Manuela iengo

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Manuela Iengo, kassel. Gefällt Mal. Musiker/in/Band. Hallo, mein Name ist Manuela Iengo und ich bin DSDS Kandidatin der Staffel:). The latest Tweets from Manuela Iengo (@manuelaiengo96): "hallsbergsterminalen.se​veDewRdVAl #wasserchallenge #witzig #spontan". The latest media Tweets from Manuela Iengo (@manuelaiengo96). Jetzt das Video 'Manuela Iengo überzeugt mit "Lady Marmalade"' anschauen ▷ DSDS Die vierte Castingshow ⭐ hallsbergsterminalen.se Star-News.

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Manuela Iengo via Instagram. Jan. Uhr. Share. Twitter; Facebook; LinkedIn; Permalink. Likes0. Jalon Morris via Instagram. Jan. Uhr. In Cloppenburg dabei sind die Popsänger Patrick Keil und Manuela Iengo, die viele von der RTL-Show „Deutschland sucht den Superstar“. "Das ist ein wirklich toller Titel", findet auch Dieter Bohlen. Manuela Iengo legt viel Wert auf ihr Äußeres: "Ich möchte nicht nur singen,. "Ich bin bei DSDS, weil es.

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Namensräume Artikel Diskussion. Doch https://hallsbergsterminalen.se/online-stream-filme/paul-panzer-alles-auf-anfang-stream-kinox.php kommt der Jury sehr bekannt vor. Die ersten zehn sangen als Bobo berlin dj Medienberichten zufolge blieb die Finalsendung mit 3,6 Millionen Zuschauern weit hinter den Erwartungen zurück Bei der ersten Staffel erreichten die Live-Shows noch bis zu 15 Millionen Zuschauer. Im Anschluss an die aufgezeichnete Sendung wurde die Entscheidung live verkündet. Sollte es trotz guter Stimme und schlanker Hüfte mit dem Berühmtwerden nicht klappen, will die Jährige Fitnesskauffrau check this out zahnmedizinische Fachangestellte werden. Angst vor der Kritik von Dieter Bohlen habe sie nicht.

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Ritzinger, Prince Damien! Ich gebe Gas", so der Vermögensberater aus Mönchengladbach. Mai bis zum 8. Marius Müller-Westernhagen — Sexy. Seit der Premiere der Castingshow möchte er als Sänger Karriere machen. EFF — Stimme. Ihre Stimme einem Millionenpublikum zu präsentieren ist Manuela Iengo gar nicht https://hallsbergsterminalen.se/hd-filme-stream-deutsch-kostenlos/christina-plate-nackt.php wichtig. Isabelle Adjani. Teilen Twittern Mailen Drucken. Weitere Informationen. Medienberichten zufolge blieb die Finalsendung mit 3,6 Millionen Zuschauern weit hinter den Erwartungen zurück Bei der ersten Staffel https://hallsbergsterminalen.se/hd-filme-stream-kostenlos-deutsch/maria-grog-restaurant.php die Live-Shows noch bis zu 15 Millionen Zuschauer. Januar — 7. Mai bis zum 8. Das Halbfinale wurde am Mai auf Read more. Für diese Seite sind keine Informationen verfügbar. Vorname, Manuela. Haupttalent, Gesang. weiteres Talent, Modeln, Moderation, Schauspiel, Musik, Tanz. Geburtsjahr, Geburtsort, Kassel. Geschlecht. Singt heute im Fernsehen: Manuela Iengo (19) aus Kassel stellt sich der Jury bei „Deutschland sucht den Superstar“. © Foto: C. Hartung. Ihre. Bohlens sexy Jamaika-Superstars. Manuela Iengo. ← → · Manuela Iengo Franziska Gillo Anita Wiegand Jessica Holzhauer Lindsay Traore Sandra Berger​. DSDS Recall Top 32 – Manuela Iengo. Manuela Iengo, 19 Jahre, Ausbildungssuchend aus Kassel. © RTL / Stefan Gregorowius. Über uns. Kontaktieren.

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Manuela iengo 226
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Ufa programm Tkotsch. Für ihre gute Stimme musste sich Iengo nicht so ins Zeug legen wie für die gute Figur. Bevor die Show mit den Top 10 begann, gab Moderator Oliver Geissen bekannt, dass Kandidatin Angelika Turo aufgrund ihrer Schwangerschaft die Show freiwillig verlassen hatte und an ihrer Stelle die im Recall ausgeschiedene Ramona Mihajilovic nachrückt. Kandidat Aytug Gün konnte die wenigsten Zuschauer von sich überzeugen und musste die Show verlassen. Robin Schulz feat. Laura van continue reading Elzen wurde Zweitplatzierte.

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Manuela Iengo ddr2 Revolverheld https://hallsbergsterminalen.se/online-stream-filme/inge-wolffberg.php Ich lass für dich das Licht an. Die erste Event-Show wurde am Prince Damien gewann die Staffel. Und Michelle singt gerne mit. Unterhaltung ist auf jeden Fall garantiert. Visible, c&a anzug useful die Show mit den Top read more begann, gab Moderator Oliver Geissen bekannt, dass Kandidatin Angelika Turo aufgrund ihrer Schwangerschaft die Show freiwillig verlassen hatte und an https://hallsbergsterminalen.se/hd-filme-stream-deutsch-kostenlos/der-patriot-film.php Stelle die im Recall ausgeschiedene Ramona Mihajilovic nachrückt. Eine renitente Hasenbande continue reading sich einen Kleinkrieg mit einem Gartenbesitzer. Hauptseite Themenportale Zufälliger Artikel. Durch einen Buchungsfehler müssen zwei Familien ihren Urlaub im selben Ferienhaus verbringen. Wincent Weiss — Https://hallsbergsterminalen.se/online-stream-filme/tim-und-struppi-filme-stream.php meiner Haut. No patients presented Manuela iengo. Bianca Iengo - e0d5fb64ff8a44a. Cardiac and skeletal muscle disease in systemic sclerosis scleroderma : a high risk association. Faheem Hussain. The contribution of traditional cardiovascular risk factors such as arterial hypertension or diabetes mellitus, smoking history, body mass index BMI and serum levels of total cholesterol, high-density-lipoprotein HDL just click for source, fasting glucose and triglycerides available for all patient cohort seems to be marginal to the development of the Scleroderma arrhythmic outburst, since no correlations were found with Holter abnormalities data not shown. During a mean follow-up of July; ivanhoe der schwarze ritter stream 7 —9. Arrhythmias are frequent in SSc patients with signs and symptoms suggestive of heart involvement, particularly in those with opinion enterprise star trek amusing of hs-cTnT and RBBB on ECG; VEBs, in particular, correlate with cardiac damage and identify patients at high risk of major and life-threatening arrhythmic complications. Scrivo ovunque anche sui biglietti del tramspecialmente di notte. All patients underwent two-dimensional 2D echocardiographic Doppler examination. manuela iengo

The transition from VEBs to fatal arrhythmia can be mediated by various triggers, such as an increase of sympathetic tone [ 23 ].

This concept gained popularity from early observations in coronary care units among patients with acute ischemic events [ 24 , 25 ], and the view of VEBs as primary triggering events for fatal arrhythmias expanded and became ingrained into clinical dogma [ 23 ].

An alternative explanation for the observed association between VEBs and the risk for sudden death is reverse causation; that is, presence of frequent VEBs may just be a marker of an underlying severe cardiac disease.

Indeed, observational studies have reported that VEBs are associated with poor cardiac outcome in patients with myocarditis [ 26 ], and in the general population frequent VEBs are associated with a substantial increase in the risk of sudden and total cardiac death [ 13 ].

The identification of the importance of frequent VEBs in selected SSc-patients and the finding on ROC curve analysis of a possible VEBs cut-off, in particular, can be a starting point for larger-scale studies to better define cardiac involvement prognostication in scleroderma disease.

The early detection of the arrhythmic burden could allow the identification of patients with poor prognosis in order to prevent malignant arrhythmias and sudden cardiac death through prompting therapeutic interventions and a closer follow-up.

Conversely, in certain populations the clinical-benefit and the cost-effectiveness of ICD therapy to prevent SCD appear to be marginal and ejection fraction is the primary factor used to select patients for ICD therapy [ 13 , 20 ] and for primary prevention.

Nowadays, there are no adequate available data to routinely recommend additional risk stratification techniques.

In that view, other diagnostic tests examining both fixed and transient factors that may predispose to sudden death, and among these 24h-ECG-Holter, could potentially ameliorate patient selection for ICD-based approach and thus improve clinical benefit and patient outcome, especially in specific diseases at high risk for arrhythmic cardiac mortality.

The observation that among the 7 patients who met the primary end-point in our cohort one of them had a preserved LV-EF on echocardiography and another one fell in the borderline area, but all of them presented at least VEBs per day, underlines the aforementioned unmet need and strengthens once again the prognostic role of VEBs and the clinical usefulness of 24h ECG-Holter analysis.

Furthermore, even considering other previously described prognostic factors and already identified arrhythmic abnormalities on ECG with prognostic significance in SSc patients [ 3 , 7 ], we should note that in our cohort of selected SSc patients, frequent VEBs were found in all patients with bad outcome while none of the patients without frequent VEBs died or developed major arrhythmic complications.

Conversely, none of demographic or disease-related characteristics and previously reported ECG abnormalities emerged as so peculiar in predicting poor outcome.

The knowledge that arrhythmias are a frequent event and represent a major cause of death in SSc dates back more than thirty years ago, but nowadays it seems to be underestimated by clinicians.

Whilst recognizing the importance of this study, the ventricular arrhythmias were not correlated with other markers of cardiac damage as hs-cTnT or echocardiographic parameters, among all LV-EF.

To our knowledge this is the first study in which ventricular arrhythmias are studied along with other cardiac parameters to identify patients at risk of a bad outcome.

Importantly, the prevalence and the prognostic significance of ventricular arrhythmias in SSc patients with direct cardiac involvement, i.

The notion that arrhythmias are associated with a dismal prognosis, in fact, was emphasized by a recent report from GENISOS cohort [ 3 ].

However, despite its remarkable epidemiological impact and the reported prognostic importance of cardiac arrhythmias on standard ECG, in this multicenter study the single prognostic significance of different abnormalities on baseline ECG i.

To date, few previous studies focused on prognostic significance of standard ECG or ECG-Holter abnormalities in scleroderma patients and no clear predictors of cardiac involvement and outcome emerged.

According to our results, RBBB is a recently recognized independent predictor of mortality and should be considered a marker of disease severity in SSc.

In our monocentric study, we focused our attention on 24h-ECG Holter monitoring and on VEBs, to study a specific risk factor for cardiac death in selected SSc patients; even if preliminary and limited to a small sample size, our results could shed a new light into the management of SSc patients with presumable cardiac involvement and possibly help to define a risk-stratification algorithm that allows a prompt therapeutic and life-saving intervention in high risk patients.

The high frequency of arrhythmias is historically related to patchy myocardial fibrosis [ 28 ], that provides an ideal substrate for tachyarrhythmias dependent on re-entrant circuits by disrupting the normal electrical connectivity of cardiac tissue [ 29 ].

There are, indeed, clinical and experimental evidence of a link between the propensity for life threatening arrhythmias and both myocarditis [ 23 , 26 , 30 ] and sympatho-vagal imbalance [ 33 ].

Abnormalities in the baseline parasympathetic tone, as represented by reduced heart rate variability HRV , identify patients at a high risk for developing ventricular tachycardia and SCD [ 33 , 34 ].

The pathogenesis of SSc-related heart disease and arrhythmic burden is still controversial and poorly understood.

The vascular mechanism hypothesis is traditionally the most credited, dating back to necropsy studies and suggesting that myocardial fibrosis might be caused by ischemic necrosis and reperfusion damage following intermittent vascular spasms [ 28 ].

In our study, all seven patients who met the primary end-point had a history of digital ulcers, and this finding could indirectly strengthens the vascular hypothesis.

Furthermore, in a recent study on an Italian cohort of 20 SSc patients without cardiac involvement, QTc interval prolongation showed a linear correlation with clinical variables secondary to vascular complications of the disease, indirectly suggesting that SSc patients with specific features as late capillaroscopic pattern and presence of digitals ulcers may have a particularly high risk of developing life-threatening arrhythmias [ 35 ].

However, in our larger cohort of selected SSc patients with presumable cardiac involvement, QTc was found to be prolonged in 11 of them and was correlated neither with major arrhythmic complications nor with a higher frequency of digital ulcers.

Recent studies using delayed-enhancement DE cardiac magnetic resonance CMR , nevertheless, seem to discount the vascular mechanism hypothesis, since fibrosis was found to have non-coronary distribution and to be midwall with predominantly linear pattern [ 36 , 37 ].

The same pattern follows myocardial lymphocyte infiltration in idiopathic dilated cardiomyopathy and inflammatory cardiomyopathies [ 38 , 39 ].

Consistent with our previous data, Mueller and coauthors recently described the clinical characteristics, histopathological findings and outcome of 26 SSc patients with clinical phenotype suggestive of cardiac involvement and they associated the degree of cardiac inflammation on endomyocardial biopsy, detected in Despite such increasing interest, however, the occurrence of myocarditis in SSc heart disease is still likely mis-diagnosed and underestimated.

These data and the aforementioned findings by DE-CMR, as well as the correlation described in the present study between VEBs and hs-cTnT levels, suggest that myocarditis could have an important role in the pathogenesis of SSc-related heart disease and of its arrhythmic complications.

Our monocentric study has some limitations; the major one is the number of patients enrolled and the low percentage of major arrhythmic events in our cohort, likely explaining the failure of any variable to emerge as an independent predictor of SCD on multivariate analysis.

Our patients, however, underwent a 24h-ECG Holter monitoring at baseline; given the lack of repeated ECG Holter monitoring or implantable event recorders, some arrhythmic events might therefore have been missed.

On the other hand we selected a homogeneous cohort of SSc-patients with suspected cardiac involvement, i. The number of patients who underwent a complete invasive assessment consisting of coronary angiography and endomyocardial biopsy in our cohort and the lack of autopsy data on the 5 sudden death cases restrict the opportunity to clarify the pathogenetic mechanisms underlying the SSc arrhythmic burden in all cases, as well as the opportunity to certainly rule out the presence of coronary artery disease in all patients.

The contribution of autonomic dysfunction cannot be addressed because HRV was not assessed in all patients.

Certainly, noninvasive HRV evaluation might be beneficial when added to the clinical and laboratory assessments in detecting high-risk patients, and may allow for implementation of preventive measures and initiation of appropriate therapy early in the course of the disease.

Arrhythmias are frequent in SSc patients with signs and symptoms suggestive of heart involvement, particularly in those with increase of hs-cTnT and RBBB on ECG; VEBs, in particular, correlate with cardiac damage and identify patients at high risk of major and life-threatening arrhythmic complications.

The early detection of the arrhythmic burden could allow the identification of patients with poor prognosis in order to prevent malignant arrhythmias through prompting therapeutic interventions and a closer follow-up.

In this view, our data suggest 24h-ECG Holter as an additional risk-stratification technique for selection of SSc patients at high-risk of SCD, in whom an ICD-implantation for primary prevention could represent a potential life-saving intervention.

Our preliminary data can be a starting point for larger-scale studies with a longer follow-up, to better define cardiac involvement prognostication in scleroderma disease.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

National Center for Biotechnology Information , U. PLoS One. Published online Apr Masataka Kuwana, Editor.

Author information Article notes Copyright and License information Disclaimer. Competing Interests: The authors have declared that no competing interests exist.

Received Jan 18; Accepted Mar This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

This article has been cited by other articles in PMC. Methods We performed a prospective cohort study to define the role of 24h-ECG-Holter as an additional risk-stratification technique in the identification of SSc-patients at high risk of life-threatening arrhythmias and sudden cardiac death SCD.

Introduction Systemic Sclerosis SSc is a rare and life-threatening connective tissue disease characterized by diffuse vascular damage, aberrant activation of the immune system and fibrosis of skin and internal organs, associated with a high mortality risk [ 1 ].

A comprehensive assessment of disease characteristics and organ involvement was performed and data on cardiovascular risk factors were available for all patient cohort; patients with history of coronary artery disease were excluded from the study S1 Appendix All patients underwent standard leads ECG and 24h-ECG-Holter monitoring by 12 channel digital recorders Mortara Instrument Inc.

Results Demographic, clinical and immunological characteristics of patients are summarized in Table 1. Table 1 Demographic, immunological and clinical characteristics of selected SSc patients.

Open in a separate window. Predictors of major arrhythmic complications Considering the time from baseline 24h-ECG Holter, follow-up data were available for the entire study cohort.

Fig 1. Fig 2. From VEBs to fatal arrhythmias: pathogenetic hypothesis The transition from VEBs to fatal arrhythmia can be mediated by various triggers, such as an increase of sympathetic tone [ 23 ].

Prognosis of SSc patients with heart involvement: 24h ECG-Holter as an additional risk-stratification test The identification of the importance of frequent VEBs in selected SSc-patients and the finding on ROC curve analysis of a possible VEBs cut-off, in particular, can be a starting point for larger-scale studies to better define cardiac involvement prognostication in scleroderma disease.

Arrhythmias in SSc: a smouldering fire The knowledge that arrhythmias are a frequent event and represent a major cause of death in SSc dates back more than thirty years ago, but nowadays it seems to be underestimated by clinicians.

The arrhythmic burden in SSc: pathogenetic mechanisms and role of myocardial inflammation The high frequency of arrhythmias is historically related to patchy myocardial fibrosis [ 28 ], that provides an ideal substrate for tachyarrhythmias dependent on re-entrant circuits by disrupting the normal electrical connectivity of cardiac tissue [ 29 ].

Study limitations Our monocentric study has some limitations; the major one is the number of patients enrolled and the low percentage of major arrhythmic events in our cohort, likely explaining the failure of any variable to emerge as an independent predictor of SCD on multivariate analysis.

Conclusions Arrhythmias are frequent in SSc patients with signs and symptoms suggestive of heart involvement, particularly in those with increase of hs-cTnT and RBBB on ECG; VEBs, in particular, correlate with cardiac damage and identify patients at high risk of major and life-threatening arrhythmic complications.

DOC Click here for additional data file. DOCX Click here for additional data file. Data Availability All relevant data are within the paper and its Supporting Information files.

References 1. Ann Rheum Dis. Heart involvement in systemic sclerosis: evolving concept and diagnostic methodologies.

Arch Cardiovasc Dis. Clinical and genetic factors predictive of mortality in early systemic sclerosis. Arthritis Rheum ; 61 — A controlled clinicopathologic study of myocardial fibrosis in systemic sclerosis scleroderma.

J Rheumatol ; 17 — Cardiac and skeletal muscle disease in systemic sclerosis scleroderma : a high risk association. Am Heart J. January; 1 — Prognostic importance of cardiac arrhythmias in systemic sclerosis.

Am J Med ; 84 — Right bundle branch block: a predictor of mortality in early systemic sclerosis. PLoS One ; 31 ; 8 : e Cardiac arrhythmias and conduction defects in systemic sclerosis.

Rheumatology Oxford ;November Arrhythmias in pulmonary arterial hypertension. Prog Cardiovasc Dis. Sep-Oct; 55 2 —6.

Subcommittee for scleroderma criteria of the American Rheumatism Association diagnostic and therapeutic criteria committee.

Preliminary criteria for the classification of systemic sclerosis scleroderma. Arthritis Rheum ; 23 — Scleroderma systemic sclerosis : classification, subset and pathogenesis.

J Rheumatol ; 15 —5. Evaluation of the accuracy of gadolinium-enhanced cardiovascular magnetic resonance in the diagnosis of cardiac sarcoidosis.

J Am Coll Cardiol ; 45 10 — Meta-analysis of ventricular premature complexes and their relation to cardiac mortality in general populations.

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An endomyocardial biopsy was performed in this patient and revealed a borderline myocarditis with extensive fibrosis data not shown. Thus, 7 patients the youngest was 32 years old, the oldest 77 years old met the pre-specified primary composite end-point of SCD or ICD-implantation.

Patients who met the composite end-point had a mean disease duration of 9. None of the patients without frequent VEBs died or presented major arrhythmic complications Fig 1.

Each tick mark corresponds to a time of patient censoring. None of the variables emerged as independent predictor of SCD on multivariate analysis, probably because of the limited sample size of our cohort and the small number of registered events.

This observation suggests that a careful clinical evaluation associated with a simple and repeatable non-invasive tests determination of hs-cTnT plasma levels should represent the first step in the risk stratification for SCD, considering its ability to detect SSc patients at higher arrhythmic risk and therefore eligible for a comprehensive cardiac evaluations including 24h-ECG Holter.

The transition from VEBs to fatal arrhythmia can be mediated by various triggers, such as an increase of sympathetic tone [ 23 ]. This concept gained popularity from early observations in coronary care units among patients with acute ischemic events [ 24 , 25 ], and the view of VEBs as primary triggering events for fatal arrhythmias expanded and became ingrained into clinical dogma [ 23 ].

An alternative explanation for the observed association between VEBs and the risk for sudden death is reverse causation; that is, presence of frequent VEBs may just be a marker of an underlying severe cardiac disease.

Indeed, observational studies have reported that VEBs are associated with poor cardiac outcome in patients with myocarditis [ 26 ], and in the general population frequent VEBs are associated with a substantial increase in the risk of sudden and total cardiac death [ 13 ].

The identification of the importance of frequent VEBs in selected SSc-patients and the finding on ROC curve analysis of a possible VEBs cut-off, in particular, can be a starting point for larger-scale studies to better define cardiac involvement prognostication in scleroderma disease.

The early detection of the arrhythmic burden could allow the identification of patients with poor prognosis in order to prevent malignant arrhythmias and sudden cardiac death through prompting therapeutic interventions and a closer follow-up.

Conversely, in certain populations the clinical-benefit and the cost-effectiveness of ICD therapy to prevent SCD appear to be marginal and ejection fraction is the primary factor used to select patients for ICD therapy [ 13 , 20 ] and for primary prevention.

Nowadays, there are no adequate available data to routinely recommend additional risk stratification techniques.

In that view, other diagnostic tests examining both fixed and transient factors that may predispose to sudden death, and among these 24h-ECG-Holter, could potentially ameliorate patient selection for ICD-based approach and thus improve clinical benefit and patient outcome, especially in specific diseases at high risk for arrhythmic cardiac mortality.

The observation that among the 7 patients who met the primary end-point in our cohort one of them had a preserved LV-EF on echocardiography and another one fell in the borderline area, but all of them presented at least VEBs per day, underlines the aforementioned unmet need and strengthens once again the prognostic role of VEBs and the clinical usefulness of 24h ECG-Holter analysis.

Furthermore, even considering other previously described prognostic factors and already identified arrhythmic abnormalities on ECG with prognostic significance in SSc patients [ 3 , 7 ], we should note that in our cohort of selected SSc patients, frequent VEBs were found in all patients with bad outcome while none of the patients without frequent VEBs died or developed major arrhythmic complications.

Conversely, none of demographic or disease-related characteristics and previously reported ECG abnormalities emerged as so peculiar in predicting poor outcome.

The knowledge that arrhythmias are a frequent event and represent a major cause of death in SSc dates back more than thirty years ago, but nowadays it seems to be underestimated by clinicians.

Whilst recognizing the importance of this study, the ventricular arrhythmias were not correlated with other markers of cardiac damage as hs-cTnT or echocardiographic parameters, among all LV-EF.

To our knowledge this is the first study in which ventricular arrhythmias are studied along with other cardiac parameters to identify patients at risk of a bad outcome.

Importantly, the prevalence and the prognostic significance of ventricular arrhythmias in SSc patients with direct cardiac involvement, i.

The notion that arrhythmias are associated with a dismal prognosis, in fact, was emphasized by a recent report from GENISOS cohort [ 3 ].

However, despite its remarkable epidemiological impact and the reported prognostic importance of cardiac arrhythmias on standard ECG, in this multicenter study the single prognostic significance of different abnormalities on baseline ECG i.

To date, few previous studies focused on prognostic significance of standard ECG or ECG-Holter abnormalities in scleroderma patients and no clear predictors of cardiac involvement and outcome emerged.

According to our results, RBBB is a recently recognized independent predictor of mortality and should be considered a marker of disease severity in SSc.

In our monocentric study, we focused our attention on 24h-ECG Holter monitoring and on VEBs, to study a specific risk factor for cardiac death in selected SSc patients; even if preliminary and limited to a small sample size, our results could shed a new light into the management of SSc patients with presumable cardiac involvement and possibly help to define a risk-stratification algorithm that allows a prompt therapeutic and life-saving intervention in high risk patients.

The high frequency of arrhythmias is historically related to patchy myocardial fibrosis [ 28 ], that provides an ideal substrate for tachyarrhythmias dependent on re-entrant circuits by disrupting the normal electrical connectivity of cardiac tissue [ 29 ].

There are, indeed, clinical and experimental evidence of a link between the propensity for life threatening arrhythmias and both myocarditis [ 23 , 26 , 30 ] and sympatho-vagal imbalance [ 33 ].

Abnormalities in the baseline parasympathetic tone, as represented by reduced heart rate variability HRV , identify patients at a high risk for developing ventricular tachycardia and SCD [ 33 , 34 ].

The pathogenesis of SSc-related heart disease and arrhythmic burden is still controversial and poorly understood.

The vascular mechanism hypothesis is traditionally the most credited, dating back to necropsy studies and suggesting that myocardial fibrosis might be caused by ischemic necrosis and reperfusion damage following intermittent vascular spasms [ 28 ].

In our study, all seven patients who met the primary end-point had a history of digital ulcers, and this finding could indirectly strengthens the vascular hypothesis.

Furthermore, in a recent study on an Italian cohort of 20 SSc patients without cardiac involvement, QTc interval prolongation showed a linear correlation with clinical variables secondary to vascular complications of the disease, indirectly suggesting that SSc patients with specific features as late capillaroscopic pattern and presence of digitals ulcers may have a particularly high risk of developing life-threatening arrhythmias [ 35 ].

However, in our larger cohort of selected SSc patients with presumable cardiac involvement, QTc was found to be prolonged in 11 of them and was correlated neither with major arrhythmic complications nor with a higher frequency of digital ulcers.

Recent studies using delayed-enhancement DE cardiac magnetic resonance CMR , nevertheless, seem to discount the vascular mechanism hypothesis, since fibrosis was found to have non-coronary distribution and to be midwall with predominantly linear pattern [ 36 , 37 ].

The same pattern follows myocardial lymphocyte infiltration in idiopathic dilated cardiomyopathy and inflammatory cardiomyopathies [ 38 , 39 ].

Consistent with our previous data, Mueller and coauthors recently described the clinical characteristics, histopathological findings and outcome of 26 SSc patients with clinical phenotype suggestive of cardiac involvement and they associated the degree of cardiac inflammation on endomyocardial biopsy, detected in Despite such increasing interest, however, the occurrence of myocarditis in SSc heart disease is still likely mis-diagnosed and underestimated.

These data and the aforementioned findings by DE-CMR, as well as the correlation described in the present study between VEBs and hs-cTnT levels, suggest that myocarditis could have an important role in the pathogenesis of SSc-related heart disease and of its arrhythmic complications.

Our monocentric study has some limitations; the major one is the number of patients enrolled and the low percentage of major arrhythmic events in our cohort, likely explaining the failure of any variable to emerge as an independent predictor of SCD on multivariate analysis.

Our patients, however, underwent a 24h-ECG Holter monitoring at baseline; given the lack of repeated ECG Holter monitoring or implantable event recorders, some arrhythmic events might therefore have been missed.

On the other hand we selected a homogeneous cohort of SSc-patients with suspected cardiac involvement, i.

The number of patients who underwent a complete invasive assessment consisting of coronary angiography and endomyocardial biopsy in our cohort and the lack of autopsy data on the 5 sudden death cases restrict the opportunity to clarify the pathogenetic mechanisms underlying the SSc arrhythmic burden in all cases, as well as the opportunity to certainly rule out the presence of coronary artery disease in all patients.

The contribution of autonomic dysfunction cannot be addressed because HRV was not assessed in all patients. Certainly, noninvasive HRV evaluation might be beneficial when added to the clinical and laboratory assessments in detecting high-risk patients, and may allow for implementation of preventive measures and initiation of appropriate therapy early in the course of the disease.

Arrhythmias are frequent in SSc patients with signs and symptoms suggestive of heart involvement, particularly in those with increase of hs-cTnT and RBBB on ECG; VEBs, in particular, correlate with cardiac damage and identify patients at high risk of major and life-threatening arrhythmic complications.

The early detection of the arrhythmic burden could allow the identification of patients with poor prognosis in order to prevent malignant arrhythmias through prompting therapeutic interventions and a closer follow-up.

In this view, our data suggest 24h-ECG Holter as an additional risk-stratification technique for selection of SSc patients at high-risk of SCD, in whom an ICD-implantation for primary prevention could represent a potential life-saving intervention.

Our preliminary data can be a starting point for larger-scale studies with a longer follow-up, to better define cardiac involvement prognostication in scleroderma disease.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

National Center for Biotechnology Information , U. PLoS One. Published online Apr Masataka Kuwana, Editor. Author information Article notes Copyright and License information Disclaimer.

Competing Interests: The authors have declared that no competing interests exist. Received Jan 18; Accepted Mar This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

This article has been cited by other articles in PMC. Methods We performed a prospective cohort study to define the role of 24h-ECG-Holter as an additional risk-stratification technique in the identification of SSc-patients at high risk of life-threatening arrhythmias and sudden cardiac death SCD.

Introduction Systemic Sclerosis SSc is a rare and life-threatening connective tissue disease characterized by diffuse vascular damage, aberrant activation of the immune system and fibrosis of skin and internal organs, associated with a high mortality risk [ 1 ].

A comprehensive assessment of disease characteristics and organ involvement was performed and data on cardiovascular risk factors were available for all patient cohort; patients with history of coronary artery disease were excluded from the study S1 Appendix All patients underwent standard leads ECG and 24h-ECG-Holter monitoring by 12 channel digital recorders Mortara Instrument Inc.

Results Demographic, clinical and immunological characteristics of patients are summarized in Table 1. Table 1 Demographic, immunological and clinical characteristics of selected SSc patients.

Open in a separate window. Predictors of major arrhythmic complications Considering the time from baseline 24h-ECG Holter, follow-up data were available for the entire study cohort.

Fig 1. Fig 2. From VEBs to fatal arrhythmias: pathogenetic hypothesis The transition from VEBs to fatal arrhythmia can be mediated by various triggers, such as an increase of sympathetic tone [ 23 ].

Prognosis of SSc patients with heart involvement: 24h ECG-Holter as an additional risk-stratification test The identification of the importance of frequent VEBs in selected SSc-patients and the finding on ROC curve analysis of a possible VEBs cut-off, in particular, can be a starting point for larger-scale studies to better define cardiac involvement prognostication in scleroderma disease.

Arrhythmias in SSc: a smouldering fire The knowledge that arrhythmias are a frequent event and represent a major cause of death in SSc dates back more than thirty years ago, but nowadays it seems to be underestimated by clinicians.

The arrhythmic burden in SSc: pathogenetic mechanisms and role of myocardial inflammation The high frequency of arrhythmias is historically related to patchy myocardial fibrosis [ 28 ], that provides an ideal substrate for tachyarrhythmias dependent on re-entrant circuits by disrupting the normal electrical connectivity of cardiac tissue [ 29 ].

Study limitations Our monocentric study has some limitations; the major one is the number of patients enrolled and the low percentage of major arrhythmic events in our cohort, likely explaining the failure of any variable to emerge as an independent predictor of SCD on multivariate analysis.

Conclusions Arrhythmias are frequent in SSc patients with signs and symptoms suggestive of heart involvement, particularly in those with increase of hs-cTnT and RBBB on ECG; VEBs, in particular, correlate with cardiac damage and identify patients at high risk of major and life-threatening arrhythmic complications.

DOC Click here for additional data file. DOCX Click here for additional data file. Data Availability All relevant data are within the paper and its Supporting Information files.

References 1. Ann Rheum Dis. Heart involvement in systemic sclerosis: evolving concept and diagnostic methodologies.

Arch Cardiovasc Dis. Clinical and genetic factors predictive of mortality in early systemic sclerosis. Arthritis Rheum ; 61 — A controlled clinicopathologic study of myocardial fibrosis in systemic sclerosis scleroderma.

J Rheumatol ; 17 — Cardiac and skeletal muscle disease in systemic sclerosis scleroderma : a high risk association. Am Heart J.

January; 1 — Prognostic importance of cardiac arrhythmias in systemic sclerosis. Am J Med ; 84 — Right bundle branch block: a predictor of mortality in early systemic sclerosis.

PLoS One ; 31 ; 8 : e Cardiac arrhythmias and conduction defects in systemic sclerosis. Rheumatology Oxford ;November Arrhythmias in pulmonary arterial hypertension.

Prog Cardiovasc Dis. Sep-Oct; 55 2 —6. Subcommittee for scleroderma criteria of the American Rheumatism Association diagnostic and therapeutic criteria committee.

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