Author: Gianpiero Pescarmona
Date: 08/04/2007


Calcium and...


Più fibrillazione atriale con glucocorticoidi
L'impiego di glucocorticoidi risulterebbe associato a una maggiore incidenza di fibrillazione e di flutter atriale. Sebbene la somministrazione di questi farmaci sia stata da tempo correlata al rischio di infarto del miocardio e ictus, per la prima volta ricercatori danesi ne hanno indagato l'effetto su episodi di fibrillazione e di flutter atriale attraverso uno studio caso controllo. L'analisi di tre database nazionali e regionali ha consentito di valutare pazienti con diagnosi di fibrillazione atriale o di flutter, nel periodo compreso tra il 1999 e il 2005. Per ogni caso sono stati selezionati 10 individui sani dello stesso sesso ed età. Tra i pazienti è stato identificato un gruppo che utilizzava i farmaci al momento dell'indagine e uno che lo aveva fatto in precedenza. In sintesi, coloro che stavano assumendo glucocorticoidi sono risultati esposti a un rischio notevolmente più elevato sia di fibrillazione atriale sia di flutter rispetto a individui che non ne avevano mai fatto uso (odds ratio=1,92). In aggiunta, per impieghi a breve termine è stato registrato un odds ratio di 3,62 mentre per quelli più duraturi di 1,66 (L.A.).

Archives of Internal Medicine 2009, 169, 1677-1683

2011-02-24T16:14:31 - Luca Amendolia


Failure of impulse initiation may result in slow heart rates (bradyarrhythmias), whereas failure of impulses to propagate normally from atrium to ventricle results in dropped beats (heart block) that usually reflect an abnormality in either the AV node or the His–Purkinje system. These abnormalities may be caused by drugs or by structural heart disease. Abnormally rapid heart rhythms (tachyarrhythmias) are common clinical problems that may be treated with antiarrhythmic drugs. Three major underlying mechanisms have been identified: enhanced automaticity, triggered automaticity, and reentry.

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Enhanced Automaticity
Enhanced automaticity may occur in cells that normally display spontaneous diastolic depolarization— the sinus and AV nodes and the His–Purkinje system. β-adrenergic stimulation, hypokalemia, and mechanical stretch of cardiac muscle cells increase phase 4 slope and so accelerate pacemaker rate, whereas acetylcholine reduces pacemaker rate both by decreasing phase 4 slope and by hyperpolarization (making the maximum diastolic potential more negative). In addition, automatic behavior may occur in sites that ordinarily lack spontaneous pacemaker activity; e.g., depolarization of ventricular cells by ischemia) may produce such “abnormal” automaticity.

Afterdepolarizations and Triggered Automaticity
Under some pathophysiological conditions, a normal cardiac action potential may be interrupted or followed by an abnormal depolarization. If this abnormal depolarization reaches threshold, it may give rise to secondary upstrokes that can propagate and create abnormal rhythms. These abnormal secondary upstrokes occur only after an initial normal, or “triggering,” upstroke and so are termed triggered rhythms. Under conditions of intracellular Ca2+ overload (e.g., myocardial ischemia, adrenergic stress,
digitalis intoxication, or heart failure), a normal action potential may be followed by a delayed afterdepolarization (DAD). If this afterdepolarization reaches threshold, a secondary triggered beat or beats may occur. In a second type of triggered activity, the key abnormality is marked prolongation of the cardiac action potential. When this occurs, phase 3 repolarization may be interrupted by an early afterdepolarization (EAD). EAD-mediated triggering clinical arrhythmias are most common when the underlying heart rate is slow, extracellular K+ is low, and certain drugs that prolong action potential duration are present. EAD-related triggered upstrokes probably reflect inward current through Na+ or Ca2+ channels or Na+–Ca2+ exchange. When cardiac repolarization is markedly prolonged, polymorphic ventricular tachycardia with a long QT interval, known as torsades de pointes, may occur. This arrhythmia is thought to be caused by EADs, which trigger “functionally defined” reentry owing to heterogeneity of action potential durations across the ventricular wall. Congenital long QT syndrome, a disease in which torsades de pointes is common, can be caused by mutations in the genes encoding the Na+ or Ca2+ channels or, more commonly, the channels underlying the repolarizing currents IKr and IKs.

Reentry can occur when impulses propagate by more than one pathway between two points in the heart, and those pathways have heterogeneous electrophysiological properties. Patients with Wolff–Parkinson–White (WPW) syndrome have accessory connections between the atrium and ventricle. With each sinus node depolarization, impulses can excite the ventricle via the normal structures (AV node) or the accessory pathway. However, the electrophysiological properties of the AV node and accessory pathways are different: Accessory pathways usually consist of fast response tissue, whereas the AV node is composed of slow-response tissue. Thus, with a premature
atrial beat, conduction may fail in the accessory pathway but continue, albeit slowly, in the
AV node and then through the His–Purkinje system; there the propagating impulse may
encounter the ventricular end of the accessory pathway when it is no longer refractory. The likelihood that the accessory pathway is no longer refractory increases as AV nodal conduction slows. When the impulse reenters the atrium, it then can reenter the ventricle via the AV node, reenter the atrium via the accessory pathway, and so on. Reentry of this type, referred to as AV reentrant tachycardia, is determined by:
- the presence of an anatomically defined circuit;
- heterogeneity in refractoriness among regions in the circuit;
- slow conduction in one part of the circuit.
Similar “anatomically defined” reentry commonly occurs in the region of the AV node (AV nodal reentrant tachycardia) and in the atrium (atrial flutter). The term paroxysmal supraventricular tachycardia (PSVT) includes both AV reentry and AV nodal reentry, which share many clinical features. It now sometimes is possible to identify and ablate critical portions of reentrant pathways (or automatic foci), thus curing the patient and obviating the need for longterm drug therapy.

Reentry also may occur in the absence of a distinct, anatomically defined pathway. If ischemia or other electrophysiological perturbations result in an area of sufficiently slow conduction in the ventricle, impulses exiting from that area may find the rest of the myocardium reexcitable, in which case fibrillation may ensue. Atrial or ventricular fibrillation is an extreme example of “functionally defined” (or “leading circle”) reentry: Cells are reexcited as soon as they are repolarized sufficiently to allow enough Na+ channels to recover. In this setting, neither organized activation patterns nor coordinated contractile activity is present.









anatomical (due its structure)

vascular (due to the local circulation)

physiopathological (due to tissue function and activity)




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