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

Citation
Jt. Walsh et al., Ventricular dilatation in the absence of ACE inhibitors: influence of haemodynamic and neurohormonal variables following myocardial infarction, HEART, 81(1), 1999, pp. 33-39
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HEART
ISSN journal
13556037 → ACNP
Volume
81
Issue
1
Year of publication
1999
Pages
33 - 39
Database
ISI
SICI code
1355-6037(199901)81:1<33:VDITAO>2.0.ZU;2-8
Abstract
Objective-To examine the relation between patterns of ventricular remodelli ng and haemodynamic and neurohormonal variables, at rest and during symptom limited exercise, in the year following acute myocardial infarction in pat ients not receiving angiotensin converting enzyme (ACE) inhibitors. Design-A prospective observational study. Patients-65 patients recruited following hospital admission with a transmur al anterior myocardial infarction. Methods-Central haemodynamics and neurohormonal activation at rest and duri ng symptom limited treadmill exercise were measured at baseline before hosp ital discharge, one month later, and at three monthly intervals thereafter. Patients were classified according to individual patterns of change in lef t ventricular end diastolic volumes at rest, assessed at each visit using t ransthoracic echocardiography. Results-In most patients (n = 43, 66%) ventricular volumes were unchanged o r reduced. Mean (SEM) treadmill exercise capacity and peak exercise: cardia c index increased at month 12 by 200 (24) seconds (p < 0.001 v baseline) an d by 0.8 (0.4) 1/min/m(2) (p<0.05 v baseline), respectively, in this group. In patients with limited ventricular dilatation (n = 11, 17%) exercise cap acity increased by 259 (52) seconds (p < 0.001 v baseline) and peak exercis e cardiac index improved by 0.8 (0.7) 1/min/m(2) (NS). In the remaining 11 patients with progressive left ventricular dilatation, exercise capacity in creased by 308 (53) seconds (p< 0.001 v baseline) and peak exercise cardiac index similarly improved by 1.3 (0.7) 1/min/m(2) (NS). There were trends t owards increased atrial natriuretic factor (ANF) secretion at rest and at p eak exercise in this group. Conclusions-Ventricular dilatation after acute myocardial infarction is a h eterogeneous process that is progressive in only a minority of patients. Co mpensatory mechanisms, including ANF release, appear capable of maintaining and improving exercise capacity in most patients for at least 12 months, e ven in those with a progressive increase in ventricular size.