ince the initial publication of ''Guidelines for Reporting Morbidity and Mortality After Cardiac Valvular Operations'' in 1988, 1 followed by a revised version in 1996, 2 valvular heart surgery has evolved to include an enhanced understanding of patient-and disease-related factors affecting outcomes, increased numbers of valve repairs, more operations performed for patients with minimal symptoms, new prostheses, novel repair methods, and the emergence of percutaneous interventional (catheter-based) valve repair and replacement. To adapt to this changing environment, the Councils of the American Association for Thoracic Surgery, The Society of Thoracic Surgeons, and The European Association for Cardio-Thoracic Surgery have directed an Ad Hoc Liaison Committee for Standardizing Definitions of Prosthetic Heart Valve Morbidity to review current clinical practice to update and clarify these reporting guidelines. The guidelines are intended to cover treatment of all four cardiac valves in both adult and pediatric patients. Further, these guidelines apply uniformly, irrespective of whether the therapy was carried out as a conventional open operation, as a minimally invasive (video-assisted or robotic) surgical procedure, or with percutaneous interventional catheter techniques. PurposeThese reporting guidelines are intended to facilitate analysis and reporting of clinical results of various therapeutic approaches to diseased heart valves such that meaningful comparisons can be made and inferences drawn from investigations of medical, surgical, and percutaneous interventional treatment of patients with valvular heart disease. Early MortalityEarly mortality is to be reported as all-cause mortality at 30, 60, or 90 days and depicted by actuarial estimates (with number remaining at risk and confidence intervals [CIs]) or as simple percentages, regardless of the patient's location, be it home or in a health care facility.

Multiple data suggest that the renin-angiotensin system contributes to the pathogenesis of atherosclerosis. The atherogenic effect of the renin-angiotensin system can only in part be explained by the influence of its effector angiotensin II on blood pressure, smooth muscle cell (SMC) growth, or antifibrinolytic activity. Because chronic inflammation of the vessel wall is a hallmark of atherosclerosis, we hypothesized that angiotensin II may elicit inflammatory signals in vascular SMCs. Human vascular SMCs were stimulated with angiotensin. Inflammatory activation was assessed by determination of interleukin-6 (IL-6) release into the culture medium, detection of IL-6 mRNA by RT-PCR, and demonstration of activation of nuclear factor-kappaB in electrophoretic mobility shift assays. Angiotensin II concentration-dependently (1 nmol/L to 1 micromol/L) stimulated IL-6 production by SMCs via activation of the angiotensin II type 1 receptor (demonstrated by the inhibitory action of the receptor antagonist losartan). Angiotensin I increased IL-6 production by SMCs, too. This effect was inhibited by captopril and ramiprilat, suggesting conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme in SMCs. Steady-state mRNA for IL-6 was augmented after stimulation with angiotensin II, suggesting regulation of angiotensin-induced IL-6 release at the pretranslational level. Moreover, the proinflammatory transcription factor nuclear factor-kappaB, which is necessary for transcription of most cytokine genes, was also activated by angiotensin II. Pyrrolidine dithiocarbamate suppressed angiotensin II-induced IL-6 release, a finding compatible with involvement of reactive oxygen species as second messengers in cytokine production mediated by angiotensin. The data demonstrate the ability of angiotensin to elicit an inflammatory response in human vascular SMCs by stimulation of cytokine production and activation of nuclear factor-kappaB. Inflammatory activation of the vessel wall by a dysregulated renin-angiotensin system may contribute to the pathogenesis of atherosclerosis.

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