Clinical and Experimental Pharmacology and Physiology (1990) 17,207-210

SHORT COMMUNICATION

PREVALENCE OF LEFT VENTRICULAR HYPERTROPHY IN ELDERLY PATIENTS WITH WELL CONTROLLED HYPERTENSION

Elizabeth Jones, Trefor 0. Morgan, Paul Califiore and Jennifer Johns

Hypertension and Cardiac Units, Repatriation Hospital, Heidelberg, Victoria, Australia

(Received 19 December 1989)

SUMMARY

1. Left ventricular hypertrophy (LVH) was measured by echocardiography in 154 patients, mostly males, aged 55 years or more, with hypertension who had been well controlled for at least 2 years.

2. Satisfactory studies with no other cardiac lesions were available for 103 patients; 52% had LVH and 48% had normal left ventricular dimensions.

3 . In patients with well controlled hypertension there was a high prevalence of LVH despite adequate control for at least 2 years. Neither the level of control nor the drugs used appeared to predict the outcome.

4. Consideration needs to be given to earlier treatment, greater lowering of blood pressure, or different drugs to reduce this high prevalence of LVH.

Key words: ACE inhibitors, cardiac hypertrophy, echocardiography, hypertension.

INTRODUCTION

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiac morbidity and mortality in hypertension (Casale et al. 1986). Several studies have demonstrated regression of LVH when hypertension is controlled with drugs such as angiotensin converting enzyme (ACE) inhibitors (Nakeshima et al. 1984), &blocking drugs (Dunn et al. 1987) and calcium antagonists (Fouad-Tarazi & Liebson 1987). However, comparable blood pressure reduction using other drugs, notably thiazide diuretics and hydralazine, does not result in regression of LVH, suggesting that factors other than blood pressure level are important in initiating and maintaining LVH in hypertension (Casale et al. 1986; Leenen et al. 1987; Messerli et al. 1989).

This study assessed the prevalence of LVH in a group of well-controlled hypertensive patients and the relationship of LVH to drug therapy, blood pressure control and age.

Correspondence: Professor T. 0. Morgan, Department of Physiology, University of Melbourne, Parkville, Vic. 3052, Australia.

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208 E. Hones et al.

METHODS

Patients were selected from the Hypertension Clinic at Repatriation General Hospital, Heidel- berg. Eligible patients had had documented diastolic blood pressure (DBP) of greater than 100 mmHg on at least two occasions either on or off therapy and had treated DBP of less than 95 mmHg on 75% of recordings over a 2 year period prior to entry to the study. All patients underwent M-mode and two-dimensional echocardiography.

LVH was judged to be present if both posterior wall and septa1 thickness exceeded 1.1 cm and if the left ventricular mass index exceeded 150 g/m2 for men and 120 g/mZ for women (Levy et al. 1987) or if a qualitative assessment of LVH was made by an experienced echocardiographer in the absence of images adequate for measurement.

Blood pressure control was graded according to DBP readings over the preceding 2 years: Grade 1 = all recordings <80 mmHg; Grade 2 = 75% readings <80 mmHg; Grade 3 = 75% readings <85 mmHg; Grade 4 = 75% readings <90 mmHg; Grade 5 = 75% readings <95 mmHg.

Blood pressure was recorded on at least four occasions during the 2 year period in all cases. Differences were compared by analysis of variance and by Chi square tests.

RESULTS

One hundred and fifty-four patients fulfilling the criteria for blood pressure control underwent echocardiography. Of these, 19 had valvular lesions or left ventricular dilatation (left ventricular internal diastolic diameter >6 cm) and in 32 patients no assessment of left ventricular dimensions was possible for anatomical and technical reasons. Thus 103 patients were suitable for analysis. Of these 94 patients were male and all were Caucasian. The age range was 45-81 years and the duration of hypertension 3-45 years.

The levels of diastolic blood pressure control for groups with and without LVH are shown in Table 1, and were not significantly different (P>0.5).

Table 1. Characteristics of patients with and without LVH

No LVH LVH n % n %

Male

Age (years) 40-49 50-59 60-69 70-79 80-89

DBP Grade 1 Grade 2 Grade 3 Grade 4 Grade 5

ACE inhibitor P-blocker Diuretic Ca antagonist Vasodilator or methyldopa

45 92

3 6 3 6

28 57 14 29 1 2

4 8 12 24 13 27 11 22 9 18

31 63 14 29 24 49

5 10 4 8

49 91

0 0 1 2

27 50 25 46

1 2

3 6 20 37 21 39

7 13 3 6

31 57 15 28 20 37 9 17 3 6

No significant differences between groups using Chi square test and analysis of variance.

LVH in control led hypertension 209

There were no significant differences between the groups in terms of therapy used to control blood pressure over the preceding 2 years. In particular, there was no difference in the use of ACE inhibitors, P-blocking drugs or calcium antagonists in patients with and without LVH.

DISCUSSION

Despite clinically acceptable control of blood pressure over a 2 year period, the prevalence of echocardiographic LVH in this group of 103 elderly hypertensive patients was 52%, using criteria which would tend to underestimate rather than overestimate the true prevalence. Other studies have used less strict criteria for the definition of echocardiography LVH and would have included patients with asymmetric septa1 hypertrophy, which may be an age-related phenomenon (Gersten- blith et al. 1977). We also excluded any patients with valvular heart disease or left ventricular dilatation which may have produced a significantly increased left ventricular mass index unrelated to hypertension.

The patients in this study did not undergo echocardiography prior to attainment of clinically acceptable blood pressure control, so we do not have baseline left ventricular dimensions to assess the initial prevalence of LVH. However, previous studies have suggested a prevalence of LVH in hypertensive patients of 23-48% (Hammond et al. 1986). Assuming that our population would have had a similar initial prevalence of LVH, we have been unable to demonstrate any reduction in prevalence after 2 years or more of adequate treatment.

Our findings do not suggest any relationship between level of treated blood pressure and prevalence of LVH. This lends support to the concept that factors other than blood pressure contribute to the development, maintenance and regression of LVH in hypertension (Tarazi & Frohlich 1987), and it is possible that age (Gerstenblith et at. 1977) was one of these factors in our population, although LVH was not significantly greater in the older age groups.

There was no evidence that use of any particular anti-hypertensive drug was associated with a lower prevalence of LVH. This is in contrast to previous studies which have demonstrated a favourable effect of ACE inhibitors, P-blocking drugs and calcium antagonists on regression of LVH in hypertension. A possible explanation may be the older age of our population, of whom 93% were over 60 years of age and 40% over 70.

If it is worthwhile to attempt reversal of LVH in hypertension (Tarazi & Frohlich 1987), then it is important to identify drugs which will achieve this goal as well as control hypertension in all age groups. Ongoing study of larger numbers of patients and prospective trials of the effect of specific drugs on LVH may help to clarify this issue.

ACKNOWLEDGEMENTS

The help of nursing staff (Leonie Carrick and Cate Wilson) and of echocardiographers (Allison McKenzie and Mala Rajah) is appreciated. This study was supported by the National Heart Foundation of Australia.

REFERENCES

Casale, P. N., Devereux, R. B., Milner, M. et al. (1986) Value of echocardiography measurements in predicting cardiovascular morbid events in hypertensive men. Annals Internal Medicine, 105, 173-178.

Dunn, F., Ventura, H., Messerli, F., Kobrin, I., Frohlich, E. (1987) Time course of regression of left ventricular hypertrophy in hypertensive patients treated with atenolol. Circulation, 76,254-258.

Fouad-Tarazi, F. & Liebson, P. (1987) Echocardiographic studies of regression of left ventricular hypertrophy in hypertension. Hypertension, 9 (Suppl. II), 1165-68.

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