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Background Surgical management of ventriculo-aortic disconnection and aortic root abscesses after prosthetic aortic valve endocarditis carries high mortality and morbidity. Initial experience with translocation of the aortic valve and distal coronary artery bypass grafting was disappointing in terms of short-term and long-term success in the few published reports. We describe a technique of translocation of the aortic valve into the ascending aorta with direct antegrade myocardial revascularization. Methods Between 1980 and 1992, we included 21 patients and evaluated their long-term outcome. The surgical technique included extracting the aortic valve prosthesis, resecting all infected tissue, restoring the left ventricular outflow tract, and translocating the aortic valve into the ascending aorta, associated with myocardial revascularization of the left main trunk and the proximal right coronary artery. Results All patients required emergency surgery: 15 patients were in severe congestive heart failure, 3 patients were in cardiogenic shock, and 3 patients had multiple neurologic and peripheral signs of distal embolization. Fifteen patients had active prosthetic valve endocarditis. Intraoperative findings dictated the translocation. The overall hospital mortality was 14%. None of the 18 hospital survivors had prosthetic aortic valve endocarditis recurrence. All patients were observed from 12 to 22 years, are alive, and have resumed normal activities. Conclusions In severe forms of prosthetic valve endocarditis, this technique provides a safe and reliable alternative to homograft replacement. The long-term results are satisfactory.

Scintigraphic images of myocardial iodine 123-labeled metaiodobenzylguanidine (MIBG) reflect the relative distribution of adrenergic neurodensity and function in the myocardium. In patients with hypertrophic cardiomyopathy or after infarction, MIBG uptake in hypertrophied myocardium and the infarct-related myocardium was found to be decreased in comparison to blood flow distribution, delineated with thallium 201. Most intriguingly, semiquantitative measurements in patients with congestive heart failure demonstrated reduced myocardial MIBG uptake. This reduction correlated directly with indexes of left ventricular function. Decreases in neuronal density, dysfunction of adrenergic neurons, or chronically elevated circulating norepinephrine levels may account for this diminished myocardial uptake, which, as demonstrated in a pilot study of 90 patients with congestive heart failure, was found to be of predictive value for survival.

The in vivo determination of the density of dihydropyridine (DHP) binding sites will allow the assessment of pathophysiological changes associated with heart disease. The calcium channel antogonist S 11568: ( + )(amino-7 dioxa-2,5 heptyl)-2(dichloro -2,3 phenyl) -4 methyl-6dihydro -1,4 pyridine has an in vitro profile of high potency and of high selectivity for the L-type Ca2+ channel. S 11568 was labelled by a reaction between 11C-diazomethane and the precursor 6-(7-amino-2,5-dioxa heptyl)-4-(2,3-dichloro phenyl)-5-(ethoxycarbonyl)-2 methyl-1,4 dihydro nicotinic acid. (+)-PN 200 110, a DHP with in vitro high affinity for the L-type Ca2+channel, was also radiolabeled. Positron emission tomographic (PET) studies of both 11C-DHP myocardial uptake were performed in Beagle dogs. 11C-(+)-PN 200 110 had a rapid wash-out from myocardium. In contrary, after a bolus injection, 11C-S 11568 myocardial concentration increased to reach a maximum in 1–2 minutes and then remained in a plateau with a slight downslope while the blood concentration fell rapidly. Myocardial uptake was 2 to 4 fold higher than lung uptake, leading to a good contrast on PET images. Pre-treatment with unlabeled S 11568 (2 μmol/kg or 6 μmol/kg over 15 minutes) reduced myocardial uptake by 60% and 80%, respectively. Specific binding was estimated during a displacement experiment: bolus of unlabeled S 11568 : 1 μmol/kg followed by a continuous infusion of 3 μmol/kg over 2 hours. It was found to represent 80% of the total binding. To assess influence of S11568 on coronary blood flow and therefore on the myocardial tracer delivery, coronary blood flow was measured using 15O-H2O and PET at baseline and following bolus injections of 0.4, 0.8, 2 μmol/kg of S 11568. Only the higher dose increased coronary blood flow. This is the in vivo demonstration of the binding characteristics to myocardial tissue of a DHP ligand. Such properties make S 11568 suitable for PET experiments. The studies of DHP binding sites will provided new insights concerning physiological situations as well as heart disease.

Background The internal thoracic artery (ITA) is considered to be the conduit of choice for coronary artery bypass grafting surgery (CABG). In triple-vessel–disease patients, CABG can be performed exclusively using both ITAs in a Y fashion with multiple sequential side-to-side coronary anastomoses. The aim of this prospective study was to evaluate by early postoperative angiographic control, the patency and particularly the quality of ITA grafts and coronary anastomoses in this configuration. Methods Between October 2002 and October 2003, 92 triple-vessel–disease patients underwent CABG with this technique and consented to immediate postoperative angiographic control. The right ITA was divided at its origin and connected to the in-situ left ITA (ITA-Y anastomosis). The left ITA was anastomosed to anterior coronary arteries and the right ITA was anastomosed to lateral and inferior coronary arteries, for a total of 374 coronary anastomoses (4.1 anastomoses per patient; range, 3 to 6). Results There was 1 hospital death by septic shock. Two patients were reoperated on for superficial wound infection. There was no postoperative myocardial infarction or stroke. On postoperative angiograms, all ITA-Y (92) and ITA-coronary anastomoses (374) were patent. Competition of flow in right ITA to the moderately stenosed right coronary artery was observed in 9 patients, and there were 4 distal ITA-coronary stenoses, both without clinical consequences. Conclusions In triple-vessel–disease patients, this procedure allows CABG without increasing operative risk. ITA-Y anastomoses and multiple sequential side-to-side ITA-coronary anastomoses are safe to perform and demonstrate excellent patency and quality in early postoperative angiographic control, particularly when coronary artery stenoses are significant (>70%).

Whether angioplasty of occluded vessels after myocardial infarction may have beneficial effects on left ventricular function remains unknown. Patients with a first myocardial infarction and thrombolytic therapy who had an occluded infarct-related vessel at delayed coronary angiography were referred systematically for an elective coronary angioplasty performed between 3 and 4 weeks after the myocardial infarction. All patients underwent stress-redistribution-reinjection thallium-201 single-photon emission computed tomography for myocardial viability assessment. Prior angioplasty, a quantitative evaluation of global and regional left ventricular function, was performed. The study group consisted of 38 patients (aged 57 +/- 10 years); 18 had anterior wall infarctions and 20 inferior wall infarctions, but before angioplasty 3 had a patent artery and were excluded. Angioplasty was successful in 30 patients. At follow-up 13 patients (43%) had an occluded coronary artery. In contrast with patients with an occluded coronary artery at follow-up, those with a patent coronary artery had no left ventricular enlargement and had an improvement in both left ventricular ejection fraction (from 48 +/- 9% to 52 +/- 9.8%, p = 0.002) and regional wall motion index (delta = +0.95 SD, p0.01). In patients with a patent vessel at follow-up, there was a positive correlation between the number of myocardial viable segments and improvement of the infarct zone wall motion (r = 0.52; p = 0.035), and the number of necrotic segments at baseline was positively correlated to the 4-month changes in end-diastolic volume indexes (r = 0.6; p = 0.04). Thus, elective revascularization of occluded coronary arteries with viable myocardium after myocardial infarction improves left ventricular function and lessens remodeling if the artery remains patent during follow-up.