Ventricular Dysfunction In Patients Research Articles

The prognostic impact of right ventricular dysfunction in patients with septic cardiomyopathy

Abstract Background Sepsis is a systemic condition of profoundly impaired health in which an infection leads to a dysregulated host response, and consecutively causes organ dysfunction, shock, and even death. Septic cardiomyopathy (SCM) is one of the multiple organ dysfunctions. SCM is typically defined as left ventricular (LV) dysfunction, presented by decreased LV ejection fraction (LVEF). However, it remains unclear about the detailed mechanism of cardiac dysfunction. In addition, the prognostic impact of right heart dysfunction in SCM patients has not been fully investigated. Purpose The purpose of this study was to investigate the prognostic impact of right heart dysfunction in patients with SCM. Methods We used the MIMIC-III (Medical Information Mart for Intensive Care III) critical care database, which is a large, freely-available database comprising deidentified health-related data associated with over forty thousand patients who stayed in critical care units of the Beth Israel Deaconess Medical Center between 2001 and 2012. We retrospectively analyzed data of patients with septic shock on admission to intensive care unit (ICU). Septic shock was defined as the presence of any suspected infections, the need for vasopressors, and the lactate level exceeding 2 mmol/L, based on the Sepsis-3 criteria. Patients were performed portable transthoracic echocardiography (TTE) during hospitalization. LVEF and right ventricular (RV) function were determined predominately by visual estimation in the parasternal long-axis view. SCM was defined as having a minimum LVEF of 50% or less during hospitalization. Patients with hyperdynamic motion of LVEF >70% were excluded. Results In total, there were 2254 patients with septic shock. Of these, 604 patients who underwent TTE were enrolled, and 314 patients were diagnosed with SCM. At baseline, age, gender, Sequential Organ Failure Assessment (SOFA) score, maximum lactate levels, and maximum norepinephrine dosage were 70 [59–79] years, 194 males, 13 [11–15], 4.0 [2.7–6.2] mmol/L, and 0.20 [0.10–0.31] mcg/kg/min, respectively. All patients were treated with vasopressors. In Kaplan-Meier survival analysis, patients with SCM had increased 28-day mortality compared with those without SCM (log-rank, p=0.09). In addition, we divided SCM patients into two groups; SCM with and without RV dysfunction. SCM patients with RV dysfunction had significant increased 28-day mortality compared with those without RV dysfunction (log-rank, p=0.01) (Figure). In Cox proportional hazard regression analysis adjusted for age, male sex, SOFA score, and maximum lactate levels, RV dysfunction was an independent determinant of 28-day mortality (hazard ratio, 1.59; 95% confidence interval, 1.03–2.46; p=0.03). Conclusions The presence of RV dysfunction increased 28-day mortality in patients with SCM. It might be useful for predicting the prognosis of SCM to evaluate not only left heart function but also right heart function. Kaplan-Meier survival curves Funding Acknowledgement Type of funding source: None

Lymphocytic myocarditis: a genetically predisposed disease?

Abstract Background Clinical presentation of myocarditis is extremely heterogeneous from asymptomatic to overt severe heart failure (HF). A complex interaction between pre-existing genetic background and inflammation might be responsible for this heterogeneity. Purpose The aim of the present study was to investigate whether positive genetic background for pathogenic cardiomyopathy-related variants might underlie a higher susceptibility to left ventricular dysfunction in patients with active lymphocytic myocarditis. Methods We prospectively performed genetic tests in 36 patients (46±15 years; 61% males; no relatives included) with biopsy-proven active lymphocytic myocarditis according to Dallas criteria and immunohistochemistry. Only pathogenic (P) or likely pathogenic (LP) variants were considered. Results After genetic test, 31% of patients (n=11) were carriers of P/LP truncating variants in structural Cardiomyopathy related genes: Titin (TTN, n=8, 73%), Desmoplakin (DSP, n=1), Filamin C (FLNC, n=1) and RNA binding protein 20 (RBM20, n=1). Among the 27 patients presenting with HF and LV dysfunction, the positive genetic yield was similar to the total cohort (n=9, 34%; 90% with TTN). Two out of six arrhythmic patients (30%) were carriers in arrhythmogenic genes (i.e. DSP and FLNC), whereas no patients with infarct-like presentation were carriers. During follow-up, 44% of patients (n=16) presented normal Left Ventricular Ejection Fraction (LVEF). Carriers had a lower rate of LVEF normalization compared to non-carriers (18% vs 56%, respectively; p=0.035). Conclusion Positive genetic testing for cardiomyopathy-related-genes might be found in a non-negligible percentage of patients with biopsy-proven myocarditis, especially if presenting with heart failure and LV dysfunction. Compared to non-carriers, carriers of P/LP variants show lower likelihood of LVEF normalization during follow-up. Funding Acknowledgement Type of funding source: None

MicroRNA-208b gene expression levels as a biomarkers of left ventricular dysfunction in patients with acute myocarditis

Abstract Purpose MicroRNAs (miRs) play a major role in protein regulation by post-transcriptional gene expression and cell to cell interaction. Recently, they have been emerged as important modulators in cardiovascular development and disease. Our aim was to determine whether cardiac related miRs such as miR-208b was differentially expressed in peripheral blood mononuclear cells from patients with acute myocarditis. We also evaluated their expression levels in peripheral blood mononuclear cells in relation with left ventricular global longitudinal peak strain (GLPS) in those patients. Methods We assessed the expression levels of miR-208b in 55 patients with acute myocarditis (48 men, mean age 33±10 years) and 22 healthy individuals (18 men, mean age 33±9 years). Blood samples were taken on admission and miR expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. All patients were also underwent an assessment with standard conventional transthoracic and a two-dimensional speckle tracking echocardiography. Results GLPS was significantly reduced in the group of myocarditis compared to healthy individuals (from −13.9±10.9% versus −22.2±6.7%, p<0.05). Myocarditis patients showed significantly higher miR-208b (28.8±16.6 versus 6.40±1.1, p<0.001) expression levels compared to control group. miR-208b gene expression levels at baseline revealed a significant negative correlation with GLPS on admission (r=−0.51, p<0.05). This correlation was independent of the patients' clinical parameters. Conclusions Our data reveal that miR-208b gene expression levels are upregulated in peripheral blood mononuclear cells from patients with acute myocarditis relative to healthy individuals. In addition, miR-208b levels have a prognostic value in the deterioration of left ventricular GLPS in those patients. Thus, miR-208b may represent a promising biomarkers in myocarditis or a potential therapeutic target in the future. Funding Acknowledgement Type of funding source: None

Validation of electrocardiographic criteria for identifying left ventricular dysfunction in patients with previous myocardial infarction.

BackgroundEleven criteria correlating electrocardiogram (ECG) findings with reduced left ventricular ejection fraction (LVEF) have been previously published. These have not been compared head‐to‐head in a single study. We studied their value as a screening test to identify patients with reduced LVEF estimated by cardiac magnetic resonance (CMR) imaging.MethodsECGs and CMR from 548 patients (age 61 + 11 years, 79% male) with previous myocardial infarction (MI), from the DETERMINE and PRE‐DETERMINE studies, were analyzed. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of each criterion for identifying patients with LVEF ≤ 30% and ≤ 40% were studied. A useful screening test should have high sensitivity and NPV.ResultsMean LVEF was 40% (SD = 11%); 264 patients (48.2%) had LVEF ≤ 40%, and 96 patients (17.5%) had LVEF ≤ 30%. Six of 11 criteria were associated with a significant lower LVEF, but had poor sensitivity to identify LVEF ≤ 30% (range 2.1%–55.2%) or LVEF ≤ 40% (1.1%–51.1%); NPVs were good for LVEF ≤ 30% (range 82.8%–85.9%) but not for LVEF ≤ 40% (range 52.1%–60.6%). Goldberger's third criterion (RV4/SV4 < 1) and combinations of maximal QRS duration > 124 ms + either Goldberger's third criterion or Goldberger's first criterion (SV1 or SV2 + RV5 or RV6 ≥ 3.5 mV) had high specificity (95.4%–100%) for LVEF ≤ 40%, although seen in only 48 (8.8%) patients; predictive values were similar on subgroup analysis.ConclusionsNone of the ECG criteria qualified as a good screening test. Three criteria had high specificity for LVEF ≤ 40%, although seen in < 9% of patients. Whether other ECG criteria can better identify LV dysfunction remains to be determined.

Serum salusin-β in relation to atherosclerosis and ventricular dysfunction in patients with type 2 diabetes mellitus

Background and aimsSalusin-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. MethodsSixty 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. ResultsSerum 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. ConclusionSerum salusin-β may be associated with atherosclerosis and LV dysfunction in T2DM.

Right ventricular dysfunction in patients with non-severe idiopathic pulmonary fibrosis: a cross-sectional prospective single-center study

ABSTRACT Background Little is known about right ventricular dysfunction in non-advanced idiopathic pulmonary fibrosis (IPF) patients without hypoxemia at rest. We evaluated it at rest and during exercise. Research design and methods 123 IPF patients were evaluated, and 27 met all the following criteria: Gender-Age-Physiology Index score ≤5, modified Medical Research Council dyspnea score ≤3, peripheral oxygen saturation ≥92% at rest, and no history of oxygen therapy. They were submitted to two-dimensional speckle-tracking echocardiography at rest and during cardiopulmonary exercise to analyze right ventricular global longitudinal strain. Results Abnormal speckle-tracking echocardiography findings were identified in 10/27 patients (37%), indicating right ventricular (RV) dysfunction. No patients had abnormalities observed in conventional echocardiographic parameters. Significant differences in mPAP were observed between patients with RV dysfunction and those without dysfunction (at rest: 26.0 ± 4.8 vs. 19.1 ± 4.2 mmHg, p = 0.001; during exercise: 51.3 ± 6.4 vs. 36.9 ± 14.7 mmHg, p = 0.002). Conclusions RV dysfunction was detected in 37% of non-advanced IPF patients and early recognition was only possible using speckle-tracking echocardiography. Special attention should be given to these patients as RV dysfunction is suggestive of worse prognosis. These patients could benefit from new specific drugs or even oxygen therapy for transitory hypoxia.

Aortic wall elasticity and left ventricular function in hypertensive patients with nonsignificant coronary artery disease.

Hypertension is an important cause of nonischemic heart failure. It is important to identify subclinical left ventricular dysfunction in patients with hypertension in an early stage to lower the risk of progression to more severe illness. The aim of our study was to assess the correlation between indices of left ventricular function and aortic stiffness in patients with hypertension. Our study was a case control study of 42 hypertensive and 40 normotensive patients with nonsignificant coronary artery disease. All the patients underwent echocardiography and left ventricular ejection fraction, global longitudinal strain, post systolic index, pulsed Doppler early transmitral peak flow velocity, early diastolic mitral annular velocity (e'), and aortic elasticity measurements were calculated. The hypertensive patients were older (58.47 ± 9.57 vs. 52.94 ± 10.38 years, p = 0.018) and had a higher body mass index (30.09 ± 5.08 vs. 27.48 ± 4.17 kg/m2, p = 0.013) and E/e' ratio (8.16 ± 1.81 vs. 6.56 ± 1.71, p < 0.001) and a lower e' velocity (8.25 ± 2.28 vs. 9.52 ± 2.34 cm/s, p = 0.015) than normotensives. They also had a lower aortic distensibility (p = 0.008) and a higher aortic stiffness index (p = 0.039) compared with the normotensive group. The hypertensive patients did not show any association between aortic elasticity and stiffness with age or e' velocity despite significant association in normotensives. Hypertension is associated with a high prevalence of diastolic dysfunction, elevated left ventricular filling pressure, and increased arterial stiffness, all of which have significant association with adverse outcomes. The measurements found in the hypertensive patients compared with the normotensive group may be due to several age-independent mechanisms.

Effects of Sacubitril/Valsartan on the Right Ventricular Arterial Coupling in Patients with Heart Failure with Reduced Ejection Fraction.

Background: right ventricle-pulmonary artery (RV-PA) coupling assessed by measuring the tricuspid anular plane systolic excursion (TAPSE)/pulmonary artery systolic pressure (PASP) ratio has been recently proposed as an early marker of right ventricular dysfunction in patients with heart failure with a reduced ejection fraction (HFrEF). Methods: As the effects of sacubitril/valsartan therapy on RV-PA coupling remain unknown, this study aimed to analyse the effect of this drug on TAPSE/PASP in patients with HFrEF. We retrospectively analysed all outpatients with HFrEF referred to our unit between October 2016 and July 2018. Results: At the 1-year follow-up, sacubitril/valsartan therapy was associated with a significant improvement in TAPSE (18.26 ± 3.7 vs. 19.6 ± 4.2 mm, p < 0.01), PASP (38.3 ± 15.7 vs. 33.7 ± 13.6, p < 0.05), and RV-PA coupling (0.57 ± 0.25 vs. 0.68 ± 0.30 p < 0.01). These improvements persisted at the 2-year follow-up. In the multivariable analysis, the improvement in the RV-PA coupling was independent of the left ventricular remodelling. Conclusions: in patients with HFrEF, sacubitril/valsartan improved the RV-PA coupling; however, further trials are necessary to evaluate the role of sacubitril/valsartan in the treatment of right ventricle (RV) dysfunction either associated or not associated with left ventricular dysfunction.

2D speckle tracking detects early left ventricular dysfunction in patients with sarcoidosis

Background: Sarcoidosis is a multisystemic granulomatous disease of unknown origin. Cardiac involvement is known to have a poor prognosis; sudden death may be its initial presentation. Conventional echocardiography remains insufficient for the detection of subclinical myocardial dysfunction. In our study we aimed to assess the prevalence of subclinical cardiac dysfunction using left ventricle global longitudinal strain. Results: we performed a cross-sectional study, 55 patients with established diagnosis of systemic sarcoidosis and 50 healthy age- and sex-matched controls underwent a transthoracic echocardiography, 9 patients were excluded, and 46 patients were included in the study. Left ventricular dimensions and ejection fraction were similar between the two groups (66% Vs 67%). Left ventricle global longitudinal strain was significantly lower in patients with sarcoidosis (-17.15 +/-3 Vs -22.4+/-2, p: 0.001). Conclusion: left ventricle global longitudinal strain may be an advanced indicator of cardiac sarcoidosis that needs to be studied further.

Artificial Intelligence ECG to Detect Left Ventricular Dysfunction in COVID-19: A Case Series

Coronavirus disease 2019 (COVID-19) can result in deterioration of cardiac function, which is associated with high mortality. A simple point-of-care diagnostic test to screen for ventricular dysfunction would be clinically useful to guide management. We sought to review the clinical experience with an artificial intelligence electrocardiogram (AI ECG) to screen for ventricular dysfunction in patients with documented COVID-19. We examined all patients in the Mayo Clinic system who underwent clinically indicated electrocardiography and echocardiography within 2 weeks following a positive COVID-19 test and had permitted use of their data for research were included. Of the 27 patients who met the inclusion criteria, one had a history of normal ventricular function who developed COVID-19 myocarditis with rapid clinical decline. The initial AI ECG in this patient indicated normal ventricular function. Repeat AI ECG showed a probability of ejection fraction (EF) less than or equal to 40% of 90.2%, corroborated with an echocardiographic EF of 35%. One other patient had a pre-existing EF less than or equal to 40%, accurately detected by the algorithm before and after COVID-19 diagnosis, and another was found to have a low EF by AI ECG and echocardiography with the COVID-19 diagnosis. The area under the curve for detection of EF less than or equal to 40% was 0.95. This case series suggests that the AI ECG, previously shown to detect ventricular dysfunction in a large general population, may be useful as a screening tool for the detection of cardiac dysfunction in patients with COVID-19.

Risk factors for right ventricular dysfunction in patients with lymphangioleiomyomatosis.

Lymphangioleiomyomatosis (LAM) is a rare disease characterized by diffuse cystic lesions of the lung. The present study was designed to evaluate the right ventricular (RV) function in LAM patients via single-beat real-time three-dimensional echocardiography (RT-3DE) and to investigate the factors affecting RV function in LAM patients. According to tricuspid regurgitation velocity (TRV), forty-five female LAM patients [(44.07 ± 10.22) years old] were divided into TRV ≤ 2.8m/s group (n = 29) and TRV > 2.8m/s group (n = 16). Relative echocardiography parameters were assessed by conventional transthoracic echocardiography, Doppler tissue imaging (DTI) and RT-3DE, respectively. Pulmonary function tests and the six-minute walk tests (SMWT) were also performed for LAM patients. We found that most of RV functional parameters in LAM patients were worse than that in control patients, although left ventricular dysfunction was not significantly observed. Correlation analysis showed that 3D echocardiographic RV ejection fraction (RVEF) was negatively correlated with pulmonary vascular resistance (PVR), TRV, and the decrease of oxygen saturation (SpO2) post SMWT, and positively correlated with Forced expiratory volume in the first second/forced vital capacity, carbon monoxide diffusion predicted value, SMWT distance, and resting SpO2 in LAM patients. Multivariate stepwise linear regression analysis showed that PVR and SpO2 before SMWT were independent influence factors of RVEF in LAM patients. In this study, we found that RV dysfunction was presented in LAM patients, although left ventricular dysfunction was not significantly obvious. The main influence factors of RVEF were PVR and hypoxia. RT-3DE is a low-cost and noninvasive way to evaluate RV function in LAM patients.

Effects of clinical depression on left ventricular dysfunction in patients with acute coronary syndrome.

Depression is associated with heart failure independent of traditional cardiovascular disease risk factors. Enhanced platelet activation has been suggested as a potential mechanism and has been associated with negative inotropic effects that can affect left ventricular ejection fraction (LVEF). We examined 131 consecutive acute coronary syndrome (ACS) patients to assess whether depression increased the risk for developing LV dysfunction, and to determine the effects of platelet serotonin signaling in this relationship. Major depression was assessed using the Structured Clinical Interview and depressive symptoms were measured using the Beck Depression Inventory (BDI), with BDI ≥ 10 defined as abnormal. LV dysfunction was defined as LVEF ≤ 45%. Platelet serotonin response was measured by serotonin augmented platelet aggregation and platelet serotonin receptor density. Mean age of ACS participants was 59years, 78.6% male and 74.0% Caucasian. 34.4% of patients had a reduced LVEF ≤ 45% on presentation. Almost half (47.0%) of patients had BDI ≥ 10 and 18.0% had major depressive disorder. Platelet serotonin response was found to be augmented in depressed patients with low LVEF compared to depressed patients with normal LVEF (p < 0.020). However, the presence of LV dysfunction was found to be similar in both depressed (32.3%) and non-depressed (36.2%) patients (p = 0.714). This suggests alternative factors contribute to poor cardiovascular outcomes in depressed patients that are independent of LV function in post ACS patients.

Fragmented QRS complexes are associated with subclinical left ventricular dysfunction in patients with Behcet's disease: Four-dimensional speckle tracking echocardiography.

Behcet's disease (BD) is a chronic systemic inflammatory disease in which early detection of cardiac involvement is essential. The aim of this study was to assess the left ventricular (LV) functions in BD patients using four-dimensional (4D) speckle tracking echocardiography (STE) and to test the correlation between LV dysfunction and the presence of QRS fragmentation. This cross-sectional study included 64 Behcet's patients and 48 healthy volunteers. The BD group was divided into two subgroups depending on the presence (fQRS+) or absence (fQRS-) of fragmented QRS (fQRS). In both groups, left ventricular global area strain (LV-GAS), global radial strain (GRS), global longitudinal strain (GLS), and global circumferential strain (GCS) were obtained with 4D echocardiography. GAS, GRS, GLS, and GCS values were significantly different in Behcet's patients and in healthy volunteers. GLS and GAS values were lower in the fQRS+ than in the fQRS- group (-15.8 ± 1.8 and -17.9 ± 1.6, P = .001 vs -25.0 ± 3.1 and -29.2 ± 4.2, P < .001, respectively). The duration of disease was longer in fQRS+ than in fQRS- patients (120.8 ± 67.4 vs 71.0 ± 40.5, P < .001). Multiple linear regression analysis showed that fQRS and disease duration were independent predictors of LV-GAS. Four-dimensional STE may be helpful for the prediction of early cardiac dysfunction in patients with BD. The presence of fQRS may be an indicator of subclinical LV dysfunction.

Effects of linagliptin on left ventricular DYsfunction in patients with type 2 DiAbetes and concentric left ventricular geometry: results of the DYDA 2 trial.

To evaluate the effect of linagliptin on left ventricular systolic function beyond glycaemic control in type 2 diabetes mellitus. A multicentre, randomised, double-blind, placebo controlled, parallel-group study, was performed (the DYDA 2 trial). Individuals with type 2 diabetes mellitus and asymptomatic impaired left ventricular systolic function were randomly allocated in a 1:1 ratio to receive for 48 weeks either linagliptin 5 mg daily or placebo, in addition to their diabetes therapy. Eligibility criteria were age 40 years and older, haemoglobin A1c 8.0% or less (≤64 mmol/mol), no history of cardiac disease, concentric left ventricular geometry (relative wall thickness ≥0.42), impaired left ventricular systolic function defined as midwall fractional shortening 15% or less at baseline echocardiography. The primary end point was the modification of midwall fractional shortening over time. The main secondary objectives were changes in diastolic and/or in longitudinal left ventricular systolic function as measured by tissue Doppler echocardiography. One hundred and eighty-eight patients were enrolled, predominantly men with typical insulin-resistance comorbidities. At baseline, mean midwall fractional shortening was 13.3%±2.5. At final evaluation, 88 linagliptin patients and 86 placebo patients were compared: midwall fractional shortening increased from 13.29 to 13.82 (+4.1%) in the linagliptin group, from 13.58 to 13.84 in the placebo group (+1.8%, analysis of covariance P = 0.86), corresponding to a 2.3-fold higher increase in linagliptin than the placebo group, although non-statistically significant. Also, changes in diastolic and longitudinal left ventricular systolic function did not differ between the groups. Serious adverse events or linagliptin/placebo permanent discontinuation occurred in very few cases and in the same percentage between the groups. In the DYDA 2 patients the addition of linagliptin to stable diabetes therapy was safe and provided a modest non-significant increase in left ventricular systolic function measured as midwall fractional shortening. ClinicalTrial.gov (ID NCT02851745).

Prevalence of left ventricular systolic dysfunction in atypical outpatient pacemaker cohort.

BackgroundRight ventricular (RV) pacing is the standard treatment for symptomatic bradycardia. RV pacing is known to cause dyssyncrony. New treatment options like His bundle pacing enhance the focus on left ventricular dysfunction in patients with pacemakers.ObjectivesThe aim of this cross-sectional study was to obtain a real-life picture of the patients in a representative cohort of outpatients with permanent pacemakers. The prevalence and causes of left ventricular dysfunction (LVD) were explored.MethodsIn total, 1869 patients of a pacemaker outpatient clinic were screened for left ventricular systolic dysfunction by transthoracic echocardiography. All patients were interviewed for symptoms and cardiologist care. Percentages of RV pacing and underlying cardiac disease were recorded.ResultsA left ventricular ejection fraction (LVEF) under 45% was found in 207 (11.1%) of all patients. Predictive factors for a reduced LVEF were a high pacing rate and long-term pacing. LVD due to RV pacing was diagnosed in 3.4% of all patients. Only 845 patients (45%) reported that they regularly visited a cardiologist.ConclusionThere is a high prevalence of unknown LVD in a typical pacemaker cohort. Therefore, regular echocardiographic examinations should be performed in outpatients of pacemaker clinics.

Exercise echocardiography demonstrates potential myocardial damage in patients with repaired tetralogy of Fallot using layer-specific strain analysis.

Exercise stress echocardiography and layer-specific strains are emerging as important tools for cardiac assessment. This study was aimed to evaluate layer-specific strains and torsion parameters during exercise in order to investigate the characteristics of cardiac dysfunction in patients with repaired tetralogy of Fallot and to detect subclinical left ventricular dysfunction. Thirteen patients with repaired tetralogy of Fallot (median age, 17.3 [interquartile range, 14.5-22.9] years; 6 males) and 13 controls (median age, 28.5 [interquartile range, 27.6-31.6] years; 13 males) underwent echocardiography at rest and during supine exercise. Layer-specific longitudinal strain and circumferential strain of three myocardial layers (endocardium, midmyocardium, and epicardium), torsion, and untwisting rate were measured using two-dimensional speckle-tracking echocardiography. Peak endocardial papillary circumferential strain (-21.1 ± 2.6% vs. -25.8 ± 3.8%, p = 0.007), midmyocardial apical circumferential strain (-11.1 ± 4.0% vs. -15.6 ± 3.2%, p = 0.001), epicardial apical circumferential strain (-11.1 ± 4.0% vs. -15.6 ± 3.2%, p = 0.021), and torsion (8.9 ± 6.0 vs. 14.9 ± 4.8 degree, p = 0.021) were significantly lower in the repaired tetralogy of Fallot group than in the control group during exercise, though no significant difference was found between patients and controls at rest. Analysis of layer-specific strains and torsion parameters during exercise could detect subclinical left ventricular dysfunction in patients with repaired tetralogy of Fallot, which might reflect potential myocardial damage, at a stage where these parameters have normal values at rest. This finding provides new insight into the mechanisms of cardiac dysfunction in patients with repaired tetralogy of Fallot.

CORRELATION OF SYSTOLIC TISSUE VELOCITY WITH LEFT VENTRICULAR DYSFUNCTION IN PATIENTS PRESENTING WITH RHEUMATIC SEVERE MITRAL REGURGITATION

Objective: To detect correlation between systolic tissue velocity and left ventricular systolic dysfunction in patients presenting with severe rheumatic mitral regurgitation (MR). Methodology: A comparative study was performed at Punjab Institute of Cardiology, Lahore between October 2016 and February 2018. Fifty eight controls and 192 patients with rheumatic severe MR were included. End systolic dimension (LVESD), end diastolic dimension (LVEDD) and ejection fraction (LVEF) of left ventricle (LV) were taken. Group-1 contained healthy controls. Groups II, III and IV contained the patients of severe MR with non-dilated LV (LVESD ≤40mm and LVEF ≥60%), dilated LV (LVESD ≤40mm and LVEF ≥60%) and decreased LVEF (LVEF&lt;60%) respectively. Tissue doppler was used to measure peak systolic tissue velocity at medial annulus (SV-Med), lateral annulus (SV-Lat) and average velocity (SV-Avg) of each subject. Results: A total of 250 study subjects contained 45.2% (n=113) males and 54.8% (n=137) females. Mean age of the study subjects was 30.8± 9.1. Group-I consisted of 58 controls. There were 69, 67 and 56 subjects in groups II, III and IV respectively. Moving from group-I to group-IV, LVEF decreased from 63.9%±2.2 to 46.2±6.5, LVESD increased from 23.2±2.3 to 49.0±2.9 and LVEDD increased from 45.9±3.5 to 64.3±3.6 respectively. Average systolic tissue velocity (SV-Avg) progressively decreased from group-I being 9.64±0.22 to group-IV being 6.32±0.47. There was a significant negative correlation between LV dysfunction and SV-Avg (spearman’s rank coefficient -0.921, p&lt;0.001). A positive correlation was also found between LVEF and SV-Avg in patients with severe MR only (pearson’s coefficient 0.859, p&lt;0.001). Conclusion: A significant negative correlation exists between the peak tissue systolic velocity and left ventricular dysfunction in patients presenting with severe rheumatic mitral regurgitation. Key words: Mitral Regurgitation, Tissue Velocity, Left ventricular dysfunction

Quantitative evaluation of subclinical left ventricular dysfunction in patients with type 2 diabetes mellitus by three-dimensional echocardiography.

Left ventricular (LV) function undergoes subtle changes (subclinical left ventricular dysfunction) in a large proportion of patients with type 2 diabetes (T2DM) who develop diabetic cardiomyopathy. This study aimed to quantify LV myocardial strain and synchrony in T2DM by real-time three-dimensional echocardiography (RT-3DE), and to evaluate subclinical LV dysfunction in T2DM at different glycemic control levels. Seventy-two patients with T2DM with an LV ejection fraction (LVEF) ≥ 55% and 45 healthy individuals as controls who underwent RT-3DE were studied. Patients were also subdivided into the DMa group (glycosylated hemoglobin < 7%, n = 38) and the DMb group (glycosylated hemoglobin ≥ 7%, n = 34). Three-dimensional strain and synchronization parameters of the left ventricle were measured by RT-3DE and compared among the three groups. Despite a similar LVEF, global longitudinal strain (GLS), global circumferential strain (GCS), and global area strain (GAS) in the DMb group were lower, and the standard deviation of peak time (Tm-SD) and the maximum difference in peak time (Tm-Dif) in the DMb group higher, than those in the control and DMa groups (all p < 0.05). Multivariable linear regression analysis showed that the duration of diabetes was independently associated with GCS (β = - 0.516, p < 0.001) and GAS (β = - 0.391, p = 0.005). HbA1c levels were independently associated with GLS (β = - 0.675, p < 0.001), Tm-SD (β = 3.363, p < 0.001), and Tm-Dif (β = 3.895, p < 0.001). RT-3DE can detect subclinical myocardial dysfunction in poor glycemic control of T2DM, and myocardial dysfunction is associated with the duration of diabetes and HbA1c.

Myocardial Ischemia Correlates with Right Ventricular Dysfunction in Patients with Noncompaction Cardiomyopathy

Noncompaction cardiomyopathy (NCM) results from an arrest of the myocardial compaction process in the embryonic period, leading to the impaired formation of the microvasculature. Predominantly left ventricle is affected, however right ventricle (RV) involvement and its functional impact in NCM remains undefined. We sought to analyze a potential correlation between myocardial ischemia and RV failure in this patient cohort. We enrolled 41 NCM patients (28 male, 13 female), aged 21 to 70 years. At baseline we performed echocardiography to measure RVID (RV inflow diastolic diameter), TAPSE (tricuspid annular plane systolic excursion), Sto (systolic tissue Doppler velocity on tricuspid annulus) and RV FAC (fractional area change). Significant myocardial ischemia was defined as summed difference score (SDS)≥2 on myocardial SPECT at rest and on stress. Myocardial ischemia has been shown in 11 patients (27%, Group A), 30 patients showed no significant ischemic changes (73%, Group B). Groups did not differ in sex (82% male vs. 63% male in Group B, P=0.454), age (48±13 years vs. 47±15 years in Group B, P=0.855), kidney function (serum creatinine 76±11µmol/L vs. 81±26µmol/L in Group B, P=0.565) or liver function (serum bilirubine 12.4±7.1µmol/L vs. 13.3±6.5µmol/L in Group B, P=0.686). When compared to Group B, Group A had significantly lower FAC (30.7±7.7% vs. 44.9±10.2%, P<0.001), greater RVID (3.3±0.6cm vs. 2.9±0.5cm, P=0.016), lower TAPSE (1.9±0.6cm vs. 2.5±0.4cm, P<0.001), higher NT-proBNP levels (1691±1883pg/mL vs. 422±877pg/mL, P=0.006). There was a trend toward lower Sto (10.7±2.6cm/s vs. 12.4±2.4cm/s, P=0.081). Overall, higher SDS was associated with lower FAC (r=-0.51, P=0.006), higher RVID (r=0.41, P=0.032), lower TAPSE (r=-0.49, P=0.008) and higher levels of NT-proBNP (r=0.66, P<0.001). In patients with NCM myocardial ischemia appears to correlate with larger RV size and worse RV function.

Bionic women and men - Part 3: Right ventricular dysfunction in patients implanted with left ventricular assist devices.

What is the topic of this review? Right heart dysfunction remains a major adverse event in patients with end stage heart failure undergoing left ventricular assist device placement. This article reviews the pathophysiology and clinical considerations of right heart failure in this patient population. What advances does it highlight? This review highlights the anatomic and physiological peculiarities of the interplay between left and right heart function in patients undergoing LVAD therapy. These would allow us to further advance our understanding of right ventricular function. The adaptation of the right ventricular (RV) output to a left ventricular assist device (LVAD) often determines the fate of patients with pulmonary hypertension secondary to left heart failure. Pre-existing right heart dysfunction in patients with advanced left heart failure is the consequence of increased (arterial) afterload and not simply the consequence of myocardial disease. If unaccounted for, it has the potential of accelerating into clinical right heart failure after LVAD, leading to significant morbidity and mortality. After LVAD implantation, the RV has to face increased flow generated by the LVAD, cardiac arrhythmias and exaggerated functional interactions between both ventricles. Understanding the key physiological mechanisms of RV dysfunction in patients with end-stage heart failure will allow us to predict and therefore prevent RV failure after LVAD implantation.