Francesco Furlanello

Prospective Assessment of Late Conduction Recurrence Across Radiofrequency Lesions Producing Electrical Disconnection at the Pulmonary Vein Ostium in Patients With Atrial Fibrillation

Background—In patients with atrial fibrillation (AF) undergoing radiofrequency (RF) electrical disconnection of multiple pulmonary veins (PVs), the incidence of late conduction recurrences has not been systematically determined. Methods and Results—Using a prospectively designed, multistep approach, we aimed at assessing the correlation between acute achievement and chronic maintenance of electrical conduction block across RF lesions disconnecting the distal tract of the PV in 43 patients (52.3±8.2 years) with AF. Forty-one left superior (LS), 42 right superior (RS), 25 left inferior (LI), and 9 right inferior (RI) PVs were targeted during 108 EP procedures (2.6±0.5 per patient). Seventeen patients underwent 2 procedures, 23 patients underwent 3 procedures, and 3 patients underwent 4 procedures. During the first attempt, electrical disconnection was achieved in 112 PVs (95.7%). During a next procedure (time interval, 4.6±1.9 months), conduction recurrence was observed in 32 of 39 LSPVs (82.1%), 29 of 40 RSPVs (72.5%), 20 of 24 LIPVs (83.3%), and 7 of 9 RIPV (77.8%). After reablation at gap sites, a later procedure (time interval, 5.1±2.4 months) revealed a second recurrence in 13 of 22 LSPVs (59.1%) and 14 of 19 RSPVs (73.7%). Conclusions—Conduction recurrence across disconnecting RF lesions can be observed in ≈80% of cases 4 months after ablation. After reablation, similar recurrence rates are observed 5 months later. This high rate of late conduction recurrence may contribute significantly to AF recurrence in patients undergoing catheter ablation aiming at disconnection of multiple PVs.

Evidence of a reentry circuit in the common type of atrial flutter in man.

To investigate the mechanism of atrial flutter (AF) in humans, we studied 13 patients during episodes of spontaneous common AF, with simultaneous multiple atrial endocavitary recordings and atrial programmed stimulation. In all patients, low paraseptal atrial activation preceded high right atrial activation, and the latter preceded mid- or low lateral right atrial activation (recorded in five patients). Programmed atrial stimulation resulted in early reset of the AF cycle, with an unchanged poststimulation AF activation pattern. The poststimulation cycle recorded from an even potential to the site of stimulation was always shorter than the basic flutter cycle length. The poststimulation cycle recorded at the site of stimulation was always equal to or longer than the flutter cycle length.These results strongly favor the existence of a reentry circuit to which the extrastimulus has access.

J wave, QRS slurring, and ST elevation in athletes with cardiac arrest in the absence of heart disease marker of risk or innocent bystander?

Background—QRS-ST changes in the inferior and lateral ECG leads are frequently observed in athletes. Recent studies have suggested a potential arrhythmogenic significance of these findings in the general population. The aim of our study was to investigate whether QRS-ST changes are markers of cardiac arrest (CA) of unexplained cause or sudden death in athletes. Methods and Results—In 21 athletes (mean age, 27 years; 5 women) with cardiac arrest or sudden death, the ECG recorded before or immediately after the clinical event was compared with the ECG of 365 healthy athletes eligible for competitive sport activity. We measured the height of the J wave and ST elevation and searched for the presence of QRS slurring in the terminal portion of QRS. QRS slurring in any lead was present in 28.6% of cases and in 7.6% of control athletes (P=0.006). A J wave and/or QRS slurring without ST elevation in the inferior (II, III, and aVF) and lateral leads (V4 to V6) were more frequently recorded in cases than in control athletes (28.6% versus 7.9%, P=0.007). Among those with cardiac arrest, arrhythmia recurrences did not differ between the subgroups with and without J wave or QRS slurring during a median 36-month follow-up of sport discontinuation. Conclusions—J wave and/or QRS slurring was found more frequently among athletes with cardiac arrest/sudden death than in control athletes. Nevertheless, the presence of this ECG pattern appears not to confer a higher risk for recurrent malignant ventricular arrhythmias.

Illicit drugs and cardiac arrhythmias in athletes.

The current management of athletes with cardiac arrhythmias has become complicated by the widespread use of illicit drugs, which can be arrhythmogenic. The World Anti-Doping Agency annually updates a list of prohibited substances and methods banned by the International Olympic Committee that includes different classes of substances namely, anabolic androgenic steroids, hormones and related substances, β2-agonists, diuretics, stimulants, narcotics, cannabinoids, glucocorticosteroids, alcohol, β-blockers and others. Almost all illicit drugs may cause, through a direct or indirect arrhythmogenic effect, a wide range of cardiac arrhythmias (focal or reentry type, supraventricular and/or ventricular) that can even be lethal and which are frequently sport activity related. A large use of illicit drugs has been documented in competitive athletes, but the arrhythmogenic effect of specific substances is not precisely known. Precipitation of cardiac arrhythmias, particularly in the presence of a latent electrophysiologic substrate including some inherited cardiomyopathies, at risk of sudden death or due to long-term consumption of the substances, should raise the suspicion that illicit drugs may be a possible cause and lead cardiologists to investigate carefully this relationship and appropriately prevent the clinical consequences.

Chronic kidney disease elicits excessive increase in left ventricular mass growth in patients at increased risk for cardiovascular events.

Background The hemodynamic alterations induced by the impairment of renal function explain only in part the development of left ventricular hypertrophy in patients with chronic kidney disease (CKD), who are theoretically exposed to an inappropriate high growth of left ventricular mass (iLVM) due to the activation of neuro-hormonal stressors. Few data are available on the relations between iLVM and renal function. Study design and measurements Three hundred and forty individuals at increased risk for cardiovascular events underwent assessment of renal function by the estimation of glomerular filtration rate (eGFR) and echocardiography: 227 patients had stages 1–2 CKD (eGFR ≥60 ml/min per 1.73 m2), and 113 stages 3–5 (eGFR <60 ml/min per 1.73 m2). LVM was predicted in each patient from height, sex and stroke work using a validated equation. iLVM was defined as LVM more than 28% of the predicted value. Sixty-eight healthy individuals served as controls. Results iLVM was detected in seven controls (10%) and in 146 study patients (43%). There was an inverse relation between observed/predicted LVM ratio and eGFR (r 0.54, P < 0.001). In linear regression analysis, iLVM was related to eGFR (β 0.40), relative wall thickness (β 0.29), diabetes (β 0.14), and maximal left atrial volume (β 0.25) (all P < 0.001). Prevalence of iLVM was 10% in patients in stage-1 CKD, 31% in stage 2, 67% in stage 3, and 100% in stages 4 and 5. Conclusion In patients at increased risk for cardiovascular events, iLVM is strongly related to the presence and magnitude of CKD. Further longitudinal studies are needed to evaluate the prognostic value of the coexistence of iLVM and CKD.

VENTRICULAR ARRHYTHMIAS AND SUDDEN DEATH IN ATHLETES

Sudden death (SD) in the athlete typically occurs during or immediately after strenuous physical exertion. It is always a dramatic, unexpected event because the victim is apparently in excellent physical condition. Whereas SD is extremely rare in professional, well-trained, and medically supervised athletes,, it more frequently occurs in a sporting population with a lesser degree of training and medical care. Although SD in athletes is no longer exceptional, relatively few complete reports are available on this topic. Moreover very little is known about the arrhythmic event that leads to cardiac arrest even if the latter is generally considered as a consequence of malignant ventricular arrhythmias. Most SD in athletes occurs in the setting of established acquired and/or congenital structural abnormalities of the heart. They are sometimes so relevant that it almost seems incredible that the subject can exercise at high levels. This study considers the problem of sudden arrhythmic death in the athlete from the standpoint of the pathologist and the arrhythmologist. We will look at the pathologists viewpoint by looking for the anatomic substrate of arrhythmias and by trying to identify the mechanisms of cardiovascular adaptation that followed a maximum level of sport activity until the final event occurred. In this regard literature and personal data are available. The arrhythmologists goal is to identify athletes at risk of sudden arrhythmic death, which we did on the basis of data gathered at our center relative both to athletes referred for arrhythmias and athletes otherwise believed normal.

Prevalence, predictors and prognostic value of acute impairment in renal function during intensive unloading therapy in a community population hospitalized for decompensated heart failure.

Background and Methods Chronic heart failure (CHF) is often associated with impaired renal function. Diuretics and vasodilators may lead to aggravated renal dysfunction (ARD), particularly among patients with decompensated CHF. Although the prevalence of ARD has been evaluated in patients awaiting heart transplantation, little is known about ARD in the community sample of CHF patients. Accordingly, we prospectively assessed the prevalence, predictors and prognostic value of ARD in 79 consecutive patients admitted to our general community hospital for decompensated CHF undergoing intensive unloading therapy (intravenous nitroprusside and furosemide). ARD was defined as a ≥ 25% increase in serum creatinine between admission and maximal value of ≥ 2 mg/dl. Results Sixteen patients (20%) developed ARD with a mean increase in serum creatinine of 31% (from 1.74 ± 0.6 to 2.27 ± 0.9 mg/dl). ARD persisted at 8-day evaluation in seven of 16 subjects (44%) whereas it was reversible in nine (56%). Lower creatinine clearance at baseline [exp β = 0.93, 95% confidence interval (CI) = 0.87–0.99] and the higher dose of furosemide (exp β = 1.02, 95% CI = 1.01–1.03) emerged as independent predictors of ARD. During a follow-up of 11 ± 8 months, death and hospitalization for worsening CHF occurred more frequently in ARD than non-ARD patients (69% versus 17%, P = 0.0001; 69% versus 29%, P = 0.003, respectively). Persistent ARD was a powerful independent predictor of long-term adverse outcome (odds ratio = 11.1; 95% CI = 1.12–36.1; P = 0.04). Conclusions Intensive unloading therapy is associated with the development of ARD in one-fifth of the community population hospitalized for decompensated CHF. The magnitude of this phenomenon is not greater than that observed in younger selected populations with advanced CHF, and depends on baseline renal function and increased diuretic dosage. ARD persisting after 8 days from starting intensive unloading is a powerful predictor of subsequent worsened clinical outcome.

Italian cardiological guidelines for sports eligibility in athletes with heart disease: part 1.

In Italy the existence of a law on health protection of competitive sports since 1982 has favored the creation and the revision of these cardiological guidelines (called COCIS), which have reached their fourth edition (1989-2009). The present article is the second English version, which has summarized the larger version in Italian. The experience of the experts consulted in the course of these past 20 years has facilitated the application and the compatibility of issues related to clinical cardiology to the sports medicine field. Such prolonged experience has allowed the clinical cardiologist to acquire knowledge of the applied physiology of exercise and, on the other hand, has improved the ability of sports physicians in cardiological diagnostics. All this work has produced these guidelines related to the judgment of eligibility for competitive sports in the individual clinical situations and in the different cardiovascular abnormalities and/or heart disease. Numerous arguments are debated, such as interpretation of the athletes ECG, the utility of a preparticipation screening, arrhythmias, congenital heart disease, cardiomyopathies, arterial hypertension, ischemic heart disease and other particular issues.

Arrhythmias and Sudden Death in Athletes

Scope of the problem of sudden death in athletes: Definitions, epidemiology and socioeconomic implications B.J. Maron. The Italian classification of different sports in relation to cardiovascular risk A. Dal Monte. Classification of sports J.H. Mitchell, et al. Cardiovascular causes and pathology of sudden death in athletes: The American experience B.J. Maron. Pathology of sudden death in young athletes: The European experience G. Thiene, et al. Markers and triggers of sudden death in athletes M.T. Subirana, et al. Competitive athletes with arrhythmias: Classification, evaluation and treatment F. Furlanello, et al. Arrhythmias in special situations P. Ferres, et al. Guidelines for competitive athletes with arrhythmias T. Al-Sheikh, D.P. Zipes. Italian guidelines for competitive athletes with arrhythmias A. Biffi, et al. Index.

Analysis of left ventricular systolic function by midwall mechanics in patients with obstructive sleep apnoea

AIMSnmidwall mechanics reveal systolic dysfunction in obese and hypertensive patients with concentric left ventricular (LV) geometry, which is frequently detected in subjects with obstructive sleep apnoea (OSA). Midwall mechanics have never been studied in these patients, who frequently experience heart failure (HF).nnnMETHODS AND RESULTSnwe analysed midwall stress-shortening relations by echocardiography in 150 controls and 200 patients with OSA (age 62 ± 13 years) without known cardiac disease. On the basis of the severity of OSA, patients were divided into mild OSA (n = 63), moderate OSA (n = 70), and severe OSA (n = 67). LV stress-corrected midwall shortening (scMS) was considered low if <87% in men and <90% in women. scMS was similar in controls and mild OSA (90 ± 13 and 91 ± 18%, respectively) and significantly lower in moderate and severe OSA (83 ± 14 and 83 ± 15%; all P < 0.001 vs. controls and mild OSA). Prevalence of low scMS was 40 and 39% in controls and mild OSA (P=NS), 62% in moderate and 61% in severe OSA (both P < 0.001 vs. controls and mild OSA). In logistic regression analysis, low scMS was associated with moderate-severe OSA (OR 3.82, P < 0.001) independent of significant associations with diabetes (OR 5.06, P < 0.01), LV hypertrophy (OR 1.89, P = 0.01), and LV concentric geometry (OR 2.79, P < 0.001).nnnCONCLUSIONnmidwall mechanics are impaired in more than half of middle-aged patients with OSA without known cardiac disease. Moderate-severe OSA predicts LV systolic dysfunction independent of diabetes, LV hypertrophy, and concentric geometry. These relations may in part explain the increased rate of HF and cardiovascular events in these patients.