Dystrophic mineralization remains the leading cause of stenotic or regurgitant failure in native human and porcine bioprosthetic heart valves. We hypothesized that cellular expression of noncollagenous matrix proteins (osteopontin, osteocalcin, and osteonectin) that regulate skeletal mineralization may orchestrate valvular calcification.Porcine bioprosthetic heart valves and native human heart valves obtained during replacement surgery were analyzed for cells, matrix proteins that regulate mineralization, and vessels.Cell accumulation and calcification were correlated for both valve types (

Angiographic CTO frequently corresponds to less than complete occlusion by histologic criteria. Age-related changes in IP composition from cholesterol laden to fibrocalcific may explain the adverse revascularization profile of older CTOs. IP NC growth derived from the adventitia increases with age and is strongly associated with IP cellular inflammation. IP NC formation may protect against the flow-limiting effects of IP growth.

(OR = 5.35, p < 0.001), cerebrovascular accident history (OR = 3.36, p = 0.023), low glomerular filtration rate (OR = 0.98, p = 0.012) and cardiac arrest on admission (OR = 17.43, p < 0.001) as robust independent predictors of long-term mortality. NLR was divided into two sub-groups based on an optimal cut off value of 7.4. This provided the best discriminatory cut off point for predicting adverse mortality outcome. (Cardiol J 2014; 21, 5: 500-508)

Selective alpha v beta 3 blockade is an effective anti-restenosis strategy that potently limits neointimal growth and lumen stenosis following deep arterial injury. The co-ordinate spatial and temporal upregulation of alpha v beta 3 expression following vessel wall injury, and the high affinity and specificity of XJ 735 for alpha v beta 3, confirms the importance of this integrin in adhesive and migratory cell-matrix events underlying coronary restenosis.

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The Bypass Angioplasty Revascularization Investigation (BARI) trial indicates 5-year cardiac mortality in patients with multivessel disease was significantly greater after initial treatment with PTCA than with CABG. The difference was manifest in diabetic patients on drug therapy. There were no significant differences overall for the composite end point of cardiac mortality or MI between treatment groups or for cardiac mortality in nondiabetic patients regardless of symptoms, left ventricular function, number of diseased vessels, or stenotic proximal left anterior descending artery.

Primary angioplasty was similarly successful in diabetics and nondiabetics and appeared to be more effective than thrombolytic therapy among diabetics with acute infarction.

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