3% of LV mass (range 5.6-11.5 %). The presence of LGE and the extent of LGE % were not significantly different in patients with moderate [3/21 (14%), 4.8% (2.8-6.9 %)] and severe LV dysfunction [21/56 (38%), P = 0.09, 8.3% (6.9-12.5 %), P = 0.2)]. However, the EAT mass in DCM patients with LGE was slightly but not statistically significant higher compared to those without LGE (26.4 ± 8.8 g/m2 vs. 23.3 ± 8.1 g/m2, P = 0.1). Compared to healthy controls, the EAT mass was significantly reduced in all patients with DCM (31.7 ± 5.6 g/m2 vs. 24.0 ± 7.5 g/m2, P < 0.0001) as well as in the subgroup analysis of DCM patients with moderate DCM (31.7 ± 5.6 g/m2 vs. 23.5 ± 9.8 g/m2, P < 0.0001) and severe LVF impairment (31.7 ± 5.6 g/m2 vs. 24.2 ± 6.6 g/m2, P < 0.0001). Although functional and volumetric parameters revealed an association with the degree of LV dysfunction, the EAT mass did not differ between DCM patients with moderate and severe LV dysfunction (23.5 ± 9.8 g/m2 vs. 24.2 ± 6.6 g/m2, P = 0.7).
|Patients with DCM
|LVF >35% (n = 28)
|LVF ≤35% (n = 84)
|All patients with DCM (n = 112)
|Healthy controls n = 48
|43.6 ± 6.9
|23.0 ± 6.7
|28.2 ± 11.2
|58.7 ± 5.2
|LV-EDMI (g/m2)
|84.2 ± 26.9
|110.3 ± 8.2
|104.1 ± 29.7
|65.1 ± 11.4
|LV-EDVI (ml/m2)
|102.8 ± 34.2
|156.9 ± 44.9
|143.9 ± 48.5
|73.7 ± 14.7
|LV-ESVI (ml/m2)
|58.1 ± 17.4
|122.9 ± 40.4
|107.2 ± 45.7
|30.5 ± 8.0
|LV-SVI (ml/m2)
|48.3 ± 18.4
|35.2 ± 11.2
|38.5 ± 14.5
|42.8 ± 9.5
|CI (l/min/m2)
|2.9 ± 0.8
|2.7 ± 1.0
|2.7 ± 0.9
|2.9 ± 0.6
|LV-EDD (mm)
|63.6 ± 7.4
|70.5 ± 7.7
|68.8 ± 8.2
|50.8 ± 5.4
|LVRI (g/ml)
|0.8 ± 0.2
|0.7 ± 0.2
|0.7 ± 0.2
|0.9 ± 0.2
|RV-EDD (ml)
|46.6 ± 6.2
|43.5 ± 8.1
|44.3 ± 7.7
|43.2 ± 5.6
|RAD (mm)
|48.6 ± 8.9
|48.4 ± 8.1
|48.4 ± 8.3
|43.8 ± 5.9
|49.1 ± 11.8
|31.9 ± 16.8
|36.2 ± 17.4
|56.4 ± 6.3
|RV-EDVI (ml/m2)
|85.4 ± 13.2
|110.8 ± 41.1
|104.4 ± 37.8
|85.1 ± 9.4
|RV-ESVI (ml/m2)
|40.6 ± 15.9
|78.3 ± 44.4
|68.9 ± 42.5
|40.8 ± 11.7
|RV-SVI (ml/m2)
|44.5 ± 9.7
|34.6 ± 10.5
|37.1 ± 11.2
|42.5 ± 5.9
|Presence of LGE
|3/21 (14%)
|21/56 (38%)
|24/77 (31%)
|% LGE Extent
|4.8% (2.8–6.9 %)
|8.3% (6.9–12.5 %)
|8.3% (5.6–11.5 %)
|EAT volume (ml)
|50.0 ± 21.9
|50.2 ± 13.9
|50.2 ± 16.2
|66.0 ± 15.3
|indexed EAT volume (ml/m2)
|25.0 ± 10.4
|25.7 ± 7.0
|25.5 ± 8.0
|33.5 ± 6.4
|EAT mass (g)
|47.0 ± 20.6
|47.2 ± 13.1
|47.2 ± 15.2
|62.1 ± 14.4
|indexed EAT mass (g/m2)
|23.5 ± 9.8
|24.2 ± 6.6
|24.0 ± 7.5
|31.7 ± 5.6
|EAT/LV mass ratio
|0.3 ± 0.1
|0.23 ± 0.1
|0.24 ± 0.1
|0.5 ± 0.1
|EAT/LV volume ratio
|0.3 ± 0.5
|0.16 ± 0.1
|0.20 ± 0.3
|0.45 ± 0.1
Correlation between EAT mass and parameters of LV remodeling
In DCM patients, the EAT mass /LV mass ratio as well as the EAT mass /LV volume ratio were significantly reduced compared to healthy controls, and the reduction was most pronounced in patients with severe LV dysfunction (Table 2, Figure 1). According to the values of LV-EDMI and RWT, 13 of the 112 patients with DCM (11.6%) showed a non-hypertrophied geometric pattern. The other 99/112 (88.4%) showed eccentric LV hypertrophy (LVH) with increased LV-EDMI and normal RWT. 47/99, (47.5%) of DCM patients with an eccentric LVH had concomitant arterial hypertension. Looking at the EAT mass in the patients with eccentric LVH, we found that it was significantly elevated compared to the DCM patients without LVH (24.4 ± 7.1 g/m2 vs. 18.5 ± 6.4 g/m2, P = 0.01), however, significantly less than that in healthy controls (24.4 ± 7.1 g/m2 vs. 31.7 ± 5.6 g/m2, P < 0.0001). Compared to the EAT mass in the 54/112 DCM patients with arterial hypertension and the 58/122 DCM patients without arterial hypertension, we did not find a difference (24.0 ± 6.8 vs. 24.0 ± 8.1, P = 0.97).
Association between the indexed EAT and CMR parameter
By univariate regression analysis (Table 3), increasing indexed EAT mass in all 112 patients with DCM correlated with increasing LV end-diastolic mass index (LV-EDMI) (P < 0.0001), increasing LV end-diastolic volume index (LV-EDVI) (P = 0.01), increasing LV end-systolic volume index (LV-ESVI) (P = 0.01), increasing LV end-diastolic diameter (LV-EDD) (P = 0.02) as illustrated in Figure 2. Among these parameters, multiple regression analysis adjusted for age and BMI revealed that LV-EDMI (P = 0.001) was the only independent correlate with EAT. Besides, male DCM patients showed more indexed EAT mass than women (P = 0.04). However, no correlation was found between indexed EAT mass and LVF (P = 0.37), LVRI (P = 0.2), RV-EDD (P = 0.3), RVF (P = 0.6), RV-EDVI (P = 0.05), RV-ESVI (P = 0.1), or presence of LGE (P = 0.1).
|All patients with DCM (n = 112)
|Healthy controls (n = 48)
|Age (years)
|Male Sex
|BMI (kg/m2)
|LV-EDMI (g/m2)
|LV-EDVI (ml/m2)
|LV-ESVI (ml/m2)
|LV-SVI (ml/m2)
|CI (l/min/m2)
|LV-EDD (mm)
|LVRI (g/ml)
|RV-EDVI (ml/m2)
|RV-ESVI (ml/m2)
|RV-EDD (ml)
|RAD (mm)
|Presence of LGEa
|LGEa extent %
In the healthy controls, increasing EAT was significantly correlated with increasing age (P = 0.001), increasing BMI (P = 0.003), and increasing LV-EDMI (P = 0.02) as shown in Figure 3.
The main findings of the study are as follows: (1) in patients with DCM, the amount of EAT is significantly reduced compared to healthy controls; (2) in patients with DCM, LV remodeling reflected by an increase in LV diameter, volumes, and mass significantly correlates with the EAT mass; and (3) the EAT amount in patients with DCM is irrespective of the LV function impairment.
EAT is a metabolically active tissue and a source of various bioactive molecules (4, 6, 24). Due to its close anatomic relationship to the adjacent myocardium, it is suggested to affect and modulate cardiac function and morphology (24–26). Both unfavorable and protective effects have been attributed to EAT (27, 28). In patients with CAD, the amount of EAT has shown to be significantly correlated with the extent and the severity of CAD (7, 29–31). However, little is known about the role of EAT in patients with DCM. In previous studies of our group (9, 10), we compared patients with HF and severely reduced LVF (<35%) due to ICM or DCM and healthy controls. We could show that in patients with HF, EAT mass was significantly reduced, compared to healthy controls. This reduction was irrespective of the underlying etiology of HF. However, in this study, we only included patients with severely LVF impairment.
In the present study, we investigated the association between the amount of EAT and CMR parameters of ventricular remodeling solely in patients with DCM and different degrees of LV function impairment compared to age-matched controls. All patients with DCM irrespective of LV function impairment showed significantly increased LV mass, volume, and dimensions, compared to healthy controls.
Patients with DCM revealed significantly decreased EAT mass compared to healthy controls. There was a significant correlation between EAT mass and LV volume, LV diameter, and LV mass in patients with DCM. However, the EAT mass did not correlate with the degree of LV function impairment. Previous studies (32, 33) have shown that the development of LVH appears to have protective and beneficial effects in patients with DCM by reducing systemic wall stress and protecting against further dilatation of the LV. In our study cohort, patients with eccentric LVH showed significantly elevated EAT mass compared to DCM patients without LVH. However, compared to healthy controls, the EAT mass was less even in patients with LVH. The fact that the EAT mass in patients with DCM was unaffected of the presence of arterial hypertension makes a direct influence of arterial hypertension on the EAT mass unlikely. Nevertheless, whether the increased EAT mass is solely explained by the increase of EAT in line with the increase in LV mass as discussed in previous studies (34, 35) cannot be distinguished.
Since the presence of LGE has a prognostic implication in patients with DCM (22, 36), we analyzed the presence of LGE with regard to EAT mass. In our study cohort, 24/77 (31%) exhibited LGE. In the DCM patients with LGE, the EAT mass was slightly but not statistically significant higher compared to those without LGE. However, due to the small number of patients in the subgroup analysis, our study might be underpowered for this analysis.
Interestingly, EAT mass did not correlate with the degree of LV function impairment. Subgroup analysis in DCM patients according to LV function showed an indexed EAT mass of 24.2 ± 6.6 g/m2 in the 84 DCM patients with severely reduced LVF (≤35%). This result was comparable to the previously reported EAT mass in these patients (9, 10). In the 28 DCM patients with only moderate LV dysfunction (LVF >35%), indexed EAT mass was equally diminished (23.5 ± 9.8 g/m2). In addition to that, linear regression analysis revealed no correlation between EAT mass and LV function impairment. In this context, Khawaja et al. (11) using cardiac CT examined the relation of EAT volume in patients with normal and impaired LV function referred to myocardial perfusion scanning for assessment of CAD. The patients with normal LVF served as a control group. Heart failure was defined by LVF <55%. Similarly to our findings, a significantly reduced EAT volume was found in patients with reduced LVF (LVF <55%) compared to patients with normal LVF. However, in the subgroup analysis, EAT volume showed a statistically significant stepwise decrease in EAT volume in the moderate heart failure (EF 35-55%), which decreased further in the severe heart failure group (EF <35%). Thus, contrary to our findings, the results by Khawaja et al. (11) indicate a correlation of smaller EAT volumes with the degree of LVF impairment. These discrepant results are due to the difference in the examined study population and control group. In the present study, the cohort consisted solely of patients with DCM, and only healthy subjects served as a control group. Whereas the study population and the controls of Khawaja et al. (11) were heterogeneous and included mainly patients with HF due to ischemic cardiomyopathy (ICM). Since patients with ICM and DCM show a different course of LV remodeling, one could assume that the relation of EAT amount and the LVF is yet not irrespective of the underlying etiology. In patients with heart failure, severely reduced LVF (<35%) and significant LV cavity dilation, representing the end stage of the disease course, the amount of EAT seems to be reduced irrespective of the underlying etiology as we already showed (9, 10). However, we suspect that this does not hold true for the whole spectrum of LV function impairment.
We found that in patients with DCM, the amount of EAT is significantly reduced compared to healthy controls irrespective of the LV function impairment. LV remodeling coming along with an increase in LV diameter and volumes as well as LV mass seems to play a major role in the EAT changes in patients with DCM.
We speculate that with increasing LV dilatation, there is a suppression of EAT. The decrease of the EAT mass coming along with LV remodeling may result in a discontinuation of its protective effects on the heart. This may contribute in an undernourishment of the adjacent myocytes, especially under conditions of special energy demand inducing a vicious circle with a further progressive EAT reduction.
Although our DCM patients with severely impaired LVF ≤ 35% received, due to standard heart failure treatment, significantly more ACE/ARB, diuretics, and digoxin than those with LVF >35%, we do not believe that the medication has a direct effect on EAT. This assumption is supported by the fact that the EAT mass 24.2 ± 6.6 g/m2 in the 84 patients with severely reduced LVF (≤35%) was comparable to those in the 28 patients with only moderate (LVF>35) 23.5 ± 9.8 g/m2. However, we believe that medication has an indirect effect on EAT in patients with DCM. Since in patients with DCM, EAT mass showed a significant correlation with LV volume, LV diameter, and LV mass, medications influencing cardiac remodeling consequently may also have an indirect effect on EAT.
Larger study cohorts with homogeneous study populations are needed to further prove the potential different interactions between LVF and EAT in different causes of HF.
Study limitations
The diagnosis of DCM was based solely on clinical history and examination accompanied by echocardiography and normal findings at CA. In line with the current guidelines (37), none of the patients underwent myocardial biopsy for the diagnosis of DCM, since myocardial biopsy is limited by the possibility of false-negative results and is associated with a significant clinical risk (38, 39).
To date, there is no accepted method for the calculation of EAT with either CT or CMR. Magnetic resonance imaging is recognized as the "gold standard" modality for imaging adipose tissue (18, 40, 41). However, CMR has only recently evolved to assess adiposity around the heart (19). In a previous study of our group, we introduced a new volumetric method for the assessment of EAT (19), tracing the EAT from the level of the mitral valve to its most inferior margin. However, this methodology hasn't been verified against actual measurement of ex vivo mass. In the study by Nelson et al. (18), this method was applied to measure the paracardial adipose tissue with CMR and to correlate these results with ex vivo paracardial adipose tissue mass in 11 merino sheep. The authors could show that the CMR-derived paracardial adipose tissue accurately reflected ex vivo paracardial adipose tissue mass. One could assume that these results also hold true for EAT measurements.
Furthermore, using this approach, we do not include EAT surrounding the atria and the whole perivascular EAT amount. However, it is known that only minor foci of EAT are found around the atria, and therefore, their contribution to total EAT is known to be minor (24).
This is the first study to evaluate the association between the amount of EAT and CMR parameters of ventricular remodeling in patients with different degrees of LV function impairment compared to age-matched controls. We found that in patients with DCM the amount of EAT is significantly reduced compared to healthy controls irrespective of the LV function impairment. LV remodeling coming along with an increase in LV diameter and volumes as well as LV mass seems to play a major role in the EAT changes in patients with DCM.
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- 5Increased subcutaneous and epicardial adipose tissue production of proinflammatory cytokines in cardiac surgery patients: possible role in postoperative insulin resistance. J Clin Endocrinol Metab 2006; 91: 4620–4627., , , et al.
- 6Human epicardial adipose tissue is a source of inflammatory mediators. Circulation 2003; 108: 2460–2466., , , et al.
- 7Epicardial adipose tissue and coronary artery plaque characteristics. Atherosclerosis 2010; 210: 150–154., , , et al.
- 8Adipose tissue and atherosclerosis: exploring the connection. Arterioscler Thromb Vasc Biol 2007; 27: 996–1003., .
- 9Epicardial adipose tissue in patients with heart failure. J Cardiovasc Magn Reson 2010; 12: 40., , , et al.
- 10Bioimpedance analysis parameters and epicardial adipose tissue assessed by cardiac magnetic resonance imaging in patients with heart failure. Obesity (Silver Spring) 2010; 18: 2326–2332., , , et al.
- 11Epicardial fat volume in patients with left ventricular systolic dysfunction. Am J Cardiol 2011; 108: 397–401., , , et al.
- 12Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies. Circulation 1996; 93: 841–42., , , et al.
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- 21Late gadolinium enhancement by cardiovascular magnetic resonance heralds an adverse prognosis in nonischemic cardiomyopathy. J Am Coll Cardiol 2008; 51: 2414–2421., , , et al.
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- 29Relationship of epicardial adipose tissue by echocardiography to coronary artery disease. Heart 2008; 94: e7., , , et al.
- 30Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease. Nutr Metab Cardiovasc Dis 2009; 19: 211–217., , , et al.
- 31Relation of epicardial and pericoronary fat to coronary atherosclerosis and coronary artery calcium in patients undergoing coronary angiography. Am J Cardiol 2008; 102: 380–385., , , et al.
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subset: commoncrawl


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Forum - View topicNEWS: Funimation to Stream Dragon Ball Z in North America
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Daimao Raki
Posts: 591
Location: Dark Side of the Moon
|Do they mean Kai?
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Posts: 182
Nope, sounds like they mean DBZ.
Is this hinting at possible streaming for all the other series in the future do you think?
Too bad its also not open to the UK, oh well....
Last edited by Takuku on Mon Jan 03, 2011 11:49 am; edited 1 time in total
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Daimao Raki
Posts: 591
Location: Dark Side of the Moon
|Well I wonder what took them so long.
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Posts: 1356
Location: Wallington, NJ
|You might want to change the title of the article since Hulu's hosting the streams.
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Posts: 36
Location: Boston
This might not have much effect on most of us, but when you consider DBZ has been one of Funi's biggest cash cows for a very long time, and now they're finally going to give it out for free, it is a fairly significant announcement. At the very least, I presume DBZ will end up being very popular on Hulu, which might help attract attention to Funi's other titles up for streaming.
This one's more for the non-anime fans, I'd say.
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Posts: 48
Location: under your porch
|I sincerely hope that they're not going to air DBZ in that "chopscreen" job from the orange box sets, but I'm guessing that's what they might do.
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Posts: 490
Thanks but no thanks, give me Kai instead. I don't get why GT would get so much exposure because that was more or less a failure.
But whatever you do, do NOT give me Evolution, that was doomed from the start.
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Posts: 831
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Posts: 80
|took long enough and damn in america too >_> good thing i got the box sets
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Posts: 1291
Location: Winnipeg, Manitoba
|More exposure to the franchise is always a good thing. Can't wait to watch.
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Posts: 441
Location: Too Far South
|Nice to hear, but I'll continue my rewatching of the series through Kai. That is, if Nicktoons ever gets episode 49 working on their site.
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Posts: 13754
|Meh, DBZ's been done to death. I'd rather have Toupee stream me some Go Nagai already.
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Posts: 6547
Location: Maine
They were giving it away for free for over a decade on TV, now they're giving Kai away for free on TV. All this does is change where they're offering it, it's still ad supported.
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Mr. sickVisionz
Posts: 1650
|I wish it was a Kai simulcast or even delayed a week or two.
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Business New Europe: Conference to highlight Ukraine's press freedom shortcomings
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The Kyiv Post is hosting comments to foster lively public debate through the Disqus system. Criticism is fine, but stick to the issues. Comments that include profanity or personal attacks will be removed from the site. The Kyiv Post will ban flagrant violators. If you think that a comment or commentator should be banned, please flag the offending material.comments powered by Disqus


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- Miss Florida 2017 stripped of crown days after win - US Weekly
- Lindsay Lohan steps out amid relationship drama - TMZ
- Was Taylor Swift snubbed by the VMAs? - Gossip Cop
- Rachel Platten sings "Fight Song" with lots of stars - Just Jared Jr
- Farrah Abraham sizzles in a revealing bikini - Radar
- New pics from the Clooneys' Italian summer - Lainey Gossip
- Fox News snubs major DNC moment - The Hollywood Reporter
06 October 2012 at 4:54 PM
Mila Kunis: Topless 'Esquire' Magazine Cover
About this photo set: Mila Kunis bares her back while appearing topless for the November 2012 issue of Esquire magazine. Here's what the 29-year-old actress had to share with the… Read More Here
Photo #: 2734024
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The Top Ten Stocks for Tuesday, March 26
March 26 (Bloomberg) -- Bloomberg's Betty Liu, Dominic Chu and Julie Hyman report on today's ten most important stocks including Yahoo, Intel and Boeing. They speak on Bloomberg Television's "In The Loop." (Source: Bloomberg)
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Solar Impulse 2 Completes Global Epic Journey
40:45 - Solar Impulse 2 has made history, completing the first around the world flight using only the power of the sun. Bloomberg's Desley Humphrey reports on "Daybreak Asia." (Source: Bloomberg)


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Best gamepad for pc?
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text:
Dean Baker: The quest for "credibility" can have very bad outcomes, as we saw in Vietnam. It's hard to see how we gain credibility by pushing a bad trade deal.
The DNC's Rules Committee repeatedly rejected a series of reforms to its "superdelegate" system, despite the pleas of Sanders delegates.
Erik Forman has been active in the Industrial Workers of the World since 2005, working and organizing at Starbucks and Jimmy John's. He is currently compiling a report on union strategies for organizing the food service and retail sectors as a Practitioner Fellow at the Kalmanovitz Initiative for Labor and the Working Poor at Georgetown University.


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- Sharing a must in business Read More
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CHARLOTTE AMALIE - At least three people are missing and one person was dead after a small plane that was delivering newspapers crashed today in the US Virgin Islands, officials said.The Piper PA-23-250 plane went down just eight miles south of the airport in St Thomas, said Jose Nazario, airport manager for the island's Port Authority.The plane had been delivering newspapers to the island of St Croix and was returning to St Thomas after picking up a couple of passengers, said David Mapp, interim Port Authority executive director.He said rescue crews are still trying to recover more bodies. Among the dead is the pilot, identified as Kirby Hodge, Nazario said.It is unclear what led to the crash.The plane's certification status had been terminated, according to records with the U.S Federal Aviation Administration. (AP)


text:
C.J. Wilson is done after a strong outing against the Red Sox.
Wilson struck out the first two hitters in the bottom of the seventh and went to a full count before walking Daniel Nava. That was it for Wilson, who left after throwing 113 pitches with 10 strikeouts in 6 2/3 innings. He was a little wild with five walks, but the lefty held the Red Sox to just three hits and one run in a bid for his eighth win of the season.
Darren O'Day relieved and walked pinch hitter J.D. Drew before getting Marco Scutaro to pop out to Julio Borbon in shallow center. The Rangers lead, 3-1, through seven innings.


text:
Seven amusing and shocking things we learned during the equal marriage debate
Post your comment
Comments on this article are now closed.
Reader comments
I thought that every so handsome sexy Nick Herbert's comment about Chris and John's ties was hilarious, certainly not mean-spirited. Arguably, I think Nick's two speeches on Monday was the best I've heard in the entire debate. Margot James facial expression was priceless.
Erm……………….. ABBA… Ties.. yep all major contributing factors… Least there were comic moment but don't call us…
Although Margo face is a picture!! lol
That Burrowes creature to a school girl… seriously… do we need to say any more? Though it IS his job to explain… sore loser me thinks.
wow. who says politicians are out-of-date!? anyone with an ounce of intelligence would body-swerve easy rhyming couplets sang in pidgen english with facile harmonies and mushy over-production. gay dial-a-cliche crap!
To be fair to Gerald Howarth, we do see marriage equality as a stepping stone to something further – its a stepping stone to full equality!
I was pulling a similar face to Margot throughout the equality debate. I just couldn't believe how stupid and openly bigoted so many MP's were. Shocking.
Parliament broadcasts live video on the internet, so I was able to watch the entire debate. The opponents said many things that were repulsive to put it mildly. The people you mention seemed to go out of their way to be offensive to gays and people who support them. The supporters didn't do this, but then it is always harder to be a loser especially if you think God will punish you.
This reminds me of the DUP, the party whose leader Ian Paisley was on one occasion kicked out of the European Parliament for calling the Pope the Anti-Christ and refusing to be silent. Several members of this party feel that God will judge anyone who supports gay equality. Hopefully people taking part in the debate in the House of Lords will remember the way the antis behaved during this debate and act accordingly.
"Touche Mr Burrowes, touche."
Surely you meant to write "douche"?
Now that Lord Tebbitt has declared himself to be one of us, perhaps we should honour him with the title "Normal Norman."
Daniel Kawczynski could take a chance on me any day of the week. Arguably the hunkiest MP ever. How lucky his boyfriend is.
John Bercow in my view tied his tie a bit better than Chris Bryant.
These comments are un-moderated and do not necessarily represent the views of PinkNews. If you believe that a comment is inappropriate or libellous, please contact us.
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July 24, 2016
Let joshua get his early leave this December without delay or incident or problem or snare or evil in Jesus Name, we pray, Amen.
July 23, 2016
Let complete love, trust, truth, passion, romance, strength, desire & commitment always flow freely between JJ & Sarah, without any kinds of blocks, whether they be people or things,etc, in Jesus Name, & I bind and remove & block the liar & thief from them and their relationship together, now & all of the time, in Jesus Name, we pray, Amen.
July 23, 2016
Please pray for my return to The LORD. My life, body, soul, mind, and spirit are ruined. Please pray for The LORD to fix me and to heal my backsliding and restore me unto Himself. Please pray for my deliverance from the devil and for my repentance toward God and faith toward The Lord Jesus Christ.
July 22, 2016
I ask for prayer for our granddaughter who is having to be taken early. I ask for prayer for a frind who is having marriage issues. I ask for a financial breakthrough . I also pray my financial aid gets worked out in time for fall classes. I pray for a new car . I ask prayer for all the officer s who lost there lives for being good and trying to do the right thing. God I prayer for a miracle.
July 22, 2016
With angels and the Holy Spirit's teachings and protection and may I be ministered as I sleep. May God cleanse me and renew me in my sleep, speak to me through dreams. May this rental of many years continue to be secure and any attempt of new owners to remove for no reason be broken. God knows the details to that.


text:
Conductive Keratoplasty Hyperopia and Presbyopia Treatment & Management
- Author: Manolette R Roque, MD, MBA, FPAO; Chief Editor: Hampton Roy, Sr, MD more...
Medical Therapy
Medical therapy is limited to broad-spectrum topical antibiotics and corticosteroids for uncomplicated cases (see Postoperative details).
Surgical Therapy
See Intraoperative details for the surgical procedure.
Preoperative Details
The procedure for CK can be performed with a local (topical) anesthetic in the form of eye drops to numb the eye. Patients who are nervous and/or have a high level of anxiety may be given a mild sedative to assist them in relaxing for the procedure.
The operative field is prepared, and the patient is prepared in the usual sterile fashion for ophthalmic surgery. A lid speculum, as shown below, is used for globe exposure.
This procedure may be performed inside the clinic.
Intraoperative Details
After appropriately preparing the patient, a lid speculum is used to hold open the eye during the CK procedure; it also serves as a return path for the radiofrequency energy applied via the instrument. CK is performed using a pen-shaped instrument to apply controlled radiofrequency energy in a ring pattern on the cornea. In performing CK, the conductive tip should be placed perpendicularly to the corneal surface prior to activation. This placement of the conductive tip ensures appropriate application of the conduction marks. The procedure is considered painless and typically requires only a few minutes (approximately 5 min) to perform. See the images below.
LightTouch technique
LightTouch is a corneal compression technique in which surgeons should apply minimal pressure to the cornea. The application of the tip is similar to the initial procedure identified above, except that after the tip is completely implanted into the cornea, it is retracted slightly until there is minimal to no indentation of the cornea, followed by application of the radiofrequency energy. See the images below.
Postoperative Details
Following the procedure, the lid speculum is removed. Postoperatively, antibiotic-corticosteroid combination drops and/or ointment are used. Antibiotic-corticosteroid combination drops are used 4 times daily for 1 week. The eye may be covered overnight with a shield.
Certain precautions should be taken following the CK procedure and are similar to those that are required with any other type of vision procedure where the cornea is altered.
Patients should take the following precautions for at least 1 week after surgery:
Avoid getting contaminated water (eg, fountains, swimming pools, spas, lakes, ocean, rivers) in the eyes.
Keep the eyes closed while showering or taking baths to avoid getting soap and dirty water into them.
When exercising, keep sweat out of the eyes.
For females, avoid applying eye makeup.
Patients should avoid vigorously rubbing the eyes for 2 weeks after the surgical procedure.
Patients are seen postoperatively on day 1; week 1; and months 1, 3, 6, and 12. Vision begins to improve within a week's time. The surgeon should monitor patients for postoperative complications; an observation timeline is outlined in Complications.
For patient education resources, see the Eye and Vision Center, as well as Vision Correction Surgery and Contact Lenses.
See the list below:
Preservation of best spectacle corrected visual acuity (BSCVA) [32, 33, 34]
- Loss of greater than 2 lines BSCVA in less than 5% of eyes
- Decrease from 20/20 preoperative to worse than 20/40 postoperative in less than 1% of eyes
Induced cylinder [35]
- Induced cylinder greater than 2.00 D in 5% of eyes (< 1% of eyes per draft ANSI guidance)
- Induced cylinder greater than 1.00 D reported in labeling for all comparable products for hyperopia treatment
- Induced cylinder greater than or equal to 1.00 D reported at request of FDA
- Effect of induced cylinder and axis shift on UCVA eyes treated with current nomogram
- Approximately 1 line impact on mean UCVA at 12 months in the following:
- Eyes with greater than 1.00 D and greater than or equal to 1.00 D induced cylinder
- Eyes with greater than 1.00 D and greater than or equal to 1.00 D induced vector cylinder
- Eyes with greater than 0.75 induced cylinder and 30° axis shift
- Correcting for residual sphere using regression models, difference in UCVA not statistically significant (P=0.82)
Induced cylinder summary
- Meets FDA safety guideline (< 5%, < 1% proposed)
- Frequency and magnitude diminish over time.
- No effect on BSCVA
- When induced cylinder is present, UCVA is affected by approximately 1 line at 6 months and improves over time as induced cylinder resolves.
- level of persistent induced cylinder is low (>1.00 D is 6.4% at 12 mo)
Endothelial cells
- Endothelial cell loss is no more than 10%.
- No change (within ±1%) in endothelial cell density over the course of follow-up in any region (central, midperipheral, and peripheral cornea)
- No polymegathism or polymorphism
- Radiofrequency energy can be safely delivered to the cornea with no effect on the endothelium.
Patient symptoms
- Increase of greater than or equal to 5% in moderate-to-severe symptoms
- Subjective questionnaire was administered at baseline and at 1, 3, 6, 9, and 12 months. Patients were asked to rate the following symptoms as none, mild, moderate, marked, or very severe: light sensitivity, headaches, pain, redness, dryness, excessive tearing, burning, foreign body sensation, glare, halos, blurred vision, double vision, fluctuation of vision, variations of vision with change in lighting, and night driving vision problems.
- Symptoms with greater than or equal to 5% increase from baseline in moderate, marked, or very severe, at months 6, 9, and 12, included dryness, glare, halos, double vision, fluctuation of vision, and variations of vision with change in lighting.
Complications and adverse events [32, 36]
- Adverse events to occur in no more than 5% of eyes; any single adverse event to occur in less than 1% of eyes
- Recurrent corneal erosions in both eyes of 1 patient (< 1%), resolved by 3 months
- Foreign body sensation in 1 eye of 1 patient (< 1%), reported at 9 months and resolved by 12 months
- Pain in both eyes of 1 patient (< 1%), reported at 3 months and resolved by 6 months
- Double/ghost images in 13 eyes of 9 patients (3%), complaint resolved in most eyes (10 out of 13 eyes)
- Keratitis and corneal melting occurred in a single case report of conductive keratoplasty enhancement.[37]
- Keratitis and corneal melt associated with nonsteroidal antiinflammatory topical medications occurred in a post-CK patient.[38]
- Other complications occurring at a rate of less than 1% include blepharitis, external hordeolum, viral conjunctivitis, allergic conjunctivitis, bacterial conjunctivitis, meibomianitis, subconjunctival hemorrhage, central striae, central stromal defects, lash loss, ecchymosis, blurry vision, starbursts, headaches, film over eye, glare, halos, and light sensitivity.[39]
Adverse events related to device/procedure
- Corneal perforation in 1 eye of 1 patient (< 1%)[40, 41]
- Resulted from detachment of Teflon stop
- Healed uneventfully; CK procedure successfully completed 2 weeks later
- Preoperative - UCVA 20/40, mean refractive spherical equivalent (MRSE) +2.00 D
- 12-month outcome - UCVA 20/16, MRSE 0.0 D
- Corrective actions implemented
- No radiofrequency energy delivered during treatment in 2 eyes of 2 patients (< 1%)
- Resulted from poor solder joint
- One eye successfully treated 3 weeks later
- Preoperative - UCVA 20/200, MRSE +2.00 D
- Twelve-month outcome - UCVA 20/32, MRSE +0.50 D
- Second eye determined to be ineligible because of previously undetected narrow angles
- Corrective action validated, implemented, and reviewed by FDA
- Corneal perforation in 1 eye of 1 patient (< 1%)[40, 41]
IOP greater than 25 mm Hg in 3 eyes of 2 patients (< 1%) [42]
- One eye of 1 patient had baseline IOP of 25 mm Hg and ineligible for enrollment
- Two eyes of 1 patient had increased IOP that resolved without treatment or sequelae
Mild iritis in 1 eye of 1 patient at 7 days (< 1%), resolved without sequelae [43]
Decrease of BSCVA of greater than 2 lines, inferior altitudinal hemianopsia, and optic atrophy secondary to spinal surgery in 1 eye of 1 patient
Retinal break in 1 eye of 1 patient
- Occurred 18 months after CK procedure
- Successfully treated with argon laser
Nonophthalmic events included terminal cancer, heart attack, breast cancer, temporal arteritis, hospitalization for tonsillectomy, and nasal septum repair.
Maloney reported that out of 50 cases of CK, no single patient complained of dryness or haziness. [32, 36]
Outcome and Prognosis
In 2001, McDonald and Maloney presented the interim results of the FDA Phase III clinical trial during the American Society of Cataract and Refractive Surgery (ASCRS) meeting in San Diego. Maloney reported that at 9-month follow-up, the UCVA was found to be 20/20 or better in 60% of the eyes treated and 20/40 or better in 96% of the eyes treated. In addition, 60% of the eyes were within 0.5 D of planned correction, whereas 80% of the eyes were within 1 D of planned correction. Maloney reported the absence of adverse events or complications after 9 months. McDonald reported that at 12-month follow-up, the UCVA was found to be 20/20 for 51% of the eyes treated, 20/25 for 73% of the eyes treated, and 20/40 or better for 91% of the eyes treated.[18, 44, 45, 19, 34, 36, 15, 46, 47, 48, 49, 50, 51, 52]
Presentation of results
- Effectiveness was reported for eyes treated with current nomogram.
- Safety and stability were reported for all eyes treated.
Effectiveness parameters [53]
- Improvement in UCVA
- UCVA 20/40 or better in greater than or equal to 85% of the eyes with preoperative BSCVA 20/20 or better
- Postoperative UCVA equal to or better than preoperative BSCVA for 32% of the eyes
- Postoperative UCVA within 1 line of preoperative BSCVA for 63% of the eyes
- Predictability
- MRSE within ±0.50 D for 50% of the eyes
- MRSE within ±1.00 D for 75% of the eyes
- Stability[54]
- Patient satisfaction
- Improvement in UCVA
In 2004, McDonald, Durrie, Asbell, et al, published the 6-month results of a 1-year clinical trial evaluating CK for the treatment of presbyopic symptoms in emmetropic and hyperopic eyes.[19]
Presentation of results
- Of the eyes treated for near, 77% had uncorrected near vision of J3 or better at 6 months postoperatively.
- A total of 85% of all patients had binocular distance UCVA of 20/25 or better along with J3 or better near, a combination that represents functional acuity for a presbyope.
- Of eyes treated for near, 66% had the MRSE within ±0.50 D of intended at 6 months.
- In 89% of eyes, the MRSE changed 0.05 D or less between 3 and 6 months postoperatively. After month 1, the incidence of variables associated with safety was 1% or lower.
- Of patients treated, 76% were very satisfied or satisfied with their procedure.
Patients with previous LASIK or PRK showed a greater treatment response to CK but regressed at a similar rate as those eyes without prior LASIK or PRK. Overall, CK is a safe procedure that inevitably regresses. [55, 56, 57]
Future and Controversies
Conductive keratoplasty is demonstrated to be safe for the treatment of presbyopia in post-LASIK patients as well as in non-LASIK patients, although longer observation in terms of factors affecting predictability is suggested. It is understood that LASIK affects the biomechanical properties and strength of the cornea, and this may be the reason for the lesser, albeit statistically insignificant, predictability.[58]
Topography-guided conductive keratoplasty may be effective in reshaping corneal configuration in eyes with keratoconus. Although the reported follow-up time is short, it theoretically may avoid or delay corneal transplantation in some cases.[59, 60]
Studies have been conducted for the safe application of conductive keratoplasty for astigmatism.[35, 61, 62, 63] Other surgical methods for the correction of hyperopia include phakic intraocular lenses (implantable contact lenses). Bifocal intraocular lenses and scleral-relaxing incision with collagen plug implantation are among the other surgical methods for the correction of presbyopia.
Duffey RJ, Leaming D. US trends in refractive surgery: 2003 ISRS/AAO survey. J Refract Surg. 2005 Jan-Feb. 21(1):87-91. [Medline].
Duffey RJ, Leaming D. US trends in refractive surgery: 2002 ISRS survey. J Refract Surg. 2003 May-Jun. 19(3):357-63. [Medline].
Duffey RJ, Leaming D. U.S. trends in refractive surgery: 2001 International Society of Refractive Surgery Survey. J Refract Surg. 2002 Mar-Apr. 18(2):185-8. [Medline].
Ocular Surgery News. Laser market provides valuable options for low levels of hyperopiaRegression may be a thing of the past as developments continue in laser and laser-like procedures for hyperopia. 2001. Available at: http://www.osnsupersite.com/. [Full Text].
Waring GO 4th, Durrie DS. Emerging trends for procedure selection in contemporary refractive surgery: consecutive review of 200 cases from a single center. J Refract Surg. 2008 Apr. 24(4):S419-23. [Medline].
Talley-Rostov A. Patient-centered care and refractive cataract surgery. Curr Opin Ophthalmol. 2008 Jan. 19(1):5-9. [Medline].
Ditzen K, Huschka H, Pieger S. LASIK for hyperopia. Burrato L, ed. LASIK Principles and Techniques. Slack Inc; 1998. Vol 22: 269-75.
Klein S, Fry K, Hersh PS. Laser in situ keratomileusis after conductive keratoplasty. J Cataract Refract Surg. 2004 Mar. 30(3):702-5. [Medline].
Kymionis GD, Aslanides IM, Khoury AN, et al. Laser in situ keratomileusis for residual hyperopic astigmatism after conductive keratoplasty. J Refract Surg. 2004 May-Jun. 20(3):276-8. [Medline].
Ocular Surgery News. Thermal keratoplasty techniques face off at ISRS meeting. Top doctors discussed the pros and cons of three thermal keratoplasty techniques for hyperopia. 2002. Available at: http://www.osnsupersite.com/. [Full Text].
Fernandez-Suntay JP, Pineda R 2nd, Azar DT. Conductive keratoplasty. Int Ophthalmol Clin. 2004 Winter. 44(1):161-8. [Medline].
Haw WW, Manche EE. Conductive keratoplasty and laser thermal keratoplasty. Int Ophthalmol Clin. 2002. 42(4):99-106. [Medline].
Huang B. Update on nonexcimer laser refractive surgery technique: conductive keratoplasty. Curr Opin Ophthalmol. 2003 Aug. 14(4):203-6. [Medline].
Rojas MC, Manche EE. Comparison of videokeratographic functional optical zones in conductive keratoplasty and laser in situ keratomileusis for hyperopia. J Refract Surg. 2003 May-Jun. 19(3):333-7. [Medline].
Asbell PA, Maloney RK, Davidorf J, et al. Conductive keratoplasty for the correction of hyperopia. Trans Am Ophthalmol Soc. 2001. 99:79-84; discussion 84-7. [Medline].
Dawson DG, Edelhauser HF, Grossniklaus HE. Long-term histopathologic findings in human corneal wounds after refractive surgical procedures. Am J Ophthalmol. 2005 Jan. 139(1):168-78. [Medline].
Wang TJ, Lo W, Hsueh CM, et al. Ex vivo multiphoton analysis of rabbit corneal wound healing following conductive keratoplasty. J Biomed Opt. 2008 May-Jun. 13(3):034019. [Medline].
McDonald M, Hersh P. A Prospective Multicenter Clinical Trial to Evaluate the Safety and Effectiveness of the ViewPoint CK System for the Correction of Hyperopia Utilizing the Conductive Keratoplasty (CK) Procedure. FDA Protocol RCS-001-HYP. 2001. Available at: http://www.fda.gov/ohrms/dockets/ac/01/briefing/3806b1_05_sponsor. [Full Text].
McDonald MB, Durrie D, Asbell P, et al. Treatment of presbyopia with conductive keratoplasty: six-month results of the 1-year United States FDA clinical trial. Cornea. 2004 Oct. 23(7):661-8. [Medline].
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