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Biomedical subjects

D M Salerno

Publications and source records attributed to D M Salerno.

At least 19 recordsLinked to original sources
PubMed1995

Reversal of flecainide-induced ventricular arrhythmia by hypertonic sodium bicarbonate in dogs.

Flecainide occasionally produces incessant ventricular tachycardia that is difficult to treat. Reports of uncontrolled clinical studies have suggested a therapeutic role for hypertonic sodium bicarbonate (NaHCO3). To test this observation, spontaneous and pacing-induced arrhythmia canine models were designed. In the spontaneous model, flecainide was infused at 0.5 mg/kg/min until ventricular tachycardia occurred spontaneously. In the pacing-induced model, flecainide was infused at 1.0 mg/kg/min load (0.5 mg/kg/min maintenance) stepwise until the QRS was widened 50%, 75%, and 100%, with programmed ventricular stimulation at each step until ventricular arrhythmia was induced. Dogs who developed spontaneous arrhythmia were treated blindly with three doses of either NaHCO3 (3 mEq/kg/dose, with 1 minute between doses) or normal saline. Dogs who were induced in the second model were treated with the same three doses, 10 minutes apart, with programmed stimulation between each dose. Before unblinding in both protocols, dogs were classified as "responders" or "nonresponders" to therapy. In the spontaneous model, of 14 dogs with spontaneous ventricular tachycardia, all 7 dogs treated with NaHCO3 showed response, compared with only 1 of 7 dogs treated with saline (P < .01). Ventricular QRS complexes/min were reduced by NaHCO3 in that protocol. In the induced arrhythmia protocol, of 14 dogs with inducible arrhythmia, 6 of 7 responded to NaHCO3, and 1 of 7 responded to placebo (P < .05). In both protocols, arterial pH and the serum sodium concentration were increased by NaHCO3 but not by normal saline control treatment. QRS interval duration was shortened by NaHCO3 therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

12-lead and continuous ECG recordings of subjects during inpatient administration of smoked cocaine.

Cocaine can cause myocardial ischemia or infarction. The incidence of these events, and the influence of specific dosing routes or regimens on their occurrence is not established. In the current study, we obtained frequent 12-lead electrocardiograms (ECGs) and continuous 2 or 3 channel ECGs from 20 subjects participating in a behavioral study of smoked cocaine. Subjects received 10 or 11 doses of cocaine 0.4 mg/kg per dose, or 10 doses of 35 mg per dose at 30 min intervals (range 233-408 mg total dose per session). ECGs were also recorded on control days on which subjects received no cocaine. The mean peak plasma cocaine concentration on cocaine days was 640 +/- 262 ng/ml. There were no changes in digitized ST segment amplitude on 12-lead ECGs obtained during cocaine administration (P = 0.098). Of 17 subjects who had technically satisfactory continuous ECGs, four had significant ST segment depression (> 1 mm below the PR segment); two on cocaine days and two on control days (P > 0.5). One subject had frequent premature beats on both cocaine and control days. One subject had an asymptomatic run of 4 ventricular beats 30 s after cocaine administration that could have been due to cocaine. All episodes of ST depression or premature beats were asymptomatic. No evidence of either symptomatic or subclinical cardiac ischemia related to cocaine administration was found. Thus no clinically important adverse events were found as a result of smoked cocaine administered by this dosing regimen to healthy males with a history of heavy cocaine use. Additional study with larger numbers of subjects will be helpful in further assessing the safety of administering smoked cocaine to research subjects.

Administration, Inhalation↗
PubMed1993

Effectiveness and costs of digoxin treatment for atrial fibrillation and flutter.

Clinical outcomes and costs associated with the use of digoxin in atrial fibrillation and flutter were evaluated in a prospective, observational study at 18 academic medical centers in the United States. Data were collected on 115 patients (aged > 18 years) with atrial fibrillation or flutter who were treated with digoxin for rapid ventricular rate (> or = 120 beats/min). The median time to ventricular rate control (i.e., resting ventricular rate < 100 beats/min, decrease in ventricular rate of > 20%, or sinus rhythm) was 11.6 hours from the first dose of digoxin for all evaluable patients (n = 105) and 9.5 hours for those only receiving digoxin (n = 64). Before ventricular rate control, the mean +/- SD dose of digoxin administered was 0.80 +/- 0.74 mg, and a mean of 1.4 +/- 1.8 serum digoxin concentrations were ordered per patient. Concomitant beta-blocker or calcium antagonist therapy was instituted in 47 patients (41%); in 19 of these, combination therapy was initiated within 2 hours. Adenosine was administered to 13 patients (11%). Patients spent a median of 4 days (range 1 to 25) in the hospital; 28% spent time in a coronary/intensive care unit and 79% in a telemetry bed. Loss of control (i.e., resting ventricular rate returned to > 120 beats/min) occurred at least once in 50% of patients and was associated with a longer hospital stay (p < 0.05). Based on 1991 data, the estimated mean hospital bed cost for patients with atrial fibrillation or flutter was $3,169 +/- $3,174.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Serum electrolytes and catecholamines after cardioversion from ventricular tachycardia and atrial fibrillation.

We have observed hypokalemia after cardioversion from spontaneous out-of-hospital ventricular fibrillation and induced ventricular tachycardia. To test the hypothesis that the hormone response to the hemodynamic stress of the arrhythmia initiated the change in potassium, we compared the electrolytes and hormones in three groups of patients. We observed a decrease in serum potassium and magnesium after cardioversion from ventricular tachycardia induced by programmed stimulation, but not after normal programmed stimulation of the ventricle or after cardioversion from stable atrial fibrillation. These changes were preceded first by a rise in norepinephrine and epinephrine, then a rise in glucose, followed by a rise in insulin. The stimulus for these changes was probably the hypotension associated with ventricular tachycardia. The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells, related to the insulin-mediated movement of glucose from the blood into cells.

Atrial Fibrillation↗
PubMed1992

Quinidine: is it a good drug or a bad drug?

Although quinidine, the oldest class I antiarrhythmic drug, has been available for several decades, recent reports have emphasized the possibility of dangerous side effects. Quinidine often successfully maintains sinus rhythm in patients with intermittent atrial fibrillation, suppresses sustained ventricular tachycardia in some patients, and minimally depresses left ventricular function. However, it can cause nonfatal and, occasionally, even fatal proarrhythmic complications. Therefore, it must be administered with caution in appropriately selected patients.

Arrhythmias, Cardiac↗
PubMed1992

Supraventricular tachyarrhythmias in the intensive care unit.

Several types of supraventricular tachyarrhythmias occur commonly during intensive care. The specific type can usually be diagnosed using standard electrocardiographic techniques. Several new drugs have significantly improved the ability to successfully manage these arrhythmias.

Adenosine↗
PubMed1992

The effects of beta 1- and beta 2-adrenergic blockade and calcium channel blockade on postresuscitation electrolyte changes.

We have previously reported in dogs after ventricular fibrillation that (1) potassium and calcium levels decrease and magnesium and glucose increase, (2) all values return to control levels by 3 hours, and (3) propranolol blocks the changes in potassium, magnesium, and glucose but not calcium. The purpose of this study was to evaluate the beta 1- and beta 2-selectivity of changes in potassium, magnesium, and glucose and assess the response of the change in calcium to calcium channel blockade. Before initiating ventricular fibrillation, we pretreated dogs with an intravenous solution of either normal saline, metoprolol, ICI 118551 (two doses), or diltiazem. After a 2-minute episode of ventricular fibrillation, dogs were resuscitated. Baseline electrolyte measurements were obtained before ventricular fibrillation and sequentially for 3 hours after fibrillation. The saline-treated control group had a maximal decrease in the serum potassium level of 0.5 +/- 0.2 mEq/L. High-dose ICI 118551 reduced this decrease to 0.3 +/- 0.3 mEq/L (p = 0.055), but the other three groups showed no difference compared with the control group. Magnesium increased in the saline control group by 0.2 +/- 0.1 mEq/L. This increase was partially reduced by high-dose ICI 118551 to 0.1 +/- 0.1 (p = 0.055) but not by the other drugs. Glucose increased to 40 +/- 13 mg/dl in the saline control group. This increase was partially reduced by high-dose ICI 118551 to 23 +/- 6 mg/dl (p = 0.007) but not by the other drugs. Calcium showed a maximal decrease of 0.6 +/- 0.3 mg/dl in the control group. This decrease was not attenuated by any of the drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

The Cardiac Arrhythmia Suppression Trial: first CAST ... then CAST-II.

The Cardiac Arrhythmia Suppression Trial (CAST) was a study designed to test the hypothesis that suppression of ventricular premature complexes after a myocardial infarction would improve survival. Preliminary results showed that suppression of ventricular premature complexes with encainide and flecainide worsened survival, and the CAST continued as the CAST-II with moricizine compared with its placebo. The protocol for the CAST-II was changed to attempt to enroll patients more likely to experience serious arrhythmias. The enrollment time was narrowed to 4 to 90 days after myocardial infarction; the qualifying ejection fraction was lowered to less than or equal to 0.40; a higher dose of moricizine could be used; early titration itself was double-blind with a placebo, and the definition of disqualifying ventricular tachycardia was changed to allow patients with more serious arrhythmias to be entered into the trial. The Cardiac Arrhythmia Suppression Trial-II was subsequently terminated prematurely because 1) patients treated with moricizine had an excessive cardiac mortality rate during the 1st 2 weeks of exposure to the drug, and 2) there appeared to be little chance of showing a long-term survival benefit from treatment with moricizine. This report outlines the rationale behind the Cardiac Arrhythmia Suppression Trial and the reasons for selection of the drugs used in the CAST and CAST-II.

Anti-Arrhythmia Agents↗
PubMed1991

Prevalence, characteristics and significance of ventricular premature complexes and ventricular tachycardia detected by 24-hour continuous electrocardiographic recording in the Cardiac Arrhythmia Suppression Trial. CAST Investigators.

The prevalence, characteristics and significance of ventricular arrhythmias detected by ambulatory electrocardiography were evaluated in 1,498 patients who were randomized to encainide, flecainide or placebo in the Cardiac Arrhythmia Suppression Trial. The mean ventricular premature complex (VPC) frequency at baseline was 133 +/- 257 VPCs/hour. Nonsustained ventricular tachycardia (VT) (rate greater than or equal to 120 beats/min) was present in 22% of patients. Accelerated idioventricular rhythm (rate less than 120 beats/min) occurred in 22% of subjects. There were 63 deaths/resuscitated cardiac arrests in the active treatment (encainide/flecainide) group and 26 in the placebo group. In the treatment group mortality increased with increasing VPC frequency, (p = 0.006), whereas in the placebo group such a relation was not present. Mortality/resuscitated cardiac arrest increased in patients with greater than or equal to 2 VT episodes than in those with less than or equal to 1 episode in the active treatment group (p = 0.04). There was no significant association between VT and mortality/resuscitated cardiac arrest in the placebo group. The presence of accelerated idioventricular rhythm was not associated with increased mortality/resuscitated cardiac arrest in either the active treatment or placebo groups. However, mortality was lower in patients with accelerated idioventricular rhythm rates less than 100 beats/min than in those with rates greater than or equal to 100 beats/min (p = 0.05). Thus, in the Cardiac Arrhythmia Suppression Trial the previously described association between mortality/resuscitated cardiac arrest and ventricular arrhythmias (VPC and VT) were only observed in the active treatment group. In addition, based on the results obtained in this highly selected population, it is suggested that the definition of accelerated idioventricular rhythm should be a rate less than 100 beats/min, and at a rate greater than or equal to 100 beats/min it should be categorized as VT.

Anti-Arrhythmia Agents↗
PubMed1991

Seismocardiographic changes associated with obstruction of coronary blood flow during balloon angioplasty.

Seismocardiography, a new noninvasive technique, detects low-frequency cardiac vibrations on the chest wall during ventricular contraction and during both early and late ventricular filling. To evaluate the ability of seismocardiography to detect ischemia caused by decreased coronary blood flow, 35 patients were studied during coronary angioplasty. Seismocardiograms and electrocardiograms were recorded twice at baseline, with the catheter across the lesion before first inflation (n = 15), every 30 seconds during the first inflation, 1 and 2 minutes after the first inflation and greater than or equal to 5 minutes after the final inflation. For comparison, sequential seismocardiograms were also obtained from 15 healthy volunteers. Electrocardiograms were blindly scored for ST change from baseline (0 = none, 1 = 0.5 mm ST depression, 2 = greater than or equal to 1.0 mm ST depression, 3 = ST elevation). Seismocardiograms were blindly scored for change from baseline (0 = none, 1 = mild, 2 = moderate, 3 = marked) for both the systolic and diastolic waves. The average maximal systolic seismocardiographic score was 2.5 +/- 0.8 for patients who had undergone angioplasty and 1.0 +/- 0.9 for volunteers (p less than 0.001). The average maximal diastolic seismocardiographic score was 2.3 +/- 0.8 for angioplasty patients and 0.7 +/- 0.9 for volunteers (p less than 0.001). The percentage of angioplasty patients with electrocardiographic, systolic and diastolic seismocardiographic scores greater than or equal to 2 was, respectively: 0, 11 and 14% at second baseline; 23, 67 and 53% with catheter across the lesion; 44, 75 and 59% after 30 seconds of inflation; 42, 71 and 61% after 60 seconds of inflation; 23, 74 and 61% after 1 minute of deflation; and 0, 71 and 47% 5 minutes after final inflation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Pirmenol: an antiarrhythmic drug with unique electrocardiographic features--a double-blind placebo-controlled comparison with quinidine.

Previous reports have stated that pirmenol is a Class IA antiarrhythmic drug that prolongs the QT interval, but did not use computerized electrocardiography. We randomized 18 patients with frequent ventricular ectopic depolarizations to pirmenol (8 patients) or quinidine (10 patients). Pirmenol was effective and tolerated for suppression of arrhythmia in all 7 patients treated (1 patient withdrew for personal reasons) but quinidine was effective and tolerated for 4 weeks in only 5 of 10 patients (p less than 0.05). Using computerized 12-lead electrocardiography, the mean change in PR interval from placebo to treatment was 5 +/- 18 ms for quinidine and 5 +/- 11 ms for pirmenol (p = NS). The mean change in QRS interval was 5 +/- 14 ms for quinidine and 10 +/- 5 ms for pirmenol (p = NS). The mean change in QT interval was 46 +/- 30 ms for quinidine and 8 +/- 9 ms for pirmenol (p less than 0.01) and the mean change in JT interval was 41 +/- 36 ms for quinidine and -2 +/- 10 ms for pirmenol (p less than 0.01). After the double-blind phase, 4 quinidine patients had computerized electrocardiographic intervals measured on pirmenol; the above findings were confirmed. These electrocardiographic features of pirmenol clearly distinguish it from quinidine, the prototype Class IA drug. However, pirmenol has minimal effect on the PR and QRS intervals, and thus does not appear to be a Class IC drug either. Although its electrocardiographic features are closest to Class IB, its electrophysiology in isolated cells and its antiarrhythmic and side effect profile are atypical for a IB agent.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1991

Rapid administration of high-dose human antibody Fab fragments to dogs: pharmacokinetics and toxicity.

The treatment of drug overdose with drug-specific antibody fragments may require very high antibody doses. To address the feasibility of this therapy, we studied the pharmacokinetics and toxicity of high-dose human nonspecific Fab fragments in beagles. Three dogs received 5.3 g/kg Fab iv over 1 hr. Because nephrotoxicity was observed, three subsequent dogs received 3.2 g/kg. The fraction of the Fab dose excreted in urine (10 +/- 6%) was lower than reported values for either high or low doses of Fab in other species. The terminal serum elimination half-life (42 hr for the higher and 48 hr for the lower dose) was also longer than reported values for other species, due to lower renal and nonrenal Fab clearance. Fab administration was tolerated without adverse hemodynamic effects. One of three dogs at each dose developed transient oliguria. All dogs developed a transient but marked increase in the serum creatinine concentration. At 2 weeks creatinine clearance had returned to normal. Urinary protein and albumin excretion at 2 weeks were within the normal range for dogs but were increased over their baseline values. The histology of all organs was normal at 3 weeks by light microscopy, and renal histology by electron microscopy was also normal. The mechanism of Fab nephrotoxicity, not observed previously with high-dose Fab in rats or lower doses of Fab in other species including dogs, is not clear. These data suggest that further study of the potential toxicity of high-dose Fab, and its reversibility, is needed to assess the feasibility of treating drug overdose with this antibody fragment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1991

Seismocardiography for monitoring changes in left ventricular function during ischemia.

Seismocardiography is a new noninvasive technique for recording cardiac vibrations. Changes in the recorded waves have been correlated with acute and chronic changes in left ventricular function. In this report, we describe a patient who developed ischemia induced by coronary angiography in the cardiac catheterization laboratory. The patient's seismocardiogram showed distinct changes during the ischemic episode that actually preceded the onset of symptoms and resolved after nitroglycerin therapy. The patient's seismocardiographic recordings were significantly different from the recordings from five control individuals. This observation suggests that seismocardiography may be helpful for monitoring left ventricular function during episodes of myocardial ischemia.

Cardiac Catheterization↗