Effects of intravenously administered digoxin on mild left ventricular failure in acute myocardial infarction in man

Morrison Hodges, Gottlieb C. Friesinger, Robert C.K. Riggins, Giles R. Dagenais

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Studies were made in 10 patients with early mild left ventricular failure in acute myocardial infarction to determine the hemodynamic correlates of the condition and evaluate the effects of intravenously administered digoxin. Studies were performed within 72 hours of infarction. Patients with basilar rales, tachycardia and ventricular (S3) gallop sound were selected for study. Findings during the control period were consistent with mild left ventricular failure. Stroke index was below normal (28 ± 7.1 ml/m2), but cardiac index was within normal limits (3.22 ± 0.60 liters/min per m2) because of tachycardia. Stroke work index was low (39 +- 13.7 g-m/m2), and pulmonary arterial end-diastolic pressure was minimally increased (15.2 ± 3.5 mm Hg). After intravenous administration of digoxin (0.75 mg in 7 patients, 1.0 mg in 3 patients), there were no statistically significant changes in any of the measured variables when the whole group was considered. Relating stroke work index to pulmonary arterial diastolic pressure, 2 types of responses were found. Four patients had a distinct inotropic response; the other 6 patients had no significant change, or a worsening of function. The reasons for a variable response in the early phase of infarction may be related to the regional nature of infarction or possibly to humoral factors influencing myocardial performance. Data suggest that digitalis is of limited value during this stage of infarction. Further studies and more precise characterization of patients may provide insight into the role of digitalis in the early phases of acute infarction.

Original languageEnglish (US)
Pages (from-to)749-756
Number of pages8
JournalThe American Journal of Cardiology
Issue number6
StatePublished - Jun 1972
Externally publishedYes

Bibliographical note

Funding Information:
Unit and Cardiovascular Division, Department of Medicine, Johns Hopkins University School of Medioine, Baltimore, Md. This research was supported by the U. S. Publ.ic Health Service, National Institutes of Health, Contract PH-43-67-1444. Manuscript received July 12, 1971, accepted October 1, 1971. * Present address: University of Rochester, Rochester, N. Y. f Dr. Friesinger was a Clayton Scholar during thse period of this investigation. $ Present address and address for reprints: Gottlieb C. Friesinger, MD, Division of Cardiology, Vanderbilt University Hoa-pital, Nashville, Tenn. 37203.


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