Diastolic Function In Hypertrophic Cardiomyopathy Research Articles

Exercise training during childhood and adolescence is associated with favorable diastolic function in hypertrophic cardiomyopathy

BackgroundDiastolic dysfunction is an important part of the clinical phenotype in hypertrophic cardiomyopathy (HCM). While exercise training is known to improve left ventricular (LV) diastolic function in normal hearts, the effects of exercise training during childhood and adolescence in carriers of HCM-associated genetic variants are unknown. MethodsIn a cross-sectional and retrospective study, we combined clinical and echocardiographic data with history of exercise training from childhood to time of examination in 187 participants with HCM or an HCM-causative genotype. Multiple linear regression was used to identify correlations between exercise training performed prior to 20 years of age and LV diastolic parameters from echocardiography. ResultsExercise training during childhood and adolescence was correlated with a favorable e’, E/e’, E deceleration time, and end-diastolic volume (EDV), when adjusting for the effects of age at examination, and presence of left ventricular hypertrophy (LVH). This correlation was evident both in patients with a HCM phenotype (HCM LVH+), and in individuals with an HCM-causative genotype without LV hypertrophy (G+ LVH-). None of the diastolic parameters correlated unfavorably with increasing exercise exposure. ConclusionMore exercise training during childhood and adolescence was associated with favorable LV diastolic function in both HCM LVH+ and G+ LVH- groups, regardless of presence of hypertrophy at the time of examination. These results indicate that exercise training initiated during childhood and adolescence has positive effects on cardiac function later in life for individuals with HCM or an HCM-causative genotype.

Strain-volume loops for assessment of diastolic function in hypertrophic cardiomyopathy

Abstract Funding Acknowledgements Type of funding sources: None. Background Diastolic function assessment in patients with hypertrophic hearts and preserved ejection fraction (EF) is a rather challenging task, necessitating the introduction of new parameters. Strain-volume loops (SVLs), based on simultaneous frame-by-frame strain and volume changes’ recordings acquired by means of three-dimensional (3D) speckle tracking imaging, is an innovative tool which has been applied in various substrates. The ability of SVLs to assess diastolic function in hypertrophic cardiomyopathy (HCM) has not been investigated until now. Purpose Aim of this study was to investigate potential correlations between SVLs, traditional diastolic function indices and phenotypic features of HCM (thickness, obstruction and fibrosis) that may also reflect myocardial "stiffness". Methods We included 40 HCM patients (54.1 ± 14.3 years, 82.5% male, maximum wall thickness 19.3 ± 4.8mm) who have consecutively undergone 3D-speckle tracking echocardiography (panel A) and cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE). Values of 3D strain were plotted vs. volume for each frame to build an SVL. Peak of radial, longitudinal and circumferential systolic strain (Rsp, Lsp, and Csp, respectively), systolic slopes of the loops (RsSl, LsSl, CsSl), strain to end-diastolic volume (EDV) ratios (Rs/V, Ls/V, Cs/V) as well as the extent of systolic-diastolic uncoupling (difference between systolic and diastolic strain for the same volume) were computed for the analysis. Left atrial volume index (LAVI), E/E’ and tricuspid regurgitation velocity (TRvel) were measured to define diastolic dysfunction (DD) stage. Burden of fibrosis was evaluated by LGE extent in CMR slices. Results All HCM patients had preserved EF (60.5 ± 5,7%), while 16 (40%) had LV outflow tract obstruction (LVOTO > 30 mm Hg at rest). Mean LV mass index was 78.9 ± 14.5 g (evaluated by 3D echocardiography). LGE was observed in 23 patients (57.5%) occupying 5.2 ± 4.5% of LV mass. Concerning SVLs the following values were recorded for radial (Rsp 30.8 ± 9.8%, RsSl 0.4 ± 0.13 and Rs/V 0.25 ± 0.09), longitudinal (Lsp -9.4 ± 3.7%, LsSl 0.12 ± 0.06 and Ls/V 0.08 ± 0.04) and circumferential deformation (Csp -14.2 ± 3.5%, CsSl 0.18 ± 0.05 and Cs/V 0.11 ± 0.03). Traditional isolated diastolic indices (E/E’, LAVI, TRvel and DD stage) did not present significant correlations with SVL parameters or HCM phenotypic features. However, potentially "stiffer" hearts (combination of increased LVMI and fibrosis) presented a leftward transition of longitudinal SVLs, which also became wider (greater uncoupling) (panel B). Conclusions Traditional diastolic indices show modest only correlations with SVLs or HCM phenotypic characteristics, necessitating new approaches to DD of HCM patients. SVLs seem to be a promising-innovative tool for indirect assessment of myocardial "stiffness" and diastolic function. Abstract Figure.

Sphingosine-1-Phosphate Receptor Modulator, FTY720, Improves Diastolic Dysfunction and Partially Reverses Atrial Remodeling in a Tm-E180G Mouse Model Linked to Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disorder, primarily involving mutations in sarcomeric proteins. HCM patients present with hypertrophy, diastolic dysfunction, and fibrosis, but there is no specific treatment. The sphingosine-1-phosphate receptor modulator, FTY720/fingolimod, is approved for treatment of multiple sclerosis. We hypothesize that modulation of the sphingosine-1-phosphate receptor by FTY720 would be of therapeutic benefit in sarcomere-linked HCM. We treated mice with an HCM-linked mutation in tropomyosin (Tm-E180G) and nontransgenic littermates with FTY720 or vehicle for 6 weeks. Compared with vehicle-treated, FTY720-treated Tm-E180G mice had a significant reduction in left atrial size (1.99±0.19 [n=7] versus 2.70±0.44 [n=6] mm; P<0.001) and improvement in diastolic function (E/A ratio: 2.69±0.38 [n=7] versus 5.34±1.19 [n=6]; P=0.004) as assessed by echocardiography. Pressure-volume relations revealed significant improvements in the end-diastolic pressure volume relationship, relaxation kinetics, preload recruitable stroke work, and ejection fraction. Detergent-extracted fiber bundles revealed a significant decrease in myofilament Ca2+-responsiveness (pCa50=6.15±0.11 [n=13] versus 6.24±0.06 [n=14]; P=0.041). We attributed these improvements to a downregulation of S-glutathionylation of cardiac myosin binding protein-C in FTY720-treated Tm-E180G mice and reduction in oxidative stress by downregulation of NADPH oxidases with no changes in fibrosis. This is the first demonstration that modulation of S1PR results in decreased myofilament-Ca2+-responsiveness and improved diastolic function in HCM. We associated these changes with decreased oxidative modification of myofilament proteins via downregulation of NOX2. Our data support the hypothesis that modification of sphingolipid signaling may be a novel therapeutic approach in HCM.

3004Pulmonary blood volume index as a quantitative biomarker of diastolic function in hypertrophic cardiomyopathy

3004Pulmonary blood volume index as a quantitative biomarker of diastolic function in hypertrophic cardiomyopathy

Abstract 6: Restoration of Impaired Diastolic Function in Hypertrophic Cardiomyopathy Induced Pluripotent Stem Cell-derived Cardiomyocytes by Re-balancing the Calcium Homeostasis

Background: Diastolic dysfunction is commonly seen in hypertrophic cardiomyopathy (HCM). However, the cellular mechanism is not fully understood, and no effective treatment so far has been developed. We hypothesize here that HCM patient-specific induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) can recapitulate the cellular mechanism, and provide us a platform for mechanistic study and for drug screening of diastolic dysfunctions in HCM. Methods and Results: We generated beating iPSC-CMs from healthy individuals and HCM patients carrying familial mutations (MYH7 R663H (n=2 lines) and MYBPC3 R943ter (n=2 lines)). Sarcomere shortening measurement in patterned iPSC-CMs with live cell confocal imaging showed significantly prolonged diastolic phase and slower relaxation velocity in HCM iPSC-CMs compared to WT cells. To elucidate the cellular mechanism, Fura-2 AM ratiometric calcium imaging showed marked elevation of resting calcium level and increased abnormal calcium handlings in HCM iPSC-CMs, which were exaggerated by β-adrenergic activation with isoproterenol. By applying calcium transient and contractile force simultaneous recording, we defined a “risk index of diastolic dysfunction” (measured as transient-contraction gain factor), which was significantly increased in HCM iPSC-CMs. Thus, both elevated basal calcium level and increased calcium sensitivity of myofilament contribute to the abnormal diastolic function in HCM iPSC-CMs. Gene expression profiling of HCM and WT iPSC-CMs indicated that increased calcium channels may underlie the increased basal calcium concentration in HCM cells. Indeed, partially blocking the calcium influx by calcium blockers reset the basal calcium level, attenuated calcium mishandling, and restored the diastolic function in HCM iPSC-CMs. Moreover, re-balancing calcium homeostasis significantly improved long-term survival rate of HCM iPSC-CMs at both basal level and under β-adrenergic stress. Conclusion: The iPSC-CM models carrying patient-specific HCM mutations recapitulated diastolic dysfunction on single cell level. Future studies using these platform may reveal additional novel cellular mechanisms and therapeutic targets of diastolic dysfunction in HCM disease.

Assessment of Diastolic Function in Hypertrophic Cardiomyopathy by Computed Tomography-Derived Analysis of Left Ventricular Filling.

Hypertrophic cardiomyopathy (HCM) is characterized by diastolic dysfunction, which is difficult to assess by noninvasive methods. We hypothesized that measurement of simultaneous left ventricular (LV) and left atrial (LA) volume changes by cardiac computed tomography would be useful in the assessment of diastolic function in HCM. We studied 21 patients with HCM and 21 age-matched controls. The LA and LV volumes were calculated and early and late diastolic volume changes derived. The HCM patients had significantly larger LA volumes and reduced LA total emptying fraction (30 ± 7% vs 42 ± 6%; P < 0.0001). Conduit volume was increased (30 ± 6 vs 22 ± 4 mL/m; P < 0.0001) and contributed a significantly higher proportion of total LV diastolic filling, suggesting that passive filling of the LV compensates for LA dysfunction, but at the expense of increased pulmonary filling pressure. This study suggests that simultaneous depiction of computed tomography-derived LV and LA volume changes can characterize diastolic dysfunction in HCM.

Left ventricular remodeling and fibrosis: Sex differences and relationship with diastolic function in hypertrophic cardiomyopathy

ObjectivesWe investigated sex differences in left ventricular (LV) remodeling and fibrosis and their relationship with LV diastolic dysfunction by cardiovascular magnetic resonance (CMR). MethodsCMR imaging was performed simultaneously in 152 age-matched patients (76 men, 76 women; mean age: 49±9 years) without LV systolic dysfunction. LV remodeling index (LVRI) was calculated as the ratio of LV mass and end-diastolic volume. Diastolic function indexes including peak filling rate (PFR) and time to PFR (tPFR) were evaluated. Extent of late gadolinium enhancement (LGE) was measured. ResultsLVRI and extent of LGE were greater in women compared with men (1.48±0.22 vs. 1.36±0.28g/ml; 13.15±2.48 vs. 11.35±2.34g, respectively, both P<0.001). Women had lower PFR and higher tPFR (both P<0.001) than men. LVRI and the extent of LGE showed significant relationships with parameters of diastolic function in both sex. In a multivariate analysis, LVRI remained a strong independent predictor of PFR and TPFR in women (β=−0.272, P=0.032; β=0.348, P=0.016, respectively), and in men (β=−0.374, P<0.001; β=0.660, P<0.001, respectively). Furthermore, the extent of LGE also remained an independent predictor of PFR in women (β=−0.283, P=0.033) and men (β=−0.492, P<0.001). ConclusionsThere are prominent sex differences in LV remodeling and myocardial fibrosis. We suggest that the effects of LV remodeling and fibrosis may lead to diastolic dysfunction with greater susceptibility to worse clinical outcome in women.

0540: Assessment of diastolic dysfunction by myocardial deformation techniques in hypertrophic cardiomyopathy

Diastolic dysfunction in hypertrophic cardiomyopathy is common, and its assessment by conventional echocardiographic parameters is difficult. Myocardial deformation techniques can be used to analyse atrial function, and therefore diastolic function. The aim of this study is to assess atrial function in hypertrophic cardiomyopathy by longitudinal atrial strain. We included 48 consecutive patients with hypertrophic cardiomyopathy (HCM group) and 48 normal subjects (control group), who underwent trans-thoracic echocardiography. The following echocardiographic parameters were systematically assessed in the two groups: mitral E-wave and A-wave velocities, Tissue Doppler Imaging of the mitral annulus, left atrial size, longitudinal strain of the left ventricle and longitudinal strain of the left atrium. Clinical status of HCM was always assessed (NYHA class) Mean age was 43±19 y.o. in each group (men: 69%). NYHA class was as follows in HCM group: class I in 46%, II in 31%, III in 29% and IV in 4%. Conventional echocardiographic parameters were significantly different in HCM as compared to control group. However, these parameters were not related to symptoms (NYHA class). Using longitudinal strain of the left atrium, endsystolic peak of left atrial longitudinal strain (ESAS) and early-diastolic left atrial longitudinal strain were altered in hypertrophic cardiomyopathy, reflecting respectively reservoir and conduit functions. ESAS was the best parameter for detecting diastolic function in HCM with a cut-off value of 15.5% (ROC curves) and was significantly correlated to symptoms (r = 0.49, p = 0.0008). Sensitivity, specificity, PPV and NPV of ESAS for predicting severe symptoms (NYHA class III and IV) were 71%, 79%, 77% and 73%, respectively. End-systolic peak of left atrial longitudinal strain is an interesting echocardiographic parameter for the assessment of diastolic function in hypertrophic cardiomyopathy.

How does morphology impact on diastolic function in hypertrophic cardiomyopathy? A single centre experience

ObjectivesIt is unclear if morphology impacts on diastole in hypertrophic cardiomyopathy (HCM). We sought to determine the relationship between various parameters of diastolic function and morphology in a large HCM...

Influence of dynamic obstruction and hypertrophy location on diastolic function in hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a disease with marked genetic and phenotypic heterogeneity. It is well known that obstructive septal forms of this disease entail worse clinical outcome compared with nonobstructive septal and apical forms. The objective of this study was to analyze the differences in left ventricular diastolic function in different subgroups of HCMs and to assess the influence of the location of myocardial hypertrophy and the presence of dynamic obstruction on impairment of diastolic function and its correlation with the clinical status. We studied 86 patients with HCM; 27 with the obstructive asymmetric septal type (OAS), 37 with the nonobstructive asymmetric septal type (NOAS) and 22 with apical hypertrophic cardiomyopathy (ApHCM). Patients underwent conventional and tissue Doppler echocardiography and were assessed applying the latest recommendations regarding diastolic dysfunction. Cardiac magnetic resonance was used to study the various morphologic subtypes and quantify left ventricular mass (LVM). The early diastolic annular velocity (e') was significantly lower in OAS with a median of 5 cm/s compared with NOAS with 7 cm/s and ApHCM with 7.5 cm/s (P = 0.0002), and the E/e' ratio was 8.5 in ApHCM, 10 in NOAS and 14 in OAS (P = 0.0001); no significant differences were found in LVM or maximal wall thickness. In HCM, the location of left ventricular hypertrophy and the presence of dynamic obstruction affect the degree of diastolic dysfunction; impairment is greater in patients with the OAS type, and markedly less in patients with apical involvement.

943Native T1 mapping correlates with echocardiographic indices of diastolic function in hypertrophic cardiomyopathy

943Native T1 mapping correlates with echocardiographic indices of diastolic function in hypertrophic cardiomyopathy

Diffuse myocardial fibrosis in hypertrophic cardiomyopathy can be identified by cardiovascular magnetic resonance, and is associated with left ventricular diastolic dysfunction.

BackgroundThe presence of myocardial fibrosis is associated with worse clinical outcomes in hypertrophic cardiomyopathy (HCM). Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) sequences can detect regional, but not diffuse myocardial fibrosis. Post-contrast T1 mapping is an emerging CMR technique that may enable the non-invasive evaluation of diffuse myocardial fibrosis in HCM. The purpose of this study was to non-invasively detect and quantify diffuse myocardial fibrosis in HCM with CMR and examine its relationship to diastolic performance.MethodsWe performed CMR on 76 patients - 51 with asymmetric septal hypertrophy due to HCM and 25 healthy controls. Left ventricular (LV) morphology, function and distribution of regional myocardial fibrosis were evaluated with cine imaging and LGE. A CMR T1 mapping sequence determined the post-contrast myocardial T1 time as an index of diffuse myocardial fibrosis. Diastolic function was assessed by transthoracic echocardiography.ResultsRegional myocardial fibrosis was observed in 84% of the HCM group. Post-contrast myocardial T1 time was significantly shorter in patients with HCM compared to controls, consistent with diffuse myocardial fibrosis (498 ± 80 ms vs. 561 ± 47 ms, p < 0.001). In HCM patients, post-contrast myocardial T1 time correlated with mean E/e’ (r = −0.48, p < 0.001).ConclusionsPatients with HCM have shorter post-contrast myocardial T1 times, consistent with diffuse myocardial fibrosis, which correlate with estimated LV filling pressure, suggesting a mechanistic link between diffuse myocardial fibrosis and abnormal diastolic function in HCM.

Myocardial Fibrosis Attenuates the Effect of Cibenzoline on Left Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

The aim of this study was to investigate the relationship between late gadolinium enhancement (LGE) and the effect of cibenzoline (CBZ) on left ventricular (LV) diastolic function in hypertrophic cardiomyopathy (HCM) patients. Echocardiography before and after intravenous CBZ (1.4 mg/kg over 5 minutes) and magnetic resonance imaging (MRI) were performed in 22 consecutive patients with HCM [mean age: 65 ± 14 years, obstructive HCM: 14, nonobstructive HCM (HNCM): 8]. The extent of LGE (%LGE = LGE volume/total LV volume) was obtained by contrast-enhanced MRI using custom software. LGE was observed in 19 patients (mean %LGE = 5.1% ± 3.9%). The propagation velocity of LV early filling flow (Vp) increased significantly in patients with obstructive HCM (26 ± 7 to 36 ± 14 cm/s, P = 0.001) and nonobstructive HCM (25 ± 9 to 36 ± 16 cm/s, P = 0.007). A significant negative correlation was observed between the change in Vp and %LGE in patients with HCM (r = 20.542, P = 0.009). Less extensive myocardial fibrosis, as demonstrated by LGE on contrast-enhanced MRI, may predict the ability of CBZ to improve LV diastolic function in HCM.

Evaluation of the diastolic function in patients with hypertrophic cardiomyopathy by tissue Doppler imaging

Objective To investigate the diagnostic value of tissue Doppler imaging(TDI)for diastolic function in hypertrophic cardiomyopathy(HCM).Methods Sixty patients with HCM and thirty age-matched control were enrolled in this study.Parameters of conventional echocardiogram and TDI were compared.Results In the HCM group,left atrial diameter,left atrial area,thickness of inter-ventricular septum(IVS),ratio of IVS to left ventricular posterior wall(IVS/LVPW),E/Em and left ventricular filling pressure were statistically higher than those of control group(P<0.01,respectively),Em was significantly lower(P<0.01).There was no statistical difference on E/A between HCM and control group(P=0.67).E/Em was correlated positively with left atrial diameter and area in the HCM group(r=0.331,P=0.017;r=0.325,P=0.019,respectively).However,E/A had no statistical correlation with left atrial diameter and area(r=0.205,P=0.142;r=0.255,P=0.066,respectively).Conclusions Compared with the conventional Doppler ecbocardiogram,the parameters of TDI(Em,E/Em)were more sensitive in evaluation of diastolic function in HCM patients. Key words: Echocardiography; Doppler; Cardiomyopathy,hypertrophic; Ventricular function,left

Diastolic Myocardial Mechanics in Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is characterized by myocardial hypertrophy, fiber disarray, and fibrosis interfering with myocardial force generation and relaxation. Because conventional Doppler echocardiographic methods inadequately assess diastolic function in HCM, the aim of this study was to determine local and global left ventricular (LV) relaxation mechanics in patients with HCM. Seventy-two patients with HCM and 32 normal controls were studied. Using Velocity Vector Imaging, longitudinal and circumferential strain, strain rate, and rotation at the base, middle, and apex of the septal and lateral LV walls were measured. Differences between patients' functional class subgroups were assessed using analysis of variance, and Tukey's post hoc analysis was used to compare patients in HCM clinical subgroups with normal controls. Longitudinal strain and systolic and early diastolic strain rates were lower than normal in patients with HCM, whereas their circumferential values were higher. This suggests that shortening and relaxation orientation in HCM was more circumferential. The ratio of peak early diastolic to peak systolic strain rate decreased longitudinally and circumferentially in moderately to severely symptomatic (New York Heart Association class III or IV) patients (0.95 +/- 0.35 vs 0.89 +/- 0.35, P < .001). LV untwist was similarly prolonged in all HCM subgroups. LV relaxation assessed using the early apical reverse rotation fraction was significantly lower in patients with worse functional status (34 +/- 14% vs 18 +/- 4% in class I or II vs class III or IV). Left atrial volume increased, paralleling the severity of symptoms and the degree of diastolic dysfunction. The evaluation of biplane myocardial mechanics offers new insights into the evaluation of diastolic function and its relationship to clinical status.

Correlation Between Late Gadolinium Enhancement and Diastolic Function in Hypertrophic Cardiomyopathy Assessed by Magnetic Resonance Imaging

Diastolic dysfunction is common in patients with overt hypertrophic cardiomyopathy (HCM). Steady-state cine magnetic resonance imaging (MRI) enables measurement of the diastolic function of the left ventricle (LV), and late gadolinium enhanced MRI can delineate the presence and extent of fibrosis in HCM. The purpose of this study was to determine the relationship between the extent of myocardial fibrosis demonstrated by late gadolinium-enhanced MRI and diastolic dysfunction. Seventeen patients (13 men, mean age 57.7+/-9.8 years) with HCM were studied. The severity index of late gadolinium enhancement was determined by scoring the extent of enhanced tissue in 30 myocardial segments. The peak filling rate (PFR), LV ejection fraction and LV mass were determined by cine MRI. Contrast-enhanced MRI demonstrated late gadolinium enhancement in 97 of 510 segments (19%) and 13 of the 17 patients (77%). The severity index of late gadolinium enhancement demonstrated a significant negative correlation with PFR (r= -0.86, p<0.01) and with the LV ejection fraction (r= -0.59, p<0.05). No significant correlation was observed between the severity index of late gadolinium enhancement and LV mass (r=0.23, p=0.30). The extent of myocardial fibrosis revealed by late gadolinium-enhanced MRI has a strong relationship to diastolic dysfunction in patients with HCM.

Quantifying Diastolic Function in Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a primary autosomal-dominant disorder of the myocardium caused by mutations in sarcomeric contractile proteins. Histopathologically, it is associated with myocardial hypertrophy, fiber disarray, increased loose connective tissue, and fibrosis, which are all thought to interfere with myocardial force generation and relaxation.1–3 There is tremendous heterogeneity in the phenotypic expression of HCM, which is generally unrelated to genotype. This is shown by the variability of the age of onset of clinical disease, degree and location of hypertrophy, and presence and site of intraventricular dynamic pressure gradients. Despite this heterogeneity, almost all patients with HCM have some degree of diastolic dysfunction. The presence of subtle changes in LV filling may even identify patients with preclinical disease without LV hypertrophy. Interventions such as medical therapy, septal alcohol ablation, and surgical myectomy improve symptoms by both reducing the left ventricular (LV) outflow tract gradients and improving diastolic function. Article p 2702 The origin of diastolic dysfunction in HCM is both multifactorial and complex, with changes at the molecular, myocardial tissue, and global LV levels. More than 400 mutations have been described in HCM, which result in the production of abnormal myocardial sarcomeric proteins that have altered contraction and relaxation characteristics. These include changes in the affinity between the various contractile proteins, in the sensitivity to Ca+2, and in the efficiency of energy use (from ATP) and its expenditure.3,4 These abnormalities may vary with the sarcomeric protein affected and the site and effect of the mutation. Myocardial ischemia also has been documented by reversible thallium perfusion defects, positron emission tomography, and abnormal lactate production. This may be due to small-vessel disease with decreased vasodilator capacity, myocardial bridging, decreased coronary perfusion pressure, obstruction to LV outflow, and myocardial supply demand mismatch. Morphological factors that influence the degree of …

Section 11: Evaluation and Management of Patients With Heart Failure and Preserved Left Ventricular Ejection Fraction

Section 11: Evaluation and Management of Patients With Heart Failure and Preserved Left Ventricular Ejection Fraction

Doppler Echocardiographic Evaluation of Right Ventricular Diastolic Function in Hypertrophic Cardiomyopathy

Left ventricular diastolic function in patients with hypertrophic cardiomyopathy has been adequately studied. In contrast there are few studies concerning right ventricular diastolic function in hypertrophic cardiomyopathy. We studied right ventricular diastolic function in patients with hypertrophic cardiomyopathy using Doppler echocardiography. We studied 20 patients with hypertrophic cardiomyopathy (mean age 43.6+/-13.8 years) and 20 healthy volunteers (control group, mean age 43+/-13.8 years). We calculated left ventricular and right ventricular diastolic indices using pulsed Doppler echocardiography. Hypertrophic cardiomyopathy patients compared with controls had significantly lower right ventricular-E/A ratio (1.01+/-0.40 vs 1.30+/-0.28, P<0.04), significantly prolonged right ventricular isovolumic relaxation time (170+/-72 vs 32+/-23 ms, P<0.001), and also significantly prolonged right ventricular deceleration time (160+/-58 vs 118+/-35 ms, P<0.01). There was also strong significant correlation between right ventricular deceleration time and left ventricular deceleration time (r=0.78), right ventricular-E/A ratio and left atrial filling fraction (r=-0.55) and between right atrial filling fraction and left atrial filling fraction (r=0.75). Right ventricular diastolic function in patients with hypertrophic cardiomyopathy is impaired, reflecting abnormal relaxation. Right ventricular diastolic indices correlate well with those of left ventricle.

633 Diminished peak J wave velocity relates to impairment of diastolic function in hypertrophic cardiomyopathy

633 Diminished peak J wave velocity relates to impairment of diastolic function in hypertrophic cardiomyopathy