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Effects of propranolol on left ventricular wall movement in patients with ischaemic heart disease
Insights
Propranolol affects normal subjects and patients with ischemic heart disease differently. Its effects on cardiac function in these groups cannot be predicted from normal subject data.
Area of Science:
- Cardiology
- Pharmacology
- Biomedical Engineering
Background:
- Assessing propranolol's impact on cardiac function is crucial for managing ischemic heart disease.
- Left ventricular wall motion analysis provides insights into myocardial performance.
Purpose of the Study:
- To evaluate the acute and chronic effects of propranolol on left ventricular wall motion in normal subjects and patients with ischemic heart disease.
- To compare propranolol's cardiac effects in patients with coordinated versus uncoordinated ventricular contractions.
Main Methods:
- Simultaneous echocardiography, apexcardiography, and phonocardiography were used.
- Measurements were taken in 10 normal subjects and 16 patients with ischemic heart disease (9 coordinated, 7 uncoordinated).
- Propranolol was administered at a dose of 0.1 mg/kg intravenously or orally for one week.
Main Results:
- Propranolol slightly reduced heart rate and peak VCF in all participants.
- In normal subjects, propranolol increased specific time intervals related to cardiac cycles.
- In ischemic heart disease patients, effects varied: group A showed early cessation of inward wall movement; group B exhibited prolonged relaxation and aggravated uncoordinated relaxation.
Conclusions:
- Propranolol's effects on ischemic heart disease patients are complex and not predictable from normal subject data.
- The drug's impact differs based on the coordination of ventricular contraction.
- Non-invasive techniques measuring time intervals are effective for assessing complex drug effects on cardiac function.
Abstract:
To assess the acute and chronic effects of propranolol on left ventricular wall motion, simultaneous, echo-, apex-, and phonocardiograms were recorded in 10 normal subjects and in 16 patients with ischaemic heart disease, nine with co-ordinate (group A) and seven with incoordinate (group B) contraction in the control site. Records were made after 0.1 mg/kg intravenous or oral therapeutic dose for one week. In all, propranolol caused small reductions in heart rate and peak VCF. In normal subjects, intravenous and oral propranolol caused rate-related increases in the intervals Q to A2, Q to minimum dimension, and Q to mitral valve opening. The effects were different in patients with ischaemic heart disease. In group A, inward wall movement ceased 80 ms early, and this was not attributable to a change in heart rate. Diastolic events were unaltered. In group B, minimum dimension already occurred early. Propranolol did not alter systolic events further, but increased delay in mitral valve opening, 'O' point, prolonged isovolumic relaxation, reduced peak rate of dimension increase, and aggravated incoordinate relaxation. It is concluded that the effects of propranolol in patients with ischaemic heart disease are modified in a manner that cannot be predicted from observations made in normal subjects. It also appears that complex drug effects can be assessed in man from the measurement of time intervals derived from multiple non-invasive techniques.