A rare case of aortocoronary dissection following percutaneous transluminal coronary angioplasty: successful treatment using off-pump coronary artery bypass grafting.

Retrograde dissection of the aorta is a rare but potentially life threatening complication of percutaneous coronary intervention. We describe a case of retrograde aortic dissection, which occurred during attempted percutaneous transluminal coroanary angioplasty (PTCA) of chronically occluded left anterior descending artery (LAD). Emergency coronary artery bypass grafting (CABG) was performed to revascularise LAD distal to the site of entry tear with pedicled left internal mammary artery (LIMA). This was achieved off-pump. Ascending aorta was not replaced as the dissection was localised.

Mitral valve replacement following a failed MitraClip procedure.

While mitral valve surgery remains the gold standard for mitral regurgitation (MR), recent innovative and less invasive procedures like percutaneous MitraClip insertion make treatment options open to patients with end-stage dilated cardiomyopathy and poor left ventricular function, since such a cohort of patients invariably represents a high surgical risk. Enthusiasts of this procedure advocate the use of MitraClip as a primary procedure for patients with Type 1 MR and end-stage cardiomyopathy. Valve repair could be reserved for those patients with ongoing regurgitation following MitraClip insertion. We describe a patient treated by MitraClip insertion in whom the unsuccessful mid-term result necessitated surgery. In this patient, damage to the mitral valve from the MitraClip insertion produced a central leaflet perforation, which precluded repair, and thereby, the patient received a mechanical valve replacement. The enthusiasm for a less invasive initial approach in such patients must be balanced against the risk of failure of the primary procedure so that the patient is not denied the prospect of repair in the first instance.

Genes regulating lymphangiogenesis control venous valve formation and maintenance in mice.

Chronic venous disease and venous hypertension are common consequences of valve insufficiency, yet the molecular mechanisms regulating the formation and maintenance of venous valves have not been studied. Here, we provide what we believe to be the first description of venous valve morphogenesis and identify signaling pathways required for the process. The initial stages of valve development were found to involve induction of ephrin-B2, a key marker of arterial identity, by venous endothelial cells. Intriguingly, developing and mature venous valves also expressed a repertoire of proteins, including prospero-related homeobox 1 (Prox1), Vegfr3, and integrin-α9, previously characterized as specific and critical regulators of lymphangiogenesis. Using global and venous valve-selective knockout mice, we further demonstrate the requirement of ephrin-B2 and integrin-α9 signaling for the development and maintenance of venous valves. Our findings therefore identified molecular regulators of venous valve development and maintenance and highlighted the involvement of common morphogenetic processes and signaling pathways in controlling valve formation in veins and lymphatic vessels. Unexpectedly, we found that venous valve endothelial cells closely resemble lymphatic (valve) endothelia at the molecular level, suggesting plasticity in the ability of a terminally differentiated endothelial cell to take on a different phenotypic identity.

Bovine pericardial versus porcine stented replacement aortic valves: early results of a randomized comparison of the Perimount and the Mosaic valves.

OBJECTIVE: A stented bovine pericardial valve might be less obstructive than a stented porcine valve. This study compared early hemodynamic function in a prospective series of 99 patients randomized to receive either a Mosaic or Perimount replacement aortic valve. METHODS: Echocardiography was performed early after surgery and at 1 year after surgery. Patients also filled in psychologic questionnaires and underwent a 6-minute walk. RESULTS: The groups were matched demographically. The Perimount valve was significantly less obstructive in terms of mean pressure difference (11 +/- 5 vs 17 +/- 7 mm Hg; P < .0001), with a trend in favor of a larger effective orifice area (1.47 +/- 0.45 vs 1.28 +/- 0.46 cm(2); P = .05) postoperatively. There were no differences in left ventricular mass regression, aortic regurgitation, 6-minute walk, psychologic questionnaires, or mortality and clinical events. CONCLUSION: The stented bovine pericardial valve was less obstructive than the stented porcine valve. Both valves were associated with similar and significant improvements in quality of life, exercise ability, and regression of left ventricular mass.

Changes in P-selectin expression on cardiac microvessels in blood-perfused rat hearts subjected to ischemia-reperfusion.

BACKGROUND: During cardiac surgery involving cardiopulmonary bypass, activation of polymorphonuclear cells is believed to contribute to ischemia-reperfusion injury and subsequent myocardial impairment of function. The early tethering of polymorphonuclear cells to blood vessel walls depends upon recognition of the adhesion molecule P-selectin on endothelium. The purpose of this study was to define the kinetic changes in expression of P-selectin on myocardial vessels in a model of global ischemia-reperfusion injury. METHODS: In a novel recirculating blood-based perfusion system, rat hearts were subjected to 30 minutes of aerobic perfusion, 60 minutes of global ischemia, and 60 minutes of reperfusion, or to 120 minutes of continuous aerobic blood perfusion (with or without leukocyte/platelet depletion). Heart function (left ventricular developed pressure), heart rate, and perfusion pressure were monitored throughout. Hearts were sampled at defined periods for microvascular expression of P-selectin, identified by immunohistochemistry. RESULTS: In control (nonperfused) hearts and in hearts subjected to perfusion and ischemia, few cardiac vessels (8% to 16%) expressed P-selectin. After 15 minutes of reperfusion, P-selectin was present on the majority of vessels (77%; p < 0.05) but expression decreased subsequently throughout the remaining duration of reperfusion. Interestingly, upregulation of P-selectin also occurred when hearts were subjected to continuous perfusion alone (no ischemia), but this upregulation was less rapid. Depletion of leukocytes/platelets from the blood perfusate did not modify P-selectin expression. CONCLUSIONS: The augmented expression of P-selectin on myocardial vessels during reperfusion of ischemic hearts probably reflects changes induced during global ischemia and by the duration of perfusion through the nonbiological tubing of the circuit. That is likely to mimic the effects initiated during cardiopulmonary bypass.