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The considerable evolution in technique and hardware, occurred over the past three decades, has greatly simplified the implantation procedure of pacemakers and cardioverter-defibrillators. Indeed, the introduction of relatively simple and safe methods of central venous access, and the miniaturization of the generator with subcutaneous placement have facilitated the implantation. However, inherent with cardiac pacing and defibrillating therapy is the potential for the occurrence of an early or delayed untoward event. Although skill, experience, and technique are all mitigating factors, every cardiologist should know potential complications and should be able to stratify overall risk related to a device implantation. Thus, both the implanting physician or the clinical cardiologist must be concerned not only with measures to avoid complications, but also with their early recognition and treatment.

Glycoprotein IIb/IIIa inhibitors have been recently proposed as a bridge to rescue transluminal coronary angioplasty in ST elevation myocardial infarction patients in whom thrombolysis fails; but data in its feasibility, safety and efficacy are still limited. In 47 consecutive acute myocardial infarction patients in whom thrombolysis failed to achieve 90 minute reperfusion, tirofiban was given at full regimen. Our results have been compared with those obtained in a control group of 48 consecutive acute myocardial infarction patients admitted two years before, period in which tirofiban and rescue angioplasty were not available in our hospital. Our preliminary data suggest this approach is feasible and safe, with possible clinical benefit in this high-risk subgroup of patients.

The HGM-CoA reductase inhibitors, blaking up intracellular synthesis of cholesterol, support the receptorial captation of cholesterol with a reduction in plasma levels. The simvastatin efficacy was evaluated in 12 patients, mean age 59 +/- 10 years with a primary hypercholesterolemia. All the patients were on a pharmacologic wash out for at least 6 weeks and dietetic treatment (according to their weight and daily needs) for a week. Total cholesterol, HDL-cholesterol and triglycerides plasma levels were taken at time 0. Then a treatment with simvastatin 10 mg/die was begin for 4 weeks and than increased to 20 mg in patients with plasma cholesterol > 200 mg/100 ml at the end of fourth week. In some patients the dose was increased up to 40 mg for the elevated levels of plasma cholesterol at the end of the second month. All the parameters above were controlled monthly for three months. A control was performed at the end of sixth month of treatment. After 4 weeks treatment, simvastatin induced reduction in cholesterol plasma levels (p < 0.005), that continued during the whole time treatment (228 mg/dl at 24 week, p < 0.005 vs basal). The mean dosage of the simvastatin at fourth month was of 25 mg/die. During the treatment an increase of HDL plasma levels was noted, but this increment wasn't statistical significant (40 +/- 7 vs 45 +/- 9 mg/100 ml). No significant impairment of principal metabolic and laboratory parameters were observed during the treatment. These data indicate that simvastatin in small dose induce a reduction in cholesterol plasma levels with a significant increase in HDL without side effects.