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We report the case of a 72-year-old male who underwent primary angioplasty for an acute myocardial infarction and developed a coronary stent infection with Staphylococcus aureus. The patient was treated with a prolonged course of IV antibiotics and underwent debridement and partial stent extraction successfully.

Background: The frequency, risk factors for, and effect on long-term survival of increased troponin I (cTnI) following elective, uncomplicated percutaneous coronary intervention (PCI) remains uncertain. Methods: We studied 907 patients undergoing elective PCI without recognized PCI complications and with at least 1 measurement of cTnI 12 or more h following the procedure. Patients with pre-PCI cTnI above 0.1 ng/ml or with myocardial infarction within the previous 48 h were excluded. Results: Maximal cTnI (TrMX) following PCI averaged 0.8 ng/ml, exceeded the upper normal of 0.1 ng/ml in 65.2% of patients and was 1.5 ng/ml or above in 13.7%. Of several demographic and procedural variables examined, the only significant predictor of TrMX was the number of stents deployed. (p<0.0023 95% confidence interval [CI]: 0.10-0.46). Significant univariate predictors of survival (Kaplan-Meier) were older age (p<0.0001), diabetes (p = 0.02), peripheral vascular disease (p<0.0001), obstructive lung disease (p<0.0001), congestive failure (p<0.0001), renal impairment (p<0.0001), and TrMX of 3.62 ng/ml or above (p = 0.0451). Independent predictors (Cox) were older age (p<0.0001), obstructive lung disease (p<0.0001), congestive failure (p<0.0001), and TrMX (p = 0.0272). Conclusions: Elevation of cTnI occurs in most patients undergoing elective, uncomplicated PCI. Deployment of multiple stents is associated with higher values of cTnI. Long-term survival is primarily influenced by age and pre-PCI comorbidities, however patients with the highest values of cTnI after PCI are also at increased risk of reduced survival. Significant independent predictors of reduced survival were older age, obstructive pulmonary disease, congestive failure (p<0.0001 for each), and maximal post-PCI cTnI (p = 0.0272).

Invasive hemodynamic assessment of MR severity could be enhanced by calculating our new ratio, V(a)/LV(a), due to its ability to account for LV work that is lost to the LA with a proportional decrease in forward or useful LV work with progressively increasing severity of MR.

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