METHODS: Twenty seven HFpEF (clinical features of HF, left ventricular EF >50%, evidence of mild diastolic dysfunction and evidence of exercise limitation as assessed by cardiopulmonary exercise test) and 14 controls underwent 1H-cardiovascular magnetic resonance spectroscopy (1H-CMRS) to measure MTG (lipid/water, %), 31P-CMRS to measure myocardial energetics (phosphocreatine-to-adenosine triphosphate - PCr/ATP) and feature-tracking cardiovascular magnetic resonance (CMR) imaging for diastolic strain rate.
RESULTS: When compared to controls, HFpEF had 2.3 fold higher in MTG (1.45 ± 0.25% vs. 0.64 ± 0.16%, p = 0.009) and reduced PCr/ATP (1.60 ± 0.09 vs. 2.00 ± 0.10, p = 0.005). HFpEF had significantly reduced diastolic strain rate and maximal oxygen consumption (VO2 max), which both correlated significantly with elevated MTG and reduced PCr/ATP. On multivariate analyses, MTG was independently associated with diastolic strain rate while diastolic strain rate was independently associated with VO2 max.
CONCLUSIONS: Myocardial steatosis is pronounced in mild HFpEF, and is independently associated with impaired diastolic strain rate which is itself related to exercise capacity. Steatosis may adversely affect exercise capacity by indirect effect occurring via impairment in diastolic function. As such, myocardial triglyceride may become a potential therapeutic target to treat the increasing number of patients with HFpEF.
INTRODUCTION: Percutaneous edge-to-edge repair of severe MR using the MitraClip device is approved for use in the USA for high risk DMR while European guidelines include its use in FMR patients as well.
METHODS: The MitraClip in the Asia-Pacific Registry (MARS) is a multicenter retrospective registry, involving eight sites in five Asia-Pacific countries. Clinical and echocardiographic characteristics, procedural outcomes and 1-month outcomes [death and major adverse events (MAE)] were compared between FMR and DMR patients treated with the MitraClip.
RESULTS: A total of 163 patients were included from 2011 to 2014. The acute procedural success rates for FMR (95.5%, n = 84) and DMR (92%, n = 69) were similar (P = 0.515). 45% of FMR had ≥2 clips inserted compared to 60% of those with DMR (P = 0.064).The 30-day mortality rate for FMR and DMR was similar at 4.5% and 6.7% respectively (P = 0.555). The 30-day MAE rate was 9.2% for FMR and 14.7% for DMR (P = 0.281). Both FMR and DMR patients had significant improvements in the severity of MR and NYHA class after 30 days. There was a significantly greater reduction in left ventricular end-diastolic diameter (P = 0.002) and end systolic diameter (P = 0.017) in DMR than in FMR.
CONCLUSIONS: The MitraClip therapy is a safe and efficacious treatment option for both FMR and DMR. Although, there is a significantly greater reduction in LV volumes in DMR, patients in both groups report clinical benefit with improvement in functional class. © 2015 Wiley Periodicals, Inc.
PATIENTS AND METHODS: Materials and methods: The study involved 134 ST-segment elevation myocardial infarction patients. Occurrence of post-percutaneous coronary (PCI) intervention epicardial blood flow of TIMI <3 or myocardial blush grade 0-1 along with ST resolution <70% within 2 hours after PCI was qualified as the no-reflow condition. Left ventricle remodeling was defined after 6-months as an increase in left ventricle end-diastolic volume and/or end-systolic volume by more than 10%.
RESULTS: Results: A logistic regression formula was evaluated. Included biomarkers were macrophage migration inhibitory factor and sST2, left ventricle ejection fraction: Y=exp(-39.06+0.82EF+0.096ST2+0.0028MIF) / (1+exp(-39.06+0.82EF+0.096ST2+0.0028MIF)). The estimated range is from 0 to 1 point. Less than 0.5 determines an adverse outcome, and more than 0.5 is a good prognosis. This equation, with sensitivity of 77 % and specificity of 85%, could predict the development of adverse left ventricle remodeling six months after a coronary event (AUC=0.864, CI 0.673 to 0.966, p<0.05).
CONCLUSION: Conclusions: A combination of biomarkers gives a significant predicting result in the formation of adverse left ventricular remodeling after ST-segment elevation myocardial infarction.
OBJECTIVE: We have conducted a systematic review of two major (FIGHT and LIVE) placebo-controlled trials of liraglutide and its clinical effect on the ejection fraction of subjects with heart failure.
METHODS: Medline data was retrieved for trials involving liraglutide from 2012 to 2020. The inclusion criteria for trials were: subjects with or without type 2 diabetes mellitus (T2DM), subjects with heart failure with rLVEF, major trials (phase II or III) on liraglutide, trials included liraglutide with defined efficacy primary outcome of patients with heart failure with rLVEF. The search was limited to the English language, whereby two trials [FIGHT and LIVE] had been included and two trials were excluded due to different primary outcomes. Participants (541) had been randomized for either liraglutide or placebo for 24 weeks.
RESULTS: In the FIGHT trial the primary intention-to-treat, sensitivity, and diabetes subgroup analyses have shown no significant between-group difference in the global rank scores (mean rank of 146 in the liraglutide group versus 156 in the placebo group; Wilcoxon rank-sum P=.31), number of deaths, re-hospitalizations for heart failure, or the composite of death or change in NT-pro BNP level (P= .94). In the LIVE trial, the change in the left ventricular ejection fraction (LVEF) from baseline to week 24 was not significantly different between treatment groups. The overall discontinuation rate of liraglutide was high in the FIGHT trial (29%, 86) as compared to that in the LIVE trial (11.6%, 28).
CONCLUSION: FIGHT and LIVE trials have demonstrated that liraglutide use in subjects with heart failure and rLVEF was implicated with an increased adverse risk of heart failure-related outcomes.
Methods: Twenty-seven patients with history of anterior myocardial infarction (MI) and baseline left ventricular ejection fraction (LVEF) of less than 35% were recruited into this study. Patients who are eligible for revascularization were grouped into group A (MSCs infusion with concurrent revascularization) or group B (revascularization only) while patients who were not eligible for revascularization were allocated in group C to receive intracoronary MSCs infusion. LV function was measured using echocardiography.
Results: Patients who received MSCs infusion (either with or without revascularization) demonstrated significant LVEF improvements at 3, 6 and 12 months post-infusion when compared to baseline LVEF within its own group. When comparing the groups, the magnitude of change in LVEF from baseline for third visits i.e., 12 months post-infusion was significant for patients who received MSCs infusion plus concurrent revascularization in comparison to patients who only had the revascularization procedure.
Conclusions: MSCs infusion significantly improves LV function in ICM patients. MSCs infusion plus concurrent revascularization procedure worked synergistically to improve cardiac function in patients with severe ICM.
METHODS: It is a prospective, open-labeled, randomized controlled study conducted at National Heart Institute, Kuala Lumpur from July 2018 to July 2019. All patients with simple and complex congenital heart diseases (CHD) with good left ventricular function (left ventricular ejection fraction [LVEF] >50%) were included while those with LVEF <50% were excluded. A total of 100 patients were randomized into two groups of 50 each receiving either del Nido or BSTH cardioplegia. Primary end points were the spontaneous return of activity following aortic cross-clamp release and ventricular function between two groups. Secondary end point was myocardial injury as assessed by troponin T levels.
RESULTS: Cardiopulmonary bypass and aortic cross-clamp time, return of spontaneous cardiac activity following the aortic cross-clamp release, the duration of mechanical ventilation, and intensive care unit stay were comparable between two groups. Statistically significant difference was seen in the amount and number of cardioplegia doses delivered (P < .001). The hemodilution was significantly less in the del Nido complex CHD group compared to BSTH cardioplegia (P = .001) but no difference in blood usage (P = .36). The myocardial injury was lesser (lower troponin T release) with del Nido compared to BSTH cardioplegia (P = .6).
CONCLUSION: Our study showed that both del Nido and BSTH cardioplegia are comparable in terms of myocardial protection. However, single, less frequent, and lesser volume of del Nido cardioplegia makes it more suitable for complex repair.
METHODS: LA reservoir strain (LASr), LA conduit strain (LAScd), and LA contractile strain (LASct) were measured using speckle-tracking echocardiography. The primary outcome was a composite of all-cause mortality, heart failure hospitalization, progression to New York Heart Association functional class III or IV, acute coronary syndrome, or syncope. Secondary outcomes 1 and 2 comprised the same end points but excluded acute coronary syndrome and additionally syncope, respectively. The prognostic performance of phasic LA strain cutoffs was evaluated in competing risk analyses, aortic valve replacement being the competing risk.
RESULTS: Among 173 patients (mean age, 69 ± 11 years; mean peak transaortic velocity, 4.0 ± 0.8 m/sec), median LASr, LAScd, and LASct were 27% (interquartile range [IQR], 22%-32%), 12% (IQR, 8%-15%), and 16% (IQR, 13%-18%), respectively. Over a median of 2.7 years (IQR, 1.4-4.6 years), the primary outcome and secondary outcomes 1 and 2 occurred in 66 (38%), 62 (36%), and 59 (34%) patients, respectively. LASr < 20%, LAScd < 6%, and LASct < 12% were identified as optimal cutoffs of the primary outcome. In competing risk analyses, progressing from echocardiographic to echocardiographic-clinical and combined models incorporating N-terminal pro-B-type natriuretic peptide, LA strain parameters outperformed other key echocardiographic variables and significantly predicted clinical outcomes. LASr < 20% was associated with the primary outcome and secondary outcome 1, LAScd < 6% with all clinical outcomes, and LASct < 12% with secondary outcome 2. LAScd < 6% had the highest specificity (95%) and positive predictive value (82%) for the primary outcome, and competing risk models incorporating LAScd < 6% had the best discriminative value.
CONCLUSIONS: In well-compensated patients with moderate to severe aortic stenosis and preserved left ventricular ejection fractions, LA strain was superior to other echocardiographic indices and incremental to N-terminal pro-B-type natriuretic peptide for risk stratification. LAScd < 6%, LASr < 20%, and LASct < 12% identified patients at higher risk for adverse outcomes.
METHODS: Between January 2013 and June 2015, a total of 116 patients underwent arterial switch operation. Of the 116 patients, 26 with TGA-IVS underwent primary arterial switch operation at more than 30 days of age.
RESULTS: The age and body weight (mean ± SD) at the operation were 120.4 ± 93.8 days and 4.1 ±1.0 kg, respectively. There was no hospital mortality. The thickness of posterior LV wall (preoperation vs postoperation; mm) was 4.04 ± 0.71 versus 5.90 ± 1.3; P < .0001; interval: 11.8 ± 6.5 days. The left atrial pressure (mm Hg; postoperative day 0 vs 3) was 20.0 ± 3.2 versus 10.0 ± 2.0; P < .0001; and the maximum blood lactate level (mmol/dL) was 4.7 ± 1.4 versus 1.4 ± 0.3; P < .0001, which showed significant improvement in the postoperative course. All cases had delayed sternal closure. The patients who belonged to the thin LV posterior wall group (<4 mm [preoperative echo]: n = 13) had significantly longer ventilation time (days; 10.6 ± 4.8 vs 4.8 ± 1.7, P = .0039), and the intensive care unit stay (days) was 14 ± 9.2 versus 7.5 ± 3.5; P = .025, compared with thick LV wall group (≥4.0 mm: n = 13).
CONCLUSIONS: The children older than 30 days with TGA-IVS can benefit from primary arterial switch operation with acceptable results under our indication. However, we need further investigation for LV function.
DESIGN: Observational study.
SETTING: A single-centre study in which eligible patients were recruited from T2DM clinic. Following consent, patients completed a questionnaire and underwent physical examinations. Patients had blood drawn for laboratory investigations and had a transthoracic echocardiography.
PARTICIPANTS: A total of 305 patients who were not known to have CVD were recruited. Patients with deranged liver function tests and end stage renal failure were excluded.
MAIN OUTCOME MEASURES: Echocardiographic parameters such as left ventricular ejection fraction, left ventricular mass index (LVMI), left ventricular hypertrophy, left atrial enlargement and diastolic function were examined.
RESULTS: A total of 305 patients predominantly females (65%), with mean body mass index of 27.5 kg/m2 participated in this study. None of them had either a history or signs and symptoms of CVD. Seventy-seven percent of patients had a history of hypertension and 83% of this study population had T2DM for more than 10 years. Mean HbA1c of 8.3% was recorded. Almost all patients were taking metformin. Approximately, 40% of patients were on newer anti-T2DM agents such as sodium-glucose cotransporter-2 and dipeptidyl peptidase 4 inhibitors. Fifty-seven percent (n=174) of the study population had SBHF at the time of study: diastolic dysfunction, increased LVMI and increased left atrial volume index (LAVI) were noted in 51 patients (17%), 128 patients (42%) and 98 patients (32%), respectively. Thirty-seven patients (12%) had both increase LVMI and LAVI.
CONCLUSION: Our study has revealed a high prevalence of SBHF in T2DM patients without overt cardiac disease in Malaysia that has one of the highest prevalence of TDM in the world.
METHODS: A total of 119 post-percutaneous coronary intervention ST elevation myocardial infarction patients with TIMI flow grade >2 were prospectively included in the study. Left ventricular global longitudinal strain was quantified by 2-dimensional speckletracking echocardiography, and left ventricular mechanical dispersion was determined at baseline and after 1 year to assess adverse cardiac remodeling. The levels of circulating biomarkers were measured at the baseline. TIMI score and the Global Registry of Acute Coronary Events score systems were used to evaluate the prognosis of patients.
RESULTS: Patients with high quartile versus low quartile of left ventricular mechanical dispersion exerted higher Global Registry of Acute Coronary Events and TIMI score grades, left ventricular endsystolic volume, global longitudinal strain, and levels of the N-terminal fragment of brain natriuretic peptide and lower left ventricular ejection fraction. Multivariate log regression showed that N-terminal fragment of brain natriuretic peptide > 953 pg/mL, global longitudinal strain > -8%, and high quartile of left ventricular mechanical dispersion remained independent predictors for adverse cardiac remodeling. Addition of left ventricular mechanical dispersion to the N-terminal fragment of brain natriuretic peptide improved the discriminative potency of the whole model.
CONCLUSION: Measurement of left ventricular mechanical dispersion might be useful in determining the risk of adverse cardiac remodeling in post-percutaneous coronary intervention ST elevation myocardial infarction patients.