Toshimitsu Jikuhara

Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction.

Motohiro M, Yuasa F, Hattori T, Sumimoto T, Takeuchi M, Kaida M, Jikuhara T, Hikosaka M, Sugiura T, Iwasaka T: Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction. Am J Phys Med Rehabil 2005;84:684–691. Objective: This study examined the cardiovascular adaptations of an exercise training program and evaluated the role of peripheral vasodilator capacity in contributing to these adaptations after myocardial infarction. Design: A total of 44 consecutive patients with uncomplicated myocardial infarction underwent 3 wks of exercise training. Controls (n = 12) with comparable myocardial infarction were selected from our database and were restricted to a program with minimal activity. All patients performed cardiopulmonary exercise testing with hemodynamic measurements. Forearm and calf reactive hyperemic flow were measured by venous occlusive plethysmography as indices of peripheral vasodilator capacity. Results: Despite no change in arteriovenous oxygen difference at peak exercise after training, training resulted in significant increases in oxygen consumption, cardiac output, and stroke volume and a significant decrease in systemic vascular resistance at peak exercise (overall, P < 0.05). Calf reactive hyperemic flow increased significantly after training (P < 0.001), but forearm reactive hyperemic flow did not. Furthermore, increase in calf reactive hyperemic flow after training had a positive correlation with increases in peak cardiac output, stroke volume, and oxygen consumption after training and an inverse correlation with peak systemic vascular resistance. Conclusions: Exercise training improved exercise tolerance by improving hemodynamic responses to exercise after myocardial infarction. This improved exercise performance was linked to a training-induced increase in calf vasodilator capacity.

Importance of left ventricular diastolic function on maintenance of exercise capacity in patients with systolic dysfunction after anterior myocardial infarction

To investigate the role of left ventricular (LV) diastolic function in the maintenance of exercise capacity in patients with systolic dysfunction, symptom-limited cardiopulmonary exercise testing combined with radionuclide ventriculography was performed in 24 patients with an LV ejection fraction < 35% after anterior myocardial infarction. The ratio of pulmonary artery wedge pressure (PAWP) to LV end-diastolic volume (EDV), an index of global diastolic function, correlated significantly with peak oxygen consumption at peak exercise (r = -0.55; p = 0.006), whereas ejection fraction at peak exercise did not. The change in PAWP/EDV ratio from rest to peak exercise was related to the increases in stroke volume (r = -0.54; p = 0.006) and cardiac output (r = -0.51; p = 0.01) during exercise, but the change in ejection fraction was not. Resting hemodynamics did not differ between patients with preserved exercise capacity (group 1, n = 8) and those with exercise impairment (group 2, n = 16). At peak exercise, stroke volume, cardiac output, and EDV were significantly higher, and PAWP and PAWP/EDV ratio were significantly lower in group 1 than in group 2, but ejection fraction and end-systolic volume were similar in both groups. Although the incidences of hypertension, LV hypertrophy, and infarct-related coronary artery lesions did not differ between the two groups, group 2 had a significantly higher incidence of non-infarct-related coronary artery lesions than group 1 (p < 0.05). Thus in patients with LV systolic dysfunction after anterior myocardial infarction, the major cause of exercise impairment and failure to increase LV performance during exercise was diastolic dysfunction associated with the presence of non-infarct-related coronary artery lesions with the potential for exercise-induced ischemia of the noninfarcted areas.

Effects of left ventricular diastolic dysfunction on exercise capacity three to six weeks after acute myocardial infarction in men

To examine the effects of left ventricular (LV) diastolic dysfunction on exercise capacity, hemodynamic and radionuclide responses were measured at rest and during exercise in 50 patients with recent myocardial infarction. The ratio of an increase in pulmonary arterial wedge pressure (PAWP) to an increase in LV end-diastolic volume (EDV) from rest to peak exercise (delta PAWP/delta EDV) was used as an index of LV diastolic function, delta PAWP/delta EDV had modest and negative correlations with peak oxygen consumption (VO2), cardiac output, and stroke volume in all patients. Among patients with peak VO2 > or = 20 ml/min/kg (group I, n = 24) and those with peak VO2 < 20 ml/min/kg (group II, n = 26), there were no differences between the 2 groups with regard to resting LV ejection fraction, EDV, PAWP, cardiac output, and stroke volume. Although there was no significant difference in LV ejection fraction at peak exercise, group II had significantly reduced EDV, increased PAWP, and decreased cardiac output and stroke volume than those in group I. As a result, delta PAWP/delta EDV was significantly higher in group II. These results suggest that LV diastolic dysfunction has a key role in determining exercise capacity in patients with reduced exercise capacity after recent myocardial infarction.

Skeletal muscle hypoperfusion during recovery from maximal supine bicycle exercise in patients with heart failure

Leg blood flow (LBF) and its relation to central hemodynamics were examined during recovery following maximal supine bicycle exercise in 11 patients with heart failure and 20 patients with normal exercise capacity after myocardial infarction. The results indicate that LBF was markedly reduced in patients with heart failure, and that decreased cardiac output response and enhanced peripheral vasoconstriction, which functioned to prevent hypoperfusion in the nonexercising vital regions and to maintain arterial blood pressure, were responsible for the reduced LBF during recovery in heart failure.

Influence of intrinsic limb vasodilator capacity on exercise tolerance in patients with recent myocardial infarction

To investigate the influence of intrinsic limb vasodilator capacity on exercise performance, limb reactive hyperemic flows and their relations to exercise capacity during upright bicycle exercise were examined in 52 patients with recent myocardial infarction. Reactive hyperemic flow was measured in the forearm and the calf by venous occlusive plethysmography after 5 min of arterial occlusion. Calf reactive hyperemic flow correlated significantly with cardiac output, systemic vascular resistance, and oxygen consumption at peak exercise, whereas flow in the forearm did not. In patients with preserved exercise capacity (group 1, n = 20) compared with those with exercise impairment (group 2, n = 32), calf reactive hyperemic flow was significantly augmented, but forearm flow was similar in the two groups. There were no significant differences in hemodynamic parameters at rest between the two groups. At peak exercise, however, cardiac output was lower and systemic vascular resistance was higher in group 2 than in group 1, whereas arterial blood pressure was maintained identically in the two groups. Thus, intrinsic calf but not forearm vasodilator capacity was linked to exercise hemodynamic responses and exercise capacity in patients with recent myocardial infarction. In addition, reduced calf vasodilation and concomitant enhanced vascular tone seemed to be useful for preserving arterial blood pressure in the setting of decreased cardiac output response to exercise in patients with exercise impairment.

Importance of intrinsic calf vasodilator capacity in determining distribution of skeletal muscle perfusion during supine bicycle exercise in patients with left ventricular dysfunction

BACKGROUND Distribution of skeletal muscle perfusion during exercise is an important factor in determining exercise capacity and is markedly impaired in patients with cardiac disease. This study examined the importance of intrinsic calf vasodilator capacity in determining distribution of skeletal muscle perfusion during supine bicycle exercise in patients with left ventricular dysfunction. METHODS We studied 19 patients with left ventricular dysfunction (left ventricular ejection fraction <45%) after myocardial infarction. All the patients underwent cardiopulmonary exercise testing with measurements of central hemodynamics, leg blood flow (LBF), and the percentage of cardiac output distributed to both legs (%LBF). Calf reactive hyperemic flow (RH) was measured by venous occlusive plethysmography at supine rest. RESULTS LBF at peak exercise was closely related to peak cardiac output and RH. Furthermore, %LBF at peak exercise had modest correlation with peak cardiac output and good correlation with RH. Although peak cardiac output and RH were independent determinants of LBF at peak exercise by multiple regression analysis, RH had higher correlation with %LBF at peak exercise than peak cardiac output. Despite marked changes in other hemodynamic variables, nonleg blood flow during exercise was constantly maintained at a level identical to resting value. CONCLUSIONS Calf vasodilator capacity, which was the major determinant of distribution of skeletal muscle perfusion during exercise, may have contributed to maintaining perfusion of important nonexercising regions during exercise in patients with left ventricular dysfunction.

The effects of infusion of trieicosapentaenoyl-glycerol emulsion on extravascular lung water during myocardial ischemia and reperfusion in dogs

To test the effects of eicosapentaenoic acid (EPA) infusion on pulmonary edema induced by coronary ligation and reperfusion, extravascular lung water (EVLW) was measured in situ by the thermal-dye double indicator dilution method in dogs. In the control group of five dogs, 30 mL of a 10% soybean oil emulsion was infused through a leg vein. One hour after infusion, the left anterior descending coronary artery below the first diagonal branch was ligated for 15 min and then reperfused for 30 min. In the EPA group, six dogs were similarly treated with an emulsion of a 10% trieicosapentaenoyl-glycerol (90% pure). EVLW, pulmonary capillary wedge pressure, mean pulmonary artery pressure, mean blood pressure, and cardiac index were measured before and 15 min after coronary ligation, and 15 min and 30 min after coronary reperfusion. There were no significant differences in the hemodynamic indices between the two groups. EVLW significantly increased up to two times of baseline during coronary ligation in the control group (P< 0.05) and more during reperfusion (P<0.01), whereas EVLW did not increase in the EPA group. In conclusion, EPA inhibited EVLW accumulation and may be useful for ameliorating one of the ischemia-reperfusion-induced complications, pulmonary edema.