Systolic Impairment Research Articles

Evaluation of the relationship between ventricular end-diastolic pressure and echocardiographic measures of diastolic function in adults with a Fontan circulation

BackgroundEchocardiographic assessment of diastolic function in the setting of Fontan physiology is not well validated. We recently demonstrated that atrioventricular systolic to diastolic duration ratio (AVV S/D ratio) independently predicts mortality in Fontan-adults and that a value >1.1 was associated with poor prognosis. PurposeTo correlate echocardiographic measures of diastolic function with direct measurement of ventricular end-diastolic pressure (VEDP). MethodsA retrospective analysis was undertaken of Fontan-adults who had transthoracic echocardiography (TTE) within 12 months of direct measurement of VEDP during cardiac catheterisation. ResultsFifteen Fontan adults (3 males, mean age 29 ± 9 years) were evaluated. Thirteen patients had dominant morphologic left ventricle and 2 had morphologic right ventricle. Four had atriopulmonary connection and 11 had total cavopulmonary connection. Twelve patients were NYHA Class I/II and 3 were Class III. Time between TTE and cardiac catheter was 46 ± 113 days; VEDP was 8 ± 5 mmHg. Ten patients had preserved ventricular function, 3 had mild and 2 had moderate systolic impairment by subjective TTE assessment. AVV S/D ratio had the strongest correlation with VEDP (r = 0.8, p = 0.001). AVV S/D ratio ≥ 1.1 had 100% positive predictive value and 92% negative predictive value for detecting VEDP >10 mmHg. The only conventional echocardiographic measure of diastolic function that correlated with VEDP was pulmonary vein A wave - atrioventricular A wave duration difference (r = 0.8, p = 0.02). ConclusionsTTE measures reflect VEDP in adults with a Fontan circulation. AVV S/D ratio is a simple parameter yet to enter standard practice that can be used to identify elevated VEDP.

Left Ventricle Function During Therapeutic Hypothermia with Beta1-Adrenergic Receptor Blockade.

Therapeutic hypothermia is an established treatment in patients resuscitated from cardiac arrest. It is usually well-tolerated circulatory, but hypothermia negatively effects myocardial contraction and relaxation velocities and increases diastolic filling restrictions. A significant proportion of resuscitated patients are treated with long-acting beta-receptor blocking agents' prearrest, but the combined effects of hypothermia and beta-blockade on left ventricle (LV) function are not previously investigated. We hypothesized that beta1-adrenergic receptor blockade (esmolol infusion) exacerbates the negative effects of hypothermia on active myocardial motions, affecting both systolic and diastolic LV function. A pig (n = 10) study was performed to evaluate the myocardial effects of esmolol during hypothermia (33°C) and during normothermia, at spontaneous and pacing-increased heart rates (HRs). LV function was assessed by a LV pressure transducer, an epicardial ultrasonic transducer (wall thickness, wall thickening/thinning velocity) and an aortic ultrasonic flow-probe (stroke volume, cardiac output). The data were compared using a paired two-tailed Students t-test, and also analyzed using a linear mixed model to handle dependencies introduced by repeated measurements within each subject. The significance level was p ≤ 0.05. The effects of hypothermia and beta blockade were distinct and additive. Hypothermia reduced myocardial motion velocities and increased diastolic filling restrictions, but end-systolic wall thickness increased, and stroke volume and dP/dtmax (pumping function) were maintained. In contrast, esmolol predominantly affected systolic pumping function, by a negative inotropic effect. In combination, hypothermia and esmolol reduced myocardial velocities in systole and diastole by ∼40%, compared with normothermia without esmolol, inducing in combination both systolic and diastolic LV function impairment. The cardiac dysfunction deteriorated at increased HRs during hypothermia. Beta1-adrenergic receptor blockade (esmolol) exacerbates the negative effects of hypothermia on active myocardial contraction and relaxation. The combination of hypothermia with beta-blockade induces both systolic and diastolic LV function impairment.

Right heart impairement in cirrhotic patients

Right ventricular dysfunction in cirrhotic patients is not well described, we suggest that cirrhosis will result in an increase of pulmonary resistance and the post-charge of RV, we aim to assess ventricle function in cirrhotic patients and the correlation between the severity of cirrhosis and the RV dysfunction. We assessed echocardiographic RV systolic function in 80 patients with cirrhosis. We compared compensated ( n = 39) and uncompensated patients ( n = 41) to controls ( n = 80). The severity of cirrhotic disease was assessed by Child and Mild scores. RV was significantly enlarged in cirrhotic patients compared to controls and in uncompensated patients compared to compensated patients (RV diastolic area = 16.7 ± 5 cm 2 , 14.5 ± 4 cm 2 , P = 0.01). The TAPSE and the S wave were significantly lower in cirrhotic patients ( P = 0.007) compared to controls but there were no difference between the sub-groups. Longitudinal peak systolic speckle tracking of lateral RV wall was significantly decreased in cirrhotic patients ( P < 0.001). There was no correlation between the different parameters of the RV and Child as well as Mild scores. The present study illustrated RV systolic function impairment in cirrhotic patients. The lack of correlation between the right ventricle dysfunction and the severity of cirrhosis suggest a complex mechanism. Right ventricular dysfunction in cirrhotic patients is not well described, we suggest that cirrhosis will result in an increase of pulmonary resistance and the post-charge of RV, we aim to assess ventricle function in cirrhotic patients and the correlation between the severity of cirrhosis and the RV dysfunction. We assessed echocardiographic RV systolic function in 80 patients with cirrhosis. We compared compensated ( n = 39) and uncompensated patients ( n = 41) to controls ( n = 80). The severity of cirrhotic disease was assessed by Child and Mild scores. RV was significantly enlarged in cirrhotic patients compared to controls and in uncompensated patients compared to compensated patients (RV diastolic area = 16.7 ± 5 cm 2 , 14.5 ± 4 cm 2 , P = 0.01). The TAPSE and the S wave were significantly lower in cirrhotic patients ( P = 0.007) compared to controls but there were no difference between the sub-groups. Longitudinal peak systolic speckle tracking of lateral RV wall was significantly decreased in cirrhotic patients ( P < 0.001). There was no correlation between the different parameters of the RV and Child as well as Mild scores. The present study illustrated RV systolic function impairment in cirrhotic patients. The lack of correlation between the right ventricle dysfunction and the severity of cirrhosis suggest a complex mechanism.

Use of Advanced Cardiac Imaging in the Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy

A 22-year-old male student presented to his general practitioner with chest discomfort and palpitations. There were no exertional symptoms or syncope and no family history of cardiac disease or sudden death. Cardiovascular examination was unremarkable. Echocardiogram demonstrated sinus bradycardia with epsilon waves in the inferior leads and abnormal T-wave morphology in the anterior leads. Seven beats of non–sustained ventricular tachycardia and frequent ventricular ectopy were present during cardiac monitoring. Transthoracic echocardiography demonstrated a dilated, dyskinetic right ventricle (RV) with systolic impairment (Figure 1) and impaired RV ventricular strain (Figure 2). There was mildly reduced left ventricular (LV) systolic function (LV ejection fraction 52%). Computed tomography coronary angiogram established normal coronary anatomy. Cardiac magnetic resonance imaging revealed segmental LV and RV dysfunction with regional fibrosis in both ventricles, predominantly affecting the right (RV ejection fraction 37%). There was severe dilatation of the RV (end diastolic volume 156 mL/m2; (Figure 3). The mid-inferior, mid-distal RV free wall, and RV outflow tract were akinetic. Post–gadolinium delayed enhancement was consistent with a non–ischaemic aetiology. The main differentials were arrhythmogenic right ventricular cardiomyopathy and cardiac sarcoidosis, the latter was excluded with a negative positron emission tomography scan. A subcutaneous implantable defibrillator was implanted for primary prevention of sudden cardiac death and the patient was started on ramipril 2.5 mg and bisoprolol 1.25 mg. He is being followed-up regularly and remains well. Proband genetic testing and family screening of first-degree relatives for arrhythmogenic right ventricular cardiomyopathy has been advised. This case illustrates the incremental value of multimodality imaging in the diagnosis of this rare but potentially life-threatening condition. Figure 2 View Large Image Figure Viewer Download Hi-res image Figure 3 View Large Image Figure Viewer Download Hi-res image

The Assessment of Left Ventricle Function and Subclinical Atherosclerosis in Patients with Acute Myeloid Leukemia.

Thirty patients diagnosed with AML with no cardiac history, having LV ejection fraction (LVEF) >50%, were evaluated at baseline and 6 months after starting four cycles of chemotherapy. We measured LV function, global longitudinal strain and subclinical atherosclerosis markers: intima-media thickness (IMT), arterial stiffness aortic pulse wave velocity (PWVAo) and ankle-brachial index (ABI). LVEF had decreased at 6 months after treatment initialization (p<0.001), the same changes being observed for LV fraction shortening (p<0.001), mitral annular plane systolic excursion and S' wave (p<0.001 and p<0.05). Bilateral IMT and PWVAo significantly increased, 12 out of 30 patients (40%) had LVEF ≤50% after 6 months of chemotherapy, five of them receiving daunorubicin at more than 500 mg/m2/injection. LV function is impaired after 6 months of chemotherapy, with early changes of subclinical atherosclerosis becoming evident.

Echocardiografic Abnormalities in Patients with Sickle Cell/β-Thalassemia Do Not Depend on the β-Thalassemia Phenotype

Introduction: Heart disease represents an important cause of mortality and morbidity in sickle cell disease and beta-thalassemia, however the impairment of cardiac function in compound heterozygotes, namely sickle cell/β-thalassemia (HbS/β-thal) remains less known. Studies with patients of Greek origin demonstrated abnormal diastolic function in both ventricules, with unchanged systolic function, and biventricular dilatation along with pulmonary hypertension (Aessopos, A., et al., Ann Hematol, 88(6), 2009, Moyssakis, I., et al., Postgrad Med J, 81(961), 2005). The aim of this study was to evaluate echocardiographic findings and clinical and laboratory parameters in a cohort of Brazilian HbS/β-thal patients to better understand the cardiac involvement in this particular ethnic background.Methods: A retrospective chart review was performed on thirty-six HbS/β-thal patients followed from 1998 to 2016. Medical records were reviewed for laboratory and clinical data, and hospital admissions were recorded for sickle related complications: acute chest syndrome, retinopathy, avascular bone necrosis, stroke, priapism, leg ulcers and venous thromboembolism. Echocardiographic evaluation was performed in all patients in steady-state disease, with pulsed, continuous, two-dimensional and color Doppler.Results: Among the studied population, 21 (58%) were women and 15 (42%) were men. The median age was 38 (18-70) years; 22 (61%) patients were diagnosed as Sβ0, and 14 (39%) as Sβ+. As expected, when the Sβ-thalassemia phenotype was considered, the two groups of patients differed significantly: hemoglobin levels were lower in Sβ0 patients, who also presented a higher proportion of HbS and HbF and higher transferrin saturation indexes. Sβ0 patients also demonstrated significantly lower body mass index and higher number of platelets highlighting disease severity in this subgroup of patients. Left atrial (LA) and left ventricular (LV) dilation were found in 19.5 and 11% of patients, respectively. These prevalences are considerably lower than observed in patients with SS phenotype: 78 and 35%, respectively (Damy et al, Eur Heart J, 37(14), 2016). Systolic LV disfunction (defined as LV ejection fraction <59%) was present in only one patient of our cohort, though also uncommon in SS patients (8.5% in the study of Damy et al). There were no significant differences in masses and volumes of cardiac chambers comparing Sβ0 with Sβ+ patients, and we found no relationship between these parameters and the occurrence of specific complications of the disease. However, a significant correlation was found regarding parameters of myocardial hypertrophy with serum creatinine, hepatic transaminases and bilirubin levels. Moreover, among the 36 patients studied, 3 of them (1 Sβ+ and 2 Sβ0) presented stroke; these patients were significantly older (median 53 years x 37.5 years, p = 0.048), had higher values of left ventricular posterior wall diastolic thickness [8 (6-14) x 10 (10-11), p= 0.03], greater left ventricular mass [147 (69-537) x 226 (194-260), p= 0.039] and a significantly higher left atrium / aortic ratio (1.26 (0.9-1,48) x 1.545 (1.48-1.61), p= 0.032). No differences were found in pulmonary artery systolic pressure (PASP) between Sβ+ and Sβ0 patients and there was no relationship between PASP and the occurrence of acute or chronic complications.Discussion: In this cohort of Brazilian patients, we observed significant differences in hematological and clinical parameters between Sβ+ and Sβ0 patients, highlighting the difference in disease severity between the two groups. However, the profile of cardiac involvement analyzed by echocardiography was similar in both groups: higher prevalence of diastolic dysfunction with little systolic function impairment, which follows the patterns of the patients of greek origin. Nevertheless, parameters of myocardial hypertrophy were related to multiorgan impairment, and rendered a higher propensity for stroke in older patients. Thus, cardiac involvement in this disease seems to not depend on the thalassemia phenotype. This may also reflect the older age of subjects evaluated, demonstrating that the exposure to the disease features (anemia/hemolysis/inflammation) renders homogeneity in cardiac damage over time, and represents an alert for greater vigilance and control of associated factors, as hypertension and diabetes. DisclosuresNo relevant conflicts of interest to declare.

Usefulness of left ventricular strain analysis in patients with takotsubo syndrome during acute phase.

Takotsubo syndrome (TTS) is peculiar clinical condition often resembling an acute coronary syndrome and mostly affecting postmenopausal women after a stressful trigger. TTS was initially thought to be a relatively benign condition. However, current data have shown it may be associated with considerable inpatient morbidity and carry a small, but important, mortality risk. We hypothesized that left ventricular (LV) regional and global longitudinal strain (GLS) assessed with 2D speckle tracking echocardiography could identify early systolic functional impairment and predict in-hospital cardiovascular events. We conducted a retrospective descriptive study reviewing patients with the discharge diagnosis of TCM between 2003 and 2016 at our institution. One hundred patients with TSS met the Modified Mayo Clinic criteria. Using 2D speckle tracking echocardiography, two independent cardiologists assessed the LV GLS as well as the longitudinal strain (LS) of 7 individual segments [basal-septal (BS); mid-septal (MS), apical-septal (AS), apex, basal-lateral (BL), mid-lateral (ML), and apical-lateral (AL)]. The inter-observer variability was <5%. Mean age was 69.1years, 87% were females, and 53% were African Americans. Mean initial LV EF was 32%±9.8%. In univariate analysis, patients with worse BL, ML, and GLS profiles (means: -5.7; -3.3, and -4, respectively) had higher in-hospital mortality (P<.05). Worse BL and ML profiles (means: -8.6 and -7.3, respectively) were associated with higher prevalence of MACE (major adverse cardiovascular outcomes) (P<.05). In a multivariate analysis, mid-lateral strain≥-7 and basolateral strain≥-10 were independent predictors of in-hospital mortality and MACE+in-hospital heart failure, respectively. Assessment of LV global and segmental longitudinal strain by speckle tracking has important prognostic value in the acute phase of TTS. Additional large-scale studies will be needed to confirm our findings.

Associations between ECG changes and echocardiographic findings in patients with acute non-ST elevation myocardial infarction

BackgroundST segment depression (STD) and T wave inversion (TWI) are typical electrocardiographic (ECG) findings in non-ST elevation myocardial infarction (NSTEMI). In ST elevation myocardial infarction, ST changes represent transmural ischemia. The pathophysiological mechanisms of the ECG changes in NSTEMI are unclear. PurposeWe studied the associations between ECG and the echocardiographic findings in NSTEMI patients. MethodsTwenty patients with acute NSTEMI were recruited during their hospital stay. A comprehensive echocardiography study was performed. The findings were compared with blinded ECG analyses. ResultsNine (45%) patients had STD, and 16 (85%) patients had TWI. In multivariable analysis, STD was independently associated with a lower global early diastolic strain rate (β=-5.061, p=0.033). TWI was independently associated with lower circumferential strain (β=0.132, p=0.032). ConclusionsThe typical ECG changes in NSTEMI patients were associated with subtle echocardiographic changes. STD was related to changes in diastolic function, and TWI was associated with systolic deterioration.

Arterial-ventricular coupling in type 1 diabetes: arterial stiffness is associated with impaired global longitudinal strain in type 1 diabetes patients-the Thousand & 1 Study.

Diabetes is associated with higher arterial stiffness-an early marker of cardiovascular disease. The coupling between arterial stiffness and myocardial function is still unresolved. We investigate associations between arterial stiffness and early myocardial impairment assessed with advanced echocardiography. In 305 type 1 diabetes (T1D) patients without known heart disease and with normal left ventricular ejection fraction (LVEF) (biplane LVEF>45%), we measured arterial stiffness as pulse wave velocity (PWV) and performed conventional and speckle-tracking echocardiography assessing global longitudinal strain (GLS) as a measure of systolic myocardial function. Associations between PWV and myocardial function were reported as standardized beta values from adjusted regression models including age, sex, mean arterial pressure, body mass index, HbA1c, diabetes duration, estimated glomerular filtration rate, degree of albuminuria, total cholesterol, heart rate and smoking. Patients were 54 (12) years [mean (SD)], 152 (50%) females, diabetes duration 31 (16) years, HbA1c 65 (12) mmol/mol, LVEF 58 (5)%, GLS -18.2 (2.6)% and PWV 10.2 (3.4) m/s. There was no association between PWV and LVEF (p=0.93). Conversely, there was a highly significant association between PWV and GLS in crude and multivariable models (standardized β-coefficient 0.25, p<0.001 and 0.16, p=0.036, respectively). Also, diastolic function measured as E/e' was highly associated with PWV in crude and multivariable models (standardized β-coefficient 0.43, p<0.001 and 0.17, p=0.016, respectively). In T1D patients with normal LVEF and without known heart disease, higher arterial stiffness is independently associated with early systolic and diastolic myocardial impairment detectable by advanced echocardiography. Although unable to demonstrate causality, we display a relationship between diabetic angiopathy and diabetic cardiomyopathy (H-3-2009-139 and PROFIL-H-B-2009-056).

Échocardiographie à la dobutamine ou étude de la déformation longitudinale au repos pour démasquer une cardiomyopathie diabétique débutante symptomatique ?

Diabetes mellitus has been associated with changes in the structure and function of the myocardium manifesting in the early stages of the disease as subtle systolic and diastolic dysfunction; myocardial strain imaging has recently been favored over dobutamine stress echocardiography for early detection of diabetic cardiomyopathy. We report a case of an elderly diabetic patient presenting with pulmonary edema in whom at rest echocardiographic parameters including strain rate were all within normal range, while dobutamine stress echocardiography induced a deep systolic deterioration unmasking an early-stage diabetic cardiomyopathy.

Differential Myocardial Fibre Involvement by Strain Analysis in Patients With Aortic Stenosis

Aortic stenosis (AS) is the most common valvular heart disease and can result in left ventricular (LV) systolic impairment. LV myocardial fibres are organised in layers: the subendocardial layer is orientated longitudinally and the subepicardial layer circumferentially. We hypothesised that there is differential involvement of myocardial fibres in patients with aortic stenosis. We performed multi-directional, multi-layered systolic strain analysis in 70 patients (aged 72±10.7years) with varying grades of AS severity (mean gradient 32.3±20mmHg, aortic valve area 1.1±0.6cm2) and in 30 controls. Clinical, demographic and resting echocardiographic data were recorded. Left ventricular subendocardial and subepicardial systolic strains were measured in the longitudinal, radial and circumferential axes. Systolic subendocardial strain was significantly higher than subepicardial strain in all three axes in patients and in controls. There were significant differences in longitudinal, but not in circumferential and radial strain, or left ventricular ejection fraction (LVEF), between patient groups. Aortic valve mean gradient (MG) and valve area (AVA) correlated better with subendocardial longitudinal strain (r=0.548, p<0.001; r=-0.54, p<0.001 respectively) than with subepicardial longitudinal strain (r=0.496, p<0.001, r=-0.544, p<0.001 respectively). Correlations between circumferential and radial strain and MG or AVA were poor. There was differential impairment in LV systolic strain in all three cardiac axes in patients with AS. Left ventricular longitudinal strain impairment was proportional to AS severity. Subendocardial longitudinal strain correlated better with AS severity than subepicardial longitudinal strain while correlations between circumferential and radial strain and AS severity were weak.

High fat diet aggravates atrial and ventricular remodeling of hypertensive heart disease in aging rats.

Left ventricular hypertrophy is a major cause of heart failure in aging population. This study is to determine whether an excess dietary fat is lipotoxic or lipoprotein to the hypertrophic aging heart. At 44-week-old, a normal chow (12% fat) was replaced a high-fat diet (HFD; 45% fat) for randomly selective spontaneously hypertensive rats (SHR+HFD, n=6) and Wistar-Kyoto rats (WKY+HFD, n=6, normotensive control). Others (SHR, n=11; WKY, n=10) were continuously fed with normal diets. After 27 weeks, electrocardiogram, echocardiography, and femoral arterial catheterization were performed before rats being sacrificed for molecular biology analyses. HFD aggravated cardiac atrial, ventricular dilation and hypertrophy in SHR (LV mass: SHR+HFD 2026.0±424.9 vs SHR 1449±461.1mg, unpaired t test P<0.05). HFD caused significant atrial dilatation in both WKY (LA diameter, 5.38±0.36 vs 4.11±0.42mm, P<0.001) and SHR (6.13±0.79 vs 4.69±1.00, P<0.01). Only in SHR, HFD induced significant left ventricular dilatation (LV diameter, 8.87±1.25 vs 7.08±1.00mm, P<0.01) and reduced ejection fraction (LVEF, 62.8±11.6 vs 75.1±9.2mm, P<0.05). The α-myosin heavy chain was significantly upregulated in atria and ventricles of HFD groups. HFD induced significant upregulation of PPARα, ACADM, and TNFα transcripts in atrial tissues (P<0.05). Hypertensive heart disease in aging rats was aggravated by HFD with worse atrial, ventricular remodeling and associated with left ventricular systolic function impairment.

P5556The use of direct heart hypothermia by METcooler reduces microvascular obstruction and left ventricular systolic function impairment in animal experimental model of myocardial infarction

P5556The use of direct heart hypothermia by METcooler reduces microvascular obstruction and left ventricular systolic function impairment in animal experimental model of myocardial infarction

Effective use of levosimendan in anthracycline-induced cardiomyopathy: A case report

BackgroundAnthracycline-induced cardiomyopathy is a serious side effect that ranges from mild left ventricular systolic impairment to congestive heart failure and cardiogenic shock. Currently, there is no evidence indicating the effective use of levosimendan in these cases. ObjectiveWe aim to present a case of life-threatening doxorubicin-induced cardiomyopathy that was successfully managed with levosimendan. CaseA 48-year-old female with formerly normal heart function, who had been treated with doxorubicin-based regimens for dedifferentiated chondrosarcoma, presented with cardiomyopathy with low left ventricular ejection fraction eight months after the last infusion. As treatment with ramipril, carvedilol, and furosemide followed by dopamine and noradrenaline was not sufficient, levosimendan was administered. Left ventricular ejection fraction increased from 15% to 45% and her clinical condition improved. DiscussionAlthough anthracycline-induced cardiomyopathy may have a poor prognosis, levosimendan was shown to be effective in this patient. Therefore, levosimendan may represent a possible therapeutic option in such cases.

Speckle Tracking Stress Echocardiography Uncovers Early Subclinical Cardiac Involvement in Pediatric Patients with Inflammatory Bowel Diseases

Inflammatory bowel disease (IBD) is an established risk factor for cardiovascular disease (CVD). However, whether cardiac consequences present early in IBD is unknown. This is the first study in children aiming to unmask altered myocardial mechanics in IBD. We enrolled 50 consecutive normotensive children with Crohn’s disease (CD) (n = 28) or ulcerative colitis (UC) (n = 22). The study groups consisted of 18 patients with active inflammatory disease (mean age 14.6 ± 2.5 years) and 32 children with IBD in remission (14.3 ± 2.3 years). 60 age- and gender-matched children served as healthy controls. Speckle tracking stress echocardiography (STE) was used to assess left ventricular (LV) myocardial strain and strain rate. Circumferential strain rate was significantly decreased in children with active IBD (−1.55 ± 0.26 s−1) and IBD in remission (−1.49 ± 0.26 s−1) versus healthy controls (1.8 ± 0.4 s−1) both at rest (p < 0.001) and during exercise (p = 0.021). Moreover, longitudinal strain rate, circumferential strain and E/E′ ratio were significantly impaired in IBD. Pediatric patients with IBD feature subclinical signs of LV systolic and diastolic myocardial impairment early in the course of CD and UC. This may not be reversible even when IBD is clinically controlled. Patients with IBD should be regularly screened for signs of CVD.

Diagnosis and assessment of dilated cardiomyopathy: a guideline protocol from the British Society of Echocardiography

Heart failure (HF) is a debilitating and life-threatening condition, with 5-year survival rate lower than breast or prostate cancer. It is the leading cause of hospital admission in over 65s, and these admissions are projected to rise by more than 50% over the next 25 years. Transthoracic echocardiography (TTE) is the first-line step in diagnosis in acute and chronic HF and provides immediate information on chamber volumes, ventricular systolic and diastolic function, wall thickness, valve function and the presence of pericardial effusion, while contributing to information on aetiology. Dilated cardiomyopathy (DCM) is the third most common cause of HF and is the most common cardiomyopathy. It is defined by the presence of left ventricular dilatation and left ventricular systolic dysfunction in the absence of abnormal loading conditions (hypertension and valve disease) or coronary artery disease sufficient to cause global systolic impairment. This document provides a practical approach to diagnosis and assessment of dilated cardiomyopathy that is aimed at the practising sonographer.

Subclinical Cardiac Dysfunction in Polymyositis and Dermatomyositis: A Speckle-tracking Case-control Study.

Subclinical heart disease occurs in up to 50% of patients with idiopathic inflammatory myopathies (IIM) and is difficult to detect through conventional imaging. We investigated the usefulness of global longitudinal strain (GLS) measurement to detect a subclinical systolic ventricular dysfunction in patients with IIM. We enrolled 28 patients with IIM and 28 matched controls in a 1:1 fashion. Standard variables for the left ventricle (LV) and right ventricle (RV) systolic and diastolic function were measured and compared between cases and controls, along with speckle-tracking GLS of the LV and RV. A possible correlation between GLS and muscle strength, disease activity, cardiovascular risk factors, and other organ systems involvement was searched. Standard variables of systolic and diastolic dysfunction were similar between patients and controls. GLS was significantly lower in patients when compared with controls for both LV (-18.7 ± 4.2% vs -21.2 ± 2.1%, p = 0.006) and RV (-19.3 ± 6.3% vs -22.5 ± 3.8%, p = 0.033). Patients with IIM had a 4.9-fold increased risk for impaired left GLS [relative risk (RR) 4.9, 95% CI 1.5-15.8, p = 0.006], which involved usually basal and mid-segments of the anterior, anterior-septal, and lateral wall. Patients with IIM had a 3.4-fold increased risk for impaired right GLS (RR 3.4, 95% CI 1.1-11.7, p = 0.04) with the basal segment of the free RV wall most frequently involved. Muscle strength, disease activity, damage and duration, other organ system involvement, and previous treatment were not associated with reduced GLS. Subclinical systolic impairment is common in patients with IIM without overt LV dysfunction. In this context, GLS is a potentially useful variable.

Pulmonary hypertension attenuates the dynamic preload indicators increase during experimental hypovolemia

BackgroundPulse pressure (PPV) and stroke volume (SVV) variations may not be reliable in the setting of pulmonary hypertension and/or right ventricular (RV) failure. We hypothesized that RV afterload increase attenuates SVV and PPV during hypovolemia in a rabbit model of pulmonary embolism (PE) secondary to RV dysfunction.MethodsSeven anesthetized and mechanically ventilated rabbits were studied during four experimental conditions: normovolemia, blood withdrawal, pulmonary embolism and fluid loading of a colloidal solution. Central venous, RV and left ventricular (LV) pressures, and infra-diaphragmatic aortic blood flow (AoF) and pressure were measured. SV was estimated by the integral of systolic AoF. We analyzed RV and LV function through stroke work output curves. PPV and SVV were obtained by the variation of beat-to-beat PP and SV, respectively. We assessed RV and LV diastolic and systolic function by the time rate of relaxation (tau) and the ratio of the first derivative of ventricular pressure and the highest isovolumic developed pressure (dP/dt/DP), respectively. The vasomotor tone was estimated by the dynamic arterial elastance (Eadyn = PPV/SVV).ResultsPPV and SVV increased significantly during hemorrhage and returned to baseline values after PE which was associated to biventricular right-downward of the stroke work curves and a decrease of AoF and SV (P < 0.05). RV systo-diastolic function and LV systolic function were impaired. All the animals were nonresponders after volume expansion. Eadyn did not show any significant change during the different experimental conditions.ConclusionsThe dynamic preload indicators (SVV and PPV) were significantly reduced after a normotensive PE in hypovolemic animals, mainly by the systo-diastolic dysfunction of the RV associated with LV systolic impairment, which makes the animals nonresponsive to volume loading. This normalization of dynamic preload indices may prevent the detrimental consequence of fluid loading.

Stress echocardiography in patients who experienced mechanical ventilation weaning failure

IntroductionCritically ill patients may suffer varying degrees of temporary myocardial dysfunction during respiratory weaning that could play an important role in weaning failure. ObjectivesIn this study, we tried to assess the existence of temporary diastolic dysfunction during respiratory weaning. MethodsInclusion period is from 2006 to 2015. In this study, we included 181 ventilated patients with cardiogenic shock that were being weaned from mechanical ventilation. Twenty of those patients were successfully weaned from mechanical ventilation, and the rest (161) experienced complications in their weaning process. All patients had a left ventricular ejection fraction >0.45 and E/E′ ratio≤8, did not require vasoactive drugs at that time, and did not have remaining significant ischemic disease. We divided our patients into 3 groups, as follows: A, patients who could not tolerate a T-tube and required pressure-support ventilation (82); B, patients who successfully tolerated a T-tube period (20); and C, patients who could not tolerate spontaneous breathing modes of mechanical ventilation and remained on assisted mechanical ventilation.We performed stress echocardiography for the last two groups; using dobutamine to assess diastolic function and using ephedrine to evaluate functional mitral regurgitation (MR). We estimated pulmonary capillary wedge pressure through the E/E′ ratio and the flow in the pulmonary veins. ResultsIn group A (ie, those patients who could not tolerate a T-tube trial), we observed an increase in the E/E′ ratio (6.32±0.77 vs 15.2±6.65; P=.0001) and a worsening of strain (S) and strain rate (SR) (−13.6±1.80 vs −11.88±5.6, P=.0001; and −1.3±1.28 vs −0.95±0.38, P=.0001; respectively). We did not observe a change in the E/E′ ratio during stress echocardiogram on those patients with successful weaning from mechanical ventilation (7.41±0.43 vs 8.38±4.57, P=.001). However, we did see in this group an increased peak velocity of the S wave and of SR (−16.11±08.72 vs −19.89±5.62 and −1.48±0.23 vs −1.59±0.21, P=.001; respectively).In 42 weaning failure patients, the dobutamine echocardiography showed an increased E/E′ ratio (7.41±0.43 vs 15.98±7.98; P=.0001) and deterioration of S (−15.41±09.56 vs −12.72±6.55; P=.0001) and SR (−1.41±0.78 vs −1.22±0.65; P=.0001). In 37 patients without systolic or diastolic impairment and functional MR grade >2, ephedrine echocardiography showed an increase of effective regurgitant volume (29.56±11.32 mL vs 46.56±0.13 mL, P=.0001) and effective regurgitant orifice area (0.19±0.09 cm2 vs 0.31±0.09 cm2, P=.0001). ConclusionsStress echocardiography may be helpful in detecting silent diastolic and systolic dysfunction or severe MR that could have a major impact on respiratory weaning.

Hypertensive Patients Have Impaired Left Ventricular Contractile Reserve Despite Normal Ejection Fraction

Hypertension (HT) may lead to LV systolic impairment through chronic pressure overload. LV hypertrophy and systolic dysfunction occur late. An impaired contractile reserve (CR) may be an early manifestation of LV dysfunction in hypertensive patients. We examined CR and its correlates in hypertensive patients and compared that with normotensive controls. Methods: 129 prospectively recruited patients (68 men, aged 58.6 ± 9.5 years) underwent dobutamine echocardiography. Patients with diabetes, coronary disease, or significant valvular disease were excluded. 72 patients (56%) had treated HT. LV global longitudinal strain (GLS) was measured at rest and at low dose dobutamine. Absolute CR was calculated as the difference in GLS between low dose and resting values. Relative CR is the ratio of absolute CR to resting GLS. Results: There was no difference in LV ejection fraction between hypertensive patients and controls (64.5 ± 6.1% vs 64.5 ± 6.6% at rest, 72.1 ± 6.6% vs 71.2 ± 6.9% at low dose dobutamine; both p = NS). LVGLS in hypertensive patients was significantly impaired at rest (-16.8 ± 2.2% vs -19.5 ± 1.5%; both p < 0.001) and at low dose dobutamine (-17.9 ± 2.7% vs -22.7 ± 2.6%; both p < 0.001). More importantly, both the absolute and relative CR were significantly lower in hypertensive patients (-1.12% vs -3.17%; 7.24% vs 16.4% respectively, both p < 0.001). CR was not correlated with LV mass, prevailing blood pressure, septal e’ velocities, E/e’ ratio. Conclusions: Compared with controls, hypertensive patients not only had impaired LV GLS at rest, but also an impaired ability to augment contractility with inotropic stimulation, i.e. CR. This impaired CR is independent of LV mass, diastolic function or filling pressures.