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Biomedical subjects

K F Browne

Publications and source records attributed to K F Browne.

36 records · Page 2Linked to original sources
PubMed1992

Adverse reactions of low osmolality contrast media during cardiac angiography: a prospective randomized multicenter study.

A multicenter study was performed to determine the incidence of adverse reactions to two contrast media with similar low osmolality during cardiac angiography. The study was of a randomized double-blind design comparing ioxaglate (an ionic dimer) and iopamidol (a nonionic compound) and included 500 patients; 250 patients received ioxaglate and 250 iopamidol. There were 58 adverse reactions attributed to the contrast media in the ioxaglate group and 29 in the iopamidol group (p less than 0.001). Chest pain occurred in 11 patients in the ioxaglate group compared with 5 in the iopamidol group (p = 0.123). Nausea or vomiting was present in 20 and 2 patients, respectively (p less than 0.0003). Allergic adverse reactions, such as bronchospasm, urticaria and itching, occurred in 15 of the ioxaglate group and only 1 of the patients receiving iopamidol (p less than 0.0007). Fifty-two patients in the ioxaglate group had a known allergic history (not to contrast medium) or asthma, whereas 77 receiving iopamidol had a similar history. Seven of the 52 ioxaglate-treated patients developed an allergic adverse reaction compared with none of the 77 in the iopamidol group (p = 0.001). Of 41 patients receiving ioxaglate who were premedicated with diphenhydramine, 4 had an allergic adverse event. In the iopamidol group 45 patients received similar premedication and none had an allergic adverse reaction (p less than 0.03). Thus, this multicenter study shows that adverse reactions occur more often with ioxaglate than with iopamidol and that patients with an allergic history have a greater risk with ioxaglate therapy compared with iopamidol.

Adult↗
PubMed1991

Five-hour balloon inflation to resolve recurrent reocclusion during coronary angioplasty.

A 63-year-old male presented with an acute inferior myocardial infarction with initial clinical reperfusion following thrombolysis. Due to recurrent reocclusion, emergency catheterization was performed, demonstrating a 90% stenosis in the mid right coronary artery. Angioplasty was complicated by multiple reocclusions, ultimately requiring 5-h autoperfusion balloon inflation to maintain patency.

Angioplasty, Balloon, Coronary↗
PubMed1991

Interventional cardiology techniques for coronary artery disease.

This review updates and extends observations made in this journal in March 1988. The focus then was on percutaneous transluminal coronary angioplasty and the clinical results of its practical application. A concern was expressed that science lagged in solving the major problems of rethrombosis and restenosis. The NHLBI Bypass Angioplasty Revascularization Investigation (BARI) study was still in the planning phase. In 1991, the scene has changed. Interventional cardiology now embraces a multitude of different catheter devices--angioplasty, atherectomy, laser, stents. Basic scientists are increasingly involved in addressing the restenosis issue. Our national heart meetings are increasingly oriented towards molecular biology approaches to solving the remaining problems. The BARI trial has nearly completed patient entry, and we eagerly await its results. The cardiologist and surgeon are faced with increasingly complex decisions with respect to interventional technologies, involving not only whether to use them, but which ones.

Angioplasty, Balloon, Coronary↗
PubMed1991

Multicenter patency trial of intravenous anistreplase compared with streptokinase in acute myocardial infarction. The TEAM-2 Study Investigators.

Thrombolytic therapy has been shown to improve clinical outcome when administered early after the onset of symptoms of acute myocardial infarction; the mechanism of benefit is believed to be reestablishment and maintenance of coronary artery patency. Anistreplase is a second generation thrombolytic agent that is easily administered and has a long duration of action. To compare anistreplase (30 units/2-5 min) and therapy with the Food and Drug Administration-approved regimen of intravenous streptokinase (1.5 million units/60 min), a randomized, double-blind, multicenter patency trial was undertaken in 370 patients less than 76 years of age with electrocardiographic ST segment elevation who could be treated within 4 hours of symptom onset. Coronary patency was determined by reading, in a blinded fashion, angiograms obtained early (90-240 minutes; mean, 140 minutes) and later (18-48 hours; mean, 28 hours) after beginning therapy. Early total patency (defined as Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion) was high after both anistreplase (132/183 = 72%) and streptokinase (129/176 = 73%) therapy, and overall patency patterns were similar, although patent arteries showed "complete" (grade 3) perfusion more often after anistreplase (83%) than streptokinase (72%) (p = 0.03). Similarly, residual coronary stenosis, determined quantitatively by a validated computer-assisted method, was slightly less in patent arteries early after anistreplase (mean stenosis diameter, 74.0%) than streptokinase (77.2%, p = 0.02). In patients with patent arteries without other early interventions, reocclusion risk within 1-2 days was defined angiographically and found to be very low (anistreplase = 1/96, streptokinase = 2/94). Average coronary perfusion grade was greater, and percent residual stenosis was less, at follow-up than on initial evaluation and did not differ between treatment groups. Enzymatic and electrocardiographic evolution was not significantly different in the two groups. Despite rapid injection, anistreplase was associated with only a small (4-5 mm Hg), transient (at 5-10 minutes) mean differential fall in blood pressure. In-hospital mortality rates were comparable for anistreplase and streptokinase (5.9%, 7.1%). Stroke occurred in one (0.5%) and three (1.6%) patients, respectively; one stroke was hemorrhagic. Other serious bleeding events and adverse experiences occurred uncommonly and with similar frequency in the two groups. Thus, for the end points of our study (patency, safety), anistreplase and streptokinase showed overall favorable and relatively comparable outcomes, with a few differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Anistreplase↗
PubMed1989

Acute reocclusion during percutaneous transluminal coronary angioplasty: immediate and long-term outcome.

Acute total occlusion of a coronary artery during percutaneous transluminal coronary angioplasty (PTCA) has previously resulted in emergency surgical intervention (CABG). We retrospectively surveyed 211 elective procedures and 65 procedures for acute myocardial infarction (AMI). There were 42 patients (pts) [29 elective (14%) and 13 AMI (20%)] in whom total occlusion occurred after initial dilation had been achieved. In 30 of 42 pts reangioplasty successfully reperfused the vessel. Ten patients (24%) required CABG and two (5%) were treated medically for AMI. Death occurred in 2 pts due to irreversible cardiogenic shock despite successful angioplasty. After 6 months follow-up 22 pts remained asymptomatic. It is concluded that aggressive redilation of total occlusions which develop during PTCA will frequently result in a successful angioplasty with a long-term restenosis rate comparable to uncomplicated angioplasty.

Adult↗
PubMed1988

Multicenter reperfusion trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: controlled comparison with intracoronary streptokinase.

The recent establishment of a firm therapeutic role for reperfusion in acute myocardial infarction has stimulated interest in the development of more ideal thrombolytic agents. Anisoylated plasminogen streptokinase activator complex (APSAC) is a new plasminogen activator possessing properties that are promising for intravenous thrombolytic application in acute myocardial infarction. To assess the reperfusion potential of intravenous APSAC, a multi-center, angiographically controlled reperfusion trial was performed. An approved thrombolytic regimen of intracoronary streptokinase served as a control. Consenting patients with clinical and electrocardiographic signs of acute myocardial infarction were studied angiographically and 240 qualifying patients with documented coronary occlusion (flow grade 0 or 1) were randomized to treatment in less than 6 h of symptom onset (mean 3.4 h, range 0.4 to 6.0) with either intravenous APSAC (30 U in 2 to 4 min) or intracoronary streptokinase (160,000 U over 60 min). Both groups also received heparin for greater than or equal to 24 h. Reperfusion was evaluated angiographically over 90 min and success was defined as advancement of grade 0 or 1 to grade 2 or 3 flow. Rates of reperfusion for the two treatment regimens were 51% (59 of 115) at 90 min after intravenous APSAC and 60% (67 of 111) after 60 min of intracoronary streptokinase (p less than or equal to 0.18). Reperfusion at any time within the 90 min was observed in 55 and 64%, respectively (p less than or equal to 0.16). Time to reperfusion occurred at 43 +/- 23 min after intravenous and 31 +/- 17 min after intracoronary therapy. The success of intravenous therapy was dependent on the time to treatment: 60% of APSAC patients treated within 4 h exhibited reperfusion compared with 33% of those treated after 4 h (p less than or equal to 0.01). Reperfusion rates were also dependent on initial flow grade (p less than or equal to 0.0001): 48% (81 of 168) for grade 0 (APSAC = 43%, streptokinase = 54%), but 78% for grade 1 (APSAC = 78%, streptokinase = 77%). APSAC given as a rapid injection was generally well tolerated, although the median change in blood pressure at 2 to 4 min was greater after APSAC than after streptokinase (-10 versus -5 mm Hg). Mean plasma fibrogen levels fell more at 90 min after the sixfold higher dose of APSAC than after streptokinase (to 32 versus 64% of control). Reported bleeding events were more frequent after APSAC but occurred primarily at the site of catheter insertion and no event was intracranial.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Electrophysiologic effects and clinical efficacy of oral propafenone therapy in patients with ventricular tachycardia.

The effects of the antiarrhythmic agent propafenone were evaluated in 25 patients with recurrent symptomatic ventricular tachycardia. Oral propafenone was given to a maximal dose of 300 mg every 8 hours. Ten of the 25 patients developed side effects or had inadequate suppression of spontaneous ventricular arrhythmias during propafenone therapy. Electrophysiologic studies were performed before and during drug therapy on the 15 patients who had a satisfactory clinical response. Propafenone increased the PR interval from 168 +/- 46 to 188 +/- 25 ms (p less than 0.007), the HV interval from 47 +/- 10 to 65 +/- 13 ms (p less than 0.005), the shortest atrial pacing cycle length to maintain 1:1 atrioventricular (AV) nodal conduction from 385 +/- 44 to 436 +/- 42 ms (p less than 0.005), the ventricular effective refractory period from 231 +/- 17 to 255 +/- 19 ms (p less than 0.001) and the ventricular functional refractory period from 260 +/- 15 to 278 +/- 17 ms (p less than 0.002). Before propafenone therapy, all 15 patients had ventricular tachycardia induced by programmed ventricular stimulation. During propafenone treatment, 12 patients still had ventricular tachycardia induced, and the tachycardia cycle length significantly increased from 236 +/- 44 to 374 +/- 103 ms (p less than 0.001). Ten patients were considered to have satisfactory electrophysiologic response to propafenone on the basis of either the inability to initiate ventricular tachycardia or a marked increase in ventricular tachycardia cycle length associated with lack of symptoms during the induced tachycardia. These patients were discharged receiving propafenone.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Functional bundle branch block: discordant response of right and left bundle branches to changes in heart rate.

Faster heart rates shorten refractoriness more in some tissues than in others. This study investigates whether faster heart rates shorten relative refractoriness more in the right than left bundle branch in humans. Premature atrial stimulation at 2 or more basic cycle lengths was performed in 314 patients with no evidence of atrioventricular conduction system disease. In 10 patients, both functional right and left bundle branch block (BBB) developed with premature atrial stimulation. Functional right BBB occurred at the longer basic cycle length, and functional left BBB at the shorter cycle length in 8 patients. In 2 patients functional right and functional left BBB were present at the same cycle length, but functional left BBB occurred at a shorter premature atrial coupling interval. For all patients, the mean functional right bundle branch relative refractoriness was 438 ms at a basic cycle length of 847 ms, and functional left bundle branch relative refractoriness was 357 ms at a cycle length of 622 ms (p less than 0.01). The HV interval was 45 +/- 15 ms at control and increased with functional left BBB to 77 +/- 19 ms (p less than 0.01), but not with functional right BBB. Thus, relative refractoriness of the right and left bundle branches are rate-dependent and discordant. At longer cycle lengths, relative refractoriness of the right bundle branch is greater than that of the left bundle branch, and at shorter cycle lengths relative refractoriness of the left bundle branch is greater than that of the right bundle branch. The relative refractory period curves "cross over" and can explain the presence of both functional right and left BBB in the same patient.

Adolescent↗
PubMed1984

Prolongation of the QT interval induced by probucol: demonstration of a method for determining QT interval change induced by a drug.

Sudden death has occurred in monkeys fed large doses of probucol, a cholesterol-lowering drug, given in combination with an atherogenic diet. These monkeys develop prolonged QT intervals and high serum levels of probucol. We investigated the effect of probucol on QT interval and the incidence of ventricular ectopy during a double-blind placebo-controlled study in 16 patients with less than 600 premature ventricular complexes (PVCs) per day and a corrected QT interval of less than 0.44 second. Seven patients received probucol and nine patients received placebo. Three 24-hour continuous ECG recordings were obtained prior to entry into the study and three additional recordings were obtained after 6 months of drug or placebo therapy. A 15-second ECG tracing was sampled from the continuous ECG recording every 30 minutes and, for the group, 15,000 QT intervals were measured permitting construction of QT versus R-R regression lines for each patient before and during therapy. Comparison of the regression lines revealed that the measured QT interval prolonged 20 +/- 18 msec during the awake state and 24 +/- 20 msec during sleep (mean + standard deviation) at matched heart rates in the seven patients receiving probucol (p less than 0.01). Using Bazett's formula to correct for rate, corrected QT interval prolonged 22 +/- 23 msec in the awake state and 20 +/- 18 msec in the asleep state (p less than 0.01). In probucol treated patients QT interval prolongation was directly related to increasing probucol plasma levels (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Clinical efficacy and electrophysiologic effects of cibenzoline therapy in patients with ventricular arrhythmias.

Cibenzoline, a new antiarrhythmic agent, was tested in 26 patients who had symptomatic ventricular tachycardia (24 patients) or premature ventricular complexes (2 patients) unresponsive to conventional drugs. Cibenzoline was given orally every 8 hours to maximal doses of 65 mg in 2 patients, 81.25 mg in 22 patients and 97.5 mg in 2 patients. Cibenzoline abolished spontaneous episodes of ventricular tachycardia in 8 of 16 patients with ventricular tachycardia during a 72 hour control electrocardiographic recording, and 7 of 22 patients had greater than 83% decrease in premature ventricular complexes compared with control. The PR interval increased 14% (p less than 0.001), QRS duration increased 17% (p less than 0.001), QT interval did not change and mean ejection fraction in 10 patients did not change. Electrophysiologic studies were performed on 10 patients in the control period and during maximal cibenzoline dosage. Cibenzoline did not affect electrophysiologic properties of the atrium or atrioventricular (AV) node. It prolonged the ventricular effective (223 +/- 16 to 241 +/- 22 ms, p less than 0.02) and functional (247 +/- 18 to 264 +/- 25 ms, p less than 0.02) refractory periods. At control electrophysiologic studies, ventricular tachycardia was induced in 9 of 10 patients (mean cycle length 210 +/- 31 ms). Cibenzoline therapy prevented ventricular tachycardia induction in two patients, and in the other seven patients the mean ventricular tachycardia cycle length increased from 210 to 260 ms. The one patient with no ventricular arrhythmia induced during the control study still had no arrhythmia induced while receiving cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Pseudobacteremia traced to cross-contamination by an automated blood culture analyzer.

Twenty-three episodes of pseudobacteremia occurring over a seven-month period were traced to cross-contamination by the automated blood culture analyzer (BACTEC 460) used in the microbiology laboratory. An epidemiologic investigation of an unusual cluster of three patients with pseudobacteremia caused by oxacillin-resistant Staphylococcus aureus led to the identification of the problem. Mock trials of the blood culture procedure confirmed that the blood culture analyzer was the source of contamination. After the needle sterilizer was replaced by the manufacturer, the problem of cross-contamination abated. Contamination of sterile blood cultures by an instrument intended to identify bacteremia rapidly may lead to incorrect diagnosis, unnecessary administration of antibiotics and prolonged hospitalization. Because of the widespread use of automated blood culture analyzers in the US, physicians, microbiologists, and infection control personnel should be alert to the possibility of cross-contamination and the subtle way in which it may present.

Blood↗
PubMed1983

Prolongation of the Q-T interval in man during sleep.

Parasympathetic blockade shortens the duration of the Q-T interval and ventricular effective refractory period independent of heart rate change. Since relative parasympathetic effect increases during sleep, it was determined whether sleep was associated with a change in the Q-T interval. Fifteen patients receiving no drugs underwent 3 to 6 days of continuous electrocardiographic recordings. Tracings were sampled every 30 minutes and recorded at a paper speed of 25 mm/s. This provided 12,000 Q-T and R-R intervals that were measured. Comparison of R-R intervals that had similar durations during sleep and awake states revealed that the duration of the Q-T interval was longer during sleep in all 15 patients (p less than 0.001). Eight patients had sufficient range of overlap of R-R intervals to compare linear regression lines of Q-T intervals recorded while awake with Q-T intervals recorded while asleep. The regression lines during sleep exhibited a mean intercept change of 38 +/- 37 ms and mean slope change of -0.021 +/- 0.040 ms when compared with the regression lines during the awake state. The difference in Q-T interval between awake and sleep states was 19 +/- 7 ms when calculated at a heart rate of 60 beats/min. These statistical comparisons of the relationship of the Q-T interval to R-R interval indicate that the Q-T interval is longer during sleep than during the awake state at the same heart rate. Prolongation of the Q-T interval during sleep may reflect increased vagal tone or sympathetic withdrawal. These changes in repolarization may be related to the diurnal variation of some ventricular arrhythmias.

Adult↗
PubMed1983

Intracardiac recording by catheter electrode of accessory pathway depolarization.

At electrophysiologic study in a patient with the Wolff-Parkinson-White syndrome, intracardiac catheter recordings demonstrated a deflection that occurred 30 ms before ventricular activation. The rapid deflection was present during ventricular preexcitation but not during normal atrioventricular conduction. All QRS complexes were preexcited to varying degrees during atrial fibrillation, yet the deflection consistently preceded ventricular activation by 30 ms. This deflection most likely represents the rare recording of a Kent bundle depolarization with an intracardiac electrode catheter.

Adult↗
PubMed1983

Modulation of the Q-T interval by the autonomic nervous system.

Recent investigations have clarified some of the effects of the autonomic nervous system on duration and spatial distribution of the Q-T interval in humans. The use of atrial pacing to fix heart rate or 24-hour continuous electrocardiographic recording to develop a regression formula for individual patients has provided a means to interpret the effects of an intervention that alters both the heart rate and the Q-T interval. Drugs that affect the autonomic nervous system can influence Q-T interval directly or by changing rate. Bazett's formula to correct for rate may be misleading after certain drug interventions. For example, the Q-T interval during sinus rhythm or atrial pacing and the ventricular effective refractory period shorten after atropine plus propranolol, but corrected Q-T interval using Bazett's formula does not change. No change occurs in the Q-T interval during sinus rhythm or atrial pacing, or in ventricular effective refractory period after administration of propranolol although corrected Q-T interval using Bazett's formula markedly shortens. Q-T interval during sinus rhythm and atrial pacing and ventricular effective refractory period decrease after atropine but correct Q-T interval lengthens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Intra-aortic balloon counterpulsation in an experimental model of myocardial infarction.

The efficacy of intra-aortic balloon counterpulsation for heart failure during acute myocardial infarction has been controversial, and early intervention has been suggested as crucial. We have examined this type of therapy in the intact anesthetized dog during complete occlusion of the proximal left anterior descending coronary artery with a balloon-tipped catheter. Group 1 (n = 8) represented untreated animals undergoing four hours of ischemia. Group 2 (n = 7) consisted of animals undergoing counterpulsation with an intra-aortic balloon after 15 minutes of ischemia. Initially, stroke volume and the mean rate of left ventricular fiber shortening were similarly diminished in both groups, while filling pressure rose proportionately. After four hours, the mean rate of fiber shortening, stroke volume, and left ventricular filling pressure rose to a greater extent in untreated compared to treated animals (p less than 0.01). The degree of swelling in ischemic tissue and the number of sites with ST-segment elevation and their sums were comparable in the two groups. Thus, intra-aortic counterpulsation applied early in the course of ischemia can improve global left ventricular dysfunction without affecting the extent of myocardial injury.

Animals↗
PubMed1982

Clinical transvenous cardioversion of recurrent life-threatening ventricular tachyarrhythmias: low energy synchronized cardioversion of ventricular tachycardia and termination of ventricular fibrillation in patients using a catheter electrode.

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was less than or equal to 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks less than or equal to 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.

Aged↗