At the end of the 1990s came an increased distrust of the concept of "sick building". A dissertation at the Karolinska Institutet in Stockholm 1999 questioned the methodology of previous research, and a Danish study from 2005 showed these flaws experimentally. It was suggested that sick building syndrome was not really a coherent syndrome and was not a disease to be individually diagnosed, but a collection of as many as to dozen semi related diseases. In 2006 the Swedish National Board of Health and Welfare recommended in the medical journal Läkartidningen that "sick building syndrome" should not be used as a clinical diagnosis. Thereafter, it has become increasingly less common to use terms such as "sick buildings" and "sick building syndrome" in research. However, the concept remains alive in popular culture and is used to designate the set of symptoms related to poor home or work environment engineering. "Sick building" is therefore an expression used especially in the context of workplace health. Sick building syndrome made a rapid journey from media to courtroom where professional engineers and architects became named defendants and were represented by their respective professional practice insurers. Proceedings invariably relied on expert witnesses, medical and technical experts along with building managers, contractors and manufacturers of finishes and furnishings, testifying as to cause and effect. Most of these actions resulted in sealed settlement agreements, none of these being dramatic.
Just like endothelial cells, nerve cells cannot regulate their glucose uptake and suffer the same type of damages listed above. Therefore, the diabetic heart shows clear denervation as the pathology progresses. This denervation correlates with echocardiographic evidence of diastolic dysfunction and results in a decline of survival in patients with diabetes from 85% to 44%. Other causes of denervation are ischemia from microvascular disease and thus appear following the development of microangiopathy. Inflammation
Diabetes is associated with increased inflammation, which is mediated by generation of abnormal fatty acids, AGEs and other mechanisms. The resulting cytokine profile promotes hypertrophy and apoptosis of cardiomyocytes, abnormal calcium signaling, impaired myocardial contractility and myocardial fibrosis. Additionally, it may lead to microvascular dysfunction, either directly or via endothelial damage, thereby promoting myocardial ischemia. Diagnosis
Diagnostic approaches for diabetic cardiomyopathy include echocardiography, cardiac MRI investigations, Multi‐slice computed tomography (MsCT), and nuclear imaging. Potential risks of the investigation (e.g. exposure to radiation) and diagnostic utility should be weighed for an optimised personalised procedure. Treatment
At present, there is no effective specific treatment available for diabetic cardiomyopathy. Treatment centers around intense glycemic control through diet, oral hypoglycemics and frequently insulin and management of heart failure symptoms. There is a clear correlation between increased glycemia and risk of developing diabetic cardiomyopathy, therefore, keeping glucose concentrations as controlled as possible is paramount. Thiazolidinediones are not recommended in patients with NYHA Class III or IV heart failure secondary to fluid retention.As with most other heart diseases, ACE inhibitors can also be administered.