ABSTRACT
Epicardial adipose tissue (EAT) has been associated with the development of many cardiovascular abnormalities, of which the development of atrial fibrillation (AFIB) in this group of patients is not an uncommon finding. Several mechanisms have been proposed to explain the role of EAT in the development of AFIB. It involves cardiac remodeling owing to the underlying fatty infiltration and the subsequent inflammation and fibrosis. This leads to the formation of ectopic foci that can lead to AFIB. Some studies propose that structural and valvular heart disease and increased hemodynamic stress further augment the development of AFIB in patients with underlying EAT. The degree of development of AFIB is also related to EAT thickness and volume. Therefore, EAT quantification can be used as an imaging technique to predict cardiovascular outcomes in these patients. Obesity also plays an important role in the development of AFIB both as an independent factor and by leading to adipose tissue deposition on the epicardial tissue. Understanding the pathophysiology of EAT is important as it can lead to the development of therapies that can target obesity as a risk factor for preventing AFIB. Some promising therapies have already been investigated for decreasing the risk of AFIB in patients with EAT. Dietary changes and weight loss have been shown to reduce the deposition of fat on epicardial tissue. Antidiabetic drugs and statin therapy have also shown promising results. Bariatric surgery has been shown to decrease EAT volume on echocardiography in obese patients.
ABSTRACT
Post-stroke complications are very common worldwide and the most common complication is infection. This contributes the most to the mortality rate in stroke patients. Among the infections, pneumonia and urinary tract infections are most common. Hyperthermia following stroke is associated with neuronal damage and worse outcomes. Post-stroke immunosuppression and activation of inflammatory mediators also cause infections. Based on the high mortality caused by post-stroke infections, various trials were done to seek the advantage that prophylactic antibiotics can give in the critical care of stroke patients. Antibiotics, including ceftriaxone (cephalosporin), levofloxacin (fluoroquinolone), penicillin, and minocycline (tetracycline), were used and the stroke patients were followed up to analyze the primary and secondary outcomes. It was concluded that early antibiotic therapy (mostly within 24 hours) leads to a reduced rate of post-stroke infections and reduced fever spikes, whereas follow-up for a longer period of time showed no better functional outcome. Furthermore, mortality and morbidity benefits were also not seen with prophylactic antibiotic therapy. This review helped us to put a nail in the coffin to the earlier thoughts that prophylactic antibiotics are necessary for the critical care of stroke patients.
ABSTRACT
Alzheimer's disease (AD) is a progressive disorder that causes brain cells to slowly degenerate and die. This leads to a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently. AD is the most common cause of dementia globally. Neuroinflammation caused by intracellular neurofibrillary tangles and extracellular amyloid deposits leads to atrophy of brain cells especially the hippocampus, which is associated with memory formation. This atrophy leads to dementia and cognitive decline. Among the many preventive factors being studied, exercise is thought to play a vital role in not only preventing the pre-clinical stage of AD but also slowing the clinical progression of AD. It is also deployed as a treatment option for late-stage AD along with pharmacological treatment options. Various studies and clinical trials in both human and animal models are of the opinion that exercise slows the onset and progression of cognitive decline in AD patients. Some studies suggest that this effect is due to a decrease in neurofibrillary tangles and amyloid deposits in brain parenchyma. Others suggest that exercise causes an increase in angiogenesis, neurogenesis, and synaptogenesis mainly due to an increase in blood flow, brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), hormones, and second messengers.
