The association between left ventricular twisting motion and mechanical dyssynchrony: a three-dimensional speckle tracking study.

Left ventricular (LV) dyssynchrony is a causal factor in LV dysfunction and thought to be associated with LV twisting motion. We tested whether three-dimensional speckle tracking (3DT) can be used to evaluate the relationship between LV twisting motion and dyssynchrony. We examined 25 patients with sick sinus syndrome who had received dual chamber pacemakers. The acute effects of ventricular pacing on LV wall motion after the switch from atrial to ventricular pacing were assessed. LV twisting motion and dyssynchrony during each pacing mode were measured using 3DT. LV dyssynchrony was calculated from the time to the minimum peak systolic area strain of 16 LV imaging segments. Ventricular pacing increased LV dyssynchrony and decreased twist and torsion. A significant correlation was observed between changes in LV dyssynchrony and changes in torsion (r = -0.65, p < 0.01). Evaluation of LV twisting motion can potentially be used for diagnosing LV dyssynchrony.

Changes in collagen metabolism account for ventricular functional recovery following beta-blocker therapy in patients with chronic heart failure.

While beta blockade improves left ventricular (LV) function in patients with chronic heart failure (CHF), the mechanisms are not well known. This study aimed to examine whether changes in myocardial collagen metabolism account for LV functional recovery following beta-blocker therapy in 62 CHF patients with reduced ejection fraction (EF). LV function was echocardiographically measured at baseline and 1, 6, and 12 months after bisoprolol therapy along with serum markers of collagen metabolism including C-terminal telopeptide of collagen type I (CITP) and matrix metalloproteinase (MMP)-2. Deceleration time of mitral early velocity (DcT) increased even in the early phase, but LVEF gradually improved throughout the study period. Heart rate (HR) was reduced from the early stage, and CITP gradually decreased. LVEF and DcT increased more so in patients with the larger decreases in CITP (r = -0.33, p < 0.05; r = -0.28, p < 0.05, respectively), and HR (r = -0.31, p < 0.05; r = -0.38, p < 0.05, respectively). In addition, there were greater decreases in CITP, MMP-2 and HR from baseline to 1, 6, or 12 months in patients with above-average improvement in LVEF than in those with below-average improvement in LVEF. Similar results were obtained in terms of DcT. There was no significant correlation between the changes in HR and CITP. In conclusion, improvement in LV systolic/diastolic function was greatest in patients with the larger inhibition of collagen degradation. Changes in myocardial collagen metabolism are closely related to LV functional recovery somewhat independently from HR reduction.

Intravenous salt supplementation with low-dose furosemide for treatment of acute decompensated heart failure.

BACKGROUND: Theoretically, salt supplementation should promote diuresis through increasing the glomerular filtration rate (GFR) during treatment of acute decompensated heart failure (ADHF) even with low-dose furosemide; however, there is little evidence to support this idea. METHODS AND RESULTS: This was a prospective, randomized, open-label, controlled trial that compared the diuretic effectiveness of salt infusion with that of glucose infusion supplemented with low-dose furosemide in 44 consecutive patients with ADHF. Patients were randomly administered 1.7% hypertonic saline solution supplemented with 40 mg furosemide (salt infusion group) or glucose supplemented with 40 mg furosemide (glucose infusion group). Our major end points were 24-hour urinary volume and GFR. Urinary volume was greater in the salt infusion group than in the glucose infusion group (2,701 ± 920 vs 1,777 ± 797 mL; P < .001). There was no significant difference in the estimated GFR at baseline. Creatinine clearance for 24 h was greater in the salt infusion group than in the glucose infusion group (63.5 ± 52.6 vs 39.0 ± 26.3 mL min(-1) 1.73 m(-2); P = .048). CONCLUSIONS: Salt supplementation rather than salt restriction evoked favorable diuresis through increasing GFR. The findings support an efficacious novel approach of the treatment of ADHF.

Elevated arterial stiffness and diastolic dysfunction in subclinical hypothyroidism.

BACKGROUND: Thyroid hormone is associated with arterial stiffness and left ventricular diastolic function in hypothyroid disease. The relationship of thyroid hormone level to cardio-ankle vascular index (CAVI) and left ventricular diastolic function, however, remains unclear in subjects with subclinical hypothyroidism. METHODS AND RESULTS: We conducted a cross-sectional study of 83 patients with untreated subclinical hypothyroidism and compared them with 83 randomly selected controls from health check-ups. Log N-terminal prohormone of brain natriuretic peptide (NT-proBNP), C-reactive protein (CRP), and arterial stiffness were measured. In addition, we measured early diastolic mitral annular velocity (E') in 43 participants with subclinical hypothyroidism and in 40 controls. When compared with the control group, patients with subclinical hypothyroidism had higher logNT-proBNP (1.9±0.5 vs. 1.7±0.3pg/ml, P<0.05), CRP (0.22±0.04 vs. 0.09±0.06mg/dl, P<0.05), and CAVI (8.8±1.7 vs. 7.8±1.4, P<0.001) and lower E' (5.8±1.7 vs. 7.5±2.1cm/s, P<0.001). CAVI was significantly associated with logNT-proBNP, CRP and E' in the subclinical hypothyroidism group. CONCLUSIONS: High logNT-proBNP was associated with a raised CAVI in patients with subclinical hypothyroidism. Subclinical hypothyroidism may be a risk factor for cardiovascular events related to arterial stiffening and left ventricular diastolic dysfunction.

The impairment of the parasympathetic modulation is involved in the age-related change in mitral E/A ratio.

The mitral early to late diastolic flow velocity ratio (E/A ratio) is age-dependent. It has been considered that its age dependency reflects the age-related lengthening of left ventricular (LV) relaxation; however, the change in E/A ratio is far larger than that expected from those in LV relaxation. We hypothesized that an age-related reduction of the parasympathetic activity increases left atrial (LA) contractility, and that this accounts for the age-related change in E/A ratio. (1) Exercise stress test was performed in 61 normal subjects (age range, 8-80 years, mean, 40 years) to assess heart rate (HR) recovery because slowed HR recovery indicates lowered parasympathetic activity. There were good interrelations among age, E/A ratio, and HR recovery. Among those aged ≤30 years, the age no longer correlated with E/A ratio or HR recovery, but there was a significant correlation between HR recovery and E/A ratio (r = 0.44, p < 0.05). (2) Pulsed Doppler and two-dimensional speckle tracking echocardiography (2DSTE) were performed before and after administration of parasympathetic blockade (atropine) in ten young healthy subjects. LA booster pump function was assessed with LA emptying index calculated by 2DSTE. LA emptying index was calculated from ([LA volume before the atrial contraction - minimal LA volume]/LA volume before the atrial contraction) × 100. Atropine increased mitral A velocity (p < 0.001) and LA emptying index (p < 0.05) along with a decrease in E/A ratio (p < 0.001). Parasympathetic withdrawal enhances LA contraction and increases mitral A velocity, which likely cause a reciprocal decrease in mitral E velocity and E/A ratio. Thus, parasympathetic deactivation with aging should be closely involved in the age-related change in mitral E/A ratio.

Sitting maneuver to uncover latent left ventricular outflow tract obstruction in patients without hypertrophic cardiomyopathy.

BACKGROUND: Left ventricular outflow tract obstruction [LVOTO; pressure gradient (PG) ≥30 mmHg] is observed in some patients without hypertrophic cardiomyopathy (HCM), and it may develop especially in older patients without HCM (non-HCM). The aim of this study is to investigate if the Valsalva or an upright sitting maneuver can unveil latent LVOTO in patients with non-HCM. METHODS: A total of 33 non-HCM patients with a late peaking or dagger-shaped pulsed Doppler waveform of the LVOT and PG <30 mmHg were included. The Doppler flow velocity of the LVOT was measured at rest, after the Valsalva and a sitting maneuver. Peak PG of ≥30 mmHg after either maneuver was defined as latent LVOTO. The angle between the left ventricular septum and the aorta in the parasternal long-axis view and the apical three-chamber view was measured. RESULTS: Twenty (61 %) of the 33 patients (mean age 74 ±â€¯9 years) were diagnosed with latent LVOTO. Of these, five (25 %) patients were diagnosed after both the Valsalva and sitting maneuver, and 15 (75 %) were diagnosed only after the sitting maneuver. The latent LVOTO group had a significantly smaller angle than the no-LVOTO group between the ventricular septum and the aorta in the parasternal long axis views (107 ±â€¯8° vs. 117 ±â€¯8°, p < 0.01). CONCLUSION: The sitting maneuver is better than the Valsalva maneuver in unveiling latent LVOTO in older, non-HCM patients.

Myocardial stretch in early systole is a key determinant of the synchrony of left ventricular mechanical activity in vivo.

BACKGROUND: Recent in-vitro observations suggest that left ventricular (LV) contraction is powered by 'stretch activation', an intrinsic mechanism by which the stretching of an activated cardiomyocyte causes delayed force redevelopment. We hypothesized that mechanical dyssynchrony is related to prolonged early systolic stretch that delays the timing of peak segmental shortening. METHODS AND RESULTS: The time intervals from R wave to segmental longitudinal stretch in early systole (Tstretch) and peak shortening (Tpeak) and the respective standard deviations (σTstretch and σTpeak) were measured by speckle-tracking echocardiography in 57 patients undergoing cardiac resynchronization therapy (CRT). The percentage of time spent in shortening, normalized to Tpeak duration [corrected ΔT=(Tpeak-Tstretch)/Tpeak] correlated with LV reverse remodeling (reduction in end-systolic volume ≥ 15%). Of the 57 patients, 40 (70.2%) demonstrated LV reverse remodeling at an average follow-up of 263 ± 125 days after CRT. At baseline, Tstretch and σTstretch correlated with Tpeak and σTpeak, respectively. Though there was no difference in Tstretch, Tpeak, σTstretch and σTpeak between responders and non-responders, corrected ΔT in the mid-lateral and mid-septal segments was shorter in the responders (P<0.05 for both) and the average of the 2 independently predicted LV reverse remodeling (area under the curve: 0.77, P=0.001). CONCLUSIONS: Mapping LV segmental shortening in relation to early systolic stretch may aid dyssynchrony assessment in patients undergoing CRT.

Beta-blocker stress echocardiography in an aortic stenosis patient with associated left ventricular outflow tract obstruction.

An 80-year-old man visited our hospital because of dyspnea on exertion from 6 months ago. Echo Doppler study showed severe calcification in the aortic valve with restricted movement and the sigmoid septum causing obstruction at the LV outflow tract (LVOT). Considering the aortic valve area (AVA) might have been inaccurately estimated, we carried out beta-blocker stress echocardiography. The transaortic pressure gradient and AVA were respectively calculated as 52 mmHg and 0.90 cm(2) before propranolol administration and as 64 mmHg and 0.86 cm(2) after propranolol administration. Thus, beta-blocker stress echocardiography may provide an accurate assessment of AS if the LVOT obstruction is concomitant.

Combination of hypertonic saline and low-dose furosemide is an effective treatment for refractory congestive heart failure with hyponatremia.

Hyponatremia often associates with heart failure. Although severe salt restriction is generally recommended in heart failure treatment, it may promote hyponatremia which is a risk factor for increased morbidity and mortality in heart failure patients. Therefore, it is not yet clear whether correction of hyponatremia is an effective treatment in congestive heart failure with hyponatremia. We experienced a successful case of refractory congestive heart failure with hyponatremia treated with hypertonic saline and furosemide. A 45-year-old man, suffering from dilated cardiomyopathy, was admitted to our hospital for heart failure worsening with hyponatremia. We started diuretics therapy without correction of hyponatremia, but his clinical status of heart failure was not improved. Therefore, we additionally started to correct hyponatremia by continuous injection of hypertonic saline. The correction of hyponatremia increased urinary volume dramatically, and improved cardiac output and clinical status of heart failure. This case strongly suggests that combination of hypertonic saline and furosemide could enhance diuretic effect, and improve the clinical status of heart failure in congestive heart failure patients with hyponatremia. .

Long-term effects of irbesartan on plasma aldosterone concentration and left atrial volume in hypertensive patients.

BACKGROUND: Plasma aldosterone concentration (PAC) is related to cardiac remodeling in patients with hypertension. However, we do not know the detailed relationship between changes in PAC and regression of left atrial (LA) volume following long-term treatment with angiotensin II receptor blocker (ARB) or calcium-channel blocker (CCB). OBJECTIVE: The aim of this study was to investigate the effects of anti-hypertensive monotherapy, an ARB irbesartan or a CCB amlodipine, on PAC and LA reverse remodeling in hypertensive patients. METHODS: A total of 48 patients with untreated hypertension were randomly assigned to irbesartan (ARB group, n=26) and amlodipine (CCB group, n=22). We examined the correlation between LA volume index (LAVI) and other echocardiographic parameters or PAC (n=40) at the baseline and after 12 months of treatment. RESULTS: After 12 months, blood pressure (BP) decreased similarly in both groups. LAVI and PAC significantly decreased in the ARB group, but not in the CCB group (-16±8% vs. 22±9%, p<0.01, -16±9% vs. 11±9%, p<0.05). Larger %-decrease in PAC was associated with larger %-reduction of LAVI in the ARB group (r=0.54, p<0.05), but not in the CCB group. CONCLUSIONS: While BP reduction was similar between the two groups, decrease in LA volume was larger in the ARB group than in the CCB group. Decrease in LA volume was larger in patients with a greater decrease in PAC than in those with smaller decrease in PAC. ARB may facilitate reverse remodeling of LA through decreases in PAC in hypertensive patients.

Speckle tracking echocardiography derived 2-dimensional myocardial strain predicts left ventricular function and mass regression in aortic stenosis patients undergoing aortic valve replacement.

Regression of left ventricular (LV) mass in severe aortic stenosis (AS) following aortic valve replacement (AVR) reduces the potential risk of sudden death and congestive heart failure associated with LV hypertrophy. We investigated whether abnormalities of resting LV deformation in severe AS can predict the lack of regression of LV mass following AVR. Two-dimensional speckle tracking echocardiography (STE) was performed in a total of 100 subjects including 60 consecutive patients with severe AS having normal LV ejection fraction (EF > 50 %) and 40 controls. STE was performed preoperatively and at 4 months following AVR, including longitudinal strain assessed from the apical 4-chamber and 2-chamber views and the circumferential and rotational mechanics measured from the apical short axis view. In comparison with controls, the patients with AS showed a significantly lower LV longitudinal (p < 0.001) and circumferential strain (p < 0.05) and higher apical rotation (p < 0.001). Following AVR, a significant improvement was seen in both strains (p < 0.001 for each respectively), however, apical rotation remained unchanged (p = 0.14). On multivariate analysis, baseline LV mass (odds ratio 1.02; p = 0.011), left atrial volume (odds ratio 0.81; p = 0.048) and circumferential strain (odds ratio 0.84; p = 0.02) independently predicted LV mass regression (>10 %) following AVR. In conclusion, STE can quantify the burden of myocardial dysfunction in patients with severe AS despite the presence of normal LV ejection fraction. Furthermore, resting abnormalities in circumferential strain at LV apex is related with a hemodynamic milieu associated with the lack of LV mass regression during short-term follow up after AVR.

CRT improves LV filling dynamics: insights from echocardiographic particle imaging velocimetry.

Echocardiographic particle imaging velocimetry allows blood flow visualization and characterization of diastolic vortex formation that may play a key role in filling efficiency. We hypothesized that abrupt withdrawal of cardiac resynchronization therapy (CRT) would alter the timing of left ventricular diastolic vortex formation and modify cardiac time intervals. In patients with heart failure (HF) who had chronically implanted CRT devices, the timing of the onset of the diastolic vortex (TDV) from mitral valve opening, transmitral flow, and cardiac time intervals was measured at baseline and after deactivation and reactivation of CRT. Compared with control patients with cardiovascular risk factors but structurally normal hearts, TDV was significantly delayed in patients with HF. Deactivation of CRT resulted in striking delay in TDV due to disorganized flow and reduced flow acceleration, and reactivation reversed these characteristics instantly. In addition, CRT deactivation also prolonged the isovolumic contraction interval, which closely correlated with the changes in the TDV. These data suggest that CRT plays an important role in optimization of left ventricular diastolic filling.