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ABSTRACT: To assess with magnetic resonance imaging (MRI) cardiovascular function in response to exercise in patients after atrial correction of transposition of the great arteries (TGA).
Cardiac function at rest and during submaximal exercise was assessed with MRI in 27 patients with TGA (mean (SD) age 26 (5) years) late (23 (2) years) after atrial correction and in 14 control participants (25 (5) years old).
At rest, only right ventricular ejection fraction was significantly lower in patients than in controls (56 (7)% v 65 (7)%, p < 0.05). In response to exercise, increases in right ventricular end diastolic (155 (55) ml to 163 (57) ml, p < 0.05) and right ventricular end systolic volumes (70 (34) ml to 75 (36) ml, p < 0.05) were observed in patients. Furthermore, right and left ventricular stroke volumes and ejection fraction did not increase significantly in patients. Changes in right ventricular ejection fraction with exercise correlated with diminished exercise capacity (r = 0.43, p < 0.05).
In patients with atrially corrected TGA, MRI showed an abnormal response to exercise of both systemic right and left ventricles. Exercise MRI provides a tool for close monitoring of cardiovascular function in these patients, who are at risk for late death.
Heart (British Cardiac Society) 07/2004; 90(6):678-84. · 4.22 Impact Factor
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ABSTRACT: After atrial correction of transposition of the great arteries (TGA), dysfunction of the systemic right ventricle at rest and during exercise has been reported. Information on changes in systemic right ventricular function during recovery from exercise is lacking. This study evaluates cardiac recovery from supine exercise using magnetic resonance (MR) imaging in patients with asymptomatic TGA after atrial correction. Flow in the ascending aorta, representing stroke volume of the systemic ventricle, was assessed with MR flow mapping in 10 asymptomatic patients with atrially corrected TGA and in 12 controls at rest during exercise and an 8-minute recovery period. In response to exercise, the patients had a smaller increase in heart rate, stroke volume, and cardiac output than did controls. After exercise, no significant difference in halftime of heart rate recovery was observed (patients, 48 +/- 7 seconds; controls, 39 +/- 4 seconds [p >0.05]). In the patients, the time course of stroke volume recovery was significantly different (p <0.001). Stroke volume in the patients, as a percent difference from rest, remained significantly elevated, from 2.5 minutes (+16 +/- 5% vs +7 +/- 6%; p <0.05) to 8 minutes (+4 +/- 7% vs -3 +/- 5%; p <0.05) after exercise. Subsequently, cardiac output remained significantly elevated, from 4.5 minutes (+27 +/- 13% vs +15 +/- 11%; p <0.05) to 7 minutes (+22 +/- 11% vs +12 +/- 12%; p <0.05) after exercise. We conclude that heart rate recovery is within normal limits in patients with atrially corrected TGA. Furthermore, cardiac recovery from exercise, assessed with MR flow mapping, is prolonged in patients with asymptomatic TGA after atrial correction. Abnormal recovery may reflect dysfunction of the systemic right ventricle and an altered metabolic response to exercise.
The American Journal of Cardiology 12/2001; 88(9):1011-7. · 3.37 Impact Factor
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ABSTRACT: In this paper, it was investigated if the ventilation-perfusion distribution can be estimated from the uptake (U) of inert gases with different solubilities during the single-breath maneuver. A model was implemented that describes U as a function of solubility for inhomogeneously distributed alveolar volume (VA) versus blood and tissue volume (Q + VTIS). The VA/(Q + VTIS) distribution describes the relative contribution of gas-exchange units with different VA/(Q + VTIS) ratios to the expiratory volume. U was derived as the sum of uptakes corresponding to different modes in the distribution, weighted with the relative contribution to the expiratory volume. This permits an estimation of the distribution parameters by fitting U as a function of solubility. The n alkanes were used because of their different solubilities. Analysis of the sensitivity of the estimated VA/(Q + VTIS) distribution parameters to measurement errors showed that mostly two modes can be discerned. The influence of fixed model parameters appeared relatively small. The model could well explain U in normal and emphysematous subjects, with a larger contribution of high VA/(Q + VTIS) ratios in the emphysematous subjects. It was concluded that the VA/(Q + VTIS) distribution can be estimated noninvasively from single-breath alkane uptake.
IEEE Transactions on Biomedical Engineering 08/2001; 48(7):772-86. · 2.28 Impact Factor
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ABSTRACT: A role of nitric oxide (NO) has been suggested in the airway response to exercise. However, it is unclear whether NO may act as a protective or a stimulatory factor. Therefore, we examined the role of NO in the airway response to exercise by using N-monomethyl-L-arginine (L-NMMA, an NO synthase inhibitor), L-arginine (the NO synthase substrate), or placebo as pretreatment to exercise challenge in 12 healthy nonsmoking, nonatopic subjects and 12 nonsmoking, atopic asthmatic patients in a double-blind, crossover study. Fifteen minutes after inhalation of L-NMMA (10 mg), L-arginine (375 mg), or placebo, standardized bicycle ergometry was performed for 6 min using dry air, while ventilation was kept constant. The forced expiratory volume in 1-s response was expressed as area under the time-response curve (AUC) over 30 min. In healthy subjects, there was no significant change in AUC between L-NMMA and placebo treatment [28.6 +/- 17.0 and 1.3 +/- 20.4 (SE) for placebo and L-NMMA, respectively, P = 0.2]. In the asthmatic group, L-NMMA and L-arginine induced significant changes in exhaled NO (P < 0.01) but had no significant effect on AUC compared with placebo (geometric mean +/- SE: -204.3 +/- 1.5, -186.9 +/- 1.4, and -318.1 +/- 1.2%. h for placebo, L-NMMA, and L-arginine, respectively, P > 0.2). However, there was a borderline significant difference in AUC between L-NMMA and L-arginine treatment (P = 0.052). We conclude that modulation of NO synthesis has no effect on the airway response to exercise in healthy subjects but that NO synthesis inhibition slightly attenuates exercise-induced bronchoconstriction compared with NO synthase substrate supplementation in asthma. These data suggest that the net effect of endogenous NO is not inhibitory during exercise-induced bronchoconstriction in asthma.
Journal of Applied Physiology 02/2001; 90(2):586-92. · 3.75 Impact Factor
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ABSTRACT: In obstructive sleep apnea syndrome (OSAS), pronounced low-frequency (LF) oscillations of blood pressure and interbeat interval (I) occur during recurrent apneas. We investigated the time relations between LF oscillations of diastolic pressure (D) and I in 12 patients with OSAS by means of spectral analysis. A high coherency between I and D was found, allowing a description of the relation by gain and phase. Oscillations in I and D were almost in counterphase in the LF range. Simple physiological models were implemented to interpret the observed features of LF oscillations. Model 1 describes the vagal and sympathetic influence by the carotid body chemoreflex on the circulation. From derivation of the frequency response of this model, gain and phase relations were obtained as would be expected from the action of the chemoreflex. We found that a range of phase relations can be induced by this reflex, depending on the relative vagal and sympathetic efferent influence on the circulation. This range of phase relations was indeed observed in 10 patients. Extended models that also included the orienting reflex (model 1a) or the baroreflex and a mechanical influence of breathing on the circulation (model 2) could not fit the data without a major contribution of the chemoreflex. We conclude that the relation between LF oscillations in I and D in OSAS can be explained by assuming that stimulation of the carotid body chemoreflex is the main source of these oscillations.
The American journal of physiology 06/1995; 268(5 Pt 2):H2145-56.
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ABSTRACT: Periodic increases in blood pressure (BP) can occur in the sleep apnea syndrome (SAS) during recurrent apneas. To investigate the mechanisms causing this periodic hypertension, we simulated SAS by imposing a matching breathing pattern on seven healthy awake male volunteers. Continuous finger arterial BP, electrocardiogram, arterial O2 saturation (SaO2), end-tidal CO2, and tidal volume were measured. The role of hypoxia was studied by comparing apneas during depletion of O2 in the spirometer with those during 100% O2 breathing. In all subjects, BP periodically reached values greater than 150/95 mmHg in the hypoxic series. During the hyperoxic apnea series, however, BP remained stable. End-apneic mean BP was shown to be inversely correlated to SaO2 in six subjects in the SaO2 range from 60 to 100%. Although the hypoxic BP pattern closely mimicked that in SAS, the heart rate pattern in four of our subjects remained distinct from that in patients. Atropine could not prevent large BP swings in the hypoxic series. We conclude that SaO2 is a major determinant of periodic hypertension in recurrent apneas. Its effect probably results from chemoreflex modulation of peripheral resistance.
Journal of Applied Physiology 04/1992; 72(3):821-7. · 3.75 Impact Factor
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ABSTRACT: Breathing patterns and associated circulatory fluctuations may reflect the action of various regulatory mechanisms as well as mechanical influences of breathing on the circulation. Thus, the study of such patterns can enhance our knowledge of these mechanisms, both in normal and pathological conditions. In this review, literature is evaluated that provides insight into the breath-to-breath variation of respiration in quietly breathing adults. Also when respiration is seemingly random, deterministic patterns in the respiratory variability can often be discerned. The various methods used in the recognition of such patterns and their possible interpretation are discussed. Furthermore, the question is addressed how respiratory variability can affect the circulation and how this can be studied by analysing the time relationships of respiratory and circulatory parameters. This may add to both the understanding of normal cardiovascular regulation and to insight into cardiovascular disturbances under unstable respiratory conditions. As examples of such circumstances, some common conditions are discussed that are often, though not always, associated with pathology, viz. Cheyne-Stokes respiration, snoring and the sleep apnoea syndrome.
Clinical Physiology 04/1991; 11(2):95-118.
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ABSTRACT: The current study tested whether "suffocation sensations" (respiratory loads) are automatically evaluated in a negative way by people fearing these sensations. It was found that, after having been primed with a slight respiratory load, participants with high suffocation fear (n=15) reacted more quickly to suffocation words and more slowly to positive words than participants with low suffocation fear (n=21). However, the effect was present only in participants who had noticed the primes. The findings are relevant to the cognitive model of panic disorder because automatic negative appraisal of sensations may play a role in initiating a panic attack.
Journal of Abnormal Psychology. 114(3):466-70.
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Journal of Abnormal Psychology, 114, 466 - 470 (2005).
