Data from experimental, clinical, and pathologic studies have suggested that the process ofrestenosis begins very early after coronary angioplasty. The present study was performed to determine prospectively the incidence of restenosis with use of the four National Heart, Lung, and Blood Institute and the 50% or greater diameter stenosis criteria, as well as a criterion based on a decrease of 0.72 mm or more in minimal luminal diameter. Patients were recatheterized at 30, 60, 90, or 120 days after successful percutaneous transluminal coronary angioplasty (PTCA). After PTCA all patients received 10 mg nifedipine three to six times a day and aspirin once a day until repeat angiography. Of 400 consecutive patients in whom PTCA was successful (<50% diameter stenosis), 342 underwent quantitative angiographic follow-up (86%) by use of an automated edge-detection technique. A wide variation in the incidence of restenosis was found dependent on the criterion applied. The incidence of restenosis proved to be progressive to at least the third month for all except NHLBI criterion II. At 4 months a further increase in the incidence of restenosis was observed when defined as a decrease of 0.72 mm or more in minimal luminal diameter, whereas the criteria based on percentage diameter stenosis showed a variable response. The lack of overlap between the different restenosis criteria applied affirms the arbitrary nature of angiographic definitions currently in use. Restenosis should be assessed by repeat angiography, and preferably ascertained according to the change in absolute quantitative measurements of the luminal diameter.

Non-invasive continuous monitoring of cardiac output could be very useful in clinical care and in research settings, particularly in elderly subjects. We studied whether Finapres arterial pulse wave analysis with Modelflow is a reliable non-invasive method for the assessment of cardiac output in healthy elderly subjects. We compared Modelflow cardiac output (MFCO) with thermodilution cardiac output (TDCO) in 28 healthy subjects, aged 70+/-4 years (mean+/-S.D.). TDCO was measured during right-sided heart catheterization, while MFCO was calculated with Modelflow(R) software from non-invasive arterial Finapres blood pressure, which was measured simultaneously. The two methods were compared using a paired t-test, by Pearson correlation, and by Bland-Altman analysis. TDCO was 6.4+/-1.1 litres/min (mean+/-S.D.) and MFCO was 4.7+/-1.3 litres/min (P<0.001). There was no significant correlation between MFCO and TDCO (r=0.28, P=0.13). Mean difference (bias) was -1.7 litres/min (S.E.M. 0.27 litres/min), with an S.D. (precision) of 1.5 litres/min. The 95% limits of agreement were -4.6 to +1.1 litres/min. In conclusion, non-invasive MFCO values differed significantly from and showed no significant correlation with invasively determined TDCO values in the normal range. Although simple, non-invasive and patient-friendly, the Modelflow method is inaccurate for assessment of cardiac output without invasive calibration.

Restenosis after coronary angioplasty is the single complication that most limits this revascularization procedure in clinical practice. The process is largely unpredictable and the lesion-related factors predisposing to restenosis are poorly understood, with little consensus in published reports. In this study using detailed quantitative angiographic measurements to assess 490 lesions, the simple lesion characteristics associated with restenosis were defined and the relation to the restenosis process documented. Restenosis was defined as an absolute deterioration in the minimal lumen diameter by greater than or equal to 0.72 mm, a criterion based on the 95% confidence intervals for repeat angiographic measurements. This was chosen in an attempt to separate spurious changes due to a poor angiographic result and the variability of angiographic measurements from significant changes due to the restenosis process. The principal determinants of restenosis were found to be a large improvement in the minimal lumen diameter at the time of dilation (1.13 mm for the restenosis group compared with 0.86 mm for the no restenosis group [p less than 0.0001]) and an optimal postangioplasty result (minimal lumen diameter 2.28 mm in the restenosis group compared with 2.05 mm [p less than 0.001] in the no restenosis group, corresponding to a 25% and a 30% diameter stenosis, respectively [p less than 0.0001]). These observations reported for the first time suggest that the distinction needs to be made between a "clinical restenosis" of greater than or equal to 50% diameter stenosis and the "restenosis process" as measured by the absolute changes occurring during and after angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the changes in stenotic and nonstenotic segments of a dilated coronary artery, detailed quantitative angiographic measurements were performed in 342 patients (398 lesions) immediately after angioplasty and at a predetermined follow-up time of 30, 60, 90 or 120 days after the dilation. Measurements of the stenotic segments were expressed as minimal luminal diameter, and the adjacent nonstenotic segments were expressed as interpolated reference diameter (both in millimeters). A follow-up rate of 86% was achieved. In the patients followed up at 30 and 60 days, there was no significant change in either the mean minimal luminal diameter or the mean reference diameter. However, at 90 and 120 days, there was significant deterioration in both the mean minimal luminal diameter (-0.37 and -0.42 mm, respectively) and the mean reference diameter (-0.17 and -0.26 mm, respectively), all of the changes being highly significant (p less than 0.00001). The reference diameter is involved in the dilation process and may be subject to the same restenosis process that takes place in initially stenotic segments. Percent diameter stenosis measurements, which are conventionally used to express the change in the severity of a stenosis after angioplasty, will tend to underestimate the change when there is a simultaneous reduction in the reference diameter.

Background-Despite the use of aspirin, reocclusion of the infarct-related artery occurs in Ϸ30% of patients within the first year after successful fibrinolysis, with impaired clinical outcome. This study sought to assess the impact of a prolonged anticoagulation regimen as adjunctive to aspirin in the prevention of reocclusion and recurrent ischemic events after fibrinolysis for ST-elevation myocardial infarction. Methods and Results-At coronary angiography Ͻ48 hours after fibrinolytic therapy, 308 patients receiving aspirin and intravenous heparin had a patent infarct-related artery (Thrombolysis In Myocardial Infarction [TIMI] grade 3 flow). They were randomly assigned to standard heparinization and continuation of aspirin alone or to a 3-month combination of aspirin with moderate-intensity coumarin, including continued heparinization until a target international normalized ratio (INR) of 2.0 to 3.0. Angiographic and clinical follow-up were assessed at 3 months. Median INR was 2.6 (25 to 75th percentiles 2.1 to 3.1). Reocclusion (ՅTIMI grade 2 flow) was observed in 15% of patients receiving aspirin and coumarin compared with 28% in those receiving aspirin alone (relative risk [RR], 0.55; 95% CI 0.33 to 0.90; PϽ0.02). TIMI grade 0 to 1 flow rates were 9% and 20%, respectively (RR, 0.46; 95% CI, 0.24 to 0.89; PϽ0.02). Survival rates free from reinfarction and revascularization were 86% and 66%, respectively (PϽ0.01). Bleeding (TIMI major and minor) was infrequent: 5% versus 3% (PϭNS). Conclusions-As adjunctive to aspirin, a 3-month-regimen of moderate-intensity coumarin, including heparinization until the target INR is reached, markedly reduces reocclusion and recurrent events after successful fibrinolysis. This conceptual study provides a mechanistic rationale to further investigate the role of prolonged anticoagulation after fibrinolytic therapy. (Circulation. 2002;106:659-665.)