The Year in Cardiology 2013: heart failure

Heart failure has become a worldwide epidemic of the 21st century with increasing impact on healthcare systems. The 2012 ESC and 2013 ACCF/AHA guidelines have set the stage for current therapy to reduce mortality and morbidity. There is a dawn of hope for therapy of acute and diastolic heart failure; it has become clearer that patients benefit from mitral reconstruction and which patients benefit from heart failure management programmes; genetics and proteomics advance in great strides; competing concepts of cell therapy seem to spiral, hopefully upwards; and we can further nurture our hope for evidence-based individualized diagnostic and therap

Intellectual and non-intellectual determinants of high academic achievement -the contribution of personality traits to the assessment of high performance potential

Abstract: In this paper a study is presented which tries to explain and predict high academic achievement in children or adolescents on the basis of intellectual and non-intellectual determinants -in this case, performance relevant personality traits as well as the social environment of stimulation. The prognosis of high academic achievement is based on a new diagnostic model, the Viennese Diagnostic Model of High Achievement Potential, which undergoes its first empirical validation here. The results show impressive evidence that performance-relevant personality traits and categories of social environment of stimulation contribute to high academic achievement in children and adolescents of above-average intelligence

Does FXIII Deficiency Impair Wound Healing after Myocardial Infarction?

Inadequate healing of myocardial infarction may contribute to local expansion of the infarct, frequently leading to chamber dilation, heart failure, or myocardial rupture. Experimental evidence in mouse models suggests that Factor XIII might play a key role in wound healing, and low persistent values lead to increased incidence of cardiac rupture following myocardial infarction. Here we would like to share our initial clinical experiences with strikingly similar observations in patients with this grave disease, and compare these observations to experimental findings

Journal of Cardiovascular Magnetic Resonance ® , 3(4), 349–360 (2001) Mechanisms of the Effects of Nicorandil in the Isolated Rat Heart During Ischemia and Reperfusion: A 31 P-Nuclear Magnetic Resonance Study

Nicorandil (SG75) is a potent K �-channel activator with an additional nitro moiety. In the present study we investigated the potential mechanisms (K �-channel activation and nitric oxide [NO] release) for the effects of nicorandil on isolated perfused rat hearts during total global ischemia using 31 P-nuclear magnetic resonance. After a 10-min control perfusion, hearts were subjected to treatment with nicorandilcontaining (100, 300, or 1000 µM) buffer for 10 min, 15 min of total global ischemia, and 30 min of reperfusion. At high dose (10 �3 M), nicorandil reduced ATP depletion during ischemia by 26 % compared with untreated hearts. Blockade of K � channels by glibenclamide prevented this protective effect. At all doses (10 �4 to 10 �3 M), nicorandil reduced the accumulation of protons during ischemia compared with untreated hearts (pH 6.22 � 0.03 vs. 6.02 � 0.05 in untreated hearts at the end of ischemia). This effect was preserved after blockade of K � channels by glibenclamide. Hearts treated with nitroglycerine before ischemia also showed reduced proton accumulation. Therefore, NO release accompanied by increased coronary flow before ischemia, which is caused by the nitro moiety of nicorandil and nitroglycerine treatment, results in reduced proton accumulation. During reperfusion, a pro-arrhythmic effect was observed in hearts treated with the nonpharmacologically high dose of nicorandil (1000 µM). Thus, we conclude that the effects of nicorandil are caused Address correspondence and reprint requests to Michael Horn

An Update Based on the SCORE-Deutschland Risk Charts

Estimation of absolute risk of cardiovascular disease (CVD), preferably with population-specific risk charts, has become a cornerstone of CVD primary prevention. Regular recalibration of risk charts may be necessary due to decreasing CVD rates and CVD risk factor levels. The SCORE risk charts for fatal CVD risk assessment were first calibrated for Germany with 1998 risk factor level data and 1999 mortality statistics. We present an update of these risk charts based on the SCORE methodology including estimates of relative risks from SCORE, risk factor levels from the German Health Interview and Examination Survey for Adults 2008–11 (DEGS1) and official mortality statistics from 2012. Competing risks methods were applied and estimates were independently validated. Updated risk charts were calculated based on cholesterol, smoking, systolic blood pressure risk factor levels, sex and 5-year age-groups. The absolute 10-year risk estimates of fatal CVD were lower according to the updated risk charts compared to the first calibration for Germany. In a nationwide sample of 3062 adults aged 40–65 years free of major CVD from DEGS1, the mean 10-year risk of fatal CVD estimated by the updated charts was lower by 29% and the estimated proportion of high risk people (10-year risk > = 5%) by 50% compared to the older risk charts. This recalibration shows a need for regular updates of risk charts according to changes in mortality and risk factor levels in order to sustain the identification of people with a high CVD risk

Differences in Fabry Cardiomyopathy Between Female and Male Patients Consequences for Diagnostic Assessment

ObjectivesWe hypothesized that Fabry cardiomyopathy in female patients might differ substantially from that in male patients and sought to prove this hypothesis in a large cohort consisting of 104 patients with Fabry disease.BackgroundFabry cardiomyopathy in male patients is characterized by left ventricular (LV) hypertrophy, impaired myocardial function, and subsequent progressive myocardial fibrosis. In contrast, the occurrence of these 3 cardiomyopathic hallmarks in female patients remains unknown.MethodsIn 104 patients (58 females, age 42 ± 16 years; 46 males, age 42 ± 13 years) with genetically proven Fabry disease, LV hypertrophy, regional myocardial deformation and myocardial fibrosis were assessed by standard echocardiography, strain rate imaging, and cardiac magnetic resonance (CMR) imaging–guided late enhancement (LE).ResultsIn men, end-diastolic left ventricular wall thickness (LVWT) ranged from 6 to 19.5 mm (LV mass CMR 55 to 200 g/m2), and LE was never seen with LVWT <12 mm (LV mass <99 g/m2). In contrast in female patients, LVWT ranged from 5 to 15.5 mm, LV mass ranged from 39 to 146 g/m2, and LE was already detectable with an LVWT of 9 mm (LV mass 56 g/m2). When LV mass was examined in CMR, LE was detected in 23% of the female patients without hypertrophy (n = 9), whereas LE was never seen in male patients with normal LV mass. LE was always associated with low systolic strain rate, but the severity of impairment was independent of LVWT in female patients (lateral strain rate in patients with LV hypertrophy with LE −0.7 ± 0.2 s−1; patients without LV hypertrophy with LE −0.8 ± 0.2 s−1; p = 0.45).ConclusionsIn contrast to male patients, the loss of myocardial function and the development of fibrosis do not necessarily require myocardial hypertrophy in female patients with Fabry disease. Thus, in contrast to actual recommendations, initial cardiac staging and monitoring should be based on LV hypertrophy and on replacement fibrosis in female patients with Fabry disease

"GOLD or lower limit of normal definition? a comparison with expert-based diagnosis of chronic obstructive pulmonary disease in a prospective cohort-study"

<p>Abstract</p> <p>Background</p> <p>The Global initiative for chronic Obstructive Lung Disease (GOLD) defines COPD as a fixed post-bronchodilator ratio of forced expiratory volume in 1 second and forced vital capacity (FEV1/FVC) below 0.7. Age-dependent cut-off values below the lower fifth percentile (LLN) of this ratio derived from the general population have been proposed as an alternative. We wanted to assess the diagnostic accuracy and prognostic capability of the GOLD and LLN definition when compared to an expert-based diagnosis.</p> <p>Methods</p> <p>In a prospective cohort study, 405 patients aged ≥ 65 years with a general practitioner's diagnosis of COPD were recruited and followed up for 4.5 (median; quartiles 3.9; 5.1) years. Prevalence rates of COPD according to GOLD and three LLN definitions and diagnostic performance measurements were calculated. The reference standard was the diagnosis of COPD of an expert panel that used all available diagnostic information, including spirometry and bodyplethysmography.</p> <p>Results</p> <p>Compared to the expert panel diagnosis, 'GOLD-COPD' misclassified 69 (28%) patients, and the three LLNs misclassified 114 (46%), 96 (39%), and 98 (40%) patients, respectively. The GOLD classification led to more false positives, the LLNs to more false negative diagnoses. The main predictors beyond the FEV1/FVC ratio for an expert diagnosis of COPD were the FEV1 % predicted, and the residual volume/total lung capacity ratio (RV/TLC). Adding FEV1 and RV/TLC to GOLD or LLN improved the diagnostic accuracy, resulting in a significant reduction of up to 50% of the number of misdiagnoses. The expert diagnosis of COPD better predicts exacerbations, hospitalizations and mortality than GOLD or LLN.</p> <p>Conclusions</p> <p>GOLD criteria over-diagnose COPD, while LLN definitions under-diagnose COPD in elderly patients as compared to an expert panel diagnosis. Incorporating FEV1 and RV/TLC into the GOLD-COPD or LLN-based definition brings both definitions closer to expert panel diagnosis of COPD, and to daily clinical practice.</p