Mechanism of altered patterns of left ventricular filling during the development of congestive heart failure.

Ohno, Michiya; Cheng, Che‐Ping; Little, William C.

doi:10.1161/01.cir.89.5.2241

Cited by 276 publications

(181 citation statements)

References 46 publications

(18 reference statements)

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“…This has been resolved by experiments in an animal model of dilated cardiomyopathy that validated an analytical expression allowing us to calculate a value for LV stiffness, K LV , from the measurement of T DEC . 11,12 More recent studies have shown that a similar equation relating K LV quantitatively to T DEC applies to patients with cardiac diseases. 13 By using this noninvasive approach, we observed that LV stiffness is abnormally increased in patients with essential hypertension.…”

Section: Discussionmentioning

confidence: 98%

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Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

et al. 2002

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Background — This study was designed to investigate whether myocardial collagen content is related to myocardial stiffness in patients with essential hypertension. Methods and Results — The study was performed in 34 patients with hypertensive heart disease. Nineteen of these patients were also evaluated after 12 months of treatment with losartan. Transvenous endomyocardial biopsies of the interventricular septum were performed to quantify collagen volume fraction (CVF). Left ventricular (LV) chamber stiffness (K LV ) was determined from the deceleration time of the early mitral filling wave as measured by Doppler echocardiography. Histological analysis at baseline revealed the presence of 2 subgroups of patients: 8 with severe fibrosis and 26 with nonsevere fibrosis. Values of CVF and K LV were significantly higher in the 2 subgroups of hypertensives than in normotensives. In addition, compared with patients with nonsevere fibrosis, patients with severe fibrosis exhibited significantly increased values of CVF and K LV . After treatment, CVF and K LV decreased significantly in patients with severe fibrosis (n=7). None of these parameters changed significantly after treatment in patients with nonsevere fibrosis (n=12). CVF was directly correlated with K LV ( r =0.415, P <0.02) in all hypertensives. Conclusions — These findings show a strong association between myocardial collagen content and LV chamber stiffness in patients with essential hypertension. Our results also suggest that the ability of losartan to induce regression of severe myocardial fibrosis is associated with diminution of myocardial stiffness in hypertensive patients.

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Section: Discussionmentioning

confidence: 98%

“…Shortened T DEC has been associated with increased LV filling pressure in patients with different types of cardiomyopathies. 8 -10 Recent studies in animals 11,12 and humans 13 with several different hemodynamic conditions have validated an analytical expression that is useful to calculate LV chamber stiffness (K LV ) from the measurement of T DEC .…”

mentioning

confidence: 99%

Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

et al. 2002

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“…These included mitral early diastolic velocity (peak velocity of mitral inflow in early diastole after mitral valve opening), deceleration time (DT of E), A velocity transit time from LV inflow to LV outflow (A wave transit time; time taken for A velocity to propagate from LV inflow to LV outflow and relates inversely to late diastolic LV stiffness), and ratio of EDV to EDP (end diastolic pressure). DT of E is an echocardiographically derived time interval that has been shown in animal 11 and human 12 investigations to have a strong and inverse correlation with LV stiffness (rϭϪ0.86 with a mean difference of 0.02Ϯ0.06 mm Hg/mL; higher LV stiffness associated with shorter DT). This measurement was applied successfully to examine changes in LV stiffness in relation to regression of fibrosis induced by losartan.…”

Section: Echocardiographic Studies and Assessment Of LV Stiffnessmentioning

confidence: 99%

Altered Titin Expression, Myocardial Stiffness, and Left Ventricular Function in Patients With Dilated Cardiomyopathy

et al. 2004

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Background-The role of the giant protein titin in patients with heart failure is not well established. We investigated titin expression in patients with end-stage heart failure resulting from nonischemic dilated cardiomyopathy, in particular as it relates to left ventricular (LV) myocardial stiffness and LV function. Methods and Results-SDS-agarose gels revealed small N2B (stiff) and large N2BA (compliant) cardiac titin isoforms with a mean N2BA:N2B expression ratio that was significantly (PϽ0.003) increased in 20 heart failure patients versus 6 controls. However, total titin was unchanged. The coexpression ratio was highest in a subsample of patients with an impaired LV relaxation pattern (nϭ7), intermediate in those with pseudonormal filling (nϭ6), and lowest in the group with restrictive filling (nϭ7). Mechanical measurements on LV muscle strips dissected from these hearts (nϭ8) revealed that passive muscle stiffness was significantly reduced in patients with a high N2BA:N2B expression ratio. Clinical correlations support the relevance of these changes for LV function (assessed by invasive hemodynamics and Doppler echocardiography). A positive correlation between the N2BA:N2B titin isoform ratio and deceleration time of mitral E velocity, A wave transit time, and end diastolic volume/pressure ratio was found. These changes affect exercise tolerance, as indicated by the positive correlation between the N2BA:N2B isoform ratio and peak O 2 consumption (nϭ10). Upregulated N2BA expression was accompanied by increased expression levels of titin-binding proteins (cardiac ankyrin repeat protein, ankrd2, and diabetes ankyrin repeat protein) that bind to the N2A element of N2BA titin (studied in 13 patients). Conclusions-Total titin content was unchanged in end-stage failing hearts and the more compliant N2BA isoform comprised a greater percentage of titin in these hearts. Changes in titin isoform expression in heart failure patients with dilated cardiomyopathy significantly impact diastolic filling by lowering myocardial stiffness. Upregulation of titin-binding proteins indicates that the importance of altered titin expression might extend to cell signaling and regulation of gene expression.

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“…Using Doppler echocardiography, distinctive diastolic transmitral filling patterns have been identified which relate to functional status and diminished exercise tolerance [7][8][9][10][11]. In advanced cases where filling pressures are high and LV chamber stiffness is often increased, the mitral filling pattern is characterized by a short deceleration time (DT) of the early diastolic filling wave and an increased ratio of peak flow velocity of early to late diastole, this has been termed a restrictive filling pattern [7,8,[12][13][14]. Restrictive filling is associated with clinical severity of heart failure and poor prognosis in patients with LV systolic dysfunction, dilated cardiomyopathy and amyloidosis [8,[15][16][17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Prognostic importance of a short deceleration time in symptomatic congestive heart failure☆

Akkan

Kjærgaard

Møller

et al. 2008

European J of Heart Fail

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Aims: A restrictive transmitral filling (RF) pattern predicts increased mortality in heart failure (HF) with reduced left ventricular (LV) systolic function. We performed a combined evaluation of LV function and RF for prognosis in patients with HF with and without systolic dysfunction. Methods and results: Doppler echocardiography was performed in 972 patients with symptomatic HF. RF was considered present when deceleration time (DT) was ≤140 ms and non-RF when N 140 ms. A DT N 240 ms was defined as delayed relaxation. During a median of 51 months the unadjusted all-cause mortality rates were significantly increased among patients with RF vs. the non-RF group (1-and 4-year mortality was 25% and 54% vs. 17% and 43%). In a multivariable model, RF was a significant predictor of all-cause mortality (hazard ratio (HR) = 2.0, 95% confidence interval (CI):1.5-2.6) whereas delayed relaxation was without prognostic importance (HR = 0.9, CI:0.5-1.6). Repeating the multivariable model in subgroups of wall motion index (WMI) showed that RF was a strong predictor of mortality independent of WMI. For patients with LVEF of at least 50%, HR for RF was 2.0 (CI:1.1-3.4; p = 0.02) and interaction between LVEF and RF was not significant. Conclusion: In a heterogeneous population hospitalised for symptomatic HF a restrictive transmitral filling pattern, defined as shortened deceleration time, during hospitalisation is an ominous prognostic sign independent of LV systolic function.

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Mechanism of altered patterns of left ventricular filling during the development of congestive heart failure.

Cited by 276 publications

References 46 publications

Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

Altered Titin Expression, Myocardial Stiffness, and Left Ventricular Function in Patients With Dilated Cardiomyopathy

Prognostic importance of a short deceleration time in symptomatic congestive heart failure☆

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