Faculty Bibliography

Percutaneous coronary intervention (PCI) is now a part of the treatment strategy of patients with both unstable syndromes and chronic angina. As our patients age and live longer with coronary artery disease, many having had PCI, they are more likely to develop potentially life-threatening comorbid conditions, including neoplastic disorders. In the United States, for example, an estimated 41% of the population will develop some form of malignancy.1 As such, they become subject to a multitude of interactions between their cardiac and oncologic diseases, and the therapies used to treat each. This is especially the case when patients have had PCI with drug-eluting stents (DES), as a careful balance between thrombosis and bleeding must be maintained, and is particularly vulnerable to the interactions described above. The following cases and accompanying review will highlight potential risks of very late stent thrombosis with acquired prothrombotic states, following coronary intervention with implantation of both 1st and second-generation DES.

Type III coronary perforations are a lethal complication of percutaneous intervention. While most involve "cavity-spilling", or extravasation of contrast into the pericardial space, a few flow into an anatomic chamber. A case of balloon angioplasty-induced Type III perforation of the ramus intermedius (RI) with iatrogenic fistula formation to the great cardiac vein is presented and, to our knowledge, is the first report involving a perforated RI with a resultant fistula to the great cardiac vein.

Anaphylaxis during diagnostic catheterization and coronary intervention is a rare and potentially life-threatening complication. Fortunately, with standard intervention, fatality is rare. We report a case of medically refractory anaphylaxis during a coronary intervention that ultimately responded to percutaneous cardiopulmonary bypass (CPB). The proposed mechanics and use of CPB for shock are discussed.

Acute right coronary artery occlusion following radiofrequency ablation. We report the first known case of acute right coronary artery occlusion following Radiofrequency (RF) ablation for atrial flutter in a patient without known prior coronary disease. Our patient developed acute chest pain and inferior ST-segment elevation immediately following the procedure. Emergent cardiac catheterization was performed, revealing an occluded distal right coronary artery, which was immediately stented. Acute coronary occlusion should be considered in the differential diagnosis of patients, with or without coronary artery disease, who experience chest pain following RF ablation for atrial flutter.

N-acetylcysteine is a remarkably active agent shown to be useful in a variety of clinical settings. The drug has actions relevant to radiocontrast-induced nephropathy (RCIN) that include vasodilatation, enhancement of renal medullary blood flow, and antioxidant properties. The drug's pharmacokinetics are remarkable for almost complete first pass metabolism after oral administration, resulting in no free drug reaching the circulation. After intravenous administration, extensive reaction with tissue and plasma proteins greatly limits the amount of circulating free drug. Given the difficulty achieving free drug in the systemic circulation, it is highly likely that the drug works via its metabolites. The primary mechanism may be through L-cysteine as a cellular source for glutathione production. Clinical studies of N-acetylcysteine in the prevention of RCIN have yielded highly mixed results; five were dramatically positive, and eight others had no demonstrable efficacy at all. The following will review the individual studies, attempt to reconcile the divergent results, and propose future research needs.

BACKGROUND:Contrast nephropathy (CN) is a common cause of renal dysfunction after cardiac angiography. Recently, N-acetylcysteine (NAC) has been found to reduce the risk of CN after CT imaging with contrast enhancement. The purpose of the current study was to evaluate the efficacy of NAC for the prevention of CN in the setting of cardiac angiography. METHODS:Eligible patients were those undergoing cardiac angiography with serum creatinine>1.7 mg/dL. Patients were randomized to one of two groups: Group 1, IV hydration and NAC, 1200 mg one hour before angiography, and a second dose 3 hours after; Group 2, IV hydration and placebo. CN was defined as an increase of 0.5 mg/dL in serum creatinine. RESULTS:Seventy-nine patients completed the study. There were no significant differences between the groups in baseline characteristics, duration of angiography, mean volume of dye infused or mean IV hydration. Contrast nephropathy developed in 24.0% of subjects, 26.3% NAC, and 22.0% placebo (P = NS). Among subjects with diabetes mellitus, there was no significant difference in the rate of CN between the groups (42.1% NAC, 27.8% placebo; P = 0.09). The independent predictors of CN risk were diabetes mellitus and preexisting chronic renal insufficiency. CONCLUSIONS:NAC was not effective for the prevention of CN after cardiac angiography.