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Hypertensive Heart Disease


Although the clinical significance of prolonged isovolumic relaxation time and other abnormalities of LV filling have not yet been fully clarified, there are numerous reports of patients with heart failure and apparently normal LV systolic function.60


Levy et al. concluded in a


study from Framingham that hypertension was the most common risk factor for chronic heart failure, and it contributed to the pathogenesis of a large proportion of heart failure cases in a population-based sample.61


70 60


There are several reports that hypertension and LV hypertrophy play an important role in the development of heart failure. Available population-based studies document significant prediction of cardiovascular events by indices of LV diastolic dysfunction,78–80


congestive heart failure among hypertensive adults. However,


but to date have not related them specifically to it


remains controversial whether heart failure patients with preserved LV systolic function by exclusion have LV diastolic heart failure.81–84


Change in Left Ventricular Diastolic Function During Antihypertensive Treatment In view of the strong relations between LV mass and relative wall thickness and transmitral flow variables, Wachtell et al. examined whether reduction in LV mass and relative wall thickness as well as blood pressure by systematic antihypertensive treatment over one year could improve diastolic transmitral flow variables.85


Blood


pressure lowering by 23/11mmHg resulted in more normal isovolumic relaxation time and E/A ratio while LV in-flow deceleration time increased. The directionally opposite changes in isovolumic relaxation time and deceleration time indicate improvements in both active LV relaxation (manifested by the shortened isovolumic relaxation time) and passive chamber stiffness during early diastole.86


Furthermore, the prevalences of


normal transmitral filling increased while prevalences of abnormal relaxation and pseudonormal pattern decreased and restrictive filling pattern remained unchanged (see Figure 7).85


Patients with LV


mass reduction had significant improvement in left atrial diameter, isovolumic relaxation time, E/A ratio and mitral valve deceleration time. However, patients without LV mass reduction had no change in their diastolic filling variables. Further multivariate analyses showed that isovolumic relaxation time shortening was independently associated with reduction in LV mass, increase in E/A ratio was independently associated with reduction in diastolic blood pressure and increase in the deceleration time was independently associated with reduced end-systolic relative wall thickness.


Although


antihypertensive therapy resulted in LV mass or relative wall thickness regression and significant improvement of diastolic filling variables, abnormalities of diastolic LV filling remained common after one year of observation.


These results support the finding by Yalcin and co-workers87 that six


months of antihypertensive treatment with perindopril in 24 patients led to a reduction in LV mass and left atrial volume and an increased E/A ratio, but contrasts with a study by Cuspidi in a small population (n=39) in which six months of antihypertensive treatment had no significant effect on LV diastolic filling parameters.88


The clinical implication is that regression of hypertensive LV hypertrophy and of concentric LV geometry is associated with partial normalisation of several LV diastolic filling variables, including the isovolumic relaxation time, E/A ratio and mitral valve deceleration time, independent of the reduction in blood pressure, thus indicating direct effects of normalisation of LV geometry on diastolic filling


EUROPEAN CARDIOLOGY


20 30 40 50


10 0


Figure 7: Changes in Transmitral Flow Patterns After One Year of Antihypertensive Treatment Reducing Blood Pressure by 23/11mmHg


Normal


Abnormal relaxation


Source: Wachtell et al., 2004.44


Figure 8: Prevalence of Normal Transmitral Valve Flow Pattern from Baseline Through Five Years of Antihypertensive Treatment


10 20 30 40 50


0


Baseline Year 1 Year 2 Year 3 Year 4 Year 5 Normal (%)


Source: Wachtell et al., 2010.94


parameters. The complexity of factors influencing LV diastolic filling is highlighted by the fact that the deceleration time of early diastolic filling passive inflow increased at the same time as the isovolumic relaxation time decreased. This implies that the deceleration time was affected in opposite directions, being lengthened by impaired relaxation and shortened by increased LV stiffness due to increased relative wall thickness and probable alterations in myocardial connective tissue. A strong relation between invasively measured early diastolic chamber stiffness and shortened deceleration time was reported in an experimental study by Little et al.86 human study by Garcia et al.89


and in a Treatment-improved relaxation


predominated in shortening the isovolumic relaxation time, while reducing passive LV chamber stiffness predominated in prolonging the deceleration time of early diastolic transmitral flow. The improvement of diastolic dysfunction parameters may contribute to the ability of blood pressure reduction to prevent congestive heart failure, and highlights the potential of normalisation of LV geometry by antihypertensive therapy to prevent or treat congestive heart failure in hypertensive patients with LV hypertrophy an LV diastolic dysfunction, a condition for which no direct treatment exists.90


29


Pseudonormal Restrictive pattern


Baseline Year 1


Not classified


Percentage


Percentage


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