What question did this study set out to answer?

To quantify the gene expression of angiotensin-converting enzyme in normal and failing human hearts.

Increased angiotensin-I converting enzyme gene expression in the failing human heart. Quantification by competitive RNA polymerase chain reaction.

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Increased cardiac ACE expression may support local RAS activation in HF; leaves open whether it drives remodeling or warrants targeted inhibition.

To quantify the gene expression of angiotensin-converting enzyme in normal and failing human hearts.
Established a competitive RNA-polymerase chain reaction for quantifying ACE and chymase mRNA in heart tissues.
Compared gene expression levels between left ventricles of normal (n = 9) and failing human hearts (n = 20).
Measured ACE RNA-PCR variability and correlated results with traditional slot blot hybridization.
ACE mRNA levels were increased threefold in failing hearts compared to nonfailing hearts (4.2 +/- 2.5 vs. 12.8 +/- 6 x 10(5), P < 0.0005).
No significant difference in chymase gene expression between normal and failing hearts.
Indicates activation of cardiac renin-angiotensin system in advanced heart failure.

Studer et al. (1994) studied this question.

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Increased cardiac ACE expression may support local RAS activation in HF; leaves open whether it drives remodeling or warrants targeted inhibition.