Active myocyte shortening during the 'isovolumetric relaxation' phase of diastole is responsible for ventricular suction; 'systolic ventricular filling'.
OBJECTIVE
To study the 'isovolumetric relaxation' phase of rapid ventricular filling by analysis of the shortening of cardiac muscle in the endocardial and epicardial segments of the left ventricle in the dual helical model of the ventricular band, described by Torrent-Guasp.


METHODS
In 10 pigs (27-82 kg), temporal shortening by sonomicrometer crystals was recorded while recording ECG, and measuring intraventricular pressure and dP/dt with Millar pressure transducers.


RESULTS
The following sequence was observed; shortening began in descending or endocardial segment, and 82+/-23 ms later it was initiated in the epicardial or ascending segment of the band. The descending segment stops shortening during the rapid filling phase of fast descent of ventricular pressure, but the ascending segment shortening continues for 92+/-33 ms, so that active shortening continues during the period of isovolumetric relaxation. During the rapid filling phase, dopamine decreased the interval between completion of endocardial and termination of epicardial contraction from 92+/-20 to 33+/-8 ms. Conversely propranolol delayed the start of epicardial shortening from 82+/-23 to 121+/-20 ms, and prolonged the duration of endocardial contraction, causing a closer (21+/-5 ms vs 92+/-20 ms) interval between termination of contraction of endocardial and epicardial fibers. The resultant slope of the rapid descent of the left ventricular pressure curve became prolonged.


CONCLUSIONS
These time sequences show that ongoing unopposed ascending segment shortening occurs during the phase of rapid fall of ventricular pressure. These active shortening phases respond to positive and negative inotropic stimulation, and indicate the classic concept of 'isovolumetric relaxation', IVR, must be reconsidered, and the new term 'isovolumetric contraction', IVC, or systolic ventricular filing may be used.
Option on Bioengineering, California Institute of Technology, Pasadena, CA, USA. gbuckberg@mednet.ucla.edu
Gerald D
GD
Buckberg
Manuel
M
Castellá
Morteza
M
Gharib
Saleh
S
Saleh
D000818:Animals; D048429:Cell Size; D003971:Diastole / Q000502:physiology*; D004562:Electrocardiography; D004699:Endocardium / Q000166:cytology / Q000502:physiology; D008955:Models, Cardiovascular; D032342:Muscle Cells / Q000166:cytology / Q000502:physiology*; D009200:Myocardial Contraction / Q000187:drug effects; D010496:Pericardium / Q000166:cytology / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D013552:Swine; D013599:Systole / Q000502:physiology*; D014160:Transducers, Pressure; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000502:physiology*
D014665:Vasodilator Agents; D011433:Propranolol