Noninvasive Detection of Fibrosis Applying Contrast-Enhanced Cardiac Magnetic Resonance in Different Forms of Left Ventricular Hypertrophy Relation to Remodeling

ObjectivesWe aimed to evaluate the incidence and patterns of late gadolinium enhancement (LGE) in different forms of left ventricular hypertrophy (LVH) and to determine their relation to severity of left ventricular (LV) remodeling.BackgroundLeft ventricular hypertrophy is an independent predictor of cardiac mortality. The relationship between LVH and myocardial fibrosis as defined by LGE cardiovascular magnetic resonance (CMR) is not well understood.MethodsA total of 440 patients with aortic stenosis (AS), arterial hypertension (AH), or hypertrophic cardiomyopathy (HCM) fulfilling echo criteria of LVH underwent CMR with assessment of LV size, weight, function, and LGE. Patients with increased left ventricular mass index (LVMI) resulting in global LVH in CMR were included in the study.ResultsCriteria were fulfilled by 83 patients (56 men, age 57 ± 14 years; AS, n = 21; AH, n = 26; HCM, n = 36). Late gadolinium enhancement was present in all forms of LVH (AS: 62%, AH: 50%; HCM: 72%, p = NS) and was correlated with LVMI (r = 0.237, p = 0.045). There was no significant relationship between morphological obstruction and LGE. The AS subjects with LGE showed higher LV end-diastolic volumes than those without (1.0 ± 0.2 ml/cm vs. 0.8 ± 0.2 ml/cm, p < 0.015). Typical patterns of LGE were observed in HCM but not in AS and AH.ConclusionsFibrosis as detected by CMR is a frequent feature of LVH, regardless of its cause, and depends on the severity of LV remodeling. As LGE emerges as a useful tool for risk stratification also in nonischemic heart diseases, our findings have the potential to individualize treatment strategies

insights on the right ventricle. A cardiovascular magnetic resonance study

OBJECTIVES Pectus excavatum (PE) is often regarded as a cosmetic disease, while its effect on cardiac function is under debate. Data regarding cardiac function before and after surgical correction of PE are limited. We aimed to assess the impact of surgical correction of PE on cardiac function by cardiovascular magnetic resonance (CMR). METHODS CMR at 1.5 T was performed in 38 patients (mean age 21 ± 8.3; 31 men) before and after surgical correction to evaluate thoracic morphology, indices and its relation to three-dimensional left and right ventricular cardiac function. RESULTS Surgery was successful in all patients as shown by the Haller Index ratio of maximum transverse diameter of the chest wall and minimum sternovertebral distance [pre: 9.64 (95% CI 8.18–11.11) vs post: 3.0 (2.84–3.16), P < 0.0001]. Right ventricular ejection fraction (RVEF) was reduced before surgery and improved significantly at the 1-year follow-up [pre: 45.7% (43.9–47.4%) vs 48.3% (46.9–49.5%), P = 0.0004]. Left ventricular ejection fraction was normal before surgery, but showed a further improvement after 1 year [pre: 61.0% (59.3–62.7%) vs 62.7% (61.3–64.2%), P = 0.0165]. Cardiac compression and the asymmetry index changed directly after surgery and were stable at the 1-year follow-up [3.93 (3.53–4.33) vs 2.08 (1.98–2.19) and 2.36 (2.12–2.59) vs 1.38 (1.33–1.44), respectively; P < 0.0001 for both]. None of the obtained thoracic indices were predictors of the improvement of cardiac function. A reduced preoperative RVEF was predictive of RVEF improvement. CONCLUSIONS PE is associated with reduced RVEF, which improves after surgical correction. CMR has the capability of offering additional information prior to surgical correction

Relation between myocardial edema and myocardial mass during the acute and convalescent phase of myocarditis – a CMR study

<p>Abstract</p> <p>Background</p> <p>Myocardial edema is a substantial feature of the inflammatory response in human myocarditis. The relation between myocardial edema and myocardial mass in the course of healing myocarditis has not been systematically investigated. We hypothesised that the resolution of myocardial edema as visualised by T2-weighted cardiovascular magnetic resonance (CMR) is associated with a decrease of myocardial mass in steady state free precession (SSFP)-cine imaging.</p> <p>Methods</p> <p>21 patients with acute myocarditis underwent CMR shortly after onset of symptoms and 1 year later. For visualization of edema, a T2-weighted breath-hold black-blood triple-inversion fast spin echo technique was applied and the ratio of signal intensity of myocardium/skeletal muscle was assessed. Left ventricular (LV) mass, volumes and function were quantified from biplane cine steady state free precession images.</p> <p>11 healthy volunteers served as a control group for interstudy reproducibility of LV mass.</p> <p>Results</p> <p>In patients with myocarditis, a significant decrease in LV mass was observed during follow-up compared to the acute phase (156.7 ± 30.6 g vs. 140.3 ± 28.3 g, p < 0.0001). The reduction of LV mass paralleled the normalization of initially increased myocardial signal intensity on T2-weighted images (2.4 ± 0.4 vs. 1.68 ± 0.3, p < 0.0001).</p> <p>In controls, the interstudy difference of LV mass was lower than in patients (5.1 ± 2.9 g vs. 16.3 ± 14.2 g, p = 0.02) resulting in a lower coefficient of variability (2.1 vs 8.9%, p = 0.04).</p> <p>Conclusion</p> <p>Reversible abnormalities in T2-weighted CMR are paralleled by a transient increase in left ventricular mass during the course of myocarditis. Myocardial edema may be a common pathway explaining these findings.</p

Dilated cardiomyopathy impairs mitochondrial biogenesis and promotes inflammation in an age- and sex-dependent manner

Dilated cardiomyopathy (DCM) belongs to the myocardial diseases associated with a severe impairment of cardiac function, but the question of how sex and age affect this pathology has not been fully explored. Impaired energy homeostasis, mitochondrial dysfunction, and systemic inflammation are well-described phenomena associated with aging. In this study, we investigated if DCM affects these phenomena in a sex- and age-related manner. We analyzed the expression of mitochondrial and antioxidant proteins and the inflammatory state in DCM heart tissue from younger and older women and men. A significant downregulation of Sirt1 expression was detected in older DCM patients. Sex-related differences were observed in the phosphorylation of AMPK that only appeared in older males with DCM, possibly due to an alternative Sirt1 regulation mechanism. Furthermore, reduced expression of several mitochondrial proteins (TOM40, TIM23, Sirt3, and SOD2) and genes (cox1, nd4) was only detected in old DCM patients, suggesting that age has a greater effect than DCM on these alterations. Finally, an increased expression of inflammatory markers in older, failing hearts, with a stronger pro-inflammatory response in men, was observed. Together, these findings indicate that age- and sex-related increased inflammation and disturbance of mitochondrial homeostasis occurs in male individuals with DCM

Characterization of Bartonella clarridgeiae Flagellin (FlaA) and Detection of Antiflagellin Antibodies in Patients with Lymphadenopathy

Cat scratch disease (CSD) is a frequent clinical outcome of Bartonella henselae infection in humans. Recently, two case reports indicated Bartonella clarridgeiae as an additional causative agent of CSD. Both pathogens have been isolated from domestic cats, which are considered to be their natural reservoir. B. clarridgeiae and B. henselae can be distinguished phenotypically by the presence or absence of flagella, respectively. Separation of the protein content of purified flagella of B. clarridgeiae by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblot analysis indicated that the flagellar filament is mainly composed of a polypeptide with a mass of 41 kDa. N-terminal sequencing of 20 amino acids of this protein revealed a perfect match to the N-terminal sequence of flagellin (FlaA) as deduced from the sequence of the flaA gene cloned from B. clarridgeiae. The flagellin of B. clarridgeiae is closely related to flagellins of Bartonella bacilliformis and several Bartonella-related bacteria. Since flagellar proteins are often immunodominant antigens, we investigated whether antibodies specific for the FlaA protein of B. clarridgeiae are found in patients with CSD or lymphadenopathy. Immunoblotting with 724 sera of patients suffering from lymphadenopathy and 100 healthy controls indicated specific FlaA antibodies in 3.9% of the patients' sera but in none of the controls. B. clarridgeiae FlaA is thus antigenic and expressed in vivo, providing a valuable tool for serological testing. Our results further indicate that B. clarridgeiae might be a possible etiologic agent of CSD or lymphadenopathy. However, it remains to be clarified whether antibodies to the FlaA protein of B. clarridgeiae are a useful indicator of acute infection