Hypertension
Figure 6: Correlation Between Left Ventricular Endocardial Fractional Shortening, Midwall Shortening and Isovolumic Relaxation Time
200
hypertrophy that the evolution of hypertensive LV hypertrophy is initiated by abnormalities of LV diastolic function, in the presence of preserved LV systolic function. It is well-established that LV relaxation is often abnormal in hypertensive patients with70
or without71 LV
hypertrophy, suggesting that abnormal relaxation might be an early response to cardiac overload caused by hypertension.71,72 cardiac myocyte volume,
Increased myocardial ischaemia caused by 140
hypertensive microvascular disease and a mismatch between increased oxygen demand and reduced coronary flow reserve may all contribute to the abnormal diastolic relaxation.73
80 20 20 30 40 Fractional shortening (%) 50
Data from the LIFE echocardiography study found very high prevalences (>80%) of abnormal diastolic LV-filling patterns in hypertensive patients with electrocardiographic LV hypertrophy.62 Most of these patients had a decreased E/A ratio and prolonged deceleration time, readily recognised manifestations of impaired early LV diastolic relaxation, but an appreciable minority had a ‘pseudonormal’ LV filling pattern. Furthermore, isovolumic relaxation time, A-peak, atrial filling fraction and left atrial dimension, an indirect index of atrial overload due to abnormal diastolic function, differed significantly among the four LV geometrical patterns.62
There was also 200
a strong association between higher LV mass and worse LV early diastolic relaxation as manifested by the prolonged isovolumic relaxation time.
140 80 20 8 10121416 Midwall shortening (%) Source: Wachtell et al., 2004.77
infarctions and 49% less incident heart failure, whereas in-treatment stress-corrected endocardial FS was not associated with any end- points. By contrast, improved in-treatment MWS was associated with a 16% reduction in the risk of the composite end-point of stroke, myocardial infarction and cardiovascular mortality, a 33% reduction in the risk of the component fatal and non-fatal myocardial infarction and 43% less incident heart failure. Improvement in stress-corrected MWS was in addition to improvement in rate of myocardial infarction (35% reduction), also associated with a 50% reduction in heart failure when adjusting for time-varying diastolic blood pressure and time- varying LVMI, relative wall thickness and randomised treatment.69
The
clinical significance of this is that antihypertensive treatment and reduction in LV hypertrophy also improve LV systolic function, and even small improvements in LV systolic function, especially at the midwall, translate into less cardiovascular morbidity and mortality.69
Left Ventricular Diastolic Function in Patients with Left Ventricular Hypertrophy It has been accepted ever since the early demonstration that electrocardiographic P-wave abnormality preceded evidence of LV
28 18 20 22
This association remained significant in regression analyses that took into account other variables also associated with longer isovolumic relaxation time, including male gender, lower peak early LV-filling velocity and higher deceleration time, briefer mitral valve opening time and lower pulse pressure/stroke volume ratio. Among the minority of LIFE patients with normal LV mass, isovolumic relaxation time was significantly longer in those with concentric LV remodelling characterised by high relative wall thickness than in those with normal relative wall thickness (i.e. normal geometry). On the other hand, in the presence of LV hypertrophy, relative wall thickness was not a significant correlate of isovolumic relaxation time. This finding suggests that increased LV mass is a stronger stimulus to impaired LV relaxation than is a concentric LV geometrical pattern. These observations also suggest that for antihypertensive therapy to be optimally beneficial for LV filling, it would be desirable to normalise not only LV mass but also relative wall thickness.
It has been speculated that LV wall thickness and cavity dimension contribute to diastolic dysfunction,75 confirmed in all studies.76
This observation of a strong association between abnormal filling and concentric LV hypertrophy has been confirmed by de Simone in data from the Hypertension Genetic Epidemiology Network (HyperGEN) study.74
but this has not been
Wachtell et al. reported from the LIFE echocardiography study a relationship between LV diastolic abnormality and abnormal LV systolic function.77
Impaired LV early diastolic relaxation, as
manifested by prolonged isovolumic relaxation time, was associated with lower LV systolic myocardial function independently of age and other relevant co-variates (see Figure 6). In addition, lower levels of stress-corrected LV MWS and early diastolic relaxation were both related to higher LV mass, but the relation between prolonged isovolumic relaxation time and reduced LV systolic midwall function remained significant when LV mass was taken into account.
EUROPEAN CARDIOLOGY
Isovolumic relaxation time (msec)
Isovolumic relaxation time (msec)
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