RESUMO
Histotripsy, an innovative ultrasonic technique, is poised to transform the landscape of cardiovascular disease management. This review explores the multifaceted applications of histotripsy across various domains of cardiovascular medicine. In thrombolysis, histotripsy presents a non-invasive, drug-free, and precise method for recanalizing blood vessels obstructed by clots, minimizing the risk of vessel damage and embolism. Additionally, histotripsy showcases its potential in congenital heart defect management, offering a promising alternative to invasive procedures by creating intracardiac communications noninvasively. For patients with calcified aortic stenosis, histotripsy demonstrates its effectiveness in softening calcified bioprosthetic valves, potentially revolutionizing valve interventions. In the realm of arrhythmias, histotripsy could play an important role in scar-based ventricular tachycardia ablation, eliminating channel-like isthmuses of slowly conducting myocardium. Histotripsy`s potential applications also extend to structural heart interventions, enabling the safe sectioning of basal chordae and potentially addressing mitral regurgitation. Furthermore, it showcases its versatility by safely generating ventricular septal defects, providing a non-invasive means of creating intracardiac communications in neonates with congenital heart disease. Yet, most supporting studies are in-vitro or animal studies and there are possible challenges in translating experimental data on cardiac histotripsy to the clinical level. As histotripsy continues to evolve and mature, its remarkable potential in cardiovascular disease management holds promise for improving patient outcomes and reducing the burden of invasive procedures in the field of cardiology.
RESUMO
Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects motor and cognition functions. The etiology of Parkinson's disease remains largely unknown, but genetic and environmental factors are believed to play a role. The neurotransmitter dopamine is implicated in regulating movement, motivation, memory, and other physiological processes. In individuals with Parkinson's disease, the loss of dopaminergic neurons leads to a reduction in dopamine levels, which causes motor impairment and may also contribute to the cognitive deficits observed in some patients. Therefore, it is important to understand the pathophysiology that leads to the loss of dopaminergic neurons, along with reliable biomarkers that may help distinguish PD from other conditions, monitor its progression, or indicate a positive response to a therapeutic intervention. Important advances in the treatment, etiology, and pathogenesis of Parkinson's disease have been made in the past 50 years. Therefore, this review tries to explain the different possible mechanisms behind the depletion of dopamine in PD patients such as alpha-synuclein abnormalities, mitochondrial dysfunction, and 3,4-dihydroxyphenylacetaldehyde (DOPAL) toxicity, along with the current therapies we have and the ones that are in development. The clinical aspect of Parkinson's disease such as the manifestation of both motor and non-motor symptoms, and the differential diagnosis with similar neurodegenerative disease are also discussed.
RESUMO
The possibility of multimodality imaging with PET/MR and the availability of ultra-high field MRI has allowed to investigate novel aspects of neuropsychiatric conditions. One of the major barriers in current studies is the lack of an instrument that allows to accurately cover the temporal aspect under the same physiological conditions. The aim of this commentary is to provide our perspective on how the integration of EEG-PET-MR could be a solution to the current challenge in molecular imaging and seems to hold great promise in future pharmacological challenging-based studies, understanding different functional states of the brain, and could furthermore aid in the diagnostic and prognostic evaluations of neurocognitive disorders.
