The incidence of nephrotoxicity occurring with the nonionic contrast agent, iohexol, and the ionic contrast agent, meglumine/sodium diatrizoate, was compared in 1196 patients undergoing cardiac angiography in a prospective, randomized, double-blind multicenter trial. Patients were stratified into four groups: renal insufficiency (RI), diabetes mellitus (DM) both absent (N = 364); RI absent, DM present (N = 318); RI present, DM absent (N = 298); and RI and DM both present (N = 216). Serum creatinine levels were measured at -18 to 24, 0, and 24, 48, and 72 hours following contrast administration. Prophylactic hydration was administered pre- and post-angiography. Acute nephrotoxicity (increase in serum creatinine of > or = 1 mg/dl 48 to 72 hours post-contrast) was observed in 42 (7%) patients receiving diatrizoate compared to 19 (3%) patients receiving iohexol, P < 0.002. Differences in nephrotoxicity between the two contrast groups were confined to patients with RI alone or combined with DM. In a multivariate analysis, baseline serum creatinine, male gender, DM, volume of contrast agent, and RI were independently related to the risk of nephrotoxicity. Patients with RI receiving diatrizoate were 3.3 times as likely to develop acute nephrotoxicity compared to those receiving iohexol. Clinically severe adverse renal events were uncommon (N = 15) and did not differ in incidence between contrast groups (iohexol N = 6; diatrizoate N = 9). In conclusion, in patients undergoing cardiac angiography, only those with pre-existing RI alone or combined with DM are at higher risk for acute contrast nephrotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of regional diastolic pressure differences within the left ventricle on the measured transmitral pressure-flow relation were determined by simultaneous micromanometric left atrial (LAP) and left ventricular pressure (LVP) measurements, and Doppler echocardiograms in 11 anesthetized, closed-chest dogs. Intraventricular pressure recordings at sites that were 2, 4, and 6 cm from the apex were obtained. Profound differences between these sites were noted in the transmitral pressure relation during early (preatrial) diastolic filling. In measurements from apex to base, minimum LVP increased (1.6+±0.7 to 3.1 ±+0.8 mm Hg, mean ± SD); the time interval between the first crossover of transmitral pressures and minimum LVP increased (31 ± 3 to 50±17 msec); the slope of the rapid-filling LVP wave decreased (74±13 to 26±5 mm Hg/sec); the m um forward (i.e., LAP>LVP) transmitral pressure gradient decreased (3.6±+1.3 to 2.1±0.7 mm Hg); the time interval between the first and second points of transmitral pressure crossover increased (71 ± 9 to 96 ± 13 msec); and the area of reversed (i.e., LVP>LAP) gradient between the second and third points of transmitral pressure crossover decreased (101± 41 to 40±33 mm Hg . msec). During atrial contraction, sigificant regional ventricular apex-to-base gradients were also noted. The slope of the LV A wave decreased (26 ± 10 to 16 ± 4 mm Hg/sec); LV end-diastolic pressure decreased (8.1±2.0 to 7.4± 2.0 mm Hg), and the upstroke of the LV A wave near the base was recorded earlier than near the apex. All differences were sigificant at the 0.05 level. Simultaneous transmitral Doppler velocity profiles and transmitral pressures were measured at the 4-cm intraventricular site. The average interval between the first and second points of pressure crossover and between the onset of early rapid filling and mamum E-wave velocity were statistically similar (81 ± 13 vs. 85 ± 12 msec; NS); and the average area of the forward transmitral pressure gradient associated with acceleration of early flow was significantly greater than the area of reversed gradient associated with deceleration of early flow (133 ±+36 vs. 80 46 msec * mm Hg;p<0.025). Finally, the average forward transmitral pressure gradient before minimum LVP was greater than the average forward gradient present after minimum LVP (2.3+0.4 vs. 1.4±0.3 mm Hg; p<0.001), with significant differences in E-wave acceleration noted before and after minimum LVP (887 ± 230 vs.455 ± 116 mm Hg/sec; p<0.001). Thus, the present study 1) confirms the existence of physiological, reversed pressure gradients during diastole, 2) shows that the magnitude and timing of the forward and reversed pressure gradients are a function of the site of intraventricular pressure measurement, 3) shows that the regional variations in pressure due to the atrial contribution to filling are opposite to that of early diastolic filling, 4) indicates that temporal features of the Doppler E wave are related in a specific manner to temporal features of transmitral pressure. These fi...

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The efficacy and safety of a 3 hr, 80 mg intravenous infusion of recombinant tissue-type plasminogen activator (rt-PA) were investigated in 47 patients with acute myocardial infarction. Coronary angiography, performed before the administration of rt-PA and for 90 min thereafter, demonstrated that 37 patients had total coronary occlusion before therapy. After 90 min of rt-PA (50 mg), reperfusion of the infarct-related artery was observed in 25 patients (68%).

Forty-five patients with acute transmural myocardial infarction and angiographically confirmed complete coronary occlusion were prospectively randomized, two for one, to treatment of acute coronary thrombosis with intravenous recombinant human tissue-type plasminogen activator (rt-PA) or placebo. Each of five additional consecutive patients was treated with a high dose of rt-PA for 2 hr. Twenty-five of 33 patients (75%) receiving 0.5 to 0.75 mg/kg of rt-PA over 30 to 120 min had angiographically proven recanalization within 90 min of initiation of therapy. Only one of 14 patients given placebo had spontaneous recanalization within 45 min (p < .001). Thirteen placebo-treated patients were crossed over to the intracoronary rt-PA group. Nine (69%) exhibited subsequent recanalization within 45 min. Levels of circulating fibrinogen decreased after treatment with rt-PA by an average of only 8% of baseline values. None of the patients manifested a depletion of fibrinogen level to below 100 mg/dl. Six patients who were completely unresponsive to rt-PA were subsequently treated with intracoronary streptokinase and none responded. Thus, either intravenous or intracoronary rt-PA induced coronary thrombolysis without eliciting clinically significant fibrinogenolysis in patients with evolving myocardial infarction due to thrombotic coronary occlusion.