Accuracy of Devereaux and Teichholz formulas for left ventricular mass calculation in different geometric patterns: comparison with cardiac magnetic resonance imaging.

Left ventricular (LV) myocardial mass is important in the evaluation of cardiac remodeling and requires accurate assessment when performed on linear measurements in two-dimensional echocardiography (Echo). We aimed to compare the accuracy of the Devereaux formula (DEV) and the Teichholz formula (TEICH) in calculating LV myocardial mass in Echo using cardiac magnetic resonance (CMR) as the reference method. Based on preceding mathematical calculations, we identified primarily LV size rather than wall thickness as the main source of bias between DEV and TEICH in a retrospective derivation cohort (n = 1276). Although LV mass from DEV and TEICH were correlated with CMR, TEICH did not show a proportional bias as did DEV (- 2 g/m2 vs. + 22 g/m2). This could be validated in an independent prospective cohort (n = 226) with symptomatic non-ischemic heart failure. DEV systematically overestimated LV mass in all tiers of LV remodeling as compared to TEICH. In conclusion, the TEICH method accounts for the changes in LV geometry with increasing LV mass and thus better reflects the different pattern of LV remodeling than the DEV method. This has important clinical implications, as TEICH may be more appropriate for use in clinical practice, rather than DEV, currently recommended.

Benefit of 3D Vena Contracta Area over 2D-Based Echocardiographic Methods in Quantification of Functional Mitral Valve Regurgitation.

BACKGROUND: The two-dimensional proximal isovelocity surface area (2D PISA) method in the quantification of an effective regurgitation orifice area (EROA) has limitations in functional mitral valve regurgitation (FMR), particularly in non-circular coaptation defects. OBJECTIVE: We aimed to validate a three-dimensional vena contracta area (3D VCA) against a conventional EROA using a 2D PISA method and anatomic regurgitation orifice area (AROA) in patients with FMR. METHODS: Both 2D and 3D full-volume color Doppler data were acquired during consecutive transoesophageal echocardiography (TEE) examinations. The EROA 2D PISA was calculated as recommended by current guidelines. Multiplanar reconstruction was used for offline analysis of the 3D VCA (with a color Doppler) and AROA (without a color Doppler). Receiver operating characteristic (ROC) analysis was used to calculate a cut-off value for the 3D VCA to discriminate between moderate and severe FMR as classified by the EROA 2D PISA. RESULTS: From 2015 to 2018, 105 consecutive patients with complete and adequate imaging data were included. The 3D VCA correlated strongly with the 2D PISA EROA and AROA (r = 0.93 and 0.94). In the presence of eccentric or multiple regurgitant jets, there was no significant difference in correlations with the 3D VCA. We found a 3D VCA cut-off of 0.43 cm2 to discriminate between moderate and severe FMR (area under curve = 0.98). The 3D VCA showed a higher interobserver agreement than the EROA 2D PISA (interclass correlation coefficient: 0.94 vs. 0.81). CONCLUSIONS: The 3D VCA has excellent validity and lower variability than the conventional 2D PISA in FMR. Compared to the 2D PISA, the 3D VCA was not affected by the presence of eccentric or multiple regurgitation jets or non-circular regurgitation orifices. With a threshold of 0.43 cm2 for the 3D VCA, we demonstrated reliable discrimination between moderate and severe FMR.

The predictive role of early CRP values for one-year mortality in the first 2 d after acute myocardial infarction.

BACKGROUND: An excessive inflammatory reaction after acute myocardial infarction (AMI) is known to be harmful. New anti-inflammatory therapies are required. PURPOSE: This study assessed the predictive role of early CRP in patients with STEMI. METHODS: A total of 1003 patients with STEMI were analysed. A total of 180 patients with proven infection were excluded. CRP after 12, 24 and 48 h after pain onset were evaluated. RESULTS: Of 823 patients, 103 (12.5%) died within one year after AMI. The deceased patients showed higher CRP, even after already 12 h (6 vs. 13 mg/l, p < .001), 24 h (13 vs. 25 mg/l, p < .001) and after 48 h (40 vs. 92 mg/l, p < .001). A CRP of ≥8 mg/l, 12 h after AMI, was found in 45% and was independently associated with long-term mortality (OR: 2.7, p = .03), after 24 h: CRP ≥ 18 mg/l in 44% (OR: 2.5, p = .03), after 48 h: CRP ≥ 53 mg/l in 44% (OR 1.9, p = .03). Early CRP values correlated strongly with the later maximum value of CRP (p < .001). CONCLUSIONS: Already early CRP values are accurate for risk-prediction following AMI. By identifying patients who are beginning to develop an excessive inflammatory response, it may be possible to identify those who benefit from anti-inflammatory therapies.

Evaluation of systemic inflammation in response to remote ischemic preconditioning in patients undergoing transcatheter aortic valve replacement (TAVR).

BACKGROUND: Systemic inflammation can occur after transcatheter aortic valve replacement (TAVR) and correlates with adverse outcome. The impact of remote ischemic preconditioning (RIPC) on TAVR associated systemic inflammation is unknown and was focus of this study. METHODS: We performed a prospective controlled trial at a single center and included 66 patients treated with remote ischemic preconditioning (RIPC) prior to TAVR, who were matched to a control group by propensity score. RIPC was applied to the upper extremity using a conventional tourniquet. Definition of systemic inflammation was based on leucocyte count, C-reactive protein (CRP), procalcitonin (PCT) and interleukin-6 (IL-6), assessed in the first 5 days following the TAVR procedure. Mortality was determined within 6 months after TAVR. RIPC group and matched control group showed comparable baseline characteristics. RESULTS: Systemic inflammation occurred in 66% of all patients after TAVR. Overall, survival after 6 months was significantly reduced in patients with systemic inflammation. RIPC, in comparison to control, did not significantly alter the plasma levels of leucocyte count, CRP, PCT or IL-6 within the first 5 days after TAVR. Furthermore, inflammation associated survival after 6 months was not improved by RIPC. Of all peri-interventional variables assessed, only the amount of the applied contrast agent was connected to the occurrence of systemic inflammation. CONCLUSIONS: Systemic inflammation frequently occurs after TAVR and leads to increased mortality after 6 months. RIPC neither reduces the incidence of systemic inflammation nor improves inflammation associated patient survival within 6 months.

Spatio-temporal regulation of calpain activity after experimental myocardial infarction in vivo.

BACKGROUND: Calpains are calcium activated cysteine proteases that play a pivotal role in the pathophysiology of cardiac remodeling. METHODS: Here, we performed left anterior descending coronary artery ligation in rats as a model for ischemic systolic heart failure and examined the time- and region-specific regulation of calpain-1 and calpain-2 in the left ventricular myocardium. RESULTS: Following anterior wall myocardial infarction, calpain activity was significantly increased restricted to the ischemic anterior area at days 1, 5 and 14. No changes in calpain activity at neither time point were detected in the borderzone and remote posterior area of the left ventricle. Of note, calpain activity in the infarcted anterior myocardium was regulated differentially in the acute vs. subacute and chronic phase. In the acute phase, calpain translocation to the plasma membrane and attenuation of the expression of its endogenous inhibitor, calpastatin, were identified as the driving forces. In the subacute and chronic phase, calpain activity was regulated at the level of protein expression that was shown to be essentially independent of transcriptional activity. CONCLUSIONS: We conclude that myocardial infarction leads to a distinct calpain regulation pattern in the left ventricular myocardium that is region specific and time dependent. Considering the results from our previous studies, a spatio-temporal interaction between calpains and calcium dependent natriuretic peptide production in the infarcted myocardium is possible. GENERAL SIGNIFICANCE: Our results shed more light in the differential regulation of calpain activity in the myocardium and might aid in the development of targeted post-infarct and/or heart failure therapeutics.

Cardiac manifestation is evident in chorea-acanthocytosis but different from McLeod syndrome.

INTRODUCTION: We aimed to study the various cardiac manifestations of the two core neuroacanthocytosis (NA) syndromes, namely chorea-acanthocytosis (ChAc) and McLeod syndrome (MLS). So far, cardiac involvement has been described as specific feature only for MLS. METHODS: We studied six patients with ChAc (mean age 44.5 years, five men, one woman) and six patients with MLS (mean age 57.1 years, all men). Cardiac evaluation included echocardiography and/or cardiac magnetic resonance imaging (cardiac MRI), 24-h ECG-recording and examination of cardiac biomarkers. RESULTS: Cardiac involvement of ChAc was found in four of six patients. Two patients showed mildly reduced left ventricular ejection fraction (LVEF), two other patients mild to moderate left ventricular (LV) dilatation. Neither an increase in ventricular ectopic beats nor ventricular tachycardia were evident in ChAc. Four of five MLS patients showed left ventricle dilatation and reduced left ventricular ejection fraction (LVEF). Two of these, in addition, had critical ventricular tachycardia. High sensitive troponin T was elevated in all patients, for whom data were available (n = 10). In contrast, elevation of high sensitive troponin I was found in one of six ChAc and one of two MLS patients. CONCLUSION: For the first time, we reveal cardiac involvement in a cohort of six ChAc patients, while the risk to develop heart failure seems lower than in MLS. Our study confirms the malignant nature of MLS in terms of ventricular arrhythmias and progression to advanced heart failure. Herein, we define disease-specific recommendations for cardiac assessment in both conditions.

Myocardial strain analysis using cardiac magnetic resonance in patients with calpainopathy.

BACKGROUND: Limb-girdle muscular dystrophy (LGMD) is a genetically and clinically heterogeneous group of rare muscular dystrophies. Subtype 2A (LGMD2A) also known as "calpainopathy" is an inherited autosomal recessive gene defect. Cardiac dysfunction is common in several forms of LGMD. Cardiac involvement in LGMD2A, however, is not clear. The aim of this study was to perform cardiac magnetic resonance (CMR)-based strain analysis in LGMD2A patients, as this is a diagnostic parameter of subclinical cardiac involvement and a powerful independent predictor of mortality. We conducted the largest prospective cardiac magnetic resonance study to date, including 11 genetically verified LGMD2A patients and 11 age- and sex-matched control subjects and performed CMR-based strain analysis of the left and right ventricles. RESULTS: Left and right global longitudinal strain (GLS) were not significantly different between the two groups and within normal reference ranges (left ventricle: control - 21.8 (5.1) % vs. patients - 22.3 (3.2) %, p = 0.38; right ventricle: control - 26.3 (7.2) % vs. patients - 26.8 (5.8) %, p = 0.85). Also, global circumferential and radial strains did not significantly differ between the two groups (p = 0.95 and p = 0.86, respectively). LGMD2A patients did not show relevant amounts of late gadolinium enhancement (LGE) or malignant ventricular arrhythmias. CONCLUSIONS: No evidence of even subtle cardiac dysfunction is evident form CMR-based strain analysis in LGMD2A patients. Malignant ventricular arrhythmias were not detected. Thus, in case of non-pathological initial echocardiographic and electrocardiographic examination, a less frequent or even no cardiac follow-up may be acceptable in these patients. However, if there are signs and symptoms that suggest an underlying cardiac condition (e.g. palpitations, angina, shortness of breath), this approach needs to be individualized to account for the unknown.

Frailty is associated with chronic inflammation and pro-inflammatory monocyte subpopulations.

AIM OF THE STUDY: Frail patients with high grade aortic valve stenosis (AS) undergoing Transcatheter Aortic Valve Implantation (TAVI) have an increased mortality. A connection between frailty and inflammation has been suggested. Monocyte subpopulations are associated with both cardiovascular diseases and chronic inflammatory diseases. This study investigates the association of frailty with monocyte subpopulations and systemic inflammatory parameters in elderly patients undergoing TAVI. METHODS: A total of 120 patients with symptomatic AS was examined. Before TAVI implantation, frailty was assessed by a bedside evaluation (eyeball test). In all patients a flow cytometry analysis has been performed. Monocyte subpopulations were defined as follows: classical (CD14++CD16-), intermediate (CD14++CD16+) and non-classical (CD14+CD16++). Expression of CD11b was measured as a marker for monocyte activation. Pro-inflammatory cytokines such as interleukin IL-8, as well as CRP were measured with Cytometric Bead Array or standard laboratory methods. RESULTS: 28 out of 120 patients were frail. These patients showed both, signs of elevated chronic systemic inflammation reflected by elevated CRP (3.7 (1.4-5.4) vs. 5.9 (3.7-29.1), p = 0.001) and an elevated level of intermediate monocytes (37 (24-54) vs. 53 (47-63), p = 0.001). At 6 months after TAVI, 19 of 120 patients died, primarily without relevant dysfunction of the implanted aortic valve. Mortality was significantly higher in the frail as compared with non-frail patients (9 of 28 frail patients vs. 10 of 92 non frail patients, p < 0.001). A binary logistic regression analysis validated frailty and intermediate monocytes as independent predictors for early mortality after TAVI. CONCLUSION: Chronic systemic inflammation and increased levels of intermediate monocytes are associated with frailty in old patients with severe aortic valve stenosis. Both the syndrome of frailty and elevated intermediate monocytes showed an association with early mortality after TAVI.

Evaluation of Myocardial Strain Using Cardiac Magnetic Resonance in Patients with Wilson's Disease.

(1) Background: Wilson's disease (WD) is an inherited autosomal recessive disorder with the excessive deposition of copper into different organs, including the heart. Previous studies showed structural cardiac changes even in patients with no signs of heart failure. The aim of this study was to perform cardiac magnetic resonance-based strain analysis in WD patients, as it is a powerful independent predictor of mortality. (2) Methods: We conducted a prospective cardiac magnetic resonance study that included 61 patients and 61 age and sex-matched controls, and performed strain analysis of the left and right ventricle. (3) Results: Left ventricular global longitudinal strain (GLS) as a prognostic marker of increased mortality was not altered (control -22.8 (4.8) % vs. WD patients -21.8 (5.1) %, p = 0.124). However, 4 of the 61 patients had a markedly reduced GLS. Global circumferential strain did not significantly differ between the groups either (p = 0.534). WD patients had significantly reduced global radial strain (p = 0.002). Right ventricular GLS was also significantly reduced in WD patients (p = 0.01). (4) Conclusions: Strain analysis revealed functional impairment of the left and right ventricle in a small number of patients as a potential early sign of cardiac manifestation in asymptomatic WD patients.

Adrenal glands enhancement in computed tomography as predictor of short-and intermediate term mortality in critically ill patients.

PURPOSE: To investigate whether adrenal gland radiodensities alone or compared to the inferior vena cava (IVC) can correctly predict hospital mortality in patients in intensive care. METHODS: One hundred thirteen intensive care patients (76 males, age: 67.2 ± 14.0 years) with an acute clinical deterioration were included in this retrospective analysis. For the venous and the arterial phase CT attenuation (Hounsfield units) of adrenal glands and IVC was ROI-based evaluated by two radiologists separately. ROC analysis, combined with the Matthews Correlation Coefficient (MCC) as a classifier, was used to assess whether one of the parameters is suitable for predicting short and medium-term mortality and, if so, which parameter is most appropriate. Interrater agreement was assessed using the intraclass correlation coefficient. RESULTS: Twenty-one patients (18.6%) died within three days in the ICU. Measurements of the adrenal glands in the portal venous phase yielded the highest discriminative power (=AUC) to distinguish between deceased and survivors. A threshold ratio of >95.5 predicted 72-hour mortality with a sensitivity of 76.19% and a specificity of 92.39% (AUC = 0.84; p < 0.0001). The positive likelihood ratio was 10.1; the positive predictive value was 69%. The predictive power for 24-hour mortality was slightly lower. Venous adrenal-to-IVC ratios and arterial measurements as a whole were substantially less suitable. All intraclass correlation coefficients indicated a high interrater agreement. CONCLUSIONS: In the portal venous phase, hyperattenuating of the adrenal glands on contrast-enhanced CT can predict short and intermediate ICU mortality quite well and may serve as a reproducible prognostic marker for individual patient outcomes.

Vascular changes of the superior mesenteric artery (SMA): A new component of the hypovolemic shock complex (HSC).

PURPOSE: To assess the type and frequency of vascular changes in the superior mesenteric artery (SMA) associated with the hypovolemic shock complex (HSC). METHODS: Twenty-six patients (14 males, 70.6 ±â€¯11.2 years) meeting the criteria for hypovolemic shock complex in computed tomography were examined for the presence of angiographic signs of non-occlusive mesenteric ischemia (NOMI) in the SMA: the string of sausages sign and spasms of the arcades of mesenteric arteries on coronal maximum intensity projection images (MIP). Interrater agreement was assessed using weighted kappa (κ). RESULTS: Vascular changes of the SMA were visible in almost all of the patients with HSC with a frequency of 88.5 %-96.2 %. Intraclass correlation coefficients indicated a substantial to almost perfect interrater agreement. CONCLUSIONS: Using computed tomography, it is possible to reliably and reproducibly detect vascular changes in SMA known from angiography in the context of hypoperfusion. The pathological vascular changes also occur more frequently than other classic signs of a CT hypoperfusion complex. Since the qualitative assessment of the SMA requires only a small amount of time, it is suitable as a further criterion for the presence of the CT hypoperfusion complex.

Remote Ischemic Preconditioning Neither Improves Survival nor Reduces Myocardial or Kidney Injury in Patients Undergoing Transcatheter Aortic Valve Implantation (TAVI).

BACKGROUND: Peri-interventional myocardial injury occurs frequently during transcatheter aortic valve implantation (TAVI). We assessed the effect of remote ischemic preconditioning (RIPC) on myocardial injury, acute kidney injury (AKIN) and 6-month mortality in patients undergoing TAVI. METHODS: We performed a prospective single-center controlled trial. Sixty-six patients treated with RIPC prior to TAVI were enrolled in the study and were matched to a control group by propensity-score. RIPC was applied to the upper extremity using a conventional tourniquet. Myocardial injury was assessed using high-sensitive troponin-T (hsTnT), and kidney injury was assessed using serum creatinine levels. Data were compared with the Wilcoxon-Rank and McNemar tests. Mortality was analysed with the log-rank test. RESULTS: TAVI led to a significant rise of hsTnT across all patients (p < 0.001). No significant inter-group difference in maximum troponin release or areas-under-the-curve was detected. Medtronic CoreValve and Edwards Sapien valves showed similar peri-interventional troponin kinetics and patients receiving neither valve did benefit from RIPC. AKIN occurred in one RIPC patient and four non-RIPC patients (p = 0.250). No significant difference in 6-month mortality was observed. No adverse events related to RIPC were recorded. CONCLUSION: Our data do not show a beneficial role of RIPC in TAVI patients for cardio- or renoprotection, or improved survival.

The infarction zone rather than the noninfarcted remodeling zone overexpresses angiotensin II receptor type 1 and is the main source of ventricular atrial natriuretic peptide.

Chromogranin B and inositol 1,4,5-trisphosphate-associated calcium signaling leading to increased natriuretic peptide production has been described in cardiac hypertrophy. Here, we performed left anterior descending coronary artery ligation in rats as a model for systolic heart failure and examined protein and gene expression clusters in the infarcted and noninfarcted myocardium and moreover under treatment with metoprolol. We found that atrial natriuretic peptide gene transcription was significantly more elevated in the infarcted compared with the noninfarcted myocardium. Chromogranin B, which facilitates calcium release from internal stores through the inositol 1,4,5-trisphosphate receptor, was upregulated in both areas. Interestingly, angiotensin II receptor type 1 gene transcription was significantly upregulated in the infarcted and unchanged in the noninfarcted myocardium. Nuclear factor ĸappa B as a calcium-dependent transcription factor showed increased activity in the infarction zone. The ß-adrenergic axis does not seem to be involved, as metoprolol treatment did not have a significant impact on any of these results. We conclude that region-specific upregulation of angiotensin II receptor type 1 is a major factor for increased atrial natriuretic peptide production in the infarcted anterior wall. This effect is most likely achieved through inositol 1,4,5-trisphosphate-mediated cytosolic calcium increase and subsequent nuclear factor ĸappa B activation, which is a known transcription factor for natriuretic peptides.

Left ventricular clefts - incidental finding or pathologic sign of Wilson's disease?

BACKGROUND: Wilson's disease is an inherited autosomal recessive multi-systemic disorder characterized by reduced excretion and consequently excessive accumulation of copper in different organs, such as the heart. RESULTS: In a prospective controlled trial, which is the largest to date, we evaluated 61 patients with Wilson's disease, age- and sex-matched to 61 healthy patients, for cardiac manifestation using cardiac magnetic resonance imaging. Patients were under stable disease and had no signs of heart failure at the time of examination. We detected a left ventricular cleft, an invagination penetrating more than 50% wall thickness of the adjoining compact myocardium in diastole, in 20% of the patients (12 out of 61) compared to 5% among control patients (3 out of 61, p = 0.013). No correlation between the incidence of cleft and a certain genotype of Wilson's disease was found. All described cases were incidental findings and none of the patients showed other signs of cardiac involvement. CONCLUSIONS: To conclude, the results of this study suggests that the increased occurrence of left ventricular clefts is due to Wilson's disease. Large studies with a long observation period are needed for further evaluation.

Influence of the plasminogen activator system on necrosis in acute myocardial infarction: analysis of urokinase- and urokinase receptor-knockout mouse models.

Serine proteases and G-protein-coupled receptors have been studied extensively as effectors of cell death. However, their roles in myocardial infarction have not been determined. In this study, we investigated the influence of the plasminogen activator system involving urokinase and urokinase receptor on necrosis after acute myocardial infarction. Myocardial infarction and reperfusion were induced in mouse hearts using the in vitro Langendorff model. DNA fragmentation and cleaved caspase-3 activity in urokinase- (uPA-/-) and urokinase receptor-knockout mice (uPAR-/-) were determined and compared with those in wild-type mice using in situ nick-end DNA labeling (TUNEL) and enzyme-linked immunosorbent assays, respectively. Infarct sizes were determined using propidium iodide and fluorescent microspheres. Following regional ischemia and reperfusion, a significant increase in the number of TUNEL-positive nuclei was observed in the ischemic zone in mouse hearts and to a lesser degree in regions remote from the ischemic area in wild-type, uPAR-/-, and uPA-/- groups compared with those in directly removed hearts. No significant differences were observed between uPAR-/- and wild-type mice. Conversely, a significant reduction in DNA fragmentation was observed in ischemic and nonischemic regions after acute myocardial infarction in uPA-/- mice when compared with that in wild-type and uPAR-/- groups. The resulting infarct sizes were significantly smaller in uPA-/- mice than in uPAR-/- and wild-type mice. These data demonstrated the involvement of uPA, but not uPAR, in protecting against necrosis during acute myocardial infarction.

Cardiac and autonomic function in patients with Wilson's disease.

BACKGROUND: The clinical effect of copper accumulation on the heart of patients suffering from Wilson's disease (WD) is not completely understood. We aimed to determine if patients with WD show signs of cardiac involvement, structural heart disease or autonomic dysfunction. In this prospective trial, we studied 61 patients (mean age 44.3 ± 15.2 years, 51% males) with WD and compared them to 61 age- and gender-matched healthy controls. All subjects underwent clinical examination, blood tests, echocardiography and 24 h electrocardiographic (ECG) recording. RESULTS: Left- and right ventricular systolic function did not differ significantly between WD patients and controls. However, 5 of the 61 patients had a reduced left ventricular ejection fraction (LVEF). Furthermore, diastolic dysfunction was more prevalent in WD patients (9 of 61 vs. 0 of 61, p = 0.001). The severity of WD based on the Unified Wilson's Disease Rating Scale was significantly correlated to NT-pro BNP (r = 0.34, P = 0.013). Patients with an exacerbation of WD in medical history had higher troponin levels compared to those without (11.3 ± 4.7 vs 4.6 ± 1.2). The autonomic function assessed by triangular index (TI) and SDNN-index was significantly reduced in WD patients compared to controls in most in almost every age category (p-value TI and SDNN: age 20-29, p < 0.001 and 0.05; age 30-39, p < 0.01 and not significant (ns); age 40-49, p < 0,01 and 0.001; age 50-59, p = ns and < 0.001, age 60-70, p < 0.05 and ns). CONCLUSION: Our data demonstrate that cardiac involvement and autonomic dysfunction in WD is possible, however the underlying cause is still not known. We suggest that patients with signs and symptoms of structural heart disease should be examined by a cardiologist in addition to the interdisciplinary treatment team of WD.

Left Ventricular Torsion　- A New Echocardiographic Prognosticator in Patients With Non-Ischemic Dilated Cardiomyopathy.

BACKGROUND: Left ventricular (LV) torsion is a key parameter in cardiac function and predicts functional capacity (FC) more appropriately than LV ejection fraction (EF). We sought to investigate LV torsion as a marker of hospitalization for worsening heart failure (HF) in non-ischemic dilated cardiomyopathy (DCM) patients. Methods and Results: The 91 outpatients with newly diagnosed DCM (53±13 years, 20% female) were evaluated with 3D speckle-tracking imaging and followed up for 12 months; 43 healthy sex- and age-matched volunteers served as controls. LV torsion, LVEF, right ventricular function, LV global longitudinal (GLS) and circumferential (GCS) strain values, peak oxygen uptake (peak V̇O2) from FC and B-type natriuretic peptide levels were measured at baseline. Peak V̇O2correlated successively with LV torsion, diastolic filling and GCS (r=0.70, -0.52 and -0.41, P<0.01) disclosing the central role of LV torsion. During follow-up (median 272 days), 24 (26%) cardiac events occurred. A reduced LV torsion (<0.59 degrees/cm) predicted cardiac events similar to a reduced peak V̇O2(<19 mL/kg/min) (unadjusted hazard ratio 6.41 and 5.90, P<0.001). LV torsion provided a significant incremental value over right ventricular function and peak V̇O2(C-index: 0.85, P=0.02). CONCLUSIONS: The results demonstrated a clear relation between LV torsion and disease severity, suggesting that LV torsion has additional prognostic relevance in DCM patients.

Reduction of atrial fibrillation burden by pulmonary vein isolation leads to a decrease of CD11b expression on inflammatory cells.

Aims: It is hypothesized that inflammation could promote structural and electrical remodelling processes in atrial fibrillation (AF). Atrial infiltration of monocytes and granulocytes has been shown to be dependent on CD11b expression. The aim of this study was to investigate whether treatment of AF by pulmonary vein isolation (PVI) may lead to reduced inflammation, as indicated by a decrease of CD11b expression on monocytes and granulocytes. Methods and results: Flow-cytometric quantification analysis and determination of systemic inflammatory markers of peripheral blood were performed in 75 patients undergoing PVI 1 day before and 6 months after PVI. The extent of activation of monocytes and granulocytes was measured by quantifying the cell adhesion molecule CD11b. The mean expression of CD11b on monocytes (20.9 ± 2.5 vs. 10.2 ± 1.4; P < 0.001) and granulocytes (13.9 ± 1.6 vs. 6.8 ± 0.5; P < 0.001), as well as the relative count of CD11b-positive monocytes (P < 0.05) and CD11b-positive granulocytes (P < 0.01) were significantly reduced when comparing the identical patients before and 6 months after PVI. Systemic inflammatory parameters showed only a declining tendency after 6 months. Patients with unsuccessful PVI and ongoing AF on the day of follow-up showed no decrease in CD11b expression. Conclusions: A significant reduction of CD11b expression on monocytes and granulocytes, as a sign of reduced cellular inflammation, was achieved by treatment of AF using PVI. These data strongly support that AF is not only a consequence of but also a cause for inflammatory processes, which, in turn, may contribute to atrial remodelling.