John R. Pepper

Early experience with the Toronto stentless porcine valve.

Stentless porcine valves in the aortic position offer many theoretic advantages, but their clinical performance has not been adequately defined. We evaluated the clinical and echocardiographic results of 103 patients who had aortic valve replacement with the Toronto stentless porcine valve over a 2-year period. There were 67 men with a mean age of 68 years. The predominant native valve lesion was aortic stenosis (64%), and 4 patients had prosthetic valve dysfunction. Forty-two patients had concomitant procedures. The 30-day mortality rate was 3.3% (n = 2) for isolated valve replacement and 5.8% (n = 6) for the series. The sole determinant of early death was poor left ventricular function. There were three late deaths due to non-valve-related complications over a median follow-up of 11.87 months. In addition, prosthetic valve endocarditis developed in 1 patient, necessitating a homograft valve replacement at 6 weeks. Doppler echocardiography performed at 3 to 6 months showed low peak and mean transvalvular gradients, with no substantial change at 1 year. None of the patients showed signs of clinically significant aortic regurgitation, although echocardiography demonstrated trivial or mild regurgitation in 12 patients at discharge or early follow-up, which was less marked or absent at 1 year. We conclude that the Toronto stentless porcine valve appears to offer promising early results.

The impact of arterial cannulation strategy on operative outcomes in aortic surgery: Evidence from a comprehensive meta-analysis of comparative studies on 4476 patients

OBJECTIVESnThere is a growing perception that peripheral cannulation through the femoral artery, by reversing the flow in the thoracoabdominal aorta, may increase the risk of retrograde brain embolization in aortic surgery. Central cannulation sites, including the right axillary artery, have been reported to improve operative outcomes by allowing antegrade blood flow. However, peripheral cannulation still remains largely used because a consensus for the routine use of central cannulation approaches has not been reached.nnnMETHODSnA meta-analysis of comparative studies reporting operative outcomes using central cannulation versus peripheral cannulation was performed. Pooled weighted incidence rates for end points of interest were obtained using an inverse variance model.nnnRESULTSnA total of 4476 patients were included in the final analysis. Central cannulation was used in 2797 patients, and peripheral cannulation was used in 1679 patients. Central cannulation showed a protective effect on in-hospital mortality (risk ratio, 0.59; 95% confidence interval, 0.48-0.7; P < .001) and permanent neurologic deficit (risk ratio, 0.71; 95% confidence interval, 0.55-0.90; P = .005) when compared with peripheral cannulation. A trend toward an increased benefit in terms of reduced in-hospital mortality was observed when only the right axillary artery was used as the central cannulation approach (risk ratio, 0.35; 95% confidence interval, 0.22-0.55; P < .001; I(2) = 0%).nnnCONCLUSIONSnCentral cannulation was superior to peripheral cannulation in reducing in-hospital mortality and the incidence of permanent neurologic deficit. This superiority was particularly evident when the axillary artery was used for central cannulation.

Induction of Cyclo-Oxygenase in Human Vessels in vitro

Cyclo-oxygenase (COX) converts free arachidonic acid to prostaglandin (PG)H2, the precursor to a group of lipid mediators including prostacyclin (PGI2), PGE2, and thromboxane (TX) A2. The predominant COX metabolite released from vessels is PGI2, which is a vasodilator, and an inhibitor of cellular proliferation, platelet adhesion and activation, and cholesterol metabolism (see Willis et al., 1986; Hajjar and Pomerantz, 1992). COX is now known to exist in at least 2 different isoforms; a constitutively expressed COX-1, and a cytokine inducible COX-2 (see Mitchell et al., 1995). Within vessels COX-1 is normally the dominant isoform, and is concentrated mainly in the endothelial cell layer. The underlying vascular smooth muscle has lower COX activity, but is a rich source of PGI2 synthetase. In animal models, COX-2 is induced in the vascular smooth muscle layer after mechanical damage to the vessel (Rimarchin et al., 1994). However, the expression of COX-2 in human vessels has not been demonstrated.