Tsutomu Sumimoto

Mixed venous oxygen saturation as a guide to tissue oxygenation and prognosis in patients with acute myocardial infarction

The relation of mixed venous oxygen saturation and the cardiac index to tissue oxygenation and prognosis was investigated in 119 patients with acute myocardial infarction. There was a positive correlation between mixed venous oxygen saturation and the cardiac index in 97 survivors and 22 nonsurvivors, but a significantly lower mixed venous oxygen saturation level at the same level of cardiac index was observed in nonsurvivors compared with survivors. Results of multivariate analysis with mixed venous oxygen saturation and the cardiac index indicated that only mixed venous oxygen saturation was significantly related to survival and to hyperlactacidemia. Oxygen delivery to tissues declined significantly in nonsurvivors because of a lower cardiac index and a lower hemoglobin concentration in these patients than in survivors. However, at the same level of oxygen delivery to tissues, nonsurvivors had a significantly higher rate of oxygen consumption leading to a correspondingly greater decrease in mixed venous oxygen saturation, suggesting that a greater increase in oxygen demand was also observed in nonsurvivors than in survivors. Thus mixed venous oxygen saturation after acute myocardial infarction is a better predictor of hyperlactacidemia and survival than the cardiac index, and this may be associated with an increased oxygen demand and an impaired oxygen transport system in seriously ill patients.

Left Ventricular Diastolic Filling Properties in Diabetic Patients during Isometric Exercise

Left ventricular diastolic filling properties during isometric handgrip exercise were measured by pulsed Doppler echocardiography in 33 noninsulin-dependent diabetic patients with a normal ejection fraction and 15 control subjects. Diabetic patients were subdivided into two groups according to their resting left ventricular filling pattern (A/E): 18 patients were in group DM-1 (A/E < or = 1.1) and 15 patients were in group DM-2 (A/E > 1.1). At rest, A/E ratio and A wave were higher, and deceleration half-time was longer in group DM-2 than in normal subjects and group DM-1, but there was no significant difference between normal subjects and group DM-1. The A/E ratio increased significantly in all three groups during isometric handgrip exercise. However, the change in A/E from rest to peak exercise in group DM-1 (0.29 +/- 0.20) was significantly greater than in normal subjects (0.09 +/- 0.07). These results suggest that diabetes mellitus patients with normal resting left ventricular (LV) filling pattern (group DM-1) had LV diastolic filling abnormalities with isometric handgrip exercise. Doppler echocardiography with isometric handgrip exercise is useful in identifying underlying left ventricular diastolic dysfunction in diabetic patients.

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.

INCREASED EXTRAVASCULAR LUNG WATER IN PATIENTS WITH LOW PULMONARY ARTERY OCCLUSION PRESSURE AFTER ACUTE MYOCARDIAL INFARCTION

ObjectiveTo evaluate the clinical characteristics of increased extravascular lung water (EVLW) in patients with low pulmonary artery occlusion pressure (PAOP) in the early phase of acute myocardial infarction. DesignConsecutive sample for descriptions of the clinical features of medical disorders. SettingA general medicine group practice in a university hospital. PatientsSixteen patients with low PAOP (>18 mm Hg) on the initial measurement obtained within 12 hr of chest pain onset. Measurements and Main ResultsEVLW was measured by the thermal indocyanine green dye double-indicator dilution method. QRS score was obtained on hospital day 7 from the Selvesters QRS Scoring System. Eleven (69%) patients had increased EVLW >7 mL/kg despite low PAOP. EVLW had no significant correlation with PAOP and the difference between plasma colloid osmotic pressure and PAOP, but did have a significant correlation with pulmonary vascular resistance index (r2 = .31, p < .05), and QRS score (r2 = .45, p < .005). ConclusionLarger infarcts led to increased EVLW even with low PAOP, and the accumulation of increased EVLW around the small arterioles might have led to increased pulmonary vascular resistance. (Crit Care Med 1991; 19:21)

Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise 6 to 8 weeks after acute myocardial infarction

The pattern of oxygen (O2) consumption (VO2), carbon dioxide (CO2) production (VCO2), ventilatory and metabolic responses during and in recovery from supine bicycle exercise was examined in 18 patients with recent myocardial infarction. An increase in VO2 with increasing work load was accomplished by proportional increases in both cardiac output and the arteriovenous O2 difference. During recovery, however, the arteriovenous O2 difference rapidly decreased below levels at rest, whereas VO2 and cardiac output remained elevated, indicating that VO2 during recovery further depended on relatively high cardiac output. The ratio of VCO2 to VO2 further increased after exercise, suggesting that such cardiac output contributed to the remaining high CO2 flow to the lung and therefore enhanced ventilation. Increased arterial catecholamines during exercise remained elevated for the first 5 minutes of recovery. Arterial lactate during this period continued to increase and resulted in profound metabolic acidosis, causing alveolar hyperventilation after exercise. These results suggest that during recovery from exercise, cardiopulmonary responses remain enhanced because of continuing high cardiac output, resulting in subsequent high CO2 flow to the lung and metabolic acidosis, and that this may be associated with profound fatigue or dyspnea after exercise.

Oxygen delivery, oxygen consumption and hemoglobin-oxygen affinity in acute myocardial infarction

The interrelations of oxygen delivery (DO2), oxygen consumption (VO2) and hemoglobin-oxygen affinity assessed by P50 were investigated in 43 patients with acute myocardial infarction. As DO2 declined due to low cardiac output, a significant decrease in VO2 (r = 0.75, p less than 0.001) and a significant increase in P50 (r = -0.74, p less than 0.001) were observed. In the DO2 range between 300 and 450 ml/min/m2, in which the DO2 of 32 survivors and 11 nonsurvivors overlapped, the P50 of nonsurvivors was significantly higher than that of survivors (31.5 +/- 1.6 vs 27.9 +/- 1.5 torr, p less than 0.001), but there were no significant differences in any other oxygen transport variable. As a result of differences in P50, VO2 in this range was significantly higher in nonsurvivors compared to survivors (169 +/- 17 vs 148 +/- 13 ml/min/m2, p less than 0.001). These data suggest that a normal or increased VO2 alone does not ensure survival in patients with acute myocardial infarction, and increased P50 leads to an increase in VO2. Nevertheless, the interpretation of an increased P50 in patients with acute myocardial infarction must be made with caution, even with adequate DO2 and VO2, because it may imply a precarious oxygen transport/requirement balance in peripheral tissue and, hence, a fatal outcome.

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.

Right ventricular ejection fraction during exercise in patients with recent myocardial infarction: Effect of the interventricular septum

To investigate the effect of interventricular septum (IVS) on right ventricular function during exercise, radionuclide angiocardiography was performed in 50 patients with recent myocardial infarction. Twenty-five patients had involvement of IVS according to thallium uptake in IVS (group I), and 25 patients were free of IVS involvement (group II). Although there was no statistical difference between the two groups in right ventricular ejection fraction (EF) at rest (45% +/- 10% vs 48% +/- 8%), patients in group I had significantly lower left ventricular (LV) EF (40% +/- 11% vs 53% +/- 11%, p < 0.01) and larger LV end-diastolic volume (129 +/- 46 vs 106 +/- 31 ml, p < 0.05) than those in group II. All parameters increased significantly during exercise in both groups, but patients in group I had significantly lower exercise right ventricular EF (50% +/- 10% vs 56% +/- 9%, p < 0.05), LVEF (44% +/- 11% vs 56% +/- 13%, p < 0.01), and larger LV end-diastolic volume (155 +/- 44 vs 129 +/- 37 ml, p < 0.05) than those of group II. Significant correlations were observed between right ventricular EF and LV end-diastolic volume at rest and during exercise (r = -0.48, p < 0.05, and r = -0.68, p < 0.01, respectively) in group I, but right ventricular EF correlated with LVEF only at peak exercise (r = 0.65, p < 0.01). In contrast, right ventricular EF did not correlate with any variables at rest or during exercise in group II.(ABSTRACT TRUNCATED AT 250 WORDS)