Search PubMed⌕ Search

Biomedical subjects

K M Kessler

Publications and source records attributed to K M Kessler.

At least 127 records · Page 7Linked to original sources
PubMed1984

Abnormal quinidine binding in survivors of prehospital cardiac arrest.

Quinidine binding was studied in 15 survivors of prehospital cardiac arrest and was compared to 18 normal individuals and 20 patients with coronary artery disease. The unbound quinidine fraction was 6.3 +/- 2.8% in the survivors of prehospital cardiac arrest, a value significantly lower than normal individuals (unbound quinidine fraction = 9.9 +/- 3.0%, p less than 0.005). Furthermore, unbound quinidine fraction correlated with interdose quinidine half-life in the six survivors of prehospital cardiac arrest where this could be measured (r = 0.79, p less than 0.05). The resultant quinidine interdose half-life was significantly prolonged (10 +/- 3 hours) when compared to normal (6 +/- 2 hours, p less than 0.02). The reduction in free drug fraction in cardiac arrest survivors was a nonspecific finding in that free drug fraction was also reduced in the patients with coronary artery disease (unbound quinidine fraction = 7.4 +/- 3%) and was independent of the alpha-1-glycoprotein concentration. Therefore survivors of prehospital cardiac arrest have a mean 40% reduction in free quinidine drug fraction which results in less free drug at any given total drug concentration and may relate to quinidine pharmacokinetics and pharmacodynamics in this patient group.

Blood Proteins↗
PubMed1984

Outcome of resuscitation from bradyarrhythmic or asystolic prehospital cardiac arrest.

Previous studies of outcome as a function of the initial electrophysiologic mechanisms recorded at the scene of prehospital cardiac arrest have demonstrated that bradyarrhythmias and asystole have the worst prognosis. In this report, our observations in bradyarrhythmic and asystolic arrests occurring from 1980 to 1982 are compared with those from 1975 to 1978. From 1980 to 1982, 61 (27%) of 225 cardiac arrest events meeting entry criteria for the study were bradyarrhythmic or asystolic. Only 2 (8%) of 24 patients with asystole and 1 (20%) of 5 patients with sinus bradycardia survived prehospital intervention. Only 1 of these 29 patients was discharged from the hospital alive. In contrast, 15 (47%) of 32 patients who presented with idioventricular rhythm at initial contact survived prehospital intervention and were hospitalized, and 8 (25%) of these 32 were ultimately discharged alive. When compared with the 1975 to 1978 patients with bradyarrhythmia and asystole, both prehospital survival (8 versus 30%, p less than 0.001) and survival after hospitalization (0 versus 15%, p less than 0.05) significantly improved, but the improvement occurred predominantly in the subgroup with idioventricular rhythm. Survivors within this subgroup tended to have a prompt response to prehospital pharmacologic interventions that were not available to the 1975 to 1978 group. The response was manifested by return to a sinus mechanism or increase in the rate of idioventricular rhythm. In conclusion, outcome has improved for a specific subgroup of victims of prehospital cardiac arrest with bradyarrhythmia or asystole; the improved outcome may relate to field interventions by rescue personnel at the scene of arrest but the mortality rate is still high.

Adult↗
PubMed1984

Dynamic variability of binding of antiarrhythmic drugs during the evolution of acute myocardial infarction.

We tested the hypothesis that the changes in free fatty acid and alpha 1-glycoprotein concentrations, which occur during acute myocardial infarction, exert asynchronous and opposing influences on the serum protein binding of selected drugs. Free drug fractions of two antiarrhythmic agents with contrasting binding characteristics, quinidine and procainamide, were related to free fatty acid and alpha 1-glycoprotein concentrations on days 1 through 5 and 10 in 20 patients with acute myocardial infarction. The mean free quinidine fraction was elevated on day 1 (9.0 +/- 4.4% vs 6.7 +/- 2.7% in patients with stable heart disease; p less than .05) and fell progressively to day 10 (4.0 +/- 2.8%; p less than .0002) as free fatty acid concentration decreased (day 1 = 464 +/- 272 meq/liter; day 10 = 264 +/- 155 meq/liter; p less than .01) and alpha 1-glycoprotein concentration increased (day 1 = 98 +/- 31 mg/dl; day 10 = 141 +/- 47 mg/dl; p less than .02). Multiple stepwise regression showed a major influence of changing alpha 1-glycoprotein concentration on the observed sequential changes in the free quinidine fraction (p less than .005). In contrast, no serial changes in procainamide binding were noted. In conclusion, metabolic changes during the course of acute myocardial infarction sequentially alter free quinidine fraction and, consequently, may influence pharmacodynamics.

Aged↗
PubMed1984

Long-term survival after prehospital cardiac arrest: analysis of outcome during an 8 year study.

We analyzed long-term follow-up data accumulated during an 8 year study of survivors of prehospital cardiac arrest. All patients included in this study were primary entrants via community-based rescue systems; patients who were tertiary referrals (survivors of cardiac arrest from other hospitals) were not included in this analysis. In the group of 61 patients entering our study between 1975 and 1980, with a follow-up to 1983, there have been a total of 24 deaths (39%). Sixteen of the 24 deaths were the result of recurrent cardiac arrest; eight were nonsudden cardiac deaths or noncardiac deaths. The mean duration from entry to death in the nonsurvivors was 27.5 +/- 19.7 months, and the time from the index event to last follow-up in the long-term survivors was 59.9 +/- 19.4 months. Life table analysis demonstrated a 10% rate of recurrence of cardiac arrest in the first year, with a 5% per year rate in each of the subsequent 3 years. Left ventricular ejection fractions at entry were not significantly different between survivors (mean = 45.3 +/- 13.6%) and nonsurvivors (mean = 37.6 +/- 12.6%), and the severity of ejection fraction abnormality at entry did not correlate with time to death in the nonsurvivors. However, ejection fraction was significantly lower in patients who died from causes other than recurrent cardiac arrest than in those who died of cardiac arrest (24.5 +/- 9.1% vs 42.7 +/- 9.2%; p less than .002).(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1983

Congestive heart failure: echocardiographic insights.

This study was designed to assess the role of echocardiography in the evaluation and management of patients with the congestive heart failure syndrome. Fifty consecutive patients with congestive heart failure referred for echocardiography were evaluated. Thirty patients (60 percent) had ejection fractions under 50 percent (mean +/- SD 30 +/- 9 percent), left ventricular dilatation (6.5 +/- 0.7 cm), and normal wall thicknesses (1.0 +/- 0.2 cm). The echocardiographic findings were predictable on clinical grounds in 18 of the 30 patients (60 percent) and worse than clinically expected in 12 patients (40 percent). Management changes after echocardiography were indicated in 11 of 30 patients (37 percent). The remaining 20 of the 50-patient cohort (40 percent) had ejection fractions above 50 percent (mean 70 +/- 9 percent, p less than 0.01), and, as a group, were characterized by normal left ventricular size (5.1 +/- 0.8 cm, p less than 0.01) and borderline wall thicknesses (1.1 +/- 0.2 cm, p less than 0.01). The largest subgroup of these 20 patients had hypertensive heart disease (seven patients, 35 percent) associated with the congestive heart failure syndrome presumably related to left ventricular diastolic (compliance) dysfunction. The normal ejection fraction was unexpected clinically in 18 of these 20 patients (90 percent). Recommended management after echocardiography changed in all 18 patients. Since standard clinical findings (history, physical examination, and chest roentgenography) failed to separate patients with normal and abnormal ejection fractions, or those in need of changes in management, echocardiography was a useful and, at times, essential part of the evaluation of these patients with the congestive heart failure syndrome.

Adult↗
PubMed1983

Determinants of recurrent atrial flutter after cardioversion.

Eighteen male patients (mean age 59 years) who were electrically cardioverted for pure atrial flutter were retrospectively studied to determine those factors influencing the maintenance of regular sinus rhythm or reversion to atrial flutter. Six months after successful cardioversion, 10 patients (55%) had recurrent atrial flutter and eight patients (45%) were still in sinus rhythm. The two groups were not significantly different with respect to age, symptomatology, abnormalities on the 12 lead electrocardiogram (during sinus rhythm), or the administration of digoxin and a class Ia antiarrhythmic agent (after cardioversion). There was a trend for those patients with recurrent atrial flutter to have a higher incidence of underlying heart disease and previous episodes of atrial flutter than the non-recurrent group. There were statistically significant differences between the recurrent and non-recurrent groups with respect to echocardiographically determined left atrial size and left ventricular ejection fraction. Patients with a left atrial size greater than 45 mm or with an ejection fraction less than 45% were all at high risk for recurrent atrial flutter after successful cardioversion.

Aged↗
PubMed1982

Evolving concepts of management of stable and potentially lethal arrhythmias.

Recent studies indicate that the eradication of premature ventricular complexes (PVCs) by antiarrhythmic agents is an inadequate end point for estimating long-term protection against potentially lethal arrhythmias. In a study of survivors of prehospital ventricular fibrillation (VF), who have a 30% risk for recurrent VF during the first year of follow-up, we observed an apparent protection against recurrent VF by antiarrhythmic agents even if chronic PVCs were not suppressed by stable therapeutic plasma levels. To expand the data base pertinent to the relationships between PVCs and advanced arrhythmias, we studied six patients with chronic recurrent ventricular tachycardia (VT) and frequent PVCs between episodes of VT. Plasma levels of procainamide (PA) required to protect against recurrent VT averaged 9.4 +/- 3.4 microgram ml, compared with mean levels of 14.9 +/- 3.8 microgram/ml for 85% suppression of PVCs (p less than 0.01). PVC frequency decreased by a mean of only 36% (range -11% to -63%) at plasma levels of PA sufficient to prevent spontaneous VT. Concentration-response relationships between (PA) and PVC suppression were also compared in patients with PVCs during acute myocardial infarction and in patients with PVCs in stable chronic ischemic heart disease. In the former group of patients the mean plasma level of PA required to suppress 85% of the PVCs was 5.0 +/- 0.5 microgram/ml, and in the latter group was 9.3 +/- 0.7 microgram/ml (p less than 0.001). We conclude that the relationship between plasma levels of PA and PVC suppression is different in the two groups of patients, and furthermore, that a high degree of PVC suppression may not be a necessary end point for protecting patients against symptomatic recurrent VT or VF.

Arrhythmias, Cardiac↗