Monoclonal gammopathy of undetermined significance in pediatric kidney transplant: a possible role of Epstein-Barr virus.

MG is a common event of hematologic malignancies. There are many papers regarding kidney transplantation patients with MGUS in adults, while data in pediatrics are scarce. The etiology and clinical significance of MGUS are unclear both in adults and children. Immunosuppressive drugs, graft antigenicity, and viral infection could play a possible role. The viruses most frequently implicated seem to be EBV or CMV in particular, but their role has to be defined better. However, many investigators have emphasized an impaired balance between an adequate immune response and reactivation of viral infection.

[Electromagnetic interference of electronic devices in workers with AICD]. / Interferenze elettromagnetiche dei dispositivi elettronici in lavoratori portatori di AICD.

The Implantable Cardioverter Defibrillators and the Pacemakers are devices that produce electric signals and consequently they are touchy to the electromagnetic interferences. This touchiness may cause a temporary or permanent device's malfunction both for short, but of high intensity, and prolonged exposures. Considered the wide diffusion in the job's environments of the technologies based on the electromagnetic waves, the aim of the study is identify the presence of electronic equipment's electromagnetic interferences in AICD bearing workers. The last aim is give to the AICD bearing workers more detailed information about the prevention of inappropriate AICD shocks.

The Snail repressor recruits EZH2 to specific genomic sites through the enrollment of the lncRNA HOTAIR in epithelial-to-mesenchymal transition.

The transcription factor Snail is a master regulator of cellular identity and epithelial-to-mesenchymal transition (EMT) directly repressing a broad repertoire of epithelial genes. How chromatin modifiers instrumental to its activity are recruited to Snail-specific binding sites is unclear. Here we report that the long non-coding RNA (lncRNA) HOTAIR (for HOX Transcript Antisense Intergenic RNA) mediates a physical interaction between Snail and enhancer of zeste homolog 2 (EZH2), an enzymatic subunit of the polycomb-repressive complex 2 and the main writer of chromatin-repressive marks. The Snail-repressive activity, here monitored on genes with a pivotal function in epithelial and hepatic morphogenesis, differentiation and cell-type identity, depends on the formation of a tripartite Snail/HOTAIR/EZH2 complex. These results demonstrate an lncRNA-mediated mechanism by which a transcriptional factor conveys a general chromatin modifier to specific genes, thereby allowing the execution of hepatocyte transdifferentiation; moreover, they highlight HOTAIR as a crucial player in the Snail-mediated EMT.

Retrospective analysis of 300 cases of paroxysmal supraventicular tachycardia by electrophysiological transesophageal study.

AIM: Paroxysmal supraventricular tachycardia (PSVT) is a very frequent type of arrhythmia. Atrioventricular nodal reciprocating tachycardia (AVNRT) and atrioventricular reciprocating tachycardia through extranodal accessory pathways (AVRT) are the most common types of paroxysmal supraventricular tachycardia. We describe our experience in diagnosing these tachycardia by electrophysiological transesophageal study (ETS). METHODS: Three hundred patients, 155 men and 145 women, (mean age, 37.2 +/- 16 years), with a history of palpitations underwent clinical evaluation and ETS. The clinical features of those with AVNRT and those with AVRT were compared. RESULTS: Of a total of 300 patients, tachycardia was diagnosed only in 234, of which 136 (58%) had AVNRT and 98 (42%) had AVRT. AVNRT patients were older than those with AVRT (P = or < 0.004); patients with AVRT had palpitations earlier (P = or < 0.0001). Dyspnea and asthenia were the most frequent symptoms in the AVNRT patients (P = or < 0,02; P = or < 0.04). There were statistically significant differences between the two patient groups in Wencke-bach time (P = or < 0.05), ventricular-atrial (V-A) interval (P = or < 0.03) and period of induced tachycardia (P = or < 0.04). CONCLUSIONS: ETS revealed important clinical and electrophysiological differences between patients with AVRT and those with AVNRT.

Superior vena cava thrombosis after intravascular AICD lead extraction: a case report.

Pacemaker lead extraction has been shown to be an effective and safe treatment in the case of infected per-manent pacemaker leads. However, it can lead to potentially serious complications, usually occurring during the ex-traction procedure. This report describes a case of a 74-year-old male with a persistent superior vena cava thrombo-sis related to an infected permanent pacemaker lead transvenous extraction. Clinical and surgical management are discussed.

Efficacy and safety of dabigatran in a "real-life" population at high thromboembolic and hemorrhagic risk: data from MonaldiCare registry.

OBJECTIVE: Dabigatran is a novel target specific oral anticoagulant for stroke prevention in non valvular atrial fibrillation. Little is still known about its real-world effectiveness and safety in the italian population. Aim of our study was to evaluate the efficacy and safety of dabigatran in a large single-center cohort of "real-life" italian population with non-valvular AF and to compare the results with those obtained from the RE-LY trial and the Medicare study. PATIENTS AND METHODS: We studied a prospective cohort of 2108 patients (1119 male; mean age 69.4 ± 9.4 years) who started the oral anticoagulant treatment with dabigatran 110 mg twice-daily (DAB 110; N = 1075; 51%) or 150 mg twice-daily (DAB 150; N = 1033; 49%). Follow-up data were obtained trough outpatients visits each 3-6 months for assessing the clinical status, adherence to treatment, occurrence of side effects and major cardiovascular complications. RESULTS: In DAB 150 group the mean age was 64.9 ± 8.8 years, 56.8% of patients was male. CHA2DS2Vasc Score was ≥ 3 in 94.3% and HAS-BLED was ≥ 3 in 59.7%. In DAB 110 group (N = 1075) the mean age was 73.9 ± 7.5 years; 49.5% of patients was male. CHA2DS2Vasc Score was ≥ 3 in 73.4% and HAS-BLED was ≥ 3 in 87.4% of DAB 110 patients. One patient taking Dabigatran 110 mg bid had ischemic stroke without significantly neurological sequelae. In both groups, no patient experienced hemorrhagic stroke during the follow-up period. 147 patients (6.9%) of MonaldiCare population reported adverse effects from treatment with dabigatran, of whom 121 patients (5.7%) discontinued therapy. We reported one case of subarachnoid hemorrhage (0.05%) in a patient with high thrombo-embolic and high hemorrhagic risk score who was taking dabigatran 150 mg bid and one case (0.05%) of bladder bleeding in a patient who was taking dabigatran 110 mg bid. No major gastrointestinal bleeding was observed in the MonaldiCare population. CONCLUSIONS: MonaldiCare registry showed a safety profile of both dosages of dabigatran regarding major of fatal bleeding in a "real life" single center italian population at high thromboembolic and hemorrhagic risk. The majority of MonaldiCare patients tolerated dabigatran treatment without significant side effects. The efficacy of dabigatran was demonstrated by very low prevalence of ictus/TIA, also when patients underwent electrical AF cardioversion independently of the transesophageal examination.

Autophagy regulates hepatocyte identity and epithelial-to-mesenchymal and mesenchymal-to-epithelial transitions promoting Snail degradation.

Epithelial-to-mesenchymal transition (EMT) and the reverse process mesenchymal-to-epithelial transition (MET) are events involved in development, wound healing and stem cell behaviour and contribute pathologically to cancer progression. The identification of the molecular mechanisms underlying these phenotypic conversions in hepatocytes are fundamental to design specific therapeutic strategies aimed at optimising liver repair. The role of autophagy in EMT/MET processes of hepatocytes was investigated in liver-specific autophagy-deficient mice (Alb-Cre;ATG7(fl/fl)) and using the nontumorigenic immortalised hepatocytes cell line MMH. Autophagy deficiency in vivo reduces epithelial markers' expression and increases the levels of mesenchymal markers. These alterations are associated with an increased protein level of the EMT master regulator Snail, without transcriptional induction. Interestingly, we found that autophagy degrades Snail in a p62/SQSTM1 (Sequestosome-1)-dependent manner. Moreover, accordingly to a pro-epithelial function, we observed that autophagy stimulation strongly affects EMT progression, whereas it is necessary for MET. Finally, we found that the EMT induced by TGFß affects the autophagy flux, indicating that these processes regulate each other. Overall, we found that autophagy regulates the phenotype plasticity of hepatocytes promoting their epithelial identity through the inhibition of the mesenchymal programme.

Impact of heart rate and atrioventricular delay on left ventricular diastolic filling in patients with dual-chamber pacing for sick sinus syndrome or atrioventricular block.

We examined the effect of left ventricular filling on different combinations of programmable heart rate and atrioventricular delay in patients with dual-chamber pacemakers. Pacing mode with heart rates of 60 beats/min and 156 ms of atrioventricular delay induced a diastolic pattern that resembles more than others the one observed in healthy subjects in sinus rhythm.

Evaluation of the antioxidant response in the plasma of healthy or hypertensive subjects after short-term exercise.

Reactive oxygen species are produced during exercise. The antioxidants prevent or limit tissue damages by these species in physiological conditions. In particular, ascorbate and urate scavenge peroxynitrite, which can alter the function of many molecules, including the lecithin-cholesterol acyltransferase (LCAT) enzyme involved in reverse cholesterol transport. The aims of the present study were to compare the plasma antioxidant response to an ergometric test (ET) in hypertensive and healthy subjects, evaluate the exercise-dependent nitrosative stress in plasma, and assess whether the LCAT activity is altered by the exercise. Plasma samples, prepared before and after ET from hypertensive or healthy volunteers, were analysed for their levels of ascorbate, urate, alpha-tocopherol, retinol, nitrotyrosine, and LCAT activity. The alpha-tocopherol and retinol levels did not significantly change in both groups during exercise, while the ascorbate level changed displaying higher increase in controls (+38.8%) than in hypertensives (+17.2%). In these patients, during ET, the urate and nitrotyrosine levels changed more than in normotensives (+13.5 and +40.6% vs -3.1 and +25.2%, respectively). The antioxidants effectively prevented loss or reduction of LCAT activity, as it was similar in hypertensives and normotensives, and did not change after ET. The results demonstrate that exercise is associated with enhanced protein nitrosation, and suggest that the ascorbate or urate levels increase to limit oxidative damage.

Prolonged corrected QT dispersion.

The anthracyclines are antibiotics effective in the treatment of many malignancies. However, their usefulness is limited by the development of potentially acute or chronic cardiotoxicity. No definitive guidelines exist for monitoring cardiac function during and after anthracyclines although methods have been suggested. Electrocardiograms and echocardiograms are routinely utilized for noninvasive assessment of myocardial function. The aim of the study was to assess the effects of doxorubicin on ventricular repolarization time indexes, as they have been shown to be effective in the identification of electrical myocardial instability and hence in the identification of the risk for either arrhythmia or heart failure. Electrocardiographic parameters were compared in 27 cancer patients before and after chemotherapy including doxorubicin. The data of the present study show that after only a short period of treatment with doxorubicin there is a significant increase in ventricular recovery time indexes (QTc dispersion and 'Adjusted' QTc dispersion). The relation between the electrophysiological response to doxorubicin and the potential cardiotoxic effect of this drug remains to be established through prospective studies.

Increased dispersion of ventricular recovery time as a new repolarization abnormality in the Wolff-Parkinson-White syndrome.

The aim of our study was to assess whether the presence of ventricular preexcitation affects the spatial distribution of ventricular recovery time. Recent reports support the hypothesis that QT and QTc dispersions (QTd and QTcd) can be reliably adopted as a non-invasive parameter to estimate regional discrepancies of ventricular repolarization. The ECGs of 32 healthy subjects with Wolff-Parkinson-White syndrome and of 29 normal individuals have been analysed using a Digitizer (Calcomp 9000), in order to obtain, for each subject, a mean QRS (M-QRS), QT (M-QTe), QTc (M-QTec), JT (M-JT), JTc (M-JTc) from all the measured intervals of the 12 standard ECG leads. QRS, QT and QTc dispersions (QRSd, QTd, QTcd) were defined as the difference between the maximal and minimal QRS, QTe and Qtec values calculated in the various leads. We attained the following results: patients with WPW syndrome exhibited, with respect to controls, longer M-QRS (P < 0.001) and M-QTec (P < 0.001) values, despite similar M-QTe (P = NS), M-JT (P = NS) and M-JTc (P = NS). QRSd did not differ in the two groups(P = NS), while QTd and QTcd both resulted significantly greater in pre-excited subjects (P < 0.001). In the WPW group, QRSd was not related either to QTd (r = 0.325, P = NS) or to QTcd (r = 0.148, P = NS), while in the controls there was a significant relation between QRSd and both QTd (r = 0.522, P = 0.004) and QTcd (r = 0.379, P = 0.042). Our findings suggest that the presence of ventricular pre-excitation does not determine a prolongation of the mean ventricular recovery time, but increases regional discrepancies of the re-polarization process. This assumption is supported by the observation of greater values of QTd and QTcd associated with a similar QRSd.

Effect of blood gas derangement on QTc dispersion in severe chronic obstructive pulmonary disease: evidence of an electropathy?

Cardiac arrhythmias are common in patients with respiratory failure from chronic obstructive pulmonary disease (COPD). Several factors may be potentially arrhythmogenic in these patients, including hypoxemia and hypercapnia, acid-base disturbances, cor pulmonale and the use of digitalis, methylxanthines, and sympathomimetic drugs. The aim of this study was to examine the effect of hypoxemia and hypercapnia on QTc dispersion (QTcD) in COPD patients, and to evaluate the effect of a partial correction of one of these pro-arrhythmic factors, the hypoxemia, on Qtc dispersion, as QTcD has been proposed as a marker of heterogeneous repolarization and, hence of ventricular electrical instability. We showed that in 15 hypoxemic/hypercapnic COPD patients, compared to 20 controls, the QTcD was significantly higher (49.7 +/- 10.6 vs. 22.9 +/- 9.8 ms; P = 0.0001); furthermore, after only 24 h of oxygen therapy, and hence after a partial correction of hypoxemia, there was a significant reduction in QTcD in COPD patients (49.7 +/- 10.6 vs. 36.3 +/- 10.1 ms; P = 0.018). The data of the present study suggest that the increase in QTcD may be an early marker of a blood gas mediated electropathy in COPD patients.

Correlation between late potentials duration and QTc dispersion: Is there a causal relationship?

QTc interval dispersion (QTcd) analysis (difference between maximum and minimum QTc calculated from at least five of the standard 12 ECG leads) and signal-averaged electrocardiograms were performed on 23 patients referred to our coronary care unit because of acute myocardial infarction. Late potentials were considered positive if all three of the following criteria were satisfied: (1) total QRS duration (QRSd) > 114 ms; (2) duration of QRS under 40 muV (LAS 40) > 38 ms; (3) root mean square voltage of the last 40 ms of QRS (RMS 40) < 25 muV. Patients were divided into two groups according to the presence (group A, 9 patients) or absence of late potentials (group B, 14 patients). Group A patients showed a significantly higher QTcd (0.0652 +/- 0.0177 s vs. 0.0448 +/- 0.0201 s; P = 0.021) and a significantly longer mean QTcm (0.43117 +/- 0.01817 s vs. 0.40472 +/- 0.03013 s; P = 0.028) than group B patients. Among the three different parameters used to define the presence of late potentials, QTcd was significantly related to LAS 40 (r = 0.418, P = 0.047) and mean QT cm to QRSd (r = 0.497; P = 0.016). We also found a significant correlation between QTcd and mean QTcm (r = 0.426; P = 0.043). In conclusion, our data suggest that (1) the presence of late potentials is associated with a greater dishomogeneity of ventricular recovery time; (2) the longer the duration of late potentials, expressed by LAS 40, the greater the QTcd, suggesting that the dispersion of repolarization could be attributed to slowly conducting areas from which late potentials arise; (3) mean QTcm is not useful to identify these areas because it is more affected by total rather than by terminal QRS duration; (4) regional discrepancies of ventricular recovery time are connected with general repolarization duration.

Compared effects of sotalol, flecainide and propafenone on ventricular repolarization in patients free of underlying structural heart disease.

Antiarrhythmic drugs are known to affect the depolarization and repolarization time in a different fashion. The aim of the present study was to compare the effects of Sotalol, Flecainide and Propafenone on some common (QT, QTc, JT, JTc) or uncommon (QTc dispersion, T-peak to T-end interval) electrocardiographic parameters in order to evaluate the effects of these antiarrhythmic drugs on ventricular repolarization time both in terms of absolute values and of dispersion across the myocardium. The analysis of these antiarrhythmic drug effects was performed on the standard 12-lead electrocardiograms of 31 patients (17F and 14M, age 38.1+/-17 years, range 11-67 years) in the free-drug state and at the steady state after oral treatment with Sotalol (160 mg daily), Flecainide (200 mg daily) and Propafenone (450 mg daily). These drugs were prescribed, separately, to all the 31 patients, free of underlying structural heart disease, for the treatment of their atrio-ventricular nodal re-entry tachycardia. Data of the present study show that Sotalol, over the range prescribed, significantly prolongs ventricular repolarization index QT (P=0.001), JT (P=0.0001) and JTc (P=0.0001) values in an homogeneous fashion, as shown by the significant decrease in QTcD (P=0.019) and Tp-Te (P=0.01). On the contrary, Flecainide treatment was associated with an increase in QTcD (P=0.029), Tp-Te (0.0001), QT (P=0.001), QTc (P=0.0001) and QRS (P=0.0001), with no significant changes in JT and JTc. Propafenone, over the range prescribed, did not affect repolarization time, resulting only in a prolongation of depolarization time as expressed by the increase of QRS (P=0.0001).

Autonomic nervous system imbalance and left ventricular systolic dysfunction as potential candidates for arrhythmogenesis in Becker muscular dystrophy.

We evaluated the arrhythmic profile in a population of 20 Becker muscular dystrophy (BMD) patients searching for possible correlations between the severity of the arrhythmic events, the cardiac autonomic balance (assessed by heart rate variability analysis in the time domain) and the degree of left ventricular systolic impairment. A population of 14 male healthy individuals served as the control group. BMD subjects exhibited lower values of SDNN (P=0.013), SDANN index (P=0.008) and 24-h mean heart rate (P=0.002). The total number of premature ventricular beats (totPVB) and the number of PVB out of 1000 heartbeats (PVB/1000) appeared also higher in BMD subjects (P=0.05 and P=0.046, respectively). No difference was found in terms of 24-h mean QTc and 24-h longest QT among the two groups. TotPVB and PVB/1000 were inversely related to both the ejection fraction (r= -0.620, P=0.004 and r= -0.517, P=0.019) and to the shortening fraction (r= -0.568, P=0.009 and r= -0.469, P=0.037). Twenty-four-h mean QTc was also inversely related to both the ejection fraction (r= -0.520, P=0.019) and the fractional shortening (r= -0.491, P=0.028). These data suggest that in BMD there is cardiac autonomic imbalance characterized by sympathetic predominance and an increased susceptibility to ventricular arrhythmias, even in the absence of overt cardiomyopathy. Furthermore, the severity of the arrhythmic profile in BMD appears closely related to the degree of left ventricular systolic dysfunction.

Ventricular tachyarrhythmias following coronary surgery: predisposing factors.

The perioperative factors potentially associated with post-coronary artery bypass grafting (CABG) ventricular tachyarrhythmias (VT) onset have not been deeply investigated. Monomorphic or polymorphic ventricular tachycardia and ventricular fibrillation represent the most dreadful arrhythmic events that can complicate the postoperative course of CABG. As a consequence, the aim of our paper was to identify which perioperative variables might predict post-CABG VT occurrence. One hundred and fifty-two consecutive patients who underwent CABG surgery at our Institution were included in the study. Post-CABG VT occurred in 13 out of 152 patients (8.5%, six cases of monomorphic ventricular tachycardia and seven cases of ventricular fibrillation). At univariate analysis, VT patients were significantly younger (54.8+/-6.6 vs. 60.1+/-8.8, P=0.038), exhibited a more severe coronary artery disease (CAD) (number of diseased vessels 2.92+/-0.3 vs. 2.45+/-0.7, P=0.023, and percentage of patients with three-vessel CAD 91.7% vs. 57.3%, P=0.043) and received a greater number of CABGs than those remaining in sinus rhythm (SR) (percentage of patients receiving three or more CABGs 76. 9% vs. 38.8%, P1000 76.9% vs. 38%, Pnormal range 72.7% vs. 30.7%, P=0.014), electrolyte derangement (84.6% vs. 45.6%, P=0.017) and a severe haemodynamic impairment (need for IABP 23% vs. 2.9%, P1000, postoperative electrolyte imbalance, the need for three or more CABGs and of IABP all were independent correlates for VT. In conclusion, post-CABG VT seem to be related to the preexistence of a severe underlying coronary artery disease along with perioperative triggering factors such as acute ischemia, electrolytic disorders and a sudden haemodynamic impairment.

Increased QT dispersion and other repolarization abnormalities as a possible cause of electrical instability in isolated aortic stenosis.

The aim of our study was to analyze the ventricular repolarization phase in patients with isolated aortic stenosis (AS) in order to search for possible abnormalities that might contribute to an explanation of the electrical instability peculiar to this valve disease. We selected a population of 39 patients with isolated AS (25 M and 14 F, mean age 60+/-16 yrs). As controls we considered a group of 31 age-matched healthy subjects 20 M and 11 F, mean age 55+/-14 yrs, P=NS. Disease severity was assessed by echocardiography, calculating the maximum and mean pressure gradients max and mean PG) and the functional valve orifice area. Various electrocardiographic intervals (QT, QT'c, JT, JTc) and indices (QT and QTc dispersion were adopted for a detailed non-invasive evaluation of the ventricular repolarization. In patients with AS, M-QT (391+/-45 ms vs 362+/-25 ms, P=0.002), M=QTc (431+/-29 ms vs 412+/-19 ms, P=0.003), M-JT (290+/-41 ms vs 265+/-26 ms, P=0.003, M-JTc 331+/-29 ms vs 302+/-19 ms, P<0.001, QTD (67+/-34 ms vs 40+/-15 ms, P<0.001), QTcD (77+/-36 ms vs 52+/-23 ms, P<0.001) all resulted significantly greater than in controls. QTD and QTcD both resulted linearly related either to max PCi (r=0.388, P=0.018 and r=0.357, P=0.03) or to mean PG (r=0.513, P=0.004 and r=0.438, P=0.015), while M-JT and M-JTc turned out to be directly related only to mean PG (r=0.436, P=0.016 and r=0.483, P=0.007). Our findings suggest a prolonged duration of ventricular recovery and a greater dispersion of ventricular repolarization in patients with AS and might account for the electrical instability proper to this valve dysfunction. Besides, the existence of a linear direct relation between the severity of AS and the degree of inhomogeneity of left ventricular recovery, together with the correlation found among mean PCr and the total duration of the repolarization phase, expressed by the intervals JT and JTc, strongly suggest the hypothesis that in AS arrhythmogenic substrates development parallels the worsening of the valve defect.

Perioperative clinical predictors of atrial fibrillation occurrence following coronary artery surgery.

OBJECTIVE: Atrial fibrillation (AF) is the most frequently encountered arrhythmic complication associated with coronary surgery. The aim of this paper was then to identify the clinical predictors of post-CABG AF occurrence. METHODS: 150 consecutive patients were included in this study and divided into two groups according to the absence (SR group, 104 male and 22 female, age 58.4+/-8.8 years) or presence (AF group, 23 male and 1 female, age 65.4+/-6.3 years) of post-CABG AF. Forty-seven perioperative variables were considered. RESULTS: After univariate analysis, advanced age (SR vs. AF: 58.4+/-8.8 vs. 65.4+/-6.3, P < 0.001), an increased BMI (SR vs. AF: 26.1+/-2.7 vs. 27.4+/-2.5, P = 0.026), a prior history of paroxysmal AF (SR vs. AF: 3.2% vs. 16.7%, P = 0.028), left atrial enlargement (SR vs. AF: 21.1% vs. 70.8%, P < 0.001) and a more severe coronary artery disease (CAD) (SR vs. AF: no. of diseased vessels: 2.42+/-0.7 vs. 2.91+/-0.3, P = 0.001; three-vessel CAD (54.1% vs. 91.3%, P = 0.002) were the only factors that statistically differed between the groups. Multivariate logistic regression analysis identified left atrial enlargement (P < 0.0001), a prior history of paroxysmal AF (P = 0.007) and a more severe CAD (P = 0.0047) to be independent correlates for AF. CONCLUSIONS: Post-CABG AF seems to require a well definite anatomical and electrical substrate that is generated by increased left atrial dimensions, a greater extension of coronary lesions and a possible electrical remodeling consequent to prior repetitive episodes of paroxysmal AF.

Arrhythmias in patients with mechanical ventricular dysfunction and myocardial stretch: role of mechano-electric feedback.

Patients with dilated cardiomyopathy, ventricular volume or pressure overload, or dysynergistic ventricular contraction and relaxation are prone to develop severe ventricular arrhythmias. In these patients it has been suggested that the abnormal mechanics of contraction can disturb 'mechano-electric feedback', also known as 'contraction-excitation feedback', which is defined as the development of electrophysiological changes during or after changes in mechanical loading. This electrical instability, expressed by significant changes in ventricular repolarization and refractoriness and by the development of afterdepolarizations, has been variously reported in isolated tissues and isolated ventricles as well as in hearts in vivo. Furthermore, it is known that many patients with supraventricular tachycardia but otherwise structurally normal hearts can develop atrial fibrillation and that atrial arrhythmias frequently occur in the setting of acute or chronic increases in atrial size and pressure. It is possible that changes in atrial load directly alter the electrophysiological properties of the atrium by an analogue mechanism of contraction-excitation feedback. This paper reviews the literature concerning mechanoelectric feedback involvement in rhythm disorders, with the aim of investigating, through basic and clinical research, the clinical and therapeutic implications.