Age- and gender-dependent left ventricular remodeling.

BACKGROUND: The effect of age and gender on left ventricular (LV) size, muscle mass, and systolic function as determined by two-dimensional echocardiography has not yet been investigated in a large population. METHODS: Normal transthoracic two-dimensional echocardiography studies of 5307 subjects (47% males) performed between March 1990 and December 2011 were analyzed. LV end-diastolic volume index (LVEDVI), LV muscle mass index (LVMMI), LV ejection fraction (LVEF), and LV fractional shortening (LVFS) were compared in different age groups. RESULTS: LVMMI increased in females from 66.4 ± 1.3 g/m(2) (7-20 years) to 76.3 ± 0.9 g/m(2) (60-80 years; P < 0.0001) and in males from 81.9 ± 1.7 g/m(2) (7-20 years) to 94.6 ± 1.3 g/m(2) (60-80 years; P < 0.0001). LVEDVI decreased in females from 49.8 ± 0.9 mL/m(2) (7-20 years) to 42.8 ± 0.6 mL/m(2) (60-80 years; P < 0.0001) and in males from 56.6 ± 0.8 mL/m(2) (7-20 years) to 49.0 ± 0.7 mL/m(2) (60-80 years; P < 0.0001). A significant increase in LVEF was observed with age (P < 0.0001 for both genders), but it was more pronounced in females (62 ± 0.5% [age 7-20 years] vs. 65 ± 0.3% [age 60-80 years]) than in males (62 ± 0.5% [age 7-20 years] vs. 64 ± 0.3% [age 60-80 years]). Similarly, LVFS increased in females from 37.7 ± 0.5% (7-20 years) to 42.4 ± 0.4% (60-80 years; P < 0.001) and in males from 37.3 ± 0.5% (7-20 years) to 39.4 ± 0.5% (60-80 years; P < 0.001). CONCLUSIONS: LVEF, LVFS, and LVMMI increase with advancing age, in particular in females. In contrast, LVEDVI decreases with age. These findings indicate that the LV undergoes a lifelong remodeling.

Evolution and triggers of defibrillator shocks in patients with arrhythmogenic right ventricular cardiomyopathy.

INTRODUCTION: Implantable cardioverter-defibrillators (ICDs) can prevent sudden cardiac death due to ventricular arrhythmias in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). The aim of our study was to assess the cumulative burden, evolution and potential triggers of appropriate ICD shocks during long-term follow-up, which may help to reduce and further refine individual arrhythmic risk in this challenging disease. METHODS: This retrospective cohort study included 53 patients with definite ARVC according to the 2010 Task Force Criteria from the multicentre Swiss ARVC Registry with an implanted ICD for primary or secondary prevention. Follow-up was conducted by assessing all available patient records from patient visits, hospitalisations, blood samples, genetic analysis, as well as device interrogation and tracings. RESULTS: Fifty-three patients (male 71.7%, mean age 43±2.2 years, genotype positive 58.5%) were analysed during a median follow-up of 7.9 (IQR 10) years. In 29 (54.7%) patients, 177 appropriate ICD shocks associated with 71 shock episodes occurred. Median time to first appropriate ICD shock was 2.8 (IQR 3.6) years. Long-term risk of shocks remained high throughout long-term follow-up. Shock episodes occurred mainly during daytime (91.5%, n=65) and without seasonal preference. We identified potentially reversible triggers in 56 of 71 (78.9%) appropriate shock episodes, the main triggers representing physical activity, inflammation and hypokalaemia. CONCLUSION: The long-term risk of appropriate ICD shocks in patients with ARVC remains high during long-term follow-up. Ventricular arrhythmias occur more often during daytime, without seasonal preference. Reversible triggers are frequent with the most common triggers for appropriate ICD shocks being physical activity, inflammation and hypokalaemia in this patient population.

Minimally invasive insertion of an equine stented pulmonary valve with a built-in sinus portion in a sheep model.

OBJECTIVES: This study evaluated the feasibility of inserting a new equine stented-valve with a sinus portion in a lamb survival model, through a minimally invasive thoracotomy with right ventricular access without cardiopulmonary bypass. BACKGROUND: Extant surgical or percutaneous methods for inserting biological valves in the right outflow tract have drawbacks and limitations. METHODS: A decellularized equine valved jugular vein, sutured to a self-expanding stent with a sinus portion, was placed through a minimal right thoracotomy using a newly developed flexible hydraulic release device in seven lambs. The approach through the right ventricle into the pulmonary valve position is achieved on a beating heart. RESULTS: The stented valves were correctly positioned in the right outflow tract, were competent up to 6 months as confirmed by angiography and echocardiography, and were well-tolerated by the animals, with endothelialization of the valve demonstrated at 6 months. CONCLUSIONS: The newly developed hydraulic release system allowed for safe and reliable insertion of an equine stented-valve with a sinus portion, through a right transventricular approach on a beating heart, in a sheep survival model.

Pharmacologic preconditioning therapy prior to atrial septal defect closure in patients at high risk for acute pulmonary edema.

OBJECTIVES: The aim of this study was to assess whether transient atrial septal defect (ASD) occlusion and, if required, vasodilator therapy would improve the safety of percutaneous ASD closure in high-risk subsets. BACKGROUND: While percutaneous ASD closure is generally considered a low risk intervention, hypertensive and elderly patients may develop pulmonary edema following the procedure because of underlying left ventricular (LV) diastolic dysfunction. METHODS: Fifty-two consecutive patients who underwent successful percutaneous ASD closures were enrolled into a single-center prospective registry. Patients with arterial hypertension and/or >60 years of age (n = 15) were considered at risk for periprocedural pulmonary edema. Those patients were tested for an increase of LV filling pressures during transient ASD occlusion and, if this was the case, treated according to a prespecified algorithm. Clinical and echocardiography data were collected in-hospital and at 6 months follow-up. RESULTS: Shunt size was comparable in high and standard-risk patients (Qp:Qs 2.1 ± 0.8 vs. 2.1 ± 0.7, P = 0.82). High-risk patients had more often pulmonary hypertension (58% vs. 14%, P < 0.05) and were more frequently symptomatic. Among them, 4/15 (27%) demonstrated a significant rise of left-sided filling pressures during transient ASD balloon occlusion and underwent pharmacologic preconditioning prior to ASD closure. None of them developed periprocedural pulmonary edema. At follow-up, patients were less symptomatic (Pre: NYHA II n = 15, NYHA III n = 9; Post: NYHA II n = 15, NYHA III n = 0; P = 0.02) and right ventricular size decreased from 23 ± 5 cm(2) to 17 ± 5 cm(2), P < 0.05. CONCLUSION: Transient ASD occlusion and, if required, pharmacologic preconditioning prior to percutaneous closure may prevent periprocedural pulmonary edema in high-risk patients.

Left ventricular non-compaction revisited: a distinct phenotype with genetic heterogeneity?

Non-compaction of the left ventricular myocardium (LVNC) has gained increasing recognition during the last 25 years. There is a morphological trait of the myocardial structure with a spectrum from normal variants to the pathological phenotype of LVNC, which reflects the embryogenic structure of the human heart due to an arrest in the compaction process during the first trimester. It must be cautioned not to overdiagnose LVNC: the morphological spectrum of trabeculations, from normal variants to pathological trabeculations with the morphological feature of LVNC must be carefully considered. The classical triad of complications are heart failure, arrhythmias, including sudden cardiac death, and systemic embolic events. Non-compaction of the left ventricular myocardium can occur in isolation or in association with congenital heart defects (CHDs), genetic syndromes, and neuromuscular disorders among others. The clinical spectrum is wide and the outcome is more favourable than in previously described populations with a negative selection bias. Familial occurrence is frequent with autosomal dominant and X-linked transmissions. Different mutations in sarcomere protein genes were identified and there seems to be a shared molecular aetiology of different cardiomyopathic phenotypes, including LVNC, hypertrophic and dilated cardiomyopathies. Thus, genetic heterogeneity, with an overlap of different phenotypes, and the variability of hereditary patterns, raise the questions whether there is a morphological trait from dilated/hypertrophic cardiomyopathy to LVNC and what are the triggers and modifiers to develop either dilated, hypertrophic cardiomyopathy, or LVNC in patients with the same mutation. The variety in clinical presentation, the genetic heterogeneity, and the phenotype of the first transgenetic animal model of an LVNC-associated mutation question the hypothesis that LVNC be a distinct cardiomyopathy: it seems to be rather a distinct phenotype or phenotypic, morphological expression of different underlying diseases than a distinct cardiomyopathy.

Impact of social characteristics on the treatment of patients with ischaemic events and patent foramen ovale.

OBJECTIVE: Percutaneous closure of a patent foramen ovale (PFO) is a technically simple and safe procedure. PFO is a common finding present in up to one third of the population. Although several conditions such as stroke, migraine, and sleep apnoea have been associated with a PFO, as underlined by observational studies, no causal relationship has been documented so far. As this setting may potentially leave more space for the involved physicians for the choice of treatment, we hypothesized that social characteristics of the patient with a PFO might play a role. METHODS: We retrospectively analysed the data of 153 patients with a cerebrovascular and/or peripheral ischaemic event with the diagnosis of a PFO as documented in echocardiography from 2000 until 2005 at the University Hospital in Zurich, Switzerland. RESULTS: Forty-four patients (= 23%) underwent catheter-based PFO closure. There was no significant difference with respect to age (<40 years: P = 0.094, ns; 40-59 years: P = 0.923, ns; > or =60 years: P= 0.234, ns), gender (P = 0.356, ns) and insurance status (<40 years: P= 0.15, ns; 40-59 years: P= 0.37, ns; 60 years: P = 0.26, ns) between those who underwent percutaneous PFO closure and those who did not. CONCLUSION: We conclude from this single-centre experience that social characteristics of patients only have a marginal impact on the indication of percutaneous closure of a PFO, if at all.

Main pulmonary artery diameter from attenuation correction CT scans in cardiac SPECT accurately predicts pulmonary hypertension.

OBJECTIVES: To establish the value of the main pulmonary artery (MPA) diameter assessed from unenhanced computer tomography (CT) scans used for attenuation correction (AC) of single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) to predict pulmonary hypertension (PHT). BACKGROUND: In contrast-enhanced chest CT scans an MPA diameter of 29 mm or greater is an established predictor of PHT. However, it is unknown, whether measurements from an unenhanced CT scan for AC may be used as predictor of PHT. METHODS: 100 patients underwent SPECT MPI for assessment of coronary artery disease. PHT was defined as a right ventriculo-atrial gradient of 30 mm Hg or greater by Doppler echocardiography. We compared MPA diameter from CT to SPECT findings (right ventricular hypertrophy/enlargement, septal wall motion abnormality/perfusion defect, and D-shape) to determine the best predictor of PHT. RESULTS: PHT was found in 37 patients. An MPA diameter of 30 mm or greater yielded a sensitivity, specificity, accuracy, positive, and negative predictive value of 78%, 91%, 86%, 83%, and 88%, respectively. This yielded an area under the ROC curve of 0.85. CONCLUSIONS: MPA diameter from low-dose unenhanced multi-slice CT reliably predicts PHT, providing an important added clinical value from AC for SPECT MPI.

Long-term follow-up of patients with isolated left ventricular noncompaction: role of electrocardiography in predicting poor outcome.

BACKGROUND: Abnormal baseline electrocardiograms (ECGs) are common in patients with isolated left ventricular noncompaction (IVNC). Whether certain electrocardiographic parameters are associated with a poor clinical outcome, however, remains elusive. The present study was therefore designed to comprehensively assess the predictive value of baseline ECG findings in patients newly diagnosed with IVNC. METHODS AND RESULTS: 74 patients diagnosed with IVNC were included in the analysis. During follow-up, 8 patients (11%) died of a cardiovascular cause or underwent heart transplantation (primary outcome measure). On univariate analysis, several variables, including repolarization abnormalities (ST segment elevation/depression, T-wave inversion) in the inferior leads (5-year estimator: 67.1 ± 10.7% vs. 98 ± 2.2%; P = 0.001), an increase in PQ- (hazard ratio (HR) 1.032, P=0.004) and QTc-duration (HR 1.037, P=0.001), were predictive of cardiovascular death or heart transplantation. On multivariate analysis, only PQ- and QTc-duration and the presence of repolarization abnormalities in the inferior leads remained significantly predictive of a poor outcome. CONCLUSIONS: PQ duration, QTc duration, and repolarization abnormalities in the inferior leads are independently predictive of a poor prognosis in IVNC. Further prospective studies are required to conclusively investigate the usefulness of baseline ECG parameters for risk stratification in patients with IVNC.

Reduced Systolic Function and Not Genetic Variants Determine Outcome in Pediatric and Adult Left Ventricular Noncompaction Cardiomyopathy.

Background: Left ventricular noncompaction cardiomyopathy (LVNC CMP) is a genetic cardiomyopathy. Genotype-phenotype correlation and clinical outcome of genetic variants in pediatric and adult LVNC CMP patients are still unclear. Methods: The retrospective multicenter study was conducted in unrelated index patients with LVNC CMP, diagnosed between the years 1987 and 2017, and all available family members. All index patients underwent next-generation sequencing for genetic variants in 174 target genes using the Illumina TruSight Cardio Sequencing Panel. Major adverse cardiac events (MACE) included mechanical circulatory support, heart transplantation, survivor of cardiac death, and/or all-cause death as combined endpoint. Results: Study population included 149 LVNC CMP patients with a median age of 27.8 (9.2-44.8) years at diagnosis; 58% of them were symptomatic, 18% suffered from non-sustained and sustained arrhythmias, and 17% had an implantable cardioverter defibrillator (ICD) implanted. 55/137 patients (40%) were ≤ 18 years at diagnosis. A total of 134 variants were identified in 87/113 (77%) index patients. 93 variants were classified as variant of unknown significance (VUS), 24 as likely pathogenic and 15 as pathogenic. The genetic yield of (likely) pathogenic variants was 35/113 (31%) index patients. Variants occurred most frequently in MYH7 (n=19), TTN (n = 10) and MYBPC3 (n = 8). Altogether, sarcomere gene variants constituted 42.5% (n = 57) of all variants. The presence or absence of (likely) pathogenic variants or variants in specific genes did not allow risk stratification for MACE. Reduced left ventricular (LV) systolic function and increased left ventricular end-diastolic diameter (LVEDD) were risk factors for event-free survival in the Kaplan-Meier analysis. Through multivariate analysis we identified reduced LV systolic function as the main risk factor for MACE. Patients with reduced LV systolic function were at a 4.6-fold higher risk for MACE. Conclusions: Genetic variants did not predict the risk of developing a MACE, neither in the pediatric nor in the adult cohort. Multivariate analysis emphasized reduced LV systolic function as the main independent factor that is elevating the risk for MACE. Genetic screening is useful for cascade screening to identify family members at risk for developing LVNC CMP.

A novel operator-independent algorithm for cardiac output measurements based on three-dimensional transoesophageal colour Doppler echocardiography.

AIMS: Cardiac output (CO) measurements from three-dimensional (3D) trans-mitral Doppler echocardiography are prone to error as manual selection of the region of interest (i.e. the site of measurement) is required. We newly developed an automated, user-independent algorithm to select the site of colour Doppler CO measurement. We aimed to validate this new method by benchmarking it against thermodilution, the current gold standard for CO measurements. METHODS AND RESULTS: Transoesophageal colour 3D Doppler echocardiographic studies were obtained from 15 patients who also had received a pulmonary catheter for invasive CO measurements. Trans-mitral flow was determined using a novel operator-independent algorithm to automatically select the optimal site of measurement. The operator-independent CO measurements were referenced against thermodilution. A good correlation was found between operator-independent Doppler flow computations and thermodilution with a mean bias of 0.09 L/min, standard deviation of bias 1.3 L/min, and a 26% error (2 SD/mean CO). Mean CO was 4.94 L/min (range 3.10-7.10 L/min). CONCLUSION: Our findings demonstrate that CO computation from transoesophageal colour 3D Doppler echo can be automated concerning the site of velocity measurement. Our operator-independent algorithm provides an objective and reproducible alternative to thermodilution.

Mutations in sarcomere protein genes in left ventricular noncompaction.

BACKGROUND: Left ventricular noncompaction constitutes a primary cardiomyopathy characterized by a severely thickened, 2-layered myocardium, numerous prominent trabeculations, and deep intertrabecular recesses. The genetic basis of this cardiomyopathy is still largely unresolved. We speculated that mutations in sarcomere protein genes known to cause hypertrophic cardiomyopathy and dilated cardiomyopathy may be associated with left ventricular noncompaction. METHODS AND RESULTS: Mutational analysis in a cohort of 63 unrelated adult probands with left ventricular noncompaction and no other congenital heart anomalies was performed by denaturing high-performance liquid chromatography analysis and direct DNA sequencing of 6 genes encoding sarcomere proteins. Heterozygous mutations were identified in 11 of 63 samples in genes encoding beta-myosin heavy chain (MYH7), alpha-cardiac actin (ACTC), and cardiac troponin T (TNNT2). Nine distinct mutations, 7 of them in MYH7, 1 in ACTC, and 1 in TNNT2, were found. Clinical evaluations demonstrated familial disease in 6 of 11 probands with sarcomere gene mutations. MYH7 mutations segregated with the disease in 4 autosomal dominant LVNC kindreds. Six of the MYH7 mutations were novel, and 1 encodes a splice-site mutation, a relatively unique finding for MYH7 mutations. Modified residues in beta-myosin heavy chain were located mainly within the ATP binding site. CONCLUSIONS: We conclude that left ventricular noncompaction is within the diverse spectrum of cardiac morphologies triggered by sarcomere protein gene defects. Our findings support the hypothesis that there is a shared molecular etiology of different cardiomyopathic phenotypes.

Protocol for measuring myocardial blood flow by PET/CT in cats.

PURPOSE: The aim of this study was to establish a protocol for measuring myocardial blood flow (MBF) by PET/CT in healthy cats. The rationale was its future use in Maine Coon cats with hypertrophic cardiomyopathy (HCM) as a model for human HCM. METHODS: MBF was measured in nine anaesthetized healthy cats using a PET/CT scanner and (13)NH(3) at rest and during adenosine infusion. Each cat was randomly assigned to receive vasodilator stress with two or three adenosine infusions at the following rates (microg/kg per minute): 140 (Ado 1, standard rate for humans), 280 (Ado 2, twice the human standard rate), 560 (Ado 4), 840 (Ado 6) and 1,120 (Ado 8). RESULTS: The median MBF at rest was 1.26 ml/min per g (n = 9; range 0.88-1.72 ml/min per g). There was no significant difference at Ado 1 (n = 3; median 1.35, range 0.93-1.55 ml/min per g; ns) but MBF was significantly greater at Ado 2 (n = 6; 2.16, range 1.35-2.68 ml/min per g; p < 0.05) and Ado 4 (n = 6; 2.11, 1.92-2.45 ml/min per g; p < 0.05). Large ranges of MBF values at Ado 6 (n = 4; 2.53, 2.32-5.63 ml/min per g; ns) and Ado 8 (n = 3; 2.21, 1.92-5.70 ml/min per g; ns) were noted. Observed adverse effects, including hypotension, AV-block and ventricular premature contractions, were all mild, of short duration and immediately reversed after cessation of the adenosine infusion. CONCLUSION: MBF can be safely measured in cats using PET. An intravenous adenosine infusion at a rate of 280 microg/kg per minute seems most appropriate to induce maximal hyperaemic MBF response in healthy cats. Higher adenosine rates appear less suitable as they are associated with a large heterogeneity in flow increase and rate pressure product, most probably due to the large variability in haemodynamic and heart rate response.

Electrophysiological findings in patients with isolated left ventricular non-compaction.

AIMS: Patients with isolated left ventricular non-compaction (IVNC) are at high risk for developing ventricular tachyarrhythmias. However, no analysis of invasive electrophysiological (EP) findings in these patients has yet been performed. METHODS AND RESULTS: We performed a retrospective analysis of EP findings in 24 patients with IVNC. Ventricular tachyarrhythmias were inducible in nine patients; of these, two patients had sustained monomorphic ventricular tachycardia (VT) and two patients had ventricular fibrillation. No specific electrocardiographic or echocardiographic finding was predictive of VT inducibility. Three of the 9 patients with inducible VT experienced ventricular tachyarrhythmias during the follow-up of 61.4+/-50 months, whereas no tachyarrhythmias or sudden deaths were noted in 12 patients without inducible VT during the follow-up of 30+/-19 months (3 patients in the latter group were lost to follow-up). Supraventricular tachyarrhythmias were inducible in seven patients. CONCLUSION: Our present study provides the first comprehensive analysis of EP findings in patients with IVNC. Ventricular and supraventricular arrhythmias can readily be induced in these patients, whereas the inducibility of a sustained monomorphic VT is relatively low. Further studies including long-term follow-up are required to investigate the role of EP testing for arrhythmic risk stratification in these patients.

The search for valved conduit tissue grafts for adults (>22 mm): an ultrasonographic study of jugular vein diameters of horses and cattle.

BACKGROUND: Natural heterologous valved conduits with a diameter greater than 22 mm that can be used for right ventricular outflow tract reconstruction in adults are not commercially available. The purpose of this study was to measure by ultrasonography the maximum diameter of the distended jugular veins of horses and cattle, respectively, to identify a population of animals that would be suitable for post-mortem collection of jugular veins at sizes greater than 22 mm. METHODS: The study population included 60 Warmblood horses, 25 Freiberger horses, 20 Brown Swiss cows, and 20 Holstein cows (including 10 Holstein and 10 Red Holstein). The maximum cross-sectional diameter of the distended jugular veins was measured at a location half-way between the mandibular angle and the thoracic inlet. The thoracic circumference (heart girth length) was used as a surrogate of body size. The jugular vein diameters of the different populations were compared by analysis of variance and the association between heart girth length and jugular vein diameter was determined in each of the four study populations by linear regression analysis. RESULTS: There was considerable individual variation of jugular vein diameters within each of the four study populations. There was no statistically significant relationship between thoracic circumference and jugular vein diameter in any of the populations. The jugular vein diameters of Brown Swiss cows were significantly larger than those of any of the other populations. Warmblood horses had significantly larger jugular vein diameters compared to Freiberger horses. CONCLUSION: The results of this study suggest that the production of bovine or equine xenografts with diameters of greater than 22 mm would be feasible. Differences between species and breeds need to be considered. However, prediction of the jugular vein diameter based on breed and heart girth length in an individual animal is inaccurate.

Diverticulum of the posterior left atrial wall.

Diverticula of the left atrium are very rare malformations of unknown etiology and may be associated with arrhythmias, thromboembolism, or mitral valve regurgitation. We report a patient with suspected coronary artery disease (CAD) in whom we performed a low-dose computed tomography coronary angiography using prospective electrocardiogram triggering. CAD could be ruled out. Incidentally, we found a diverticulum on the posterior wall of the left atrium combined with an interatrial septal aneurysm. The diagnosis was confirmed by transthoracic echocardiography.

Implantable cardioverter-defibrillators in patients with left ventricular noncompaction.

BACKGROUND: Left ventricular noncompaction (LVNC) is a rare, congenital cardiomyopathy and can be associated with heart failure, embolic events, arrhythmias, and sudden cardiac death. Implantation of implantable cardioverter-defibrillators in these patients is a treatment option, but data on long-term follow-up are limited. The aim of the study was to analyze the clinical outcome of patients with LVNC who were treated with an implantable cardioverter-defibrillator (ICD). METHODS: We conducted a retrospective study on 12 patients (mean age: 45 +/- 13 years, range 20-60) with LVNC, who underwent ICD implantation for secondary (n = 8) and primary (n = 4) prevention. RESULTS: During a median follow-up of 36 months, five patients (42%) presented with appropriate ICD therapy: in four of the eight patients (50%) in whom the ICD was implanted as a secondary prevention and in one of the four patients (25%) for whom the ICD was implanted for primary prevention. In eight patients (66%) supraventricular tachyarrhythmias were documented. Improvement of left ventricular function could be observed in one of two patients with a biventricular ICD. CONCLUSIONS: Potentially life-threatening ventricular tachyarrhythmias may occur in patients with LVNC. ICD therapy may be effective for primary and secondary prevention in these patients. Due to the high prevalence of supraventricular tachyarrhythmias devices with reliable detection enhancements should be considered.

Echocardiographic findings in former professional cyclists after long-term deconditioning of more than 30 years.

BACKGROUND: In professional cyclists, typical changes include reversible dilatation of atria and left ventricle (LV), LV hypertrophy but normal diastolic function. Data on long-term outcome are limited. METHODS: Of all 134 former Swiss professional cyclists (PC) participating >or=1x in the professional bicycle race Tour de Suisse from 1955 to 1975, 62 (42%) were recruited for a prospective case control study. The PC and a control group of 62 golfers (matched for age, gender, hypertension, present physical activity) were screened [clinical examination, history, echocardiography, measurement of proBNP (normal <227 pg/mL)]. RESULTS: The interval since the last bicycle race as PC was 38 (15-49) years. Average age at exam was equal in controls and PC (66+/-6 vs 66+/-7 years; P = 0.73). Percentage of participants undergoing >4 h of endurance training per week was identical (P = 0.72). Total kilometers (km) on the bicycle were higher in PCs with 311,000 (60,000-975,000) than in controls (2500 [0-120,000]; P < 0.0001). PC had larger atrial volume indices (P = 0.002) and tended to have higher LV muscle mass indices (P = 0.07). Multiple regression analysis identified the total number of bicycle km as an independent factor for LV muscle mass. For left atrial size, heart rate at rest, age, years since the last bicycle race and the current hours of endurance training were identified as independent predictors. Long axis function of both ventricles (systolic velocities of mitral and tricuspid annulus) was decreased in PC (P

Serological evidence for the association of Bartonella henselae infection with arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an important cause of sudden death in young adults. On the basis of histopathological findings its pathogenesis may involve both a genetic origin and an inflammatory process. Bartonella henselae may cause endomyocarditis and was detected in myocardium from a young male who succumbed to sudden cardiac death. HYPOTHESIS: We hypothesized that chronic infection with Bartonella henselae could contribute to the pathogenesis of ARVC. METHODS: We investigated sera from 49 patients with ARVC for IgG antibodies to Bartonella henselae. In this study, 58 Swiss blood donors tested by the same method served as controls. RESULTS: Six patients with ARVC (12%) had positive (>1:256) IgG titres in the immunofluorescence test with Bartonella henselae. In contrast, only 1 elevated titre was found in 58 controls (p < or = 0.05). Interestingly, all patients with increased titres had no familial occurrence of ARVC. CONCLUSIONS: Further studies in larger patient cohorts seem justified to investigate a possible causal link between chronic Bartonella henselae and ARVC, in particular its sporadic (nonfamilial) form.