Determinants of exercise capacity in patients with heart failure without left ventricular hypertrophy.

BACKGROUND: Determinants of exercise intolerance in a phenotype of heart failure with preserved ejection fraction (HFpEF) with normal left ventricular (LV) structure have not been fully elucidated. METHODS: Cardiopulmonary exercise testing and exercise-stress echocardiography were performed in 44 HFpEF patients without LV hypertrophy. Exercise capacity was determined by peak oxygen consumption (peak VO2). Doppler-derived cardiac output (CO), transmitral E velocity, systolic (LV-s') and early diastolic mitral annular velocities (e'), systolic pulmonary artery (PA) pressure (SPAP), tricuspid annular plane systolic excursion (TAPSE), and peak systolic right ventricular (RV) free wall velocity (RV-s') were measured at rest and exercise. E/e' and TAPSE/SPAP were used as an LV filling pressure parameter and RV-PA coupling, respectively. RESULTS: During exercise, CO, LV-s', RV-s', e', and SPAP were significantly increased (p < 0.05 for all), whereas E/e' remained unchanged and TAPSE/SPAP was significantly reduced (p < 0.001). SPAP was higher and TAPSE/SPAP was lower at peak exercise in patients showing lower-half peak VO2. In univariable analyses, LV-s' (R = 0.35, p = 0.022), SPAP (R = -0.40, p = 0.008), RV-s' (R = 0.47, p = 0.002), and TAPSE/SPAP (R = 0.42, p = 0.005) were significantly correlated with peak VO2. In multivariable analyses, not only SPAP, but also TAPSE/SPAP independently determined peak VO2 even after the adjustment for clinically relevant parameters. CONCLUSIONS: In HFpEF patients without LV hypertrophy, altered RV-PA coupling by exercise could be associated with exercise intolerance, which might not be caused by elevated LV filling pressure.

Determinants of altered left ventricular suction in pre-capillary pulmonary hypertension.

AIMS: Although the left ventricular (LV) dysfunction in pre-capillary pulmonary hypertension (PH) has been recently recognized, the mechanism of LV dysfunction in this entity is not completely understood. We thus aimed to elucidate the determinants of intraventricular pressure difference (IVPD), a measure of LV suction, in pre-capillary PH. METHODS AND RESULTS: Right heart catheterization and echocardiography were performed in 86 consecutive patients with pre-capillary PH (57 ± 18 years, 85% female). IVPD was determined using colour M-mode Doppler to integrate the Euler equation. In overall, IVPD was reduced compared to previously reported value in normal subjects. In univariable analyses, QRS duration (P = 0.028), LV ejection fraction (P = 0.006), right ventricular (RV) end-diastolic area (P < 0.001), tricuspid annular plane systolic excursion (P = 0.004), and LV early-diastolic eccentricity index (P = 0.009) were associated with IVPD. In the multivariable analyses, RV end-diastolic area and LV eccentricity index independently determined the IVPD. CONCLUSION: Aberrant ventricular interdependence caused by RV enlargement could impair the LV suction. This study first applied echocardiographic IVPD, a reliable marker of LV diastolic suction, to investigate the mechanism of LV diastolic dysfunction in pre-capillary PH.

Prognostic value of an echocardiographic index reflecting right ventricular operating stiffness in patients with heart failure.

PURPOSE: We recently reported a noninvasive method for the assessment of right ventricular (RV) operating stiffness that is obtained by dividing the atrial-systolic descent of the pulmonary artery-RV pressure gradient (PRPGDAC) derived from the pulmonary regurgitant velocity by the tricuspid annular plane movement during atrial contraction (TAPMAC). Here, we investigated whether this parameter of RV operating stiffness, PRPGDAC/TAPMAC, is useful for predicting the prognosis of patients with heart failure (HF). METHODS: We retrospectively included 127 hospitalized patients with HF who underwent an echocardiographic examination immediately pre-discharge. The PRPGDAC/TAPMAC was measured in addition to standard echocardiographic parameters. Patients were followed until 2 years post-discharge. The endpoint was the composite of cardiac death, readmission for acute decompensation, and increased diuretic dose due to worsening HF. RESULTS: 58 patients (46%) experienced the endpoint during follow-up. Univariable and multivariable Cox regression analyses demonstrated that the PRPGDAC/TAPMAC was associated with the endpoint. In a Kaplan-Meier analysis, the event rate of the greater PRPGDAC/TAPMAC group was significantly higher than that of the lesser PRPGDAC/TAPMAC group. In a sequential Cox analysis for predicting the endpoint's occurrence, the addition of PRPGDAC/TAPMAC to the model including age, sex, NYHA functional classification, brain natriuretic peptide level, and several echocardiographic parameters including tricuspid annular plane systolic excursion significantly improved the predictive power for prognosis. CONCLUSION: A completely noninvasive index of RV operating stiffness, PRPGDAC/TAPMAC, was useful for predicting prognoses in patients with HF, and it showed an incremental prognostic value over RV systolic function.

Visual echocardiographic scoring system of the left ventricular filling pressure and outcomes of heart failure with preserved ejection fraction.

AIMS: Elevated left ventricular filling pressure (LVFP) is a powerful indicator of worsening clinical outcomes in heart failure with preserved ejection fraction (HFpEF); however, detection of elevated LVFP is often challenging. This study aimed to determine the association between the newly proposed echocardiographic LVFP parameter, visually assessed time difference between the mitral valve and tricuspid valve opening (VMT) score, and clinical outcomes of HFpEF. METHODS AND RESULTS: We retrospectively investigated 310 well-differentiated HFpEF patients in stable conditions. VMT was scored from 0 to 3 using two-dimensional echocardiographic images, and VMT ≥2 was regarded as a sign of elevated LVFP. The primary endpoint was a composite of cardiac death or heart failure hospitalization during the 2 years after the echocardiographic examination. In all patients, Kaplan-Meier curves showed that VMT ≥2 (n = 54) was associated with worse outcomes than the VMT ≤1 group (n = 256) (P < 0.001). Furthermore, VMT ≥2 was associated with worse outcomes when tested in 100 HFpEF patients with atrial fibrillation (AF) (P = 0.026). In the adjusted model, VMT ≥2 was independently associated with the primary outcome (hazard ratio 2.60, 95% confidence interval 1.46-4.61; P = 0.001). Additionally, VMT scoring provided an incremental prognostic value over clinically relevant variables and diastolic function grading (χ2 10.8-16.3, P = 0.035). CONCLUSIONS: In patients with HFpEF, the VMT score was independently and incrementally associated with adverse clinical outcomes. Moreover, it could also predict clinical outcomes in HFpEF patients with AF.

Difference in left atrial myocardial dynamics during reservoir phase between hypertrophic cardiomyopathy and hypertensive heart determined using three-dimensional speckle tracking echocardiography.

We aimed to investigate left atrial (LA) myocardial dynamics during reservoir phase using three-dimensional speckle-tracking echocardiography (3DSTE) focusing on its longitudinal-circumferential relationship in patients with left ventricular (LV) hypertrophy and clarifying the difference in LA myocardial reservoir dynamics between hypertrophic cardiomyopathy (HCM) and hypertension with LV hypertrophy (HT-LVH). We studied 4 age-matched groups consisting of 27 patients with HCM, 16 with HT-LVH, 22 hypertensive patients without LV hypertrophy (HT), and 18 normal controls. Using 3DSTE, we measured LA global longitudinal strain (LA-LSR), global circumferential strain (LA-CSR), and global area strain (LA-ASR) during the reservoir phase, as well as LV global longitudinal strain (LV-LS), global circumferential strain (LV-CS), and global area strain (LV-AS). LA-LSR was significantly lower in the HCM and HT-LVH groups than in the controls, but there was no significant difference between the HCM and HT-LVH groups. LA-CSR and LA-ASR were significantly lower in the HCM group than in the other three groups, among which no significant difference was detected. In all subjects, LA-LSR was significantly correlated with LV-LS but not with LV-CS. LA-CSR was correlated with neither LV-LS nor LV-CS. In conclusion, both longitudinal and circumferential LA myocardial expansion during reservoir phase were reduced in HCM, while only the longitudinal one was reduced in HT-LVH. Reduction of LA circumferential expansion may reflect a more serious and intrinsic impairment of LA myocardial distensibility in HCM. Measuring LA-CSR and LA-ASR using 3DSTE would contribute to a more accurate understanding of LA reservoir function abnormality in HCM.

Influence of left ventricular systolic dysfunction on occurrence of pulsus tardus in patients with aortic stenosis.

BACKGROUND: Although the time difference between peak of left ventricular (LV) and aortic systolic pressures (TLV-Ao), which is considered to in part reflect pulsus tardus, is reported to be associated with clinical outcome in aortic stenosis (AS), its physiological determinants remain to be elucidated. We hypothesized that not only AS severity but also LV systolic dysfunction could be associated with occurrence of pulsus tardus. METHODS: TLV-Ao was measured by simultaneous LV and aortic pressure tracing in 74 AS patients and prolonged TLV-Ao was defined as ≥66 ms according to the previous report. Mean transaortic valvular pressure gradient (mPG) and effective orifice area index (EOAI) were estimated by Doppler echocardiography and severe AS was defined as EOAI ≤0.60 cm2/m2. Global longitudinal strain (GLS) was measured by using speckle-tracking method. RESULTS: Although a weak correlation was observed between EOAI and TLV-Ao, there was substantial population showing discordance between the parameters: severe AS despite normal TLV-Ao (10 of 47 patients) and moderate AS despite prolonged TLV-Ao (9 of 17 patients). In severe AS, mPG was significantly higher in patients showing prolonged TLV-Ao (57±20 vs 36±10 mmHg, p<0.0001) whereas GLS was comparable between the groups (-15.2±3.5% vs -14.8±3.2%). In contrast, in moderate AS, GLS was significantly smaller in patients showing prolonged TLV-Ao (-12.6±4.7% vs -17.4±3.4%, p=0.0271) while mPG was comparable (34±7 mmHg vs 35±8 mmHg). Multivariable analysis revealed that not only mPG but also GLS was an independent determinant of TLV-Ao. CONCLUSIONS: The occurrence of pulsus tardus could be associated with not only AS severity but also LV systolic dysfunction in AS patients.