title: Prolongation of left atrial augmentation after handgrip stress in coronary artery disease: observation using pulsed Doppler flowmetry.
abstract: Although alterations in left ventricular diastolic filling dynamics have been observed during myocardial ischemia, few data exist regarding temporal changes in left ventricular filling during recovery. Therefore, the authors evaluated transmitral inflow pattern during and after handgrip exertion in coronary artery disease (CAD) by using Doppler echocardiography. The study population consisted of 18 normal (N) subjects and 47 patients with CAD. Of the CAD patients, 17 had coronary lesions associated with a limited area of underperfused myocardium (seven with good collateral circulation and 10 with distal lesions) (MILD), 15 patients exhibited a proximal lesion in a single vessel (SVD), and 15 patients had significant multivessel disease (MVD). Transmitral inflow velocities were continuously recorded at baseline, during handgrip exercise (50% of maximal for 1 minute), and for 5 minutes of recovery. Mean blood pressure, heart rate, early diastolic (E) and late atrial (A) inflow velocities, A/E ratio, and percent changes in E, A, and A/E from baseline were measured. In N and MILD, respectively, left ventricular inflow pattern returned to baseline at 3 minutes after handgrip (%E: 0.7 +/- 7.6%, 6.4 +/- 13.7%; %A: -0.2 +/- 7.9%, 3.1 +/- 6.5%; %A/E: -0.1 +/- 9.7%, -1.7 +/- 12.9%). In SVD and MVD, respectively, change in left ventricular inflow pattern was continued at 3 minutes after handgrip (%E: 7.2 +/- 9.4%, -4.3 +/- 17.2%, %A: 15.4 +/- 11.7%, 20.4 +/- 14.6%, %A/E: 7.9 +/- 10.0%, 29.2 +/- 25.6%). Increases in A and A/E in SVD and MVD were significantly higher than in N and MILD. Impaired left ventricular inflow pattern was observed at 3 minutes after handgrip in CAD, which may be reflected from prolonged impairment of diastolic function produced by ischemia. Therefore, temporal observation of left ventricular inflow pattern using the handgrip stress Doppler method may be useful for detection or follow-up of CAD.
authors.affiliation: Second Department of Internal Medicine, Kagawa Medical University, Kita, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Mizushige
authors.forename: H
authors.initials: H
authors.lastname: Masugata
authors.forename: H
authors.initials: H
authors.lastname: Matsuo
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D016279:Atrial Function, Left / Q000502:physiology*; D001783:Blood Flow Velocity / Q000502:physiology; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015150:Echocardiography, Doppler / Q000295:instrumentation / Q000379:methods / Q000706:statistics & numerical data; D018737:Hand Strength / Q000502:physiology*; D006801:Humans; D008875:Middle Aged; D012212:Rheology / Q000295:instrumentation / Q000379:methods / Q000706:statistics & numerical data; D013312:Stress, Physiological / Q000000981:diagnostic imaging / Q000503:physiopathology*; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology