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Biomedical subjects

C E Rackley

Publications and source records attributed to C E Rackley.

At least 37 records · Page 2Linked to original sources

Late angiographic follow-up after successful coronary arterial thrombolysis and angioplasty during acute myocardial infarction.

Emergency percutaneous transluminal coronary angioplasty (PTCA) is accepted as an important reperfusion intervention for acute myocardial infarction (AMI). Although its primary success rate is well documented, the frequency of restenosis after this procedure is unclear. The frequency of restenosis was determined in patients undergoing emergency PTCA at least 6 months after PTCA was performed during AMI. Of 66 consecutive patients undergoing emergency PTCA, 25 had a second, elective catheterization at an average of 22 months after AMI and 6 underwent repeat catheterization because of recurrent chest pain. Restenosis of the PTCA site was found in 10 of the 31 patients (32%) restudied. Also, 14 (45%) of these 31 patients showed progression of narrowing in the non-infarct-related coronary arteries. In summary, patients in whom AMI is treated by PTCA are at risk for restenosis and for progressive narrowing of the non-infarct artery.

Angioplasty, Balloon↗

Assessment of residual coronary arterial stenosis after thrombolytic therapy during acute myocardial infarction.

Maximal myocardial salvage appears to be related to the severity of residual coronary arterial stenosis after thrombolysis. The degree of residual infarct vessel stenosis was assessed in 119 consecutive patients with patent arteries who received streptokinase during acute myocardial infarction. After administration of streptokinase, 99 of 119 patients (83%) had a residual stenosis 70% or more in diameter. Assuming that a residual diameter stenosis of at least 70% is flow limiting, the feasibility for percutaneous transluminal coronary angioplasty (PTCA) was determined by the following criteria: length less than 10 mm, no significant distal narrowing or left main stenosis, and an adequate-sized distal artery. In 81 of 99 patients (82%), arterial anatomy was suitable for PTCA. Thus, after therapy with streptokinase for acute myocardial infarction, most patients have a significant infarct arterial residual stenosis and are candidates for PTCA.

Aged↗

Metabolic support during coronary reperfusion.

The limitation of infarct size by thrombolysis could potentially be improved by an early metabolic intervention. We therefore evaluated the effects of a 48-hour infusion of glucose-insulin-potassium (GIK) in patients with anterior infarctions. Seventeen patients were randomized to receive intravenous GIK (n = 10) or placebo (n = 7). All patients additionally received streptokinase. Changes in left ventricular function were assessed by comparing the global ejection fractions and the regional infarct area ejection fractions of the first ventriculogram with the 10-day second ventriculogram. There was a significantly greater improvement in the global ejection fraction of patients receiving GIK (increases 0.07 +/- 0.04) than in those randomized to placebo (decreases 0.08 +/- 0.04) (p less than 0.02). There was also a much greater improvement in the area ejection fractions of the group receiving GIK vs the group receiving placebo in the anterolateral (increases 0.24 +/- 0.07 vs decreases 0.02 +/- 0.04 [p less than 0.02]) and diaphragmatic (increases 0.08 +/- 0.08 vs decreases 0.17 +/- 0.05 [p less than 0.005]) segments. Thus in patients with anterior infarctions receiving streptokinase, GIK improves ventricular function and reduces the size of the segmental wall motion abnormality.

Adult↗

Progressive heart failure secondary to a high output state.

A high cardiac output state has been an infrequent but previously reversible cause of heart failure in patients with hemodialysis fistulas. A patient with two proximal upper extremity fistulas was found to have progressive depression in his left ventricular function and a high output state. His symptoms did not respond to the removal of the most prominent fistula, suggesting that chronic volume overload from the high output state may irreversibly depress left ventricular function.

Adult↗

Noninvasive detection of coronary artery patency using continuous ST-segment monitoring.

Continuous ST-segment Holter recordings were analyzed from 46 patients with acute myocardial infarction (AMI) receiving intracoronary streptokinase (SK) during the first 48 hours of hospitalization. Changes in ST deviation and the time periods of these changes were quantitated and correlated with angiographic evidence of reperfusion. Thirty-six patients had total occlusion of the infarct vessel and 10 had subtotal occlusion. Of the 36 vessels that were totally occluded, 19 were reperfused and 17 were not. In patients in whom reperfusion was successful, an ST steady state was achieved 55 +/- 32 minutes after SK administration. In patients in whom it was not successful, a steady state was achieved in 219 +/- 141 minutes (p less than 0.001). Achievement of steady state within 100 minutes after SK reperfusion indicated successful reperfusion with 89% sensitivity and 82% specificity. All patients with subtotal occlusion achieved an ST steady state before SK infusion. No patient with total occlusion achieved a steady state before SK. Achievement of ST steady state before SK infusion was 100% sensitive and 100% specific for subtotal occlusion at initial angiography. Continuous, quantitative ST-segment analysis is a sensitive and specific noninvasive technique for following coronary artery patency during AMI.

Coronary Vessels↗

Ventricular arrhythmias during reperfusion.

Accelerated idioventricular rhythm has been used as a marker for coronary reperfusion. The incidence of accelerated idioventricular rhythm and ventricular tachycardia was evaluated in 52 consecutive patients undergoing thrombolysis with intracoronary streptokinase during acute myocardial infarction. Complete 12-hour Holter recordings during and after intracoronary streptokinase were obtained in 39 patients. Reperfusion was documented in 17 patients (44%), no reperfusion in 14 (36%), and subtotal occlusion in eight (20%). Accelerated idioventricular rhythm occurred in 83%, 57%, and 63% of patients by group, respectively (p greater than 0.05). Ventricular tachycardia occurred in 100%, 71%, and 100% of patients by group, respectively (p less than 0.05). These data demonstrate that accelerated idioventricular rhythm is not specific for reperfusion and cannot be used as a marker for this event, and that ventricular tachycardia is more common with reperfusion and subtotal occlusion.

Cardiac Catheterization↗

The assessment of contractile reserve after thrombolytic therapy for acute myocardial infarction.

"Stunned" myocardium prevents the assessment of myocardial salvage after streptokinase. In order to unmask "stunning," we sought to evaluate left ventricular inotropic contractile reserve of patients after streptokinase. Radionuclide ventriculograms were obtained in 75 consecutive patients 2 weeks after myocardial infarction, at rest and during intravenous isoproterenol infusion. Resting and isoproterenol-stressed ejection fractions were compared in the patent and closed-infarct vessel groups. Although there was no difference in the resting ejection fractions between the patent group (0.48 +/- 0.02) and the closed group (0.48 +/- 0.02), isoproterenol increased the ejection fractions in the patent group (increase 0.14 +/- 0.01) significantly more than in the closed group (increase 0.06 +/- 0.01) (p less than 0.0001). Thus, despite identical resting ventricular function, the greater inotropic contractile reserve in the patent infarct vessel group suggests that restoration of blood flow in acute myocardial infarction salvages myocardium.

Adult↗

Determinants of cardiac failure after coronary bypass surgery within 30 days of acute myocardial infarction.

Timing of coronary artery bypass grafting after acute myocardial infarction (MI) is controversial, especially if myocardial function is depressed. Early coronary artery bypass grafting may result in reperfusion injury causing cardiac failure. Delay, however, may risk a second ischemic event. This study was performed to determine if four preoperative factors--time after MI, ejection fraction, ischemia (need for intravenous administration of nitroglycerin), and failure (need for inotropic support)--independently predict postoperative cardiac failure. Postoperative failure was defined as the need for inotropic support or intraaortic balloon pumping. The study group consisted of 145 patients who underwent isolated coronary artery bypass grafting between January, 1980, and July, 1985, within 4 weeks of an acute MI. Postoperatively 38 patients (26%) had cardiac failure. Five patients, all of whom had postoperative cardiac failure, died. Univariate and stepwise logistic regression analyses showed preoperative failure (p = .0001), ejection fraction less than 45% (p = .002), and preoperative ischemia (p = .02) were predictors of postoperative cardiac failure. Time after MI was not found to be an independent predictor (p = .96). We conclude that if ischemia or threatening coronary anatomy is present early after MI and clinical improvement is not occurring, operative intervention should be strongly considered at that time, as it does not appear that delay itself reduces the risk of cardiac failure and may risk a second ischemic event.

Coronary Artery Bypass↗

Energy dependent insulin binding, internalization and degradation in isolated cardiac myocytes from normal and diabetic rats.

Insulin binding to isolated cardiac myocytes from normal and streptozotocin-induced diabetic rats was investigated. We found that at high affinity sites, the maximum numbers of insulin binding sites per cell are 33 000 and 22 000 for normal and diabetic myocytes, respectively with no discernible difference in receptor affinity. However, since the yield of myocytes from the diabetic heart was only 1/3 of the normal heart, it is suspected that the insulin function in the diabetic heart may be significantly lower than that in the normal heart. Chloroquine was found to markedly decrease insulin degradation with concomitant increase in net insulin uptake by isolated myocytes. This suggests that insulin degradation may take place within lysosomes after insulin is internalized. To determine whether internalization of insulin in myocytes is an energy dependent process, insulin binding and subsequent degradation were assessed in cells depleted of ATP by treatment with various metabolic inhibitors (2,4-dinitrophenol, NaF and iodoacetic acid). Depletion of the cellular ATP level resulted in a decrease in both insulin uptake and degradation. In diabetic myocytes, the general relationship between cellular ATP level and insulin uptake and degradation was similar to that found in normal myocytes. However, in diabetic myocytes, the cellular ATP level and insulin uptake were lower, but insulin degradation was greater than in normal myocytes. Insulin uptake by normal and ATP depleted cells at 4 degrees C (16 h) was lower than at 37 degrees C (1 h), while the ATP level was almost the same at both temperatures. This suggests that the internalization of insulin is a temperature as well as an ATP dependent process.

Adenosine Triphosphate↗

Thrombolysis in acute myocardial infarction.

Emergency cardiac catheterization and angiography in patients have resulted in an appreciation of the pathogenesis of AMI and the efficacy of thrombolytic therapy. Simple reperfusion of the infarcted myocardium, however, does not necessarily guarantee myocardial salvage, and preliminary studies have been somewhat confusing as to its beneficial effects. Metabolic support of the ventricle during early reperfusion may enhance left ventricular performance. Although the potential effects of thrombolytic therapy are still unclear, the routine administration of these agents has resulted in more frequent performance of early coronary angiography, with the result that appropriate therapeutic decisions can be made immediately regarding medical treatment, coronary angioplasty, or complete myocardial revascularization. In fact, in prolonged chest pain syndromes, emergency angiography may play a very important role in establishing appropriate initial therapy early in the course of hospitalization, potentially lowering mortality, morbidity, and cost. These issues will be answered ultimately only by carefully designed long-term randomized trials.

Fibrinolytic Agents↗

Use of hemodynamic measurements for management of acute myocardial infarction.

The modern coronary care unit now can provide hemodynamic measurements that characterize the determinants of myocardial oxygen consumption and mechanical performance. These determinants of preload, afterload, contractile state, and heart rate can be obtained from measurements with the Swan-Ganz catheter, systemic blood pressure, assessment of ventricular function, and heart rate. With the hemodynamic characterization of the determinants of left ventricular function, drugs can be selected that either decrease or increase the specific determinants in order to optimize left ventricular performance. Thus, a physiologic approach can be taken to the pharmacologic management of patients with acute myocardial infarction based on hemodynamic measurements and appropriate therapeutic strategies.

Blood Pressure↗

Ischemia during angioplasty after streptokinase: a marker of myocardial salvage.

Although thrombolytic therapy can result in lysis of a coronary artery thrombus, salvage of myocardium as measured by enzymatic, electrocardiographic and regional wall motion evaluation has not been clearly documented. Many patients after successful reperfusion continue to experience recurrent chest pain. The presence of recurrent chest pain suggests salvaged myocardium. Controlled reocclusion of the infarct vessel with the use of coronary angioplasty may support evidence for myocardial salvage. Experience in 50 patients who underwent angioplasty was reviewed retrospectively. Sixteen of the 50 patients had electrocardiographic or clinical evidence of ischemia at the time of balloon inflation. Prospectively, all patients who underwent angioplasty after they had received streptokinase were evaluated, and 5 of 5 patients had chest pain and ST-segment elevation during balloon inflation. The development of ischemic changes during balloon catheter inflation suggests the presence of persistently viable, salvaged myocardium after successful thrombolysis.

Angioplasty, Balloon↗

Improved myocardial contractility with glucose-insulin-potassium infusion during pacing in coronary artery disease.

The metabolic and mechanical effects of a solution of glucose-insulin-potassium (G-I-K) were investigated in 18 patients who underwent diagnostic cardiac catheterization for coronary artery disease. All patients were paced at a rate of approximately 140 beats/min before and after infusion of G-I-K. Basal and paced left ventricular (LV) end-diastolic pressure, dP/dt, arterial substrate levels and osmolarity were measured in all 18 patients. In 13 patients cardiac index was also measured. In 5 patients arterial-coronary sinus measurements of oxygen, carbon dioxide, glucose, free fatty acids, lactate, alanine, glutamate, glutamine, ammonia and urea were made, in addition to coronary sinus blood flow. G-I-K increased the blood sugar level to approximately 200 mg/dl and raised the serum osmolarity 9 mosmol. Pacing alone raised the cardiac index 4% and pacing with G-I-K increased the cardiac index 6% (p less than 0.05). Pacing before G-I-K augmented dP/dt (21%) and pacing with G-I-K increased it (30%) (p less than 0.01). The metabolic changes noted included a shift in the respiratory quotient from 0.77 to 0.96 with G-I-K infusion (p less than 0.05). During G-I-K infusion the myocardial oxygen consumption at rest increased from 17.1 to 21.8 ml/min (23%, p less than 0.05). Myocardial oxygen consumption during pacing was similar before and after G-I-K infusion. Before G-I-K infusion nitrogen balance was slightly positive; after G-I-K infusion it was negative with regard to the nitrogen-containing compounds measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗