RESUMEN
Parkinson's disease (PD) is one of the most common neurodegenerative illnesses, and is a major healthcare burden with prodigious consequences on life-quality, morbidity, and survival. Cardiovascular diseases are the leading cause of mortality worldwide and growing evidence frequently reports their co-existence with PD. Cardiac dysautonomia due to autonomic nervous system malfunction is the most prevalent type of cardiovascular manifestation in these patients, comprising orthostatic and postprandial hypotension, along with supine and postural hypertension. Moreover, many studies have endorsed the risk of patients with PD to develop ischemic heart disease, heart failure and even arrhythmias, but the underlying mechanisms are not entirely clear. As importantly, the medication used in treating PD, such as levodopa, dopamine agonists or anticholinergic agents, is also responsible for cardiovascular adverse reactions, but further studies are required to elucidate the underlying mechanisms. The purpose of this review was to provide a comprehensive overview of current available data regarding the overlapping cardiovascular disease in patients with PD.
RESUMEN
Atrial fibrillation (AF) is a common heart rhythm disorder with a prevalence of up to 2.9% in the general population. Its mechanism involves a particular electrophysiological profile as well as structural and biohumoral changes that are often irreversible. With the recent advances in pharmacology, amiodarone remains the cornerstone for the treatment of AF. Although it is one of the most controversial anti-arrhythmic agents due to the multitude of side effects, it is further recognised as the most effective drug available for the conversion and maintenance of sinus rhythm in the case of significant left ventricular dysfunction or severe aortic stenosis. This quality is provided by its multivalent profile, with a complex electrophysiological activity overlapped with an anti-inflammatory and vasodilatory effect. This review aims to outline the main structural and functional changes in AF and the multisite impact of amiodarone on its treatment.