Hypertension
Figure 3: Cardiovascular Death, Stroke and Myocardial Infarction Stratified by Time-varying Presence or Absence of Left Ventricular Hypertrophy
A. Cardiovascular death stratified by time-varying presence of echo–LVH
0 1 2 3 4 5 6 7
cardiac death.48 These findings support the concept of reducing
cardiac target organ damage as a goal of antihypertensive treatment. In another analysis from the LIFE study, losartan was more effective than atenolol in reducing echocardiographic LV mass49 cardiographic indices.50
or relevant electro- Further analyses of the LIFE echocardiographic
data showed that even though LV geometry changed significantly during treatment, time-varying LV geometry predicted higher risk of composite end-points (HR 2.99 [1.16–7.71] for concentric remodelling, HR 1.79 [1.17–2.73] for eccentric hypertrophy and HR 2.71 [1.13–6.45] for concentric hypertrophy when adjusting for randomised treatment, Framingham risk score, race and time-varying systolic blood pressure).51 This suggests that concentric LV geometry carries the most risk, extending an observational study by Muiesan et al. in a group of 436 hypertensive patients in which persistent or new development of concentric LV geometry was associated with higher risk of cardiovascular morbidity and mortality during prospective follow-up.52
0 6 12 18 24 30 36 42 48 54 60 LVH absent
Month LVH present
B. Fatal and non-fatal stroke stratified by time-varying presence of echo–LVH
0 1 2 3 4 5 6 7
Left Ventricular Systolic Function in Patients with Left Ventricular Hypertrophy Assessment of LV systolic performance by the ratio of observed LV endocardial fractional shortening (FS) to the value predicted by the level of end-systolic stress in normal individuals53,54
may appear to
identify LV function as ‘supranormal’ in hypertensive patients compared with normal controls, even in the absence of LV hypertrophy.53,55,56
LV midwall shortening (MWS), in relation to stress,
provides a different impression of the integrity of systolic performance; MWS may be impaired in hypertensive patients with normal or supranormal LV ejection fraction. Wachtell et al. confirmed that LV endocardial FS or MWS were lower with higher LV mass and relative wall thickness either alone or in combination.57
In the
0 6 12 18 24 30 36 42 48 54 60 LVH absent
Month LVH present
C. Fatal and non-fatal myocardial infarction stratified by time-varying presence of echo–LVH
0 1 2 3 4 5 6 7
subgroup with concentric LV hypertrophy, we found that >40% had overt LV systolic dysfunction, manifested by endocardial FS or MWS below the 2.5th percentile of normal values (see Figure 4). Even in the subgroup with normal LV geometry we found impaired LV systolic performance in 10% of cases, i.e. five times more commonly than in the reference population.30,58
Furthermore, it was observed that
hypertensive patients with normal geometry or with eccentric LV hypertrophy had high end-systolic stress compared with normal adults. Previously reported in mildly hypertensive adults,59
this result
also reflects the Laplace relationship, which indicates that high relative wall thickness tends to normalise wall stress. Moreover, impaired endocardial FS was most prevalent in eccentric LV hypertrophy, while impaired MWS was most prevalent with concentric remodelling or, especially, concentric hypertrophy.
The clinical significance of impaired LV systolic performance in hypertensive patients is not yet fully clarified; however, there are numerous reports of patients with heart failure and ‘normal’ LV systolic chamber function.60
In the Framingham Heart Study in
participants 40–89 years of age and free of chronic heart failure, Levy et al.61
found that hypertension antedated the development of heart
0 6 12 18 24 30 36 42 48 54 60 LVH absent
Month LVH present LVH = left ventricular hypertrophy. Source: Devereux et al., 2004.46
independent effect of LV mass reduction on prognosis. In addition, reduction in LV hypertrophy translates into a reduction in sudden
26
failure. After adjusting for age and heart failure risk factors in proportional hazard regression models, the hazard of developing heart failure in hypertensive compared with normotensive subjects was about two-fold higher in men and three-fold higher in women. Multivariate analyses revealed that hypertension had a high population-attributable risk of chronic heart failure, accounting for 39% of cases in men and 59% in women. Survival following the onset of hypertensive heart failure was bleak: only 24% of men and 31% of women survived for five years. Furthermore, recent reports support a
EUROPEAN CARDIOLOGY
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