Elevated potassium intake inhibits neointimal proliferation in the swine coronary artery.

BACKGROUND: Previously, we reported that elevated extracellular potassium concentration in vitro inhibited proliferation and migration of vascular smooth muscle cells, formation of free radical compounds by macrophages, and reduced platelet sensitivity to agonists. More recently, we described a reduction in neointimal proliferation after balloon angioplasty injury in the carotid arteries of rats associated with an elevation of dietary potassium intake during a 4-week experiment. In the present study we conducted a similar investigation in the swine coronary artery balloon angioplasty model. PROCEDURES: Two groups of seven castrated male swine were studied; for 28 days the normal potassium group consumed a diet containing 0.25% potassium and the high potassium group ate diet containing 2.0% potassium. After 14 days on the diet, balloon angioplasty was performed. After an additional 14 days on the same diets the hearts were removed, and normal and lesioned sections of the artery were analyzed histologically. RESULTS: The neointimal area was markedly less in the high potassium group than in the normal potassium group, 0.33+/-0.04 mm2 v 0.74+/-0.10 mm2 (P < .004). Neointimal area-to-total wall area ratio in the normal potassium group averaged 0.199+/-0.018, significantly greater than the ratio computed for the elevated potassium group, 0.120+/-0.015 (P < .006). CONCLUSION: These results support the hypothesis that a high level of dietary potassium intake inhibits neointimal proliferation after balloon angioplasty in the swine coronary artery.

Lysis of a left ventricular thrombus with recombinant tissue plasminogen activator.

A 23-year-old woman with peripartum cardiomyopathy presented with a 2.1 x 2.5-cm pedunculated, mobile, left ventricular thrombus and evidence of systemic embolization. Due to the patient's poor left ventricular function, thrombectomy was not a viable option. Treatment with high-dose IV heparin was initially utilized but was unsuccessful as the thrombus appeared to enlarge on echocardiography. An accelerated weight-adjusted dose of recombinant tissue plasminogen activator (rt-PA) successfully lysed the thrombus without evidence of embolization. Although rt-PA has been used for primary lysis of high-risk ventricular thrombi, this is the first documentation of successful lysis of a left ventricular thrombus in a patient with peripartum cardiomyopathy.

Thromboembolism in the right side of the heart.

Right-sided cardiac thromboemboli, or pulmonary emboli-in-transit, represent an unusual disease process with high morbidity and mortality. We present a detailed case report and a synopsis of our experience at the University of Mississippi Medical Center between 1990 and 1997 and review the current medical literature. These thrombi and emboli may largely be subdivided into type A--a mobile, serpiginous clot that is probably a mobilized deep vein thrombus--and type B--a rather immobile clot morphologically similar to left-sided heart thrombi that may represent intracardiac thrombosis. The mainstays of therapy include surgical embolectomy and thrombolysis, but there is no clear benefit of one over the other. Treatment should be individualized according to the clot's size and morphology, likelihood of preexisting pulmonary embolism, the patient's cardiopulmonary reserve, comorbid conditions, and local expertise with treatment modalities.

Fructose-1,6-diphosphate in the treatment of oleander toxicity in dogs.

Oleander, a flowering plant that grows in the Mediterranean and southern US, contains the cardiac glycosides oleandrin, digitoxigenin and nerium, which inhibit Na(+)-K+ ATPase. Clinical manifestations of oleander toxicity include gastrointestinal irritation, marked hyperkalemia, A-V block, ventricular dysrhythmia, and not uncommonly death. Because fructose-1,6-diphosphate (FDP) has been shown to attenuate digoxin toxicity, we determined whether this agent would be effective in the treatment of the toxicity of these similarly-structured cardiac glycosides. Anesthetized dogs (n = 12) were infused i.v. for 5 min with 40 mg oleander extract/kg and then 6 dogs randomly selected from that group received a 50 mg/kg bolus of 10% FDP followed by a constant infusion. The other control animals received the same dosage of 10% dextrose. Within 5 min after oleander administration, all dogs developed dysrhythmias. The FDP-treated animals reverted to sinus rhythm within 1.58 +/- 0.15 h; none in the control group returned to sinus rhythm. One control dog died at 3 h from ventricular fibrillation. Marked hyperkalemia was observed in the control group; plasma K+ remained unchanged in the FDP group. Throughout the 4 h experimental period the FDP group maintained normal arterial pressures; in the control dextrose group, pressures were profoundly depressed. Cardiac output declined in both groups but remained higher in the FDP group. To determine the mechanism whereby FDP attenuates oleander toxicity, we studied the in vitro effect of FDP on oleander poisoned myocardial sarcolemmal membranes. At concentrations of 1 and 2 mg oleander inhibited Na(+)-K+ ATPase activity and addition of 500 microM FDP restored myocardial sarcolemmal Na(+)-K+ ATPase function. FDP effectively prevented hyperkalemia, reversed dysrhythmias and improved hemodynamics in vivo in this canine model of oleander toxicity and also restored sarcolemmal Na(+)-K+ ATPase activity in vitro.

Hemodynamic effects of fructose 1,6-diphosphate in patients with normal and impaired left ventricular function.

We compared the short-term hemodynamic effects of intravenous fructose 1,6-diphosphate (FDP) administration in patients with coronary artery disease. Hemodynamic measurements were performed before and after administration of FDP in two groups of patients: those with impaired left ventricular (LV) function, elevated LV end-diastolic pressures (LVEDP > or =12 mm Hg, n = 30), and those with normal LV function (LVEDP <12 mm Hg, n = 17). In those with impaired LV function, FDP induced a decrease in LVEDP from 22 +/- 1.31 to 16.73 +/- 1.46 mm Hg (p< 0.0001). The cardiac index increased (2.50 +/- 0.11 to 2.81 +/- 0.13 L/m2 [p < 0.0001]), as did the LV stroke work index (31.7 +/- 2.04 to 40.3 +/- 2.67 gm x m x m2 [p < 0.0001]). FDP induced no significant change in heart rate and mean aortic pressure. Pulmonary pressure and resistance declined (p<0.002 and p< 0.0001, respectively). Systemic vascular resistance decreased because of increased cardiac output and unchanged arterial pressure (p < 0.001). In those patients with normal baseline LVEDP (5.06 +/- 0.27 mm Hg), FDP decreased heart rate (p< 0.0001) and systemic and pulmonary resistance (p < 0.03 and p < 0.004, respectively), whereas LVEDP and mean aortic and pulmonary pressures remained unchanged. FDP moderately increased cardiac output (p < 0.05), stroke volume index, and LV stroke work index (p< 0.002 and p< 0.003, respectively). The observed improvement in LV function in those patients with elevated LV filling pressures is thought to be a result of an increased energy production by the Embden-Meyerhoff pathway and to act as a positive inotrope.

Problems in the recognition of aortoembolic stroke.

Recent reports suggest aortoembolism is an important cause of stroke. Although transesophageal echocardiography visualizes the aortic arch, diagnosis of aortoembolism stroke is not common. We investigated reasons for this discrepancy at our institution. We reviewed charts and transesophageal echocardiography videotapes of 16 patients with recent ischemic stroke or transient ischemic attack who had undergone transesophageal echocardiography. For each patient, we determined the most likely cause of cerebral ischemia, and we compared the official transesophageal echocardiography report to our interpretation of the videotape. In our videotape review, 13 patients had good visualization of the aortic arch. Of 6 patients with atherosclerosis in the arch, 1 had high-grade carotid stenosis, 1 had atrial fibrillation, 1 had "small-vessel disease," and 3 had cerebral ischemia of unknown cause. The official reports did not mention aortic arch disease in 4 of 6 patients. A possible cause of cerebral ischemia was identified in 6 of 7 patients with normal aortic arches. Of 3 patients who had poor visualization of the aortic arch, one had "small-vessel disease," and 2 had ischemic stroke of unknown cause despite extensive workups. We conclude that aortic arch disease is common in patients with ischemic stroke and transient ischemic attack and may be a cause of cerebral ischemia, especially in patients with stroke or transient ischemic attack due to small-vessel occlusion or of unknown cause. Aortic arch disease may not be identified as the cause of stroke or transient ischemic attack because (a) transesophageal echocardiography is not done, (b) transesophageal echocardiography is done but the aortic arch is not visualized, (c) transesophageal echocardiography is done, the aortic arch is visualized, but the examiner does not comment on aortic arch disease, or (d) despite transesophageal echocardiography identification of arotic arch disease, the treating physician does not consider the aorta to be a potential source of embolization.

Plasma oxidase assay for screening of myocardial infarction.

The availability of techniques such as surgical reperfusion, angioplasty, and thrombolysis for the treatment of acute myocardial infarction (AMI) has revived interest in seeking an early detectable biochemical marker diagnostic for AMI. Therefore, we investigated whether an unidentified oxidase that is released by activated neutrophils at the onset of AMI could be used as an early diagnostic assay. The conversion by plasma oxidase of 1 microM of adrenaline to 1 microM of adrenochrome represents the plasma oxidase activity (POA) of 1 U/L. Fifty patients suspected of having AMI, 40% of whose electrocardiograms were nondiagnostic for AMI, were admitted to the coronary care unit, and venous blood samples were obtained for determination of the POA and creatine phosphokinase-MB levels. Healthy volunteers (n = 12) served as control subjects, and 8 patients with pneumonia whose leukocyte counts were greater than 15,000 microL were included in the study. In those with AMI (n = 22), as determined by serial creatine phosphokinase-MB, the mean POA (+/- standard error of the mean) was 233 +/- 13 U/L, and in those with angina and no AMI (n = 28) was 127 +/- 5 U/L (P < 0.0001). In the control group, mean POA (+/- standard error of the mean) was 84 +/- 5 U/L (control versus angina; P < 0.01) and for those with infection was 214 +/- 10 U/L. At admission, the creatine phosphokinase-MB was diagnostic for only 12 of the 22 patients with AMI (sensitivity rate of 54%), whereas in 21 of those patients, the POA values were diagnostic for AMI (sensitivity rate of 95%).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of preload recruitable stroke work, end-systolic pressure-volume and dP/dtmax-end-diastolic volume relations as indexes of left ventricular contractile performance in patients undergoing routine cardiac catheterization.

The end-systolic pressure-volume relation, the relation between stroke work and end-diastolic volume, termed the preload recruitable stroke work relation, and the relation between the peak of the first derivative of left ventricular pressure (dP/dtmax) and end-diastolic volume have been employed as linear indexes of left ventricular contractile performance in laboratory animals. The purpose of this study was to examine the relative utility of these indexes during routine cardiac catheterization in seven human subjects (mean age 48 +/- 18 [SD] years) with a normal left ventriculogram and coronary angiogram. Left ventricular pressure was recorded continuously with a micromanometer catheter, and left ventricular volume was derived from digital subtraction contrast ventriculograms obtained at 30-ms intervals. Transient occlusion of the inferior vena cava with a balloon-tipped catheter was employed to obtain beat to beat reductions in left ventricular pressure and volume over 8.7 +/- 1.7 cardiac cycles. Stroke work declined by 49 +/- 13% during vena caval occlusion, but end-systolic pressure fell by only 26 +/- 11%, and changes in dP/dtmax were small and inconsistent (12 +/- 22%). Consequently, the range of data available for determination of the preload recruitable stroke work relation greatly exceeded that for the end-systolic pressure-volume relation and the dP/dtmax-end-diastolic volume relation, and much less linear extrapolation from the measured data was required to determine the volume-axis intercept. Preload recruitable stroke work relations were highly linear (r = 0.95 +/- 0.07), and much more so than end-systolic pressure-volume relations (r = 0.79 +/- 0.23).(ABSTRACT TRUNCATED AT 250 WORDS)

Serial left ventricular performance evaluated by cardiac catheterization before, immediately after and at 6 months after balloon aortic valvuloplasty.

Although impaired ventricular function has been shown to improve after aortic valve replacement, there are few data on hemodynamic changes after balloon aortic valvuloplasty based on follow-up catheterization. Of 71 patients surviving 6 months after balloon aortic valvuloplasty, 41 agreed to late recatheterization. All patients had pre- and postvalvuloplasty and 6 month catheterization data measured with high fidelity micromanometer pressure recordings and simultaneous digital subtraction left ventriculography. The hemodynamic result immediately after valvuloplasty included a reduction in the aortic valve gradient and a moderate increase in aortic valve area (0.51 +/- 0.14 to 0.81 +/- 0.19 cm2, p less than 0.0001). Ejection fraction increased slightly (52 +/- 18 to 55 +/- 17%, p less than 0.0001) despite a decrease in peak positive rate of rise of left ventricular pressure (dP/dt 1,650 +/- 460 to 1,500 +/- 490 mm Hg/s, p less than 0.05). There was also a decrease in left ventricular afterload and a small decrease in preload. At 6 month recatheterization, the mean aortic valve gradient and area were similar to baseline values, with 31 (76%) of 41 patients demonstrating valvular restenosis. At 6 months many left ventricular hemodynamic variables, including peak positive dP/dt and stroke work, also resembled prevalvuloplasty values. However, left ventricular end-diastolic volume was reduced (111 +/- 40 ml at 6 months versus 136 +/- 52 ml before valvuloplasty, p less than 0.01). The mean left ventricular ejection fraction was unchanged from prevalvuloplasty values in the study group of 41 patients, but was significantly improved in 9 of 15 patients with a baseline ejection fraction less than 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in left ventricular diastolic performance after aortic balloon valvuloplasty: acute and late effects.

To evaluate acute and follow-up changes in left ventricular diastolic performance, simultaneous digital left ventriculography and micromanometry were performed in 49 patients undergoing aortic balloon valvuloplasty. All patients improved symptomatically after valvuloplasty, and 26 returned 6.3 +/- 1.5 months later for follow-up catheterization. Immediately after valvuloplasty, aortic valve area increased (before 0.5 +/- 0.2 versus after 0.8 +/- 0.2 cm2, p less than 0.01), cardiac output (before 4.3 +/- 1.2 versus after 4.4 +/- 1.3 liters/min) and ejection fraction (before 51 +/- 18% versus after 52 +/- 17%) did not change and diastolic indexes worsened, signified by a decrease in peak filling rate (before 247 +/- 80 versus after 226 +/- 78 ml/s, p less than 0.01) and increase in the time constant of isovolumetric relaxation (tau) (before 78 +/- 29 versus after 96 +/- 40 ms, p less than 0.01) and the modulus of chamber stiffness (before 0.107 +/- 0.071 versus after 0.141 +/- 0.083, p less than 0.01). At follow-up catheterization, 16 patients continued to have symptomatic improvement (group 1) and 10 had recurrence of symptoms (group 2). Aortic valve area, cardiac output and ejection fraction at follow-up catheterization in both groups were similar and unchanged from values before valvuloplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Early and late changes in left ventricular systolic performance after percutaneous aortic balloon valvuloplasty.

To evaluate early and late hemodynamics after aortic valvuloplasty, 17 patients underwent first-pass radionuclide angiocardiography with simultaneous high-fidelity micromanometer pressure before, 10 minutes after and 6 months after aortic valvuloplasty. Pressure-volume and stress data were assessed. Immediately after the procedure, no significant change was observed in heart rate, systemic blood pressure, cardiac output or aortic insufficiency (as measured by visual or quantitative aortography). The mean and peak transvalvular gradient decreased from 64 to 36 mm Hg (p less than 0.001) and 76 to 38 mm Hg (p less than 0.001), respectively. The mean aortic valve area increased from 0.5 to 0.8 cm2 (p less than 0.001). Using echocardiography, meridional end-systolic wall stress decreased from 81 to 63 x 10(3) dynes/cm2 (p less than 0.001). Left ventricular ejection fraction increased from 0.48 to 0.54 (p less than 0.01), end-diastolic volume decreased from 161 to 143 ml (p less than 0.001) and end-diastolic pressure decreased from 18 to 13 mm Hg (p less than 0.01). Left ventricular stroke work (the area of the pressure-volume loop) also decreased from 17.5 to 14.7 x 10(6) ergs (p less than 0.001). The loop shifted to the left and downward. At the 6-month study, the mean and peak aortic valve gradient increased from 36 to 56 mm Hg (p less than 0.001) and 38 to 61 mm Hg (p less than 0.001), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in left ventricular systolic performance immediately after percutaneous aortic balloon valvuloplasty.

To evaluate the acute changes in left ventricular (LV) performance before and immediately after percutaneous aortic valvuloplasty, 25 patients underwent first-pass radionuclide angiocardiography for construction of pressure-volume loops. Simultaneously, high-fidelity micromanometric aortic and LV pressures were recorded. Echocardiographic wall thickness was used to define wall stress. After valvuloplasty, no acute changes were observed in the heart rate, aortic systolic pressure, cardiac output or degree of aortic insufficiency. Valvuloplasty decreased the peak aortic valve gradient from 73 to 40 mm Hg (p less than 0.001) and the mean gradient from 61 to 30 mm Hg (p less than 0.001); aortic valve area increased from 0.55 to 0.80 cm2 (p less than 0.001). Meridional end-systolic wall stress decreased from 83 to 55 X 10(3) dynes/cm2 (p less than 0.01). LV ejection fraction increased from 0.41 to 0.48 (p less than 0.01). LV end-diastolic volume decreased from 186 to 160 ml (p less than 0.001), end-systolic volume decreased from 115 to 87 ml (p less than 0.001) and end-diastolic pressure decreased from 22 to 17 mm Hg (p less than 0.01). LV stroke work decreased from 16.0 to 14.0 X 10(6) erg (p less than 0.001). No change was observed in peak positive LV dP/dt or the end-systolic pressure-volume ratio. This study documents variable and complex changes in the measures of cardiac function after aortic valvuloplasty. A decrease in the amount of LV outflow obstruction with maintenance of the cardiac output at a decreased level of LV filling occurs.

Exercise treadmill testing is a poor predictor of anatomic restenosis after angioplasty for acute myocardial infarction.

This study evaluated whether an exercise treadmill test could predict restenosis in 289 patients 6 months after a successful emergency angioplasty of the infarct-related artery for acute myocardial infarction. After excluding those with interim interventions (64), medical events (36), or medical contraindications to follow-up testing (25), both a treadmill test and a cardiac catheterization were completed in 144 patients, 88% of those eligible for this assessment. Four patients with left bundle branch block or pacemaker rhythm at the time of treadmill testing were also excluded from analysis. Of six follow-up clinical and treadmill variables examined by multivariable logistic regression analysis, only exercise ST deviation was independently correlated with restenosis at follow-up (chi 2 = 5, p = 0.02). The clinical diagnosis of angina at follow-up, although marginally related to restenosis when considered by itself (p = 0.04), did not add significant information once ST deviation was known. The sensitivity of ST deviation of 0.10 mV or greater for detecting restenosis was only 24% (13 of 55 patients), and the specificity was 88% (75 of 85 patients). The sensitivity of exercise-induced ST deviation for detection of restenosis was not affected by extent or severity of wall motion abnormalities at follow-up, by the timing of thrombolytic therapy or of angioplasty, or by the presence of collateral blood flow at the time of acute angiography. A second multivariable analysis evaluating the association of the same variables with number of vessels with significant coronary disease at the 6-month catheterization found an association with both exercise ST deviation (p = 0.003) and exercise duration (p = 0.04). Angina symptoms and exercise treadmill test results in this population had limited value for predicting anatomic restenosis 6 months after emergency angioplasty for acute myocardial infarction.

Validation of pressure-volume data obtained in patients by initial transit radionuclide angiocardiography.

In order to validate the measurement of pressure-volume loops and stroke work in humans, simultaneous digital subtraction ventriculography (DSA) and first-pass radionuclide angiocardiography (RNA) coupled with high-fidelity micromanometer left ventricular pressure measurements were undertaken in 34 patients, mean age 75 +/- 9 years, with aortic stenosis. Twenty-nine patients had a repeat study after balloon valvuloplasty, for a total of 63 DSA and RNA pressure-volume loops. All data were analyzed in a systemic fashion in order to minimize intra- and interobserver error. Linear regression analysis was used to calculate the degree of agreement between the two technologies. Left ventricular ejection fraction (RNA: 0.47 +/- 0.17, DSA: 0.49 +/- 0.18) had a correlation coefficient of 0.96; left ventricular end-diastolic volume (RNA: 171 +/- 42 ml, DAS: 168 +/- 52 ml) and end-systolic volume (RNA: 95 +/- 50 ml, DSA: 89 +/- 50 ml) had correlation coefficients of 0.89 and 0.95, respectively. Left ventricular stroke volume (RNA: 75 +/- 26 ml, DSA: 75 +/- 27 ml) had a correlation coefficient of 0.92, while integrated pressure-volume loop or stroke work (RNA: 15.6 +/- 6.6 ergs 10(6), DSA: 15.9 +/- 6.3 ergs 10(6] had a correlation coefficient of 0.89. These data demonstrate that RNA measurements of left ventricular chamber dynamics concur with that obtained with DSA. With semiautomated data analysis, the portable first-pass RNA pressure-volume data are also less labor-intensive. Moreover, multiple measurements of ventricular performance during hemodynamic manipulations in the catheterization laboratory or operating room would allow for a more precise estimation of left ventricular performance.

Doppler left ventricular diastolic filling abnormalities in aortic stenosis and their relation to hemodynamic parameters.

Doppler mitral flow indexes and their relation to invasively measured hemodynamic diastolic indexes were assessed in 13 patients with isolated aortic stenosis (AS), and compared to Doppler indexes in 10 normal subjects matched for age, heart rate, left ventricular (LV) ejection fraction and LV load. Patients with AS showed no difference in Doppler early filling (E) indexes, but demonstrated greater Doppler atrial filling (A) indexes in comparison to normal subjects: atrial velocity (89 +/- 31 vs 56 +/- 7 cm/s), atrial integral (11.4 +/- 4.8 vs 5.7 +/- 1.6 cm), A/E velocity (1.69 +/- 0.89 vs 1.06 +/- 0.26) and A/E integral (3.53 +/- 6.64 vs 0.81 +/- 0.27) (all p less than 0.05). Doppler indexes in patients with AS did not correlate with hemodynamic indexes of LV relaxation or chamber stiffness. Significant correlations were observed between Doppler and angiographic peak filling rates (r = 0.70) and between Doppler atrial filling velocity and LV end-diastolic volume (r = -0.66), LV end-diastolic pressure (r = -0.48) and LV ejection fraction (r = 0.53) (all p less than 0.05). These data indicate that, compared to matched normal subjects, most patients with AS have an increased atrial contribution to LV filling. However, in patients with decreased LV function, atrial function may also be depressed, as indicated by a decreased atrial contribution to LV filling, resulting in "normalization" of the Doppler mitral flow pattern.

Prediction of early recurrent myocardial ischemia and coronary reocclusion after successful thrombolysis: a qualitative and quantitative angiographic study.

To determine the association of qualitative and quantitative measurements of the myocardial infarct-related coronary narrowing with subsequent recurrent ischemia/reocclusion after successful thrombolysis, 47 patients treated with high-dose (150 mg) tissue plasminogen activator over 6 to 8 hours were studied in the setting of acute myocardial infarction. No patient underwent emergent coronary angioplasty. All patients had Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow or higher at the baseline (90-minute) angiogram; 31 patients had a protocol 24-hour catheterization as well. Eighteen patients had recurrent ischemia/reocclusion whereas 29 had an uneventful hospital course. There was no significant difference in baseline clinical characteristics between the 2 groups. Twenty-five (86%) of those with an uneventful course had TIMI grade 3 flow at baseline angiogram compared with 56% of patients with recurrent events. No significant difference in angiographic morphologic characteristics was found between the 2 groups at baseline catheterization. At 24 hours, however, none of the patients who subsequently had recurrent events had a concentric narrowing, while 13 (58%) of them had a complex morphology. In contrast, quantitative parameters of minimal lumen diameter, percent area stenosis and percent diameter stenosis at baseline and 24 hours were not significantly different between those who did and did not have recurrent ischemia/reocclusion. These findings suggest that the degree and quality of coronary flow at baseline catheterization are more important determinants of sustained patency and event-free hospitalization than are quantitative dimensions or coronary morphology. In addition, narrowings that fail to become concentric within the first 24 hours are more likely to be associated with subsequent ischemia or reocclusion during the early periinfarct period.

Analysis of the early rise in aortic transvalvular gradient after aortic valvuloplasty.

The relationship between dynamic changes in aortic valve gradient and left ventricular ejection performance in the early period after successful percutaneous aortic valvuloplasty has not been described in detail. Accordingly 20 adult patients with severe symptomatic calcific aortic stenosis underwent first-pass radionuclide angiography and Doppler echocardiography before, immediately after, and 2 to 4 days after the valvuloplasty procedure. A significant (p less than 0.001) reduction in peak-to-peak (72 +/- 24 mm Hg to 36 +/- 11 mmHg) and mean (60 +/- 20 mm Hg to 34 +/- 9 mm Hg) transaortic gradient and an increase in aortic valve area (0.5 +/- 0.2 cm2 to 0.8 +/- 0.2 cm2) were measured by high-fidelity micromanometer catheters immediately after aortic valvuloplasty. Results of Doppler echocardiography showed a significant (p less than 0.001) immediate decrease in peak instantaneous (81 +/- 22 mm Hg to 53 +/- 15 mm Hg) and mean (48 +/- 14 mm Hg to 31 +/- 9 mm Hg) aortic gradients. However, 2 to 4 days later a significant (p less than 0.001) return of peak (56 +/- 15 mm Hg to 65 +/- 20 mm Hg) and mean (31 +/- 9 mm Hg to 39 +/- 12 mm Hg) transvalvular gradient occurred. Aortic valve area as determined by the continuity equation also increased from 0.4 +/- 0.2 cm2 to 0.6 +/- 0.2 cm2 immediately after the procedure (p less than 0.001), then partially returned to baseline (0.5 +/- 0.2 cm2; p less than 0.005) at 2 to 4 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular and renal toxicity of a nonionic radiographic contrast agent after cardiac catheterization. A prospective trial.

STUDY OBJECTIVE: To determine the incidence of cardiovascular and renal toxicity of a nonionic contrast agent when used for cardiac catheterization, and to assess the value of electrolytes and urinalysis results as predictors of nephropathy induced by a contrast agent. STUDY DESIGN: Nonrandomized trial using a criterion standard and a cohort analytic study with a 48-hour follow-up. SETTING: Referral-based university hospital. PATIENTS: Convenience sample of patients having diagnostic cardiac catheterization. Renal function and clinical status were evaluated at baseline in 1,144 patients; at 24 hours in 1,077 (94%); and at 48 hours in 663 (57%). INTERVENTIONS: After patients received saline for hydration, coronary angiography and left ventriculography were done with iopamidol (average dose, 203 +/- 56 cc). MEASUREMENTS AND MAIN RESULTS: The definite and possible incidence of major acute cardiovascular complications from nonionic contrast media was 0.2% and 0.7%, respectively. The mean serum creatinine level increased 11.5 mumol/L from baseline at 24 hours (P less than 0.0001) and 16.8 mumol/L from baseline at 48 hours (P less than 0.0001). Results in a randomly selected training sample were studied to determine predictors of a rise in serum creatinine of 44.2 mumol/L or more. The baseline serum creatinine level and age were significant predictors of renal injury, but hypertension, diabetes mellitus, congestive heart failure, vascular disease, the volume of contrast agent injected or baseline values of urinary variables did not predict nephrotoxicity. In an independent validation sample, only the baseline serum creatinine level was confirmed as a predictor of nephrotoxicity, whereas age was not. A model that predicted contrast-induced nephropathy by the serum creatinine level showed an exponential increase in the risk for nephrotoxicity if the baseline level was 106.1 mumol/L or higher. CONCLUSIONS: Patients have a small but significant rise in serum creatinine after cardiac catheterization with a nonionic contrast agent. Baseline renal insufficiency is the only confirmed predictor of nonionic contrast-induced nephrotoxicity.