Epicardial adipose tissue in patients with heart failure.

PURPOSE: The aim of this study was to evaluate the extent of epicardial adipose tissue (EAT) and its relationship with left ventricular (LV) parameters assessed by cardiovascular magnetic resonance (CMR) in patients with congestive heart failure (CHF) and healthy controls. BACKGROUND: EAT is the true visceral fat deposited around the heart which generates various bioactive molecules. Previous studies found that EAT is related to left ventricular mass (LVM) in healthy subjects. Further studies showed a constant EAT to myocardial mass ratio in normal, ischemic and hypertrophied hearts. METHODS: CMR was performed in 66 patients with CHF due to ischemic cardiomyopathy (ICM), or dilated cardiomyopathy (DCM) and 32 healthy controls. Ventricular volumes, dimensions and LV function were assessed. The amount of EAT was determined volumetrically and expressed as mass indexed to body surface area. Additionally, the EAT/LVM and the EAT/left ventricular remodelling index (LVRI) ratios were calculated. RESULTS: Patients with CHF had less indexed EAT mass than controls (22 +/- 5 g/m2 versus 34 +/- 4 g/m2, p < 0.0001). In the subgroup analysis there were no significant differences in indexed EAT mass between patients with ICM and DCM (21 +/- 4 g/m2 versus 23 +/- 6 g/m2, p = 0.14). Linear regression analysis showed that with increasing LV end-diastolic diameter (LV-EDD) (r = 0.42, p = 0.0004) and LV end-diastolic mass (LV-EDM) (r = 0.59, p < 0.0001), there was a significantly increased amount of EAT in patients with CHF. However, the ratio of EAT mass/LV-EDM was significantly reduced in patients with CHF compared to healthy controls (0.54 +/- 0.1 versus 0.21 +/- 0.1, p < 0.0001). In CHF patients higher indexed EAT/LVRI-ratios in CHF patients correlated best with a reduced LV-EF (r = 0.49, p < 0.0001). CONCLUSION: Patients with CHF revealed significantly reduced amounts of EAT. An increase in LVM is significantly related to an increase in EAT in both patients with CHF and controls. However, different from previous reports the EAT/LVEDM-ratio in patients with CHF was significantly reduced compared to healthy controls. Furthermore, the LV function correlated best with the indexed EAT/LVRI ratio in CHF patients. Metabolic abnormalities and/or anatomic alterations due to disturbed cardiac function and geometry seem to play a key role and are a possible explanation for these findings.

CMR findings in patients with hypertrophic cardiomyopathy and atrial fibrillation.

OBJECTIVES: We sought to evaluate the relation between atrial fibrillation (AF) and the extent of myocardial scarring together with left ventricular (LV) and atrial parameters assessed by late gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: AF is the most common arrhythmia in HCM. Myocardial scarring is also identified frequently in HCM. However, the impact of myocardial scarring assessed by LGE CMR on the presence of AF has not been evaluated yet. METHODS: 87 HCM patients underwent LGE CMR, echocardiography and regular ECG recordings. LV function, volumes, myocardial thickness, left atrial (LA) volume and the extent of LGE, were assessed using CMR and correlated to AF. Additionally, the presence of diastolic dysfunction and mitral regurgitation were obtained by echocardiography and also correlated to AF. RESULTS: Episodes of AF were documented in 37 patients (42%). Indexed LV volumes and mass were comparable between HCM patients with and without AF. However, indexed LA volume was significantly higher in HCM patients with AF than in HCM patients without AF (68 +/- 24 ml.m-2 versus 46 +/- 18 ml.m-2, p = 0.0002, respectively). The mean extent of LGE was higher in HCM patients with AF than those without AF (12.4 +/- 14.5% versus 6.0 +/- 8.6%, p = 0.02). When adjusting for age, gender and LV mass, LGE and indexed LA volume significantly correlated to AF (r = 0.34, p = 0.02 and r = 0.42, p < 0.001 respectively). By echocardiographic examination, LV diastolic dysfunction was evident in 35 (40%) patients. Mitral regurgitation greater than II was observed in 12 patients (14%). Multivariate analysis demonstrated that LA volume and presence of diastolic dysfunction were the only independent determinant of AF in HCM patients (p = 0.006, p = 0.01 respectively). Receiver operating characteristic curve analysis indicated good predictive performance of LA volume and LGE (AUC = 0.74 and 0.64 respectively) with respect to AF. CONCLUSION: HCM patients with AF display significantly more LGE than HCM patients without AF. However, the extent of LGE is inferior to the LA size for predicting AF prevalence. LA dilation is the strongest determinant of AF in HCM patients, and is related to the extent of LGE in the LV, irrespective of LV mass.

The role of hormonal treatment in prostate cancer.

In 1941 Huggins and Hodges published for the first time the favorable effects of surgical castration and estrogen treatment on the progression of metastatic prostate cancer. However, this hormonal therapy is not without side effects. Since this pioneering milestone in history of prostate cancer, a further tremendous innovation did not take place. Today, due to intensive clinical, biochemical, nuclear-biological and molecular-biological research, many hormone active treatment variations are available. Besides traditional hormonal therapy, surgical or chemical castration, maximal androgen blockade, nontraditional forms of hormonal therapy, intermittent hormonal therapy, antiandrogens, 5-alpha-reductase inhibitors, and their combinations, we discuss options toward creating an increased number of side effect-oriented offers of hormonal treatment options, guaranteeing a longer and more comfortable exhaustion of the individual hormonal period of response and probably a longer survival. The prerequisite is a closer-than-ever monitoring by tumor marker and an early observation of symptomatic changes.

Extent of myocardial hyperenhancement on late gadolinium-enhanced cardiovascular magnetic resonance correlates with q waves in hypertrophic cardiomyopathy.

PURPOSE: Despite several electrocardiographic, echocardiographic, electrophysiologic and pathologic studies, the cause of abnormal Q waves in patients with HCM remains unclear. Cardiovascular magnetic resonance (CMR) is a powerful in vivo diagnostic tool for evaluating cardiac morphology and function. We hypothesized that estimation of segmental and transmural extent of myocardial enhancement by late gadolinium enhancement (LGE) CMR could clarify the basis of Q waves. The purpose of this prospective study was to evaluate the morphological basis of abnormal Q waves in hypertrophic cardiomyopathy (HCM) as assessed by CMR. METHODS: Thirty-eight patients with HCM underwent gadolinium-enhanced CMR and 12 lead electrocardiography (ECG). Left ventricular function, volumes, segmental and transmural extent of myocardial LGE were assessed and analysed in relation to the presence of abnormal Q waves. RESULTS: Twelve (31%) of the 38 patients had abnormal Q waves on the ECG. Patients with Q waves exhibited significantly more myocardial LGE segmentally as well as transmurally than patients without Q waves. As the segmental and the transmural extent of LGE increased, the probability of Q wave increased (anterior: segmental extent chi2 = 10, p = 0.0013, transmural extent chi2 = 10, p = 0.0013; inferior: segmental extent chi2 = 13, p = 0.0003, transmural extent chi2 = 15, P < 0.0001: lateral: segmental extent chi2 = 10, p = 0.0016, transmural extent chi2 = 10, p = 0.0012). Additionally, the ratio of septal to posterior wall thickness was significantly higher in patients with Q waves than in patients without Q waves (2.3 vs. 1.6, p = 0.012). CONCLUSIONS: It seems that segmental and transmural extent rather than the mere presence of myocardial LGE is the underlying mechanism of abnormal Q waves in HCM. Additionally, distribution of hypertrophy as indicated by differences in the ratio of septal to posterior wall thickness seems to play an important role.

Volumetric assessment of epicardial adipose tissue with cardiovascular magnetic resonance imaging.

OBJECTIVE: Previous studies determined the amount of epicardial fat by measuring the right ventricular epicardial fat thickness. However, it is not proven whether this one-dimensional method correlates well with the absolute amount of epicardial fat. In this prospective study, a new cardiovascular magnetic resonance imaging (CMR) method using the three-dimensional summation of slices method was introduced to assess the total amount of epicardial fat. RESEARCH METHODS AND PROCEDURES: CMR was performed in 43 patients with congestive heart failure and in 28 healthy controls. The absolute amount of epicardial fat was assessed volumetrically in consecutive short-axis views by means of the modified Simpson's rule. Additionally, the right ventricular epicardial fat thickness was measured in two different imaging planes: long-axis view (EFT-4CV) and consecutive short-axis views (EFT-SAX). RESULTS: Using the volumetric approach, patients with congestive heart failure had less epicardial fat mass than controls (51 g vs. 65 g, p=0.01). This finding was supported by EFT-SAX (2.9 mm vs. 4.3 mm, p<0.0001) but not by EFT-4CV (3.5 mm vs. 3.8 mm, p=not significant). Epicardial fat mass correlated moderately with EFT-SAX in both groups (r=0.466, p=0.012 in controls and r=0.590, p<0.0001 in patients) and with EFT-4CV in controls (r=0.387, p=0.042). There were no significant differences between EFT-4CV and EFT-SAX in controls (4.3 mm vs. 3.8 mm, p=0.240). However, in the heart failure group, EFT-4CV was significantly higher compared with EFT-SAX (3.5 mm vs. 2.9 mm, p=0.003). Interobserver variability and reproducibility were superior for the volumetric approach compared with thickness measurements. DISCUSSION: Quantitative assessment of epicardial fat mass using the CMR-based volumetric approach is feasible and yields superior reproducibility compared with conventional methods.

Cerebral infarction: incidence and risk factors after diagnostic and interventional cardiac catheterization--prospective evaluation at diffusion-weighted MR imaging.

PURPOSE: To prospectively evaluate incidence of clinically silent and clinically apparent embolic cerebral infarction following diagnostic and interventional coronary angiography and associated risk factors. MATERIALS AND METHODS: Written informed consent was obtained from all patients, and the study was approved by the research ethics committee of University of Heidelberg, Germany. Fifty-two patients, including 37 men (mean age, 66.1 years +/- 11.9 [standard deviation]) and 15 women (mean age, 65.3 years +/- 10.3), undergoing elective cardiac catheterization were examined 3-26 hours (mean, 15.3 hours +/- 6) before and 12-48 hours (mean, 25.9 hours +/- 10.4) after cardiac catheterization. Magnetic resonance imaging protocol included isotropic and anisotropic diffusion-weighted single-shot echo-planar sequences. T2-weighted turbo spin-echo and T1-weighted spin-echo sequences also were performed. Apparent diffusion coefficient maps were calculated to exclude false-positive reading results on diffusion-weighted images because of T2 shine-through effect. Images were assessed by two experienced radiologists blinded to clinical data. Cardiac catheterization was performed by 11 experienced cardiologists to exclude operator-related risk. A neurologic examination according to the National Institutes of Health Stroke Scale and Barthel index was performed by a senior cardiologist before acquisition of each image. Sixteen clinical and angiographic variables were analyzed with univariate analysis for ability to predict occurrence of cerebral infarction. RESULTS: No embolic cerebral lesions could be detected at diffusion-weighted imaging before catheterization. After coronary angiography, seven (15%) of 48 patients demonstrated nine focal cerebral infarcts affecting anterior and posterior circulation. Patients remained asymptomatic. Of all tested variables, only duration of the procedure was identified as an independent predictor of occurrence of cerebral infarction (P < .05). CONCLUSION: In this prospective study, asymptomatic cerebral infarction following cardiac catheterization occurred in 15% of patients in whom duration of the procedure was significantly longer than in those without infarction (P = .017).

[Sex, erectile dysfunction, and the heart: a growing problem]. / Sexualität, erektile Dysfunktion und das Herz: ein zunehmendes Problem.

BACKGROUND: Erectile dysfunction (ED) is defined as the inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance. ED may also be an early sign of cardiovascular disease. The main risk factors for coronary heart disease (high LDL, smoking, hypertension, diabetes) and ED are the same. ED after the diagnosis of coronary artery disease or myocardial infarction is also common. CARDIOVASCULAR EFFECTS AND RISK OF SEXUAL ACTIVITY: Cardiac and metabolic expenditures during sexual intercourse will vary depending on the type of sexual activity. When oxygen uptake was measured in men, an average metabolic expenditure during stimulation and orgasm of 2.5 metabolic equivalents (METs) was found for woman-on-top coitus, and of 3.3 METs for man-on-top coitus (range 2.0-5.4 METs). However, coital death is rare, encompassing only 0.6% of all sudden death cases. A retrospective case-crossover study has shown that although sexual activity can trigger the onset of myocardial infarction, the relative risk in the 2 h after sexual activity was low (2.5; 95% confidence interval [CI] 1.7-3.7). Sexual activity was a likely contributor to the onset of myocardial infarction only 0.9% of the time. Regular exercise appears to prevent triggering. It has to be cautioned that these reassuring data should not be extrapolated to patients taking sildenafil, if they perform at higher cardiac and metabolic expenditures during coitus. The hemodynamic changes associated with sexual activity may be far greater with an unfamiliar partner, in unfamiliar settings, and after excessive eating and drinking. The Princeton Consensus Table for estimation of cardiovascular risk during sexual intercourse gives a first orientation regarding the question which patients can perform sex safely and which subgroup needs further diagnosis and treatment. PHOSPHODIESTERASE-5 INHIBITORS FOR ED TREATMENT: The introduction of sildenafil has been a valuable contribution to the treatment of ED. Sildenafil acts as a selective inhibitor of cyclic guanosine monophosphate-(cGMP-)specific phosphodiesterase type 5 (PDE 5), resulting in smooth muscle relaxation, vasodilation, and enhanced penile erection. Reported cardiovascular side effects in healthy males are headache, flushing, and < 10% decreases in systolic and diastolic blood pressures. Significant hypotension can be found in patients who are concurrently taking nitrates. On the basis of the pharmacokinetic profile of sildenafil, the co-administration of a nitrate within the first 24 h is likely to produce a severe, potentially lifethreatening hypotensive response and is therefore contraindicated. The risk of precipitating a cardiotoxic, hypotensive, or hemorrhagic event secondary to combining sildenafil (a PDE 5 inhibitor) with specific PDE 3 inhibitors such as milrinone and enoximone or with nonspecific PDE inhibitors such as theophylline and pentoxifylline is unlikely. Sildenafil is predominantly metabolized by both the P450 2C9 pathway and the P450 3A4 pathway. Thus, potent inhibitors of the P450 3A4 pathway may increase the plasma concentrations of sildenafil, like cimetidine, erythromycin, digitoxin, and CSE inhibitors (simvastatin, atorvastatin, etc.). A creatinine clearance < 30 ml/min also increases plasma levels of sildenafil. SAFETY PROFILE OF SILDENAFIL: Sildenafil is safe in healthy subjects. In a postmarketing study on 6,527 males, no increase of cardiovascular events was found. However, in older males with coronary heart disease, the risk of sildenafil and the risk of physical exercise during sexual intercourse contribute both to fatal outcomes. Of 69 cases reported to the FDA, 46 patients might have had a cardiovascular event, and in twelve a possible interaction with nitrate use has been reported. Sildenafil is absolutely contraindicated in patients taking long-acting nitrates, those with severe aortic stenosis, and patients with hypertrophic obstructive cardiomyopathy (HOCM). No nitrates should be used within 24 h of sildenafil use. Caution is necessary in patients with a combination of antihypertensive medications, and in patients with cardiac insufficiency. A "pre-Viagra" treadmill test to assess for the presence of stress-induced ischemia can be helpful for both the patient and the physician. If the patient can achieve > or = 5 METs without demonstrating ischemia, the risk of ischemia during coitus is low. MANAGEMENT OF SEVERE ADVERSE EVENTS: If severe hypotension occurs, aggressive fluid resuscitation is the first step, followed by administration of vasoactive drugs and, if necessary, by intraaortic balloon counterpulsation. If unstable angina or myocardial infarctions occurs after the use of sildenafil, the patient is treated according to the guidelines, but without nitrates. CONCLUSION: Sexual activity is a cornerstone of quality of life. However, giving the incidence of "occult" cardiovascular disease in patients with ED and the indications and contraindications of PDE 5 inhibitors in patients with cardiovascular diseases, all patients with ED must be evaluated by a cardiovascular specialist.

Magnetic resonance imaging findings in patients with Brugada syndrome.

INTRODUCTION: Cardiac magnetic resonance imaging (CMR) is a powerful diagnostic tool for evaluating cardiac structure and function. Recently, right ventricular wall-motion abnormalities were described using electron beam tomography in patients with Brugada syndrome. In the present study, we prospectively evaluated CMR findings in patients with Brugada syndrome compared to matched controls. METHODS AND RESULTS: CMR was performed on 20 consecutive patients with proven Brugada syndrome. The imaging protocol included breath-hold dark blood prepared T1-weighted multislice turbo spin-echo and gradient-echo images. Ventricular volumes and dimensions were compared to age- and sex-matched normal volunteers. The right ventricular outflow tract area was significantly enlarged in patients with Brugada syndrome compared to controls (11 vs 9 cm2, P = 0.018). There was a trend to larger right ventricular end-diastolic and end-systolic volumes and lower right ventricular ejection fraction in patients with Brugada syndrome compared to controls. However, none of the differences reached significance (P = 0.3, P = 0.08, and P = 0.06, respectively). There was no statistically significant difference in the left ventricular parameters between patients and controls. High intramyocardial T1 signal similar to fat signal was observed in 4 (20%) of the 20 patients compared to none of the controls. CONCLUSION: The findings support the view that subtle structural changes, such as right ventricular outflow tract dilation may point to a localized arrhythmogenic substrate in patients with Brugada syndrome.