Functional mitral regurgitation: a 30-year unresolved surgical journey from valve replacement to complex valve repairs.

Functional mitral regurgitation remains one of the most complex and controversial aspect--for both clinicians and surgeons--in the management of mitral valve disease in the context of left ventricular dysfunction. Given the current absence of clear guidelines, as well as of results from randomized trials comparing the outcome of different surgical strategies potentially available for this complex scenario, surgical decision making for these high-risk patients poses a real dilemma in the daily practice. The resulting surgical choices often represent a questionable combination of surgeons' personal feeling, local supplies, patients' life expectancy and risk/benefit ratios, opinions and statements of the experts, and so on. This review provides an overview of the present knowledge about the complex pathophysiology underlying functional mitral regurgitation, the different pathophysiology-guided surgical techniques suggested in the last decades, as well as the current results following these different surgical techniques.

The CIAO (Coronary Interventions Antiplatelet-based Only) Study: a randomized study comparing standard anticoagulation regimen to absence of anticoagulation for elective percutaneous coronary intervention.

OBJECTIVES: We sought to evaluate, in a double-blind, randomized, prospective study, safety and efficacy of elective percutaneous coronary intervention (PCI), with pharmacotherapy consisting of antiplatelet therapy and no anticoagulation therapy. BACKGROUND: Available guidelines recommend systemic anticoagulation agent use during PCI. Significant debate remains, however, with regard to the correlation between the effects of systemic anticoagulation therapy and ensuing ischemic and hemorrhagic complications. METHODS: From June 2005 to January 2007, 700 patients undergoing elective PCI of an uncomplicated lesion have been prospectively enrolled in the protocol. Patients should have been on aspirin and thienopyridine therapy and were assigned either to the control arm (70 to 100 UI/kg unfractionated heparin) or to the no-heparin arm. A clinical assessment was obtained before hospital discharge and at 30 days after PCI. RESULTS: Procedural success was obtained in 100% of the cases. No acute or subacute thrombosis was observed. The absence of anticoagulation therapy was associated with a significant decrease in post-procedural myocardial damage (p = 0.03) and bleeding events (p = 0.048). At 30 days, the primary end point (death, myocardial infarction, or urgent target vessel revascularization) was more frequent in the control arm than in the no-heparin arm (2.0% vs. 3.7%, respectively; absolute risk reduction 1.7% [95% confidence interval: -0.1% to 4.5%], p for superiority = 0.17, p for noninferiority <0.001). CONCLUSIONS: In the treatment of uncomplicated lesions and in the presence of dual antiplatelet therapy, elective PCI can be safely performed without systemic anticoagulation and is associated with a reduced incidence of bleeding complications.

[Mechanism of troponin and CK-MB release after percutaneous coronary interventions]. / Meccanismo del rilascio delle troponine e del CK-MB durante procedure interventistiche percutanee.

Cardiac troponins are highly sensitive and specific markers of early detection of myocardial injury. The incidence of cardiac troponin increase is of 5-40% after percutaneous coronary interventions and is significantly higher in patients undergoing stenting than in patients with balloon angioplasty only. Four mechanisms are responsible for myocardial necrosis during coronary angioplasty: 1) distal embolization of small fragments of the atherosclerotic plaque; 2) side branch occlusion; 3) intimal dissection, and 4) temporary vessel occlusion. The multiple and/or complex lesions, the diabetic status and plaque instability increase the probability of troponin elevation during coronary angioplasty. Moreover, the long time needed for interventional as well as atherectomy procedures may induce myocardial necrosis. In conclusion, after successful percutaneous coronary interventions, minor elevation of troponin may occur. In this setting cardiac troponin I is a highly specific marker of myocardial injury.