Why the study?
Does transient afterload increase with intravenous angiotensin II detect subclinical heart failure using echocardiography?
Does transient afterload increase with intravenous angiotensin II detect subclinical heart failure using echocardiography?
A transient increase in afterload using intravenous angiotensin II combined with echocardiography can reliably detect subclinical heart failure by revealing suppressed left ventricular posterior wall motion.
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May detect subclinical heart failure on angiotensin II stress echocardiography; hypothesis-generating and requires prospective validation before any clinical use.
In an attempt to diagnose latent heart failure, a transient increase of afterload to left ventricle was produced by angiotensin II, and the ventricular movement was assessed by echocardiography. Angiotensin II was administered in a dose of 0.075 micrograms/kg body weight. Blood pressure was elevated by 40.5 +/- 14.5 mmHg in 38 cases with latent heart failure and by 41.2 +/- 4.5 mmHg in 30 normal subjects. Yet, only in the former group, posterior wall excursion of left ventricle reduced from 11.4 +/- 2.4 mm to 7.3 +/- 2.3 mm and mean posterior wall velocity from 41.4 +/- 10.1mm/sec to 26.5 +/- 8.8 mm/sec. The rates of these reductions were inversely correlated to the rate of elevation of left ventricular endodiastolic pressure as determined in 5 cases by cardiac catheterization. There was no change in 30 subjects. The data indicate the usefulness of angiotensin-induced echocardiographic changes in detecting latent cadiac failure.
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Kanaya et al. (1979) studied this question.
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