[Arrhythmogenicity in left ventricular hypertrophy in mild to moderate arterial hypertension].

BACKGROUND

Several studies have evidenced that hypertensive patients (pts) with left ventricular hypertrophy (LVH) have an increased incidence of malignant ventricular arrhythmias and sudden death. The purpose of our study was to investigate the prevalence of risky ventricular arrhythmias in uncomplicated hypertensive pts (untreated during last 10 days) in comparison with normotensive ones. In this context, not only the value of left ventricular mass index (LVMI) was taken into account, but also the type of LVH and the related functional behaviour.

PATIENTS AND METHODS

59 untreated mild to moderate essential hypertensives (EH), without symptoms or signs of coronary artery disease, were classified in 3 groups: normal (i.e. without hypertrophy) EH (NEH: 12 pts, 6 M and 6 F, mean age +/- SD 52 +/- 10 yrs), concentric hypertrophic EH (CEH: 30 pts, 15 M and 15 F, mean age +/- SD 59 +/- 10 yrs), and eccentric hypertrophic EH (EEH: 17 pts, 7 M and 10F, mean age +/- SD 60 +/- 10 yrs), according to echocardiographic measurements. Values and duration of arterial hypertension were comparable among the groups. A normotensive, age-matched group was studied as control (C: 21 pts, 11 M and 10 F, mean age +/- SD, 57 +/- 10 yrs). 24-hour Holter electrocardiographic monitoring (ECG-H) and Signal-Averaged electrocardiography (SAECG) were performed seeking to identify the arrhythmogenic risk. Echocardiographic analysis was accomplished by means of a computerized system: LVMI, ratio of LV wall thickness to LV internal radius (relative wall thickness = RWTh), systolic velocity of circumferential fractioning (VCFs), peak of LV relaxation rate (pLVRr) and peak-systolic stress (pSS) were evaluated.

RESULTS

Normal LV systolic function was generally found, but both NEH and EEH groups showed a significant reduction in pLVRr in comparison with C and CEH groups (mean values +/- SD: 3.52 +/- 1,3 and 3.40 +/- 0.9 vs 4.92 +/- 0.4 and 4.27 +/- 1.4 sec-1, respectively, p < .05 for both). pSS was significantly higher in EEH and NEH than in CEH and C (mean values +/- SD: 149 +/- 42 and 157 +/- 66 vs 116 +/- 28 and 122 +/- 15 10(3) dynes/cm2, respectively; p < .05 for both). At ECG-H, EEH had a prevalence of potentially malignant ventricular arrhythmias (PMVA: ventricular extrasystoles > or = 30/h; ventricular couplets, > or = 2 episodes/24h, or triplets, > or = 1 episode/24h; R on T), significantly larger than in C (35.3% vs 4.8%, p < .05) and almost significantly larger than in NEH and CEH (8.3% and 10%, respectively). No differences in LVMI were found between EEH with or without PMVA. In respect of functional LV behaviour, the former group showed lower values of VCFs (2.33 +/- 0.6 vs 3.71 +/- 1.32 sec-1, (p < .005) than the latter group. At SAECG, the EEH exhibited again a greater prevalence of abnormal findings than C (35.3% vs 0%, p < 0.5). No correlations were found between ECG-H and SAECG abnormalities, nor between the latter group and LVMI or LV functional indexes. Among pts showing a more pronounced impairment of diastolic function (pLVRr < 4 sec-1), EEH exhibited the highest prevalence of both PMVA (50%) and late potentials (41%).

CONCLUSIONS

Our data suggest that uncomplicated mild to moderate essential hypertension may be associated with higher risk of ventricular arrhythmias, particularly when cardiac involvement is characterized by eccentric LVH. On the contrary, in this stage of hypertensive disease, LVMI as well as LV function do not seem to influence the ventricular arrhythmogenesis. The clinical importance of these findings is uncertain, and further studies are needed.