Journal of the American College of Cardiology Vol. 44, No. 5, 2004 2004 by the American College of Cardiology Foundation ISSN 0735-1097/04/$30.00 Published by Elsevier Inc.
Impact of Physical Deconditioningon Ventricular Tachyarrhythmias in Trained AthletesAlessandro Biffi, MD,* Barry J. Maron, MD, FACC,‡ Luisa Verdile, MD,* Fredrick Fernando, MD,*Antonio Spataro, MD,* Giuseppe Marcello, MD,* Roberto Ciardo, MD,* Fabrizio Ammirati, MD,†Furio Colivicchi, MD,† Antonio Pelliccia, MD*Rome, Italy; and Minneapolis, Minnesota The purpose of this research was to evaluate the impact of athletic training and, in particular,physical deconditioning, on frequent and/or complex ventricular tachyarrhythmias assessed by24-h ambulatory (Holter) electrocardiogram (ECG).
Sudden deaths in athletes are usually mediated by ventricular tachyarrhythmias.
Twenty-four hour ambulatory ECGs were recorded at peak training and after a decondi-tioning period of 19 ⫾ 6 weeks (range, 12 to 24 weeks) in a population of 70 trained athletesselected on the basis of frequent and/or complex ventricular tachyarrhythmias (i.e., ⱖ2,000premature ventricular depolarization [PVD] and/or ⱖ1 burst of non-sustained ventriculartachycardia [NSVT]/24 h).
A significant decrease in the frequency and complexity of ventricular arrhythmias was evidentafter deconditioning: PVDs/24 h: 10,611 ⫾ 10,078 to 2,165 ⫾ 4,877 (80% reduction; p ⬍0.001) and NSVT/24 h: 6 ⫾ 22 to 0.5 ⫾ 2, (90% reduction; p ⫽ 0.04). In 50 of the 70athletes (71%), ventricular arrhythmias decreased substantially after detraining (to ⬍500PVDs/24 h and no NSVT). Most of these athletes with reduced arrhythmias did not havestructural cardiovascular abnormalities (37 of 50; 74%). Over the 8 ⫾ 4-year follow-up period,each of the 70 athletes survived without cardiac symptoms.
CONCLUSIONS Frequent and/or complex ventricular tachyarrhythmias in trained athletes (with and without cardiovascular abnormalities) are sensitive to brief periods of deconditioning. In athletes withheart disease, the resolution of such arrhythmias with detraining may represent a mechanismby which risk for sudden death is reduced. Conversely, in athletes without cardiovascularabnormalities, reduction in frequency of ventricular tachyarrhythmias and the absence ofcardiac events in the follow-up support the benign clinical nature of these rhythmdisturbances as another expression of athlete's heart.
(J Am Coll Cardiol 2004;44:1053– 8) 2004 by the American College of Cardiology Foundation "Athlete's heart" is a complex physiologic and structural arrhythmias in an athletic population is unresolved. There- cardiac syndrome that develops in response to intensive and fore, the primary aim of this study was to assess the chronic athletic training. A growing body of literature has relationship between physical deconditioning and the oc- distinguished physiologic left ventricular (LV) remodeling currence of ventricular tachyarrhythmias in our unique with increased LV chamber size, wall thickness, and mass population of highly trained athletes.
from the pathologic form of hypertrophy characteristic ofcardiomyopathies One of the parameters differenti- See page 1059
Study population. The case records of the Institute of
Sports Science (Rome) from 1984 to 2001 were reviewed.
ating these two forms of LV hypertrophy is regression in During this time period, 355 athletes had been assessed by cavity dimension and/or wall thickness, which is confined to 24-h ambulatory (Holter) electrocardiogram (ECG), by "athlete's heart," typically occurring within weeks to months virtue of meeting the following criteria: 1) ⱖ3 premature after cessation of training ventricular depolarizations (PVDs) on resting 12-lead ECG We have reported that frequent and/or complex ventric- (n ⫽ 337), and/or 2) history of palpitations (n ⫽ 18). Of the ular arrhythmias occur not uncommonly in trained athletes 355 athletes, 71 with particularly frequent and/or complex with physiologic LV hypertrophy However, at present, ventricular arrhythmias (arbitrarily defined as ⱖ2,000 PVDs the potential impact of deconditioning on such ventricular and/or ⱖ1 burst of non-sustained ventricular tachycardia[NSVT]/24 h) were initially considered for inclusion. One From the *National Institute of Sports Medicine, Italian Olympic Committee, athlete (2,100 PVDs and 2 bursts of NSVT on 24-h Holter Rome, Italy; †San Filippo Neri Hospital, Department of Heart Disease, Rome, Italy; recording) with arrhythmogenic right ventricular cardiomy- and ‡Minnneapolis Heart Institute Foundation, Minneapolis, Minnesota.
opathy (ARVC), who died suddenly while participating in a Manuscript received February 14, 2004; revised manuscript received May 13, 2004, accepted May 18, 2004.
competitive field hockey game (against medical advice), was Biffi et al.
JACC Vol. 44, No. 5, 2004 Ventricular Arrhythmias in Deconditioned Athletes September 1, 2004:1053– 8 dimensional images LV ejection fraction was measured Abbreviations and Acronyms
from end-diastolic and end-systolic volumes in the apical ARVC ⫽ arrhythmogenic right ventricular four-chamber view.
Left ventricular mass was calculated by the formula of ⫽ left ventricle/ventricular Devereux and normalized to body surface area. Param- NSVT ⫽ non-sustained ventricular tachycardia eters of LV filling were obtained with pulsed Doppler PVD ⫽ premature ventricular depolarization echocardiography Diagnostic criteria. ARVC. Echocardiographic criteria
excluded from the study group because he did not undergo used for the clinical diagnosis of ARVC included right detraining, and relevant Holter data were not obtained.
ventricular cavity dilation and/or segmental thinning, bulg- Therefore, the final study group comprises 70 athletes with ing or aneurysm formation, and wall motion abnormalities, frequent and/or complex ventricular tachyarrhythmias on as suggested by the Task Force of the European Society of Cardiology and Federation of Cardiology In the study subjects, 24-h Holter ECGs were initially Myocarditis. Diagnosis of myocarditis was based on labo-
recorded during periods of peak training, including a con- ratory evidence of an inflammatory condition involving ditioning session (an average of 1 h in duration), similar to myocardium, associated either with segmental LV wall that usually performed by the athlete; the remaining time motion abnormalities and cavity enlargement, and con- was occupied by usual daily activities that may have involved firmed in selected cases (n ⫽ 4) by biopsy showing histo- non-competitive and recreational physical activity.
pathology in accord with the Dallas criteria At the time of Holter monitoring during peak training, Dilated cardiomyopathy. Dilated cardiomyopathy was di-
no athlete was taking antiarrhythmic or other cardioactive agnosed based on marked LV cavity dilation (end-diastolic medications. However, eight athletes (all with cardiovascu- dimension ⱖ60 mm) associated with systolic LV dysfunc- lar abnormalities) were taking medications at the time of the tion (ejection fraction ⬍50%) and/or segmental wall motion deconditioning Holter ECG, including beta-blockers (n ⫽ abnormalities, and differentiated from physiologic cavity 5), propafenone (n ⫽ 2), or enalapril (n ⫽ 1).
enlargement as previously reported Mean age of the athletes was 25 ⫾ 12 years (range, 15 to Mitral valve prolapse. Mitral valve prolapse was identified
33 years); 51 subjects (72%) were male. These athletes were by evidence of elongated, thickened, and redundant leaflets engaged in a variety of sports disciplines, most commonly billowing beyond the mitral annulus plane during systole, in soccer (n ⫽ 15; 21%), basketball (n ⫽ 10; 14%), and the parasternal long-axis echocardiographic view volleyball (n ⫽ 7; 10%). They also presented a broad Deconditioning. Based on the Italian guidelines for deter-
spectrum of athletic achievement with 25 (35%) participat- mining eligibility in competitive athletes with cardiovascular ing at an elite level, including 18 competing in the Olympic abnormalities (which closely resemble those of the 26th Games or World Championships (five finalists or medal- Bethesda Conference) each of the 70 athletes with frequent and/or complex ventricular tachyarrhythmias was Control group. A total of 148 athletes without structural
disqualified from competitive sports.
heart disease, of similar age (26 ⫾ 10 years) and gender The 70 athletes underwent a deconditioning period of at (78% males) as the study population, with less frequent least three consecutive months (mean, 19 ⫾ 6 weeks; range, ventricular arrhythmias (ⱖ100 to ⬍2,000 PVDs/24 h and 12 to 24 weeks). This time period was selected because it no episode of NSVT) were assembled as a control group.
has been shown to be sufficient to reverse the cardiac The 148 controls underwent a second Holter ECG 3 to 6 remodeling induced by physical training After decon- months after the first study, and at the same level of training ditioning, each athlete had a second cardiovascular assess- (without deconditioning). The time period between these ment, which also included a 24-h Holter ECG performed two Holter recordings obtained during training (19 ⫾ 4 under the same conditions as at peak training, except for weeks; range, 12 to 24 weeks) was the same as between the eight athletes who were receiving pharmacologic treatment active and deconditioned phases in the 70 athletes with with propafenone, sotalol, or enalapril at the time of the frequent and/or complex ventricular tachyarrhythmias.
most recent Holter. This second 24-h Holter ECG also Echocardiography. Echocardiographic studies were per-
included a conditioning session similar to that usually formed using Hewlett-Packard 77020 AC or Sonos 5500 performed by the athlete (of about 1 h in duration).
(Andover, Massachusetts). Images of the heart were ob- Ventricular tachyarrhythmias were regarded as having tained in multiple cross-sectional planes using standard partial reversibility when PVDs decreased to ⬍500 transducer positions. The LV cavity dimensions, anterior PVDs/24 h (in the absence of NSVT) on the second Holter ventricular septal and posterior free wall thicknesses, and ECG. Arrhythmias were considered to show complete left atrial dimension were obtained from M-mode echocar- reversibility when PVDs and NSVT decreased to 0/24 h.
diograms in accordance with previous recommendations Electrophysiologic study. Of these 70 athletes, 24 were
To enhance the accuracy of LV wall thickness measure- selected on clinical and Holter indications for electrophysi- ments, these dimensions were verified from two- ologic study: ⱖ10,000 PVDs/24 h (n ⫽ 10), ⱖ10,000 JACC Vol. 44, No. 5, 2004 Biffi et al.
September 1, 2004:1053– 8 Ventricular Arrhythmias in Deconditioned Athletes Figure 1. Number of premature ventricular depolarizations (PVD), ventricular couplets, and bursts of non-sustained ventricular tachycardia (NSVT) during24-h Holter electrocardiogram recording at peak training and after the period of deconditioning in 70 trained athletes.
PVDs and NSVT (n ⫽ 9), or ⱖ2,000 PVDs and NSVT ventricular tachyarrhythmias (i.e., to ⬍500 PVDs and (n ⫽ 5). Ventricular stimulation was performed using a absence of NSVT/24 h) was evident in 34 athletes; com- programmable stimulator (Medtronic 5328, Medtronic plete abolition of arrhythmias (no PVDs and NSVT/24 h) Inc., Minneapolis, Minnesota), delivering rectangular pulses occurred in 16 athletes (Figs. 2 and 3). In the remaining 20 of 2 ms duration at twice the diastolic threshold. Up to three athletes (29%), frequency of ventricular arrhythmias showed extrastimuli were introduced after eight ventricular paced no significant reduction in frequency after detraining (i.e., beats at three drive cycle lengths (600, 500, and 400 ms) and persistence of ⱖ500 PVDs/24 h), including 6 in whom runs in two right ventricular sites (apex and outflow tract).
of NSVT persisted. No athlete showed an increase of Programmed stimulation during isoproterenol infusion was ventricular arrhythmias after deconditioning.
subsequently performed in athletes who otherwise were not Ventricular tachyarrhythmias in the control group. Con-
trol group athletes did not show significant variability in Statistics. Data are expressed as mean ⫾ SD. Differences
ventricular arrhythmias between the two Holter ECGs ob- between means were assessed by unpaired or paired Student tained during training (19 ⫾ 4 weeks interval training period).
t test, where appropriate. A two-tailed p value of ⬍0.05 was For example, mean number of PVDs on the first Holter was considered statistically significant.
1,211 ⫾ 850 and on the second was 1,050 ⫾ 648 (p ⫽ NS) Relation of change in ventricular tachyarrhythmias with
deconditioning to cardiovascular abnormalities.
Of the
Ventricular tachyarrhythmias at peak conditioning and
50 athletes who showed reversibility of ventricular arrhyth- after deconditioning. PEAK CONDITIONING. Frequency of
mias after deconditioning, most (37; 74%) had no cardio- PVDs on 24-h Holter ECG performed during the period of vascular abnormalities, and 13 (26%) had cardiac abnormal- peak training and competition ranged from 2,089 to 43,151 ities, including mitral valve prolapse (n ⫽ 5), myocarditis (n (mean, 10,611 ⫾ 10,078), including 21 athletes (34%) with ⫽ 3), dilated cardiomyopathy (n ⫽ 3), and ARVC (n ⫽ 2).
10,000 PVDs. Each of the 70 athletes had ⱖ1 couplet (mean, 48 ⫾ 131; range, 1 to 280); 37 athletes (53%) also
had 1 to 179 bursts of NSVT (mean, 6) consisting of 3 to 28
consecutive beats at heart rates of 130 to 270 beats/min. Of
the 70 athletes, 8 (11%) reported frequent or prolonged
palpitations (each with ⬎10,000 PVDs or NSVT), but none
had episodes of impaired consciousness or other cardiac
DECONDITIONING. After the deconditioning period, the
overall study group showed significant reduction in PVDs,
couplets, and NSVT; PVDs decreased from 10,611 ⫾
10,078 to 2,165 ⫾ 4,877 (80% reduction; p ⬍ 0.001);
couplets from 48 ⫾ 131 to 9 ⫾ 45 (80% reduction; p ⬍
0.02); and NSVT from 6 ⫾ 22 to 0.5 ⫾ 2 (90% reduction;
p ⫽ 0.038)
Individual subject analysis showed that after decondition- Figure 2. Effect of deconditioning on frequent and/or complex ventriculartachyarrhythmias in 70 trained athletes. C-V abn. ⫽ cardiovascular ing, 50 of 70 athletes (71%) showed partial or complete abnormalities; NSVT ⫽ non-sustained ventricular tachycardia; PVDs ⫽ reversibility of ventricular arrhythmias. Partial reversal of premature ventricular depolarizations.
Biffi et al.
JACC Vol. 44, No. 5, 2004 Ventricular Arrhythmias in Deconditioned Athletes September 1, 2004:1053– 8 Relation of change in ventricular tachyarrhythmias to
electrophysiologic findings.
Of the 24 athletes who un-
derwent electrophysiologic study, 23 (10 with and 13
without cardiovascular abnormalities) showed no ventricular
arrhythmias or only non-sustained runs of ventricular tachy-
cardia during programmed ventricular stimulation; most of
these 23 athletes (17; 74%) had shown reduced arrhythmia
frequency after deconditioning (i.e., 4,376 ⫾ 754 to 336 ⫾
112 PVDs/24 h).
Only one athlete, a 32-year-old cyclist with ARVC and 12,000 PVDs and 5 NSVT bursts on Holter ECG, hadinduced sustained ventricular tachycardia (by two extra-stimuli); oral administration of sotalol reduced ventriculararrhythmias (to ⬍500 PVDs and absence of NSVT).
Follow-up. The 70 study athletes and the 148 controls
Arrhythmia trends during 24-h Holter electrocardiogram (ECG) recordings showing marked reversibility of premature ventricular were periodically examined at our institute over 8 ⫾ 4 years depolarizations (PVDs) after three months of deconditioning in a 32-year- after identification of ventricular tachyarrhythmias. Over old elite bobsledder. (Top panel) The 24-h ECG performed during peak
training shows 3,288 PVDs, distributed relatively homogeneously, with a
this follow-up period, each of the 70 athletes and each of the slight reduction evident during the evening hours. (Bottom panel) Marked
148 controls survived without experiencing cardiac symp- reduction in ventricular arrhythmias (to 73 PVDs) is evident after three toms or events. The 37 of the 70 athletes with partial or months of physical deconditioning. The reduction of ventricular arrhyth-mia after detraining has occurred throughout the 24-h recording period.
complete reversibility of the ventricular tachyarrhythmiasafter deconditioning (and without cardiovascular abnormal- In particular, each of the 16 athletes who showed complete ities) resumed competitive sports without restriction. In reversibility of ventricular arrhythmias after detraining had addition, six athletes with cardiovascular abnormalities no cardiovascular abnormalities.
(three with mitral valve prolapse and without significant In the remaining 20 athletes for whom ventricular ar- regurgitation, and three with healed myocarditis), who had rhythmias remained substantially unchanged after detrain- shown partial and substantial reduction of ventricular ar- ing, 13 had no cardiovascular abnormalities (65%), and 7 rhythmias after deconditioning, were also allowed to resume (35%) had either ARVC (n ⫽ 4), mitral valve prolapse (n ⫽ 1), myocarditis (n ⫽ 1), or dilated cardiomyopathy (n ⫽ 1) The remaining 27 of the 70 athletes were permanently Therefore, the absence of structural heart disease disqualified because of structural cardiovascular diseases was similar in athletes with or without reversibility of such as dilated cardiomyopathy or ARVC, and/or frequent, ventricular arrhythmias after deconditioning (37/50; 74% vs.
and/or complex ventricular arrhythmias, which were not 13/20; 65%; p ⫽ NS).
reversible after deconditioning (either in the presence or Relation of change in ventricular tachyarrhythmias with
absence of cardiovascular abnormalities).
deconditioning to LV mass. During peak training, LV
Pharmacologic treatment. Pharmacologic treatment, with
mass index was 115 ⫾ 24 g/m2 (range, 77 to 170 g/m2) and beta-blocker or propafenone at the time of the first Holter after deconditioning decreased to 93 ⫾ 20 g/m2 (range, 53 ECG, did not influence reversibility of ventricular tachyar- to 140 g/m2). The decrease in LV mass after detraining did rhythmias with deconditioning. The proportion of athletes not differ between athletes who experienced partial or with partial or complete reversal of ventricular arrhythmias complete reversibility of ventricular arrhythmias with de- was similar in those taking cardioactive drugs (5 of 8; 63%) conditioning and athletes with no change in arrhythmias as in those without medications (42 of 62; 70%; p ⫽ NS).
(116 ⫾ 22 g/m2 to 94 ⫾ 18 g/m2; 19% reduction vs. 114 ⫾22 g/m2 to 93 ⫾ 26 g/m2; 18% reduction; p ⫽ NS).
Table 1. 24-H Holter Monitoring ElectrocardiographicRecordings in 148 Control Group Athletes We have previously shown that intense athletic condition- First 24-H
Second 24-H
ing may be associated with the occurrence of frequent and/or complex ventricular tachyarrhythmias on ambulatory (Holter) ECG These observations are extended in the present study where we demonstrate that detraining can reverse this process, whether or not structural cardiovascular abnormalities are present. Indeed, frequent and/or complex ventricular tachyarrhythmias in 70 highly trained and eliteathletes were particularly sensitive to short periods of NSVT ⫽ non-sustained ventricular tachycardia; PVD ⫽ premature ventriculardepolarization.
deconditioning (19 weeks on average), including complete JACC Vol. 44, No. 5, 2004 Biffi et al.
September 1, 2004:1053– 8 Ventricular Arrhythmias in Deconditioned Athletes reversibility in about one-fourth and partial reversibility in data in the context of certain clinical circumstances. For almost one-half.
example, we cannot exclude the possibility that in an The mechanisms that explain reduction in ventricular occasional athlete the observed reduction in ventricular tachyarrhythmias with deconditioning are probably com- arrhythmias was due to the resolution of previously unrec- plex, but likely are related to autonomic nervous system ognized structural heart disease (such as myocarditis), rather changes associated with high-intensity training and detrain- than to a deconditioning effect. Nevertheless, given the large ing. Intensive endurance training has been shown to shift number of trained athletes with ventricular tachyarrhyth- autonomic modulation from parasympathetic to sympa- mias in our cohort (and the rarity of cardiovascular abnor- thetic predominance which may predispose to an malities in a young athletic population) this explana- electrical instability of the ventricles and eventually trigger tion seems very unlikely for the vast majority of athletes in ventricular tachyarrhythmias Alternatively, sinus bra- the present analysis.
dycardia, characteristic of athlete's heart (with lengthening Recommendations for the eligibility of athletes without of the R-R interval) could facilitate the emergence of PVDs cardiovascular disease or abnormalities, but with frequent The increase in cardiac mass induced by training is and/or complex ventricular tachyarrhythmias on ambulatory an unlikely explanation for the ventricular tachyarrhythmias Holter ECG, are presently unresolved and have not yet been in our athletes, given the mild degree of cardiac remodeling definitively addressed in formal expert consensus panels present in our study group, and the observation that such as the Bethesda Conference or the Italian guide- decreased cardiac dimensions after deconditioning was sim- lines However, it is our current practice to initially ilar in athletes with and without reversible ventricular withdraw such athletes from all training and competition for arrhythmias. The possibility of significant spontaneous vari- three to six months and then reevaluate with ambulatory ability of ventricular arrhythmias in our study group is Holter ECG monitoring for the presence of these arrhyth- unlikely, given the lack of arrhythmia variation documented mias. If ventricular tachyarrhythmias are greatly reduced in in the control group of trained athletes.
frequency or abolished at the end of the detraining period, The removal of athletes with cardiovascular disease (such then competitive sports participation can be resumed. Close as hypertrophic cardiomyopathy) from intense training and follow-up of athletes with frequent and/or complex ventric- competition has been promoted as a strategy to reduce the ular arrhythmias is recommended for the assessment of new risk for sudden death Recently, Corrado et al.
symptoms, and/or to detect worsening of arrhythmias, or showed that the risk for sudden death in young the possible expression of a previously undiagnosed cardio- competitive athletes with cardiovascular disease was 2.5-fold vascular abnormality with late clinical onset On the greater than in non-athletes. These data suggest that sports other hand, no limitation in sports activity is recommended activity itself may act as a trigger for life-threatening for athletes without cardiovascular abnormalities and less ventricular tachyarrhythmias during intense physical exer- frequent arrhythmias (such as in the 148 control group tion in susceptible individuals with silent cardiovascular athletes), due to their favorable prognosis and the observa- diseases, thereby predisposing to cardiac arrest. Based on tion that sports training and competition were not associ- our present data, in which no athlete (with or without ated with an increase in arrhythmia frequency.
cardiovascular abnormalities) experienced a clinical event or In those athletes with underlying cardiovascular disease or sudden death during follow-up after deconditioning, we abnormalities, and with frequent and/or complex ventricular propose that such a favorable outcome may be related to the tachyarrhythmias, permanent (or temporary in selected reduction in ventricular arrhythmias associated with de- cases) disqualification from most competitive sports is indi- training. Therefore, the deconditioning effect on arrhyth- cated. These guidelines are based primarily on recommen- mias is a potential mechanism by which disqualification dations for the athlete's particular structural heart disease from intense competitive sports may reduce the risk for (i.e., hypertrophic cardiomyopathy, ARVC, dilated cardio- sudden cardiac death in those athletes with structural heart myopathy, or myocarditis) With particular regard to disease and frequent and/or complex ventricular arrhyth- mitral valve prolapse, exertion-related sudden cardiac death mias. Our data support, therefore, the restriction from is a known, albeit uncommon, consequence, particularly in competitive sports in athletes with frequent and/or complex those athletes with frequent and/or complex ventricular ventricular tachyarrhythmias and structural heart disease, as arrhythmias Therefore, it is prudent to disqualify from suggested by the present recommendations competitive sports athletes with mitral valve prolapse asso- Conversely, this study also identified a subset of athletes ciated with frequent and/or complex ventricular arrhythmias without cardiovascular abnormalities, and with reversibility of ventricular arrhythmias, who resumed training and com- In conclusion, frequent and/or complex ventricular tachy- petition and experienced a benign course. Therefore, reso- arrhythmias in highly trained athletes are sensitive to short lution of ventricular tachyarrhythmias with deconditioning periods of deconditioning. This reversibility of arrhythmias may justify resumption of competition without risk in these after deconditioning was observed both in athletes with and athletes without heart disease.
without cardiovascular abnormalities. In athletes with heart However, some caution is suggested in interpreting our disease, resolution of arrhythmias after detraining could Biffi et al.
JACC Vol. 44, No. 5, 2004 Ventricular Arrhythmias in Deconditioned Athletes September 1, 2004:1053– 8 explain the mechanism by which the restriction of these heart" from hypertrophic cardiomyopathy. Am J Cardiol athletes from intense sports competition may reduce their 1992;68:296 –300.
10. McKenna WJ, Thiene G, Nava A, et al. Diagnosis of arrhythmogenic risk for sudden death. Conversely, in athletes without right ventricular dysplasia/cardiomyopathy. Br Heart J 1994;71:215– 8.
cardiovascular abnormalities, the reversibility of ventricular 11. Aretz HT, Billingham ME, Edwards WD, et al. Myocarditis: a tachyarrhythmias (and the absence of cardiac events in the histopathologic definition and classification. Am J Cardiovasc Pathol1987;1:3–14.
follow-up period) support the benign clinical nature of these 12. Gavazzi A, De Maria R, Renosto G, et al. The spectrum of left arrhythmias as another expression of athlete's heart.
ventricular size in dilated cardiomyopathy: clinical correlates andprognostic implications. Am Heart J 1993;125:410 –22.
Reprint requests and correspondence: Dr. Alessandro Biffi,
13. Levine RA, Triulzi MO, Harrigan P, Weyman AE. The relationship of mitral annular shape to the diagnosis of mitral valve prolapse.
National Institute of Sports Medicine, Italian Olympic Commit- Circulation 1987;75:756 – 67.
tee, Via dei Campi Sportivi, 46, 00197 - Rome, Italy. E-mail: 14. Organizing Cardiologic Committee on Eligibility for Sports (COCIS). Cardiological protocols on determining eligibility for com-petitive sports. J Ital Cardiol 1996;26:949 – 83.
15. Maron BJ, Mitchell JE. 26th Bethesda Conference: recommendations for determining eligibility for competition in athletes with cardiovas-cular abnormalities. J Am Coll Cardiol 1994;24:848 –99.
1. Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The upper 16. Iellamo F, Legramante JM, Pigozzi F, et al. Conversion from vagal to limit of physiologic cardiac hypertrophy in highly trained elite athletes.
sympathetic predominance with strenuous training in high- N Engl J Med 1991;324:295–301.
performance world class athletes. Circulation 2002;105:2719 –24.
2. Maron BJ, Pelliccia A, Spirito P. Cardiac disease in young trained 17. Grassi G, Seravalle G, Bertinieri G, Mancia G. Behavior of the athletes: insights into methods for distinguishing athlete's heart from adrenergic cardiovascular drive in atrial fibrillation and cardiac arrhyth- structural heart disease, with particular emphasis on hypertrophic mias. Acta Physiol Scand 2003;177:399 – 404.
cardiomyopathy. Circulation 1995;91:1596 – 601.
18. Pitzalis MV, Mastropasqua F, Massari F, et al. Dependency of 3. Pelliccia A, Culasso F, Di Paolo FM, Maron BJ. Physiologic left premature ventricular contractions on heart rate. Am Heart J 1997; ventricular cavity dilatation in elite athletes. Ann Intern Med 1999; 133:153– 61.
19. Sapoznikov D, Luria MH, Gotsman MS. Changes in sinus RR 4. Martin WH, III, Coyle EF, Bloomfield SA, Eshani AA. Effects of physical deconditioning after intense endurance training on left ven- interval patterns preceding ventricular ectopic beats: assessment with tricular dimensions and stroke volume. J Am Coll Cardiol 1986;7: rate enhancement and dynamic heart rate trends. Int J Cardiol 5. Maron BJ, Pelliccia A, Spataro A, Granata M. Reduction in left 20. Estes NAM, III, Link MS, Cannom D, et al. Report of the NASPE ventricular wall thickness after deconditioning in highly trained policy conference on arrhythmias and the athlete. J Cardiovasc Olympic athletes. Br Heart J 1993;69:125– 8.
Electrophysiol 2001;12:1208 –19.
6. Biffi A, Pelliccia A, Verdile L, et al. Long-term clinical significance of 21. Corrado D, Basso C, Schiavon M, Thiene G. Screening for hyper- frequent and complex ventricular tachyarrhythmias in trained athletes.
trophic cardiomyopathy in young athletes. N Engl J Med 1998;339: J Am Coll Cardiol 2002;40:446 –52.
7. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations 22. Corrado D, Basso C, Rizzoli G, Schiavon M, Thiene G. Does sport regarding quantitation in M-mode echocardiography: results of a activity enhance the risk of sudden death in adolescents and young survey of echocardiographic measurements. Circulation 1978;58: adults? J Am Coll Cardiol 2003;40:446 –52.
23. Maron BJ. Sudden death in young athletes. N Engl J Med 2003;349: 8. Devereux RB, Alouso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison with necropsy 24. Heidbuchel H, Hoogsteen J, Fagard R, et al. High prevalence of right findings. Am Heart J 1986;57:450 – 8.
ventricular involvement in endurance athletes with ventricular arrhyth- 9. Lewis JF, Spirito P, Pelliccia A, et al. Usefulness of Doppler echocar- mias: role of an electrophysiologic study in risk stratification. Eur diographic assessment of diastolic filling in distinguishing "athlete's Heart J 2003;24:1473– 80.


Microsoft word - 12-lecture.doc

Pt. Govind Ballabh Pant Memorial Lecture - XI Medicinal Plants for Health Care Prof. S.S. Handa Senior Specialist, Earth Environment and Marine Sciences & Technologies, UNIDO September 10, 2006, Mohal-Kullu, H.P. Anbout Prof. S.S. Handa Ex-Director, RRL-Jammu (CSIR) and formerly Professor and Head of the University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh; Presently Senior specialist Industrial utilization of Medicinal and Aromatic Plants, Earth Environment and Marine Sciences & Technologies United Nations Industrial Development Organization (UNIDO) International Centre for Science & High Technologies Area Science Park, Padriciano 99. 34012 Trieste, Italy. (Permanent residence: C-522A, Sushant Lok-1,Gurgaon – 122 002)

Microsoft word - 7.14.06 wegman report fact sheet.doc

Chairman, R-Texas Report Raises New Questions About Climate Change Assessments ‘It is important to note the isolation of the paleoclimate community; even though they rely heavily on statistical methods they do not seem to be interacting with the statistical community. Additionally, we judge that the sharing of research materials, data and results was haphazardly and grudgingly done. In this case we judge that there was too much reliance on peer review, which was not necessarily independent. Moreover, the work has been sufficiently politicized that this community can hardly reassess their public positions without losing credibility. Overall, our committee believes that Dr. Mann's assessments that the decade of the 1990s was the hottest decade of the millennium and that 1998 was the hottest year of the millennium cannot be supported by his analysis.'