title: Decreased and abnormal left ventricular filling in acute heart failure: role of pericardial constraint and its mechanism.
abstract: Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.
authors.affiliation: First Department of Medicine, Osaka University School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Masuyama
authors.forename: J
authors.initials: J
authors.lastname: Tanouchi
authors.forename: M
authors.initials: M
authors.lastname: Uematsu
authors.forename: Y
authors.initials: Y
authors.lastname: Doi
authors.forename: J
authors.initials: J
authors.lastname: Naito
authors.forename: M
authors.initials: M
authors.lastname: Hori
authors.forename: M
authors.initials: M
authors.lastname: Tada
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D000208:Acute Disease; D000818:Animals; D016279:Atrial Function, Left / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology*; D002303:Cardiac Output, Low / Q000503:physiopathology*; D003971:Diastole; D004285:Dogs; D004452:Echocardiography; D015150:Echocardiography, Doppler; D008943:Mitral Valve / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology; D010492:Pericardiectomy; D010496:Pericardium / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology*