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Prognostic evaluation of heart failure in women: insight from the MECKI score database
Full text linkBackground: Heart failure is a multi-organ disease often associated with comorbidities. Heart failure in women assumes extremely peculiar characteristics. The pathophysiology of the damage is profoundly different; the endothelial dysfunction, the damage to the microcirculation and the comorbidities that cause chronic heart failure are in fact frequently associated with a type of decompensation that has a better ejection fraction than those in the male population. Symptoms are often vague and not "typical", which often delays diagnosis, bringing patients to the doctor's attention only belatedly. This aspect frequently leads to having a much older age than the male gender at diagnosis, which determines higher co-pathology degree and polypharmacy. In this situation, female patients are highly exposed to risk of iatrogenic damage and poor compensation and therapeutic unsuccess. Age is often a limiting factor also for enrollment in clinical trials, which therefore frequently have a gender-related bias.
To identify the prognosis, it is necessary to take into account several variables. The cardiopulmonary test allows a comprehensive assessment of the patient during physical activity as physical exercise involves the cardiovascular, hematopoietic, sympathetic/parasympathetic, neuro-hormonal, respiratory and motor systems. The oxygen consumption at the peak and at the anaerobic threshold mainly depend on the cardiovascular and motor systems while the VE/VCO2 is an index not only of ventilatory efficiency and of the ventilation/perfusion mismatch of the lung, but also of activation of metabo- and chemoreceptors.
The proposed risk scores are very numerous but mostly based on data obtained in male populations. Few use the cardiopulmonary exercise test. Among these, the Metabolic Exercise Cardiac Kidney Indexes -MECKI score- was obtained by evaluating about 80 variables of which 6 have independent prognostic significance: hemoglobin, natremia, renal function (MDRD), left ventricular ejection fraction (LVEF), oxygen consumption at the peak of the exercise [%] and VE/VCO2 slope. The MECKI score demonstrated in patients with systolic heart failure, considering the combined cardiovascular death, urgent heart transplant and LVAD as an end-point, AUC = 0.804 (0.754-0.852) at 1 year, 0.789 (0.750-0.828) at 2 years, 0.762 (0.726-0.799) at 3 years and 0.760 (0.724-0.796) at 4 years.
Aim of the study: identify parameters and variables which could be associated to a different prognosis in men and women enrolled in the MECKI Score database. Thus, the objectives of the present study: 1) achievement in 2 years of at least 7000 cases with about 1400 cases of female gender; 2) evaluation of the prognosis in systolic heart failure in the female gender, differentiating by: a) etiology (ischemic non-ischemic), b) presence/absence of atrial fibrillation, c) presence of CRT, d)
presence/absence of diabetes/hypertension/dyslipidemia; 3) evaluation in the female gender of the prognostic cut-offs of the variables that generate the MECKI score.
Results: In reviewing the MECKI Score database, numerous, mostly expected, gender differences emerged which reinforce the initial hypothesis. In the population examined, there is no substantial difference in age, women have, although overweight, a lower BMI than men, a better LVEF, significant differences in renal function and hemoglobin concentration (these parameters are already corrected for sex); no difference in terms of natremia. Other differences were observed about pharmacological therapy among the two groups.
Kaplan-Meier survival curves showed that the MECKI Score is accurate in predicting the risk also in the female population, as there are no overall differences in the prevalence of events in the two sexes at two years. Differences in survival curves begin to be observed over longer follow-up periods.
Conclusions: gender-specific characteristics have a critical impact on heart failure in women and it should be valuable to concentrate future analysis for the identification of any specific subpopulation that have peculiarities that can impact on the prognosis. However, the MECKI Score maintains its prognostic power at two years follow up, even in the female population, guaranteeing appropriate clinical and therapeutic choices
Il QT variability index come strumento per stratificare il rischio di morte improvvisa
No full textLa morte cardiaca improvvisa (MCI) è costituisce la principale causa di mortalità in paziente con scompenso cardiaco e pregresso infarto del miocardio. Lo studio e l’individuazione dei pazienti a rischio è di vitale importante per garantire il giusto approccio e la corretta terapia al paziente. Il QT variability index (QTVI) è un marker non invasivo di labilità della ripolarizzazione che è stato applicato ad un ampio spettro di soggetto con patologia cardiovascolare. E’ un rapporto tra la variabilità del QT e la Heart Rate Variability (HRV) normalizzate, costituendo quindi un valore riferibile all’attività del sistema nervoso autonomo. Contrariamente a quanto avviene per altri metodi di valutazione, come l’alternanza dell’onda T, il QTVI non risente delle modificazioni della frequenza cardiaca. Gli ultimi studi ci inducono a ritenere che il QTVI potrebbe essere di aiuto al clinico nella scelta del timing per l’impianto del ICD, sia nel paziente con cardiopatia dilatativa che in quelli con cardiomiopatia ipertrofica e scompenso, prestandosi con grande efficacia alla valutazione e il follow-up di questi pazienti.Sudden cardiac death is the main cause of mortality in patients affected by chronic heart failure (CHF) and with history of myocardial infarction. Selection of patients at risk of sudden cardiac death is dramatically important to choose the correct therapeutic approach. The QT variability index (QTVI) is a non-invasive measure of repolarization lability that has been applied to a wide variety of subjects with cardiovascular disease. It is a ratio of normalized QT variability to normalized heart rate variability, and therefore includes an assessment of autonomic nervous system tone. As opposed to T wave alternans, QTVI assesses variance in repolarization at all frequencies. Last studies suggests that QTVI should help clinicians choosing the correct ICD timing implantation, in patients with dilatative or hypertrophic cardiomyopathy ore CHF, seen its efficacy in patients evaluation and follow up
La sincope. fisiopatologia, diagnosi e terapia. [syncope: physiopathology, diagnosis and therapy].
No full textL’inquadramento diagnostico della sincope è un problema complicato per il medico per l’allarme che determina questo sintomo nel paziente, ma al contempo per l’estrema numerosità delle cause
che possono generare l’episodio di perdita di coscienza transitoria. In circa due terzi dei casi la sincope è neuromediata, nel giovane èvasovagale, mentre nell’anziano è dovuta ad ipersensibilità senocarotidea. Queste due sincopi hanno, però, un percorso diagnostico e terapeutico completamente diverso, soprattutto nel secondo caso andràconsigliato l’impianto di un pacemarker come profilassi per possibili altri episodi ed eventuali traumi che ne conseguono. In un quinto dei casi la causa è aritmica e più spesso è una bradiaritmia e anche in questo caso l’impianto di pacemaker ridurrà il rischio di recidiva. Inuna piccola parte dei casi la sincope è dovuta a tachiaritmie ventricolari che possono recidivare ed indurre anche morte improvvisa, in questo caso l’impianto di defibrillatore insieme all’uso corretto di farmaci antiaritmici ridurrà il rischio di morte improvvisa. Nell’articolo vengono esaminate dettagliatamente tutte le cause di sincope, e il loro razionale percorso diagnostico e terapeutico.Nowadays, syncope still generates complicated challenges for clinicians for the alarm it arises in patients and, at the same time, for the multiple causes it has determined by. In almost one third of cases, syncope is neuromediated, in young subjects in vasovagal, whereas in elderly is often determinated by carotid sinus hypersensitivity. These two kinds of syncope have two completely different diagnostic approach. In some cases pace-maker implantation will be suggested to avoid new syncope episodes. In a 20% of cases, the underlying cause is arrhythmic, most of all bradiarrhythmia which is treated with pace-maker implantation. In a little number of cases, syncope is caused by ventricular arrhythmias, that require the implantation of a defibrillator device. In this review, we analyze in detail every cause of syncope with its diagnostic and therapeutic approac
Authonomic nervous system and heart activity. old and new (review) [sistema nervoso autonomo e attività cardiaca. vecchie e nuove acquisizioni]
No full textThe autonomic nervous system plays an important role in the modulation of cardiac electrophysiology and arrhythmo-genesis. The mechanisms by which autonomic activation is arrhythmogenic or antiarrhythmic are complex and different for specific arrhythmias. In atrial fibrillation, simultaneous sympathetic and parasympathetic activations are the most common trigger. In contrast, in ventricular fibrillation in the setting of cardiac ischemia, sympathetic activation is proar-rhythmic, whereas parasympathetic activation is antiarrhythmic. In inherited arrhythmia syndromes, sympathetic stimulation precipitates ventricular tachyarrhythmias and sudden cardiac death except in Brugada and J-wave syndromes where it can prevent them. Heart rate variability (an index of myocardial temporal dispersion), analyzed with QT variability index (QTVI), specifics segment of QT interval (QT peak-end) or intra-QT phase spectral coherence, may be considered a possible tool in stratifying the arrhythmic susceptibility in patients at risk of FV and sudden cardiac death (SCD). Moreover, direct nerve activity recordings (stellate ganglion and vagal nerve) in diseased animal models have provided insights into the understanding of the role of cardiac ANS in arrhythmogenesis. The identification of specific autonomic triggers in different arrhythmias has brought the idea of modulating autonomic activities for both preventing and treating these arrhythmias
QT variability before premature ventricular contraction as a short term predictor of non sustained ventricular tachycardia in chronic heart failure
No full textBackground – Myocardial repolarization lability before and after premature ventricular complex (PVC) has been recently suggested as a potential marker of malignant ventricular arrhythmias. We therefore sought to investigate possible different behavior of QT and Tpeak-Tend (Te) interval variability index (VI) when calculated before and after a PVC with respect a non-sustained ventricular tachycardia (nsVT).
Method and Results – QTVI, TeVI and other short-term repolarization indexes were calculated before and after PVC (PVC group) as well as before and after nsVT (nsVT group). QTVI and TeVI before PVC were significantly lower in the nsVT group than PVC group (p<0.05), whereas QTVI and TeVI differences resulted significantly higher in the nsVT than the counterpart (p<0.01). At multivariate logistic regression analysis, low QTVI and TeVI values before PVC were significantly associated to higher risk of imminent nsVT (QTVI: OR, 6.44; 95% CI, 1.33-31.18, p<0.05; TeVI: OR, 6.87; 95% CI, 1.25-37.72, p<0.05).
Conclusion – QTVI and TeVI before PVC seem be predicative for imminent nsVT. Further studies needed to assess possible utility of these findings for monitoring patients with chronic heart failure at high risk of sudden cardiac death
Menopausal hormone therapy and breast cancer risk. the cardiological point of view
No full textWe felt the compulsory and urgent need to highlight some peculiar risk factors' prevention in women, on the basis of evidence that certain typical or exclusive conditions in women could alter their personal risk, clinical presentation, therapeutic response and prognosis in cardiovascular diseases. In a recent metanalysis, hormone replacement therapy (HRT) has been connected to an increased risk for breast cancer in postmenopausal women. So, we are worried about the possible future, incorrect underuse of HRT to avoid breast cancer in women with high cardiovascular risk.We would like to stimulate a proper awareness in clinicians, in order to elite the need of a responsible, appropriate and patient-customized approach to personal risk factors, undertaking all possible prevention strategies in order to avoid future damaging and expensive diseases
Influence of aging and chronic heart failure on temporal dispersion of myocardial repolarization
No full textQT and Tpeak-Tend (Te) intervals are associated with sudden cardiac death in patients with chronic heart failure (CHF). We studied age-dependent influence on short-term temporal dispersion of these two variables in patients with postischemic CHF. Method: We grouped 75 CHF and 53 healthy control subjects into three age subsets: ≤50 years, >50 years and ≤65 years, and >65 years. We then calculated the following indices: QT and Te variability index (QTVI and TeVI), the ratio between the short-term variability (STV) of QT or Te, and the STV of resting rate (RR) (QT/RR STV and Te/RR STV). Results: In all different age subgroups, patients with CHF showed a higher level of QTVI than age-matched control subjects (≤50 years: P 50 years and ≤65 years: P 65 years: P 2: 0.178, P 2: 0.433, P < 0.001) were positively related to age in normal subjects, even if the first correlation was weaker than the second one. Conclusion: Our data showed that QTVI could be used in all ages to evaluate repolarization temporal liability, whereas the other indices are deeply influenced by age. Probably, the age-dependent increase in QTVI was more influenced by a reduction of RR variability reported in older normal subjects. © Piccirillo et al, publisher and licensee Dove Medical Press Ltd
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