Left ventricular filling after long-term angiotensin converting enzyme inhibition in congestive heart failure.
As a rule, left ventricular relaxation is impaired in patients with coronary artery disease and congestive heart failure. In addition, the passive elastic properties in early and late diastole change when the ventricle dilates. Diastolic properties of the left ventricle were studied in 11 patients with congestive heart failure class II-IV (NYHA) before and 3 months after 10-20 mg enalapril was added to their regimen of salt restriction, a diuretic and occasionally digitalis. Haemodynamic studies were performed using radionuclide angiography and simultaneous pressure-volume measurements. Systemic vascular resistance decreased from 1479 to 1182 dynes.s.-1 cm-5 (P < 0.05) and left ventricular end-diastolic pressure from 19.2 to 15.9 mmHg (P < 0.05). Left ventricular end-diastolic volume index decreased from 130 +/- 22 to 81 +/- 22 ml (P < 0.01). Indices of early diastolic relaxation, such as peak filling rate (1.43 +/- 0.46 to 1.49 +/- 0.84 EDV/s), time to peak filling rate (460 +/- 70 to 490 +/- 70 ms), peak negative dP/dt (-903 +/- 190 to -891 +/- 190 mmHg/s) and tau, the time constant of isovolumic pressure decay (58.7 +/- 14.4 to 48.4 +/- 15.2 ms) did not change significantly. In nine patients pressure-volume loops shifted to the left in all patients but one due to reduction in end-systolic and end-diastolic volume. The steepness of the diastolic part of the pressure-volume relationship increased, indicating an increase in chamber stiffness. The stiffness constant increased about 25% towards a more normal value. The alteration in stiffness seemed to be mainly due to the change of the geometry of the ventricle and not to a major change in the visco-elastic properties of the ventricular wall. In conclusion, regression of remodelling induced by enalapril does not change diastolic function parameters in patients with chronic congestive heart failure beyond the changes caused by regression of ventricular dilation.
Baur
L H
LH
Department of Cardiology, University Hospital Leiden, The Netherlands.
Schipperheyn
J J
JJ
Cats
V M
VM
van der Wall
E E
EE
Baan
J
J
van Dijk
A D
AD
Bruschke
A V
AV
D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D006328:Cardiac Catheterization / Q000295:instrumentation; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D002303:Cardiac Output, Low / Q000188:drug therapy / Q000503:physiopathology; D002306:Cardiac Volume / Q000187:drug effects / Q000502:physiology; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology; D003971:Diastole / Q000187:drug effects / Q000502:physiology; D004656:Enalapril / Q000627:therapeutic use*; D015637:Gated Blood-Pool Imaging; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D008134:Long-Term Care; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D013599:Systole / Q000187:drug effects / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
D004656:Enalapril