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MicroRNA(miR)-143 and miR-145 are mainly expressed in vascular smooth muscle cells. However, the relationship between plasma miR-143 or miR-145 levels and the left ventricular (LV) function in patients with heart diseases remains unclear. Blood samples were taken from the antecubital vein in patients with heart diseases (n = 52), such as coronary artery disease, old myocardial infarction, cardiomyopathy, and valvular heart disease, and controls without heart diseases (n = 22). We measured plasma miR-143 and -145 levels by quantitative RT–PCR using TaqMan MicroRNA Assays and THUNDERBIRD Probe qPCR Mix. Plasma BNP levels were also measured. Echocardiography was performed to measure the LV ejection fraction (LVEF) and LV dilation. Plasma miR-143 and miR-145 levels were significantly higher in patients with heart diseases than in controls, respectively. Plasma miR-143 and miR-145 levels were significantly higher in patients with LVEF < 50% than in those with LVEF ≧ 50%, respectively. Plasma miR-143 and miR-145 levels were inversely correlated with LVEF, respectively. Plasma miR-143 and miR-145 levels were positively correlated with LV end-systolic dimension, respectively. Plasma miR-143 and -145 levels were positively correlated with plasma BNP levels, respectively. Plasma BNP levels were inversely correlated with LVEF. Plasma miR-143 and miR-145 levels are elevated in patients with LV dysfunction and may counteract LV dysfunction. [ABSTRACT FROM AUTHOR]

Abstract Background Cancer therapy is considered to cause accelerated ischemia. Ankle-Brachial Index (ABI) measurement is an inexpensive, simple, available test for the early diagnosis of peripheral artery disease (PAD); however, it is not performed routinely. We aimed to evaluate the role of routine ABI measurement for the diagnosis of PAD among patients diagnosed with cancer and whether it correlates with left ventricular (LV) dysfunction. Methods A retrospective, single-center study including patients diagnosed with cancer at Tel Aviv Sourasky Medical Center. The cohort included patients performing routine ABI and LV global longitudinal strain (GLS) echocardiography. The primary endpoint was the prevalence of PAD and whether it correlates with LV dysfunction, defined by LV GLS absolute value

Key Clinical Message: With increased complexity in both medical comorbidities and coronary anatomy, the proportion of surgically turndown patients and high‐risk PCI will continue to rise. Impella‐assisted complex PCI can be performed with high technical success and can improve quality of life, angina score, and potentially left ventricular ejection fraction. [ABSTRACT FROM AUTHOR]

Purpose: We sought to detect left ventricular (LV) adverse alterations in structure and function in type 2 diabetes mellitus (T2DM) patients with or without mild renal dysfunction (MRD) using comprehensive echocardiography techniques and to explore the independent risk factors for LV remodeling (LVR) and dysfunction in these patients. Methods: The study included 82 T2DM patients with normal LV ejection fraction (presence (n = 42)/absence (n = 40) of MRD). Age- and gender-matched controls (n = 40) were also recruited. LV structure and function were evaluated using conventional echocardiography and three-dimensional speckle tracking echocardiography (3DSTE). Global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were all measured using 3DSTE. Results: Compared with the controls with absolute advantage of LV normal geometry, LVR was more frequently present in the two T2DM groups, with the largest proportion in those with T2DM and MRD (P < 0.001). Fasting plasma glucose (FPG) and MRD were both significant risk factors for LVR in T2DM patients. The detection rates of LV diastolic dysfunction and subclinical systolic dysfunction were significantly higher in the T2DM groups than in the controls (P = 0.000). Moreover, the two case groups also showed significantly lower strain values in multiple directions than the controls (all P < 0.05). FPG was significantly associated with LV diastolic dysfunction, whereas FPG and MRD were both significantly associated with subclinical LV systolic dysfunction in T2DM patients. Conclusions: The combined use of conventional echocardiography and 3DSTE allowed the timely detection of early cardiac damage in T2DM patients with or without MRD. [ABSTRACT FROM AUTHOR]

Key Clinical Message With increased complexity in both medical comorbidities and coronary anatomy, the proportion of surgically turndown patients and high‐risk PCI will continue to rise. Impella‐assisted complex PCI can be performed with high technical success and can improve quality of life, angina score, and potentially left ventricular ejection fraction.

Objective: To study the prevalence of non‑alcoholic fatty liver disease (NAFLD) and its association of with microvascular complications and ventricular dysfunction in patients with type 2 diabetes mellitus (T2DM). Methods: In this cross‑sectional study, 100 T2DM patients were screened randomly for detection of fatty liver in ultrasonography. Patients with fatty liver (NAFLD group, n = 36) were compared with subjects without fatty liver (non‑NAFLD group, n = 64). Detailed clinical, biochemical, and imaging parameters like lipid profile, LFT, fasting plasma glucose, 2‑hour post‑prandial plasma glucose, HbA1C, fasting insulin, spot urinary albumin/creatinine ratio, and 2‑D ECHO (M‑mode) were performed. Results: The prevalence of NAFLD was found to be 36%. NAFLD group had significantly higher BMI, WHR, blood pressure, glycemic profile, and lipid parameters compared to non‑NAFLD group. HOMA IR was elevated significantly in NAFLD group (3.16 ± 1.96) compared to non‑NAFLD group (1.73 ± 1.59). There was significantly higher prevalence of all the diabetes‑related microvascular complications and LV diastolic dysfunction in NAFLD patients with higher odds for the occurrence of neuropathy (OR = 4.74; P = 0.001), nephropathy (OR = 3.92; P = 0.003), retinopathy (OR = 5.95; P = 0.002), and LV diastolic dysfunction (OR = 1.84; P = 0.043). Conclusions: NAFLD is significantly associated with various diabetes‑related microvascular complications as well as LV diastolic dysfunction in T2DM patients. [ABSTRACT FROM AUTHOR]

Aim: The present aim of the study is to study cardiac dysfunction in chronic liver disease using 2D Echo cardiography and tissue Doppler Imaging. Methodology: This was a hospital-based cross-sectional descriptive study conducted over 16 months (between March 2021 and June 2022) among patients seeking medical attention at Narayana Medical College & Hospital, Nellore. Results: A total of 100 cirrhosis patients were recruited. The average age was 46.6±11.13 years (Range 23 to 80 years). 80% patients were males. Most of the male patients (30 patients) were in 41 to 50 years age group but most female patients (7 patients) were less than 40 years in age group. Alcohol was the most common etiology (69%). Abdominal distention due to ascites (59 patients) was the most common clinical presentation and eleven among them had spontaneous bacterial peritonitis. 53 patients were found to have some echocardiographic abnormalities at the time of assessment. All 53 patients had diastolic dysfunction. However, only 18 patients had an ejection fraction less than 55%, indicating significant LV dysfunction. 8% of patients had RV Systolic dysfunction, and 8% of patients had pulmonary arterial hypertension. Based on the complications developed by the patients, 53.19% of hepatic encephalopathy, 72.73% of SBP, 50% of cases with GI Bleeding and HRS had Echo changes. Likewise, 21.15% of cases with esophageal varices and 10% of cases with PHG & GAVE had Echo changes respectively. Conclusion: The study concluded that to assess the cardiac dysfunction in chronic liver disease patients, it is preferable to do 2D Echo-Tissue Doppler Imaging rather than a conventional Colour Doppler study. [ABSTRACT FROM AUTHOR]

Background: The presence of a chronic total occlusion (CTO) and severe left ventricular (LV) systolic dysfunction are known negative prognostic factors in patients with coronary artery disease. Several studies have examined the effect of CTO revascularization on mortality, symptoms, occurrence of myocardial infarction (MI), and cardiac function in patients with normal or reduced LV function. However, the effect of CTO revascularization on heart failure-related events in patients with LV dysfunction, such as heart failure hospitalization (HFH), the occurrence of atrial fibrillation (AF), and a worsening renal function (WRF), has not yet been evaluated. To assess the success rate and safety of CTO percutaneous coronary interventions (PCIs) in coronary patients with LV ejection fractions of =40% and evaluate the impact of successful CTO revascularization on HFH, occurrence of AF, and WRF. Methods: Prospectively, data were collected from CTO PCIs performed at three referral centers and analyzed. From a total of 1435 CTO PCIs, 132 (9.2%) patients with a left ventricular ejection fraction (LVEF) of =40% were included in this analysis. The median follow-up duration was 23.18 months (interquartile range (IQR): 11.02-46.66 months). Results: A successful CTO PCI was achieved in 109 of these patients, while the procedure was unsuccessful in 23 patients (82.5% procedural success rate). Overall, the intervention had an acceptable number of peri-procedural (or in-hospital) complications (9.1%). During the follow-up period, the rates of all-cause death, cardiovascular death, and non-fatal MI were not significantly different between the two groups. The rates of HFH were significantly lower in the successful PCI group, while WRF and AF did not differ between successful and unsuccessful PCI groups. Successful PCI and higher estimated glomerular filtration rate (eGFR) were independent predictors of a lower risk of HFH, while prior stroke and diabetes were independent predictors of a higher risk of HFH. Conclusions: In patients with reduced LV systolic function (ejection fraction, EF =40%), CTO PCI is a safe and effective procedure and successful CTO PCI is independently associated with a lower risk of HFH during follow-up. Further expansion of this cohort is necessary to confirm these results. [ABSTRACT FROM AUTHOR]

Objective: To study the prevalence of non-alcoholic fatty liver disease (NAFLD) and its association of with microvascular complications and ventricular dysfunction in patients with type 2 diabetes mellitus (T2DM). Methods: In this cross-sectional study, 100 T2DM patients were screened randomly for detection of fatty liver in ultrasonography. Patients with fatty liver (NAFLD group, n = 36) were compared with subjects without fatty liver (non-NAFLD group, n = 64). Detailed clinical, biochemical, and imaging parameters like lipid profile, LFT, fasting plasma glucose, 2-hour post-prandial plasma glucose, HbA1C, fasting insulin, spot urinary albumin/creatinine ratio, and 2-D ECHO (M-mode) were performed. Results: The prevalence of NAFLD was found to be 36%. NAFLD group had significantly higher BMI, WHR, blood pressure, glycemic profile, and lipid parameters compared to non-NAFLD group. HOMA IR was elevated significantly in NAFLD group (3.16 ± 1.96) compared to non-NAFLD group (1.73 ± 1.59). There was significantly higher prevalence of all the diabetes-related microvascular complications and LV diastolic dysfunction in NAFLD patients with higher odds for the occurrence of neuropathy (OR = 4.74; P = 0.001), nephropathy (OR = 3.92; P = 0.003), retinopathy (OR = 5.95; P = 0.002), and LV diastolic dysfunction (OR = 1.84; P = 0.043). Conclusions: NAFLD is significantly associated with various diabetes-related microvascular complications as well as LV diastolic dysfunction in T2DM patients.

Peripartum Cardiomyopathy is a rare type of cardiomyopathy that occurs during late pregnancy or in early postpartum period and is a life threatening condition. It presents with heart failure secondary to left ventricular systolic dysfunction. Here the LVEF is < 45%, with/without LV dilatation. The condition shows overlapping symptoms with pregnancy related pathology like preeclampsia, myocarditis or underlying genetic diseases and hence underestimated. Underlying pathophysiology is poorly understood with lack of specific biomarkers. Timely diagnosis and multidisciplinary team approach helps in determining the outcome. [ABSTRACT FROM AUTHOR]

Right ventricular (RV) pacing is associated with a reduction in left ventricular (LV) systolic function, thought to be mediated by pacing-induced ventricular dyssynchrony. The prevalence of heart failure after RV pacing is reported to range from 31±3%. We studied 60 subjects with high-grade atrioventricular block and Complete Heart Block (CHB) scheduled to undergo right ventricular apical pacing. 2D echocardiography was done at baseline, 1 month and 12 months. Pacing-induced cardiomyopathy was defined as a reduction in LVEF to

Abstract Background Subclinical LV dysfunction (LVD) identifies heart failure (HF) risk in type 2 diabetes mellitus (T2DM). We sought the extent to which clinical scores (ARIC-HF, WATCH-DM), natriuretic peptides (NTpBNP) and troponin (hs-TnT) were associated with subclinical LV dysfunction (LVD). These associations could inform the ability of these tests to identify which patients should undergo echocardiography. Methods Participants with T2DM were prospectively recruited from three community-based populations. ARIC-HF risk at 4 years and WATCH-DM scores were calculated from clinical data. NTpBNP and hs-TnT were measured using an electro-chemiluminescence assay. All underwent a comprehensive echocardiogram. We calculated the sensitivity and specificity of clinical scores and biomarkers to identify abnormal global longitudinal strain (GLS ≥ −16%)), diastolic function (E/e’ ≥ 14 or e’ 34 ml/m2) and LV hypertrophy (LV mass index > 88 g/m2 (F) > 102 g/m2(M)). Results Of 804 participants (median age 69 years [inter-quartile range (IQR) 65–73], 36% female), clinical scores suggested significant HF risk (median ARIC-HF 8% [IQR 4–12]; WATCH-DM 10 points [IQR 8–12]), and the median NTpBNP was 50 pg/mL [IQR 25–101] and hs-TnT 9.6 pg/mL [IQR 6.8–13.6]. Abnormal GLS was present in 126 (17%), elevated E/e’ in 114 (15%), impaired e’ in 629 (78%), increased LAV in 351 (44%) and LV hypertrophy in 113 (14%). After adjustments for age, body-mass index, and renal function, each standard deviation increase in NTpBNP was associated with a GLS increase of 0.32 (p

Rheumatic heart disease (RHD) remains a significant cardiovascular burden in the world even though it is no longer common in affluent countries. Centuries of history surrounding this disease provide us with a thorough understanding of its pathophysiology. Infections in the throat, skin, or mucosa are the gateway for Group A Streptococcus (GAS) to penetrate our immune system. A significant inflammatory response to the heart is caused by an immunologic cascade triggered by GAS antigen cross-reactivity. This exaggerated immune response is primarily responsible for cardiac dysfunction. Recurrent inflammatory processes damage all layers of the heart, including the endocardium, myocardium, and pericardium. A vicious immunological cycle involving inflammatory mediators, angiotensin II, and TGF-β promotes extracellular matrix remodeling, resulting in myocardial fibrosis. Myocardial fibrosis appears to be a prevalent occurrence in patients with RHD. The presence of myocardial fibrosis, which causes left ventricular dysfunction in RHD, might be utilized to determine options for treatment and might also be used to predict the outcome of interventions in patients with RHD. This emerging concept of myocardial fibrosis needs to be explored comprehensively in order to be optimally utilized in the treatment of RHD.

Background: The presence of a chronic total occlusion (CTO) and severe left ventricular (LV) systolic dysfunction are known negative prognostic factors in patients with coronary artery disease. Several studies have examined the effect of CTO revascularization on mortality, symptoms, occurrence of myocardial infarction (MI), and cardiac function in patients with normal or reduced LV function. However, the effect of CTO revascularization on heart failure-related events in patients with LV dysfunction, such as heart failure hospitalization (HFH), the occurrence of atrial fibrillation (AF), and a worsening renal function (WRF), has not yet been evaluated. To assess the success rate and safety of CTO percutaneous coronary interventions (PCIs) in coronary patients with LV ejection fractions of ≤40% and evaluate the impact of successful CTO revascularization on HFH, occurrence of AF, and WRF. Methods: Prospectively, data were collected from CTO PCIs performed at three referral centers and analyzed. From a total of 1435 CTO PCIs, 132 (9.2%) patients with a left ventricular ejection fraction (LVEF) of ≤40% were included in this analysis. The median follow-up duration was 23.18 months (interquartile range (IQR): 11.02–46.66 months). Results: A successful CTO PCI was achieved in 109 of these patients, while the procedure was unsuccessful in 23 patients (82.5% procedural success rate). Overall, the intervention had an acceptable number of peri-procedural (or in-hospital) complications (9.1%). During the follow-up period, the rates of all-cause death, cardiovascular death, and non-fatal MI were not significantly different between the two groups. The rates of HFH were significantly lower in the successful PCI group, while WRF and AF did not differ between successful and unsuccessful PCI groups. Successful PCI and higher estimated glomerular filtration rate (eGFR) were independent predictors of a lower risk of HFH, while prior stroke and diabetes were independent predictors of a higher risk of HFH. Conclusions: In patients with reduced LV systolic function (ejection fraction, EF ≤40%), CTO PCI is a safe and effective procedure and successful CTO PCI is independently associated with a lower risk of HFH during follow-up. Further expansion of this cohort is necessary to confirm these results.

BackgroundModerate severity aortic stenosis (AS) is poorly understood, is associated with subclinical myocardial dysfunction, and can lead to adverse outcome rates that are comparable to severe AS. Factors associated with progressive myocardial dysfunction in moderate AS are not well described. Artificial neural networks (ANNs) can identify patterns, inform clinical risk, and identify features of importance in clinical datasets.MethodsWe conducted ANN analyses on longitudinal echocardiographic data collected from 66 individuals with moderate AS who underwent serial echocardiography at our institution. Image phenotyping involved left ventricular global longitudinal strain (GLS) and valve stenosis severity (including energetics) analysis. ANNs were constructed using two multilayer perceptron models. The first model was developed to predict change in GLS from baseline echocardiography alone and the second to predict change in GLS using data from baseline and serial echocardiography. ANNs used a single hidden layer architecture and a 70%:30% training/testing split.ResultsOver a median follow-up interval of 1.3 years, change in GLS (≤ or >median change) could be predicted with accuracy rates of 95% in training and 93% in testing using ANN with inputs from baseline echocardiogram data alone (AUC: 0.997). The four most important predictive baseline features (reported as normalized % importance relative to most important feature) were peak gradient (100%), energy loss (93%), GLS (80%), and DI

Background: Subclinical LV dysfunction (LVD) identifies heart failure (HF) risk in type 2 diabetes mellitus (T2DM). We sought the extent to which clinical scores (ARIC-HF, WATCH-DM), natriuretic peptides (NTpBNP) and troponin (hs-TnT) were associated with subclinical LV dysfunction (LVD). These associations could inform the ability of these tests to identify which patients should undergo echocardiography. Methods: Participants with T2DM were prospectively recruited from three community-based populations. ARIC-HF risk at 4 years and WATCH-DM scores were calculated from clinical data. NTpBNP and hs-TnT were measured using an electro-chemiluminescence assay. All underwent a comprehensive echocardiogram. We calculated the sensitivity and specificity of clinical scores and biomarkers to identify abnormal global longitudinal strain (GLS ≥ −16%)), diastolic function (E/e' ≥ 14 or e' < 8 cm/s), left atrial volume index (LAV > 34 ml/m2) and LV hypertrophy (LV mass index > 88 g/m2 (F) > 102 g/m2(M)). Results: Of 804 participants (median age 69 years [inter-quartile range (IQR) 65–73], 36% female), clinical scores suggested significant HF risk (median ARIC-HF 8% [IQR 4–12]; WATCH-DM 10 points [IQR 8–12]), and the median NTpBNP was 50 pg/mL [IQR 25–101] and hs-TnT 9.6 pg/mL [IQR 6.8–13.6]. Abnormal GLS was present in 126 (17%), elevated E/e' in 114 (15%), impaired e' in 629 (78%), increased LAV in 351 (44%) and LV hypertrophy in 113 (14%). After adjustments for age, body-mass index, and renal function, each standard deviation increase in NTpBNP was associated with a GLS increase of 0.32 (p < 0.001) and hs-TnT increase by 0.26 (p < 0.001). Similar trends were observed with ARIC-HF (standardised β = 0.22, p < 0.001) and WATCH-DM (standardised β = 0.22, p < 0.001) in univariable analyses. However, none of the risk assessment tools provided satisfactory discrimination for abnormal GLS (AUC 63%), diastolic indices (e' AUC 54–61%) or LV mass (AUC 59–67%). At a sensitivity of 90%, there was an unacceptably low (< 50%) specificity. Conclusion: Although risk assessment based on clinical scores or biomarkers would be desirable to stratify HF risk in people with T2DM, they show a weak relationship with subclinical LVD. [ABSTRACT FROM AUTHOR]

Background: Although studies have proven that liver cirrhosis affects cardiac hemodynamics by means of circulatory overload, they present with definite cardiac functional alteration mostly with end-stage disease. There is limited data on relationship between progression of cirrhosis, cardiac mechanics and sub-clinical dysfunction. This study was done to assess ventricular myocardial mechanics using speckle tracking and deformation imaging among Child-Turcotte-Pugh (CTP) classification A and B cirrhosis. Method: Seventy patients with cirrhosis of Child-Pugh A/B class and sixty-two healthy subjects were prospectively evaluated by standard conventional echocardiography and deformation imaging with rotational echocardiography. Clinical stage of liver cirrhosis was assessed by model for end-stage liver disease (MELD) scores and CTP classification. Results: Mean ages of patients with cirrhosis and controls were 55.64±14 years and 52.24±12 years, respectively. Though left ventricular (LV) dimensions (end diastolic dimension: 47.27±4.6 mm vs. 45.03±3.8 mm, p = 0.003; end systolic dimension: 30.33±4.9 mm vs. 28.40±2.91 mm, p = 0.006) and volumes (end diastolic volume: 82.08±22.53 mL vs. 68.18±15.75 mL, p = 0.001; end systolic volume: 28.60±8.42 mL vs. 22.18±7.48 mL, p = 0.001) were significantly higher in patients with cirrhosis, mean ejection fraction (EF) by Simpsons method was higher among controls (65.83±5.79% vs. 68.35±5.79%, p = 0.009). Left atrial volume was higher in cirrhosis group indicating presence of diastolic dysfunction (41.24±14.10 mL vs. 26.08±6.4 mL, p = 0.001). Global longitudinal strain as assessed by speckle tracking echocardiography did not show statistical significant difference between two groups (−22.35±4.08% vs. −21.80±2.54%, p = 0.348). Median value of torsion parameters in patients with cirrhosis did not differ compared to controls (torsion in degrees: 2.46 vs. 2.79, p = 0.268). Conclusion: Patients with Child-Pugh A and B stages of cirrhosis present with preserved longitudinal strain, normal torsion but with subtle diastolic dysfunction. Higher MELD score may correlate with increased longitudinal strain possibly due to hyperdynamic state. [ABSTRACT FROM AUTHOR]

Background: Covid-19 is multi-system viral infection caused by SARS-CoV-2 virus. Apart from having acute severe respiratory illness causing high mortality, the disease also has a variety of cardiovascular manifestations contributing to morbidity as well as mortality. Cardiac dysfunction and myocarditis are well established complications of Covid-19 as evident in multiple studies after the Covid-19 pandemic. However it is not sufficiently studied in Indian patients either by Echocardiography or by any other imaging modalities like cardiac magnetic resonance imaging (MRI). Methodology: In this study, we analysed the severity of Left ventricular(LV) dysfunction in Covid-19 survivors. A total of 100 consecutive patients of Covid-19 after one month of discharge who had no underlying cardiovascular diseases underwent echocardiography and global longitudinal strain (GLS) imaging. This study cohort included patients with mild 42 (42%),moderate 46(46%) and severe 12(12%) Covid-19 disease as defined by computerised tomography (CT) severity score. Result: We observed that total 36(36%) patients had reduced ejection fraction(EF) which included 11 patients having EF

The treatment of heart failure with reduced ejection fraction HFrEF (< 40%) uses hygienic-dietary rules combined with beta-blockers, renin-angiotensin system blockers RASB (alone or in combination with Sacubitril) and spironolactone. Dapagliflozin (SGLT2 inhibitor) has proven its effectiveness in reducing morbi-mortality in patients with HF. However, its effects on echocardiographic parameters are less known. To describe the impact of the addition of Dapagliflozin to conventional treatment on echocardiographic parameters in patients with HFrEF < 40%. Observational, single-center and non-randomized study involving patients with HFrEF < 40%. This group was compared to a cohort of 50 patients with HfrEF < 40% under conventional treatment without Dapagliflozin (taken from the HF register of our center and whose management dates back to before the adoption of this molecule in the HF ESC-2021 guidelines) to assess the ultrasound impact of Dapagliflozin. 43 patients aged between 40 and 68 years with HfrEF < 40% on Beta-blocker, BSRA, Spironolactone and Dapagliflozin 10 mg/d. The mean EF was 33% ± 3 (30–39%), mean LVd diameter 64 mm ± 6 (55–71 mm) and mean longitudinal strain at -11% ± 4. These patients were compared to a cohort of 50 patients with the same profile without Dapagliflozin. After a follow-up of 7 months (5–8 months): The average EF increased to 37% with 11 patients EF > 40% against 35% and 5 patients EF > 40% for the group without Dapagliflozin (P 0.057), average LVd at 61 mm versus 66 mm in the group without Dapagliflozin (P 0.095), Mean longitudinal strain at −14% (6 patients < −15) versus −12% (1 patient <−15) in the group without Dapagliflozin (P 0.046). In a population of patients with HfrEF < 40% under conventional treatment for HF, the prescription of Dapagliflozin is associated with an improvement of echocardiographic parameters (EF and longitudinal strain). Série;Dapagliflozine;insuffisance cardiaque;strain;ProBNP;dysfonction VG [ABSTRACT FROM AUTHOR]

The purpose of this study was to evaluate the early alterations of left ventricular (LV) structure and function in type 2 diabetes mellitus (T2DM) patients with or without obstructive sleep apnoea (OSA) using 3 D speckle tracking echocardiography (3DSTE). Eighty T2DM patients with preserved LVEF were included, half of whom had OSA as co-morbidity. Forty age- and sex-matched controls were also enrolled. LV structure and function were evaluated by conventional echocardiography and 3DSTE. LV global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS) were all measured by 3DSTE. Four geometric patterns (normal geometry, concentric remodelling, concentric and eccentric hypertrophy) occupied significantly different proportions within the three groups (p =.014). LV remodelling made up higher shares in two T2DM groups than in the controls, whereas LV hypertrophy appeared most frequently in the patients with T2DM and OSA. The patients with T2DM alone had significantly lower GLS and GCS than the controls (both p <.01). The patients with T2DM and OSA had significantly lower GLS, GCS, GAS, and GRS than the controls and the patients with T2DM alone (all p <.01). Fasting plasma glucose (FPG), OSA and BMI had negative impacts on all and part of the strain values in T2DM patients. The T2DM patients with moderate-to-severe OSA showed significantly lower GLS, GCS, GAS, and GRS than those with mild OSA (all p <.05). The 3DSTE plus conventional echocardiography could detect the sub-clinical LV alterations in T2DM patients with or without OSA. [ABSTRACT FROM AUTHOR]

Abstract Background The purpose of this study is to evaluate cardiac functions using transthoracic echocardiography, change in lead parameters and electrocardiogram (ECG) morphology in patients undergoing permanent pacemaker implantation over a follow-up period of 6 months. Methods This is a prospective study in patients undergoing permanent pacemaker implantation in a tertiary care hospital. Patients undergoing permanent pacemaker implantation were enrolled for up to one year and Echocardiographic parameters (by 2 blind operators) and ECG parameters were recorded at admission (within 24 h), before discharge (within 7 days of pacemaker implantation), after 1 month (± 7 days) and after 6 months (± 7 days) of follow-up. Results A total of 96 patients (60.4% males and 39.6% female, mean age 66.65 years) were implanted with permanent pacemaker. The mean QRS duration was 133.18 ms and increased significantly to 146.03 ms by 6 months despite septal lead placement in majority (92%) of patients. The mean baseline ejection fraction of 51.47 decreased significantly to 47.83 by 6 months. Diastolic parameters like left atrial volume index, early to late diastolic transmitral flow velocity (E/A) and early diastolic mitral annular tissue velocity (E/e′) showed a significant increase (> 5%) from baseline by the end of first week. By the end of first month, systolic dysfunction of RV sets in with significant (> 5%) change from baseline in parameters like Right ventricle myocardial performance index, transannular plane systolic excursion and right ventricle systolic excursion velocity (RVS′). Conclusion We have observed that pacemaker recipients with baseline reduced left ventricle (LV) systolic functions perform significantly worse compared to those with baseline normal cardiac functions and had a higher rate of deterioration of LV function. RV dysfunction is the first abnormality that occurs, by 1 week followed by LV dysfunction which starts by 1 month and the diastolic dysfunctions precede the systolic dysfunction. QRS duration also showed a gradual increase despite septal lead placement in majority (92%) and lead parameters showed no significant change over 6 months.

Abstract Background Doxorubicin (DOX) is widely used as an effective chemotherapeutic agent for cancers; however, DOX induces cardiac toxicity, called DOX-induced cardiomyopathy. Although DOX-induced cardiomyopathy is known to be associated with a high cumulative dose of DOX, the mechanisms of its long-term effects have not been completely elucidated. Pioglitazone (Pio) is presently contraindicated in patients with symptomatic heart failure owing to the side effects. The concept of drug repositioning led us to hypothesize the potential effects of Pio as a premedication before DOX treatment, and to analyze this hypothesis in mice. Methods First, for the hyperacute (day 1) and acute (day 7) DOX-induced dysfunction models, mice were fed a standard diet with or without 0.02% (wt/wt) Pio for 5 days before DOX treatment (15 mg/kg body weight [BW] via intraperitoneal [i.p.] administration). The following 3 treatment groups were analyzed: standard diet + vehicle (Vehicle), standard diet + DOX (DOX), and Pio + DOX. Next, for the chronic model (day 35), the mice were administrated DOX once a week for 5 weeks (5 mg/kg BW/week, i.p.). Results In the acute phase after DOX treatment, the percent fractional shortening of the left ventricle (LV) was significantly decreased in DOX mice. This cardiac malfunction was improved in Pio + DOX mice. In the chronic phase, we observed that LV function was preserved in Pio + DOX mice. Conclusions Our findings may provide a new pathophysiological explanation by which Pio plays a role in the treatment of DOX-induced cardiomyopathy, but the molecular links between Pio and DOX-induced LV dysfunction remain largely elusive.

We present a case of reversible left ventricular (LV) dysfunction with characteristic stress or "Takotsubo" cardiomyopathy (SCM) after therapeutic pericardiocentesis in a patient with tubercular pericardial effusion. SCM following pericardiocentesis is uncommon, as opposed to the well-defined entity, pericardial decompression syndrome (PDS). PDS is defined as a paradoxical deterioration of hemodynamics and development of severe biventricular dysfunction, cardiogenic shock, and pulmonary edema after uneventful, often large volume pericardiocentesis in patients of pericardial effusion.

We present a case of reversible left ventricular (LV) dysfunction with characteristic stress or «Takotsubo» cardiomyopathy (SCM) after therapeutic pericardiocentesis in a patient with tubercular pericardial effusion. SCM following pericardiocentesis is uncommon, as opposed to the well-defined entity, pericardial decompression syndrome (PDS). PDS is defined as a paradoxical deterioration of hemodynamics and development of severe biventricular dysfunction, cardiogenic shock, and pulmonary edema after uneventful, often large volume pericardiocentesis in patients of pericardial effusion. [ABSTRACT FROM AUTHOR]

This study identified predictors of clinical (CR) and echocardiographic response (ER) following immunosuppressive therapy (IST) in patients with cardiac sarcoidosis (CS). IST has been the cornerstone of treatment for patients with CS and active myocardial inflammation. However, there are little data to explain the variable response to IST in CS. Data of 96 consecutive patients with CS from the Granulomatous Myocarditis Registry were analyzed. All patients underwent a 18fluorodeoxy glucose positron emission tomography−computed tomography (18FDG-PET-CT) before initiation of IST. Response was assessed after 4 to 6 months of therapy. CR was defined as an improvement in functional class (New York Heart Association functional class ≥I) and freedom from ventricular arrhythmias and heart failure hospitalizations. ER was defined as an improvement in left ventricular ejection fraction (LVEF) ≥10%. ER was assessed only in patients with a LVEF <50%. Complete responders had no residual myocardial FDG uptake and fulfilled both response criteria. Partial responders fulfilled only 1 response criteria or had residual FDG uptake. Nonresponders did not fulfill either CR or ER criteria. The uptake index (UI) was defined as the product of maximum standardized uptake value and the number of LV segments with abnormal uptake on 18FDG-PET-CT. Among 91 patients included in the final analysis, 54.9%, 20.9%, and 24.2% of patients were classified as complete and partial responders and nonresponders, respectively. Cox regression analysis (all responders vs. nonresponders) identified the following as independent predictors of response following immunosuppression: LVEF >40% (hazard ratio: 1.61; 95% confidence interval: 1.06 to 7.69; p = 0.031) and myocardial UI >30 (hazard ratio: 1.28; 95% confidence interval: 1.05 to 6.12; p = 0.010). The final model had a good discriminative power (area under the curve [AUC]: 0.85) and predictive accuracy (sensitivity: 85.5%; specificity: 86.4%). Pre-treatment myocardial UI had a strong positive correlation with change in LVEF following immunosuppression. Pre-treatment 18FDG myocardial uptake was a predictor of CR and ER response to immunosuppression in patients with CS. [Display omitted] [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX, an anthracycline) is a widely used chemotherapy agent against various forms of cancer; however, it is also known to induce dose-dependent cardiotoxicity leading to adverse complications. Investigating the underlying molecular mechanisms and strategies to limit DOX-induced cardiotoxicity might have potential clinical implications. Our previous study has shown that expression of microRNA-377 (miR-377) increases in cardiomyocytes (CMs) after cardiac ischemia-reperfusion injury in mice, but its specific role in DOX-induced cardiotoxicity has not been elucidated. In the present study, we investigated the effect of anti-miR-377 on DOX-induced cardiac cell death, remodeling, and dysfunction. We evaluated the role of miR-377 in CM apoptosis, its target analysis by RNA sequencing, and we tested the effect of AAV9-anti-miR-377 on DOX-induced cardiotoxicity and mortality. DOX administration in mice increases miR-377 expression in the myocardium. miR-377 inhibition in cardiomyocyte cell line protects against DOX-induced cell death and oxidative stress. Furthermore, RNA sequencing and Gene Ontology (GO) analysis revealed alterations in a number of cell death/survival genes. Intriguingly, we observed accelerated mortality and enhanced myocardial remodeling in the mice pretreated with AAV9-anti-miR-377 followed by DOX administration as compared to the AAV9-scrambled-control-pretreated mice. Taken together, our data suggest that in vitro miR-377 inhibition protects against DOX-induced cardiomyocyte cell death. On the contrary, in vivo administration of AAV9-anti-miR-377 increases mortality in DOX-treated mice.

Background Subclinical left ventricular dysfunction detected by 2‐dimensional global longitudinal strain post breast radiotherapy has been described in patients with breast cancer. We hypothesized that left ventricular dysfunction postradiotherapy may be site specific, based on differential segmental radiotherapy dose received. Methods and Results Transthoracic echocardiograms were performed at baseline, 6 weeks, and 12 months postradiotherapy on 61 chemotherapy‐naïve women with left‐sided breast cancer undergoing tangential breast radiotherapy. Radiation received within basal, mid, and apical regions for the 6 left ventricular walls was quantified from the radiotherapy treatment planning system. Anterior, anteroseptal, and anterolateral walls received the highest radiation doses, while inferolateral and inferior walls received the lowest. There was a progressive increase in the radiation dose received from basal to apical regions. At 6 weeks, the most significant percentage deterioration in strain was seen in the apical region, with greatest reductions in the anterior wall followed by the anteroseptal and anterolateral walls, with a similar pattern persisting at 12 months. There was a within‐patient dose–response association between the segment‐specific percentage deterioration in strain at 6 weeks and 12 months and the radiation dose received. Conclusions Radiotherapy for left‐sided breast cancer causes differential segmental dysfunction, with myocardial segments that receive the highest radiation dose demonstrating greatest strain impairment. Percentage deterioration in strain observed 6 weeks postradiotherapy persisted at 12 months and demonstrated a dose–response relationship with radiotherapy dose received. Radiotherapy‐induced subclinical cardiac dysfunction is of importance because it could be additive to chemotherapy‐related cardiotoxicity in patients with breast cancer. Long‐term outcomes in patients with asymptomatic strain reduction require further investigation.

Background: Doxorubicin (DOX) is widely used as an effective chemotherapeutic agent for cancers; however, DOX induces cardiac toxicity, called DOX-induced cardiomyopathy. Although DOX-induced cardiomyopathy is known to be associated with a high cumulative dose of DOX, the mechanisms of its long-term effects have not been completely elucidated. Pioglitazone (Pio) is presently contraindicated in patients with symptomatic heart failure owing to the side effects. The concept of drug repositioning led us to hypothesize the potential effects of Pio as a premedication before DOX treatment, and to analyze this hypothesis in mice. Methods: First, for the hyperacute (day 1) and acute (day 7) DOX-induced dysfunction models, mice were fed a standard diet with or without 0.02% (wt/wt) Pio for 5 days before DOX treatment (15 mg/kg body weight [BW] via intraperitoneal [i.p.] administration). The following 3 treatment groups were analyzed: standard diet + vehicle (Vehicle), standard diet + DOX (DOX), and Pio + DOX. Next, for the chronic model (day 35), the mice were administrated DOX once a week for 5 weeks (5 mg/kg BW/week, i.p.). Results: In the acute phase after DOX treatment, the percent fractional shortening of the left ventricle (LV) was significantly decreased in DOX mice. This cardiac malfunction was improved in Pio + DOX mice. In the chronic phase, we observed that LV function was preserved in Pio + DOX mice. Conclusions: Our findings may provide a new pathophysiological explanation by which Pio plays a role in the treatment of DOX-induced cardiomyopathy, but the molecular links between Pio and DOX-induced LV dysfunction remain largely elusive. [ABSTRACT FROM AUTHOR]

Background: The superiority of surgical revascularization in ischemic cardiomyopathy is established beyond doubt, and off‐pump CABG (OP‐CABG) is a safe way of revascularization in this high‐risk subset. Data on the effect of postoperative ventricular function and size on their midterm outcome is scarce. Materials and Methods: A retrospective study was done on 211 consecutive patients with severe LV dysfunction who underwent OP‐CABG from January 2017 to December 2018. Data were collected from the institutional database. Their operative and midterm outcomes were statistically analyzed. Results: The mean age of the cohort was 58.4 ± 8.3 years. An average number of grafts was 3.1 ± 0.8 (cumulative intended number of grafts—3). Operative mortality was 10.9%. Preoperative NYHA class (p <.0001; OR, 19.72) and postoperative IABP insertion (p <.008; OR, 88.75) were independent predictors of operative mortality. The mean follow‐up period was 3.14 ± 0.07 years, was 97.4% complete with cardiac mortality of 5.8%. Postoperative LVEF (p =.002; OR, 0.868) and LV dimensions (systole & diastole) (p =.013, OR = 1.182 and p =.036, OR = 1.184, respectively) were independent predictors of midterm mortality. Midterm major adverse cardiovascular event‐free survival of operative survivors was 89%. There was no correlation between postoperative LV dimension and NYHA status(p >.05). Myocardial viability was not associated with early (p =.17) or midterm mortality (p =.676). Conclusion: OP‐CABG can achieve complete revascularization in patients with severe LV dysfunction with good midterm outcomes, albeit with high early operative mortality. Postoperative change in LV dimension and EF are predictors of midterm mortality. [ABSTRACT FROM AUTHOR]

Abstract Supplemental oxygen (O2) therapy in preterm infants impairs lung development, but the impact of O2 on long‐term systemic vascular structure and function has not been well‐explored. The present study tested the hypothesis that neonatal O2 therapy induces long‐term structural and functional alterations in the systemic vasculature, resulting in vascular stiffness observed in children and young adults born preterm. Newborn Sprague‐Dawley rats were exposed to normoxia (21% O2) or hyperoxia (85% O2) for 1 and 3 weeks. A subgroup exposed to 3 weeks hyperoxia was recovered in normoxia for an additional 3 weeks. Aortic stiffness was assessed by pulse wave velocity (PWV) using Doppler ultrasound and pressure myography. Aorta remodeling was assessed by collagen deposition and expression. Left ventricular (LV) function was assessed by echocardiography. We found that neonatal hyperoxia exposure increased vascular stiffness at 3 weeks, which persisted after normoxic recovery at 6 weeks of age. These findings were accompanied by increased PWV, aortic remodeling, and altered LV function as evidenced by decreased ejection fraction, cardiac output, and stroke volume. Importantly, these functional changes were associated with increased collagen deposition in the aorta. Together, these findings demonstrate that neonatal hyperoxia induces early and sustained biomechanical alterations in the systemic vasculature and impairs LV function. Early identification of preterm infants who are at risk of developing systemic vascular dysfunction will be crucial in developing targeted prevention strategies that may improve the long‐term cardiovascular outcomes in this vulnerable population.

Gastrointestinal stromal tumors (GISTs) are rare and current estimates range from 4,000 to 6,000 number of GIST cases in the USA annually. Imatinib, a tyrosine kinase inhibitor, has shown a survival benefit in GISTs, and the presence of KIT mutation status is predictive of response. The current case discusses rapidly progressive dyspnea and heart failure in an elderly male with metastatic GIST who was started on imatinib. Although reported as a rare and sporadic side effect of imatinib, the current case illustrates rapidity and the clinical significance of cardiotoxicity, with onset at 2 weeks. Cases of imatinib-induced cardiotoxicity can range from being mild ventricular dysfunction to overt heart failure. Prior to starting imatinib, our patient had a history of hypertension. He subsequently ended up developing heart failure as acknowledged by the echocardiogram (ECHO). In general, elderly with preexisting cardiovascular comorbidity are at greater risk. The goal in such situations is immediate discontinuation or reduction of the imatinib dosage. The case prompts for awareness of imatinib cardiotoxicity. Moreover, a pretreatment cardiac assessment along with monitoring throughout therapy is therefore advisable. Also, imatinib-induced cardiotoxicity should be differentiated from imatinib-associated fluid retention, in which ECHO findings can be normal. This case report raises the concern for accelerated cardiotoxicity profile of imatinib. Further prospective studies with multidisciplinary input are needed to establish this association further.

Salusin-β is a newly defined biomarker that plays a role in atherogenesis and in homeostasis. The study aimed to assess serum salusin-β level in relation to atherosclerosis and ventricular dysfunction in type 2 diabetes mellitus (T2DM) patients. Sixty T2DM patients and twenty-five age-matched healthy controls were included. Serum salusin-β was determined by ELISA. Echocardiography and carotid ultrasonography were carried out for all individuals. Serum salusin-β level was significantly elevated in patients with T2DM than in controls (P < 0.001). It was positively correlated with obesity parameters, insulin resistance index (r = 0.280,P < 0.001), atherogenic dyslipidemia and with carotid intima media thickness (CIMT) (r = 0.411, P < 0.001). Echocardiographic findings showed a positive correlation between salusin-β and left ventricular hypertrophy (LVH) parameters and a negative correlation with left ventricular (LV) diastolic and systolic functions. Regression analysis showed that serum salusin-β level was a significant predictor of diastolic dysfunction. Serum salusin-β may be associated with atherosclerosis and LV dysfunction in T2DM. ∙ Serum levels of Salusin-β were found to be elevated in type 2 diabetes patients. ∙ Salusin-β positively correlated with obesity indices, insulin resistance index, dysglycemic and dyslipidemic variables. ∙ Serum salusin-β levels correlated with carotid mean-IMT, left ventricular hypertrophy and dysfunction. ∙ Serum salusin-β may serve as a predictor of diastolic dysfunction in type 2 diabetes patients. [ABSTRACT FROM AUTHOR]

Patients with severe aortic stenosis are classified according to flow-gradient patterns. We investigated whether left ventricular (LV) mechanical dispersion, a marker of dyssynchrony and predictor of mortality, is associated with low-flow status in aortic stenosis. 316 consecutive patients with aortic stenosis and QRS duration < 120 ms were included in the retrospective analysis. Patients with severe aortic stenosis (aortic valve area ≤ 1.0 cm2) were classified as normal-flow (NF; stroke volume index > 35 ml/m2) high-gradient (HG; mean transvalvular gradient ≥ 40 mmHg) (n = 79), NF low-gradient (LG) (n = 62), low-flow (LF) LG ejection fraction (EF) ≥ 50% (n = 57), and LF LG EF < 50% (n = 23). Patients with moderate aortic stenosis (aortic valve area 1.5-1.0 cm2; n = 95) served as comparison group. Mechanical dispersion (calculated as standard deviation of time from Q/S onset on electrocardiogram to peak longitudinal strain in 17 left ventricular segments) was similar in patients with NF HG (49.4 ± 14.7 ms), NF LG (43.5 ± 12.9 ms), LF LG EF ≥ 50% (47.2 ± 16.3 ms) and moderate aortic stenosis (44.2 ± 15.7 ms). In patients with LF LG EF < 50%, mechanical dispersion was increased (60.8 ± 20.7 ms, p < 0.05 vs. NF HG, NF LG, LF LG EF ≥ 50% and moderate AS). Mechanical dispersion correlated with global longitudinal strain (r = 0.1354, p = 0.0160) and heart rate (r = 0.1587, p = 0.0047), but not with parameters of aortic stenosis. Mechanical dispersion was similar among flow-gradient subgroups of severe aortic stenosis with preserved LVEF, but increased in patients with low-flow low-gradient and reduced LVEF. These findings indicate that mechanical dispersion is rather a marker of systolic myocardial dysfunction than of aortic stenosis. [ABSTRACT FROM AUTHOR]

Purposes: The purposes of our study were to determine the risk factors related to metabolic left ventricular remodeling (LVR) in type 2 diabetes mellitus (T2DM) patients and to assess the LV function with different geometry in such population. Methods: Seventy‐eight T2DM patients with normal 2D‐LVEF (≥55%) were enrolled and divided into two groups with LV normal geometry (LVN) and with LV remodeling (LVR). The control group was composed of forty age‐ and sex‐matched healthy individuals with LVN. A multifactor logistic regression was used to determine the risk factors for LVR, and their diagnostic values were evaluated using the area under the ROC curves (AUC). Three‐dimensional speckle tracking echocardiography (3DSTE) was used to measure LV global longitudinal strain (GLS), global circumferential strain (GCS), global area strain (GAS), and global radial strain (GRS). Results: Fasting plasma glucose (FPG), hyperlipidemia, and BMI were independently associated with LVR in T2DM patients, and the AUC values were 0.699, 0.697, and 0.732, respectively. The T2DM patients with LVN showed significantly lower GLS than the controls (P < 0.05), whereas the T2DM patients with LVR showed significantly lower GLS, GCS, GAS, and GRS than the T2DM patients with LVN (all P < 0.01). Additionally, GLS, GAS, and GRS values decreased significantly in the T2DM patients with LV hypertrophy than in those with LV concentric remodeling (all P < 0.05). Conclusions: The routine echocardiography and 3DSTE could be used in combining way to detect the metabolic LV remodeling and accompanied dysfunction in T2DM patients. [ABSTRACT FROM AUTHOR]

Aim: Role of PET-CT in assessment of myocardial viability in patients with LV dysfunction. Methods: This prospective study included 120 patients with LV dysfunction who underwent 99mTechnetium-Sestamibi myocardial perfusion SPECT-CT and 18FFDG cardiac PET-CT. They also underwent serial echocardiography and coronary angiography along with myocardial perfusion and FDG PET study. Results: Thirty-three patients had single vessel disease, 48 had triple vessel disease, and rest had double vessel disease. Among 786 segments, matched defects were seen in 432 (55%) and mismatched defects in 354 (45%) segments. 78 patients were surgically managed, and 42 were medically managed. The change in LVEF after surgical management was statistically significant compared to medical management. Conclusion: Viability assessment should be performed in patients who present after 12 h of acute myocardial infarction or with LV dysfunction due to ischemic heart disease to decide upon appropriate surgical management.

Background: Landiolol effectively controls rapid heart rate in atrial fibrillation or flutter (AF/AFL) patients with left ventricular (LV) dysfunction. However, predicting landiolol Responders and Non-Responders and patients who will experience adverse effects remains a challenge. The aim of this study was to clarify the potential applicability of landiolol for rapid AF/AFL and refractory ventricular tachyarrhythmias (VTs) in patients with heart failure. Methods: A total of 39 patients with AF/AFL with ventricular response ≥120 bpm and 12 VTs were retrospectively enrolled. Landiolol Responders for rapid AF/AFL were defined as patients whose ventricular response was suppressed to less than 110 bpm or decreased by ≥20% from the initial heart rate after administration of landiolol. Responders for VTs were defined as patients with no recurrent VTs during the 24 h after the initiation of landiolol. Results: For AF/AFL, 29 patients (74%) were Responders. In nine patients (31%), AF was spontaneously terminated after starting landiolol. Eight Non-Responders (80%) needed to have AF terminated by cardioversion. Left ventricular ejection fraction (LVEF) at baseline was significantly associated with landiolol efficacy. For VTs, seven patients (58%) were Responders, and smaller LV diastolic and systolic diameters were associated with landiolol efficacy. Hypotension after landiolol treatment occurred in 5 of 51 patients, and lower LV systolic function was associated with the development of adverse events. Conclusions: Landiolol is effective in patients with heart failure not only due to rapid AF/AFL but also due to VTs. However, preserved LVEF is important for efficacy and safety in landiolol treatment.

Fever with rash is one of the most common causes of referral to a dermatologist. A plethora of conditions need to be considered in the differential diagnosis. They may be broadly classified into infectious causes, drug reactions, and autoimmune disorders. Here we present a rare case of rickettsial fever with cardiac involvement in an elderly male patient with no comorbidities.

Gastrointestinal stromal tumors (GISTs) are rare and current estimates range from 4,000 to 6,000 number of GIST cases in the USA annually. Imatinib, a tyrosine kinase inhibitor, has shown a survival benefit in GISTs, and the presence of KIT mutation status is predictive of response. The current case discusses rapidly progressive dyspnea and heart failure in an elderly male with metastatic GIST who was started on imatinib. Although reported as a rare and sporadic side effect of imatinib, the current case illustrates rapidity and the clinical significance of cardiotoxicity, with onset at 2 weeks. Cases of imatinib-induced cardiotoxicity can range from being mild ventricular dysfunction to overt heart failure. Prior to starting imatinib, our patient had a history of hypertension. He subsequently ended up developing heart failure as acknowledged by the echocardiogram (ECHO). In general, elderly with preexisting cardiovascular comorbidity are at greater risk. The goal in such situations is immediate discontinuation or reduction of the imatinib dosage. The case prompts for awareness of imatinib cardiotoxicity. Moreover, a pretreatment cardiac assessment along with monitoring throughout therapy is therefore advisable. Also, imatinib-induced cardiotoxicity should be differentiated from imatinib-associated fluid retention, in which ECHO findings can be normal. This case report raises the concern for accelerated cardiotoxicity profile of imatinib. Further prospective studies with multidisciplinary input are needed to establish this association further. [ABSTRACT FROM AUTHOR]

Background: In the American College of Cardiology/American Heart Association guidelines, patients are considered to have true-severe stenosis when the mean gradient (MG) is ≥40 mm Hg with an aortic valve area (AVA) ≤1 cm2 during dobutamine stress echocardiography (DSE). However, these criteria have not been previously validated.Objectives: The aim of this study was to assess the value of these criteria to predict the presence of true-severe AS and the occurrence of death in patients with low-flow, low-gradient aortic stenosis (LF-LG AS).Methods: One hundred eighty-six patients with low left ventricular ejection fraction (LVEF) LF-LG AS were prospectively recruited and underwent DSE, with measurement of the MG, AVA, and the projected AVA (AVAProj), which is an estimate of the AVA at a standardized normal flow rate. Severity of AS was independently corroborated by macroscopic evaluation of the valve at the time of valve replacement in 54 patients, by measurement of the aortic valve calcium by computed tomography in 25 patients, and by both methods in 8 patients. According to these assessments, 50 of 87 (57%) patients in the study cohort had true-severe stenosis.Results: Peak stress MG ≥40 mm Hg, peak stress AVA ≤1 cm2, and the combination of peak stress MG ≥40 mm Hg and peak stress AVA ≤1 cm2 correctly classified AS severity in 48%, 60%, and 47% of patients, respectively, whereas AVAProj ≤1 cm2 was better than all the previous markers (p < 0.007), with 70% correct classification. Among the subset of 88 patients managed conservatively (47% of the cohort), 52 died during a follow-up of 2.8 ± 2.5 years. After adjustment for age, sex, functional capacity, chronic kidney failure, and peak stress LVEF, peak stress MG and AVA were not predictors of mortality in this subset. In contrast, AVAProj ≤1 cm2 was a strong predictor of mortality under medical management (hazard ratio: 3.65; p = 0.0003).Conclusions: In patients with low LVEF LF-LG AS, the DSE criteria of a peak stress MG ≥40 mm Hg, or the composite of a peak stress MG ≥40 mm Hg and a peak stress AVA ≤1 cm2 proposed in the guidelines to identify true-severe AS and recommend valve replacement, have limited value to predict actual stenosis severity and outcomes. In contrast, AVAProj better distinguishes true-severe AS from pseudo-severe AS and is strongly associated with mortality in patients under conservative management. (Multicenter Prospective Study of Low-Flow Low-Gradient Aortic Stenosis [TOPAS]; NCT01835028). [ABSTRACT FROM AUTHOR]