Angiology

Primary cardiac lymphoma is a very rare malignancy, which is typically of a non-Hodgkin type, and involves only the heart and pericardium with no or minimal evidence of extracardiac involvement. Primary cardiac lymphoma account for about 1% of the primary cardiac tumors and 0.5% of the extranodal lymphomas. On the other hand, disseminated lymphoma with cardiac involvement can occur in up to 20% of patients with lymphoma. About 80% of cases of the primary cardiac lymphoma in immunocompetent hosts are of diffuse B-cell lymphoma, and in patients with immunodeficiency states, small noncleaved or immunoblastic lymphomas are more frequent. The right atrium and right ventricle are the 2 most frequently involved sites. Clinical presentation is heterogeneous and is generally related to the site of involve ment in the heart. The diagnosis is suspected when patients present with a cardiac mass or an unexplained refractory pericardial effusion. A thorough workup should include transtho racic and transesophageal echocardiography, computed tomography, and magnetic resonance imaging. Diagnosis is confirmed by cytology of the serous fluid from pericardial or pleural effusion or biopsy of the pericardial mass or endomyocardial tissue. The exploratory thoraco tomy should not be delayed if indicated. Chemotherapy has been used alone or combined with radiotherapy. Similarly, palliative cardiac surgery has been performed, mainly for tumor debulking. Combination of chemotherapy and radiation therapy is considered as the treatment of choice. The survival is generally less than a month without treatment but has been prolonged up to 5 years with palliative treatments in selected cases.

Peripheral arterial disease (PAD)-related exertional leg pain may limit physical activity, thereby contributing to mobility loss and increasing cardiovascular morbidity and mortality in men and women with PAD. The objectives of this study were: (1) to compare objectively measured physical activity levels between patients with and without PAD, (2) to assess the validity of two physical activity questionnaires in patients with PAD. Twenty PAD patients from a noninvasive vascular laboratory and 21 patients without PAD from a general medicine practice wore an accelerometer continuously for 7 days to measure physical activity objectively. After 7 days, participants completed the leisure time physical activity questionnaire (LTPAQ), derived from the Health Interview Survey, and the Stanford 7-day physical activity recall questionnaire (PARQ). PAD participants had markedly lower physical activity levels than non-PAD participants as measured by accelerometer (803 kcal/week ±364 (range=284-2,000, median=708) vs 1,750 kcal/week ±1,296 (range=882-6,586, median=1,278), p<0.001). For the LTPAQ, physical activity levels in PAD and non-PAD participants were 609 kcal/week ±576 (range=0-2,085, median=529) vs 832 kcal/week ±784 (range=53-2,820, median= 623), p=0.128. For the PARQ, physical activity levels in PAD and non-PAD participants were 234 METS/week ±21 (range=214-301, median=229) vs 238 METS/week ±11 (range=225-268, median=234), p=0.454, respectively. Pearson's correlation coefficient for the association between the accelerometer and the log-transformed LTPAQ measure was 0.419 (p=0.006). Pearson's correlation coefficient was 0.348 for the association between the accelerometer and the log-transformed PARQ measure of physical activity (p=0.026). In conclusion, PAD patients have significantly lower physical activity levels than non-PAD patients. Two commonly used physical activity questionnaires were less sensitive than objective measurement to the association between PAD and inactivity.

Background: Cardiovascular diseases are prevalent in people with chronic obstructive pulmonary disease (COPD). We hypothesized that endothelial dysfunction could be a marker of the proatherogen status in COPD. Methods and results: We measured endothelial dysfunction by flow-mediated dilation (FMD) and after sublingual administration of nitroglycerin (nitrate-mediated dilation: NMD) in 44 COPD patients and 48 controls. Compared with controls COPD patients had worse mean FMD (5.4% vs 8.2%, P < .001) and NMD (12.0% vs 13.9%, P = .007). FMD was inversely related to FEV1/VC ratio ( r = −0.327, P = .030). The negative association between COPD and FMD was confirmed after correction for potential confounders in a multiple linear regression model (β = −0.019, P = .002). In the same model NMD (β = 0.396, P < .001) was positively associated with FMD. Conclusions: Endothelial-dependent and, to a lesser extent, endothelial-independent dilations are significantly impaired in COPD, and the impairment is proportional to the severity of bronchial obstruction.

Evidence suggests that psoriasis together with other cardiovascular (CV) risk factors is associated with increased vascular morbidity, but it is not clear whether psoriasis is an independent risk factor. Consecutive patients (n = 33; 35.6 ± 5.7 years; 13 females) with mild psoriasis (Psoriasis Area and Severity Index <10) without comorbidities and 33 healthy participants (36.3 ± 5.9 years; 15 females) were enrolled. Both groups underwent echocardiography, speckle tracking (2-dimensional strain echocardiography [2D-SE]), and pulse wave velocity (PWV) testing. Clinical and conventional echocardiographic characteristics were comparable between both groups. Global longitudinal strain (GLS) was significantly lower ( P = .002) in the psoriasis group (22.39% ± 2.28%) than in controls (24.15% ± 2.17%). The PWV was significantly lower ( P = .004) in controls (8.06 ± 1.68 m/s) than in the psoriasis group (9.23 ± 1.53 m/s). Significant correlations between GLS and disease duration ( r = −.66, P < .0001) and between GLS and patient age at diagnosis ( r = .48, P = .0043) were found. Psoriasis may be an independent CV risk factor, causing cardiac and vascular impairment. Both 2D-SE and PWV may be useful tools for the screening of CV risk in these patients.

It is well known that the relative risk of developing type 2 diabetes mellitus increases with increasing body mass index. The presence of not only excessive body fat but also the pattern of fat distribution (central obesity) is important for other metabolic abnormalities included in the metabolic syndrome. The possible mechanisms linking obesity to type 2 diabetes including high concentrations of free fatty acids, altered adipokines expression (low adiponectin levels and high expression of tumor necrosis factor-α), and low-grade inflammation are reviewed. Finally, the author refers to the theory that the primary defect is β-cell failure that leads to diabetes as well as to obesity.