Echocardiographic assessment of mitral valve morphology after Percutaneous Transvenous Mitral Commissurotomy (PTMC)

<p>Abstract</p> <p>Aims</p> <p>PTMC produces significant changes in mitral valve morphology as improvement in leaflets mobility. The determinants of such improvement have not been assessed before.</p> <p>Methods and results</p> <p>The study included 291 symptomatic patients with mitral stenosis undergoing PTMC. Post-PTMC subvalvular splitting area was a determinant of post-PTMC excursion in both the anterior (B 0.16, 95% CI 0.03 to 0.30, p < 0.05) and the posterior (B 0.12, 95% CI 0.01 to 0.24, p < 0.05) leaflets. Another determinant was the post-PTMC transmitral pressure gradient for anterior (B -0.02, 95% CI -0.04 to -0.005, p < 0.01) and posterior (B -0.01, 95% CI -0.04 to -0.005, p < 0.05) leaflets excursion. The relationship between post-PTMC MVA and leaflet excursion was non-linear "S curve". There was a steep increase of both anterior (p, 0.02) and posterior (p, 0.03) leaflets excursion with increased MVA till the MVA reached a value of about 1.5 cm²; after which both linear and S curves became nearly parallel.</p> <p>Conclusion</p> <p>The improvement in leaflets excursion after PTMC is determined by several morphologic and hemodynamic changes produced in the valve. The increase in MVA improves mobility within limit; after which any further increase in MVA is not associated by a significant improvement in mobility in both leaflets.</p

Mast Cell-Derived Histamine Mediates Cystitis Pain

Background: Mast cells trigger inflammation that is associated with local pain, but the mechanisms mediating pain are unclear. Interstitial cystitis (IC) is a bladder disease that causes debilitating pelvic pain of unknown origin and without consistent inflammation, but IC symptoms correlate with elevated bladder lamina propria mast cell counts. We hypothesized that mast cells mediate pelvic pain directly and examined pain behavior using a murine model that recapitulates key aspects of IC. Methods and Findings: Infection of mice with pseudorabies virus (PRV) induces a neurogenic cystitis associated with lamina propria mast cell accumulation dependent upon tumor necrosis factor alpha (TNF), TNF-mediated bladder barrier dysfunction, and pelvic pain behavior, but the molecular basis for pelvic pain is unknown. In this study, both PRV-induced pelvic pain and bladder pathophysiology were abrogated in mast cell-deficient mice but were restored by reconstitution with wild type bone marrow. Pelvic pain developed normally in TNF- and TNF receptor-deficient mice, while bladder pathophysiology was abrogated. Conversely, genetic or pharmacologic disruption of histamine receptor H1R or H2R attenuated pelvic pain without altering pathophysiology. Conclusions: These data demonstrate that mast cells promote cystitis pain and bladder pathophysiology through the separable actions of histamine and TNF, respectively. Therefore, pain is independent of pathology and inflammation, an

Anesthetic considerations in the patient with valvular heart disease undergoing noncardiac surgery

Valvular heart disease can be an important finding in patients presenting for noncardiac surgery. Valvular heart disease and resulting comorbidity, such as heart failure or atrial fibrillation, significantly increase the risk for perioperative adverse events. Appropriate preoperative assessment, adequate perioperative monitoring, and early intervention, should hemodynamic disturbances occur, may help prevent adverse events and improve patient outcome. This review article aims to guide the practitioner in the various aspects of anesthetic management in the perioperative care of patients with valvular heart disease. The pharmacological approach to optimization of patient outcome with drugs, such as βblockers and lipid-lowering medications (statins), is an evolving field, and recent developments are discussed in this article

Interventional and surgical occlusion of the left atrial appendage

With a steadily increasing prevalence, atrial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide and an independent risk factor for stroke caused by thromboembolic events. The left atrial appendage (LAA) is the primary source of thromboemboli in patients with nonvalvular AF who have a stroke. Novel strategies (such as mechanical and nonpharmacological intervention) targeting the LAA in patients with AF for stroke prevention have become a major focus during the past decade. Some devices for percutaneous LAA occlusion are supported by robust clinical data obtained from randomized trials or large registries, and are a valid alternative to pharmacological stroke prevention. However, the incidence of periprocedural complications and the presence of device-related thrombi or residual LAA leaks, whose long-term clinical implications are still unknown, are limiting factors in wider acceptability of these techniques. In this Review, we discuss the available techniques for LAA occlusion in patients with nonvalvular AF at high risk of stroke. We describe the pharmacological and mechanical approaches to LAA occlusion, and provide the current clinical evidence for various strategies. We particularly focus on the current management of the LAA, and discuss the challenges and future implications of the available approaches to LAA occlusion