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Free access | 10.1172/JCI109250
The Peter Belfer Laboratory for Myocardial Research, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Cardiovascular Division, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Find articles by Weisfeldt, M. in: JCI | PubMed | Google Scholar
The Peter Belfer Laboratory for Myocardial Research, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Cardiovascular Division, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Find articles by Frederiksen, J. in: JCI | PubMed | Google Scholar
The Peter Belfer Laboratory for Myocardial Research, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Cardiovascular Division, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Find articles by Yin, F. in: JCI | PubMed | Google Scholar
The Peter Belfer Laboratory for Myocardial Research, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Cardiovascular Division, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205
Find articles by Weiss, J. in: JCI | PubMed | Google Scholar
Published December 1, 1978 - More info
Although it has been proposed that incomplete relaxation explains certain increases in left ventricular end diastolic pressure relative to volume, there has been no clear demonstration that incomplete relaxation occurs in the intact working ventricle. To identify incomplete relaxation, left ventricular pressure-dimension relationships were studied in 10 canine right heart bypass preparations during ventricular pacing. The fully relaxed, exponential diastolic pressure-dimension line for each ventricle was first determined from pressure and dimension values at the end of prolonged diastoles after interruption of pacing. For 167 beats during pacing under widely varying hemodynamic conditions, diastolic pressure-dimension values encountered this line defining the fully relaxed state during the filling period indicating that relaxation was complete before end diastole. The time constant for isovolumic exponential pressure fall (T) was determined for all beats. For this exponential function, if no diastolic filling occurred, 97% of pressure fall would be complete by 3.5 T after maximal negative dP/dt. For the 167 beats the fully relaxed pressure-dimension line was always encountered before 3.5 T.
With very rapid pacing rates (170-200 beats/min) and(or) with pharmacologic prolongation of relaxation, incomplete relaxation occurred as evidenced by the fact that the line defining the fully relaxed state was never reached during diastole (n = 15). This evidence of incomplete relaxation occurred only when the subsequent beat began before 3.5 T but did not always occur under these conditions. Thus, an increase in end diastolic pressure relative to diastolic volume may result from incomplete relaxation under conditions of sufficiently rapid heart rate or sufficiently prolonged ventricular relaxation. Incomplete relaxation does not occur when the next beat begins more than 3.5 T after maximum negative dP/dt.