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.

Cineangiograms of 138 patients who underwent percutaneous transluminal coronary angioplasty (PTCA) were analyzed with a computer-based coronary angiography analysis system. The results before and after dilatation are presented. In a first study group (120 patients), the severity of the obstructive lesions derived from the automatically detected contours was evaluated in absolute terms and in percent-diameter reduction. In a second group of patients, 18 coronary lesions were selected for their extreme severity and symmetric aspect before angioplasty as assessed from multiple views. In the second group, the densitometric percent-area stenosis was used to assess the changes in cross-sectional area after PTCA and was compared with the circular percent-area stenosis computed from the diameter measurements. Before PTCA, a good agreement exists between the densitometric percent-area stenosis and the circular percent-area stenosis. After PTCA, important discrepancies between these 2 types of measurements are observed. It is suggested that these discrepancies in results after PTCA can be accounted for by asymmetric morphologic changes in luminal cross section, which cannot be assessed accurately from diameter measurements in a single-plane view.

No abstract

In 11 patients, 1 mg of i.v. nifedipine was administered over 3 minutes and regional wall motion was studied during atrial pacing. The dominant effect of nifedipine at basal heart rate (HR) was a lowering of peak left ventricular pressure (152 to 128 mm Hg) with an increase in HR from 70 to 86 beats/min. During pacing, nifedipine produced (p < 0.02) a similar reduction in pressure at all rates, which is a mechanism reducing or sparing myocardial oxygen consumption. At the highest paced rate, the maximal velocity (Vmax) of the contractile element was significantly (p < 0.02) increased from 61 to 68 sec-' and the regional shortening fractions were increased over the entire pacing range: basal HR, 13.7% to 14.6% (p < 0.025); HR 120 beats/min, 11.6% to 13.5% (p < 0.005); maximal HR, 10.9% to 11.8% (p < 0.05). No evidence of a negative inotropic effect after i.v. administration of nifedipine was observed, myocardial oxygen consumption was probably reduced and there was an increase in regional function.Nifedipine (0.1 mg within 10 seconds) was selectively injected into bypass grafts at a constant paced rate in 10 patients. Seventeen marker pair regions were directly supplied by bypasses selectively injected with nifedipine (group A), and nine were independently perfused (group B). The pressure-derived variables showed a direct negative inotropic effect and a slowed relaxation phase. Thirty seconds after injection, minimal marker separation in group A occurred 78 msec after end-systole (ES), whereas before injection, minimal marker separation occurred 39 msec before ES (p < 0.0001). At the same time, the relation between minimal marker separation and ES in group B was unaffected. In consequence, the regional shortening fraction in group A contributing to left ventricular ejection decreased significantly 30 seconds after injection (-32%, p < 0.01), while that calculated simply from minimal and maximal marker separation remained unchanged (-9%, NS). Active regional contraction starting after the beginning of ejection and ending after ES must be considered as asynchrony and can be considered responsible for the slowed isovolumic contraction and relaxation of the whole ventricle. The dominant effect of i.v. nifedipine at clinical dosage levels is a lowering of systemic blood pressure, possibly reducing oxygen demand. When regionally administered, nifedipine exerts a direct negative inotropic effect, but after i.v. injection, this effect is overridden by reflex increases in contractility and in heart rate as a result of lowered systemic arterial pressure.INIFEDIPINE has been classified as a calcium antagonist that inhibits the electromechanical coupling process' and results in the relaxation of the muscle fiberr For the blood vessel, this means vasodilation and for the myocardium, a negative inotropic effect. Therefore, early investigations of the effects of nifedipine on myocardial contractility described nrimarily a reduction in contractility and oxygen consumotion for the isolated papillary muscle and for the isolated he...

The prognostic value of QRS score (Selvester), ST depression, ST elevation, extrasystoles, P terminal force in V1, and QTc derived from the predischarge 12 lead electrocardiogram was assessed after myocardial infarction in 474 patients without intraventricular conduction defects, ventricular hypertrophy, or atrial fibrillation. The usefulness of these results in risk assessment was compared with that of other clinical data. During follow up 45 patients died. Logistic regression analysis showed that QRS score, ST depression, and QTc were independently predictive of cardiac mortality. When multivariate analysis was applied to clinical and electrocardiographic data together, however, the 12 lead electrocardiogram did not provide independent information additional to that provided by other routine clinical findings and laboratory tests such as a history of previous myocardial infarction, clinical signs of persistent heart failure, indication for digitalis or antiarrhythmic drugs at discharge, and enlarged heart on chest x ray. In conclusion, the electrocardiogram has important prognostic value; however, it is not powerful enough to further improve the risk assessment of post-infarction patients.