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Background We have previously reported an increased risk for non-hematological malignancies in young patients with moderate or severe aortic stenosis (AS) (1). These findings were the result of a post-hoc analysis from a large echocardiography database and needed verification. Purpose To determine, using a different study population, whether young patients with AS are at increased risk for cancer. Methods A large echocardiographic database was used to identify patients (age≥20 years) with moderate or severe AS (study group) and patients without aortic stenosis (comparative group). The new occurrence of non-hematological malignancies was determined after the index date (first echo with moderate or severe AS or first recorded echo in the control group). Results The final study group included 7,013 patients with AS and 98,884 without AS. During a median follow-up of 6.9 years (3.0–11.1) there were 10,705 new cases of non-hematological cancer. The crude incidence rate of cancer was higher in AS compared to non-AS patients (22.3 vs. 13.7 per 1,000 patient-year, crude HR 1.58 (95% CI 1.46–1.71). After adjustment for relevant covariates, there was no difference between groups (HR 0.93, 95% CI 0.86–1.01). Only patients in the lowest age quartile (20–49.7 years), had an increased adjusted risk of cancer (HR 1.91, 95% CI 1.08–3.39). The HR for the risk of cancer in AS was inversely proportional to age (P Conclusion Young patients with moderate or severe AS are at increased risk for cancer. Cancer surveillance should be considered for young patients with AS. Funding Acknowledgement Type of funding sources: None. Figure 1

Background: Atherosclerosis is a complex histopathologic process that is analogous to chronic inflammatory conditions. Several factors have been shown to correlate with the extent of atherosclerosis. Whereas hypertension, obesity, hyperlipidemia, diabetes, smoking, and family history are all well documented, recent literature points to additional associated factors. Thus, antibodies to oxidized low-density lipoprotein (oxLDL), cytomegalovirus (CMV), Chlamydia pneumonia, Helicobacter pylori, as well as homocysteine and C-reactive protein (CRP) levels have all been implicated as independent markers of accelerated atherosclerosis. Hypothesis: In the current study we attempted to formulate a system by which to predict the extent of coronary atherosclerosis as assessed by angiographic vessel occlusion. Methods: The 81 patients were categorized as having single-, double-, triple-, or no vessel involvement. The clinical data concerning the “classic” risk factors were obtained from clinical records, and sera were drawn from the patients for determination of the various parameters that are thought to be associated with atherosclerosis. Results: Using four artificial neural networks, we have found the most effective parameters predictive of coronary vessel involvement were (in decreasing order of importance) antibodies to oxLDL, to cardiolipin, to CMV, to Chlamydia pneumonia, and to β2-glycoprotein I (β2GPI). Although important in the prediction of vessel occlusion, hyperlipidemia, hypertension, CRP levels, and diabetes were less accurate. Conclusion: The results of the current study, if reproduced in a larger population, may establish an integrated system based on the creation of artificial neural networks by which to predict the extent of atherosclerosis in a given subject fairly and noninvasively.

Although specific echocardiographic features of the mitral valve (MV) have been shown to predict the likelihood of a successful outcome of percutaneous mitral valvuloplasty (PMV), they do not identify those patients who are more likely to be a risk for significant mitral regurgitation (MR) post- PMV. Based on pathologic data from patients who developed severe post-PMVMR, an echocardiographic score was developed. (MR-Echo Score) which included uneven distribution of thickness and calcification of both mitral leaflets, degree of commissural disease and subvalvular involvement. Each component was graded fro 0–4 and a total score (0–16) was calculated. Intraobserver and interobserver variability for score assessment were 6% and 7% respectively. From 566 consecutive patients who underwent PMV, 36 (6.5%) developed severe post-PMV MR (g 3 + by angiography.) The MR-Echo Score was applied to 31 of these patients (28 women; mean age 54 + 14 yr.) for whom pre-PMV echocardiograms were available and 31 randomly selected patients who did not develop severe post-PMV MR but were matched for age, sex, pre-PMV MV area and degree of MR. The total MR- Echo Score was significantly greater in the severe MR group (11.7 ± 1.9 vs. 8 ± 1.2; P l 0.001). Using a total score ∼ 10 as a cutoff point for predicting severe post PMV MR, a sensitivity of 90 ± 5% and a specificity of 97 ± 3% were obtained. Stepwise logistic regression analysis identified the MR-Echo Score as the only independent predictor for the development of severe post-PMV MR (p l 0.0001). Conclusions Specific morphologic features of the mitral valve apparatus in mitral stenosis as identified in this new MR-Echo Score predict the development of severe post PMV MR and therefore can be useful in the selection of patients for PMV.

To assess the progression of chronic aortic regurgitation (AR), 127 patients 169 men; 59 ± 21 yr) with AR (59 mild, 8 mild-to-moderate, 41 moderate, 4 moderate-to-severe, 15 severe) who had ≥ 6 months of follow-up (6–47 months) by color Doppler and 2-D echo were studied. The degree of AR was established at entry and follow-up studies using an algorithm (semi-quantitative) that takes into account several Doppler criteria (jet area and jet height ratios, jet length, pressure half-time, reversal of flow in descending aorta) and the jet height/LV outflow tract (LVOT) height ratio (quantitative). LV volume (Simpson) and LV mass (Devereux) were calculated. A significant increase in jet/LVOT height ratio was observed in the whole population (30 ± 17 vs. 35 ± 20%; p l 0.00001) and in the subsets of patients with mild (18 ± 7 vs. 22.3 ± 9%; p l 0.01), moderate (40 ± 14 vs. 44 ± 16%; p l 0.01) and severe (54 ± 19 vs. 65 ± 15%; p l 0.05) AR. An increase in the degree of AR (semi-quantitative) during the follow-up was observed in 38 (30%) of patients: 25% with mild, 37% with mild-to-moderate, 44% with moderate and 50% with moderate-to-severe AR (p l 0.006). Patients were further divided according to the rank order in the rate of progression of jet/LVOT height ratio into “progressives” (n = 18; rate g 5.64%/yr) and “non-progressives” (n = 109). Patients with “progressive” AR had a faster rate of progression of LV end-diastolic volume, LV end-systolic volume and LV mass than “non-progressives” (p l 0.025). Conclusions AR is a progressive disease even in patients with mild insufficiency. The progression in the degree of AR is more frequent in patients with more severe disease. The rate of progression of regurgitation appears to playa role in LV overload in patients with AR.