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


METHODS
A prospective observational study.


METHODS
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.
Walsh
J T
JT
Department of Cardiovascular Medicine, University Hospital, Nottingham NG7 2UH, UK.
Batin
P D
PD
Hawkins
M
M
McEntegart
D
D
Cowley
A J
AJ
D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D009320:Atrial Natriuretic Factor / Q000097:blood; D002302:Cardiac Output; D004837:Epinephrine / Q000097:blood; D017079:Exercise Tolerance; D005260:Female; D005500:Follow-Up Studies; D006339:Heart Rate; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption; D012083:Renin / Q000097:blood; D013997:Time Factors; D014655:Vascular Resistance; D020257:Ventricular Remodeling / Q000502:physiology*
D009320:Atrial Natriuretic Factor; D012083:Renin; D009638:Norepinephrine; D004837:Epinephrine