1,720,982 research outputs found
Genotype in hypertrophic cardiomyopathy: clinical implications
Full text linkLa cardiomiopatia ipertrofia (CMPI) è una malattia genetica del muscolo cardiaco caratterizzata da una notevole eterogeneità genetica e fenotipica. Lo scopo del nostro studio è stato quello di valutare la prevalenza e il tipo di mutazioni in un’ampia popolazione di pazienti affetti da CMPI e di ricercare eventuali correlazioni fra il genotipo ed il fenotipo del paziente, valutando le caratteristiche cliniche, ecocardiografiche e soprattutto funzionali, mediante l’utilizzo del test da sforzo cardiopolmonare. Infine abbiamo valutato l’impatto prognostico dei dati genetici, clinici e funzionali nella nostra popolazione. Abbiamo analizzato retrospettivamente i dati clinici e strumentali di 317 pazienti con diagnosi di CMPI sottoposti ad analisi genetica per la ricerca di mutazioni a carico principali geni sarcomerici coinvolti nella patogenesi della CMPI e seguiti per un tempo medio di follow-up di 5,3±4,4 anni. L’analisi genetica, condotta nella maggior parte dei casi con tecnica NGS su una mediana di 10 geni, ha documentato una mutazione patogenetica o probabilmente patogenetica in 182 pazienti (G+ 57,4%) ed una mutazione di incerto significato in 43 pazienti (VUS 13,5%), mentre nel 29% dei pazienti non è stato possibile identificare una mutazione (G-). A differenza dei pazienti G-, i pazienti G+ presentavano un’età inferiore alla diagnosi e alla prima visita, avevano più spesso una storia familiare positiva per CMPI e morte cardiaca improvvisa, all’ecocardiogramma presentavano valori più bassi di frazione d’eiezione e, al test cardiopolmonare, mostravano una ridotta tolleranza allo sforzo ed un minor incremento della pressione arteriosa con l’esercizio. L’analisi univariata e multivariata hanno dimostrato come il dato genetico non risulti un predittore indipendente di prognosi, a differenza dei valori di circulatory power, importante indice funzionale, che risulta un predittore indipendente sia di morte cardiaca improvvisa sia di scompenso cardiaco. In conclusione, i pazienti affetti da CMPI portatori di una mutazione sarcomerica patogenetica o probabilmente patogenetica sono più giovani e presentano forme più aggressive di malattia, associate ad una maggior compromissione della capacità funzionale. Tuttavia il dato genetico non presenta una significativa rilevanza in termini di prognosi a differenza degli indici funzionali del singolo paziente. In particolare, è emerso come il circulatory power rappresenti un importante fattore predittivo di morte cardiaca improvvisa e di scompenso cardiaco nella CMPI
Anemia and heart failure. Is there still a role for erythropoiesis-stimulating agents?
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Integrated preclinical cardiovascular prevention: a new paradigm to face growing challenges of cardiovascular disease
Full text linkCardiovascular disease (CVD) still represents the leading cause of mortality and morbidity worldwide. Despite considerable improvements in the prognosis of CVD and the significant reduction of CVD mortality obtained during the past half century, patients developing CVD, even though satisfactorily treated, still carry coronary artery disease and remain at risk for advanced CVD. Thus, the healthcare and socioeconomic burden linked to CVD remains high. As a result, more effective CVD prevention strategies remain crucial. 'Population strategies' and 'high-risk' approaches both have limitations and have often been viewed as alternative solutions. This persistent dualism could be overcome with the promotion of integrated prevention strategies based on a systematic evaluation of the total risk of disease, at both a population and an individual level. New approaches are also needed to reach people earlier in the course of the vascular disease and, possibly, to prevent risk factors and reduce CVD clinical manifestation
Reducing Cardiovascular and Cancer Risk. How to Address Global Primary Prevention in Clinical Practice
No full textEmerging evidence suggesting the possibility that interventions able to prevent cardiovascular disease (CVD) may also be effective in the prevention of cancer have recently stimulated great interest in the medical community. In particular, data from both experimental and observational studies have demonstrated that aspirin may play a role in preventing different types of cancer. Although the use of aspirin in the secondary prevention of CVD is well established, aspirin in primary prevention is not systematically recommended because the absolute cardiovascular event reduction is similar to the absolute excess in major bleedings. By adding to its cardiovascular prevention benefits, the potential beneficial effect of aspirin in reducing the incidence of mortality and cancer could tip the balance between risks and benefits of aspirin therapy in primary prevention in favor of the latter and broaden the indication for treatment with aspirin in populations at average risk. Prospective and randomized studies are currently investigating the effect of aspirin in prevention of both cancer and CVD; however, clinical efforts at the individual level to promote the use of aspirin in global (or total) primary prevention already could be made on the basis of a balanced evaluation of the benefit/risk ratio
The natriuretic peptides system in the pathophysiology of heart failure. From molecular basis to treatment
Full text linkAfter its discovery in the early 1980s, the natriuretic peptide (NP) system has been extensively characterized and its potential influence in the development and progression of heart failure (HF) has been investigated. HF is a syndrome characterized by the activation of different neurohormonal systems, predominantly the renin-angiotensin (Ang)-aldosterone system (RAAS) and the sympathetic nervous system (SNS), but also the NP system. Pharmacological interventions have been developed to counteract the neuroendocrine dysregulation, through the down modulation of RAAS with ACE (Ang-converting enzyme) inhibitors, ARBs (Ang receptor blockers) and mineralcorticoid antagonists and of SNS with β-blockers. In the last years, growing attention has been paid to the NP system. In the present review, we have summarized the current knowledge on the NP system, focusing on its role in HF and we provide an overview of the pharmacological attempts to modulate NP in HF: from the negative results of the study with neprilysin (NEP) inhibitors, alone or associated with an ACE inhibitor and vasopeptidase inhibitors, to the most recently and extremely encouraging results obtained with the new pharmacological class of Ang receptor and NEP inhibitor, currently defined ARNI (Ang receptor NEP inhibitor). Indeed, this new class of drugs to manage HF, supported by the recent results and a vast clinical development programme, may prompt a conceptual shift in the treatment of HF, moving from the inhibition of RAAS and SNS to a more integrated target to rebalance neurohormonal dysregulation in HF
Natriuretic peptides and volume handling in heart failure. The paradigm of a new treatment
No full textThis article refers to ‘Chronic subcutaneous brain natri- uretic peptide therapy in asymptomatic systolic heart failure’†, by PM McKie et al., published in this issue on pages 433–441
Tailored Angiogenesis Inhibition in Cancer Therapy: Respecting the Heart to Improve the Net Outcome
No full textEven though cancer therapies attain nowadays as many as 10 million survivors, some studies surprisingly report a higher risk of cardiovascular death compared with that of tumor recurrence. Cancer survivors are thus candidates for a thorough cardiovascular evaluation, because they acquire cardiovascular risk together with oncologic cure. VEGF or tyrosinkinase inhibitors, increasingly used in a large variety of tumours with a significant survival advantage, are prototypical drugs simultaneously realizing oncologic care and cardiotoxicity, by targeting angiogenic replicative pathways, involved in both cardiac health and cancer progression. The pathophysiology of cardiovascular disease, mainly consisting in defective angiogenesis, is indeed opposite to that of tumorigenesis and metastasis spreading, both crucially sustained by enhanced blood vessel development. The clinical expression of cardiotoxicity includes not only the development of a dilated hypokinetic cardiomyopathy, currently generally treated with cardiological drugs, but also hypertension, clinical or subclinical atherothrombotic ischemic heart disease and ischemic cardiomyopathy. These clinical syndromes deserve a more adequate cardiovascular assessment and appropriate advanced treatment strategies including percutaneous coronary intervention, coronary artery bypass graft, or device implantation. If not proactively suspected, diagnosed and treated, these manifestations may lead to cardiac events, and reduce overall survival. This review analyzes the available evidence about molecular pathways, predictors and monitoring of impaired angiogenesis-driven cardiotoxicity. Even clinical relevance, pharmacodynamics and markers of efficacy of various intended or "accidental" antiangiogenic drugs will be discussed with the purpose of easing appropriate cardiological surveillance and treatment. Drug tailoring aimed at outcome and cost-effectiveness, according to both drug susceptibility and cardiovascular vulnerability will be finally revised. © 2012 Bentham Science Publishers
Erythropoietin in cardiac disease: effective or harmful?
No full textDiscovered as the primary regulator of erythropoiesis, erythropoietin (EPO) is involved in a broad variety of processes that play a major role in cardiovascular diseases. In particular, the antiapoptotic and pro-angiogenic properties of EPO have prompted a growing interest in the use of EPO for the treatment of myocardial infarction and heart failure. In a variety of myocardial ischemic injury animal models, EPO administration has been shown to acutely reduce infarct size, thereby preserving ventricular function. In addition, cardiac long-term effects of EPO, such as prevention of ventricular remodeling and heart failure, have been described. In recent years, several trials have tested the effects of recombinant human erythropoietin (rhEPO) administration in patients with myocardial infarction and chronic heart failure, in the attempt to translate the cardioprotection found in experimental models to human patients. In view of the generally controversial findings, in this updated review we provide an overview of the results of the most recent trials that investigated the role of erythropoiesis-stimulating agents (ESAs), including rhEPO and its analogue darbepoetin, in the treatment of acute myocardial infarction and heart failure. The problems related to safety and tolerability of ESA therapy are also discussed. Our analysis of the available literature demonstrates that the results of clinical studies in patients with cardiac disease are not uniform and the conclusions are contradictory. Further larger prospective studies are required to test clinical efficacy and safety of EPO
[Role of adherence to chronic drug therapy in patients with cardiovascular disease: an Italian intersocietary consensus document].
No full textChronic therapy with statins, antihypertensive and antiplatelet drugs is one of the most important interventions for primary and secondary prevention of cardiovascular disease. Adherence to drug treatment is key to successful therapeutic intervention, especially in chronic conditions. This holds particularly true in the setting of cardiovascular diseases, because poor adherence may have serious adverse effects in terms of morbidity and mortality. Many factors may contribute to poor adherence, which can be either patient-related or dependent on the healthcare system, the physician and the environment. The identification and appropriate correction of these factors may result in both clinical and economic benefits. In this setting it is also important to assess the implications of the increasing use of generic or equivalent drugs on adherence to pharmacological therapy
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