Changes in myocardial microcirculation are a characteristic feature of essential hypertension. Research has shown that in hypertensive patients, the myocardium has decreased perfusion reserve and increased minimal vascular resistance. These abnormalities may relate to changes, such as narrowing, in resistance artery structure.

Previous investigations have shown that angiotensin-converting enzyme (ACE) inhibitor treatment improved resistance artery structure. By contrast, beta-blocker treatment did not improve resistance artery structure, even though it reduced blood pressure to a similar degree.

Based on those findings, Dr. Buus and co-investigators hypothesized that an ACE inhibition would also improve minimal myocardial vascular resistance, while beta-blockade would not. To test this, they compared long-term treatment with the ACE inhibitor perindopril or the beta-blocker atenolol in patients with essential hypertension. They evaluated the effect of treatment on myocardial perfusion and vascular resistance.

The researchers randomized 30 patients (mean age 50 years) with previously untreated essential hypertension to perindopril (4-8 mg) or atenolol (50-100 mg). Researchers allowed dosage adjustment to reach a diastolic blood pressure of less than 90 mmHg. They measured myocardial perfusion at rest and during dipyridamole-induced hyperemia using positron emission tomography. These measurements occurred before and after 12 months of treatment.

Reduction in blood pressure was similar between the two treatment groups. Ambulatory blood pressure decreased in the perindopril group from 160/105 to 138/88 mmHg (p < 0.01). Blood pressure reduction decreased from 158/105 to 131/86 mmHg in the atenolol group (p < 0.01).

Both drugs decreased resting myocardial perfusion. In the atenolol group, the decrease was from 0.91 to 0.67 ml/g/min. There was a smaller decrease in the perindopril group, from 0.95 to 0.84 ml/g/min. However, there was no difference between treatments when investigators corrected for changes in myocardial workload (expressed as the rate-pressure product). On the other hand, atenolol markedly reduced hyperemic myocardial perfusion, while perindopril did not.

In addition, atenolol significantly increased hyperemic vascular resistance compared with perindopril.

These results suggest that there is a difference in the way ACE inhibition and beta-blockade affect myocardial circulation. This difference occurs despite similar reduction in blood pressure. Both drugs reduce resting myocardial perfusion. However, atenolol markedly reduces hyperemic myocardial perfusion, while perindopril does not. Atenolol increases hyperemic vascular resistance compared with perindopril.

Based on these results, it appears that patients may require a vasodilating therapy to improve hypertensive myocardial microcirculation.