LEFT VENTRICULAR LATE POTENTIALS IN VENTRICULAR HYPERTROPHY MAY SIGNAL ABOUT INCREASED ARRHYTHMOGENICITY AFTER ACUTE MYOCARDIAL INFARCTION

A. Kaasik, T. Ristimäe,  R. Teesalu
                     Department of Cardiology, University of Tartu, Tartu, Estonia

Abstract:  The associations between left ventricular mass (LVM) and the presence of ventricular late potentials (VLPs) in patients with first acute myocardial infarction (AMI) have not been well described.

Methods and results: In 48 hypertensive patients with first AMI, signal-averaged electrocardiography analysis and echocardiographic examination after admission to the hospital were performed. Twenty-four patients had left ventricular hypertrophy (LVH), and 24 patients had normal LVM. In patients with LVH, LVMI correlated significantly with fQRS and HFLA (r=0.53 and r=0.29, p<0.05, respectively). Although the prevalence of VF episodes was higher in LVH-group when compared to subjects without LVH, this difference did not reach the statistical power (11 (45%) in LVH group versus 7(29%) without LVH, p=NS).

Conclusion: According to this study, in hypertensive AMI-patients with higher value of LVH detected with echocardiography, LVH might serve as a possible contributing factor to the development of VLPs and life-threatening ventricular arrhythmias.

INTRODUCTION

Both left ventricular hypertrophy (LVH) and the presence of ventricular late potentials (VLPs) have been suggested to predict arrhythmogenic events after acute myocardial infarction (AMI) (1,2). The aim of this study was to investigate the relationship between left ventricular mass (LVM) and the VLPs parameters in hypertensive patients in early stage of AMI which is known to be highly vulnerable to the development of life-threatening ventricular arrhythmias.

METHODS

We studied 48 hypertensive male patients with the first AMI. Arterial hypertension was defined as systolic blood pressure ³140 mmHg or current antihypertensive medication. During hospitalisation, 37% of study patients have had ventricular fibrillation (VF) requiring resuscitation. In these patients signal-averaged electrocardiograms were recorded 8.11±3.8 days after AMI. Signal-averaging (40-to 250-Hz filtering) was obtained according to previously described technique (3). The total QRS duration (fQRS), the root mean square voltage of the last 40 ms of the QRS complex (RMS), and the terminal low (<40microV) amplitude signal duration (HFLA). VLPs were considered to be positive when 2 of three criteria (fQRS ³ 114 ms, RMS voltage < 20microV, or HFLA ³ 38ms) were met (4).

LVM was determined by 2-dimensional echocardiography (Hewlett Pacard, Sonos 5500) according to the formula introduced by Devereux et al (5): LVM (in grams) = 0.80 {1.04 × [left ventricular internal diameter (EDD) + septal thickness (VS) + posterior wall thickness (PW)) ³ – (EDD)³]}. LVM was corrected (LVMI) by body surface area (g/m²) (BSA). End-diastolic and end-systolic volume, and left ventricular ejection fraction (LVEF) were calculated by Simpson’s formula (6). Subjects with LVMI greater than 125 g/m² we considered to have LVH (7).

RESULTS

Table 1 shows clinical characteristics of the study population and signal-averaged ECG data according to the presence or absence of LVH. The two groups were age-, BSA-, and LVEF-matched. Although the prevalence of VF episodes was higher in LVH-group when compared to subjects without LVH this difference did not reach the statistical power (11 (45%) in LVH group versus 7 (29%) without LVH, p=NS). In patients with LVH, LVMI correlated significantly with fQRS and HFLA (r=0.53 and r=0.29, p<0.05, respectively).

TABLE 1. Clinical characteristics and signal-averaged ECG data of the study population.

Variable	LVH        (n=24)	Without LVH (n=24)
Age	60.3 ± 11.3	57.8 ± 10.9
LVEF	45.0 ± 13.2	48.9 ± 8.2
VF episodes	11(45%)	7 (29%)
LVMI (g/m2)	159.4± 23.2	117.3± 12.4
fQRS	124.3 ± 23.4	112.4 ± 7.7*
HFLA	41.1± 15.2	30.1 ± 11.6*
RMS	23.9 ± 12.3	34.8 ± 9.8
VLPs(%)	36%	28%

Data are given as mean ± SD, with * p<0.05 for differences between groups.

                              (1)

DISCUSSION

The main finding of the present study was the significant correlation detected between the LVMI and measures of VLPs in hypertensive patients with the first AMI. Although there was a tendency towards higher prevalence of episodes of ventricular fibrillation in LVH patients, no statistically significant difference was revealed when comparison with subjects having no LVH was made. Recently the prognostic value of LVH has been described in the setting of AMI patients with an increased incidence of ventricular arrhythmias for patients presenting an increased LVM (8). However, it is not known whether this relationship exists in early stage of AMI. Whereas the electrophysiological basis of VLPs is a slow, delayed, and fragmented activation in the vicinity of the AMI scar (9) the detection VLPs in patients with LVH in early stage of AMI carries on complementary information to the arrhythmogenic risk stratification of these patients. The LVH with the irregular hypertrophy pattern could impede the homogeneous propagation of the electric impulse throughout the myocardium that may provide the anatomic substrate for re-entrant ventricular arrhythmias. According to the present study, LVH might serve as a possible contributing factor to the development of VLPs and life-threatening ventricular arrhythmias in hypertensive patients after acute myocardial infarction.

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