RESUMEN
Spontaneous Coronary Artery Dissection (SCAD) is one of the nonatherosclerotic causes of Acute Coronary Syndrome. It's extremely rare for SCAD to present in an asymptomatic male, with incidental finding of Left Ventricular (LV) thrombus on echocardiogram. This report presents the case of a 36-year-old male with such an atypical presentation of Spontaneous Coronary Artery Dissection with Left Ventricular apical thrombus as a complication. The patient received successful medical management, with excellent clinical outcomes. This case highlights the importance of an early recognition and treatment strategy for both conditions using medical therapy.
RESUMEN
The last decade has witnessed a proliferation of neuroimaging studies characterising brain changes associated with Alzheimer's disease (AD), where both widespread atrophy and 'signature' brain regions have been implicated. In parallel, a prolonged latency period has been established in AD, with abnormal cerebral changes beginning many years before symptom onset. This raises the possibility of early therapeutic intervention, even before symptoms, when treatments could have the greatest effect on disease-course modification. Two important prerequisites of this endeavour are (1) accurate characterisation or risk stratification and (2) monitoring of progression using neuroimaging outcomes as a surrogate biomarker in those without symptoms but who will develop AD, here referred to as preclinical AD. Structural neuroimaging modalities have been used to identify brain changes related to risk factors for AD, such as familial genetic mutations, risk genes (for example apolipoprotein epsilon-4 allele), and/or family history. In this review, we summarise structural imaging findings in preclinical AD. Overall, the literature suggests early vulnerability in characteristic regions, such as the medial temporal lobe structures and the precuneus, as well as white matter tracts in the fornix, cingulum and corpus callosum. We conclude that while structural markers are promising, more research and validation studies are needed before future secondary prevention trials can adopt structural imaging biomarkers as either stratification or surrogate biomarkers.