Uncorrected pre-ejection period: A simple non-invasive measurement for pharmacodynamic screening of inotropic activity

Rousson, D.; Galleyrand, Jacques; Silie, M; Boissel, Jean-Pièrre

doi:10.1007/bf00606630

Cited by 14 publications

(4 citation statements)

References 23 publications

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“…In contrast, PEP is not substantially altered by changes in HR (Harris et al, 1967; Cokkinos et al, 1976). Thus, while it is widely acknowledged that LVET and PEP:LVET should be corrected for the underlying HR, the need for HR-correction of PEP (Weissler et al, 1968; Lewis et al, 1982) is contentious (Cokkinos et al, 1976; Spodick et al, 1984; Rousson et al, 1987; Cacioppo et al, 1994). As a result, PEP appears to be the STI measure of choice for reflecting cardiac sympathetic β-adrenergic activity (Rousson et al, 1987; Cacioppo et al, 1994).…”

Section: Systolic Time Intervalsmentioning

confidence: 99%

Cardiac Autonomic Responses during Exercise and Post-exercise Recovery Using Heart Rate Variability and Systolic Time Intervals—A Review

2017

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Cardiac parasympathetic activity may be non-invasively investigated using heart rate variability (HRV), although HRV is not widely accepted to reflect sympathetic activity. Instead, cardiac sympathetic activity may be investigated using systolic time intervals (STI), such as the pre-ejection period. Although these autonomic indices are typically measured during rest, the “reactivity hypothesis” suggests that investigating responses to a stressor (e.g., exercise) may be a valuable monitoring approach in clinical and high-performance settings. However, when interpreting these indices it is important to consider how the exercise dose itself (i.e., intensity, duration, and modality) may influence the response. Therefore, the purpose of this investigation was to review the literature regarding how the exercise dosage influences these autonomic indices during exercise and acute post-exercise recovery. There are substantial methodological variations throughout the literature regarding HRV responses to exercise, in terms of exercise protocols and HRV analysis techniques. Exercise intensity is the primary factor influencing HRV, with a greater intensity eliciting a lower HRV during exercise up to moderate-high intensity, with minimal change observed as intensity is increased further. Post-exercise, a greater preceding intensity is associated with a slower HRV recovery, although the dose-response remains unclear. A longer exercise duration has been reported to elicit a lower HRV only during low-moderate intensity and when accompanied by cardiovascular drift, while a small number of studies have reported conflicting results regarding whether a longer duration delays HRV recovery. “Modality” has been defined multiple ways, with limited evidence suggesting exercise of a greater muscle mass and/or energy expenditure may delay HRV recovery. STI responses during exercise and recovery have seldom been reported, although limited data suggests that intensity is a key determining factor. Concurrent monitoring of HRV and STI may be a valuable non-invasive approach to investigate autonomic stress reactivity; however, this integrative approach has not yet been applied with regards to exercise stressors.

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Section: Systolic Time Intervalsmentioning

confidence: 99%

Cardiac Autonomic Responses during Exercise and Post-exercise Recovery Using Heart Rate Variability and Systolic Time Intervals—A Review

2017

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“…It should be noted, however, that conflicting results have been reported in the literature concern ing the influence of heart rate on STIs. While Weissler et al [10] and Wolf et al [11] recommend heart rate correction, other authors use uncorrected preejection period (PEP) [12,13]. In the present study, PEP was not heart rate corrected.…”

Section: Methodsmentioning

confidence: 41%

Twenty-Four-Hour Hemodynamic Effects of Two Different Dihydropyridine Derivatives Assessed by Noninvasive Methods in Patients with Congestive Heart Failure

Halabi¹,

Kirch²

1993

Am J Noninvas Cardiol

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In a placebo-controlled randomized double-blind cross-over study, 16 patients with congestive heart failure (NYHA class II; 12 males and 4 females; 60.6 ± 6.2 years; body weight 72.2 ± 11.7 kg; mean ± SD) received single oral doses of either 10 mg felodipine extended release, 20 mg nitrendipine, or placebo. The patients were crossed over to the subsequent treatments after 4-day washout intervals. Mechanocardiography (systolic time intervals), impedance cardiography, venous occlusion plethysmography, heart rate, and blood pressure were measured before as well as 2, 6, 12, and 24 h after drug administration. Felodipine and nitrendipine significantly increased stroke volume and the Heather index in impedance cardiography, whereas the preejection period significantly decreased in mechanocardiography. Two hours after drug administration, the effect of felodipine on mechano- and impedance cardiographie parameters was more pronounced than that of nitrendipine. In conclusion, in the present study, felodipine had a longer-lasting and more pronounced influence on the cardiovascular parameters determined than nitrendipine.

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“…The systolic time intervals were corrected for heart rate, although it is debatable whether this should be done for PEP (Rousson et al 1987;Joubert and Belz 1987). STI indexes and PEP/LVET were lower during treatment with digoxin plus epanolol than with digoxin plus placebo.…”

Section: Discussionmentioning

confidence: 99%

Investigation of possible pharmacokinetic and pharmacodynamic interactions between epanolol and digoxin

Lefebvre

Bogaert

Duprez

1990

Eur J Clin Pharmacol

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The possibility of a pharmacokinetic and/or pharmacodynamic interaction between epanolol and digoxin has been investigated in 10 healthy male subjects taking digoxin 0.375 mg daily for 14 days. During that period epanolol 200 mg daily or matching placebo was also given, each for 7 days, according to a double-blind, randomized cross-over plan. The plasma digoxin concentration-time profiles after 7 days of concomitant placebo or epanolol were comparable. Trough and peak plasma digoxin levels were similar (placebo: 0.84 and 2.62 ng.ml-1; epanolol: 0.87 and 2.46 ng.ml-1). The renal clearances of digoxin and creatinine were lower during treatment with epanolol, but the differences were not significant (placebo 142.0 and 126.5 ml.min-1; epanolol 105.7 and 109.3 ml.min-1). STI indexes were lower during treatment with digoxin plus epanolol, than after digoxin alone. The difference was significant for QS2I (513 versus 503 ms), PEPI (119 versus 112 ms) and PEP/LVET (0.286 versus 0.304). The observations suggest that in healthy volunteers there is no pharmacokinetic interaction between epanolol and digoxin, and that epanolol does not interfere with the positive inotropic action of digoxin.

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Uncorrected pre-ejection period: A simple non-invasive measurement for pharmacodynamic screening of inotropic activity

Cited by 14 publications

References 23 publications

Cardiac Autonomic Responses during Exercise and Post-exercise Recovery Using Heart Rate Variability and Systolic Time Intervals—A Review

Cardiac Autonomic Responses during Exercise and Post-exercise Recovery Using Heart Rate Variability and Systolic Time Intervals—A Review

Twenty-Four-Hour Hemodynamic Effects of Two Different Dihydropyridine Derivatives Assessed by Noninvasive Methods in Patients with Congestive Heart Failure

Investigation of possible pharmacokinetic and pharmacodynamic interactions between epanolol and digoxin

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