Restenosis in the months following a successful percutaneous transluminal coronary angioplasty (PTCA) remains the main limitation to this technique for myocardial revascularisation. Despite intensive investigation in this area, no pharmacological therapy has yet been found to be useful in preventing restenosis after conventional balloon angioplasty. The occurrence of restenosis, which is now known to be caused by both vessel remodelling and neointimal hyperplasia, might be reduced in the future by a combined mechanical and pharmacological approach. Although systemic administration of 'antirestenosis' drugs has not yet been tested to prevent restenosis after coronary stenting, it is very likely that pharmacological inhibition of neointimal hyperplasia within coronary stents will take advantage of local delivery techniques. In addition to local drug delivery catheters that are available, the stent itself may be coated with polymers and serve as a platform for drug delivery. The continued attractiveness of PTCA, as an alternative to medical treatment or bypass surgery for patients with coronary artery disease, will depend upon our ability to control the restenotic process.
Exercise training can induce important haemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examined the impact of exercise rehabilitation on cardiac neuronal function using iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy, Fourteen patients (11 men, 3 women; mean age 48 years; range: 36-66 years) with stable chronic heart failure of NYHA class II-III and an initial resting radionuclide left ventricular ejection fraction (LVEF) < 50% were enrolled in the study. Patients underwent progressive, supervised endurance training (treadmill test, Bruce protocol) during a 6-month period (60 sessions, 3 sessions per week) at a cardiac rehabilitation referral centre in order to measure exercise parameters. Planar 123I-MIBG scintigraphy provided measurements of cardiac neuronal uptake (heart-mediastinum ratio activity, 4 h after intravenous injection of 185 MBq of MIBG). Radionuclide LVEF was also assessed at the outset and after 6 months of exercise training. Workload (801 +/- 428 vs 1229 +/- 245 kpm.min-1, P = 0.001), exercise duration (504 +/- 190 vs 649 +/- 125 s, P = 0.02), and myocardial MIBG uptake (135% +/- 19% vs 156% +/- 25%, P = 0.02) increased significantly after rehabilitation. However, LVEF did not change significantly (23% +/- 9% vs 21% +/- 10%, p = NS). It is concluded that exercise rehabilitation induces improvement of cardiac neuronal function without having negative effects on cardiac contractility in patients with stable chronic heart failure.
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