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Electrocardiographic Diagnosis of Atrial Tachycardia: Classification, P-Wave Morphology, and Differential Diagnosis with Other Supraventricular Tachycardias
Get PDFAtrial tachycardia is defined as a regular atrial activation from atrial areas with centrifugal spread,
caused by enhanced automaticity, triggered activity or microreentry. New ECG classification
differentiates between focal andmacroreentrant atrial tachycardia. Macroreentrant atrial tachycardias
include typical atrial flutter and other well characterized macroreentrant circuits in right and left
atrium. Typical atrial flutter has been described as counterclockwise reentry within right atrial and it
presents a characteristic ECG “sawtooth” pattern on the inferior leads. The foci responsible for focal
atrial tachycardia do not occur randomly throughout the atria but tend to cluster at characteristic
anatomical locations. The surface ECG is a very helpful tool in directing mapping to particular
areas of interest. Atrial tachycardia should be differentiated from other supraventricular tachycardias.
We propose a diagnostic algorithm in order to help the physician to discriminate among those.
Holter analysis could offer further details to differentiate between atrial tachycardia and another
supraventricular tachycardia. However, if the diagnosis is uncertain, it is possible to utilize vagal
maneuvers or adenosine administration. In conclusion, in spite of well–known limits, a good
interpretation of ECG is very importan
L’alimentazione del circuito del sapere attraverso la generazione di nuova imprenditorialità: i processi di spin-off da STMicroelettronics
No full textIl radicamento della STMicroelettronics nel territorio: il potenziamento degli stabilimenti produttivi
No full textRelazioni tra imprese e saperi locali. I risultati di un’indagine sui fornitori di STMicroelettronics a Catania
No full textStruttura e dinamiche competitive del settore microelettronico: il caso della STMicroelettronic
No full textEffects of physical exercise on inflammatory markers of atherosclerosis.
Get PDFIt is well established that physically fit individuals have a reduced risk of developing CVD (cardiovascular disease) and other age-related chronic disorders. Regular exercise is an established therapeutic intervention with an enormous range of benefits. Chronic low-grade systemic inflammation may be involved in atherosclerosis, diabetes and in pathogenesis of several chronic pathological conditions; recent findings confirm that physical activity induces an increase in the systemic levels of a number of cytokines and chemokines with anti-inflammatory properties. The possibility that regular physical exercise exerts anti-inflammation activity, being the interaction between contracting muscle and the other tissues and the circulating cells mediated through signals transmitted by "myokines" produced with muscle contractions. To date the list of myokines includes IL-6, IL-8, and IL-15. During muscle contractions are also released IL-1 receptor antagonis and sTNF-R, molecules that contribute to provide anti-inflammatory actions. Nevertheless discrepancies, analysis of available researches seem to confirm the efficacy of regular physical training as a nonpharmacological therapy having target chronic low-grade inflammation. Given this, physical exercise could be considerate a useful weapon against local vascular and systemic inflammation in atherosclerosis. Several mechanisms explain the positive effect of chronic exercise, nevertheless, these mechanisms do not fully enlighten all pathways by which exercise can decrease inflammation and endothelial dysfunction, and hence modulate the progression of the underlying disease progres
Antivitamin K drugs in stroke prevention.
Get PDFAmong the different subtypes of ischaemic strokes, almost 20 % are of cardiac origin. Different are the causes of cardioembolic stroke, but the most common is the atrial fibrillation, a supraventricular arrhythmia. Appropriate use of antiplatelet drugs and anticoagulants after transient ischaemic attack (TIA) or ischaemic stroke depends on whether the underlying cause is cardioembolic or of presumed arterial origin. Adequate antiplatelet therapy is recommended for secondary prevention after cerebral ischaemia of presumed arterial origin, whether for patients with TIA and ischaemic stroke of cardiac origin, mainly due to atrial fibrillation. Vitamin K antagonists (VKAs) are highly effective in preventing recurrent ischaemic stroke but have important limitations and are thus underused. Current guidelines still regard Vitamin K Antagonists at INR 2·0-3·0 to be the standard treatment after cerebral ischaemia of cardiac origin for patients who can tolerate them. In this setting antiplatelet therapy provides an alternative when oral anticoagulation is contraindicated or when patient choice or compliance limits choice of therapy, but is much less effective than VKAs. Recent trial data performed with new anticogulants such as the factor Xa and thrombin inhibitors will need to be taken into account, in order to prevent several of the clinical problems actually related to VKAs use
Effects of ACE-inhibitors and angiotensin receptor blockers on inflammation.
Get PDFThe role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosterone system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Receptor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflammatory effect of drugs blocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors
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