[The percutaneous treatment of pulmonary atresia with intact ventricular septum]. / Traitement percutané de l'atrésie pulmonaire à septum interventriculaire intact.

OBJECTIVE: Describe a mechanical method of perforation-dilatation of the pulmonary valve in pulmonary atresia with intact interventricular septum (PA-IVS), with or without stenting the patent ductus arteriosus (PDA) and medium-term results. METHOD: Since 2007, all patients with PA-IVS and a right ventricle adequate for biventricular repair, benefited from a transcatheter attempt to perforate-dilate the valve with or without stenting the PDA, and were included in this retrospective study. TECHNIQUE: A catheter was percutaneously introduced through the femoral vein and positionned in front of the atretic pulmonary valve. A lasso catheter was introduced through the femoral artery to the other side of the pulmonary valve. The tip of a rigid guidewire was then pushed through the atretic valve and taken with the lasso, creating a loop that allowed for balloon valvuloplasty. If the child remained ductal dependant following PGE1 withdrawal, a stent is placed in the ductus arteriosus. RESULTS: Five patients were included in this series. Four patients were successfully dilated, and two patients necessitated stents. The procedure had to be interrupted in one patient. FOLLOW-UP: One patient with a patent stent was operated at the age of one year and died in the postoperative period. The other patient with a stent is now 16 months old with a patent stent and an oxygen saturation of 98%. The two remaining patients without stent are now 3- and 18-month-old with oxygen saturation of 85% and 96% respectively. CONCLUSION: The percutaneous treatment of PA-IVS is feasible and avoids early high risk surgery. Stenting the ductus arteriosus may replace a Blalock shunt. However, the prognosis is still related to the severity of the anomaly.

Effect of high bolus dose tirofiban on the inflammatory response following percutaneous coronary intervention.

BACKGROUND: Tirofiban at the bolus dose of 10 microg/kg does not suppress the inflammatory response following percutaneous coronary intervention (PCI). This may be due to less than optimal inhibition of platelet aggregation. High bolus dose tirofiban (25 microg/kg) allows better inhibition of platelet aggregation but its anti-inflammatory effect remains unknown. HYPOTHESIS: High bolus dose tirofiban exhibits anti-inflammatory activity. METHODS: A total of 100 patients referred for PCI were randomized to receive high bolus dose tirofiban followed by a 24-h infusion or a bolus and an infusion of saline. Patients with elevated troponin or with thrombus in the culprit lesion were excluded. Inflammatory markers were measured at baseline and at 24 h. RESULTS: Levels of soluble CD40 ligand (sCD40L) were not affected by PCI while those of interleukin-6 (IL-6) and of high sensitivity C-reactive protein (hs-CRP) significantly increased. Despite inhibiting platelet's aggregation by > 90%, tirofiban did not suppress the rise of IL-6 and hs-CRP. Median (interquartile range) elevation of IL-6 was 0.6 pg/mL (-1.5-3.6) versus 0.4 pg/mL (-0.7-1.8) and that of hs-CRP was 2.1 mg/L (0.7-5.2) versus 2.4 mg/L (1-4.7) in the tirofiban and the control groups, respectively (p = ns). However, in patients with diabetes mellitus, tirofiban significantly suppressed the rise of hs-CRP by 65% (p = 0.01), but did not significantly affect the rise of IL-6. CONCLUSION: In low-risk patients undergoing PCI, tirofiban did not attenuate the rise of inflammatory markers. However, the significant effect in diabetics suggests that tirofiban may have anti-inflammatory activity in higher risk patients.

Combined coronary surgery and aortic valve replacement after previous right pneumonectomy.

Cardiac surgery in patients with previous pneumonectomy is infrequently reported. We report a case of combined coronary artery bypass grafting and aortic valve replacement in a patient with left ventricular ejection fraction less then 35% and a previous right pneumonectomy. All steps in operative management of this rare condition are discussed.

Percutaneous coronary intervention increases leptin and decreases adiponectin levels.

OBJECTIVE: The study was designed to examine the effect of percutaneous coronary intervention (PCI) on adiponectin and leptin levels. We have previously demonstrated that PCI triggers a systemic inflammatory response. We hypothesized that inflammation participates in the pathogenesis of diabetes mellitus and the metabolic syndrome by modulating levels of adiponectin and leptin. DESIGN: Prospective study in which inflammation was induced by PCI. PATIENTS: Forty-eight patients with stable coronary artery disease and without diabetes mellitus. MEASUREMENTS: High-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), leptin and adiponectin were measured at baseline and 48 h after the procedure. RESULTS: Following PCI, hs-CRP increased by 211%, IL-6 by 87% and leptin by 19%, while adiponectin decreased by 14% (P < 0.001 for all). The change in IL-6 correlated with that in hs-CRP (rho = 0.32; P = 0.027), as did the changes in IL-6 and leptin (rho = 0.31; P = 0.03). The change in adiponectin, however, did not correlate with the change in any of the other markers. CONCLUSION: This study demonstrates that PCI affects the levels of adiponectin and leptin within 48 h. These effects may be secondary to the inflammatory response triggered by PCI.

Effects of tirofiban and statins on high-sensitivity C-reactive protein, interleukin-6, and soluble CD40 ligand following percutaneous coronary interventions in patients with stable coronary artery disease.

This study assessed the effects of tirofiban and statins on high-sensitivity C-reactive protein, interleukin-6, and soluble CD40 ligand after percutaneous coronary intervention in patients who had stable coronary artery disease. Tirofiban insignificantly limited the increase of soluble CD40 ligand after revascularization, especially in patients who had high levels of this marker at baseline (p = 0.06), whereas statins significantly inhibited increases in interleukin-6 and, to a lesser extent, high-sensitivity C-reactive protein without affecting the soluble CD40 ligand.

[Coronary angioplasty for primary cardiogenic shock following acute myocardial infarction]. / L'angioplastie à la phase aiguë de l'infarctus du myocarde compliqué d'un choc cardiogénique primaire.

BACKGROUND: In the setting of acute myocardial infarction (AMI), several investigators have demonstrated that emergency coronary angioplasty (PTCA) reduces in-hospital mortality of primary cardiogenic shock (CS) from 90% to less than 50% ; however, few studies have focused on the current outcome of non selected patients in whom the onset of AMI is immediately complicated by CS. PURPOSE OF THE STUDY: To evaluate in-hospital mortality of the patients admitted to our institution for Q wave AMI presented in CS. MATERIAL AND METHOD: Between 05/93 and 05/03, 30 consecutive pts, 26 men and 4 women, in CS following AMI were treated with direct PTCA, 26 without thrombolysis and 4 as rescue after failed streptokinase. AMI was defined by prolonged chest pain and > or =1 mm ST segment elevation in > or =2 contiguous peripheral leads or > or =2 mm for precordial leads on the admission ECG. The diagnosis of CS was based on the combination of systolic blood pressure of <90 mm Hg, unresponsive to volume expansion, signs of acute circulatory failure (cyanosis, cold extremities, restlessness, mental confusion or coma) and congestive heart failure secondary to myocardial dysfunction. In 40% of cases the diagnosis of CS was only clinical and in 60% of cases was confirmed by a Swan Ganz catheter. Mean age was 62.3 +/- 12.3 years, 7 had triple vessel disease, 14 a double vessel disease, 8 a single vessel disease and in one case a left main disease. The AMI was anterior in 22 pts (73%), inferior in 8 (27%). Intraaortic balloon was used in 3 pts, CPR in 16 (47%), transitory pacemaker in 1 pt, inotropes in 25 pts, emergency coronary artery bypass grafting (CABG) in 1 pt. RESULTS: Success for PTCA with a residual stenosis < 50% and a TIMI flow III was obtained in 26 pts (87%). Mean time between CS and revascularization was 219 +/- 302 minutes. 19 pts (63%) survived and 11 pts (37%) died while at the hospital, 6 from intractable shock, 4 from multiple organ failure and in 1 case from pulmonary hemorrhage. Mean time of revascularization for the surviving was 190 +/- 329 min, and for the dead 295 +/- 212 min. Hospital mortality for inferior infarction is 12.5% after successful angioplasty. Comparison of surviving and non surviving number of patients according to revascularization time showed a significant difference of these groups whether the revascularization was accomplished before or after 120 minutes. [table: see text] CONCLUSION: Direct PTCA for AMI immediately complicated by CS, can be achieved with a high success rate, and can significantly reduce in-hospital mortality; this improvement of survival is most evident if revascularizarion is performed early.