Pericarditis is a common disorder that has multiple causes and presents in various primary-care and secondary-care settings. New diagnostic techniques have improved the sampling and analysis of pericardial fluid and allow comprehensive characterisation of cause. Despite this advance, pericarditis is most commonly idiopathic, and radiation therapy, cardiac surgery, and percutaneous procedures have become important causes. Pericarditis is frequently self-limiting, and non-steroidal anti-inflammatory agents remain the first-line treatment for uncomplicated cases. Integrated use of new imaging methods facilitates accurate detection and management of complications such as pericardial effusion or constriction. Differentiation of constrictive pericarditis from restrictive cardiomyopathy remains a clinical challenge but is facilitated by tissue doppler and colour M-mode echocardiography. Most pericardial effusions can be safely managed with an echo-guided percutaneous approach. Pericardiectomy remains the definitive treatment for constrictive pericarditis and provides symptomatic relief in most cases. In the future, the pericardial space might become a conduit for treatments directed at the pericardium and myocardium.
The ratio of component velocity (E) over the color M-mode propagation velocity during early LV filling, by correcting for the effect of LV relaxation, provides a better estimate of pw than standard measurements of transmitral Doppler flow.
CPFs are generally small and single, occur most often on valvular surfaces, and may be mobile, resulting in embolization. Because of the potential for embolic events, symptomatic patients, patients undergoing cardiac surgery for other lesions, and those with highly mobile and large CPFs should be considered for surgical excision.
Prior epidemiologic studies have shown that increasing body mass index (BMI) is associated with higher total cholesterol and low-density lipoprotein cholesterol (LDL). However, these studies were limited by underrepresentation of obese subjects. The aim of this study was to determine whether there is an association between BMI and lipid profiles in a population of patients with a broad spectrum of BMI values. A case-control study was performed involving patients seen at the Cleveland Clinic Florida. Cases (BMI >30 kg/m(2)) were obtained from the obesity surgery database between August 31, 2000, and April 4, 2002. Controls (BMI ≤ 30 kg/m(2)) were obtained from a database of primary care physicians between May 1, 2004, and November 18, 2004. Pearson correlation coefficients were used to assess the relationship between BMI and lipid fractions. Multiple linear regression was performed to assess the independent effect of BMI on lipid levels while adjusting for potential confounders and propensity scores. Six hundred thirty-seven patients were analyzed (females, n = 362, 57%). There was no association between higher BMI and LDL (r = 0.19 p = 0.07), a negative association with high-density lipoprotein cholesterol (HDL; r = 0.45, p < 0.001), and a positive association with the log transformation of triglycerides (r = 0.32, p = 0.005).Higher BMI was inversely associated with HDL and directly associated with TG. BMI showed no significant association with LDL. Although the association between BMI and both HDL and TG may be explained by insulin resistance, the lack of a significant association between BMI and LDL remains an unexpected finding that requires further investigation.
The correlation between formal coronary artery calcium scoring (CACS) determined by multi-detector CT (MDCT) and the presence of coronary calcium on standard non-gated CT chest examinations was evaluated. In 163 consecutive healthy participants, we performed screening same-day standard non-gated, non-enhanced CT chest exams followed by high-resolution, ECG-synchronized MDCT exams for CACS. For the standard CT examinations, a scoring system (Weston score, range 0-12) was developed assigning a score (0-3) for each coronary vessel including the left main trunk. Overall, 30% and 39% of patients had CAC on standard CT and MDCT exams, respectively (P = 0.13). CAC on standard CT was highly correlated to the Agatston CACS on the MDCT (Spearman correlation coefficient 0.83, P < 0.001). Absence of calcium on the standard CT exam was associated with a very low CACS (mean Agatston 0.5, range 0-19). A Weston score >2 identified a CACS > 100 with an area under the curve of 0.976, sensitivity of 100%, and specificity of 85%. A Weston score >7 identified a CACS > 400 with an area under the curve of 0.991, sensitivity of 100%, specificity of 98%. The intra-observer variability was low as was the inter-observer variability between a cardiac specialized radiologist and a non-specialized reader. A visual coronary artery scoring system on standard, non-gated CT correlates well with traditional methods for CACS. Further, a non-expert cardiac radiologist performed equally well to a cardiac expert. This information suggests that a visual scoring system, at least in a descriptive manner can be utilized for a general statement about coronary artery calcification seen on standard CT imaging to guide clinicians in risk stratification.
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