Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis.

BACKGROUND: To investigate the prevalence and prognostic relevance of cardiac involvement in an ANCA-associated vasculitis (AAV) population of eosinophilic granulomatosis with polyangiitis (EGPA) and granulomatosis with polyangiitis (GPA) patients. METHODS: Prospective cohort study of fifty EGPA and forty-one GPA patients in sustained remission without previous in-depth cardiac screening attending our clinical immunology outpatient department. Cardiac screening included clinical evaluation, ECG, 24-hour Holter registration, echocardiography and cardiac magnetic resonance imaging (CMR) with coronary angiography and endomyocardial biopsy upon indication. Fifty age-, sex- and cardiovascular risk factor-matched control subjects were randomly selected from a population study. Long-term outcome was assessed using all-cause and cardiovascular mortality. RESULTS: A total of 91 AAV-patients (age 60±11, range 63-87years) were compared to 50-matched control subjects (age 60±9years, range 46-78years). ECG and echocardiography demonstrated cardiac abnormalities in 62% EGPA and 46% GPA patients vs 20% controls (P<0.001 and P=0.014, respectively). A total of 69 AAV-patients underwent additional CMR, slightly increasing the prevalence of cardiac involvement to 66% in EGPA and 61% in GPA patients. After a mean follow-up of 53±18months, presence of cardiac involvement using ECG and echocardiography in AAV-patients showed increased all-cause and cardiovascular mortality (Log-rank P=0.015 and Log-rank P=0.021, respectively). CONCLUSION: Cardiac involvement in EGPA and GPA patients with sustained remission is high, even if symptoms are absent and ECG is normal. Moreover, cardiac involvement is a strong predictor of (cardiovascular) mortality. Therefore, risk stratification using cardiac imaging is recommended in all AAV-patients, irrespective of symptoms or ECG abnormalities.

Right ventricular function in dilated cardiomyopathy and ischemic heart disease: assessment with non-invasive imaging.

BACKGROUND: Dilated cardiomyopathy and ischaemic heart disease can both lead to right ventricular (RV) dysfunction. Direct comparisons of the two entities regarding RV size and function using state-of-the-art imaging techniques have not yet been performed. We aimed to determine RV function and volume in dilated cardiomyopathy and ischaemic heart disease in relation to left ventricular (LV) systolic and diastolic function and systolic pulmonary artery pressure. METHODS AND RESULTS: A well-characterised group (cardiac magnetic resonance imaging, echocardiography, coronary angiography and endomyocardial biopsy) of 46 patients with dilated cardiomyopathy was compared with LV ejection fraction (EF)-matched patients (n = 23) with ischaemic heart disease. Volumes and EF were determined with magnetic resonance imaging, diastolic LV function and pulmonary artery pressure with echocardiography. After multivariable linear regression, four factors independently influenced RVEF (R(2) = 0.51, p < 0.001): LVEF (r = 0.54, p < 0.001), ratio of peak early and peak atrial transmitral Doppler flow velocity as measure of LV filling pressure (r = - 0.52, p < 0.001) and tricuspid regurgitation flow velocity as measure of pulmonary artery pressure (r = - 0.38, p = 0.001). RVEF was significantly worse in patients with dilated cardiomyopathy compared with ischaemic heart disease: median 48 % (interquartile range (IQR) 37-55 %) versus 56 % (IQR 48-63 %), p < 0.05. CONCLUSIONS: In patients with dilated cardiomyopathy and ischaemic heart disease, RV function is determined by LV systolic and diastolic function, the underlying cause of LV dysfunction, and pulmonary artery pressure. It was demonstrated that RV function is more impaired in dilated cardiomyopathy.

Idiopathic dilated cardiomyopathy: possible triggers and treatment strategies.

Despite recent advances in the management of patients with heart failure, morbidity and mortality rates remain high. Common causes of heart failure are ischaemic heart disease, uncontrolled hypertension and valvular disease. However, in up to 50 % of the cases its exact cause remains initially unknown; this condition is called idiopathic dilated cardiomyopathy (DCM). Improved diagnostic methods, most notably the advancements in molecular and immunohistological biopsy techniques and genetic research, have endorsed a new era in the diagnosis and classification of patients with idiopathic DCM. These insights have led to novel aetiology-based treatment strategies and improved outcome. The present article will briefly discuss all causes of DCM with a special focus on inflammatory- and virus-mediated forms of DCM.

Unmappable ventricular tachycardia after an old myocardial infarction. Long-term results of substrate modification in patients with an implantable cardioverter defibrillator.

PURPOSE: The frequent occurrence of ventricular tachycardia can create a serious problem in patients with an implantable cardioverter defibrillator. We assessed the long-term efficacy of catheter-based substrate modification using the voltage mapping technique of infarct-related ventricular tachycardia and recurrent device therapy. METHODS: The study population consisted of 27 consecutive patients (age 68 ± 8 years, 25 men, mean left ventricular ejection fraction 31 ± 9%) with an old myocardial infarction and multiple and/or hemodynamically not tolerated ventricular tachycardia necessitating repeated device therapy. A total of 31 substrate modification procedures were performed using the three-dimensional electroanatomical mapping system. Patients were followed up for a median of 23.5 (interquartile range 6.5-53.2) months before and 37.8 (interquartile range 11.7-71.8) months after ablation. Antiarrhythmic drugs were not changed after the procedure, and were stopped 6 to 9 months after the procedure in patients who did not show ventricular tachycardia recurrence. RESULTS: Median ventricular tachycardias were 1.6 (interquartile range 0.7-6.7) per month before and 0.2 (interquartile range 0.00-1.3) per month after ablation (P = 0.006). Nine ventricular fibrillation episodes were registered in seven patients before and two after ablation (P = 0.025). Median antitachycardia pacing decreased from 1.6 (interquartile range 0.01-5.5) per month before to 0.18 (interquartile range 0.00-1.6) per month after ablation (P = 0.069). Median number of shocks decreased from 0.19 (interquartile range 0.04-0.81) per month before to 0.00 (interquartile range 0.00-0.09) per month after ablation (P = 0.001). One patient had a transient ischemic attack during the procedure, and another developed pericarditis. Nine patients died during follow-up, eight patients due to heart failure and one patient during valve surgery. CONCLUSION: Catheter-based substrate modification using voltage mapping results in a long-lasting reduction of cardioverter defibrillator therapy in patients with multiple and/or hemodynamically not tolerated infarct-related ventricular tachyarrhythmia.

Reversal of ventricular premature beat induced cardiomyopathy by radiofrequency catheter ablation.

Frequent monomorphic ventricular premature beats (VPBs) may lead to left ventricular dysfunction. We describe two patients with frequent monomorphic VPBs and dilated cardiomyopathy in whom left ventricular function normalised after elimination of the VPBs by radiofrequency catheter ablation. The recent literature on this topic is summarised and potential candidates for catheter ablation are discussed. (Neth Heart J 2010;18:493-8.).

Giant cell myocarditis triggered by a parvovirus B19 infection.

Giant cell myocarditis (GCM) is an uncommon inflammatory heart disease with a rapid progression and a devastating outcome. Its exact cause is unknown, but it has been associated with various inflammatory and autoimmune disorders. The authors report a case where GCM is triggered by a parvovirus B19 (PVB19) infection.

Superior vena cava syndrome as a complication of colon carcinoma.

Superior vena cava syndrome is a group of signs and symptoms resulting from the impairment of blood flow through the SVC into the right atrium. We present a case of a 54-year-old female with superior vena cava syndrome due to metastasis of colon carcinoma into the SVC leading to an intraluminal obstruction. To our knowledge this is the first published report of an intraluminal metastasis of colon adenocarcinoma into the superior vena cava causing SVC syndrome.

[Therapy of cervico-brachialgia. Controlled clinical comparison of a high-dose combination of neurotropic vitamins with an analgesic]. / Zur Therapie der Zerviko-Brachialgie. Kontrollierter klinischer Vergleich einer hochdosierten Kombination neurotroper Vitamine mit einem Analgetikum

The study revealed that cervicobrachialgias (cervical syndrome) can be effectively treated with high-dosed neurotropic vitamins. This refers in particular to pain caused by pressure on the cervical plexus and paravertebral pain on pressur, Regarding paravertebral pain on pressure, it was possible to prove a significant superiority of the therapy with Neurotrat forte. The duration of therapy in both groups was, however, too short in order to prove a significant improvement regarding the lateral listing of the cervical spine. Both forms of treatment produced similar results in view of an improvement of impaired sensibility, paresthesia and alleviation of pain. In both groups side effects were only occasionally observed.

[Radiologic differentiation between pathologic osteoporosis and bone atrophy due to age (author's transl)]. / Zur röntgenologischen Unterscheidung zwischen pathologischer Osteoporose und altersbedingtem Knochenabbau

Loss of architecture within the femoral neck due to ageing follows a distinct pattern. This may serve as an index of physiologic ageing of bone. In pathologic osteoporosis (e.g. Cushing's disease, thyreotoxicosis and idiopathic osteoporosis) this systematic reduction of trabecular structure cannot be seen in the femoral neck although the vertebral bodies show all the signs of severe osteoporosis. Radiographic comparison between the proximal end of femur and the spine may, therefore, serve as a useful means of differentiation between pathologic and age-osteoporosis.

[Loosening of the acetabular implant after replacement of the hip-joint due to age-related loss of bone structure (author's transl)]. / Pfannenlockerung bei Hüfttotalendoprothesen infolge alters-abhängigen Knochensubstanzverlustes

Radiographs of the pelvis of 17 patients who after replacement of the hip joint showed loosening of the acetabular component have been examined as to the degree of osteoporosis by the method of Singh et al. Comparing aseptic and infective loosening showed that in aseptic cases age-related loss of bone-substance was on average more pronounced than in loosening due to infection. Since we have stopped opening the cancellous space in patients with advanced osteoporosis but only fill anchorholes or ridges with cement, we have not seen any more aseptic loosening.

[The cell-independent influence on calcification in living bone and in vitro (author's transl)]. / Die zellunabhängige Beeinflussung der Calcifikation im lebenden Knochengewebe und in vitro

While there is no doubt that collagen is an important extra-cellular factor in the calcification of bone tissues, the exact nature of the process remains unclear. It has been explained in turn by the nucleation effect of corresponding lattice distances of apatite and collagen, that is, an oriented crystal overgrowth of the two substances which decreases the energy of nucleus formation, or by conformity between fibril-bundles and calciumphosphate crystal, or by the binding of phosphate to anionic positions of the collagen, as well as by the bone-forming effect of a non-collagen protein which is, however, separable from collagen. Because of their high viscosity proteo-polysaccharides inhibit crystal formation. Alkaline soluble proteo-pholysaccharides, however, appear to promote calcification in vitro and also in tissue of living bone. Lathyrogene and penicillamine impair the cross-linking in the bone collagen; this probably explains their disturbing effect on ossification. Diphosphonates would, like anorganic pyrophosphate, inhibit both the formation and dissolution of apatite crystal. Our research shows, however, that methanie-bis-phosphonate clearly promotes calcification, in vitro and in vivo. In vitro, and probably also in vivo, magnesium inhibits the formation of apatite crystal nucleus. Our research indicates moreover that magnesium also slows down the reduction of calcified bone tissue on account of its inhibiting effect on parathormone emission.