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Biomedical subjects

M Hodges

Publications and source records attributed to M Hodges.

At least 73 records · Page 4Linked to original sources
PubMed1990

A comparison of antiarrhythmic drugs for the suppression of ventricular ectopic depolarizations: a meta-analysis.

This article reports the results of a meta-analysis of the effectiveness of antiarrhythmic drugs for the suppression of ventricular ectopic depolarizations. We analyzed 97 published articles that referred to a total of 27 drugs and contained data from 2989 patient-treatment trials; our goal was to determine the number of patients responding to therapy, defined as greater than or equal to 80% suppression of ventricular ectopic depolarizations. By means of logistic regression we tested the effect of 10 clinical and experimental variables on the likelihood of response to therapy. The likelihood of a drug response was significantly affected by the following six variables: increased by the use of dose titration (t = 3.59, p less than 0.0001), increased by the use of a higher daily dose (t = 3.21, p less than 0.0001), decreased by older age (t-2.67, p = 0.004), decreased by the use of blinding (t = -2.28, p = 0.011), increased by treating more male patients (t = 1.72, p = 0.043), and decreased by the presence of cardiovascular disease (t = -1.52, p = 0.064). Incorporating these six variables into our logistic regression model, we adjusted the response rate in each published study and calculated the mean response and standard error for each drug. Of the drugs tested in at least 100 patients, the most effective were amiodarone (estimated response rate 90%), encainide (80%), flecainide (79%), and propafenone (74%). Class IC drugs were significantly more effective than class IB and II drugs (p less than 0.05). With the exception of lorcainide and moricizine, class IC drugs were also more effective than class IA drugs (p less than 0.05). Amiodarone was significantly more effective than all drugs except encainide and flecainide (p less than 0.05). We found no significant differences among the response rates to class IA, IB, and II drugs. Whereas several patient and study characteristics affect the likelihood of response to antiarrhythmic drugs, class IC drugs and amiodarone are significantly more effective than other drugs in suppressing ventricular ectopic depolarizations.

Anti-Arrhythmia Agents↗
PubMed1990

Thrombolysis in Myocardial Infarction (TIMI) phase II trial: outcome comparison of a "conservative strategy" in community versus tertiary hospitals. The TIMI Research Group.

In the conservative strategy arm of phase II of the Thrombolysis in Myocardial Infarction (TIMI) trial, 1,461 patients were treated with intravenous recombinant tissue-type plasminogen activator (rt-PA). Coronary angiography, with angioplasty if feasible, was to be performed only for recurrent spontaneous or exercise-induced ischemia. In this study results in patients treated by this strategy in community and tertiary hospitals are compared. Despite similar baseline findings in the two groups, coronary angiography was performed within 42 days in more patients (542 [48%] of 1,155) initially admitted to a tertiary hospital (on-site coronary angiography/angioplasty available) than in those (94 [32%] of 306) admitted to a community hospital (transfer to tertiary hospital for coronary angiography/angioplasty) (p less than 0.001). This different approach resulted in a greater use of coronary angioplasty (203 [18%] of 1,155 versus 32 [11%] of 306, p less than 0.01), coronary artery bypass surgery (133 [12%] of 1,155 versus 23 [8%] of 306, p less than 0.05) and blood transfusions (139 [12%] of 1,155 versus 17 [5.5%] of 306, p less than 0.001) in patients admitted to a tertiary than to a community hospital. However, there were no significant differences between the two groups in mortality, recurrent myocardial infarction or left ventricular function. These results demonstrate that a conservative strategy after treatment of acute myocardial infarction with rt-PA is applicable in the community hospital setting.

Angioplasty, Balloon, Coronary↗
PubMed1989

An analysis of time delays preceding thrombolysis for acute myocardial infarction.

For a patient to derive maximal benefit from intravenous thrombolytic therapy for acute myocardial infarction, early treatment is essential. As part of the Thrombolysis in Myocardial Infarction II trial, this study investigated the time delays that preceded treatment of 236 consecutive patients with intravenous tissue-plasminogen activator (TPA) during acute myocardial infarction. The average (+/- SD) time from the onset of symptoms to treatment with TPA was 153 +/- 54 minutes. After arrival in the emergency department, patients waited an average of 19.9 +/- 17.8 minutes for the initial electrocardiogram. Following the diagnosis of acute myocardial infarction by electrocardiogram, an additional 70 +/- 40 minutes elapsed before thrombolytic therapy began. The interval between the initial electrocardiogram and initiation of treatment with TPA was less when the drug was first administered in the emergency department (46.8 +/- 23.4 minutes) rather than after transfer to the coronary care unit (82.1 +/- 34.7 minutes). In-hospital delays at the two academic and two private hospitals accounted for more than half of the total time from the onset of symptoms to initiation of thrombolytic therapy. We conclude that significant in-hospital delays are likely to occur before a patient receives thrombolytic therapy for acute myocardial infarction. Various factors conspire to create these delays, but a well-organized team approach to treatment will help to minimize delays in the implementation of this new form of therapy.

Adult↗
PubMed1988

Serial changes in left ventricular wall motion by two-dimensional echocardiography following anterior myocardial infarction.

To evaluate the time course of spontaneous changes in wall motion following anterior infarction, we prospectively performed serial apical four-chamber two-dimensional echocardiography on 45 consecutive long-term survivors of initial transmural anterior infarction. Studies were performed on admission (1 +/- 1 days), 1 week after admission (6 +/- 2 days), at discharge (15 +/- 8 days), and at long-term follow-up (235 +/- 186 days). Ventricular size was expressed as end-diastolic area in square centimeters. Wall motion for this tomographic section was evaluated as the percent change in left ventricular area from end diastole to end systole (% LVA). Patients were grouped on the basis of significant differences for %LVA between the first and fourth studies. Group I (n = 14) had improved wall motion (23 +/- 5% to 38 +/- 9%); group II (n = 23) did not change (22 +/- 9% to 23 +/- 11%); and group III (n = 8) had worsened wall motion (28 +/- 6% to 18 +/- 7%). End-diastolic area did not change over the study period for groups I and II but increased significantly for group III (30 +/- 6 to 35 +/- 4 cm2, p less than 0.05). Most of the increase in end-diastolic area for group III was between the third and fourth study. The percent improvement (%IMP) in wall motion for patients in group I who did not have ventricular fibrillation outside the hospital expressed in days (t) following infarction fit an exponential curve (%IMP = 100-100e-(.108t) that predicts that 70% of eventual recovery will occur in the first 15 days post-infarction. We conclude that changes in left ventricular size and wall motion occur following anterior infarction with improvement or worsening occurring spontaneously in some patients. If improvement occurs, it should be evident within 2 weeks of infarction; infarct expansion in this select group of long-term survivors occurred primarily after discharge.

Clinical Enzyme Tests↗
PubMed1988

Encainide-induced hyperglycemia.

Twenty-three patients were treated for at least one month with encainide, a new antiarrhythmic drug. No patient was treated for hyperglycemia prior to encainide therapy. During encainide administration, five episodes of marked hyperglycemia (serum glucose level greater than or equal to 200 mg/dl) developed in four patients. (One patient received encainide twice.) The mean pretreatment glucose level was 190 +/- 69 mg/dl and rose to 397 +/- 163 mg/dl after one month of encainide therapy in patients in whom hyperglycemia developed (p less than 0.025). The glucose level was 111 +/- 27 mg/dl in nonhyperglycemic patients before encainide administration and 108 +/- 22 mg/dl after one month of encainide therapy (p = NS). There was no difference in age or encainide dosage between hyperglycemic and nonhyperglycemic patients. Treatment for hyperglycemia was given during four of the five encainide treatment periods in hyperglycemic patients. Encainide was discontinued in each of the five hyperglycemic episodes; therapeutic requirements for hyperglycemia markedly decreased. Hypoglycemic reactions to insulin occurred in two patients when encainide was stopped. Thus, encainide exacerbates hyperglycemia in some patients. These patients usually have mild hyperglycemia not requiring therapy before administration of encainide but may require insulin while receiving encainide. Treatment requirements for hyperglycemia decrease following withdrawal of encainide. The mechanism of this effect and the consequences of long-term encainide therapy on glucose metabolism are unknown.

Aged↗
PubMed1988

Increasing precordial QRS voltage correlates with improvement in left ventricular function following anterior myocardial infarction.

To evaluate whether changes in QRS voltage reflect changes in left ventricular function after myocardial infarction, 28 patients were studied following anterior myocardial infarction. Two-dimensional echocardiograms and 12-lead electrocardiograms were obtained during the acute phase of the infarction and again after at least 30 days of recovery (mean, 8 +/- 8 months). At follow-up, 11 patients (group A) showed improvement in left ventricular systolic function; 9 had increased net QRS voltage in V1-6 and 8 in V1-4. No improvement in ventricular function was found in 17 patients (group B); 7 had increased QRS voltage in V1-6 (p less than 0.05 vs group A) and only 5 in V1-4 (p less than 0.05 vs group A). For detection of improved left ventricular function, the sensitivity, specificity, and predictive value of the change in net QRS voltage for leads V1-6 was 82%, 59%, and 56% respectively, and for leads V1-4 was 73%, 71%, and 62% respectively. Neither R wave voltage, Q wave voltage, nor the total number of Q waves was reliable for identifying patients with improving left ventricular function. Thus, increasing net QRS voltage in the precordial electrocardiographic leads during long-term follow-up after anterior myocardial infarction correlates with and has a reasonable sensitivity for detection of improvement in left ventricular systolic performance.

Adult↗
PubMed1988

Indecainide for treatment of ventricular ectopic depolarizations: efficacy, pharmacokinetics, hemodynamic effects and safety.

Ten patients were treated with oral indecainide for frequent ventricular ectopic depolarizations during a short-term, dose-ranging, single blind inpatient trial followed by open label long-term therapy for 2 years. During dose ranging, patients received placebo followed by 50, 75 and 100 mg of indecainide three times daily. Eight of the 10 patients achieved greater than or equal to 80% reduction in ventricular ectopic depolarizations during inpatient therapy. Mean ventricular ectopic depolarizations decreased from 15,792/24 h to 2,357/24 h on optimal dosage (p less than 0.01). Nine patients had paired ventricular ectopic depolarizations; four of the nine had greater than or equal to 99% reduction of these beats. Among seven patients with nonsustained ventricular tachycardia, five had 100% elimination of these events with indecainide and all had greater than or equal to 90% reduction in these events. Indecainide prolonged the PR interval 44 +/- 27 ms (p less than 0.0001) and the QRS interval 11 +/- 9 ms (p less than 0.0001) from baseline without prolongation of the QTc or JTc interval. The mean trough plasma level of indecainide on optimal dosage was 409 +/- 173 ng/ml and the mean plasma elimination half-life was 10.3 +/- 2.3 h (range 7.1 to 14.2). No adverse hemodynamic effects of indecainide were detected. Side effects during short-term therapy were mild and did not require discontinuation of the drug. Efficacy was maintained for some patients during long-term therapy for 2 years, although five patients discontinued therapy because of loss of efficacy or side effects. Indecainide is a highly effective and well tolerated antiarrhythmic drug for suppression of frequent and repetitive ventricular ectopic depolarizations.

Administration, Oral↗
PubMed1988

Mesothelioma of the AV node: potential utility of pacing.

Mesothelioma of the atrioventricular node are rare benign tumors with well-described potential for resulting in sudden death. The presentations have varied: the majority of patients have been predominantly female aged 15 to 40, dying suddenly; however, other patients have had documented heart block for many decades and a noncardiac cause of death. A 19-year-old female expired after presenting with ventricular fibrillation and was subsequently discovered to have a mesothelioma involving the AV node. Although high degree heart block is present in many patients, most episodes of sudden death probably are secondary to ventricular tachyarrhythmias. Either form of dysrhythmia may potentially benefit from ventricular pacing.

Adult↗
PubMed1987

Accuracy of commercial 24-hour electrocardiogram analyzers for quantitation of total and repetitive ventricular arrhythmias.

The accuracy of 2 commercial 24-hour electrocardiogram analyzers was tested for quantitation of ventricular premature complexes (VPCs). Scanner 1 was the Cardiodata Systems Mark III and scanner 2 was the Avionics Trendsetter DCG VII. Twenty-four-hour electrocardiographic recordings from 19 consecutive ambulatory patients with frequent VPCs were analyzed by each device. Results were compared with those from hand counts of complete printouts of each of the 19 recordings. For total VPCs, scanner 1 had an average error of 13% (range 0 to 58%) and scanner 2 had an average error of 24% (range (1 to 80%). Scanner 1 had an error of more than 10% for 9 of the 19 recordings and scanner 2 more than 10% for 11 of the 19 recordings. For paired VPCs, scanner 1 had a mean error of 23% (range 4 to 77%), and scanner 2 of 56% (range 34 to 79%). For nonsustained ventricular tachycardia, scanner 1 had an average error of 20% (range 8 to 41%) and scanner 2 had an error of 56% (range 34 to 78%). Thus, when recordings from consecutive ambulatory patients with frequent VPCs were analyzed, neither device was consistently accurate for quantitation of total VPCs. Both analyzers had an unacceptable error for quantitation of repetitive VPCs. All currently available devices may have comparably large errors. This possibility is confirmed by recalculation of the reported data from a third scanner.

Arrhythmias, Cardiac↗
PubMed1987

Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation.

To ascertain if myocardial ischemia is the mechanism of out-of-hospital ventricular fibrillation (VF), left ventricular (LV) function was assessed at rest and during submaximal exercise in 15 patients who survived out-of-hospital VF. They were separated into asymptomatic (9 patients, group A) and symptomatic (6 patients, group S) groups for a history of angina or myocardial infarction. Both groups had significant (at least 70% diameter stenosis) coronary artery disease. At catheterization no patient had angina during exercise, but 12 of 15 had ST depression or increased ST depression (group A, 1.9 +/- 1.4 mm; group S, 1.1 +/- 1.2 mm) and 11 had abnormal wall motion. From rest to exercise, patients in group S had increased LV end-diastolic pressure (from 21 +/- 9 to 37 +/- 11 mm Hg, p = 0.009) and volume (from 100 +/- 25 to 107 +/- 26 ml/m2, p = 0.006), with no significant change in LV ejection fraction (from 40 +/- 13 to 42 +/- 12%). In group A LV end-diastolic pressure increased from 19 +/- 4 to 31 +/- 8 mm Hg (p = 0.001), but neither end-diastolic volume nor ejection fraction changed significantly (from 83 +/- 13 to 92 +/- 23 ml/m2 and from 55 +/- 13% to 46 +/- 13%, respectively). Thus, patients with coronary artery disease who survive out-of-hospital VF may have evidence of myocardial ischemia during exercise without pain. Painless ischemia may have a role in out-of-hospital VF.

Adult↗
PubMed1987

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction.

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.

Acute Disease↗
PubMed1987

The Thrombolysis in Myocardial Infarction (TIMI) phase II pilot study: tissue plasminogen activator followed by percutaneous transluminal coronary angioplasty.

The Thrombolysis in Myocardial Infarction (TIMI) Study Group is investigating whether percutaneous transluminal coronary angioplasty or intravenous beta-receptor blockers, or both, are useful adjuncts to recombinant tissue-type plasminogen activator (rt-PA) in the treatment of patients with acute myocardial infarction (TIMI II study). A total of 317 patients with acute myocardial infarction were treated an average of 2.7 hours after the onset of chest pain during the course of a nonrandomized pilot investigation with 150 mg of rt-PA given over 6 hours. This dose of rt-PA resulted in a high rate of infarct-related coronary artery patency (82 and 87% of patients catheterized an average of either 1 or 32 hours after entry, respectively) and a low 21 day mortality rate of 4.4%. Coronary angioplasty was performed successfully in greater than 90% of patients with appropriate anatomy and in greater than 50% of those treated with rt-PA. In 75 patients treated within 2 hours of the onset of chest pain only 2 (2.7%) were dead by 6 weeks. However, five cases of intracranial hemorrhage were noted, and the rt-PA dose was subsequently reduced to 100 mg given over 6 hours. The TIMI II design and the results of the TIMI II pilot study are discussed.

Adrenergic beta-Antagonists↗
PubMed1987

Efficacy, safety, hemodynamic effects, and pharmacokinetics of high-dose moricizine during short- and long-term therapy.

Moricizine, 15 mg/kg, was given to 10 patients with frequent ventricular ectopic depolarizations, eight of whom had previously been treated unsuccessfully with antiarrhythmic drugs. A single-blind inpatient study was followed by therapy for up to 6 months. Two patients developed aggravation of arrhythmia during inpatient therapy. Of the eight patients who completed the inpatient study, seven achieved greater than or equal to 80% suppression of total ventricular ectopic depolarizations (P less than 0.001). During inpatient therapy the mean of the individual patients' suppression of total ventricular ectopic depolarizations was 87.9%, paired ventricular beats 99.3%, nonsustained ventricular tachycardia 99.6%, and premature atrial contractions 89.0%. Suppression was maintained during long-term therapy. The PR interval increased 27% (P less than 0.001), QRS interval increased 10% (P less than 0.0001), QTc increased 1% (P not significant), and JTc decreased 2% (P not significant). Heart rate, blood pressure, and left ventricular performance at rest and exercise were unchanged by moricizine. Moricizine half-life was 9.2 +/- 3.4 hours. Plasma levels of moricizine decreased after 10 days of therapy, suggesting induction of metabolic enzyme systems.

Adult↗
PubMed1986

Pharmacodynamics and side effects of flecainide acetate.

We compared side effects with flecainide trough levels and ECG intervals among 43 patients who received flecainide for up to 34 months. Flecainide plasma levels were higher when associated with cardiovascular side effects (mean 1063 ng/ml; range 296 to 2050 ng/ml) than when no side effects occurred (mean 609 ng/ml; range 89 to 1508 ng/ml; P less than 0.001). The PR interval (P less than 0.001), QRS interval (P less than 0.001), and the rate-corrected QT interval (P less than 0.001) were greater at the time of cardiovascular side effects, but the rate-corrected JT interval was not. The therapeutic-toxic window for flecainide plasma level was 381 ng/ml (at least 50% probability of efficacy) to 710 ng/ml (less than 10% probability of cardiovascular side effects). The risk of cardiovascular side effects increases at higher plasma levels of flecainide and is associated with greater increases in the PR and QRS intervals from baseline than are routinely observed during flecainide dosing.

Aged↗
PubMed1984

Double-blind placebo-controlled evaluation of propafenone in suppressing ventricular ectopic activity.

The effectiveness of oral propafenone in treating ventricular premature complexes (VPCs) was assessed with a single-blind dose-ranging trial followed by a double-blind, randomized, crossover comparison of propafenone and placebo. Patients subsequently were treated with propafenone for up to 24 months. During dose ranging, the average of individual percent suppressions was 83% at the largest dose (300 mg/8 hours). During the double-blind trial, the effectiveness of propafenone was confirmed, with 7 of 12 patients achieving greater than or equal to 80% reduction in VPCs (p less than 0.05 versus double-blind placebo study). Propafenone was also effective in controlling couplets and nonsustained ventricular tachycardia. Seven patients were treated with propafenone for 24 months, during which effectiveness continued, with mean suppression ranging from 67 to 79% (p less than 0.05 versus initial single-blind placebo). Propafenone prolonged PR and QRS intervals by 16 and 18%, respectively; these prolongations continued during long-term therapy. Propafenone increased serum digoxin levels in 5 of 5 patients (mean increase 83%). Cardiovascular side effects included congestive heart failure (1 patient) and conduction abnormalities (3 patients). Thus, propafenone was effective in the treatment of total and repetitive VPCs. Side effects were few, but congestive heart failure, conduction disturbances and increases in serum digoxin were observed.

Aged↗