Second, follow-up data are lacking. In ischemic stroke, low IGF-I concentrations may predict poor outcome in humans. Further studies are needed to determine whether serum IGF-I levels predict outcomes after a stroke in our population. Furthermore, the biological effects and bioavailability of IGF-I are modulated through IGFBPs, which control IGF-I access to cell surface receptors. Unfortunately, we did not have IGFBPs; therefore, our results do not fully represent biologically active IGF-I. Finally, IGF-I measurements were done after the stroke and thus may not accurately reflect pre-stroke exposure. In conclusion, lower IGF-I levels are significantly related to risk of stroke, independent from other traditional and emerging risk factors, suggesting that they may play a role in the pathogenesis of AIS. Thus, IGF-I levels should be considered as a routine risk factor for stroke in the Chinese population, and further post-ischemic IGF-I therapy may be beneficial for stroke. We suggest routing screening of serum IGF-I levels to prevent stroke in the Chinese population. However, before a broad implementation of this recommendation, additional studies are needed for external validation. A network of extracellular matrix maintains the structural integrity of the myocardium. Due to several etiologies increased deposition of collagen and other extracellular matrix proteins can occur leading to Saikosaponin-B2 cardiac fibrosis. After myocardial infarction, cardiomyocytes are replaced by connective tissue leading to reparative fibrosis. In contrast, in nonischemic cardiomyopathies, an increase in collagen synthesis by myofibroblasts results in diffuse interstitial reactive fibrosis. In arrhythmogenic cardiomyopathy, fibrosis is accompanied by an increase of adipocytes leading to so-called fibrofa y replacement. Myocardial fibrosis is an important part of the histological characteristics in heart failure with preserved and reduced ejection fraction and may act as a substrate 
for cardiac arrhythmias. Adequate detection of the amount and distribution of fibrosis in the heart is important for diagnosis, predicting prognosis, treatment planning and follow-up after therapy. The reference noninvasive standard for indirect detection of myocardial fibrosis is late gadolinium enhancement on cardiac magnetic resonance imaging. Thus far, detailed histological correlation studies to validate this MRI technique are scarce. Histological assessment of cardiac fibrosis is mostly limited by the small amount of tissue available in diagnostic endomyocardial biopsies that only provides regional information. In addition, quantification of histological fibrosis is usually performed semiquantitatively, classifying the fibrosis in limited categories. The aim of this study was to determine the exact pa erns of fibrosis and fa y changes in the myocardium of patients with the PLN p.Arg14del mutation associated cardiomyopathy in relation to their clinical phenotype. This study population was used as proof-of-principle for a novel Procyanidin-B2 method of high resolution systematic digital quantification of fibrosis and fa y tissue in transversal cardiac slides. In the future this method may be used for detailed histological quantification and determination of the distribution paern of cardiac fibrosis in different types of heart disease.