Effect of Diphenylhydantoin on Left Ventricular Function in Patients with Heart Disease

Lieberson, Alan D.; Schumacher, Ralph; Childress, Richard H.; Boyd, Daniel L.; Williams, John F.

doi:10.1161/01.cir.36.5.692

Cited by 38 publications

(3 citation statements)

References 26 publications

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“…However, recently it has been demonstrated that diphenylhydantoin also is not totally devoid of adverse hemodynamic effects since it will depress myocardial function in patients with heart disease. 5 Key: BSA = body surface area in M2; ASHD = arteriosclerotic heart disease; PMD = primary myocardial disease. Time = time in minutes after drug injection with 0 representing the control period; HR = heart rate in beats/min; Mean art pr = mean arterial pressure in mm Hg; CI = cardiac index in L/min/m2; LVEDP = left ventricular end-diastolic pressure in mm Hg; SVI = stroke volume index in mI/M2; SWI = left ventricular stroke work index in g-m/m2; dp/dt = maximum rate of rise of left ventricular pressure as per cent of control.…”

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confidence: 99%

Hemodynamic Effects of Lidocaine in Patients with Heart Disease

et al. 1968

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The intravenous administration of 50 mg of lidocaine as a single bolus to four patients with heart disease did not result in a significant change in cardiac output or left ventricular end-diastolic pressure (LVEDP). Two patients had moderate decrease in systemic arterial pressure which was not accompanied by symptoms, was of short duration, and did not require therapeutic intervention. Left ventricular function, as assessed by the relationship of changes in stroke volume index (SVI) and stroke work index (SWI) to changes in LVEDP, was not significantly affected nor was the maximum rate of rise of left ventricular pressure (dp/dt).

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confidence: 99%

Hemodynamic Effects of Lidocaine in Patients with Heart Disease

et al. 1968

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“…They noted a direct vasodilating effect on the coronary vessels, with no change in the myocardial consumption of oxygen during a constant work load. Lieberson et al (11) have shown that diphenylhydantoin does not significantly reduce cardiac output or greatly elevate left ventricular end‐diastolic pressure. Thus, improvement in ventricular ectopic activity not related to digitalis may be secondary to an improvement in coronary perfusion and a decrease in ventricular automaticity.…”

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confidence: 99%

Treatment of Ventricular Ectopic Rhythms with Diphenylhydantoin

Kemp

1972

Journal of the American Geriatrics Society

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For the treatment of non‐digitalis‐induced ventricular ectopic rhythms, the effect of diphenylhydantoin was studied in 5 patients and compared with the effect of placebo in 5 control patients. For the first three weeks the dosage of diphenylhydantoin was 100 mg four times daily. Then, for maintenance therapy during the rest of the three‐month study, the dosage was reduced to 100 mg three times daily. The numbers of premature ventricular contractions during a five‐minute continuous ECG monitoring period were recorded before therapy, after three weeks of therapy, and after three months of therapy. There was a marked reduction in the number of ventricular ectopic beats in the diphenylhydantoin group compared with the control group.

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“…Propyl ene glycol, the solvent for DPH, also has cardiotoxic properties (49). DPH is a negative inotropic agent, although the depression of myocardial function appears to be slight and transient (50)(51)(52). It is also a peripheral vasodila tor-producing hypotension, and may cause central nervous system toxicity ataxia, psychoses, and excitability (50).…”

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confidence: 99%

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Selzer¹,

Cohn²

1970

Annu. Rev. Med.

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Two developments at the beginning of this decade exerted a profound influence upon clinical management of acute myocardial infarction: the in troduction of closed-chest resuscitation with electric shock therapy for ven tricular fibrillation, and the availability of continuous monitoring of the electrocardiogram by means of the cathode-ray oscilloscope. As a result of this, the coronary care unit has become a standard facility for the treatment of myocardial infarction. I t should be recognized that the concept of thera peutic centers for patients with myocardial infarction encompasses a broad range of facilities available in such units (1). On the one end of the spectrum, one can place the comprehensive cardiology center, equipped to treat all as pects and complications of myocardial infarction, including the use of emer gency surgery and artificial pump-support. On the other end, is the small area in a hospital in which nurses can observe the patient's rhythm displayed upon the monitoring oscilloscope. The great majority of coronary care units ap proach the latter end of the spectrum-based primarily on the availability of electrocardiographic monitoring units. Thus, the role of such units is the identification, early recognition, treatment, and prevention of dangerous arrhythmias. The most common arrhythmias that are potentially life-threat ening are related to increased "irritability" of the ventricular myocardium. The purpose of this review is to examine the rationale for the therapy of ventricular arrhythmias in acute myocardial infarction-both the fundamen tal and practical considerations. INCIDENCE OF ARRHYTHMIASDuring the earlier era, when the diagnosis of arrhythmias was based on their occurrence during routine examination of the patient or during record ing of an electrocardiographic tracing, the incidence of arrhythmias was es timated to range between 9 and 27 percent, with an average of 18 percent

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Effect of Diphenylhydantoin on Left Ventricular Function in Patients with Heart Disease

Cited by 38 publications

References 26 publications

Hemodynamic Effects of Lidocaine in Patients with Heart Disease

Hemodynamic Effects of Lidocaine in Patients with Heart Disease

Treatment of Ventricular Ectopic Rhythms with Diphenylhydantoin

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

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