Contrast induced nephropathy (CIN) is the third leading cause of hospital aquired renal failure and is associated with significant morbidity and mortality. Chronic kidney disease is the primary predisposing factor for CIN. As estimated glomerular filtration rate <60 ml/1.73 m 2 represents significant renal dysfunction and defines patients at high risk. Modifiable risk factors for CIN include hydration status, the type and amount of contrast, use of concomitant nephrotoxic agents and recent contrast administration. The cornerstone of CIN prevention, in both the high and low risk patients, is adequate parenteral volume repletion. In the patient at increased risk for CIN it is often appropriate to withhold potentially nephrotoxic medications, and consider the use of n-acetylcysteine. In patients at increased risk for CIN the use of low or iso-osomolar contrast agents should be utilized and strategies employed to minimize contrast volume. In these patients serum creatinine should be obtained forty-eight hours post procedure and it is often appropriate to continue withholding medications such as metformin or non steroidal anti-inflammatories until renal function returns to normal.' 2006 Wiley-Liss, Inc.

The goal of this study was to verify whether myocardial protection could be achieved via the intracoronary administration of propranolol in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Accordingly, 21 patients undergoing PTCA were randomly assigned to receive either intracoronary placebo (group A, n = 10) or intracoronary propranolol (group B, n = 11). Three balloon inflations (i.e., coronary artery occlusions) were performed in each patient. Inflations I and II (maximum duration 60 sec) served as control occlusions. Inflation III (maximum duration 120 sec) was performed either after intracoronary administration of saline (2 ml) or propranolol (1.1 + 0.2 mg). The following electrocardiographic index of myocardial ischemic injury were measured: (1) time to the development of ST segment elevation equal to 0.1 mV and (2) magnitude of ST segment elevation after 60 sec of coronary artery occlusion. Both indexes did not differ significantly between the groups during inflations I and LI. In group A the time to development of ST segment elevation of 0.1 mV remained unchanged between the second and third occlusions (25 + 5 and 26 ± 4 sec during inflations II and III, respectively). In group B subselective injection of propranolol into the affected coronary artery significantly prolonged the time to ST segment elevation of 0. 1 mV from 19 + 4 sec (inflation II) to 53 ± 9 sec (inflation III; p < .001). Administration of placebo did not change the magnitude of ST segment elevation 60 sec after coronary artery occlusion between the second and third occlusion in group A (0. 16 + 0.02 and 0. 18 ± 0.03 mV, respectively). In group B, after intracoronary administration of propranolol, ST segment elevation 60 sec after occlusion decreased significantly from 0.23 0.06 mV (inflation II) to 0.12 ± 0.04 mV (inflation III; p < .005). There were no significant differences in heart rate and mean aortic pressure between groups A and B during inflations I, II, and III. In conclusion, our results suggest that (1) repetitive episodes of transient coronary artery occlusion are associated with similar degrees of myocardial ischemic injury, (2) intracoronary propranolol significantly reduces the electrocardiographic indexes of myocardial ischemic injury, and (3) the myocardial protection afforded by intracoronary propranolol is most likely mediated by a regional effect of the drug.

Of 47 consecutive patients referred for coronary angioplasty, the procedure was attempted in 13 patients despite occlusion of the involved vessel. This included four patients with total coronary occlusion and nine with functional coronary occlusion (faint, late antegrade opacification in the absence of a discernible luminal continuity). All procedures were performed with an angioplasty system in which the leading guide wire could be moved independently of the dilatation catheter. Primary success was obtained in 54% (7/13) of patients with coronary occlusion compared with 85% (29/34) in the remaining patients with conventional stenoses between 75% and 95% (91 + 5%, mean + SD; p < .02). In patients with coronary occlusion, the mean residual stenosis after angioplasty (41%), the abrupt reclosure rate (8%), and the incidence of angiographically evident dissection (29%) were similar to those seen in the 34 patients who underwent angioplasty of conventional stenoses, although restenosis tended to be more common (43% vs Received April 11, 1983; accepted June 2, 1983. This work was done during the tenure of a research fellowship from the American Heart Association, Greater Boston Massachusetts Division, No. 13-435-812 (J. P. D.). 776in totally occluded vessels.' Angioplasty systems in which the leading guide wire can be moved independently of the balloon catheter have recently been developed and offer advantages over fixed wire systems in the performance of coronary angioplasty.4 I These advantages now appear to extend to coronary angioplasty of functionally occluded vessels, and this report describes our experience in 13 such patients, with attention to the unique technical and coronary hemodynamic considerations present in this patient population. MethodsOf 47 consecutive patients (ages 35 to 81 years) who underwent coronary angioplasty at the Beth Israel Hospital between December 1981 and February 1983, 13 patients (group A) did so despite total occlusion (100%) or functional total occlusion (99%) of the involved vessel. Total vessel occlusion (figure 1) was defined as absent antegrade filling beyond the lesion. Functional total occlusion (figure 2) was defined as faint, late antegrade opacification of the distal segment in the absence of a discernible luminal continuity on detailed review of the cineangiogram. The remaining 34 patients (group B) had conventional stenoses between 75% and 95% (mean 91 + 5%) with evident luminal continuity. CIRCULATION

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