Left Ventricular Remodeling Changes Research Articles

Left ventricular remodeling and its association with mineral and bone disorder in kidney transplant recipients

Background The assessment of left ventricular (LV) remodeling and its association with mineral and bone disorder (MBD) in kidney transplant recipients (KTRs) have not been systematically studied. We aimed to evaluate LV remodeling changes one year after kidney transplantation (KT) and identify their influencing factors. Methods Ninety-five KTRs (68 males; ages 40.2 ± 10.8 years) were followed before and one year after KT. Traditional risk factors and bone metabolism indicators were assessed. Left ventricular mass index (LVMI), left ventricular ejection fraction (LVEF) and left ventricular diastolic dysfunction (LVDD) were measured using two-dimensional transthoracic echocardiography. The relationship between MBD and LV remodeling and the factors influencing LV remodeling were analyzed. Results One year after KT, MBD was partially improved, mainly characterized by hypercalcemia, hypophosphatemia, hyperparathyroidism, 25-(OH) vitamin D deficiency, elevated bone turnover markers, and bone loss. LVMI, the prevalence of left ventricular hypertrophy (LVH), and the prevalence of LVDD decreased, while LVEF increased. LVH was positively associated with postoperative intact parathyroid hormone (iPTH) and iPTH nonnormalization. ΔLVMI was positively associated with preoperative type-I collagen N-terminal peptide and postoperative iPTH. LVEF was negatively associated with postoperative phosphorous. ΔLVEF was negatively associated with postoperative iPTH. LVDD was positively associated with postoperative lumbar spine osteoporosis. Preoperative LVMI was negatively associated with ΔLVMI and positively associated with ΔLVEF. Advanced age, increased BMI, diabetes, longer dialysis time, lower albumin level, and higher total cholesterol and low-density lipoprotein levels were associated with LV remodeling. Conclusions LV remodeling partially improved after KT, showing a close relationship with MBD.

Association Between Progression of Arterial Stiffness and Left Ventricular Remodeling in a Community-Based Cohort

BackgroundCross sectionally measured, elevated arterial stiffness is associated with unfavorable left ventricular (LV) remodeling, suggesting its important role in the pathophysiology of heart failure. However, data linking the degree of arterial stiffness progression with LV remodeling are scarce. ObjectivesThe purpose of this study was to investigate the association between longitudinal change in arterial stiffness and changes in LV remodeling. MethodsSerial measurements of arterial stiffness by cardio-ankle vascular index (CAVI) were performed in 317 participants without cardiovascular disease and with normal arterial stiffness. LV size, mass, and function were assessed by transthoracic echocardiography and including LV global longitudinal strain (LVGLS) by speckle-tracking and tissue Doppler velocity (e’) of the mitral annulus (diastolic function). ResultsDuring a median follow-up of 26.8 mo, there was a significant increase in CAVI (P < 0.001). Generalized estimating equation analyses showed that longitudinal increase in CAVI was associated with impaired LVGLS (estimate 0.46, 95% CI: 0.11-0.82; P = 0.010) after adjustment for demographics and baseline cardiovascular factors, but not with changes of LV mass index and e’ velocity. When controlling for longitudinal change of covariates, CAVI progression remained associated with change in LVGLS (estimate 0.50, 95% CI: 0.16-0.85; P = 0.004). In sex stratified analysis, progression of CAVI was significantly associated with LVGLS deterioration only in women (estimate 0.92, 95% CI: 0.27-1.58; P = 0.006). ConclusionsLongitudinal increase in arterial stiffness is associated with deterioration in LVGLS. Vascular-ventricular coupling plays an important role in the progressive decline in ventricular function even at an early, subclinical stage.

An audit of Heart failure management among ambulatory adult patients at Queen Elizabeth Central Hospital (QECH), Malawi.

There are limited data on the clinical characteristics and use of guideline directed medical therapy among patients with heart failure in Malawi. We conducted a study to assess patient characteristics and clinical management given to heart failure patients at Queen Elizabeth Central hospital in Malawi. In a cross sectional study, patients with a diagnosis of heart failure who were followed up in the adult chest clinic at QECH were recruited to ascertain their characteristics and the therapy they were receiving. Echocardiograms and electrocardiograms were performed to identify abnormalities. A total of 79 patients were recruited and 62% (49 out of 79) were female. The median age was 60 years (IQR 40.5-70.5). Most patients were hypertensive with NYHA (New York Heart Association) class I and II symptoms. Left ventricular(LV) systolic dysfunction was found in 55% (36 out of 65), with 68% (39 out of 65) having features of left ventricular remodeling. Most patients were on at least a single neurohormonal drug with 77% (61 out of 79) on ACEI (angiotensin converting enzyme inhibitor), 52% (42 out of 79) on a beta blocker and 34%(27 out of 79) on aldosterone antagonists. The recommended doses of medications were achieved in 14% (9 out 61), 24% (10 out 42), 22% (6 out of 27) on ACEI, beta blockers and aldosterone antagonists respectively. Hypertension is the commonest comorbidity in patients with heart failure, who are mostly females with NYHA class I or II symptoms. Most had LV remodeling changes and are on at least one neurohormonal antagonist but most remain sub optimally treated.

Changes of left ventricular remodeling due to increased afterload in patients with essential hypertension

BackgroundIt is unclear whether afterload mismatch occurs during the initial stage of essential hypertension (EHT). Additionally, critical left ventricular hypertrophy (LVH) between preserved and reduced systolic functions in hypertension is also unclear. Thus, we aimed to clarify these points. MethodsForty-five normal control subjects (NCS) and 140 EHT patients participated. EHT patients were subdivided into three groups: group I, without LVH (n = 37); group II, with LVH (n = 80); and group III, with LVH and LV heart failure (LVHF) (n = 23). Routine electrocardiographic and echocardiographic parameters, V5R/V6R ratio, relative wall thickness (RWT), LV mass (LVM) index, and peak systolic wall stress (PSWS) were measured. ResultsIn group I, LV systolic functions were preserved despite the increase of PSWS. In group II, LVH advanced, but LV systolic functions remained normal. A negative T-wave was observed in 69% of group II and 100% of group III. A significant correlation between RWT and LVM index was seen in NCS and groups I and II (r2 = 0.545, P < 0.0001) but not in group III. Afterload mismatch occurred in group III due to the decrease in V5R/V6R ratio, the increase of LV end-diastolic dimension, and the LV systolic dysfunctions, which are caused by exhaustion of preload reserve. The boundary of the LVM index between groups II and III was approximately 180 g/m2. ConclusionAfterload mismatch did not occur in group I, but it was observed in group III due to the exhaustion of preload reserve.

Left ventricular remodeling and systolic function changes in patients with obstructive sleep apnea: a comprehensive contrast-enhanced cardiac magnetic resonance study.

BackgroundA comprehensive assessment of left ventricular (LV) remodeling and systolic function using contrast-enhanced cardiac magnetic resonance (CMR) imaging in patients with obstructive sleep apnea (OSA) has not yet been reported. This retrospective case-control study aimed to explore and assess the myocardial structure, function, and tissue characteristic changes of LV remodeling in patients with OSA using the CMR method.MethodsFifty-one selected participants 32 OSA and 19 non-OSA underwent overnight polysomnography and CMR examination using T1 mapping and feature tracking techniques. Twenty age- and sex-matched healthy controls were also enrolled for comparison between the groups.ResultsPatients were grouped by apnea-hypopnea index (AHI): AHI <5 events/h as non-OSA group (n=19, 40.7±8.0 years), 5–30 events/h as mild-moderate OSA (n=13, 47.8±9.4 years), and >30 events/h as severe OSA (n=19, 39.0±10.0 years). The OSA group had a higher LV mass index (LVMI) to height2.7 than the non-OSA and healthy control groups (21.0±3.8 vs. 16.4±3.1 and 16.3±3.2 mL/m2.7, P<0.001). Compared with healthy controls, OSA patients had lower global circumferential strain values, although the LV ejection fraction was preserved. Late gadolinium enhancement was not detected in all participants, whereas the extracellular volume fraction was lower in patients with OSA than in the non-OSA and healthy control groups (24.4%±1.9% vs. 26.2%±2.5%, P=0.006 and 24.4%±1.9% vs. 26.5%±2.3%, P=0.004, respectively). The indexed cellular volume (iCV) of the myocardium was significantly higher in subjects with mild-to-moderate and severe OSA than in those without OSA (14.2±2.3 and 15.8±3.1 vs. 11.6±2.4 mL/m2.7, P<0.05). On multivariate linear regression analysis of patients with two different models, OSA severity remained significantly associated with increased LVMI (β=0.348, P=0.004 and β=0.233, P=0.048, respectively) and iCV (β=0.337, P=0.004 and β=0.231, P=0.047, respectively) after adjusting for clinical risk factors.ConclusionsLVMI is elevated in OSA with a normal LV ejection fraction, mainly with cellular hypertrophy. Cellular hypertrophy without focal fibrosis in OSA may be our main finding.

Reshaping the Preterm Heart: Shifting Cardiac Renin-Angiotensin System Towards Cardioprotection in Rats Exposed to Neonatal High-Oxygen Stress.

Background:Approximately 10% of infants are born preterm. Preterm birth leads to short and long-term changes in cardiac shape and function. By using a rat model of neonatal high-oxygen (80%O2) exposure, mimicking the premature hyperoxic transition to the extrauterine environment, we revealed a major role of the renin-angiotensin system peptide Angio II (angiotensin II) and its receptor AT1 (angiotensin receptor type 1) on neonatal O2-induced cardiomyopathy. Here, we tested whether treatment with either orally active compounds of the peptides Angio-(1–7) or alamandine included in cyclodextrin could prevent postnatal cardiac remodeling and the programming of cardiomyopathy induced by neonatal high-O2 exposure.Methods:Sprague-Dawley pups were exposed to room air or 80% O2 from postnatal day 3 (P3) to P10. Neonatal rats were treated orally from P3 to P10 and assessed at P10 and P28. Left ventricular (LV) shapes were characterized by tridimensional computational atlases of ultrasound images in addition to histomorphometry.Results:At P10, high O2-exposed rats presented a smaller, globular and hypertrophied LV shape versus controls. Treatment with cyclodextrin–Angio-(1–7) significantly improved LV function in the O2-exposed neonatal rats and slightly changed LV shape. Cyclodextrin-alamandine and cyclodextrin–Angio-(1–7) treatments similarly reduced hypertrophy at P10 as well as LV remodeling and dysfunction at P28. Both treatments upregulated cardiac angiotensin-converting enzyme 2 in O2-exposed rats at P10 and P28.Conclusions:Our findings demonstrate LV remodeling changes induced by O2-stress and the potential benefits of treatments targeting the cardioprotective renin-angiotensin system axis, supporting the neonatal period as an important window for interventions aiming at preventing cardiomyopathy in people born preterm.

Effects of diabetes mellitus on left ventricular function and remodeling in hypertensive patients with heart failure with reduced ejection fraction: assessment with 3.0T MRI feature tracking.

BackgroundHeart failure with reduced ejection fraction (HFrEF) is a major health burden worldwide with high morbidity and mortality. Comorbidities of HFrEF complicate treatment and lead to poor prognosis, among which hypertension (HTN) and diabetes mellitus (DM) are common and frequently cooccur. DM was found to have additive effects on cardiac function and structure in hypertensive patients, while its effects on the HFrEF cohort in the context of HTN remain unclear.MethodsA total of 171 patients with HFrEF were enrolled in our study, consisting of 51 HFrEF controls, 72 hypertensive HFrEF patients (HTN-HFrEF [DM−]) and 48 hypertensive HFrEF patients with comorbid DM (HTN-HFrEF [DM+]). Cardiac MRI-derived left ventricular (LV) strains, including global radial (GRPS), circumferential (GCPS) and longitudinal (GLPS) peak strain, and remodeling parameters were measured and compared among groups. The determinants of impaired LV function and LV remodeling in HFrEF patients were investigated by multivariable linear regression analyses.ResultsDespite a similar LV ejection fraction, patients in the HTN-HFrEF (DM+) and HTN-HFrEF (DM−) groups showed a higher LV mass index and LV remodeling index than those in the HFrEF control group (all p < 0.05). Compared with the HTN-HFrEF (DM−) and HFrEF control groups, the HTN-HFrEF (DM+) group exhibited the most severe GLPS impairment (p < 0.001). After adjustment for covariates in HFrEF patients, DM was found to be an independent determinant of impaired LV strains in all three directions (GRPS [β = − 0.189; p = 0.011], GCPS [β = 0.217; p = 0.005], GLPS [β = 0.237; p = 0.002]). HTN was associated with impaired GLPS (β = 0.185; p = 0.016) only. However, HTN rather than DM was associated with LV remodeling in HFrEF patients in the multivariable regression analysis (p < 0.05).ConclusionsDM aggravated LV longitudinal dysfunction in hypertensive HFrEF patients without further changes in LV remodeling, indicating that HFrEF patients with comorbid HTN and DM may have a hidden high-risk phenotype of heart failure that requires more advanced and personalized management.

Perspective on the development of a bioengineered patch to treat heart failure: rationale and proposed design of phase I clinical trial

This perspective focuses on the development of tissue engineered (TE) cell-based therapies to treat left ventricular (LV) dysfunction and chronic heart failure (CHF). The development of induced pluripotent stem cells enabled investigators to seed or co-culture human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) alone and in combination with other cells onto bioengineered scaffolds applied to the epicardial surface of the damaged left ventricle. Using our work as an example, we show how a xenograft implant of a bioengineered scaffold embedded with human neonatal fibroblasts and seeded with hiPSC-CMs partially reversed maladaptive LV remodeling and improved LV systolic/diastolic function in an immune-competent rat model of CHF. The fibroblasts lay down an extracellular matrix and secrete growth factors that increase myocardial blood flow. This approach provides an improved cell payload that covers a larger area of the damaged left ventricle as opposed to direct cell injections into the heart or down the coronary arteries. These studies combined with ongoing studies in immune-competent Yucatan mini swine treated with the same xenograft led to the preliminary design of a proposed Phase I clinical trial that will be presented to the Federal Drug Administration. For the proposed Phase I clinical, this TE patch will be implanted onto the epicardial surface of non-immunosuppressed patients undergoing elective Coronary Artery Bypass Grafting with Ejection Fractions ≥ 20% and ≤ 45%. The primary endpoints will be adverse events/severe adverse events associated with placing the TE patch on the heart. While Phase I trials are primarily safety trials, this proposed trial is designed to obtain some potential efficacy endpoints to help with the design of future Phase II/III clinical trials. These endpoints include changes in LV remodeling that were seen in the pre-clinical animal models as well as including endpoints that focus on patient well-being.

Abstract 11256: Longitudinal Changes of Left Ventricular Hemodynamics and Geometry After Myocardial Infarction in a Chronic Swine Model with Functional Mitral Regurgitation

Introduction: Ischemic mitral regurgitation (IMR) is a frequent complication of left ventricular (LV) pathological remodeling after myocardial infarction (MI), which doubles morbidity and mortality. Longitudinal LV remodeling after an MI is not fully understood, therefore large animal studies are needed. In this study, we developed a chronic swine model with IMR and investigated temporal changes of LV remodeling with transesophageal echo (TEE) and pressure-volume (PV) loops. Methods: Yorkshire swine (n=14) underwent induction of a lateral MI through ethanol injection percutaneously into the left circumflex artery (LCX) distal to the first obtuse marginal branch. The animals were survived for 3 months with monthly follow-up TEE. PV loops were performed at baseline, immediately after MI induction, and 3 months post-MI ( Fig.A ). Results: 12 animals survived the MI procedure and developed IMR (average MR grade was 2.6±1.0). LCX occlusion was confirmed with coronary angiogram at 3 months post-MI. EDV and ESV were significantly increased at 3months compared to baseline (156.5±53.0 vs 63.3±7.2ml, p&lt;0.0001, and 83.2±31.4 vs 25.5±5.1ml, p&lt;0.0001, respectively). EF decreased 39.7±7.2% just after infarction compared to 59.4±4.3% at baseline (p=0.0001) and increased at 1 and 2 months, then decreased again at 3 months (53.6±8.1, 55.9±6.3, and 46.7±7.6%, respectively) ( Fig.B ). In invasive hemodynamics, end-systolic elastance, preload adjusted dP/dt max , and end-diastolic pressure-volume relationship significantly decreased at 3 months indicating both systolic and diastolic dysfunction. Arterial elastance at 3 months was significantly lower than baseline indicating a reduction of afterload due to MR ( Fig.C ). Conclusions: A lateral MI resulted in an acute reduction in EF, followed by development of IMR, chronic LV dilation, and decreased systolic and diastolic function over 3 months. Temporary improvement of EF after MI may indicate reduced afterload due to MR.

P3461Sex-specific pattern of left ventricular hypertrophy and diastolic function in patients with type 2 diabetes mellitus

Abstract Background Few prospective studies have evaluated sex-specific pattern, natural progression of left ventricular (LV) remodeling and diastolic dysfunction in patients with type 2 diabetes (T2DM). Purpose The aim of this study was to study the sex-specific prevalence, longitudinal changes of LV remodeling and diastolic dysfunction in patients with T2DM. Further the prognostic value of diastolic function in women and men was also evaluated. Methods A total of 386 patients with T2DM (mean age 61±11 years; women, 48.2%) was recruited. Detailed echocardiography was performed and LV geometry, systolic and diastolic function were measured at baseline and follow-up. A major adverse cardiovascular event (MACE) was defined as cardiovascular death, heart failure hospitalization or myocardial infarction. Multivariable cox-regression adjusted for age, hypertension, LVEF and HbA1c was used to assess the association between sex-specific diastolic function and the development of a MACE. Results Despite a similar age, prevalence of hypertension and body mass index, women had a higher prevalence of LV hypertrophy and diastolic dysfunction at baseline and follow-up compared with men. A total of 26 patients developed a MACE (4 cardiovascular death, 14 hospitalization for heart failure, 8 myocardial infarction) during follow-up. Women with diastolic dysfunction had a higher incidence of MACE than those with normal diastolic function but this association was neutral in men. Multivariable Cox-regression analysis indicated that diastolic dysfunction was associated with MACE in women (hazard ratio 6.35, 95% confidence interval 1.18–34.19, P&lt;0.05) but not men (hazard ratio 1.85, 95% confidence interval 0.58–5.92, P=0.30). Conclusions LV hypertrophy and diastolic dysfunction, both at baseline and follow-up, were more common in women than men. Pre-clinical diastolic dysfunction was independently associated with MACE only in women with T2DM but was neutral in men.

Secondhand Smoke Exposure Enhances Cardiac Fibrosis Effects on the Aging Rat Hearts.

Examining aging rats exposed to secondhand smoke (SHS) engenders changes in left ventricular remodeling due to age- or disease-dependent alterations. Rats were placed in whole-body exposure chambers and exposed to 10 cigarettes. Filtered air was introduced into the chamber at a low rate. Rats were exposed to SHS for 30 min, twice a day, 5 days per week for 1 month. After 4 weeks SHS exposure, rats were sacrificed for morphological study with trichome staining and left ventricular remodeling related protein analysis using western blot. Characteristic fibrotic morphology in the left ventricle increased significantly with aging and exposure to SHS. Exposure to SHS elevated TGFβ1/p-Smad2/3/CTGF and MMP2/MMP9 protein expression levels (p < 0.05). No significant differences in FGF-2 and UPA protein expression were noted as a result of SHS exposure. However, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 protein expression were suppressed by SHS exposure. We also observed increased TGFβ1/p-Smad2/3/CTGF (p < 0.01), FGF-2/UPA (p < 0.05) and decreased TIMPs protein expression levels. Corresponding MMP2 and MMP9 upregulation occurred with aging and exposure to SHS. TGFβ1/p-Smad2/3/CTGF and FGF-2/UPA protein expression from SHS exposure were higher than that from aging. In contrast, MMP2 and MMP9 were increased in aging rats compared with SHS exposed rats (p < 0.05); however, TIMP-1 (p < 0.01), TIMP-2 (p < 0.01) and TIMP-3 (p < 0.05) were decreased. TIMP-4 protein expression levels were decreased compared with SHS exposed rats (p < 0.01). Aging and SHS exposure in rats will produce elevated fibrosis. Exposure to SHS will accelerate aging and left ventricular fibrosis.

Gated-SPECT Functional Assessment in Overweight and Obese Patients

Introduction: Obesity could be implicated in the modification of myocardial structure and function. Mexico has a 70% prevalence of overweight/obesity; therefore, we suggest assessing these changes with a non-invasive technique as the Gated-SPECT. Methods: This is retrospective observational study. Gated-SPECT assessment was conducted in patients suggesting ischemic heart. Multiple regression analysis was used for predicting the value of age, sex, BMI, DM and hypertension for functional parameters. T-test was used to compare DM groups and one-way ANOVA to compare BMI groups. Results: The model statistically significantly predict BMI and smoking to contribute to the prediction of LVEF, p<0.005, adj. R2 = 0.155. BMI, sex and hypertension added statistically significantly to the EDV prediction, p<0.05. EDV, p < 0.005, adj. R2 = 0.202; and sex, age and hypertension to the ESV prediction, p<0.005, adj. R2 = .251. Significant differences between men and women groups in ESV and EDV were found, p<0.000. Conclusions: BMI is associated with the decrease in LVEF and the elevation of EDV without ventricular dysfunction. Sex, age and hypertension counted for predictors for an increase in ESV. There were no significant differences in the diabetic and non-diabetic groups, however obese diabetic patients have an increase in their EDV values. These alterations could be secondary to preliminary changes in left ventricular remodeling. Gated-SPECT is an effective non-invasive technique to discover alterations in structures before fatal events.

Effects of atrioventricular nodal ablation on permanent atrial fibrillation patients with cardiac resynchronization therapy: a systematic review and meta-analysis.

Cardiac resynchronization therapy (CRT) is a well-established therapy for patients with heart failure (HF) and wide QRS configuration, especially for those in sinus rhythm. However, for those with permanent AF, atrioventricular nodal (AVN) ablation use remains under debate. Our objective was to evaluate clinical outcomes and mortality of AVN ablation in HF patients with permanent AF receiving CRT. Electronic publication database and reference lists through October 1, 2013 were searched. Observational cohort studies comparing CRT patients with AF who received either AVN ablation or medical therapy were selected. Outcomes included mortality, CRT nonresponse, changes in left ventricular remodeling, and functional outcomes, such as New York Heart Association (NYHA) functional class, quality of life, and 6-minute hall walk distance. Of 1641 reports identified, 13 studies with 1256 patients were included. Among patients with permanent AF and insufficient biventricular pacing (< 90%), those who had undergone AVN ablation compared to those who did not had numerically lower all-cause mortality (risk ratio [RR]: 0.63, 95% confidence interval [CI]: 0.42 to 0.96, P = 0.03) and significantly lower nonresponse to CRT (RR: 0.41, 95% CI: 0.31 to 0.54, P < 0.00001). Furthermore, AVN ablation was not associated with additional improvements on left ventricular ejection fraction, NYHA functional class, 6-minute hall walking distance, and quality of life. In patients with permanent AF undergoing CRT, AVN ablation tended to reduce mortality potentially and improved clinical response when it was applied to patients with inadequate biventricular pacing (< 90%). Randomized controlled trials are needed to further address the efficacy of AVN ablation among this population.

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Impact of Diet and Exercise Training‐Induced Weight Loss on Myocardial Mechanics in Severely Obese Adolescents

Recent findings indicated silent incipient myocardial dysfunction in juvenile obesity despite normal global cardiac function. The present study investigated whether lifestyle intervention is able to favorably impact these obesity-related myocardial abnormalities and whether improvements are related to changes in insulin resistance and cardiac remodeling. Twenty-eight severe obese adolescents (OB) participated in a 9 month lifestyle intervention program (LIP) based on aerobic exercise and diet. Twenty healthy adolescents (CG) served as controls. Conventional echocardiography and myocardial mechanics were obtained at baseline and follow-up along with insulin resistance. Insulin sensitivity improved (P < 0.001) and body weight decreased (P < 0.001) consecutive to LIP. At baseline, OB had depressed longitudinal (L) strain (CG: -18.3 ± 2.6, OB: -14.2 ± 3.6%, P < 0.001) and enhanced twist compared to controls. The LIP in OB restored L strain to normal values (-16.9 ± 3.5%, NS), whereas it did not affect twist mechanics. From stepwise multiple regression analysis, only baseline L strain and changes in BMI Z-score (r(2) -adjusted = 0.49, P < 0.001) emerged as independent predictors of L strain changes. Juvenile obesity is associated with myocardial mechanic abnormalities that can be partly corrected by lifestyle intervention. Restoration of longitudinal myocardial function occurs in the absence of left ventricular remodeling changes and is not associated with insulin resistance improvements.

Surgical treatment of post-infarction left ventricular aneurysm: clinical analysis

To explore the clinical experiences, efficacies and postoperative left ventricular remodeling changes of surgical ventricular reconstruction in the treatment of post-infarction left ventricular aneurysm. The investigators reviewed retrospectively the clinical data, operative approaches and follow-up outcomes of consecutive 194 patients with post-infarction left ventricular aneurysm, who underwent surgical ventricular reconstruction between January 1997 and December 2009. There were 54 cases in the linear group and 137 cases in the endoventricular patch plasty group. The changes of ventricular remodeling were measured by peri-operative and follow-up echocardiography. All patients underwent surgery with a mean cardiopulmonary bypass duration of (103 ± 35) min and aortic cross clamp duration of (62 ± 26) min. There were 8 per-operative deaths with a mortality rate of 2.2%. Angina pectoris of other cases disappeared and heart function greatly improved. After operation, the ventricular remodeling results showed that in the linear group, there was not significant difference in the changes of ventricular remodeling of post-op 2 weeks, 6 months, 1 year and 5 years versus pre-operation. However, in the endoventricular patch group, the changes of ventricular remodeling of post-op 2 weeks and follow-up 6 months versus pre-operation were significantly reduced (P < 0.05). End-systolic volume (LVESV) reduced from (129 ± 27) ml to (65 ± 8) ml and end-systolic volume index (LVESVI) decreased from (104 ± 14) ml/m(2) to (44 ± 6) ml/m(2) and the subgroup of LVEF < 35% was the most significant in the changes of LVESV and LVESVI. But LVEF improved significantly at post-operation and follow-up (from preoperation 42% ± 11% to 52% ± 7% during follow-up). For patients with infarction left ventricular aneurysm, left ventricular reconstruction is quite effective. The choice of operative approaches is determined by the size and range of ventricular aneurysm. Both string suture and endoventricular patch plasty technique can yield similarly satisfactory surgical outcomes. After operation, ventricular volume significantly decreases and cardiac function greatly improves.

The Effects of Antihypertensive Treatment on the Doppler‐Derived Myocardial Performance Index in Patients with Hypertensive Left Ventricular Hypertrophy: Results from the Swedish Irbesartan in Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA)

To investigate the effects of antihypertensive treatment on the Doppler-derived myocardial performance index (MPI) in patients with hypertensive left ventricular hypertrophy. The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol. Antihypertensive treatment lowered MPI (mean difference -0.03 +/- 0.01, P = 0.04). Changes in MPI by treatment were associated with changes in left ventricular ejection fraction (beta-coefficient -0.35 P = 0.005), stroke volume/pulse pressure (reflecting arterial compliance, beta-coefficient -0.39 P < 0.001) and peripheral vascular resistance (beta-coefficient 0.28 P < 0.04). Furthermore, there was a borderline significant association between changes in MPI and changes in E-wave deceleration time (reflecting diastolic function, beta-coefficient 0.23, P = 0.06). No associations were found between changes in MPI and changes in blood pressure, E/A-ratio, left ventricular mass index, relative wall thickness or heart rate. A stepwise multivariable regression model confirmed the association between changes in MPI and changes in ejection fraction and stroke volume/pulse pressure (all P < 0.05), as well as the trend for E-wave deceleration time (P = 0.08), but not in the case of peripheral vascular resistance. The MPI exhibited a modest decrease after 48 weeks of antihypertensive treatment in patients with hypertensive left ventricular hypertrophy. Changes in MPI were associated with changes in left ventricular function and vascular compliance, rather than with changes in left ventricular remodeling or blood pressure.

Abnormal Segmental Relaxation Patterns in Hypertensive Disease and Symptomatic Diastolic Dysfunction Detected by Strain Echocardiography

An abnormal segmental relaxation pattern exists as an early sign of diastolic dysfunction (DD), detectable by strain (S) echocardiography. The objective of this study was to investigate the relation of segmental relaxation patterns with longitudinal systolic function and symptomatic DD in patients with hypertension (HTN). We evaluated 30 healthy volunteers and 78 volunteers with HTN, divided as follows: (1) patients without DD (n: 28); (2) patients with asymptomatic DD (n: 25); and (3) patients with symptomatic DD (n: 25). All groups had normal ejection fraction greater than or equal to 55%. The symptomatic group had mild exertional dyspnea. All participants underwent 2-dimensional and color Doppler myocardial imaging, and the mean longitudinal strain (S) and S rate (SR) were estimated. Early and late diastolic SR parameters (SR(E) and SR(A)) were also recorded from the basal, mid, and apical segments for each wall. Altered segmental relaxation (SR(E)/SR(A) < 1.1) was regarded as an index of segmental DD. Patients who were symptomatic with DD were found to have more segments with an abnormal relaxation pattern (segmental DD) and more deteriorated longitudinal systolic function based on S and SR, compared with patients with asymptomatic HTN and control subjects. Segmental DD was correlated with structural changes of left ventricular (LV) remodeling such as wall thickness (r: 0.64), relative wall thickness (r: 0.58), and LV mass index (r: 0.59), as well as mean S (r: -0.61), SR (r: -0.62), systolic blood pressure (r: 0.44), age (r: 0.49), and filling pressures (r: 0.50), all P less than .01. In multiple regression analysis, segmental DD and systolic blood pressure were independently related to symptomatic status (segmental DD: beta = 0.33, P = .003; systolic blood pressure: beta = 0.24, P = .009, R(2): 0.33). Compared with conventional indices of DD (deceleration time of the E wave, isovolumic relaxation time, E, A, and E/A), segmental DD was the only parameter that predicted symptomatic status (coefficient: 0.3817, SE: 0.1101, P = .0005, odds ratio: 1.4648, 95% confidence interval: 1.1761-1.7485). LV segmental relaxation demonstrates progressive deterioration in HTN disease, which is more pronounced in patients with symptomatic DD. Altered segmental relaxation is related to structural changes of LV remodeling and constitutes an independent predictor for the presence of a symptomatic status.

COMPARE: Comparison of the Effects of Carvedilol CR and Carvedilol IR on Left Ventricular Ejection Fraction in Patients with Heart Failure

Left ventricular ejection fraction (LVEF) is an important measure of ventricular function in the evaluation of heart failure. Immediate-release (IR) carvedilol twice daily has been shown to improve LVEF in subjects with ischemic and nonischemic chronic heart failure. A once-daily formulation, controlled-release (CR) carvedilol, is expected to improve quality of care through improved adherence as a result of the reduced frequency of dosing. This multicenter, randomized, double-blind study in subjects with stable chronic heart failure will compare the change in LVEF in patients receiving carvedilol IR with those receiving carvedilol CR. LVEF will be measured by 2-dimensional echocardiography at 6 months after entry into the maintenance period of the study drug. The secondary objectives of this study are to assess changes in left ventricular remodeling and function, to evaluate changes in brain natriuretic peptide levels, and to determine the incidence of all-cause and heart failure-related hospitalizations and all-cause mortality after treatment with carvedilol CR or carvedilol IR.

Autoantibody against β1‐adrenergic receptor and left ventricular remodeling changes in response to metoprolol treatment

Autoantibodies specific for the beta(1)-adrenoceptor (beta(1)-AR) have been implicated in the pathology of congestive heart failure (CHF). We hypothesized that the presence of autoantibodies against beta(1)-AR (anti-beta(1)-AR) is associated with left ventricular (LV) remodelling in response to metoprolol. Synthetic beta(1)-AR peptides served as the target antigen in an ELISA (enzyme-linked immunosorbent assay) were used to screen the sera of 106 CHF patients. Patients were separated into positive (+) anti-beta(1)-AR or negative (-) anti-beta(1)-AR groups according to their anti-beta(1)-AR reactivity. Echocardiography (ECG) was performed at baseline and after one year of metoprolol therapy in combination with standard treatment regime for CHF, that is, digoxin, diuretics and an ACEI (angiotensin-converting enzyme inhibitor). The dose of metoprolol was doubled on a biweekly basis up to 50 mg x 2 daily (b.i.d./day) or attainment of maximum tolerated dose. Ninety-six patients completed final data analysis. Fifty-four patients with (+) anti-beta(1)-AR had greater improvements than 42 patients with (-) anti-beta(1)-AR in LVEDD (left ventricular end-diastolic dimension) (P < 0.01, from 69 +/- 0.8 to 58.0 +/- 0.5 mm vs. 69.0 +/- 0.8-63.6 +/- 0.9 mm) and LVESD (left ventricular end-systolic dimension) (P < 0.01, from 57.1 +/- 1.4 to 43.9 +/- 0.8 mm vs. 56.2 +/- 0.9-48.6 +/- 1.0 mm), and LVEF (left ventricular ejection fraction) (P < 0.01, from 35.4 +/- 1.3 to 49.8 +/- 0.6% vs. 34.4 +/- 1.0-44.3 +/- 1.1%) by metoprolol therapy in combination with standard treatment regime for one year. Of the CHF patients with (+) anti-beta(1)-AR, 65.4% responded to target metoprolol dose as compared to 21.4% of CHF patients without anti-beta(1)-AR (P < 0.01). Response to target metoprolol dose occurred more rapidly in (+) anti-beta(1)-AR than (-) anti-beta(1)-AR of CHF patients (67.5 +/- 2.4 vs. 100.8 +/- 3.0 days, P < 0.01). These results demonstrated that CHF patients with (+) anti-beta(1)-AR had greater improvements in LV remodelling and heart function by metoprolol as compared to (-) anti-beta(1)-AR patients. Moreover, patients with (+) anti-beta(1)-AR have better tolerance to metoprolol therapy than patients without anti-beta(1)-AR.