SUMMARYWe treated an 88-year-old man with aortic valvular stenosis/insufficiency and paroxysmal atrial fibrillation, who developed ventricular tachycardia due to pilsicainide toxicity.He was treated at the outpatient clinic of his local hospital, and was administered pilsicainide (100 mg/day) for atrial fibrillation. The electrocardiographic findings on admission to our hospital indicated wide QRS with frequent episodes of ventricular tachycardia. We diagnosed him as having pilsicainide toxicity because of a low cardiac output and renal dysfunction. His creatinine level was 2.4 mg/dL and the serum pilsicainide level was 2.42 µg/mL on admission. Fluid infusion and continuous hemodiafiltration were performed to achieve an early reduction in the serum pilsicainide level. His serum pilsicainide concentration was significantly decreased by these treatments, and the prolongation of the QTc and ventricular tachycardia improved in parallel to the decrease in the serum pilsicainide level. The changes in the serum pilsicainide level showed a significant positive correlation with the changes in the electrocardiographic findings (PQ, QRS, ST intervals, and QTc).Pilsicainide should be administered with great care to elderly patients, especially patients with cardiac dysfunction and renal dysfunction. Estimation of the serum level may be possible from the electrocardiographic findings if the pilsicainide toxicity occurs.
SUMMARYAlthough several investigations have reported that stent implantation is an option for the treatment of vasospastic angina (VSA) that is resistant to medical treatment, we are concerned about the occurrence of new stent-edge spasms after stenting. The purpose of this study was to determine the incidence of new stent-edge spasms after stenting. Twenty-seven patients with VSA and 23 patients without VSA were enrolled. About 6 months after stent implantaion, a spasm provocation test was performed by intracoronary infusion of acetylcholine or ergonovine in 26 patients with VSA and all patients without VSA, and the induced stent-edge spasms were classified as either moderate (stent-edge spasm > 75% and < 95% reduction in coronary artery diameter) or severe (stent-edge spasm > 95% reduction in coronary artery diameter). In one patient with VSA, stent-edge spasm and acute thrombosis occurred several hours after stent implantation. The remaining 26 patients with VSA had no complications during or after stent implantation. However, during the chronic phase, severe stent-edge spasm was provoked in 5 patients with VSA (19.2%) and in 2 patients without VSA (8.7%). Moderate stent-edge spasm was provoked in 5 patients with VSA (19.2%) and 5 patients without VSA (21.7%). The results suggest new onset stent-edge spasm in patients either with or without VSA should not be neglected. (Int Heart J 2005; 46: 23-33)
Objectives: To analyse clinical, echocardiographic, and prognostic characteristics of Staphylococcus aureus infective endocarditis (IE) compared with endocarditis caused by other pathogens. Design: Cohort study. Methods: 194 consecutive patients with definite IE according to the Duke criteria prospectively examined by transthoracic and transoesophageal echocardiography were enrolled. Patients without identified microorganisms were excluded. The S aureus IE group (n = 61) was compared with the group with IE caused by other pathogens (n = 133). Results: Compared with IE caused by other pathogens, S aureus IE was characterised by severe comorbidity, a shorter duration of symptoms before diagnosis, and a higher prevalence of right sided IE, cutaneous portal of entry, and history of renal failure. Severe sepsis, major neurological events, and multiple organ failure were more frequent during the acute phase in S aureus IE. In-hospital mortality (34% v 10%, p , 0.001) was higher in patients with S aureus IE and the 36 month actuarial survival rate was lower in S aureus IE than in IE caused by other pathogens (47% v 68%, p = 0.002). Multivariate analyses identified S aureus infection as a predictive factor for in-hospital mortality and for overall mortality. Conclusions: S aureus IE compared with IE caused by other pathogens occurs in a more debilitated clinical setting and is characterised by a higher prevalence of severe sepsis, major neurological events, and multiple organ failure leading to higher mortality.
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