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Water drinking elicits a profound pressor response in autonomic failure patients. It increases blood pressure to a lesser degree in tetraplegic patients, cardiac transplant recipients, and older healthy subjects. Blood pressure does not change in healthy young subjects. The haemodynamic response to water drinking appears to be mediated through sympathetic activation via an unknown mechanism. Water drinking improves orthostatic responses in patients with orthostatic hypotension and orthostatic tachycardia, and delays the onset of neurocardiogenic syncope in healthy subjects. Thus, water drinking may be a promising and essentially cost-free intervention for all these conditions, either as monotherapy or in conjunction with other non-pharmacological or pharmacological treatments.

Patients with right ventricular pacing and heart failure may be candidates for resynchronisation therapy with the upgrading to biventricular pacing.

The procedure has been shown to be simple and safe. In addition, the results of the above-mentioned studies are encouraging and show that upgraded patients may profit from a better quality of life. However, the life expectancy of these patients remains to be investigated.

Both triggers and an atrial electrophysiologic substrate contribute to the development of AF episodes. In the absence of structural heart disease, AF itself promotes a substrate due to electrical remodeling by shortening of refractoriness. However, before this remodeling susceptibility to AF is due to an initiating substrate. This substrate facilitates reentrant mechanisms and appeared to be due to enhanced spatial dispersion of refractoriness. The initiating substrate is associated with a minor form of Cx40 polymorphism in selected patients. Further studies are needed to confirm this relationship in other patient categories and to assess causation.

The diagnosis of an idiopathic RVOT-VT is made by exclusion of ARVC or any other structural heart disease. If there are no signs of RV myocardial changes, such as dilatation, dyskinesia, hypokinesia, or aneurysms and wall thickening, and there are no electrocardiographic signs of ARVC, the patient most likely has an idiopathic RVOT-VT. However, especially in families with a history of sudden death, close follow-up may be useful. When enough minor or major criteria are met, the patient should be risk-stratified and treatment options should be tailored to the individual, taking into consideration the risks and benefits. In some younger patients with, e.g. syncope and one other minor criterion and RVOT-VT, this decision is often very difficult and will probably remain difficult. Genetic testing should be performed in all patients with a family history in order to detect relatives at risk.

Patients with recurrent vasovagal syncope frequently display mild to moderate psychiatric disorders, and the presence of psychiatric illness seem to predict the risk of recurrence. Thus, in our opinion, psychiatric evaluation should be included in the clinical management of patients with severe vasovagal syncope, because it may be valuable in identifying which subjects are at high risk of recurrence and really need long-term treatment. Psychiatric and psychological interventions seem to represent a promising treatment, at least in patients with refractory vasovagal syncope and in those with blood/injury phobia. However, before becoming a first-line therapy for most vasovagal fainters, the positive effects of psychiatric treatment need to be verified in larger, randomised and placebo-controlled trials.

Disturbances in autonomic function can result in a wide variety of conditions that may ultimately culminate in the loss of consciousness. Success in identification of genes conferring susceptibility to hypotension and its clinical sequelae is expected to provide new insights into the pathophysiology of this condition and lead to development of highly accurate genetic tests, permitting identification of subjects with specific inherited susceptibility. These insights may permit intervention at preclinical stages with therapies tailored to underlying primary abnormalities, improving efficacy of treatment (nowadays, mostly empirical), and reducing morbidity from these diseases.