Hypertension and Left Ventricular Diastolic Function

Shepherd, Roger F.J.; Zachariah, Prince K.; Shub, Clarence

doi:10.1016/s0025-6196(12)65708-5

Cited by 34 publications

(29 citation statements)

References 53 publications

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“…3 30 31 In hypertrophic cardiomyopathy, however, it has been found that the Doppler pattern of left ventricular filling is largely independent of the extent of left ventricular hypertrophy 30. Focusing on the entire ventricle, our present study confirms these findings, showing an independence of the conventional Doppler diastolic relaxation indices from the extent of left ventricular hypertrophy (that is, left ventricular wall thickness index) in hypertrophic cardiomyopathy.…”

Section: Discussionsupporting

confidence: 85%

Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function

Marchì¹

2000

Heart

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Aim-To determine the relation between the extent and distribution of left ventricular hypertrophy and the degree of disturbance of regional relaxation and global left ventricular filling. Methods-Regional wall thickness (rWT) was measured in eight myocardial regions in 17 patients with hypertrophic cardiomyopathy, 12 patients with hypertensive heart disease, and 10 age matched normal subjects, and an asymmetry index calculated. Regional relaxation was assessed in these eight regions using regional isovolumetric relaxation time (rIVRT) and early to late peak filling velocity ratio (rE/A) derived from Doppler tissue imaging. Asynchrony of rIVRT was calculated. Doppler left ventricular filling indices were assessed using the isovolumetric relaxation time, the deceleration time of early diastolic filling (E-DT), and the E/A ratio. Results-There was a correlation between rWT and both rIVRT and rE/A in the two types of heart disease (hypertrophic cardiomyopathy: r = 0.47, p < 0.0001 for rIVRT; r = −0.20, p < 0.05 for rE/A; hypertensive heart disease: r = 0.21, p < 0.05 for rIVRT; r = −0.30, p = 0.003 for rE/A). The degree of left ventricular asymmetry was related to prolonged E-DT (r = 0.50, p = 0.001) and increased asynchrony (r = 0.42, p = 0.002) in all patients combined, but not within individual groups. Asynchrony itself was associated with decreased E/A (r = −0.39, p = 0.01) and protracted E-DT (r = 0.69, p < 0.0001) and isovolumetric relaxation time (r = 0.51, p = 0.001) in all patients. These correlations were still significant for E-DT in hypertrophic cardiomyopathy (r = 0.56, p = 0.02) and hypertensive heart disease (r = 0.59, p < 0.05) and for isovolumetric relaxation time in non-obstructive hypertrophic cardiomyopathy (n = 8, r = 0.87, p = 0.005). Conclusions-Non-invasive ultrasonographic examination of the left ventricle shows that in both hypertrophic cardiomyopathy and hypertensive heart disease, the local extent of left ventricular hypertrophy is associated with regional left ventricular relaxation abnormalities. Asymmetrical distribution of left ventricular hypertrophy is indirectly related to global left ventricular early filling abnormalities through regional asynchrony of left ventricular relaxation. (Heart 2000;83:678-684) Keywords: hypertrophic cardiomyopathy; hypertensive heart disease; isovolumetric relaxation; diastolic function Hypertrophic cardiomyopathy is a primary myocardial disease. It is characterised by left ventricular hypertrophy which develops independently of loading conditions. Hypertrophy in hypertensive heart disease is considered to be a response to increased afterload. 1 In both types of hypertrophy, abnormal left ventricular relaxation is a hallmark of the disease. Even in the presence of normal left ventricular systolic performance, this abnormality results in a rise in left atrial pressure, pulmonary congestion, and oedema. Dyspnoea is thus a very common symptom in these patients. Myocardial hypertrophy has been shown to be the crucial morphological change accoun...

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Section: Discussionsupporting

confidence: 85%

Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function

Marchì¹

2000

Heart

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“…This finding supports the concept of pathophysiological similarities between patients with white coat and persistent hypertension, which are not dependent on ambulatory blood pressure values. Our data seem consistent with previous observations of an altered E/A ratio already present in very mild forms of hypertension, 31 in young borderline essential hypertensive patients, 32 and even before the development of true clinical hypertension. 33 …”

Section: Cardiac End-organ Changessupporting

confidence: 93%

Psychophysiological reactivity and cardiac end-organ changes in white coat hypertension.

et al. 1993

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This study aimed 1) to assess whether patients with an exaggerated blood pressure response to the doctor's presence ("white coat" effect) also display a pattern of enhanced blood pressure reactivity to mental stress and physical exercise and 2) to determine the presence of left ventricular structural and filling abnormalities in patients with white coat hypertension. We studied 56 (40 men) consecutive patients (mean [SD] age, 46.4 [9.1] years) whose clinic blood pressure was repeatedly high. Patients were classified as having white coat hypertension («=20) if both their mean daytime (from 7 AM to 11 PM) ambulatory systolic and diastolic blood pressures were less than 134 and 90 mm Hg, respectively. Patients were considered to have persistent hypertension (n=36) if daytime systolic blood pressure was 134 mm Hg or more or diastolic blood pressure was 90 mm Hg or more. Eighteen subjects with clinic blood pressure lower than 140/90 mm Hg served as a normotensive control group. Blood pressure reactivity from baseline to mental arithmetic, isometric handgrip, and cycle ergometry did not display any difference among the three groups. The white coat hypertensive group had left ventricular mass index lower than the persistent hypertensive group but higher than the normotensive group. Doppler indexes of left ventricular diastolic filling displayed similar abnormalities in the white coat and persistent hypertensive groups compared with the normotensive group. We conclude that 1) we cannot distinguish white coat hypertensive patients by a pattern of blood pressure hyperreactivity to mental and physical laboratory tasks, and 2) white coat hypertension is characterized by mild cardiac enlargement and shares with persistent hypertension similar abnormalities in left ventricular filling. These latter findings suggest that white coat hypertension may not be considered an entirely innocuous clinical condition. One possible explanation for this observation might be the "white coat" phenomenon, the exaggerated blood pressure rise related to the doctor's visit, 3 which may cause the misclassification of some normotensive subjects as hypertensive patients. Despite the long-standing recognition of white coat hypertension, 4 some aspects of it are still unclear.5 In fact, there is no agreement about its prevalence, and the factors responsible for it are not clearly understood; moreover, its long-term prognostic significance has not been established, and consequently, whether it needs to be treated is unknown.We hypothesized that patients who are normotensive during daily life and respond to the stress of a clinic visit with an exaggerated increase in blood pressure might have an exaggerated blood pressure rise also during exposure to other stressful situations. To test this hy-

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“…41 This demands a speedier energy-dependent myocardial relaxation and accentuated atrial topping off (atrial kick) of end-diastolic ventricular volume. Ventricular pumping problems and heart failure may reflect compromised filling and are elicited or accentuated by exercise or by a dobutamine stress test if ergometric exercise is unfeasible.…”

Section: What Goes Out Must Come Back In—before It Can Go Out Againmentioning

confidence: 99%

LV twisting and untwisting in HCM: Ejection begets filling

Pasipoularides

2011

American Heart Journal

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Conventional and emerging concepts on mechanisms by which hypertrophic cardiomyopathy (HCM) engenders diastolic dysfunction are surveyed. A shift from familiar left ventricular (LV) diastolic function approaches to large-scale (twist-untwist) and small-scale (titin unfoldingrefolding, etc.) wall rebound models, incorporating interaction and dynamic distortions and rearrangements of myofiber sheets and ultrastructural constituents, is suggested. Such an emerging new paradigm of diastolic dynamics, emphasizing the relationship of myofiber sheet and ultraconstituent distortion to LV mechanics and end-systolic shape, might clarify intricate patterns of early diastolic rebound and suction, needed for LV filling in many of the polymorphic phenotypes of HCM.Janus was a Roman deity with 2 faces (Janus bifrons), looking backward and forward simultaneously just as gates look in both directions (Figure 1). He too watched entrances and exits, and his shrines were located at crossing places or intersections. The left ventricle as Janus bifronsThe pumping left ventricle forms the intersection or central link (Figure 1) between the lowpressure and the high-pressure systems of the circulatory ensemble. 1 It is a suctioncompression positive-displacement pump, exhibiting both self-regulating properties as an independent organ and dependent properties as part of the overall circulation. In diastole, it adapts to the low-pressure system from which it draws blood, whereas, in systole, it adjusts to the high-pressure system into which it must force blood. For that reason, it needs to alternate between the widely disparate functional-structural requirements of systole and diastole. 1 Since like Janus it can look directly backward and forward, into the low-and high-pressure systems, it displays remarkable Janus-like characteristics. Hence, it subserves at times incongruous functions, such as when excessive wall hypertrophy in response to a systolic pressure overload is associated with diminished diastolic distending wall stress levels and, not uncommonly, with increased muscle stiffness, both of which may then be responsible for impaired left ventricular (LV) diastolic filling. [2][3][4] Almost all forms of heart disease and most strikingly hypertrophic cardiomyopathy (HCM) alter ventricular structure. The changes in

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Hypertension and Left Ventricular Diastolic Function

Cited by 34 publications

References 53 publications

Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function

Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function

Psychophysiological reactivity and cardiac end-organ changes in white coat hypertension.

LV twisting and untwisting in HCM: Ejection begets filling

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