Improvement In Left Ventricular Diastolic Function Research Articles

The role of Ivabradine in Diastolic Heart Failure with preserved Ejection Fraction. A Doppler-Echocardiographic study.

Background:Ivabradine (IVA) is effective in patients with coronary artery disease (CAD) or systolic heart failure in sinus rhythm. Its action consists in reducing heart rate (HR) and improving the time of left ventricular (LV) diastolic filling. The aim of this study was to evaluate the effects of IVA added to conventional therapy on patients with diastolic heart failure (DHF) and preserved ejection fraction (HFpEF).Methods:We evaluated 25 patients with DHF in the New York Heart Association (NYHA) Class II-III and sinus rhythm. In these, IVA per os (5 mg/twice a day) was added to the conventional medical therapy and given for 12 weeks. Immediately before the beginning of IVA therapy and 3 months later, patients underwent echocardiographic evaluation by two-dimensional (2D) ultrasound and tissue Doppler imaging (TDI). The patterns of diastolic mitral inflow and pulmonary venous flow were recorded using 2D echocardiography, while the diastolic phase of mitral flow was recorded by TDI, from the lateral mitral annulus.Results:Three months after the addition of IVA to conventional treatment, HR significantly decreased in comparison to the baseline values. On the contrary, the echocardiographic indexes of LV diastolic dysfunction improved.Conclusions:These results testify that the addition of IVA to conventional therapy in patients with HFpEF can improve LV diastolic function evaluated by 2D and tissue Doppler-echocardiographic patterns. These Doppler-echocardiographic results match with the clinical improvement of patients evaluated.

PS 17-54 EFFECTS OF CILNIDIPINE VERSUS ATENOLOL ON LEFT VENTRICULAR DIASTOLIC FUNCTION AND HYPERTROPHY IN ESSENTIAL HYPERTENSION - CANDLE TRIAL

Objective: Effects of Cilnidipine versus Atenolol on Left Ventricular Diastolic Function and Hypertrophy in Essential Hypertension (CANDLE) study was designed as a prospective, randomized, double-blind, parallel-group to test whether cilnidipine achieves greater left ventricular (LV) mass reduction and improves LV diastolic function than does atenolol. Design and method: Seventy-two patients with uncomplicated essential hypertension and increased LV mass index at screening echocardiography (55 ± 2 years; 59% male; BP 157 ± 4/99 ± 3 mmHg) were enrolled and were randomly assigned and forced-titrated to 20 mg/d cilnidipine or 100 mg of atenolol treatment for 36 weeks. Echocardiography, 24-hours ambulatory blood pressure monitoring, biochemical studies including N-terminal pro-B-type natriuretic peptide and 24-hours urine protein and microalbumin were measured at baseline and after 36-weeks therapy. Results: Clinical examination and blinded echocardiogram in a per-protocol analysis of 28 cilnidipine-treated and 26 atenolol-treated patients revealed similar reductions in systolic/diastolic pressure (−16.5/8.9 versus −23.9/14.8 mmHg, both P > 0.05) and LV mass index (−21.4 versus −19.5 g/m2, both P > 0.05). No significant between-treatment difference was detected in population subsets defined by monotherapy treatment, sex, age, or severity of baseline hypertrophy. Similarly, there was no between-treatment difference in change in biochemical parameters. As we expected, cilnidipine-treated group showed lesser reduction on night-time heart rate (−2.4 versus −5.6 %, p = 0.021) rather than atenolol-treated group. Interestingly, cilnidipine-treated group showed reduction on left atrial (LA) volume index but on the contrary, atenolol-treated group showed more enlarged LA after treatment (−5.1 versus 7.3 %, p = 0.035). Conclusions: Both cilnidipine and atenolol similarly and effectively reduced blood pressure and LV mass index. However, only cilnidipine reduced LA volume index, whereas atenolol increased. Cilnidipine may provide more beneficial effect on the management in essential hypertension with diastolic dysfunction.

Immediate recovery of the left atrial and left ventricular diastolic function after transcatheter aortic valve implantation: A transesophageal echocardiography study.

Chronic increased afterload due to severe aortic stenosis (AS) results in com-pensatory concentric left ventricular (LV) hypertrophy and LV dysfunction. These in turn cause remodeling of the left heart. The aim of this study was to investigate the acute effect of transcatheter aortic valve implantation (TAVI) on left atrial (LA) mechanics and LV diastolic function. The study consisted of a total of 35 consecutive patients (mean age was 77.7 ± 5.0 years, 25 female) undergoing TAVI. All TAVI procedures have been performed under the transesophageal echocardiography (TEE) guidance. Before and 24 h after TAVI, all patients underwent transthoracic echocardiography (TTE) and mitral inflow velocities with pulsed-wave (PW) Doppler including early filling wave (E), late diastolic filling wave (A), and E/A ratio were obtained. LV diastolic function was also explored by pulsed tissue Doppler imaging (TDI). Early (E') and late (A') diastolic annular velocities, E'/A' ratio and E/E' ratio were obtained. In addition, during the procedure before and minutes after the valve implantation, the left atrial appendage-peak antegrade flow velocity (LAA-PAFV) was measured and recorded with TEE. Compared with baseline, the mean mitral E, septal E' and E'/A' ratio increased significantly after TAVI. In addition, the LAA-PAFV increased significantly within minutes of TAVI (32.45 ± 10.7 cm/s vs. 47.6 ± 12.6 cm/s, p < 0.001). TAVI improves LV diastolic function and LA performance immediately.

Effect of selective heart rate reduction through sinus node If current inhibition on severely impaired left ventricular diastolic dysfunction in patients with chronic heart failure

Aims The aim of the study was the assessment of heart rate reduction effect through selective If current inhibition on several left ventricular (LV) diastolic function parameters and left atrial (LA) volumetric parameters in patients with systolic heart failure (HF).Methods and results In total 54 patients with systolic HF and pseudonormal/restrictive type of diastolic dysfunction were randomly allocated to either the ivabradine (27) or control group (27) during a 3-month period. Left atrial volume index (LAVI) and the following diastolic function parameters were determined by transmitral pulsed wave and mitral annulus tissue Doppler study before and after the therapy period: deceleration time (DT), peak early to late mitral inflow wave velocity ratio (E/A) and the ratio of mitral peak velocity of early filling (E) to early diastolic mitral annular velocity (Em) (E/Em). Parametric variables were compared by a two-set analysis of variance with a repeated measurement for the time factor. Ivabradine treatment was accompanied by increase of DT (30.19 ± 30.21 msec in ivabradine, versus 4.07 ± 16.93 msec in controls, 95% CI, P= 0.00001), decrease of E/A ratio (-0.83 ± 1.2, in ivabradine versus –0.05 ± 0.42 in controls, P= 0.0001) and decrease of E/Em ratio (-5.16 ± 3.9 in ivabradine versus 0.99 ± 4.34, P= 0.0002 in controls). Ivabradine also improved LAVI (-6.14 ± 5.17 ml/m² versus 0.65 ± 4.29 ml/m² in controls, P < 0.0001). After 3 months of treatment heart rate was significantly reduced in the ivabradine group (P <0.0001).Conclusion Treatment with ivabradine improves LV diastolic function through reducing E/A ratio, E/Em ratio and increasing DT. These changes may contribute to the improvement of intracardiac haemodynamics with decrease of LAVI and improvement of LV filling.

Statin Induced Regression of Cardiomyopathy Trial: A Randomized, Placebo-controlled Double-blind Trial.

Background:Hypertrophic cardiomyopathy (HCM), characterized by a thickened, fibrotic myocardium, remains the most common cause of sudden cardiac death in young adults. Based on animal and clinical data, we hypothesized that atorvastatin would induce left ventricular (LV) mass regression.Methods:Statin Induced Regression of Cardiomyopathy Trial (SIRCAT) was a randomized, placebo-controlled study. The primary endpoint was change in LV mass measured by cardiac magnetic resonance imaging 12 months after treatment with once-daily atorvastatin 80 mg or placebo. A key secondary endpoint was diastolic dysfunction measured echocardiographically by transmitral flow velocities. SIRCAT is registered with www.clinicaltrials.gov (NCT00317967).Results:Of 222 screened patients, 22 were randomized evenly to atorvastatin and placebo. The mean age was 47 ± 10 years, and 15 (68%) were male. All subjects completed the protocol. At baseline, LV masses were 197 ± 76 g and 205 ± 82 g in the placebo and atorvastatin groups, respectively. After 12 months treatment, the LV masses in the placebo and atorvastatin groups were 196 ± 80 versus 206 ± 92 g (P = 0.80), respectively. Echocardiographic indices were not different in the two groups at baseline. After 12 months, diastolic dysfunction as assessed using transmitral flow velocities E/E', A/A', and peak systolic mitral velocity showed no benefit from atorvastatin.Conclusions:In patients with HCM, atorvastatin did not cause LV mass regression or improvements in LV diastolic function.

Selective Heart Rate Reduction Improves Metabolic Syndrome-related Left Ventricular Diastolic Dysfunction.

Enhanced heart rate observed in metabolic syndrome (MS) contributes to the deterioration of left ventricular (LV) function via impaired LV filling and relaxation, increased myocardial O2 consumption, and reduced coronary perfusion. However, whether heart rate reduction (HRR) opposes LV dysfunction observed in MS is unknown. We assessed in Zucker fa/fa rats, a rat model of MS, the cardiovascular effects of HRR induced by the If current inhibitor S38844 (3 mg · kg(-1) · d(-1)). Delayed short-term (4 days) and long-term (90 days) HRR induced by S38844 reduced LV end-diastolic pressure and LV end-diastolic pressure-volume relation, increased myocardial tissue perfusion, decreased myocardial oxidized glutathione levels, and preserved cardiac output, without modifying LV end-systolic pressure and LV end-systolic pressure-volume relation, although only long-term S38844 opposed LV collagen accumulation. Long-term S38844 improved flow-induced endothelium-dependent dilatation of mesenteric arteries, while metabolic parameters, such as plasma glucose levels, and Hb1c, were never modified. In rats with MS, HRR induced by the If inhibitor S38844 improved LV diastolic function and endothelium-dependent vascular dilatation, independent from modifications in metabolic status. Moreover, this improvement in cardiac function involves not only immediate effects such as improved myocardial perfusion and reduced oxidative stress but also long-term effects such as modifications in the myocardial structure.

Association between high arterial stiffness and left ventricular filling pressures in patients with acute myocardial infarction

High arterial stiffness increases the left ventricular (LV) filling pressures in different cardiac disorders. The association between arterial stiffness and LV filling pressures has not been studied so far in patients with acute myocardial infarction (MI). The aim of the study was to assess the association between arterial stiffness and LV filling pressures in patients with acute MI. Arterial stiffness, measured using the digital volume pulse stiffness index (SIDVP), and LV filling pressures, quantified as the ratio of early transmitral flow velocity to early diastolic septal mitral annulus velocity (E/e'), were evaluated in 263 patients with acute MI (mean age, 63.8 ±11 years; 69 women). The association between high E/e' (>15) and very stiff arteries (SIDVP >18 m/s) was analyzed by logistic regression, with data presented as odds ratios (OR s) and 95% confidence intervals (CIs). A multivariate logistic regression analysis revealed an association between E/e' >15 and SIDVP >18 m/s (OR, 4.7; 95% CI, 1.8-12.3), independently of female sex (OR, 4.3; 95% CI, 1.4-10.2), LV ejection fraction <35% (OR, 3.1; 95% CI, 1.2-8.2), left atrial volume >34 ml/m2 (OR, 17.4; 95% CI, 5.8-52.0). There was no significant association between E/e' >15 and previous MI (OR, 2.2; 95% CI, 0.9-5.7). High arterial stiffness is an independent risk factor for LV diastolic dysfunction in patients with acute MI. A reduction in arterial stiffness may improve LV diastolic function in this patient group.

PP.05.10

Objective: Patients with essential hypertension (EH) complicated by type 2 diabetes mellitus (DM) have a high risk of cardiovascular events.The aim of the present study was to evaluate the effects of combination therapy with Valsartan and Amlodipine on BP,left ventricular (LV) hypertrophy,LV diastolic function in patients with EH, type 2 DM and LV hypertrophy. Design and method: Fifty-eight patients with moderate EH,type 2 DM and LV hypertrophy were randomly assigned to Valsartan (80 mg)+Amlodipine (5 mg) in combination once a day(30 males and 28 females).Doppler -and 2-dimensional echocardiography were performed at baseline and after 12 months of therapy.The parameters of LV hypertrophy,ratio of the early filling velocity (E) to the late filling velocity (A)-E/A ratio,isovoluming relaxation time (IVRT) and deceleration time (DT) were evaluated.LV mass index (LV mass/body surface area) was calculated according to the Devereux formula.Statistical comparisons were performed by 2-tailed Student's t test for quantitative parameters. Results: All patients comleted the study without showing intolerance or side effects to the drugs.At the end of the study therapy normalized BP (126,2 ± 3,3/74,5 ± 1,9 mm Hg vs 166,41 ± 5,4/104,3 ± 4,1 mm Hg,p < 0,01) in 94,8% of patients.LV mass index reduced from 158,1 ± 5,7 to 132,5 ± 2,8 g/m2.(p < 0,01) in 79,3 % of patients.At the end of the study E/A ratio increased from 0,91 ± 0,01 to 1,36 ± 0,02 (p < 0,001) in 82,8 % of patients.IVRT decreased from 103,2 ± 5,2 to 74,2 ± 3,1 msec (p < 0,01) in 81,0% of patients.DT passed from 168,2 ± 7,9 to 128,1 ± 3,0 msec (p < 0,01) in 84,5% of patients. Conclusions: BP control was stable and effective until the end of the study.Combination therapy with Valsartan+Amlodipine,wich have complementary mechanisms of action,demonstrated qualitative regression of LV hypertrophy and improvement of LV diastolic function in patients with moderate EH complicated by type 2 DM.In addition,this combination attenuated the side effects of each component.

PDE 5 inhibition with udenafil improves left ventricular systolic/diastolic functions and exercise capacity in patients with chronic heart failure with reduced ejection fraction; A 12-week, randomized, double-blind, placebo-controlled trial

Impaired nitric oxide-mediated pulmonary vascular tone is commonly found in heart failure with reduced ejection fraction (HFrEF), and is associated with derangement of left ventricular (LV) hemodynamics and decreased exercise capacity, which may be reversed by PDE5 inhibitor. This study investigated the effects of a new, long-acting PDE5 inhibitor on LV hemodynamics and exercise capacity in HFrEF. Patients with chronic HFrEF on optimal medical therapy for >30 days before enrollment were randomly assigned to placebo or udenafil at a dose of 50mg 2x/day for the first 4 weeks followed by 100mg 2x/day for the next 8 weeks. All patients underwent cardiopulmonary exercise echocardiography before and after the 12-week treatment. Improvement of subjective functional capacity was more frequently reported in the udenafil group (P = 0.002). Also, a higher increase in peak VO2 (Δpeak VO2, 21.6% (6.9 ~ 106.4%) vs 1.9% (-15.7 ~ 21.0%) in the placebo group, P = 0.04) and a larger decrease in ventilatory efficiency were observed in the udenafil group (Δ-6.4 ± 9.7 vs Δ1.9 ± 12.1 in the placebo group, P = 0.03). Regarding LV systolic function, the extent of increment in LV ejection fraction was significantly greater in the udenafil group (6.6 ± 6.4% vs 2.3 ± 4.8% in the placebo group, P = 0.02). In the udenafil group, an echocardiographic surrogate of LV filling pressure was more prominently decreased (P = 0.006) along with a significant reverse remodeling of left atrial volume index (57 ± 25mL at baseline to 44 ± 23 at 12th week, P = 0.04) and a progressive fall in B-type natriuretic peptide level (589 ± 679pg/mL at baseline to 220 ± 225pg/mL at 12th week, P < 0.001), indicating LV diastolic function improvement. Udenafil was well tolerated without excess of adverse events compared to placebo. Udenafil improves LV systolic/diastolic functions and exercise capacity in conjunction with established conventional pharmacotherapy, without significant adverse events in HFrEF.

Effect of Cardiac Resynchronization Therapy on Left Ventricular Diastolic Function

Aims: Cardiac Resynchronization Therapy (CRT) improves systolic performance in Heart Failure (HF). However, the effects of CRT on Left Ventricular (LV) diastolic function were variable and not fully understood. The aim of this study was to determine the effects of cardiac resynchronization therapy on LV diastolic filling pattern and the relation between the diastolic filling pattern and the response to CRT. Methods and Results: Twenty nine patients (mean age, 66 ± 8 years; 26 men; mean LV ejection fraction 25±7%) with severe HF were included. Measurements included LV volumes and Ejection Fraction (EF), pulsed-wave Doppler (PWD)-derived transmitral filling indices (E- and A-wave velocities, E/A ratio, Ewave deceleration time). Clinical responders were defined as survived patients with an improvement by one or more NYHA functional class, echocardiographic response to CRT was defined as a decline in LV end-systolic volume >15% during follow-up. In clinical responder group, both diastolic and systolic LV volumes decreased significantly (p=0.02 and p<0.001 respectively) and LVEF increased significantly (p=0.001) in 26 of 29 patients (89%) and were accompanied by reduction in mitral E-wave velocity and E/A ratio (both p<0.001), and increased A-wave velocity and Ewave deceleration time (p=0.03 and p<0.001). In echocardiographic responders, reverse remodelling (52%) was coupled to the improvement in LV diastolic function but diastolic filling pattern improved also in 42% in patients without reverse remodelling. Conclusion: Left ventricular diastolic indices after CRT improved in the clinical responder group, but there was no significant change in these indices among non-responders. CRT enhances diastolic filling patterns in both echocardiographic responder and nonresponder patients. This may be related to improvement in symptoms even in echocardiographic nonresponders who were clinical responders.

Effects of alcohol septal ablation on left ventricular diastolic filling patterns in obstructive hypertrophic cardiomyopathy.

Alcohol septal ablation (ASA) has been shown to improve left ventricular (LV) diastolic function in patients with obstructive hypertrophic cardiomyopathy (HCM). However, its beneficial effect on diastolic function assessed by cardiac magnetic resonance (CMR) has not been reported. We investigated the mid-term changes of diastolic function by CMR combined with echocardiography in HCM patients after ASA at a median of 14-month follow-up. CMR parameters of diastolic function including peak filling rate (PFR), and time to peak filling rate (TPFR) were evaluated in 43 patients (aged 48±9years). LV diastolic function improved significantly measured by echocardiography with the decrease in ratio of transmitral early LV filling velocity (E) to early diastolic mitral lateral annular velocity (E') (14.20±1.17 to 11.58±1.16, p<0.001) and E-wave deceleration time (194.04±19.30 to 168.45±12.58 ms, p<0.001). PFR increased significantly with associated decrease in TPFR after ASA (both p<0.001) at follow-up. Furthermore, patients with larger decrease in LVOT gradients had a greater improvement of LV diastolic function, as measured by the reduction of E/E' (p<0.001) and increase of PFR (p<0.001). In conclusion, this study demonstrated that successful ASA results in both echocardiographic and CMR indices of diastolic function improvement after ASA at 14-month follow-up. ASA therapy can significantly reduce LVOT gradient and mitral regurgitation, both of which may contribute to the improvement of diastolic function.

Heart rate reduction with ivabradine improves left ventricular function and reverses multiple pathological maladaptations in dogs with chronic heart failure.

We tested the hypothesis that heart rate (HR) reduction with ivabradine (IVA) leads to reversal of structural, biochemical, and molecular maladaptations characteristic of the heart failure (HF) state. HR reduction with IVA has been shown to improve left ventricular (LV) systolic function and clinical outcome in patients with HF. Studies were performed in 16 HF dogs produced by intracoronary microembolizations [LV ejection fraction (EF) ~35%]. Dogs were randomized to 3-month oral therapy with IVA (30 mg Bid, n = 8) or to no therapy (Control, n = 8). LV tissue was obtained from all dogs at the end of therapy and used for molecular, biochemical, and histological studies. Average 24-h ambulatory Holter monitoring showed a significant decrease of HR in IVA-treated dogs compared with controls. Compared with pre-therapy, LV EF decreased at 3 months in controls (36 ± 1 vs. 32 ± 2%, P < 0.05) but increased significantly with IVA (40 ± 3 vs. 35 ± 3%, P < 0.05). Treatment with IVA was associated with (i) improved LV diastolic function; (ii) increased sarcoplasmic reticulum Ca2+ uptake and ATPase activity; (iii) decreased plasma levels of vasoactive neurohormones, natriuretic peptides, and pro-inflammatory cytokines; (iv) normalization of messenger RNA gene expression of multiple signalling pathways; and (v) reduced cardiomyocyte apoptosis and hypertrophy. In dogs with HF, HR reduction with IVA reversed many of the structural, biochemical, and molecular maladaptations characteristic of HF. The findings support the concept that HR reduction in HF can elicit benefits, albeit indirect, on a host of maladaptations implicated in the progressive worsening of the HF state.

Effects of Septal Myectomy on Left Ventricular Diastolic Function and Left Atrial Volume in Patients With Hypertrophic Cardiomyopathy

Ventricular septal myectomy in patients with obstructive hypertrophic cardiomyopathy (HC) has been shown to reduce left ventricular (LV) outflow tract (LVOT) gradient and improve symptoms, although little data exist regarding changes in left atrial (LA) volume and LV diastolic function after myectomy. We investigated changes in LA size and LV diastolic function in patients with HC after septal myectomy from 2004 to 2011. We studied 25 patients (age 49.2 ± 13.1 years, 48% women) followed for a mean of 527 days after surgery who had serial echocardiography at baseline and at most recent follow-up, at least 6 months after myectomy. In addition to myectomy, 3 patients (12%) underwent Maze surgery and 13 (52%) underwent mitral valve surgery, of whom 5 had a mitral valve replacement or mitral annuloplasty. Patients with mitral valve replacement or mitral annuloplasty were excluded from LV diastolic function analysis. LA volume index decreased (from 47.2 ± 17.6 to 35.9 ± 17.0 ml/m(2), p = 0.001) and LV diastolic function improved with an increase in lateral e' velocity (from 7.3 ± 2.9 to 9.8 ± 3.1 cm/sec, p = 0.01) and a decrease in E/e' (from 14.8 ± 6.3 to 11.7 ± 5.5, p = 0.051). Ventricular septal thickness and LVOT gradient decreased, and symptoms of dyspnea and heart failure improved, with reduction in the New York Heart Association functional class III/IV symptoms from 21 (84%) to 1 (4%). In conclusion, relief of LVOT obstruction in HC by septal myectomy results in improved LV diastolic function and reduction in LA volume with improved symptoms.

Structural and functional cardiac adaptations to 6 months of football training in untrained hypertensive men.

We investigated the effects of 3 and 6 months of regular football training on cardiac structure and function in hypertensive men. Thirty-one untrained males with mild-to-moderate hypertension were randomized 2:1 to a football training group (n = 20) and a control group receiving traditional recommendations on healthy lifestyle (n = 11). Cardiac measures were evaluated by echocardiography. The football group exhibited significant (P < 0.05) changes in cardiac dimensions and function after just 3 months: Left ventricular (LV) end-diastolic volume increased from 104 ± 25 to 117 ± 29 mL. LV diastolic function improved measured as E/A ratio (1.15 ± 0.32 to 1.54 ± 0.38), early diastolic velocity, E' (11.0 ± 2.5 to 11.9 ± 2.6 cm/s), and isovolumetric relaxation time (74 ± 13 to 62 ± 13 ms). LV systolic function improved measured as longitudinal displacement (10.7 ± 2.1 to 12.1 ± 2.3 mm). Right ventricular function improved with respect to tricuspid annular plane systolic excursion (21.8 ± 3.2 to 24.5 ± 3.7 mm). Arterial blood pressure decreased in both groups, but significantly more in the football training group. No significant changes were observed in the control group. In conclusion, short-term football training improves LV diastolic function in untrained men with mild-to-moderate arterial hypertension. Furthermore, it may improve longitudinal systolic function of both ventricles. The results suggest that football training has favorable effects on cardiac function in hypertensive men.

Physical Activity and Improved Diastolic Function in Spinal Cord–Injured Subjects

Subjects with spinal cord injury (SCI) have been reported to present impaired left ventricular (LV) diastolic function in comparison with able-bodied (AB) ones. The present study investigated the effect of regular physical activity on the cardiac structure and function of SCI subjects. Fifty-eight SCI men (29 sedentary [SCI-S] and 29 athletes [SCI-A]) and 29 AB men were cross-sectionally evaluated by clinical, laboratory, hemodynamic, and echocardiographic analysis. All enrolled subjects were normotensive, nondiabetic, nonsmoker, and normolipemic, and the studied groups presented similar age and body mass index. SCI-S presented similar LV structural and systolic parameters but higher E/Em (8.0 ± 0.5) and lower Em/Am (1.18 ± 0.09) ratios than SCI-A and AB (E/Em = 6.4 ± 0.3 and 5.9 ± 0.3, respectively; Em/Am = 1.57 ± 0.12 and 1.63 ± 0.08, respectively; all P < 0.05 compared with SCI-S). Analysis of SCI individuals according to injury level revealed that tetraplegic athletes had similar features compared with sedentary tetraplegic subjects, except for higher Em (10.9 ± 0.6 vs 8.6 ± 0.7 cm s, P < 0.05) and lower E/Em ratio (6.3 ± 0.4 vs 8.8 ± 0.8, P < 0.05), whereas paraplegic athletes had similar features compared with sedentary paraplegic individuals, except for higher LV end-diastolic diameter (49.4 ± 1.4 vs 45.0 ± 1.0 mm, P < 0.05) and Em/Am ratio (1.69 ± 0.20 vs 1.19 ± 0.08, P < 0.05) and lower LV relative wall thickness (0.330 ± 0.012 vs 0.369 ± 0.010, P < 0.05) and heart rate (67.1 ± 4.2 vs 81.9 ± 2.8 bpm, P < 0.05). Regular physical activity is associated with improved LV diastolic function in SCI subjects and might exert distinct cardiac structural effects in tetraplegic and paraplegic subjects.

Pyridostigmine ameliorates cardiac remodeling induced by myocardial infarction via inhibition of the transforming growth factor-β1/TGF-β1-activated kinase pathway.

Autonomic imbalance characterized by sympathetic predominance coinciding with diminished vagal activity is an independent risk factor in cardiovascular diseases. Several studies show that vagus nerve stimulation exerted beneficial effects on cardiac function and survival. In this study, we investigated the vagomimetic effect of pyridostigmine on left ventricular (LV) remodeling in rats after myocardial infarction. After myocardial infarction, surviving rats were treated with or without pyridostigmine (31 mg·kg⁻¹·d⁻¹) for 2 weeks, and hemodynamic parameters were measured. LV tissue was used to assess infarct size and interstitial fibrosis by Masson's trichrome and 0.1% picrosirius red staining. Protein expression of heart tissues was used to assess the efficacy of the treatment. Pyridostigmine markedly reduced myocardial infarct size and improved cardiac diastolic function. These improvements were accompanied with a significant decrease in matrix metalloproteinase-2 expression and collagen deposition. Additionally, pyridostigmine inhibited both transforming growth factor-β1 (TGF-β1) and TGF-β1-activated kinase expression in hearts postmyocardial infarction. Thus, pyridostigmine reduces collagen deposition, attenuates cardiac fibrosis, and improves LV diastolic function after myocardial infarction via TGF-β1/TGF-β1-activated kinase pathway inhibition.

Effects of Bariatric Surgery on Cardiac Structure and Function: A Systematic Review and Meta-Analysis

Morbid obesity, a condition increasingly treated with bariatric procedures, is strongly associated with left ventricular (LV) hypertrophy and impaired LV function. We analyzed the literature to provide comprehensive information on cardiac structural and functional changes, as assessed by imaging techniques, after bariatric surgery. The studies were identified by the following search terms: "bariatric surgery," "obesity," "left ventricle," "left ventricular hypertrophy," "cardiac hypertrophy," "ventricular dysfunction," "left ventricular hypertrophy regression," "echocardiography," "magnetic resonance imaging," and "cardiac imaging techniques." In a pooled population of 1,022 obese subjects with preserved systolic function included in 23 studies, bariatric procedures induced (i) a decrease in LV mass (standardized mean difference (SMD) = -0.46; P < 0.001) and relative wall thickness (SMD = -0.20; P < 0.001); (ii) an improvement of LV diastolic function, as reflected by the increase in mitral flow E/A ratio (SMD = +0.39; P < 0.001); (iii) a decrease in left atrium diameter (SMD = -0.26; P < 0.001); or (iv) no changes in LV ejection fraction (SMD = +0.03; P = 0.46). The present meta-analysis, the largest to date focusing on cardiac structural and functional changes in morbidly obese subjects after bariatric surgery, documents that this therapeutic approach exerts important cardioprotective effects in terms of regression of LV hypertrophy, improvement of LV geometry and diastolic function, and reduction of left atrial size.

Improvement of left ventricular diastolic function and left atrial reverse remodeling after catheter ablation of premature ventricular complexes

Catheter ablation of premature ventricular complexes (PVC) improves left ventricular (LV) systolic performance in certain patients; however, the effect on diastolic function and left atrial (LA) remodeling is unclear. We assessed the effects of catheter ablation of PVCs on parameters of LV diastolic function and LA remodeling. Forty-seven patients (age 65 ± 10 years, 46 men) who underwent catheter ablation for symptomatic PVCs were evaluated using two-dimensional echocardiography before and 6 ± 2 months after ablation. The measured diastolic indices included mitral inflow parameters (E wave, A wave, E/A ratio, and deceleration time (DT)), mitral lateral annulus early diastolic velocity (Ea), and E/Ea ratio. The LA volume was measured using modified biplane Simpson's method. We also compared the changes in the left atrial volumes and left atrial volume index (LAVI) after PVC ablation. After catheter ablation of PVCs, the mean LV ejection fraction (EF) increased significantly (49.9 ± 10.3 vs. 42.8 ± 11.8, p < 0.01). Significant improvement was also seen in A wave velocity (71.3 ± 17.1 vs. 59.5 ± 15.1 cm/s, p = 0.039), E/A ratio (1.42 ± 0.6 vs. 1.07 ± 0.5 ml, p = 0.034), Ea (8.9 ± 3.9 vs. 6.8 ± 2.9 cm/s, p = 0.04), and E/Ea ratio (15.4 ± 5.8 vs. 10.6 ± 3.4, p = 0.027), whereas mitral E and DT did not show significant change. LAVI decreased significantly after ablation (44.4 ± 14.8 vs. 36.7 ± 12.5, p < 0.001). Significant improvement in LAVI was also seen in patients with normal baseline LVEF (p = 0.04). Catheter ablation of PVCs improved LV diastolic function and resulted in left atrial reverse remodeling.

Sustained cardiac remodeling after a short-term very low calorie diet in type 2 diabetes mellitus patients

A very low calorie diet (VLCD) results in cardiac remodeling and improved diastolic function. It is unknown how long these effects sustain after reintroduction of a regular diet. We aimed to assess the long-term effects of initial weight loss by VLCD on cardiac dimensions and function in type 2 diabetes mellitus (T2DM) patients. Fourteen insulin-dependent T2DM patients (mean ± SEM: age 53 ± 2 years; BMI 35 ± 1 kg/m(2)) were treated by a VLCD (450 kcal/day) during 16 weeks. Cardiac function and myocardial triglyceride (TG) content were measured by magnetic resonance imaging and spectroscopy at baseline, after a 16-week VLCD and after 14 months of follow-up on a regular diet. BMI decreased from 35 ± 1 to 28 ± 1 kg/m(2) after VLCD and increased again to 32 ± 1 kg/m(2) at 18 months (both P < 0.05 vs. baseline). Left ventricular (LV) end-diastolic volume index increased after the 16-week VLCD (80 ± 3 to 89 ± 4 ml/m(2), P < 0.05) and remained increased after follow-up (90 ± 3 ml/m(2); P < 0.05 vs. baseline) at comparable filling pressures. The improvement in LV diastolic function after the 16-week VLCD, was sustained at 18 months [early (E)/atrial (A) diastolic filling phase ratio: 0.96 ± 0.07 (baseline); 1.12 ± 0.06 (after VLCD); 1.06 ± 0.07 (18 months, P < 0.05 vs. baseline)]. Myocardial TG content decreased after the 16-week VLCD [0.74 (0.41-1.10) to 0.45 (0.31-0.54) %, P < 0.05], but returned to baseline levels at 18 months [0.76 (0.65-1.32) %]. Weight reduction by a 16-week VLCD in T2DM patients results in sustained cardiac remodeling and improved diastolic function after 14 months of follow-up, despite weight regain on a regular diet.

Reductions of left-ventricular mass and improvements in left-ventricular diastolic function following renal denervation do not correlate with blood pressure or heart rate reduction

Reductions of left-ventricular mass and improvements in left-ventricular diastolic function following renal denervation do not correlate with blood pressure or heart rate reduction