Angiotensin converting enzyme (ACE) inhibitors are of proven value in patients with severe chronic heart failure (CHF). Studies of the effects of ACE inhibitors on exercise capacity and quality of life in mild CHF have produced conflicting results. We have studied the effects of quinapril, a new ACE inhibitor with a relatively short plasma half-life, in mild CHF. Once daily (o.d.) dosing was compared with twice daily (b.i.d.) dosing in a three-way cross-over, double-blind, placebo-controlled trial. Thirty-two patients (two female), mean age 59 (range 32-76) years were enrolled in three cardiology centres in the U.K. in 29 patients, and non-ischaemic in three. The mean (range) radionuclide ejection fraction was 20.4% (8%-47%). Following full familiarization with the protocol, the treadmill exercise time (modified Bruce protocol) was determined for each patient during a placebo run-in phase, and at the end of each of three 8-week double-blind treatment phases with quinapril o.d., quinapril b.i.d. (maximal total daily dose 20 mg) and placebo. Three patients were withdrawn due to adverse events while receiving quinapril (unstable angina, exacerbation of CHF and arrhythmia); there were no deaths and no patient was withdrawn due to hypotension. Mean exercise time (the primary end-point) was 65 s and 53 s longer in patients receiving quinapril o.d. and b.i.d. respectively compared to placebo (both P < 0.01, ANOVA). There was no significant period effect during the trial and no significant difference between the two quinapril dosing regimens. Quinapril had no significant effect on secondary end-points including ejection fraction, functional class and quality of life.(ABSTRACT TRUNCATED AT 250 WORDS)
1. The non-invasive method of near-infrared spectroscopy was used to measure myocardial oxygenation and haemodynamics in response to left anterior descending coronary artery occlusion in a porcine model. 2. Near-infrared spectroscopy measures changes in haemoglobin (and myoglobin) oxygenation and blood volume to yield information on tissue perfusion and flow. It also measures the redox state of cytochrome aa3, thus providing information about intracellular oxygen utilization. 3. Left anterior descending coronary artery occlusion was induced to produce periods of ischaemia lasting between 24s and 13.5 min (n = 13). The changes in deoxyhaemoglobin, oxyhaemoglobin and cytochrome aa3 measured during occlusion were all highly significant compared with baseline variation. In all occlusions (n = 13) a rapid decrease in oxyhaemoglobin concentration (-75.83 +/- 3.27 mumol/l, mean +/- SEM) with a simultaneous increase in deoxyhaemoglobin of 9.27 +/- 1.69 mumol/l was measured. The total haemoglobin concentration also fell by -71.3 +/- 5.32 mumol/l. Cytochrome aa3 was also reduced during occlusion (-8.35 +/- 1.044) mumol/l. 4. Over the range 24-60s occlusion, the magnitude of the fall in total haemoglobin and oxyhaemoglobin correlated with the duration of occlusion (P < 0.003 and 0.013 respectively). For total haemoglobin only the magnitude of the fall correlated with the increase upon release of occlusion (r = 0.89, P < 0.003). 5. Release of occlusion (n = 8) resulted in an immediate increase in the concentration of deoxyhaemoglobin at 9.88 +/- 1.06s, then total haemoglobin at 13.62 +/- 1.23s and finally oxyhaemoglobin at 29.75 +/- 5.96s. The difference between the timing of the maxima after reperfusion is significant (P < 0.002 and P < 0.007 respectively). Moreover, the time for the deoxyhaemoglobin signal to reach maximum values was found to correlate with the duration of occlusion (P < 0.04). This could be indicative of the PO2 of the ischaemic tissues and an immediate off-loading of oxygen from oxyhaemoglobin. The results are reliable, reproducible and sensitive enough to detect the kinetics of haemoglobin oxygenation from a beating heart in situ.
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