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Inflammation plays a key role in atherosclerosis. A number of different biomarkers of inflammation are measurable in blood. These include cytokines, chemokines, soluble adhesion molecules, and acute-phase reactants. The first three of these groups of molecules are not routinely available in clinical laboratories. In contrast, however, C-reactive protein is readily measurable, and numerous clinical studies have demonstrated its usefulness as a marker of atherosclerotic risk [12, 13]. Other independent predictive risk factors of cardiovascular events are: myeloperoxidase, serum CD40L (sCD40L), adiponectin, and vWF.

Given its pro-inflammatory properties, myeloperoxidase, produced by the activated PMNs, could be utilised as a marker and mediator of vascular inflammation, confirming the importance of activated PMNs in the physiopathology of the acute coronary syndrome.

The different combinations of immunocompetent cells (macrophage-monocytes and T lymphocytes), of the vascular wall cells, of atheronecrotic material, and of fibrous material regulated by cytokines and growth factors produced by the same cells, allow us to say that every plaque is different from the next. This combination is responsible for the clinical manifestations of coronary atherosclerosis that affect only 5–10% of the individuals who have these lesions.

This hypothesised physiopathological and pathogenetic paradigm is a useful reference point for therapeutic strategies and prevention.

Evidence-based large clinical trials have undoubtedly demonstrated the benefits of ICD in specific populations. Guidelines are intended only as a tool to aid in the decision whether to implant an ICD or CRT device. The responsibility of physicians is primarily towards their patients, but judicious use of health care resources is critical to be able to provide a fair share to all the patients in need of these devices.

The MADIT II study and the SCD-HeFT studies suggest that the ICD reduces total mortality in patients with patients with LV dysfunction. However, the cost-effectiveness of this treatment makes it far from affordable. Better selection of patients that could benefit from an ICD might increase the cost-effectiveness and decrease the percentage of patients in whom an ICD will only produce inappropriate discharges and other undesirable effects. Subgroup analysis has demonstrated a progressive increase in effectiveness of the ICD as QRS duration increases. Little benefit was derived in patients with a QRS of less than 0.12 s, whereas if a QRS duration of 0.15 s was used as a cut-off, a marked reduction in SCD was observed, comparable to that in MUSTT and MADIT I. Similarly, in the SCD-HeFT trial the relative benefits of ICD therapy appeared greater in patients with NYHA class II heart failure, the group in which sudden death is expected to predominate. There seemed to be no benefit in patients with NYHA class III heart failure.

Acute coronary syndromes without persistent ST segment elevation (NSTE-ACS) are common manifestations of coronary artery disease and represent one of the most important reasons for emergency medical care and hospitalisation, accounting for approximately 2.5 million hospital admissions annually worldwide [1]. Although conventional antithrombotic therapy (e.g. unfractionated heparin and aspirin) have proved to reduce the incidence of ischaemic complications, a substantial burden of death and (re-)infarction still remains.

Considerable progress has been made recently in the optimal management of these patients, particularly with regard to (1) the introduction of new powerful antiplatelet drugs (mainly the IIb/IIIa platelet receptor inhibitors) and (2) the demonstration that, in selected cases, an aggressive approach with early coronary angiography and percutaneous coronary interventions (PCI) can be safely performed with low risk of procedural complications and with improved in-hospital and long-term outcome.

Diabetes is a source of significant morbidity and mortality resulting from long-term micro- and macrovascular complications after coronary angioplasty in patients with ACS. Optimal pre-procedural glycaemic control and inhibition of intimal hyperplasia would reduce or impede re-stenosis, resulting in better clinical results.

ARVD is part of the group of cardiomyopathies characterised pathologically by fibrofatty replacement of the right ventricular myocardium and clinically by right ventricular arrhythmias of the LBBB pattern. Pathogenesis, prevalence, and aetiology are yet not fully known. The diagnosis of ARVD is based on the presence of structural, histological, electrocardiographic, and genetic factors. Therapeutic options include antiarrhythmic medication, catheter ablation, implantable cardioverter defibrillation, and surgery. Angiography and echocardiography lack sensitivity and specificity in the diagnosis of ARVD. MR imaging allows a three-dimensional evaluation of especially the right ventricle, and provides the most important anatomical, functional, and morphological criteria for diagnosis of ARVD within one single study. Although demonstration of morphological/functional abnormalities of the right ventricle, especially fat in the right ventricular myocardium, shows high specificity but low sensitivity, MR imaging appears to be the optimal imaging technique for detection and follow-up of clinically suspected ARVD. Positive MR imaging findings, based on the criteria of McKenna et al. [16], should be used as important additional criteria in the clinical diagnosis of ARVD, although negative MR imaging findings do not rule out ARVD.

Available data from controlled clinical trials comparing different drug classes seem to indicate a similar benefit in preventing cardiovascular morbidity and mortality in hypertensive patients. Although some differences in secondary end-points were detected, the overall benefit of various antihypertensive regimens seems to be linked to the extent of BP reduction. The cost of antihypertensive drugs (cost minimisation) is not an overwhelming consideration until cost-benefit analyses are correctly performed. Moreover, although the cost of drugs should be taken into account both for individual patients and for the health provider, cost considerations should not predominate over those of efficacy and tolerability in individual patients.

We therefore believe that liberality of choice among various antihypertensive drugs could offer an appropriate possibility of selecting the right drug for the right patient in order to achieve BP control, a goal which often requires rational combinations of antihypertensive drugs.

Platelets play a pivotal role in the development and progress of atherosclerotic vascular disease, as well as in the pathogenesis of its unstable clinical manifestations (e.g., unstable angina, non-ST elevation myocardial infarction (MI), ST elevation MI, and stroke) [1].

Therefore, antiplatelet therapy is an integral component in the treatment of patients with atherosclerotic cardiovascular disease, which represents the leading cause of death and disability worldwide.

Aspirin is the cornerstone of oral antiplatelet therapy and is effective for the prevention and treatment of cardiovascular events [2].

The availability and cost-effectiveness of aspirin have made it the most widely employed antiplatelet agent for the prevention and treatment of vascular disease.

In November 2003 the American College of Cardiology (ACC) and the European Society of Cardiology (ESC) published in the an expert consensus document on hypertrophic cardiomyopathy (HCM) to inform practitioners about the state of the art in managing this particular disease [1]. HCM is a genetic disease which can cause sudden cardiac death (SCD), particularly in young people (including athletes). As HCM is uncommon (1:500 in the general population) [2], many cardiologists do not see many patients with this disease, and may therefore have some difficulty in managing the cases of the patients they do see.

This document has been written by specialists with extensive experience of managing HCM. However, the statements and treatment strategies put forward by the panel are very cautious owing to the considerable difficulties involved in reaching conclusions: (1) because the disease is uncommon, the available data are relatively limited; (2) HCM has a broad disease spectrum, so individual patients may have very different risk profiles; (3) large-scale controlled and randomised study designs (as in coronary artery disease) are not available. Consequently most information derives from non-randomised and retrospective studies.

Although lowering the blood pressure stands out as the fundamental mechanism for preventing any complication of hypertension, recent data suggest that ARBs might play an important and perhaps independent contribution in the prevention of AF. By inhibiting the effects of angiotensin II, ARBs reduce both blood pressure and myocardial fibrosis, with important potential implications for atrial and ventricular electric remodelling and atrial pressure and stretch. The LIFE study has shown the beneficial effect of losartan in reducing the risk of AF in hypertensive subjects in sinus rhythm. Further studies should clarify to what extent this effect applies to other ARBs.