Determinants of stroke volume response to exercise in patients with mitral stenosis: a Doppler echocardiographic study.

OBJECTIVES: The aim of this study was to assess exercise-induced changes in stroke volume and their main determinants in mitral stenosis. BACKGROUND: The mechanisms of the stroke volume response to exercise in mitral stenosis are not clearly established. METHODS: Twenty-seven patients with mitral stenosis, aged 47 +/- 13 years, and 10 healthy control subjects, aged 46 +/- 11 years, were examined by Doppler echocardiography to obtain stroke volume, mitral velocity-time integral and calculated mitral valve area (by continuity equation) at rest and during submaximal supine bicycle exercise. Measured mitral valve area at rest and total mitral score were also obtained. RESULTS: During exercise, stroke volume increased significantly (p < 0.001) in the control subjects (+25 +/- 6%) but remained unchanged in the patients. In 10 patients (Group I), stroke volume increased by > or = 14% (+23 +/- 10%, p < 0.001); in the other 17 (Group II), it decreased or increased by < 14% (-5 +/- 14%, p = NS). Mitral velocity-time integral did not change in the three groups, whereas calculated mitral valve area increased significantly (p < 0.001) and similarly in Group I and the control group but remained unchanged in Group II. The exercise change in calculated mitral valve area correlated significantly with both measured mitral valve area at rest (r = 0.46, p < 0.05) and total mitral score (r - 0.53, p < 0.005). However, at constant mitral score, exercise change in calculated mitral valve area no longer correlated significantly with measured mitral valve area at rest. CONCLUSIONS: In mitral stenosis, the change in stroke volume during exercise depends on the change in mitral valve area, which itself depends on the degree of mitral valve damage.

Comparison of oxygen uptake during bicycle exercise in patients with chronic heart failure and in normal subjects.

Prediction of oxygen uptake (VO2) during exercise from relations established in normal subjects between VO2 and work load in watts (W) may be inaccurate in patients with chronic heart failure because these patients could manifest delayed VO2 kinetics at final stages of exercise. To test the hypothesis that even at low levels of work, patients exhibit a lower VO2 than do normal subjects, 77 patients with heart failure and 27 control subjects with a normal heart or with disease other than heart failure underwent bicycle exercise with respiratory gas analysis. Work load was increased by 10 W/min from an initial 20 W. VO2 (ml/min per kg) was measured every 15 s. The delta VO2/delta W ratio was significantly reduced only in the most severely impaired patients in heart failure class C-D (8.75 +/- 2.14 versus 11.05 +/- 0.38, p less than 0.05). Class B patients showed a lower ratio at a work load of greater than or equal to 80 W, whereas class C-D patients manifested a lower ratio at greater than or equal to 20 W. Even with a low incremental work rate protocol, compared with sedentary normal subjects or patients without heart failure, patients with heart failure demonstrate impaired oxygen uptake. This observation suggests the presence of anaerobic metabolism or delayed VO2 uptake, or both; accordingly, indirect estimates of VO2 requirements derived from intensity or duration of exercise in such patients are overestimated.

Influence of preload reserve on stroke volume response to exercise in patients with left ventricular systolic dysfunction: a Doppler echocardiographic study.

OBJECTIVES: This study evaluated the role of preload reserve in the stroke volume response to exercise in patients with left ventricular systolic dysfunction by assessing the relation between stroke volume and late left ventricular diastolic filling during exercise. BACKGROUND: In patients with left ventricular diastolic dysfunction, the absence of left ventricular distension is the fundamental mechanism explaining the nonaugmentation of stroke volume during exercise. METHODS: In 32 patients with left ventricular systolic dysfunction and 16 healthy control subjects, mitral and aortic velocities were recorded by Doppler echocardiography at rest and during submaximal supine bicycle exercise. Stroke volume, peak early (E) and late (A) mitral velocities, A/E ratio and end-diastolic filling were measured at rest and during exercise. RESULTS: Stroke volume increased significantly in control subjects but did not change in patients. Peak early mitral velocity increased significantly and to the same extent in both groups, whereas peak late mitral velocity and end-diastolic filling increased significantly in both groups but more so in control subjects; the A/E ratio increased significantly in control subjects but did not change in patients. In addition, stroke volume correlated significantly with peak late mitral velocity during exercise in patients (r = 0.72, p < 0.001). CONCLUSIONS: Compared with control subjects, patients with left ventricular systolic dysfunction exhibited limited increases in both stroke volume and late left ventricular filling during exercise. Furthermore, their stroke volume response correlated with the capacity of the left ventricle to increase late diastolic filling, that is, preload reserve.

Cardiac metaiodobenzylguanidine uptake in patients with moderate chronic heart failure: relationship with peak oxygen uptake and prognosis.

OBJECTIVES: This prospective study was undertaken to correlate early and late metaiodobenzylguanidine (MIBG) cardiac uptake with cardiac hemodynamics and exercise capacity in patients with heart failure and to compare their prognostic values with that of peak oxygen uptake (VO2). BACKGROUND: The cardiac fixation of MIBG reflects presynaptic uptake and is reduced in heart failure. Whether it is related to exercise capacity and has better prognostic value than peak VO2 is unknown. METHODS: Ninety-three patients with heart failure (ejection fraction <45%) were studied with planar MIBG imaging, cardiopulmonary exercise tests and hemodynamics (n = 44). Early (20 min) and late (4 h) MIBG acquisition, as well as their ratio (washout, WO) were determined. Prognostic value was assessed by survival curves (Kaplan-Meier method) and uni- and multivariate Cox analyses. RESULTS: Late cardiac MIBG uptake was reduced (131+/-20%, normal values 192+/-42%) and correlated with ejection fraction (r = 0.49), cardiac index (r = 0.40) and pulmonary wedge pressure (r = -0.35). There was a significant correlation between peak VO2 and MIBG uptake (r = 0.41, p < 0.0001). With a mean follow-up of 10+/-8 months, both late MIBG uptake (p = 0.04) and peak VO2 (p < 0.0001) were predictive of death or heart transplantation, but only peak VO2 emerged by multivariate analysis. Neither early MIBG uptake nor WO yielded significant insights beyond those provided by late MIBG uptake. CONCLUSIONS: Metaiodobenzylguanidine uptake has prognostic value in patients with wide ranges of heart failure, but peak VO2 remains the most powerful prognostic index.

A statistical prognostic study of pump failure in acute myocardial infarction.

Repeated measurements of maemodynamic status were made and were subsequently subjected to analysis to assess prognosis in a group of patients with acute myocardial infarction and pump failure. Two multivariate methods were used: correspondence analysis and discriminant analysis. Both these methods agreed with the highest prognostic reliability of left ventricular function indices. Using various discriminant functions a prospective study was carried out on a test sample and a rate for well-classified subjects ranging from 80% to 90% was obtained. For each discriminant function the different causes of misclassification were analysed; among them a right ventricular dysfunction was allowed to account for discrepancies between expected and observed data on inferior infarction.

Evaluation of the elasticity and characteristic impedance of the ascending aorta in man.

In 30 patients, simultaneous measurements of ascending aortic pressure and diameter were performed, allowing one to evaluate: (1) the influence of age, the aortic diastolic pressure, and the radius on the aortic elasticity; (2) the correlations between characteristics impedance of the aorta (Zo), systemic arterial resistance, age and diastolic aortic pressure; and (3) the importance of Zo when comparing two indices of left ventricle performance; one during isovolumic phase ([dP/dt]/Pt)max and the other during the outflow phase (maximum acceleration of aortic blood flow).

Post-extrasystolic left ventricular peak pressure with and without left ventricular failure.

18 patients without valvular pathology, coronary artery disease, or idiopathic hypertrophic subaortic stenosis were haemodynamically and angiographically investigated in order to analyse the effects of a ventricular extrasystolic beat upon the post-extrasystolic left ventricular peak pressure. In eight normal patients (group I), the post-extrasystolic peak pressure (P.ES.P.P.) was lower than that of the pre-extrasystolic beat; in 10 patients with symptoms of left ventricular failure (group II) the P.ES.P.P. significantly increased. The reasons are: 1) cardiac origin: stroke volume increased more in group II; 2) arterial origin. a) aortic compliance was lower in group II (this is probably related to the older age of patients in group II), and by decrease in end-diastolic aortic pressure was smaller in group II. Part of this arterial effect (2b) may probably be explained from the fact that post-extrasystolic compensatory pauses are equal in both groups, but the decay time of arterial pressure during diastole (assuming an exponential decay) is larger in group II. At the same age and with the identical aortic compliance only the two factors 1 and 2b play a part in the changes in P.ES.P.P.

Aortic input impedance in normal man and arterial hypertension: its modification during changes in aortic pressure.

The purpose of this work was to study the factors determining aortic input impedance in hypertensive patients. Aortic input impedance (simultaneous measurements of aortic pressure and blood flow), mean (Wm) and pulsatile (Wp) powers and the Wp/Wm ratio were compared in normal subjects (n = 13) and hypertensive patients (n = 12) under basal conditions and during blood pressure manipulation--angiotensin infusion in five normal patients and nitroprusside infusion in six hypertensive patients. Pulse wave velocity (Möens-Korteweg equation; simultaneous measurement of aortic pressure and radius) was determined under basal conditions in normal subjects and in 11 hypertensive patients. The results show that: 1) the changes in impedance curves in hypertensive patients are related to increased peripheral resistance, pulse wave velocity, wave reflection and aortic radius; 2) in most hypertensive patients impedance curves are normalised when blood pressure is reduced, whereas the Wp/Wm ratio remains higher. This latter result demonstrates that pulsatile energy losses are greater in hypertensive patients and suggests either that the aortic wall remains stiffer, despite the reduction in aortic pressure, or that the flow wave becomes more pulsatile since impedance curves of hypertensive patients seen after lowering blood pressure are similar to those of normal subjects.

Left ventricular-arterial coupling in systemic hypertension: analysis by means of arterial effective and left ventricular elastances.

OBJECTIVE: To clarify the spectrum of the left ventricular responses in hypertension in man by means of coupled analysis of elastances. In the present study we analysed the 'functional' coupling of the left ventricle and the arterial system in terms of the arterial effective elastance (E(a)) divided by a value of end-systolic left ventricular elastance approximated by the end-systolic pressure-volume ratio (E(lv)). METHODS: Twenty-five normotensive and 19 hypertensive males without heart failure underwent a haemodynamic and angiographic study. The hypertensives were divided into three subgroups: group 1 had normal ejection fraction, group 2 had ejection fraction > 70% and group 3 had ejection fraction 50-58%. RESULTS: The ejection fraction was similar in hypertensives and controls and E(lv) was significantly increased in the hypertensives. E(a) was identical in the three hypertensive subgroups, which differed only for E(lv). Hypertensives with a normal ejection fraction (n = 8) had a normal E(a)/E(lv) ratio and end-systolic stress, and a significantly increased E(lv), related mainly to an increase in the left ventricular mass divided by the end-diastolic volume (m/VED) with normal systolic function of the left ventricular muscle. The significantly increased systolic pump function of group 2 (n = 5) seems to be related to a significant increase in both m/VED and left ventricular muscle contractility. Group 3 (n = 6) was more heterogeneous, some patients having insufficient hypertrophy and others impaired muscle function. CONCLUSIONS: The left ventricle and the arterial system remain correctly coupled in hypertensives overall, but with marked heterogeneity of the systolic pump (and sometimes muscle) function and mainly of the geometry of the left ventricle. Regarding the relatively unequivocal changes in Ea, the differences in ejection fraction and in left ventricular-arterial coupling in hypertensives are related mainly to changes in the left ventricular systolic pump function.

Assessment of exercise tolerance in chronic congestive heart failure.

In patients with chronic heart failure, exercise capacity is poorly related to cardiac hemodynamics, and peripheral circulation is an important determinant of exercise tolerance. The ability of the muscle vasculature to dilate is markedly impaired, in part, because of exaggerated neurohumoral activity increasing vascular wall stiffness. For this reason, increasing cardiac output is not sufficient to increase exercise capacity if not accompanied by improving vascular reactivity. The poor reliability and reproducibility of exercise tolerance assessed by maximal exercise duration or maximal attained work load (particularly on a treadmill) has led to widespread measurement of respiratory gas during exercise. Peak oxygen consumption (peak VO2), even if it is symptom-limited, has been shown to be a very reproducible criterion of exercise tolerance; moreover, because VO2 is the product of cardiac output and arteriovenous oxygen difference, it also has a qualitative hemodynamic significance. Ventilatory threshold can be determined before maximal exercise; however, problems of determination limit the practical value of this criterion. Unfortunately, peak VO2 lacks sensitivity to detect minor improvement or impairment of symptoms during daily life, although these are significant to the patient. Submaximal exercises have been proposed for this purpose and are currently being evaluated.

Hemodynamic action of nicorandil in chronic congestive heart failure.

Nicorandil is a new compound that has shown potent vasodilator activities on venous and arterial beds in experimental pharmacology. This study was designed to evaluate the magnitude and the time course of hemodynamic effects of different doses of nicorandil in congestive heart failure. Eleven patients with severe congestive heart failure (New York Heart Association class III or IV), with a cardiac index less than 3 liters/min/m2 and a pulmonary wedge pressure greater than 15 mm Hg were enrolled in the study. Three patients had ischemic dilated cardiomyopathy and 8 had idiopathic dilated cardiomyopathy. Hemodynamic assessments were performed by right-sided cardiac catheterization (Swan-Ganz catheter) with cardiac output determination (thermodilution) at baseline and from 30 minutes to 12 hours after single oral administration of nicorandil; 3 patients were given 40 mg, 6 patients 60 mg, and 2 patients 80 mg. Maximal hemodynamic changes were observed 30 minutes after dosing and remained statistically significant at 3 hours. Thirty minutes after drug administration, pulmonary wedge pressure decreased 34 +/- 6%, cardiac index increased by 55 +/- 13% and diastolic and mean arterial pressures decreased by 15 +/- 3% and 9 +/- 2%, respectively, from baseline values. The decrease in systolic blood pressure was slight (5 +/- 2%) and not statistically significant. Calculated systemic vascular resistances decreased by 36 +/- 6% and heart rate did not significantly change. Nicorandil was well tolerated. Thus, the results of this first study of nicorandil in congestive heart failure demonstrated the unloading action of this compound on the failing heart, leading to an improvement in cardiac function; further investigation of nicorandil in this therapeutic area is needed.

Patterns of myoglobin and MM creatine kinase isoforms release early after intravenous thrombolysis or direct percutaneous transluminal coronary angioplasty for acute myocardial infarction, and implications for the early noninvasive diagnosis of reperfusion.

Early noninvasive detection of reperfusion after thrombolysis for acute myocardial infarction may enable detection of unsuccessful thrombolysis in time for rescue percutaneous transluminal coronary angioplasty (PTCA). It has been suggested that repeated measurement of myoglobin or of MM creatine kinase (CK) isoforms enables early detection of reperfusion. Twenty consecutive patients with acute myocardial infarction treated by intravenous thrombolysis underwent serial determination of myoglobin, MM3 and MM1 CK isoforms every 30 minutes after the beginning of thrombolysis. At 90 minutes, coronary angiography was performed, enabling classification of patients as with (group A) and without (group B) reperfusion. A third group of 7 patients (group C) underwent direct PTCA without antecedent thrombolysis. In all groups, there were increases in myoglobin, percentage of MM3 isoform, and ratio of MM3/MM1. These increases appeared on the average steeper and faster in group B, but the large dispersion of values in this group resulted in a wide overlap with group A. Retrospective analysis suggests that an increase in the MM3/MM1 ratio > 0.35 after 60 minutes is very specific for reperfusion (sensitivity 60% and specificity 100%). In group C, PTCA always led to a sharp increase in all biochemical parameters measured within 30 minutes. Thus, macromolecular markers can be used for very early, noninvasive detection of reperfusion with a high specificity. This could help reduce the need for emergency angiography to select candidates for rescue PTCA. Furthermore, the patterns of biochemical markers of reperfusion differ when reperfusion is initiated by either thrombolysis or PTCA.

A patency-oriented strategy for early management of acute myocardial infarction using emergency coronary angiography and selective coronary angioplasty.

From June 1988 to March 1991, an unselected cohort of 150 consecutive patients with acute myocardial infarction (AMI) (less than 6 hours) was managed according to a strategy designed to ensure early patency of the infarct-related artery in the maximum number of patients. The following procedures were used: (1) intravenous thrombolysis, which was the usual treatment (n = 103), followed in 98 cases by emergency coronary angiography 90 minutes after the beginning of thrombolysis. This identified 31 thrombolysis failures (32%) and led to 19 rescue angioplasties (18 successes). All patients were then scheduled for predischarge angiography. (2) Direct angioplasty, which was performed in 40 patients because of contraindications to thrombolysis (n = 23), cardiogenic shock (n = 3), diagnostic doubt (n = 7) or "ideal" conditions for direct angioplasty (n = 7). Success (defined as Thrombolysis in Myocardial Infarction [TIMI] flow greater than 1, with a residual stenosis less than 50% in the infarct-related artery) was achieved in 36 of 40 patients (90%). (3) The 7 remaining patients were given conventional medical treatment because of advanced age, contraindications to thrombolysis and angioplasty, or spontaneous reperfusion (confirmed by emergency angiography). In all, emergency angioplasty was performed in the acute phase in 39% of the 150 patients in this nonselected cohort.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence and significance of left ventricular filling abnormalities determined by Doppler echocardiography in young type I (insulin-dependent) diabetic patients.

In 16 insulin-dependent diabetic patients, 36 +/- 8 years old with no microangiopathy, hypertension or coronary artery disease, and 16 healthy control subjects matched for sex, age and body surface area, the following parameters were obtained by Doppler-echocardiography: (1) end-diastolic left ventricular thickness and radius; (2) aortic pulse wave velocity; (3) mitral flow with measurement of early and late (atrial) peak velocities (E and A), pressure half-time and the velocity time integrals of the entire mitral curve and of the atrial wave; and (4) isovolumic relaxation time (i.e., the time between aortic closure and the mitral opening signals recorded simultaneously by continuous-wave Doppler). Heart rate and systolic blood pressure were not different in the 2 groups. Aortic pulse wave velocity and the wall thickness to radius ratio were significantly increased in the diabetic patients compared to the controls. E was significantly reduced whereas A/E, pressure half-time, the atrial contribution to the left ventricular filling (i.e., the ratio of the atrial velocity time integral to the mitral velocity time integral) and the isovolumic relaxation time were significantly increased in the diabetic group versus the control subjects. Lastly, 11 of 16 diabetic patients (69%) had at least 2 of the following abnormalities: A/E greater than 0.71, an atrial contribution to the left ventricular filling greater than 0.25, a pressure half-time greater than 50 ms and an isovolumic relaxation time greater than 88 ms. No correlations were found between the wall thickness to radius ratio, aortic pulse wave velocity and the filling indexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Serial assessment of cardiopulmonary exercise capacity after cardiomyoplasty for either ischemic or idiopathic dilated cardiomyopathy.

Cardiomyoplasty is a surgical procedure aimed at assisting the left ventricle during ejection. We describe the long-term effects of cardiomyoplasty on peak exercise capacity, with serial assessments for up to 3 years after operation. Sixteen patients (12 in New York Heart Association class III and 4 in class IV) were enrolled. The mean left ventricular ejection fraction was 18 +/- 8%. Bicycle exercise tests with respiratory gas analysis were performed preoperatively and 6, 12, 18, 24, and 36 months after operation. Mean follow-up was 12 +/- 5 months (range 6 to 24). At 6 months, peak oxygen consumption and the ventilatory threshold were unchanged (from 17.8 +/- 5.8 to 15.8 +/- 5.3 ml/min/kg, and from 12.1 +/- 2.7 to 11.4 +/- 3.4 ml/min/kg, respectively). Ventilation at 50 W, viewed as an index of polypnea at submaximal exercise, was also unchanged. Serial assessment of exercise capacity thereafter showed no changes. However, ejection fraction tended to increase from 18 +/- 8% to 21 +/- 9% (p=0.08) and 14 patients reported an improvement in their functional status, resulting in a significant change in New York Heart Association functional class (3.3 +/- 0.5 to 2.2 +/- 0.4 at 6 months and 2.4 +/- 0.4 at the last visit, p <0.005) and improvement in quality-of-life scores. Thus, cardiomyoplasty does not appear to increase peak exercise capacity in the long term, despite an improvement in the left ventricular ejection fraction. Symptoms and quality of life, however, appear to improve. This may be related in part to an insufficient number of assisted systoles during exercise, persistent deconditioning, or changes in pulmonary mechanics.

Primary coronary angioplasty for acute myocardial infarction with contraindication to thrombolysis.

Patients with acute myocardial infarction (AMI) and contraindication to thrombolysis have a high mortality and morbidity with conventional medical treatment. Among 226 consecutive patients hospitalized within 6 hours of the onset of Q-wave AMI, 45 (20%) had contraindications to thrombolysis. All were treated by emergent primary angioplasty. Mean age of the 45 patients was 60 +/- 11 years and 8 (18%) were > or = 70 years old; 17 (38%) had multivessel disease and 5 (11%) presented with cardiogenic shock. Successful angioplasty was achieved in 42 of the 45 patients (93%) 52 +/- 27 minutes after admission and 238 +/- 100 minutes after the onset of pain. Overall in-hospital mortality was 9% (4 of 45). Neither major bleeding nor stroke occurred. There was 1 case of early symptomatic reocclusion, treated with emergent repeat angioplasty without reinfarction. Predischarge angiography in 33 patients showed only 1 silent reocclusion (3%). Ejection fraction at discharge was 46 +/- 13%. Repeat catheterization at 6 months in 19 patients showed 4 restenoses (21%) and 4 reocclusions (21%) of the infarct-related artery. There were 3 late deaths (2 noncardiac), which gave survival rates of 87 and 85% at 1 and 3 years, respectively, and event-free survival rates of 71 and 69% including in-hospital deaths. There were no cases of late reinfarction. Consequently, in this series, primary coronary angioplasty proved safe and highly effective in rapidly restoring sustained infarct-vessel patency during AMI, and led to a greater improvement in early and late outcomes than that reported in the literature for medically treated subjects in this high-risk subset for which thrombolytic therapy is contraindicated.

Comparison using dynamic vectorcardiography and MIBI SPECT of ST-segment changes and myocardial MIBI uptake during percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery.

The quantitative relation between ST-segment changes and the severity and extent of myocardial ischemia during coronary occlusion remains unclear. This study assesses whether ST-segment changes during percutaneous transluminal coronary angioplasty (PTCA) correlate with the amount of myocardium at risk, measured with technetium-99m hexakis 2-methoxyisobutyl isonitrile (MIBI; also called sestamibi) single-photon emission computed tomography (SPECT). Quantitative continuous dynamic vectorcardiography was performed during PTCA of the left anterior descending coronary artery in 11 patients (mean age 64.3 years) without previous myocardial infarction. Change in the magnitude of the ST vector (STc-VM) was continuously recorded. A standardized protocol of balloon inflations was used and technetium-99m MIBI was injected intravenously at the onset of the third inflation. SPECT imaging was performed 60 minutes later and compared to a rest acquisition. SPECT was quantified by bull's-eye analysis using: (1) the change in the pathologic/normal area count ratio (delta P/N) as an index of the severity of ischemia; and (2) planimetered defect size during PTCA as an indicator of the size of the area at risk. The delta P/N from baseline to balloon occlusion (22 +/- 11%) was correlated, albeit loosely, to the maximum value of STc-VM (245 +/- 186 microV, r = 0.62, p < 0.05), but there was no correlation between the size of the scintigraphic defect and STc-VM. Likewise, the sum of ST-segment elevation was correlated to delta P/N (r = 0.72, p < 0.02), but not to the size of the scintigraphic defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of left ventricular responses to the six-minute walk test, stair climbing, and maximal upright bicycle exercise in patients with congestive heart failure due to idiopathic dilated cardiomyopathy.

Submaximal exercise tests have been advocated to assess exercise capacity in chronic heart failure, but hemodynamic responses have not been characterized. To determine left ventricular (LV) responses during submaximal exercise, the LV ejection fraction (EF) and volumes were evaluated by using an ambulatory radionuclide detector in 13 patients with idiopathic dilated cardiomyopathy during upright maximal graded bicycle exercise, stair climbing and a 6-minute walk test. The 3 tests elicited different responses in volumes and, to a lesser degree, in LVEF. The maximal bicycle exercise led to a decrease in LVEF from 22 +/- 9% to 17 +/- 8% (p <0.05), with marked increases in both end-diastolic volume (EDV) (+15 +/- 10%, p <0.001) and end-systolic volume (ESV) (+23 +/- 18%, p <0.001). Stair climbing tended to reduce LVEF (from 24 +/- 11% to 21 +/- 10%, p = 0.05), with a lesser increase in volumes, which was more marked for ESV (+8 +/- 9%, p <0.01) than for EDV (+4 +/- 4%, p <0.01). The 6-minute walk test did not significantly change LVEF (23 +/- 10% vs 22 +/- 10%), but increased both EDV (+10 +/- 6%, p <0.001) and ESV (+8 +/- 8%, p <0.01) moderately and proportionally. Exercise capacity indexes (peak oxygen consumption, maximal bicycle work rate, stair climbing time, and the distance covered during the 6-minute walk test) correlated significantly with one another. There was no correlation between submaximal exercise tolerance indexes and resting or exercise LVEF. This study shows that (1) LVEF changes are inadequate to report on LV volume changes during exercise; (2) the 3 tests induce different LV volume changes; (3) the 6-minute walk test induces significant changes in LV volumes but no change in LVEF.

Transient fall in oxygen intake during exercise in congestive heart failure.

We report four cases in which oxygen intake abruptly decreased during a graded exercise test. In all these cases, there was an acute event (arrhythmia, mitral regurgitation) that had very likely resulted in a decrease in cardiac output. These studies provide new evidence of oxygen intake dependence on oxygen transport, even in nonsteady-state situations.

Left ventricular-arterial system coupling at peak exercise in dilated nonischemic cardiomyopathy.

We assessed the ventricular-arterial coupling at peak exercise in 20 patients with dilated cardiomyopathy (ejection fraction, 27+/-12%) and 7 normal subjects by radionuclide ventriculography during exercise, coupled with respiratory gas analysis. The end-systolic pressure-volume ratio, taken as an index of contractility, and the effective arterial elastance were calculated at rest and at peak exercise. The end-systolic pressure/volume ratio increased from 3.7+/-2.7 to 6.9+/-4.0 mm Hg/mL at peak exercise in the normal subjects, but did not change significantly (from 0.9+/-0.5 to 1.0+/-0.6 mm Hg/mL) in the patients. Arterial elastance did not change significantly in the patients (+17+/-32%, not significant [NS] vs rest) or in the normal subjects (+22+/-28%, NS vs rest). The change in ejection fraction during exercise correlated both with the end-systolic pressure/volume ratio and with effective arterial elastance changes (r=0.60 and 0.68, respectively). We conclude that ventricular arterial coupling is further altered at peak exercise in these patients because of the lack of increase in contractility and not of altered effective arterial elastance response.