Noninvasive assessment of clinical response to oral propranolol therapy

Frishman, William H.; Smithen, Charles; Befler, Barbara; Kligfield, Paul; Killip, Thomas

doi:10.1016/0002-9149(75)90049-1

Cited by 79 publications

(9 citation statements)

References 29 publications

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“…hemodynamic parameters and intraventricular indices of contractility [10][11][12], Prolongation of ratecorrected PEP and shortening of the rate-cor rected LVET are indicative of a reduction in myocardial performance. The PEP/LVET ra tio has been found to correlate well with the contractility index and ejection fraction of the left ventricle [13,14], Studies on the effect of propranolol on STI indicate that with progressively larger doses of this drug the PEP/LVET ratio increases and the ven tricular ejection fraction decreases [15], It was also shown that lengthening of rate-cor rected PEP and a slight shortening of ratecorrected LVET are the result of increasing doses of propranolol. However, it has also been concluded that equipotent doses of oxprenolol and propranolol induce equal ino tropic effects [16].…”

Section: Discussionmentioning

confidence: 99%

Effects of Oxprenolol versus Propranolol on Myocardial Performance and Myocardial O<sub>2</sub> Consumption in Hypertensive Patients

Schlesinger¹,

Ravid²,

Meshulam³

1983

Cardiology

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The purpose of the study was to compare the effects of oxprenolol, a beta-adrenergic blocking agent with intrinsic sympathomimetic activity, to propranolol, a beta-blocker without intrinsic sympathomimetic activity, on myocardial performance and myocardial O₂ consumption (MVO₂). Myocardial performance was reflected by the systolic time intervals (STI) and MVO₂ by the triple product of heart rate × left ventricular ejection time × systolic blood pressure (HR × LVET × SBP). The trial, a double-blind cross-over study, included 32 hypertensive patients, 17 males and 15 females, with a mean age of 50.9 years. The patients were divided into two groups: group A – 16 patients who were treated with effective antihypertensive doses of oxprenolol and diuretics (Esidrex K) for the first 8 weeks (period I) and with similar doses of propranolol and diuretics for the following 8 weeks (period II); Group B – the same number of patients who received the same drugs in the reverse order. All patients were examined during both periods at 2- and 3-week intervals, blood pressure and heart rate were recorded, and patients were provided with the appropriate study medication. At the end of periods I and II, myocardial function was assessed on the basis of STI, and MVO₂ was evaluated on the basis of the triple product of HR × LVET × SBP. Four measurements of STI and MVO₂ were carried out for each patient at the end of periods I and II: prior to intake of medication and 1½, 3 and 4½ h after intake of medication. The results of the study indicated in all four measurements a tendency for lower myocardial performance in both groups following propranolol treatment as compared to oxprenolol. This tendency was more marked on the third and fourth measurements, during which higher blood levels are expected, and was statistically significant on measurement IV (p < 0.001, t = 3.5 for the ratios PEP/LVET). A slight tendency for lower values of MVO₂ following the treatment with propranolol as compared to oxprenolol was obtained (measurement I: t = 2.04, p < 0.05; measurement IV: t = 1.56, p < 0.05). It can be concluded that treating hypertensive patients with propranolol is accompanied by a somewhat lower myocardial function and a tendency for lower MVO₂ as compared to treatment with oxprenolol. Treatment with oxprenolol seems, therefore, to be superior to propranolol in patients with impaired myocardial function.

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Section: Discussionmentioning

confidence: 99%

Effects of Oxprenolol versus Propranolol on Myocardial Performance and Myocardial O<sub>2</sub> Consumption in Hypertensive Patients

Schlesinger¹,

Ravid²,

Meshulam³

1983

Cardiology

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“…A number of explanations have been offered for this fact: the first is the difference in sympathetic tone between patients, possibly requiring a greater level of ~-blocker effect in an individual with heightened sympathetic tone. The wide range of variability in plasma concentrations to achieve the same therapeutic effect has been demonstrated with propranolol (Frishman et al 1975). The second suggestion is that the pharmacokinetics of those ~-blockers that are lipid soluble may be disturbed in patients with a larger amount of body fat, without interference with the clinical efficacy (Galletti et al 1989).…”

Section: Relationship Between Dose Plasma Concentration and Clinicalmentioning

confidence: 96%

Pharmacokinetic Optimisation of Therapy with ??-Adrenergic Blocking Agents

Frishman

Lazar

Gorodokin

1991

Clinical Pharmacokinetics

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beta-Adrenergic blockade has provided one of the major pharmacotherapeutic advances of this century. The drugs in this class have the common property of blocking the binding of catecholamines to beta-adrenergic receptor sites; however, there are pharmacodynamic and pharmacokinetic differences between the individual agents which are of clinical importance. Among these differences are the completeness of gastrointestinal absorption, degree of hepatic first-pass metabolism, lipid solubility, protein binding, brain penetration, concentration within cardiac tissue, rate of hepatic biotransformation, and renal clearance of drug and/or metabolites. Long-acting formulations of existing beta-blockers are currently in use, and ultrashort-acting agents are also available. The pharmacokinetics of beta-blocking drugs can also be influenced by race, age, cigarette smoking and concomitant drug therapy. The wide interpatient variability in plasma drug concentration observed with beta-blockers makes this parameter unreliable in routine patient management. Despite the pharmacokinetic differences among the beta-blockers, these drugs should always be titrated in the individual patient to achieve the desired clinical response.

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“…Fig. 6 6 Response of left ventricular ejection fraction to exercise before and after propranolol treatment. Each solid line represents the change in the response of exercise left ventricular ejection fraction during propranolol treatment in an individual patient.…”

Section: Left Ventricular Ejection Fractionmentioning

confidence: 99%

“…[2][3][4][5] In addition, the effects of oral propranolol on myocardial function at rest have not been characterised completely. [6][7][8] Since the effects of propranolol should be most pronounced during periods of sympathetic stimulation (such as exercise), and since the chronic oral effects of propranolol may be different from those produced by single dose intravenous treatment it seems important to evaluate the influence of chronic oral propranolol treatment on left ventricular function both at rest and during exercise. Several preliminary reports and one recent detailed communication have sug.…”

mentioning

confidence: 99%