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Heart 1999;81:33-39; doi:10.1136/hrt.81.1.33
Copyright © 1999 BMJ Publishing Group Ltd & British Cardiovascular Society

Heart 1999;81:33-39 ( January )

Ventricular dilatation in the absence of ACE inhibitors: influence of haemodynamic and neurohormonal variables following myocardial infarction

J T Walsh, P D Batin, M Hawkins, D McEntegart, A J Cowley

Department of Cardiovascular Medicine, University Hospital, Nottingham NG7 2UH, UK

Correspondence to: Dr J T Walsh, Department of Cardiology, Papworth Hospital, Papworth Everard, Cambridge CB3 8RE, UK.

Accepted for publication 31 July 1998

Objective---To examine the relation between patterns of ventricular remodelling and haemodynamic and neurohormonal variables, at rest and during symptom limited exercise, in the year following acute myocardial infarction in patients not receiving angiotensin converting enzyme (ACE) inhibitors.
Design---A prospective observational study.
Patients---65 patients recruited following hospital admission with a transmural anterior myocardial infarction.
Methods---Central haemodynamics and neurohormonal activation at rest and during symptom limited treadmill exercise were measured at baseline before hospital discharge, one month later, and at three monthly intervals thereafter. Patients were classified according to individual patterns of change in left ventricular end diastolic volumes at rest, assessed at each visit using transthoracic echocardiography.
Results---In most patients (n = 43, 66%) ventricular volumes were unchanged or reduced. Mean (SEM) treadmill exercise capacity and peak exercise cardiac index increased at month 12 by 200 (24) seconds (p < 0.001 v baseline) and by 0.8 (0.4) l/min/m2 (p<0.05 v baseline), respectively, in this group. In patients with limited ventricular dilatation (n = 11, 17%) exercise capacity increased by 259 (52) seconds (p < 0.001 v baseline) and peak exercise cardiac index improved by 0.8 (0.7) l/min/m2 (NS). In the remaining 11 patients with progressive left ventricular dilatation, exercise capacity increased by 308 (53) seconds (p< 0.001 v baseline) and peak exercise cardiac index similarly improved by 1.3 (0.7) l/min/m2 (NS). There were trends towards increased atrial natriuretic factor (ANF) secretion at rest and at peak exercise in this group.
Conclusions---Ventricular dilatation after acute myocardial infarction is a heterogeneous process that is progressive in only a minority of patients. Compensatory mechanisms, including ANF release, appear capable of maintaining and improving exercise capacity in most patients for at least 12 months, even in those with a progressive increase in ventricular size.

Keywords: ventricular remodelling;  myocardial infarction;  neurohormones;  atrial natriuretic factor

© 1999 by Heart
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This article has been cited by other articles:

  • HETMANSKI, D J, SPARROW, N J, CURTIS, S, COWLEY, A J (2000). Failure of plasma brain natriuretic peptide to identify left ventricular systolic dysfunction in the community. Heart 84: 440-441 [Full Text]  
  • (1999). Post-MI Ventricular Remodeling Reexamined. Journal Watch Cardiology 1999: 7-7 [Full Text]  

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