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Biomedical subjects

A H Gradman

Publications and source records attributed to A H Gradman.

At least 37 records · Page 2Linked to original sources
PubMed1992

Supraventricular tachycardia in patients with right hemisphere strokes.

BACKGROUND AND PURPOSE: The physiological basis for the arrhythmias commonly observed after a stroke is not well understood. Based on evidence that the right and left cerebral hemispheres influence cardiac function in different ways, we sought to determine whether the nature and severity of cardiac arrhythmias in the context of an acute stroke vary in relation to whether the stroke is located in the left or the right hemisphere. METHODS: Data were obtained from the medical records of nineteen patients with left hemisphere strokes and nineteen patients with right hemisphere strokes who had also had 24-hour electrocardiographic (Holter) recordings within 2 weeks of admission to a stroke unit. Written Holter monitor reports already on file were used for the data analysis. RESULTS: All four patients with supraventricular tachycardia had right hemisphere strokes (p = 0.05). There was a nonsignificant trend for left hemisphere stroke patients to have more severe ventricular arrhythmias. CONCLUSIONS: These data provide partial support for the hypothesis that the two cerebral hemispheres have a differential influence on the nature and severity of arrhythmias following an acute stroke. We speculate that parasympathetic tone was diminished ipsilateral to the affected hemisphere associated with a reciprocal rise in sympathetic tone on that side and recommend that a prospective study be undertaken to test this hypothesis more definitively.

Arrhythmias, Cardiac↗
PubMed1989

Lack of correlation between clinic and 24 hour ambulatory blood pressure in subjects participating in a therapeutic drug trial.

Although previous studies document that blood pressure measured in the clinic may differ significantly from blood pressure recorded over 24 hours, the impact of these differences on patient selection for therapeutic drug trials is unknown. A placebo controlled double-blind evaluation of an experimental antihypertensive agent was conducted. Of 30 patients entered, 21 were admitted to the active drug phase of the protocol on the basis of a clinic supine diastolic blood pressure greater than or equal to 95 mmHg; 9 subjects with lower levels of diastolic blood pressure were dropped. Noninvasive ambulatory blood pressure monitoring was performed during the placebo period. Comparison of the two subgroups demonstrated similar levels of 24 hour blood pressure (142 +/- 13/86 +/- 7 vs 137 +/- 10/82 +/- 10). Analysis of individual patient data showed that 24 hour mean diastolic blood pressure was apparently normal (less than or equal to 80 mmHg) in 5/21 (24%) "admitted" and 3/9 (33%) "dropped" subjects. Circadian blood pressure pattern were similar in the two subgroups. A statistically large difference was noted between clinic and 24 hour blood pressures in the "admitted" subgroup (20 +/- 18/13 +/- 7 vs 7 +/- 12/4 +/- 6, p less than 0.08/p less than 0.001), suggesting that patients exhibiting a marked blood pressure rise in the clinic setting were preferentially selected.

Antihypertensive Agents↗
PubMed1989

Lisinopril dose-response relationship in essential hypertension.

1. This was a multicentre, double-blind, parallel study in 216 patients with mild to moderate (supine diastolic blood pressure = 95-115 mm Hg) essential hypertension. 2. After a 4-week placebo washout, patients were randomized to placebo or lisinopril 1.25, 5.20 or 80 mg once daily for 6 consecutive weeks. Supine and erect blood pressure was measured 24 h postdose at the end of weeks -2, 0, 2, 4, and 6. 3. There was a linear dose-response relationship for both supine and erect blood pressure. Diastolic blood pressure reductions in the lisinopril 20 and 80 mg day-1 groups were significantly greater than in the placebo or lisinopril 1.25 and 5 mg day-1 groups. 4. Lisinopril, at doses up to 80 mg day-1, was well tolerated.

Adult↗
PubMed1987

Situational panic attacks. Behavioral, physiologic, and biochemical characterization.

To investigate the pathophysiology of nonpharmacologically induced panic attacks, 18 drug-free agoraphobic patients and 13 matched healthy subjects underwent structured exposure to phobic situations. Heart rate, blood pressure, and plasma free 3-methoxy-4-hydroxyphenylglycol (MHPG), cortisol, growth hormone, and prolactin levels were measured before, during, and after exposure. Fifteen patients experienced situational panic attacks during exposure. Panicking patients displayed significantly greater increases in heart rate but not blood pressure or plasma free MHPG or cortisol in comparison with the healthy subjects. Growth hormone and prolactin responses tended to be smaller in the patients. If brain noradrenergic hyperactivity occurs during situational panic attacks, it may be too brief or too restricted in regional localization to affect MHPG levels in plasma. Chronically recurrent attacks may cause an adaptation of neuroendocrine mechanisms activated by anxiety or stress.

Adult↗
PubMed1985

Ambulatory electrocardiographic correlates of ventricular inducibility during programmed electrical stimulation.

To determine the relation between spontaneous and induced ventricular arrhythmias, ambulatory electrocardiographic (Holter) monitoring and programmed electrical stimulation were performed in 48 adult patients with suspected life-threatening ventricular arrhythmias. Nine had no inducible arrhythmia, 11 demonstrated 1 to 2 beats of intraventricular reentry, 19 exhibited non-sustained ventricular tachycardia and 9 exhibited sustained ventricular tachycardia during electrophysiologic studies. Patients without arrhythmia inducibility had a high incidence of multiformity (56%) and bigeminy (44%), but a low incidence of either couplets (11%) or spontaneous ventricular tachycardia (11%) on Holter monitoring. An increasing incidence of all "complex" ectopic features was found with increasing degrees of ventricular inducibility. In patients with inducible sustained ventricular tachycardia, multiformity was present in 100%, bigeminy and couplets in 89% and spontaneous ventricular tachycardia in 78%. Premature ventricular complex frequency, couplet frequency and the repetition index (the ratio of couplets to premature ventricular complexes) were also found to be directly correlated with the degree of ventricular inducibility. Three quantitative arrhythmia variables were identified which predicted ventricular tachycardia inducibility. Seven (78%) of 9 patients with a mean premature ventricular complex frequency of 100 or more/1,000 normal beats, 11 (85%) of 13 with a mean couplet frequency of 1 or more/1,000 normal beats and 19 (83%) of 23 with a mean repetition index value of 15 or more/1,000 premature ventricular complexes proved to have inducible ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

Effects of oral digoxin on ventricular ectopy and its relation to left ventricular function.

The ventricular antiarrhythmic properties of oral digoxin were examined in 13 patients with chronic ventricular ectopy using serial 24-hour electrocardiographic monitoring. Mean premature ventricular complex frequency (per 1,000 normal beats) decreased from 56 +/- 47 during the placebo period to 40 +/- 27 (p = not significant [NS]) and 25 +/- 17 (p less than 0.05) during daily administration of digoxin, 0.25 and 0.375 mg. Digoxin had no significant effect on the qualitative occurrence of complex ventricular arrhythmia patterns (multiformity, bigeminy, couplets, ventricular tachycardia). Radionuclide left ventricular (LV) ejection fraction was measured during the placebo period. Seven patients had normal (ejection fraction greater than 50%) and 6 abnormal global LV performance. In the normal group, the mean premature ventricular complex frequency decreased from 69 +/- 58 to 20 +/- 18 (p less than 0.05) and the mean couplet frequency decreased from 0.59 +/- 0.85 to 0.07 +/- 0.06 (p less than 0.04) during the placebo and 0.375 mg digoxin dosing periods, respectively. In contrast, no significant changes in either variable occurred after digoxin in subjects with depressed LV function. This study indicates that oral digoxin is moderately effective in suppressing premature ventricular complexes, and that its effects are greatest in patients with normal overall LV performance.

Administration, Oral↗
PubMed1978

Antiarrhythmic drug effect assessed from ventricular arrhythmia reduction in the ambulatory electrocardiogram and treadmill test: comparison of propranolol, procainamide and quinidine.

A 5 week study was performed in 17 patients with frequent ventricular ectopic complexes. The study design comprised an initial control period, 1 week each of treatment with propranolol (240 mg daily), procainamide (3.0 g daily) and quinidine (1.8 g daily) and a final control period. Twenty-four hour ambulatory electrocardiograms and maximal exercise tests were performed each week. For the group, the total number and qualitative types of ventricular ectopic complexes were similar during the two control periods; however, there were large variations among individual patients. Each drug reduced the total number of ventricular ectopic impulses and the percent of patients with each qualitative type. There was agreement between the ambulatory electrocardiogram and treadmill test in three quarters of the drug evaluations. Although it is possible to determine antiarrhythmic drug effects for a group, spontaneous variability in the occurrence of ventricular arrhythmias makes it difficult to evaluate the effects in individual patients.

Adult↗
PubMed1977

Sudden death during ambulatory monitoring. Clinical and electrocardiographic correlations. Report of a case.

A man with known coronary heart disease underwent treadmill exercise testing to determine his functional capacity. The test was negative for ischemia. Ventricular ectopic activity was noted at rest and in the recovery period. On the same day, while viewing a sporting event at home, the patient died suddenly. An ambulatory electrocardiographic recording documented ventricular fibrillations as the terminal mechanism. Ventricular ectopic activity and heart rate increased in the two hours prior to death, and ischemic ST-segment depression was noted at the time of the terminal arrhythmia. It is postulated that myocardial ischemia and catecholamine response lowered the threshold to ventricular fibrillation, thus facilitating the emergence of the fatal arrhythmia.

Ambulatory Care↗
PubMed1977

Suppression of premature ventricular contractions by acebutolol.

The antiarrhythmic action of the beta-blocking drug, acebutolol, was evaluated in patients with frequent premature ventricular contractions (PVCs). In the 12 hours following administration of a single 300 mg oral dose, 8 of 10 patients showed a greater than 50% reduction in PVC frequency, and statistical analysis indicated that PVC reduction persisted for 10 hours after the single dose. Analysis of plasma concentrations of acebutolol and an acetyl metabolite indicated that after single oral doses of plasma concentrations of the metabolite exceed those of unchanged acebutolol. When patients were studied during periods of 300 mg doses every 8 hours, eight of 11 showed a 70% reduction in PVC frequency, and analysis showed that the therapeutic effect was present throughout the 24-hour monitoring period. Acebutolol slowed the heart rate and prolonged the PR interval without affecting the QT interval. Significant clinical or laboratory toxicity was not encountered. In the small group studied, acebutolol was found to be safe and effective for short-term administration to patients with frequent PVCs and possessed a relatively long duration of antiarrhythmic action.

Acebutolol↗
PubMedDate not supplied

Long-term efficacy, tolerability, and safety of the combination of enalapril and felodipine ER in the treatment of hypertension. Enalapril-Felodipine ER Factorial Study Group.

A recent 8-week, double-masked, placebo-controlled, 3 x 4 factorial-design study demonstrated that enalapril-felodipine extended-release (ER) combinations had statistically significant additive effects for reducing both sitting systolic blood pressure (SiSBP) and sitting diastolic blood pressure (SiDBP) and were generally well tolerated in hypertensive patients with SiDBPs ranging from 95 to 115 mm Hg. The present open-label study was undertaken to assess the long-term efficacy, tolerability, and safety of such combinations. Patients from the factorial study were eligible for the 1-year, open-label extension. Initially, all patients received enalapril 5 mg-felodipine ER 2.5 mg once daily; if SiDBP was not controlled (< 90 mm Hg) after 4 weeks of treatment, the dose was titrated upward at 2- to 4-week intervals to a maximum of enalapril 10 mg-felodipine ER 10 mg. Hydrochlorothiazide (HCTZ) 12.5 mg was added to the regimen of patients whose hypertension was not controlled at the highest enalapril-felodipine ER dose. A total of 507 patients were enrolled, of whom 502 were assessable. At their last study visit, 391 (78%) of the assessable patients were receiving only an enalapril-felodipine ER combination. The enalapril-felodipine ER combinations resulted in mean trough SiDBPs of 85 to 89 mm Hg (decreases of 13 to 16 mm Hg from baseline) and SiSBPs of 137 to 140 mm Hg (decreases of 13 to 21 mm Hg). Overall, 407 (81%) of the 502 assessable patients achieved an SiDBP < 90 mm Hg or a reduction from baseline > or = 10 mm Hg (responders); such a response was recorded in 331 patients (66%) taking a combination of enalapril-felodipine ER alone and 76 patients (15%) taking the combination with the addition of HCTZ 12.5 mg. Blood pressure reductions were maintained throughout the treatment period. Drug-related adverse events were relatively infrequent, often transient, usually mild, and apparently not dose related. The most frequently reported drug-related adverse events were edema/swelling, asthenia/fatigue, dizziness, cough, and headache. These results suggest that combination therapy with enalapril-felodipine ER is effective for long-term blood pressure reduction, has an excellent safety profile, and is generally well tolerated. Addition of low-dose HCTZ to the enalapril-felodipine ER combination appears to provide further blood pressure control without increasing drug-related adverse events.

Adult↗
PubMedDate not supplied

Comparative effects of candesartan cilexetil and losartan in patients with systemic hypertension. Candesartan Versus Losartan Efficacy Comparison (CANDLE) Study Group.

The antihypertensive efficacy and tolerability of the novel angiotensin-II (A-II) receptor blocker candesartan cilexetil and the prototype A-II receptor blocker, losartan, were compared in an 8-week, multicenter, double-blind, randomized, parallel-group, titration-to-effect study of 332 adults (42% women, 12% black) with systemic hypertension (sitting diastolic blood pressure [DBP] 95-114 mmHg, inclusive). In patients with a mean trough (24 +/- 3 hours after dose) sitting DBP of 90 mmHg or higher after 4 weeks of once daily administration of candesartan 16 mg or losartan 50 mg, dose was titrated up to candesartan 32 mg or losartan 100 mg once daily. The candesartan regimen was significantly more effective than the losartan regimen in reducing trough sitting DBP at week 8 (11.0 mmHg versus 8.9 mmHg). Candesartan also produced numerically greater reductions in secondary blood pressure parameters, including sitting systolic blood pressure (SBP), trough standing DBP and SBP, and peak (6 +/- 2.5 hours after dose) sitting and standing DBP and SBP. Responder rates (sitting DBP < 90 mmHg or reduction in blood pressure of > or = 10 mmHg) and control rates (sitting DBP <90 mmHg) were higher with candesartan (64% versus 54% and 54% versus 43%, respectively). A total of 1.9% of the patients taking candesartan and 6.5% of those taking losartan discontinued prematurely because of adverse events or lack of efficacy.

Analysis of Variance↗
PubMedDate not supplied

Cardiac effects of cocaine: a review.

Over the past 15 years, there has been a dramatic increase in the abuse of purified cocaine preparations throughout the industrialized world. The potential lethality of the drug is now recognized, and a growing series of case reports indicate that cardiotoxicity may be an important factor in the morbidity and mortality associated with the drug. Acute myocardial infarction is a demonstrated risk both in subjects with and without pre-existent coronary artery disease. The arrhythmogenic potential of cocaine is less clear and appears to have been overemphasized, although several documented cases of ventricular arrhythmia following cocaine use have been reported. Cardiomyopathy and myocarditis associated with cocaine have also been described, but an etiologic relationship is presently inferential. Based upon presumed pathophysiologic mechanisms, beta adrenergic blocking agents are recommended for arrhythmias, and calcium channel blocking agents and/or nitrates for ischemic syndromes related to cocaine. It is emphasized that these recommendations are based upon a paucity of relevant clinical studies, and controlled clinical trials to establish their efficacy have not been performed.

Animals↗