The aim of this study was to evaluate the role of left ventricular (LV) dysfunction
(global and regional, systolic and diastolic) acute dyssynchrony, ischemic mitral
regurgitation (MR), and afterload changes in acute hypertensive pulmonary edema (AHPE).
Forty-four consecutive patients were evaluated by comprehensive echocardiography during
clinical and radiologic pulmonary edema (63 ± 29 minutes after first dose of treatment)
and after 48 to 92 hours. Twenty age- and gender-matched asymptomatic hypertensive
and diabetic subjects served as controls. AHPE was associated with increased afterload
(estimated arterial elastance 3.0 vs 2.3 mm Hg/ml, p = 0.024) and subsequent decreased
longitudinal LV systolic function (mean strain of 6 basal segments −11.0% vs −15.4%;
p = 0.015) compared to the stable follow-up state. However, global LV systolic function
was maintained (estimated ventricular elastance 1.7 vs 1.6 mm Hg/ml, stroke work 76.7
vs 84.5 cJ, ejection fraction 0.33 vs 0.37, all nonsignificant). Except for diastolic
filling time (ratio to cardiac cycle 0.41 vs 0.49, p <0.001), other indexes of diastolic
function, dyssynchrony, and MR severity were similar between evaluations. Patients
with AHPE had worse ventricular–arterial coupling, systolic function, estimated diastolic
stiffness, and filling pressures compared to asymptomatic controls, suggesting a decreased
capacity to adapt to changes in loading. In conclusion, acute alterations of systolic
and diastolic LV function, myocardial synchrony, and ischemic MR are unlikely mechanisms
of AHPE. Rather, AHPE is likely to develop in patients with decreased systolic and
diastolic capacity to adapt to acute changes in loading.
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Article Info
Publication History
Published online: March 22, 2012
Accepted:
January 3,
2012
Received in revised form:
January 3,
2012
Received:
November 2,
2011
Footnotes
This work was supported by Research Grant PNII-IDEI 242/2007 from the CNCSIS-UEFISCSCU , Romania and Investment Grant 135/2007 from the Romanian Ministry of Education and Research .
Identification
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© 2012 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
