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Effects of digitalis on normal and abnormal left ventricular segmental dynamics
Insights
Digoxin improved overall heart function in patients with coronary disease. However, it worsened performance in some heart segments, suggesting potential risks despite overall benefits.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Coronary artery disease (CAD) often leads to regional left ventricular (LV) dysfunction.
- Understanding how positive inotropic agents affect regional LV performance in CAD is crucial.
Purpose of the Study:
- To investigate the effects of digoxin on regional left ventricular (LV) performance in patients with stable coronary disease.
- To assess whether digoxin improves or exacerbates segmental LV abnormalities.
Main Methods:
- Nine patients with stable coronary disease underwent continuous ventricular dynamics assessment.
- Computer-assisted analysis of fluoroscopic motion of surgically implanted myocardial markers was used to define LV segments.
- Measurements included mean velocity of circumferential fiber shortening and ejection fraction before and after digoxin administration.
Main Results:
- Digoxin significantly increased mean velocity of circumferential fiber shortening (19%) and ejection fraction (4.5%) in patients with coronary disease.
- While 83-91% of normal LV segments improved, only 45-55% of initially abnormal segments showed benefit.
- Segmental dyssynergy increased in some areas, even with enhanced overall ventricular function.
Conclusions:
- Digoxin enhances overall left ventricular (LV) performance in patients with coronary disease.
- However, digoxin may deteriorate performance in abnormal LV regions due to increased afterload and improved dynamics in normal areas.
- These findings highlight potential risks of digoxin in patients with heterogeneous LV dysfunction from coronary artery disease.
Abstract:
To study the effects of digoxin on regional left ventricular performance, continuous ventricular dynamics were assessed in nine patients with stable coronary disease. Computer-assisted analysis of the fluoroscopic motion of surgically implanted mid wall myocardial markers was used. The markers define six minor ventricular radii and outline the left ventricle. One and one-half hours after administration of 1 mg of intravenous digoxin, mean velocity of circumferential fiber shortening for all segments increased 19 percent, from 0.67 +/- 0.06 to 0.78 +/- 0.06 circumference/sec (P less than 0.01) and ejection fraction increased 4.5 percent, from 0.50 +/- 0.03 to 0.53 +/- 0.03 (P less than 0.05). Segmental velocity of circumferential fiber shortening, total segmental shortening and early segmental systolic shrtening increased in 83 percent to 91 percent of normal segments, depending on which index was used. Only 45 to 55 percent of initially abnormal segments benefited from digoxin. In general, segmental dyssynergy increased even when net ventricular function was enhanced. These results suggest that in pateints with chronic left ventricular contraction abnormalities due to coronary disease, deterioration of performance in abnormal regions after administration of digoxin may result from increased stress imposed by increased afterload and by improved segmental dynamics in more normal areas.
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