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Effects of digoxin on left ventricular function in coronary artery disease patients
Insights
Acute digoxin administration improves resting left ventricular function but does not enhance exercise tolerance or prevent deterioration during ischemia in patients with coronary artery disease.
Area of Science:
- Cardiology
- Pharmacology
- Nuclear Medicine
Background:
- Coronary artery disease (CAD) can lead to left ventricular dysfunction during ischemia.
- Digitalis (digoxin) is a medication used to treat heart conditions.
- The effect of acute digoxin administration on ventricular function during ischemia is not fully understood.
Purpose of the Study:
- To evaluate if digoxin modifies or prevents the decline in left ventricular ejection fraction (LVEF) and wall motion during acute ischemia.
- To assess the impact of intravenous digoxin on exercise tolerance and angina in patients with CAD.
Main Methods:
- Gated blood pool radionuclide ventriculograms were performed in 15 patients with CAD.
- Studies were conducted at rest and during maximal exercise, before and after intravenous digoxin administration.
- Left ventricular ejection fraction, wall motion, and exercise tolerance were assessed.
Main Results:
- Digoxin significantly improved resting LVEF (53% to 58%, P < 0.05).
- No significant difference was observed in exercise tolerance, exercise-induced wall motion abnormalities, or LVEF during exercise post-digoxin.
- Ten patients developed angina during exercise, regardless of digoxin administration.
Conclusions:
- Acute intravenous digoxin improves resting left ventricular function in patients with CAD.
- Digoxin does not improve exercise tolerance to the point of angina or prevent the deterioration of LVEF and wall motion during exercise-induced ischemia.
Abstract:
To assess whether digitalis modifies or prevents the deterioration of the left ventricular ejection fraction and wall motion during acute ischemia, we performed gated blood pool radionuclide ventriculograms in 15 patients with angiographically documented coronary artery disease. All patients were studied in the resting state and during maximal supine bicycle exercise, both before and 1 hour after 1 mg intravenous digoxin. There was no significant difference, pre-digoxin vs post-digoxin, in exercise tolerance (415 +/- 84 vs 418 +/- 107 seconds), number of segments with abnormal resting wall motion (12 vs 11) or exercise wall motion (21 vs 19). Ten patients developed angina during the same exercise load, irrespective of digoxin administration. Twelve patients had subnormal left ventricular ejection fraction during exercise pre-digoxin, vs 13 patients post-digoxin (P = ns). In the resting state, the left ventricular ejection fraction was higher after digoxin (53 +/- 14% pre vs 58 +/- 14% post, P less than 0.05). During exercise, however, the left ventricular ejection fraction was not significantly improved after digoxin (50 +/- 16% pre vs 53 +/- 17% post, P = ns). These data indicate that although acute administration of digoxin improves the resting left ventricular function, it does not improve exercise tolerance to angina. Furthermore, intravenous digoxin does not appear to prevent the deterioration of left ventricular wall motion and ejection fraction during exercise induced ischemia.