Relation of exercise capacity to left ventricular systolic function and diastolic filling in idiopathic or ischemic dilated cardiomyopathy

Lapu-Bula, Rigobert; Robert, Annie; Kock, Martine De; D'hondt, Anne-Marie; Detry, Jean-Marie R.; Melin, Jacques; Vanoverschelde, Jean-Louis

doi:10.1016/s0002-9149(98)00979-5

Cited by 70 publications

(40 citation statements)

References 27 publications

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“…Moreover, these individuals differed also in E-wave characteristics: increased E peak (peak of the E wave), decreased acceleration time, and decreased deceleration time. These findings are in agreement with other studies and are consistent with the "constrictive-restrictive" (tall-narrow) Ewave pattern encountered in significant HF (2,18,25,32). The trend in the magnitude of k in our subjects reflects the fact that as NYHA class increases so does LV chamber stiffness (class I, k ϭ 167.8; class II, k ϭ 216.2; class III, k ϭ 253.8; and class IV, k ϭ 307.9).…”

Section: Resultssupporting

confidence: 93%

“…Our statistical approach is commonly used in the literature to analyze similar physiological relationships. Specifically, it is similar to the analysis used by Lapu-Bula et al (18) in their study assessing the relation of exercise capacity to LV systolic function and diastolic filling in idiopathic or ischemic dilated cardiomyopathy. Univariate predictors of V O 2 peak are reported in Table 2.…”

Section: Resultsmentioning

confidence: 93%

“…Exercise intolerance in HF patients is a poorly understood multifactorial pathological entity and is mediated by numerous mechanisms encompassing central limitations (i.e., cardiac limitations) peripheral limitations that are predominantly muscular and metabolic in origin, or a combination of both (18). Apart from age, gender, and habitual physical activity that affect V O 2 peak , the relative contribution of central and peripheral factors to the modulation in V O 2 peak continues to be investigated (6).…”

Section: Discussionmentioning

confidence: 99%

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Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Meyer¹,

Karamanoglu²,

Kovács

2004

Journal of Applied Physiology

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. Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction. J Appl Physiol 97: 1667-1672. First published June 18, 2004 doi:10.1152/japplphysiol.00078.2004.-Impaired exercise tolerance, determined by peak oxygen consumption (V O2 peak), is predictive of mortality and the necessity for cardiac transplantation in patients with chronic heart failure (HF). However, the role of left ventricular (LV) diastolic function at rest, reflected by chamber stiffness assessed echocardiographically, as a determinant of exercise tolerance is unknown. Increased LV chamber stiffness and limitation of V O2 peak are known correlates of HF. Yet, the relationship between chamber stiffness and V O2 peak in subjects with HF has not been fully determined. Forty-one patients with HF New York Heart Association [(NYHA) class 2.4 Ϯ 0.8, mean Ϯ SD] had echocardiographic studies and V O2 peak measurements. Transmitral Doppler E waves were analyzed using a previously validated method to determine k, the LV chamber stiffness parameter. Multiple linear regression analysis of V O2 peak variance indicated that LV chamber stiffness k (r 2 ϭ 0.55) and NYHA classification (r 2 ϭ 0.43) were its best independent predictors and when taken together account for 59% of the variability in V O2 peak. We conclude that diastolic function at rest, as manifested by chamber stiffness, is a major determinant of maximal exercise capacity in HF. diastole; echocardiography; oxygen consumption CHRONIC HEART FAILURE (HF) is a major health problem that carries a high mortality rate despite continued significant advances in medical therapy. With ϳ400,000 new cases of HF diagnosed each year, 4.7 million Americans suffer from this debilitating disease (1). It has been established that patients with HF have impaired exercise tolerance that is predictive of mortality and the need for cardiac transplantation (10). Characteristically, the failing heart demonstrates an inability to maintain an adequate cardiac output, first during effort and later also at rest. Cardiac decompensation ultimately leads to impaired exercise capacity, fatigue, and exertional dyspnea. Patients with HF thus may have a decreased left ventricular (LV) ejection fraction (LVEF), large end-diastolic volume, and impaired contractile reserve (33, 34). Ventricular dysfunction as quantitated by a decreased LVEF is the main manifestation of HF that ultimately results in circulatory failure. Advanced LV dysfunction is associated with a variety of neurohumoral, peripheral circulatory, skeletal muscle, and respiratory adaptations that determine the syndrome's overall clinical presentation and prognosis (33, 34). The known mechanisms that lead to HF are highly complex, involving chamber enlargement and remodeling and decreased LV contractile reserve (10). The factor common to all types of HF regardless of etiology is increased LV end-diastolic pressure (LVEDP), which compromises LV filling, diminishes stroke volume and cardiac outpu...

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Section: Resultssupporting

confidence: 93%

Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Meyer¹,

Karamanoglu²,

Kovács

2004

Journal of Applied Physiology

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“…6 In addition to the usual indices, end-diastolic (largest dimension or onset of QRS complex) and end-systolic (smallest dimension or aortic valve closure) LV volumes and ejection fraction were calculated by use of the Simpson biplane method. LV shape was assessed by computation of end-diastolic and end-systolic sphericity indexes, ie, the ratio of the major to the minor axis at end diastole and end systole.…”

Section: Gas Exchange Analysismentioning

confidence: 99%

“…[1][2][3][4][5][6] Although the mechanisms of exercise intolerance are multifactorial, they depend at least in part on the maximal pumping capacity of the heart, ie, maximal stroke volume and cardiac output.…”

mentioning

confidence: 99%

Contribution of Exercise-Induced Mitral Regurgitation to Exercise Stroke Volume and Exercise Capacity in Patients With Left Ventricular Systolic Dysfunction

et al. 2002

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Background-Functional mitral regurgitation (MR) is common in patients with heart failure and left ventricular (LV) dysfunction, and its severity may vary over time, depending primarily on the loading conditions. Because dynamic changes in the severity of functional MR may affect forward stroke volume, we hypothesized that exercise-induced changes in MR severity influence the stroke volume response of patients with LV dysfunction to exercise, and hence their exercise capacity. Methods and Results-Heart failure patients (nϭ25; mean age 53Ϯ12 years) with LV dysfunction underwent dynamic bicycle exercise at steady-state levels of 30%, 60%, and 90% of predetermined peak V O 2 . During each exercise level, right heart pressures, cardiac output, V O 2 , and MR severity were measured simultaneously. During exercise, MR severity, as evaluated by the ratio of MR jet over left atrium area, increased from 15Ϯ8% to 33Ϯ15%. Peak V O 2 , exercise-induced changes in stroke volume, and those in capillary wedge pressure correlated with the changes in MR (rϭϪ0.55, Ϫ0.87, and 0.62, respectively, PϽ0.01). The changes in MR severity also correlated with those in end-diastolic (rϭϪ0.75, PϽ0.01) and end-systolic (rϭϪ0.72, PϽ0.01) sphericity indexes and those in the coaptation distance (rϭ0.86, PϽ0.01). Conclusions-Our data indicate that in patients with LV dysfunction, exercise-induced changes in MR severity limit the stroke volume adaptation during exercise and therefore contribute to limitation of exercise capacity.

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Worsening of left ventricular diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension

Nair

Tekin²,

Khan

et al. 2000

Clinical Cardiology

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SummaryBackground: Exercise tolerance is reduced in hypertension. Hypertension affects left ventricular (LV) diastolic filling by causing abnormal relaxation and decreasing compliance.Hypothesis: This study was designed to determine whether worsening of LV diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension.Merhods: Left ventricular diastolic filling parameters were examined at mitral valve by Doppler echocardiography at rest and at peak exercise in hypertensive patients and were compared with those of age-and gender-matched normotensive individuals. Treadmill exercise stress test was performed according to the Bruce protocol and the exercise time was recorded.Results: Exercise time was significantly shorter in the hypertensive group than that in the normotensive group (320 k 29 vs. 446 k 38 s, p 0.03). The hypertensive group demonstrated abnormal relaxation pattern of diastolic mitral inflow at rest, which became pseudonormal at peak exercise (HA velocity ratio, rest 0.86 k 0.06 vs. exercise 1.19 k 0.09, p

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Relation of exercise capacity to left ventricular systolic function and diastolic filling in idiopathic or ischemic dilated cardiomyopathy

Cited by 70 publications

References 27 publications

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction

Contribution of Exercise-Induced Mitral Regurgitation to Exercise Stroke Volume and Exercise Capacity in Patients With Left Ventricular Systolic Dysfunction

Worsening of left ventricular diastolic dysfunction during exercise causes decreased exercise tolerance in hypertension

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