Masayoshi Korenaga

Oxygen uptake kinetics are determined by cardiac function at onset of exercise rather than peak exercise in patients with prior myocardial infarction.

BACKGROUND Resting cardiac function does not necessarily affect exercise capacity. However, to determine whether it affects early dynamics of oxygen uptake (VO2) during exercise, we measured VO2 during a constant work rate and during incremental exercise testing in patients with a history of myocardial infarction. VO2 kinetics and exercise capacity were compared between patients with relatively high left ventricular ejection fractions (LVEF > or = 35%, group 1) and those with lower ejection fractions (LVEF < 35%, group 2). METHODS AND RESULTS Forty patients with a history of prior myocardial infarction (age, 57 +/- 10 years) were monitored during 6 minutes of moderate constant work rate testing (40 +/- 8 W) and during symptom-limited incremental exercise testing with a cycle ergometer. VO2 was calculated from respired gas analysis on a breath-by-breath basis. Cardiac output determinations were made with a computerized cadmium telluride detector every 10 seconds during exercise. The VO2 time constant during constant work rate exercise was slower in group 2 (58.0 +/- 7.6 seconds) compared with group 1 (45.8 +/- 10.5 seconds, P = .0002), indicating slower kinetics in group 2. The time constant for the rise in cardiac output during exercise was also slower in patients with lower EFs (63.0 +/- 12.8 versus 50.0 +/- 12.2 seconds). However, there were no differences in exercise capacity parameters, such as the VO2 or cardiac output at peak exercise, obtained during incremental exercise testing among the two groups. CONCLUSIONS The prolonged time constant of VO2, which is primarily determined during early parts of exercise, reflects delayed cardiac output response in patients with severely impaired LV function. The time constant of VO2 during submaximal constant work rate exercise can be used as a sensitive and discriminant measure of impaired cardiac reserve in these patients.

Effects of nicorandil on kinetics of oxygen uptake at the onset of exercise in patients with coronary artery disease

The beneficial effects of coronary vasodilators on exercise capacity in patients with angina pectoris are well known. However, their effects on oxygen uptake (VO2) kinetics at the onset of exercise have not been elucidated. The present study was undertaken to determine the acute effects of nicorandil, a newer coronary vasodilator, on the kinetics of VO2 at the onset of exercise in patients with ischemic heart disease. Ten patients with significant coronary stenosis performed constant mild-intensity cycle exercise (32 +/- 3 W) for 6 minutes after oral administration of 10 mg of nicorandil or an identical placebo in a double-blind, crossover manner. Nicorandil had no effect on resting heart rate, blood pressure, or VO2. However, the time constant for the increase in VO2 during constant work rate exercise was significantly shorter (the kinetics of VO2 were faster) after administration of nicorandil than after placebo (46.5 +/- 13.3 vs 51.1 +/- 11.9 seconds; p = 0.039). The increase in VO2 at 6 minutes compared with 3 minutes of constant work, which reflects the VO2 kinetics, also was reduced with nicorandil (3.8 +/- 37.9 vs 27.5 +/- 27.1 ml/min; p = 0.022). Nicorandil was found to increase the rate of VO2, increase during the onset of constant work rate exercise, probably as a result of an improved response in cardiac output. Analysis of VO2 kinetics provides new and useful parameters for the evaluation of circulatory adjustments at the onset of exercise in patients with ischemic heart disease.

Longitudinal Dissociation in the His Bundle: A Possible Mechanism of Two Distinct Cycle Lengths in Atrioventricular Reentrant Tachycardia

Two wide QRS tachycardias with identical morphology but different cycle lengths (CLs) developed in a 63‐year‐old man. Electrophysiological study demonstrated inducible atrioventricular reentrant tachycardia (AVRT) due to a concealed left posterior accessory pathway (AP), which was successfully ablated by radiofrequency application. Neither dual AV nodal pathways nor other APs were documented. Splitting of the His‐bundle electrogram was shown, and programmed stimulation induced sudden prolongation of intra‐hisian conduction time. These results suggest longitudinal dissociation in the His bundle may be responsible for two distinct CLs in AVRT without dualAV nodal physiology.