Duration of diastole and its phases as a function of heart rate during supine bicycle exercise
ABSTRACT The duration of diastole can be defined in terms of mechanical events. Mechanical diastolic duration (MDD) is comprised by the phases of early rapid filling (E wave), diastasis, and late atrial filling (A wave). The effect of heart rate (HR) on diastolic duration is predictable from kinematic modeling and known cellular physiology. To determine the dependence of MDD of each phase and the velocity time integral (VTI) on HR, simultaneous transmitral Doppler flow velocities and ECG were recorded during supine bicycle exercise in healthy volunteers. Durations, peak values, and VTI using triangular approximation for E- and A-wave shape were measured. MDD, defined as the interval from the start of the E wave to end of the A wave, was fit as an algebraic function of HR by MDD=BMDD + MLMDD.HR + MIMDD/HR, derivable from first principles, where BMDD is a constant, and MLMDD and MIMDD are the constant coefficients of the linear and inverse HR dependent terms. Excellent correlation was observed (r2=0.98). E- and A-wave durations were found to be very nearly independent of HR: 100% increase in HR generated only an 18% decrease in E-wave duration and 16% decrease in A-wave duration. VTI was similarly very nearly independent of HR. Diastasis duration closely tracked MDD as a function of HR. We conclude that the elimination of diastasis and merging of E and A waves of nearly fixed durations primarily govern changes in MDD. These observations support the perspective that E- and A-wave durations are primarily governed by the rules of mechanical oscillation that are minimally HR dependent.
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ABSTRACT: Although catheterization is the gold standard, Doppler echocardiography is the preferred diastolic function (DF) characterization method. The physiology of diastole requires continuity of left ventricular pressure (LVP)-generating forces before and after mitral valve opening (MVO). Correlations between isovolumic relaxation (IVR) indexes such as tau (time-constant of IVR) and noninvasive, Doppler E-wave-derived metrics, such as peak A-V gradient or deceleration time (DT), have been established. However, what has been missing is the model-predicted causal link that connects isovolumic relaxation (IVR) to suction-initiated filling (E-wave). The physiology requires that model-predicted terminal force of IVR (FtIVR) and model-predicted initial force of early rapid filling (Fi E-wave) after MVO be correlated. For validation, simultaneous (conductance catheter) P-V and E-wave data from 20 subjects (mean age 57 years, 13 men) having normal LV ejection fraction (LVEF>50%) and a physiologic range of LV end-diastolic pressure (LVEDP) were analyzed. For each cardiac cycle, the previously validated kinematic (Chung) model for isovolumic pressure decay and the Parametrized Diastolic Filling (PDF) kinematic model for the subsequent E-wave provided FtIVR and Fi E-wave respectively. For all 20 subjects (15 beats/subject, 308 beats), linear regression yielded FtIVR = α Fi E-wave + b (R = 0.80), where α = 1.62 and b = 1.32. We conclude that model-based analysis of IVR and of the E-wave elucidates DF mechanisms common to both. The observed in vivo relationship provides novel insight into diastole itself and the model-based causal mechanistic relationship that couples IVR to early rapid filling.03/2014; 2(3). DOI:10.1002/phy2.258
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ABSTRACT: Recent studies have reported evidence of both a short-term and a more sustained reduction in left ventricular diastolic function after prolonged strenuous exercise. Interpretation of this data is confounded by alterations in heart rate (HR) post-exercise. The purpose of this study was to investigate the association between HR and diastolic function during recovery from supine exercise, and to reassess the impact of increasing HR on early diastolic flow and tissue velocities during supine exercise. Repeat echocardiograms in 16 young, trained, volunteers were obtained at rest (50 +/- 6 beats.min-1), during steady-state supine cycling at HR of 60, 80, and 100 beats.min-1, and then during supine recovery at HR of 80 and 60 beats.min-1. Doppler flow velocities and tissue Doppler myocardial annular velocities were recorded in early (E and E', respectively) and late diastole (A and A', respectively). The ratios E/A, E'/A', and E/E' were calculated. Data were compared via analyses of variance (ANOVA; exercise) and t tests (recovery). Peak E, A, E', and A' all increased in line with HR during exercise (p < 0.05) although relatively greater changes in A and A' resulted in a significant decline in E/A and E'/A' with increasing HR (p < 0.05). During recovery E, A, E', and A' all declined from peak values during exercise (p < 0.05). At 80 beats.min-1, flow and tissue Doppler data were still elevated above resting values and only A was significantly reduced compared with assessments made at the same HR during exercise. Diastolic flow and tissue velocities tended to increase (during supine exercise) and return to baseline (during recovery from exercise) in line with changes in HR. The interpretation of diastolic functional indices measured after physical exertion should be made in light of the present data.Applied Physiology Nutrition and Metabolism 11/2008; 33(5):896-902. DOI:10.1139/H08-078 · 2.23 Impact Factor
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ABSTRACT: A system for non-invasive and automatic assessment of systolic and diastolic duration is presented. The method is based on a accelerometer sensor which was positioned in the mid-sternal precordial region. The acceleration signal, together with an ECG signal, was recorded by a laptop PC and systole and diastole durations were computed for each cardiac beat. The system was tested in 103 patients who performed semi-supine bicycle exercise (71M/32F, age 57plusmn14 years, 17 healthy people 86 patients with cardiovascular diseases). A consistent signal was obtained in 98% patients and systolic/diastolic time ratio as a function of the heart rate was computed. At higher heart rates (for example 100 bpm), this ratio was lower in the 17 control subjects (0.74plusmn0.12) than in the patients with systemic hypertension (0.94plusmn0.12), coronary (0.88plusmn0.11), valvular (0.93plusmn0.14) or dilated heart (0.86plusmn0.10) disease.Computers in Cardiology, 2008; 10/2008