1,721,072 research outputs found
Peak oxygen uptake in heart failure. Look behind the number!
No full textAn impaired peak oxygen uptake (V̇O2peak) during a maximal cardiopulmonary exercise test (CPET) has been shown extensively to correlate with a poor prognosis in heart failure (HF) patients. Even, the abovementioned relationship remains effective irrespective of the left ventricular ejection fraction (LVEF), a most recent study by Sato showing an unaltered V̇O2peak prognostic power also in the early defined HF with mid-range ejection fraction class (HFmrEF). The advantage of adopting V̇O2peak to evaluate and, possibly, to manage clinically this setting of patients is linked to its composite character which enables it to account for most of the mechanisms underlying the HF pathophysiology. In fact, as per the well-known Fick Law, V̇O2 represents arithmetically the resulting number of the product between cardiac output (CO = stroke volume*heart rate) and artero-venous O2 difference (ΔavO2). Thus, a reduced V̇O2peak, as a single variable, mirrors variably a reduced LVEF and/or a concomitant chronotropic incompetence as well as a huge number of conditions able to impact negatively on the O2 transport and deliver
Cardiopulmonary exercise testing in heart failure: from ugly duckling to swan
No full text[No abstract available
Cardiopulmonary exercise testing: An increasingly important step in managing hypertrophic cardiomyopathy.
No full textHypertrophic cardiomyopathy, the most common genetic heart disease, inherited with an autosomal dominant pattern, incomplete penetrance and variable expressivity, is characterized by markedly heterogeneous morphologic and clinical spectra [...]. In such a context, as it is yet worldwide recognized in heart failure with reduced ejection fraction (HFrEF) [...], the cardiopulmonary exercise test (CPET) is becoming an essential tool in the contemporary HCM clinical management [...]. Indeed, also in this setting of patients, a well-reasoned CPET assessment might be extremely useful to evaluate objectively the true functional capacity [...] as well as to better understand mechanisms underlying the exercise impairment [..]. Properly the latter aspect represents one of the most challenging field in the HCM scenario where, besides the disease-related complications, a number of factors have been advocated as possibly implied [...], including left ventricular (LV) hypertrophy with myocardial fiber disarray and interstitial fibrosis, LV outflow tract obstruction, microvascular ischemia, chronotropic incompetence, peripheral muscle changes and, in nearly 5% of cases, even LV systolic dysfunction (progression to the “end-stage” phase) (Figure 1). Contextually, growing evidences suggest a possible role of the CPET variables also in stratifying the HCM risk of adverse cardiac events both in terms of sudden cardiac death (SCD) as well as of HF development [...], the latter gaining even more in significance in the last decades due to the improvements in pharmacological and no-pharmacological HCM management
Short-term RR-interval power spectral analys as a tool to stratify the risk of sudden deah in various cardiovascular condition
No full textRecently short-term power spectral analysis of heart rate variability (HRV) has been used also to stratify the risk of sudden death in subjects with chronic heart failure (CHF). Short-term spectral analysis of RR variability in normotensive healthy subjects shows two distinct components of HRV: high-frequency power (HF), which synchronizes with breathing and therefore reflects vagal modulation of the sinus node, and low-frequency power (LF) oscillating around 0.1 Hz influenced also, though not solely, by sympathetic modulation of the sinus node. Among factors that strongly influence autonomic control of the sinus node and HRV are aging, hypertension and CHF. CHF, markedly reduces both spectral components of HRV and the paradoxical LF reduction is a risk factor for sudden death. It is reasonable that, in a next future, LF could become a useful tool to identify more precisely subjects at high risk of sudden death in various cardiovascular conditionsRecently short-term power spectral analysis of heart rate variability (HRV) has been used also to stratify the risk of sudden death in subjects with chronic heart failure (CHF). Short-term spectral analysis of RR variability in normotensive healthy subjects shows two distinct components of HRV: high-frequency power (HF), which synchronizes with breathing and therefore reflects vagal modulation of the sinus node, and low-frequency power (LF) oscillating around 0.1 Hz influenced also, though not solely, by sympathetic modulation of the sinus node. Among factors that strongly influence autonomic control of the sinus node and HRV are aging, hypertension and CHF. CHF, markedly reduces both spectral components of HRV and the paradoxical LF reduction is a risk factor for sudden death. It is reasonable that, in a next future, LF could become a useful tool to identify more precisely subjects at high risk of sudden death in various cardiovascular condition
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
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
Letter regarding the article ‘Changes in 6‐min walk test is an independent predictor of death in chronic heart failure with reduced ejection fraction’
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