Estimation of regional stress in the left ventricular septum and free wall: An echocardiographic study suggesting a mechanism for asymmetric septal hypertrophy

Heng, Ming K.; Janz, R. F.; Jobin, Jean

doi:10.1016/0002-8703(85)90519-8

Cited by 61 publications

(28 citation statements)

References 16 publications

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“…Following Bernoulli's theory, the septal wall of the outflow tract has the smallest radius of curvature and is thus exposed to the strongest stress. Heng et al (24) showed that regional wall stress is greater in the IVS than in the free wall, and the base of the IVS shows the greatest stress according to echographic data and analysis of the shape of the LV cavity. An echocardiographic study has revealed that, in hypertensive patients with LVH, diastolic dysfunction is more evident at the basal septum than in other parts of the LV (25).…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Regional Variations in Myosin Isoform Shift in Dahl Salt-Sensitive Hypertensive Rats.

et al. 2003

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To evaluate the effects of chronic pressure overload on different parts of the left ventricle (LV), we examined a myosin isoform shift from V1 to V3 as a biochemical marker of LV hypertrophy in Dahl salt-sensitive (DS) rats. Six-week-old DS rats were fed an 8% (high salt, HS; n 24) or a 0.3% (low salt, LS; n 12) NaCl diet. After 2 or 4 weeks, the hearts were dissected and the LVs were separated into four parts (the base and mid- after blood pressure is controlled (12). Studies have confirmed this prominence of the basal septal hypertrophy in hypertensives, and especially in elderly hypertensives (13,14). These observations suggest that myocardial hypertrophy as a response to pressure overload may develop differently at individual regions of the left ventricle (LV). Thus, we surmised that the base of the IVS is exposed to the greatest pressure overload, and that LVH begins at this site in hypertensive patients. Using the transformation of the myosin isoform from V1 to V3 as a biochemical marker of pressure overload, the present study was carried out to determine which part of the ventricular wall is most stressed by systemic hypertension in Dahl salt-sensitive rats (DS). MethodsSix-week-old male inbred DS rats (n 36) were obtained

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Section: Discussionmentioning

confidence: 99%

Left Ventricular Regional Variations in Myosin Isoform Shift in Dahl Salt-Sensitive Hypertensive Rats.

et al. 2003

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“…14 The latter is usually compensated for by transseptal pressure from the right ventricle that acts to reduce wall stress. 14,34 When this compensation becomes insufficient, local stress increases, leading to the development of the characteristic basal septal bulge and regional longitudinal dysfunction. 14,25,34,35 LV concentric hypertrophy is known to be accompanied by subendocardial fibrosis both in hypertensive subjects and from autopsy data.…”

Section: Systolic Function and Heart Remodelingmentioning

confidence: 99%

Maternal Cardiac Dysfunction and Remodeling in Women With Preeclampsia at Term

et al. 2011

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Abstract-Preeclampsia is a disease associated with significant cardiovascular morbidity during pregnancy and in later life.This study was designed to evaluate cardiac function and remodeling in preeclampsia occurring at term. This was a prospective case-control study of 50 term preeclampsia and 50 normal pregnancies assessed by echocardiography and tissue Doppler analysis. Global diastolic dysfunction was observed more frequently in preeclampsia versus control pregnancies (40% versus 14%, Pϭ0.007). Increased cardiac work and left ventricular mass indices suggest that left ventricular remodeling was an adaptive response to maintain myocardial contractility with preeclampsia at term. Approximately 20% of patients with preeclampsia at term have more evident myocardial damage. Diastolic dysfunction usually precedes systolic dysfunction in the evolution of ischemic or hypertensive cardiac diseases and is of prognostic value in the prediction of long-term cardiovascular morbidity. The study findings also have significant implications for the acute medical management of preeclampsia. (Hypertension. 2011;57:85-93.) • Online Data Supplement Key Words: diastolic dysfunction Ⅲ echocardiography Ⅲ left ventricular remodeling Ⅲ preeclampsia Ⅲ pregnancy Ⅲ strain rate Ⅲ tissue Doppler P reeclampsia (PE) is a pregnancy complication of placental etiology with acute onset of predominantly cardiovascular manifestations. 1 The pathological changes in this disorder are primarily ischemic in nature and are known to affect the placenta, kidney, liver, and brain, whereas there is scant and conflicting information about the impact on the heart. [1][2][3][4][5][6][7] Cardiopulmonary morbidity is seen in a significant proportion of preeclamptic cases 8 and autopsy data have demonstrated that preeclamptic women have a 10-fold higher prevalence of myocardial contraction band necrosis than deaths in pregnancy from other causes. 9 Epidemiological data have also highlighted the strong relationship between preeclampsia and premature morbidity and mortality from cardiovascular disease 10,11 thought to be related to shared cardiovascular risk factors. 12 All these data suggest that preeclampsia may be associated with the potential for significant myocardial damage. Tissue Doppler (TD) velocity and deformation indices are highly sensitive at detecting even mild myocardial damage. [13][14][15][16][17][18] The aim of this study is to test the hypothesis that PE provokes significant myocardial damage/dysfunction by using both conventional echocardiography and TD analysis in women with and without PE. Methods Study SubjectsThis was a prospective case-control study carried out over a 2-year period from January 2008. All women with singleton pregnancy and PE at term (37 to 42 completed weeks of gestation) were recruited consecutively as cases after informed consent and with local institutional review committee approval. Only women without comorbidities, nonsmokers, and before starting any medication were asked to take part in the study. PE and nonprotein...

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“…Some authors have suggested that the asymmetric septal hypertrophy of hemodialysis patients is due to sympathetic nervous system overactivitv and increased circulating catecholamine levels [28]. However, the reason seems more probably to be stereometric: the geometry of the ventricular cavity makes for a parietal stress that is higher at the level of the septum because of its more eccentric position and of its greater radius of the curvature [29], Besides the mechanical factors, hypertro phy and growth of myocardial cells are also influenced by neural and humoral factors with 280 London/Guerin/Marchais Cardiac Hypertrophy in Uremia…”

Section: Left Ventricular Mass In Esrdmentioning

confidence: 99%

Pathophysiology of Left Ventricular Hypertrophy in Dialysis Patients

London¹,

Guérin²,

Marchais³

1994

Blood Purif

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Left ventricular hypertrophy is a frequent cardiovascular alteration in end-stage renal disease patients on hemodialysis which is associated with increased morbidity and mortality. Hypertrophy results from chronic flow and pressure overload and from poorly understood neurohumoral alterations. Clinical symptomatology associated with ventricular hypertrophy is related to diastolic dysfunction which characterizes this condition. The symptoms are (1) an unusual sensitivity to volume changes such that hypotension and hemodynamic instability and/or pulmonary edema occur with small volume variations and (2) a high frequency of supraventricular arrhythmias.

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Estimation of regional stress in the left ventricular septum and free wall: An echocardiographic study suggesting a mechanism for asymmetric septal hypertrophy

Cited by 61 publications

References 16 publications

Left Ventricular Regional Variations in Myosin Isoform Shift in Dahl Salt-Sensitive Hypertensive Rats.

Left Ventricular Regional Variations in Myosin Isoform Shift in Dahl Salt-Sensitive Hypertensive Rats.

Maternal Cardiac Dysfunction and Remodeling in Women With Preeclampsia at Term

Pathophysiology of Left Ventricular Hypertrophy in Dialysis Patients

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