Global Diastolic Dysfunction Research Articles

Global molecular calcium score: is there a link between sodium fluoride uptake and cardiovascular risk burden?

Abstract Background Sodium fluoride (18F-NaF) uptake in positron emission tomography with computed tomography (PET-CT) identifies active microcalcification both in atherosclerotic plaques and the aortic valve. Purpose We aimed to evaluate global cardiac microcalcification activity with 18F-NaF, as a measure of the microcalcification burden, in high cardiovascular (CV) risk patients. Additionally, as an exploratory endpoint, we evaluated the association between global cardiac microcalcification and diastolic dysfunction. Methods High CV-risk individuals without previous CV events from a single centre were prospectively scanned with 18F-NaF PET-CT. Total cardiac 18F-NaF uptake was measured as global molecular calcium score (GMCS), which was calculated by summing the product of mean standardized uptake value and volume of the region of interest on every slice within the borders of the heart. The result was then divided by the number of slices to adjust for the volume. Results We included sixty-five patients with a mean age of 64.0 ± 9.0 years and 38.5% females. There was a high rate of CV risk factors, including hypertension (95.4%), diabetes (84.6%), dyslipidemia (78.5%), obesity (58.5%), smoking (26.2%) chronic kidney disease (18.5%), and family history of premature coronary disease (9.2%). The mean 10-year risk of fatal and nonfatal cardiovascular events predicted by ASCVD risk score was 30.54 ± 18.4. Median GMCS was 221.42 [IQR 144.55-317.58]. Individuals with > 5 CV risk factors (46.2%) had increased overall GMCS compared to those with a lower number of CV risk factors (295.29, IQR 159.37-356.87 vs 186.16, IQR 122.57-281.78; p=0.03). Thirty-three patients underwent diastolic dysfunction evaluation by echocardiography. All patients had normal left ventricle ejection fraction, mean of 62.86 ± 3.58%. Mean E/A was 0.88 ± 0.27, mean septal e’ velocity 0.07 ± 0.02 m/s, mean lateral e’ velocity 0.08 ± 0.02 m/s, and mean average E/e’ 10.7 ± 3.3. The mean peak tricuspid regurgitation velocity was 2.14 ± 0.59 m/s and the median indexed left atrium volume was 37, IQR 29-44mL/m2. After applying the algorithm for diagnosis of diastolic dysfunction in subjects with normal ejection fraction, 21.2% had diastolic dysfunction and 36.4% had a normal diastolic function, while 42.4% were indeterminate. There was no correlation between echocardiographic variables of diastolic function and GMCS, except for indexed left atrium volume (r = 0.83, p<0.01). There was no association between GMCS and diastolic function categories. Conclusions In a high CV risk cohort, the global cardiac microcalcification assessed by GMCS was associated with the burden of CV risk factors. Additionally, despite a strong positive correlation between GMCS and indexed left atrium volume, we found no association between GMCS and echocardiographic variables of diastolic function.

Associations Between Albuminuria, Estimated GFR and Cardiac Phenotype in a Cohort with Chronic Kidney Disease: The CPH-CKD ECHO Study

ObjectiveEchocardiographic findings in chronic kidney disease (CKD) vary. We sought to estimate the prevalence of abnormal cardiac structure and function in patients with CKD and their association to estimated glomerular filtration rate (eGFR) and urine albumin/creatinine ratio (UACR). MethodsWe prospectively enrolled 825 outpatients with non-dialysis-dependent CKD, mean age 58± 13 yrs, and 175 matched healthy controls, mean age 60±12 yrs. Echocardiography included assessment of left ventricular (LV) hypertrophy, LV ejection fraction (LVEF), global longitudinal strain (GLS) and diastolic dysfunction according to ASE/EACVI guidelines. ResultsLV hypertrophy was found in 9% of patients vs. 1.7% of controls (p=0.005) was independently associated with UACR (p=0.002). Median LVEF was 59.4% (IQR 55.2, 62.8) in patients vs. 60.8% (57.7, 64.1) in controls (p=0.002). GLS was decreased in patients with eGFR <60ml/min/1.73m² (-17.6%±3.1%) vs. patients with higher eGFR (19.0%±2.2%, p<0.001), who were similar to controls. Diastolic dysfunction was detected in 55% of patients and in 34% of controls. LimitationsNon-random sampling, cross-sectional analysis. ConclusionsWe report lower prevalence of hypertrophy than previous studies, but similar measurements of systolic and diastolic function. Cardiac remodeling in CKD may be influenced by treatment modalities, demographics, comorbidities and renal pathology.

Cardiac impairments in postacute COVID-19 with sustained symptoms: A review of the literature and proof of concept.

Although acute COVID‐19 is known to cause cardiac damage in some cases, there is still much to learn about the duration and relative permanence of the damage that may occur. Long COVID is a condition that can occur when COVID‐19 symptoms remain in the postviral acute period. Varying accounts of long COVID have been described across the literature, however, cardiac impairments are sustained in many individuals and cardiovascular assessment is now considered to be an expected follow‐up examination. The purpose of this review and proof of concept is to summarize the current research related to the assessment of cardiac function, including echocardiography and blood biomarker data, during the follow‐up period in patients who recovered from COVID‐19. Following a literature review, it was found that right ventricular dysfunction along with global longitudinal strain and diastolic dysfunction are common findings. Finally, more severe acute myocardial injury during the index hospitalization appears to exacerbate cardiac function. The available literature implies that cardiac function must be monitored in patients recovered from COVID‐19 who remain symptomatic and that the impairments and severity vary from person‐to‐person. The proof‐of‐concept analysis of patients with cardiac disease and respiratory disease in comparison to those with sustained symptoms from COVID‐19 suggests elevated systolic time interval in those with sustained symptoms from COVID‐19, thus reducing heart performance indices. Future research must consider the details of cardiac complications during the acute infection period and relate this to the cardiac function in patients with long COVID during mid‐ and long‐term follow‐up.

Кардиогемодинамические показатели миокарда у пациентов с истинной полицитемией

The aim of the research. To study structural and functional parameters of the heart in patients with polycythemia vera. Material and methods. A total of 63 patients with stage I-IIB polycythemia vera (27 male and 36 female) and 52 healthy subjects underwent echocardiography, dopplerography, tissue dopplerography of fibrous rings of atrioventricular valves as well as evaluation of longitudinal strain of the left ventricular myocardium. Results. In patients with polycythemia vera, there is enlargement of heart chambers, interventricular septum hypertrophy develops in 20.6% of the cases, pulmonary hypertension in 39.7% of the cases, global diastolic dysfunction of the left ventricle in 84.1% of the cases, as well as diastolic dysfunction of the fibrous rings of the mitral and tricuspid valves and a decrease in longitudinal strain parameters of the left ventricle indicating impairment of its contractile function. Conclusion. The decline in parameters of tissue dopplerography of the fibrous rings of the atrioventricular valves and longitudinal strain of the left ventricular myocardium may serve as early criteria for diagnosis of myocardial dysfunction in patients with polycythemia vera.

Anabolic Steroids Use Is Associated with Impairments in Atrial and Ventricular Cardiac Structure and Performance in Athletes.

Despite potential severe cardiac side effects, anabolic androgenic steroids (AAS) are increasingly used by strength athletes. However, previous echocardiographic studies focused on the left ventricular (LV) strains but did not assess LV twist and untwist mechanics. Moreover, left atrial (LA) function has been often neglected, and its stiffness, an important determinant of LA reservoir function, has never been challenged. The aim of this study was to investigate the effects of AAS on LA and LV morphologies and functions in strength athletes. Fifty subjects including 20 strength-trained young athletes age 32.0 ± 8.5 yr with a mean duration of AAS use of 4.7 ± 1.8 yr (users), 15 athletes with no history of AAS use (nonusers) and 15 sedentary controls underwent speckle tracking echocardiography to assess LA and LV morphology and function. Users showed higher LA reservoir dysfunction than nonusers (33.7% ± 10.9% vs 44.9% ± 9.9% respectively, P = 0.004) and higher LA stiffness (0.13 ± 0.05 vs 0.19 ± 0.08 A.U., respectively; P = 0.02), higher LV mass index and lower global and regional LV diastolic and systolic dysfunction (global longitudinal strain: -15.5% ± 3.2% vs -18.9% ± 1.8% respectively; P = 0.003), with a drop of LV twist-untwist mechanics (untwisting velocity: 61.5°·s-1 ± 20.2°·s-1 vs 73.7°·s-1 ± 16.1°·s-1 respectively, P = 0.04). There were significant correlations between LV mass and LV apical rotation (P = 0.003, r = 0.44) and diastolic longitudinal strain rate (P = 0.015, r = 0.33). Our results showing significant LA and LV remodeling and dysfunctions in young AAS using athletes are alarming. Screening echocardiography based on speckle tracking echocardiography parameters for early diagnosis, as well as a stronger awareness in athletes and in physicians are warranted in this context.

Prevalence of cardiac amyloidosis in patients with unexplained left ventricle hypertrophy

Abstract Background Amyloid cardiomyopathy (CA) it is more frequently diagnosed due to rapidly developing imaging modalities. Misfolding of transthyretin (TTR) is the source of two distinct forms of amyloidosis (ATTR): acquired wild-type (ATTRwt) and hereditary (ATTRm). Types of TTR gene variants display genetic and ethnic variability. The aim of this prospective study was to assess the prevalence and types of pathogenic genetic variants associated with ATTRm amyloidosis in patients with unexplained left ventricle (LV) hypertrophy. Methods We evaluated prospectively 101 consecutive patients (37 (37%) females, age: 69.7±13.6 y.o.) in years 2016–2021. Analysis included clinical data, free light chain blood immunoglobulins and urine immunofixation, transthoracic echocardiography (TTE), single-photon emission computed tomography (SPECT) with 3,3-disphono-1,2-propanodicarboxylic acid (DPD), and in selected cases cardiac or soft tissue biopsy. Patients with DPD cardiac uptake in SPECT or positive histopathology or family history of ATTR were subjected to genetic testing by an amplicon-based next-generation TTR sequencing approach. Results Enrolled patients presented with marked LV hypertrophy with maximum wall thickness of 18.9±4 mm. Based on performed tests 34 patients (33.7%) were diagnosed with amyloidosis, including 17 cases of light-chain amyloidosis (AL), 16 of ATTR, and 1 case of other type of amyloidosis. Overall, patients with CA presented with mean 2.6±0.9 NYHA class. In TTE there was LV maximum wall thickness of 19.5±4 mm and LV mass value index value of 182±48 g/m2, decreased global longitudinal strain value (GLS, −14.1±5%) and advanced diastolic dysfunction (EA 2.2±1.1, E/E' 22±9). Overall, there were 8 cases of ATTRwt and eight patients were diagnosed ATTRm. There were detected following types of TTR variants - c.302C&amp;gt;T p.(Ala101Val) in a single male patient, c.325G&amp;gt;A p.(Glu109Lys) in a single male patient and c.157T&amp;gt;C p.(Phe53Leu) in six patients. Overall, 10 patients with ATTR presented with polyneuropathy, additionally six had diagnosed carpal tunnel syndrome. All patients with ATTRm had positive family history for CA. Conclusions In patients with unexpected LV hypertrophy evaluated in a cardiology referral center a high number of patients may suffer from underlying CA. Types of detected TTR gene variants associated with CA included most often Phe53Leu, and rare variants Ala101Val, Glu109Lys. Funding Acknowledgement Type of funding sources: None.

Scintigraphic and echocardiographic evaluation of patients with cardiac transthyretin amyloidosis and first-degree relatives

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Pfizer Research Grant (ID#57165999) Background Misfolding of transthyretin (TTR) is the source of two distinct forms of amyloidosis (ATTR): acquired or wild-type (ATTRwt) and hereditary (ATTRm), which is transmitted in an autosomal dominant inheritance with a variable penetrance. Types of transthyretin (TTR) gene mutations display genetic and ethnic variability. Purpose The aim of this prospective study was to assess the TTR gene variants, echocardiographic parameters and regional left ventricle 99mTc-DPD uptake among patients with ATTR and first-degree relatives. Methods We present data based on evaluation of first 25 patients (13 (52%) females), including 10 (40%) index patients with ATTR (age 66.4 ± 13 years) and 15 (60%) first-degree relatives who were studied between June 2020 and February 2021. Analysis included clinical data, free light chain blood immunoglobulins and urine immunofixation, transthoracic echocardiography (TTE) with global longitudinal strain (GLS) analysis, single-photon emission computed tomography (SPECT) with 3,3-disphono-1,2-propanodicarboxylic acid (DPD), genetic testing by an amplicon-based next-generation TTR sequencing approach, and in selected cases cardiac or soft tissue biopsy. Results Overall, 6 index patients were diagnosed with ATTRm and 4 with ATTRwt presenting mixed, cardiac or neuropathic phenotype. There were detected following types of TTR variants - Phe53Leu, Ala101Val, Glu112Lys, Glu109Lys. Nine out of 10 index patients were diagnosed with amyloid cardiomyopathy (CA) with grade 2-3 tracer uptake in SPECT and symptomatic heart failure (NYHA 2.2 ± 1.1; NT-proBNP value 2224 ± 2799 pg/ml). In both ATTRm and ATTRwt there were patients presenting with either focal or diffuse tracer pattern evaluated by SPECT technique. In TTE there was marked left ventricle (LV) hypertrophy with maximum wall thickness of 22 ± 5 mm and LV mass value index value of 382 ± 111 g/m2. All patients with CA had abnormal global longitudinal strain (GLS, -14.5 ± 5%) and diastolic dysfunction (EA 1.56 ± 0.76, E/E’ 16 ± 11). None of relatives expressed tracer uptake in scintigraphy. Overall, 5 first-degree relatives were diagnosed with Phe53Leu variant, among them two patients presented with decreased GLS value. Conclusions Patients with ATTR presented in TTE with LV hypertrophy, decreased GLS value, diastolic dysfunction and grade 2-3 in scintigraphy with either focal or diffuse tracer uptake in SPECT technique. None of first-degree relatives expressed increased tracer uptake in scintigraphy. However, some of relatives who were diagnosed with pathogenic TTR variant presented with decreased GLS value.

Prevalence and pathophysiology of subclinical cardiac dysfunction in obesity patients detected by multimodality diagnostics

Abstract Background Obesity doubles the lifetime risk of developing heart failure. Current knowledge on the role of obesity in causing cardiac dysfunction is insufficient for optimal risk stratification. Purpose The aim of the study was first to identify the prevalence of subclinical cardiac dysfunction in obesity patients and second to investigate the underlying pathophysiology by comparing obesity patients with and without cardiac dysfunction. Methods The CARDIOBESE-study is a cross-sectional multicentre study of 100 obesity patients (BMI ≥35 kg/m2) without known cardiovascular disease, and 50 age- and gender-matched non-obese controls (BMI ≤30 kg/m2). Echocardiography was performed, blood samples were collected and a Holter monitor was affixed. Cardiac dysfunction was defined as either reduced LV ejection fraction, decreased global longitudinal strain (GLS), diastolic dysfunction, sustained supraventricular or (non)sustained ventricular arrhythmia or an increased BNP. Results Figure 1a shows the characteristics of the obesity patients and the non-obese controls. 59 obesity patients (48 [42–50] years, 70% female) showed subclinical cardiac dysfunction: 57 patients had decreased GLS, 2 patients with normal GLS had either diastolic dysfunction or increased brain natriuretic peptide. Only 1 non-obese control had diastolic dysfunction, none had another sign of cardiac dysfunction. Figure 1b shows the characteristics of obesity patients with and without cardiac dysfunction. Multivariable logistic analysis identified male gender and SDNN-index, which is a heart rate variability parameter and thereby a measure of autonomic dysfunction, as independent significant risk factors for subclinical cardiac dysfunction in obesity patients. Conclusions There was a high prevalence (61%) of subclinical cardiac dysfunction in obesity patients without known cardiovascular disease, which appeared to be best identified by GLS. Subclinical cardiac dysfunction in obesity was linked to autonomic dysfunction and male gender, and not to the presence of traditional cardiac risk factors, inflammation, increased cardiac filling pressure, cardiomyocyte damage or increased left ventricular mass. Figure 1 Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Stichting BeterKeter

Right and left ventricular interaction in pulmonary hypertension: Insight from velocity vector imaging.

To evaluate whether global peak systolic strain (PSS) and peak systolic strain rate (PSSR) derived from velocity vector imaging (VVI) allow early recognition of regional and global right ventricular (RV) dysfunction and the impact of this on left ventricular (LV) function in patients with pulmonary hypertension (PHT). RV function is an important determinant of prognosis in patients with heart failure, pulmonary hypertension, heart transplant, and congenital heart diseases. However, evaluation of the right ventricle is often limited by its complex geometry and inadequate visualization of RV free wall. Furthermore, the impact of RV dysfunction on the LV function is not well elucidated. Ninety-nine participants, 35 control patients with normal RV systolic pressure (RVSP) (<30mm Hg) and 64 patients with PHT (25 with mild-to-moderate increase in RVSP [≥36 and <60mm Hg] and 39 with severe increase in RVSP [≥60mm Hg]), underwent comprehensive echo-Doppler assessment and velocity vector imaging (VVI) for strain rate analysis. RV regional peak systolic and diastolic tangential velocity, strain, and strain rate were obtained from the basal, mid and apical segments of the RV free wall and interventricular septum (IVS) from apical 4-chamber view at end-expiration. Similar data were obtained from eighteen LV segments from apical 4-chamber, 2-chamber, and long-axis views. Peak systolic strain, strain rate, and tangential velocity at all segments in the RV free wall and IVS were decreased compared to controls in patients with PHT (P<0.001). Significant correlation (r>0.60; P<0.001) was noted between RVSP and systolic and diastolic strain and strain rate at basal segment in IVS and global RV function. Peak early diastolic strain rate at all segments was also decreased in PHT patients compared with control patients (P<0.01). Furthermore, RV systolic and diastolic strain and strain rate were lower in group 2 with mild-to-moderate hypertension while the conventional echo parameters were normal. Except for IVS segments, other LV segments had no statistical differences in systolic and diastolic velocity, strain, and strain rate compared to controls. However, they were lower than the published normal range. Strain and strain rate derived from VVI demonstrates early recognition of systolic and diastolic RV dysfunction in patients with PHT compared to controls. PHT is associated with global and regional RV systolic and diastolic dysfunction. Systolic and diastolic strain and strain rate from LV was lower compared to controls but were not statistically significant. This may indicate subclinical LV dysfunction in these patients, suggesting that conventional LV function parameters may not be sensitive to recognize subclinical LV dysfunction.

Diagnosis of Nonischemic Stage B Heart Failure in Type 2 Diabetes Mellitus: Optimal Parameters for Prediction of Heart Failure

ObjectivesThis study sought to identify whether impaired global longitudinal strain (GLS), diastolic dysfunction (DD), or left atrial enlargement (LAE) should be added to stage B heart failure (SBHF) criteria in asymptomatic patients with type 2 diabetes mellitus. BackgroundSBHF is a precursor to clinical heart failure (HF), and its recognition justifies initiation of cardioprotective therapy. However, original definitions of SBHF were based on LV hypertrophy and impaired ejection fraction. MethodsPatients with asymptomatic type 2 diabetes mellitus ≥65 years of age (age 71 ± 4 years; 55% men) with preserved ejection fraction and no ischemic heart disease were recruited from a community-based population. All underwent a standard clinical evaluation, and a comprehensive echocardiogram, including assessment of left ventricular hypertrophy (LVH), LAE, DD (abnormal E/e′), and GLS (<16%). Over a median follow-up of 1.5 years (range 0.5 to 3), 20 patients were lost to follow-up, and 290 individuals were entered into the final analyses. ResultsIn this asymptomatic group, LV dysfunction was identified in 30 (10%) by DD, 68 (23%) by LVH, 102 (35%) by LAE, and 68 (23%) by impaired GLS. New-onset HF developed in 45 patients and 4 died, giving an event rate of 112/1,000 person-years. Survival free of the composite endpoint (HF and death) was about 1.5-fold higher in patients without a normal, compared with an abnormal echocardiogram. LVH, LAE, and GLS <16% were associated with increased risk of the composite endpoint, independent of ARIC risk score and glycosylated hemoglobin, but abnormal E/e′ was not. The addition of left atrial volume and GLS provided incremental value to the current standard of clinical risk (ARIC score) and LVH. In a competing-risks regression analysis, LVH (hazard ratio: 2.90; p < 0.001) and GLS <16% (hazard ratio: 2.26; p = 0.008), but not DD and LAE were associated with incident HF. ConclusionsSubclinical left ventricular systolic dysfunction is prevalent in asymptomatic elderly patients with type 2 diabetes mellitus, and impaired GLS is independent and incremental to LVH in the prediction of incident HF.

The effect of kidney transplantation on speckled tracking echocardiography findings in patients on hemodialysis.

Introduction: Cardiac dysfunction is a major cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Previous studies have shown that kidney transplantation can reverse some of the gross changes in the myocardial structure such as left ventricular ejection fraction (LVEF) and volumes. Whether kidney transplantation can reverse the subtle and early myocardial changes in ESRD patients who do not suffer from gross alternations in myocardial function is not yet studied. The aim of this study was to answer this question. Methods: We followed 25 patients with ESRD at baseline that all of them had a kidney transplant and were reassessed 1 month after the transplantation. Conventional and speckle tracking echocardiography (STE)was done at baseline and 1 month after kidney transplantation in patients. Results: LV hypertrophy was the most prevalent finding at baseline (58%), followed by diastolic dysfunction (53%). Kidney transplantation significantly improved the ejection fraction (EF) (treatment effect = 4.23 ± 2.06%; P = 0.046) and apical 4-chamber strain (treatment effect = -0.89 ± 0.37%; P = 0.021) in the patients. It also reduced the LV mass index (treatment effect = -73.82 ± 11.6; P < 0.001) and relative wall thickness (treatment effect = -0.056±0.023; P = 0.021). Other variables including global longitudinal strain and diastolic dysfunction were not improved significantly. Conclusion: STE may show early improvements in myocardial function 1 month after renal transplantation.

Ivabradine improves left ventricular twist and untwist during chronic hypertension

BackgroundLeft ventricular (LV) dysfunction develops during LV hypertrophy and particularly during tachycardia. Thus we investigated the effects of heart rate (HR) reduction with ivabradine, an If-channel blocker, on LV twist and untwist which represents myocardial deformation occurring during the overall systole and diastole and therefore provide valuable evaluation of global LV systolic and diastolic function. MethodsEight chronically instrumented pigs receiving continuous angiotensin II infusion during 28days to induce chronic hypertension and LV hypertrophy. Measurements were performed at Days 0 and 28 after stopping angiotensin II infusion in the presence and absence of ivabradine. ResultsAt Day 0, reducing HR from 75±3 to 55±2beats/min with ivabradine did not affect LV twist but slowed LV untwist along with an increase in LV end-diastolic pressure. At Day 28, LV posterior and septal wall thickness as well as the estimated LV mass increased, indicating LV hypertrophy. LV twist and untwist were significantly reduced by 33±4% from 16±1° and 32±6% from −154±9°/s, respectively, showing global LV systolic and diastolic dysfunction. In this context, ivabradine decreased HR by 25% from 86±5beats/min and significantly improved LV twist from 11±1 to 14±1° and LV untwist from −104±8 to −146±5°/s. ConclusionsAdministration of ivabradine during chronic hypertension and LV hypertrophy improved LV twist and untwist. This further supports the beneficial effect of this drug on both LV systolic and diastolic function during the development of LV hypertrophy.

Maternal cardiovascular dysfunction in women with early onset preeclampsia and late onset preeclampsia: A cross-sectional study.

To compare the cardiovascular changes associated with early onset (EOPE) and late onset (LOPE) subtypes of preeclampsia. A prospective matched cross-sectional study involving 50 women each with early and late onset subtypes of preeclampsia conducted in a tertiary hospital in South India. Cardiac function and remodelling were assessed by conventional 2D, M-mode and doppler echocardiography. Women with EOPE had a significantly more altered left ventricular (LV) geometry, global LV diastolic dysfunction, impairment in myocardial contractility (40% vs. 24%) and a higher total vascular resistance index (863.0 vs 704.0 dynes/s/cm5/m2) compared to LOPE. Stroke volume index (55.3 vs. 62.2 ml/m2) and cardiac work index (520.7 vs. 584.9mmHg×L/min/m2) were higher in women with LOPE. However, the systolic function was found to be preserved in the LV in both the groups. Women with EOPE have a more severe cardiac impairment than those with LOPE. The difference in the hemodynamic indices may provide a chance to tailor patient-specific treatment strategies to improve the pregnancy outcome as well as in early identification and initiation of preventive measures for those at risk of cardiovascular diseases later in life. Adaptation of the heart in women with early onset subtype differs with that of late onset subtype of preeclampsia. Total vascular resistance is higher in early onset group compared to late onset group having a higher cardiac output. These differences in the hemodynamic indices may provide a chance to tailor patient-specific treatment strategies to improve the pregnancy outcome as well as in early identification and initiation of preventive measures for those at risk of cardiovascular diseases later in life.

Appearance of Local Abnormalities of Left Ventricular Contraction on Top of Global Diastolic Dysfunction in the Hypertensive mRen2 Rat

Hypertension is a major co‐morbidity of diastolic dysfunction. Appearance of systolic dysfunction on top of diastolic dysfunction further increases the risk of cardiac failure and mortality. We hypothesized that a hypertensive rat model with diastolic dysfunction can give insight into the pathomechanism of progressing human heart failure.To this end we compared 15 weeks old male rats (n=9‐9) with hypertension due to a renin transgene (mRen2, 228.9±4.9 mmHg; P&lt;0.05) with geno‐/phentoype controls (SD, 121.3±4.4 mmHg).Invasive parameters of left ventricular (LV) active relaxation (Tau, mRen2: 16.9±0.8 ms vs. SD: 12.6±0.6 ms; P&lt;0.05) and passive stiffness (slope of EDPVR, mRen2: 0.050±0.004 mmHg/μL vs. SD:0.040±0.002 mmHg/μL; P&lt;0.05) confirmed diastolic dysfunction with preserved ejection fraction (EF, mRen2: 52.5±0.7% vs. SD:53.3±0.7%) in the mRen2 animals.In contrast, regional echocardiography (n=8‐8) and histology (n=5‐5) showed worse Tei index (0.78±0.04; P&lt;0.05) and relatively higher wall thickness (0.74±0.06; P&lt;0.05) of the LV free wall in mRen2 rats than those of the interventricular septum (0.68±0.02 and 0.54±0.03, respectively).At the cellular level, both lower Ca2+ sensitivity (pCa50) and higher troponin I (cTnI) phosphorylation of LV cardiomyocytes from the free wall and the septum (n=mean of 3‐3/4‐4 rats) suggest abnormal systolic function in the mRen2 group as compared to the control. LV heterogeneity of mRen2 rats is further supported by lower cardiomyocyte maximal Ca2+‐activated force (21.2±1.4 kN/m2), higher Ca2+ sensitivity (5.85±0.01) and phosphorylation of cTnI at Thr‐144 (1.62±0.19; P&lt;0.05) in the free wall than those in the septum (30.0±0.6 kN/m2, 5.76±0.02 and 1.00±0.15, respectively).The local abnormalities of LV contraction on top of global diastolic dysfunction may provide a pathomechanism for the clinical progression with increasing mortality seen in human.

Echocardiographic characterization of hypertrophic cardiomyopathy in Chinese patients with myosin-binding protein C3 mutations

Hypertrophic cardiomyopathy (HCM) is a common autosomal dominant cardiac disease, affecting 1 in 500 people. Myosin-binding protein C3 (MyBPC3) gene mutations are the most common genetic cause of HCM. However, the prevalence of the MyBPC3 gene mutation in Chinese patients with HCM, and their echocardiographic characteristics, remain unknown. In the present study, 48 Chinese patients with HCM were sequenced to identify the MyBPC3 gene and were characterized by their clinical features using 2-dimensional echocardiography and real-time 3-dimensional echocardiography. Nine MyBPC3 mutations were identified in seven unrelated patients out of 48 cases, which accounts for a 15% prevalence of MyBPC3 mutations in Chinese patients with HCM. Family members of the seven patients were further tested and divided into the following two groups based on HCM phenotype and MyBPC3 mutations: Positive genotype with left ventricular (LV) hypertrophy (LVH) (G+/LVH+, n=18); and positive genotype without LVH (G+/LVH-, n=23). These groups were compared with matched normal control subjects (n=30). G+/LVH+ patients showed significantly lower septal and lateral Tissue Doppler imaging (TDI)-derived systolic, early and late diastolic mitral annular velocities compared with the controls. In addition, diastolic dyssynchrony index (DDI) was markedly higher in the G+/LVH+ subjects. However, only septal Ea was significantly lower in G+/LVH- subjects in comparison with controls, with no significant difference in lateral Sa, Ea and Aa, and DDI. In conclusion, the patients in the present study demonstrated a 15% prevalence of MyBPC3 gene mutations in the Chinese HCM population. MyBPC3 gene mutations may cause regional LV hypertrophic remodeling first and further proceed to global hypertrophic remodeling and myocardial diastolic dysfunction.

New and Evolving Concepts Regarding the Prognosis and Treatment of Cardiac Amyloidosis.

Systemic amyloidoses are rare and proteiform diseases, caused by extracellular accumulation of insoluble misfolded fibrillar proteins. Prognosis is dictated by cardiac involvement, which is especially frequent in light chain (AL) and in transthyretin variants (ATTR, both mutated, (ATTRm), and wild-type, (ATTRwt)). Recently, ATTRwt has emerged as a potentially relevant cause of a heart failure with preserved ejection fraction (HFpEF). Cardiac amyloidosis is an archetypal example of restrictive cardiomyopathy, with signs and symptoms of global heart failure and diastolic dysfunction. Independent of the aetiology, cardiac amyloidosis is associated with left ventricular concentric "hypertrophy" (i.e. increased wall thickness), preserved (or mildly depressed) ejection fraction, reduced midwall fractional shortening and global longitudinal function, as well as evident diastolic dysfunction, up to an overly restrictive pattern of the left ventricular filling. Cardiac biomarkers such as troponins and natriuretic peptides are very robust and widely accepted diagnostic as well as prognostic tools. Owing to its dismal prognosis, accurate and early diagnosis is mandatory and potentially life-saving. Although pathogenesis is still not completely understood, direct cardiomyocyte toxicity of the amyloidogenic precursor proteins and/or oligomer aggregates adds on tissue architecture disruption caused by amyloid deposition. The clarification of mechanisms of cardiac damage is offering new potential therapeutic targets, and several treatment options with a relevant impact on prognosis are now available.

Research status on pathogenesis of myocardial depression in sepsis

The cardiovascular system plays a key role in sepsis, and septic myocardial depression is a common finding associated with increased morbidity and mortality.Myocardial depression during sepsis is not clearly defined, but it can perhaps be best described as a global (systolic and diastolic) dysfunction of both the left and right sides of the heart.The pathogenesis of septic myocardial depression involves a complex mix factor of genetic, molecular, metabolic, and structural.Now, the research status on pathogenesis of myocardial depress in sepsis was reviewed. Key words: Myocardial depression; Dysfunction of heart; Sepsis; Septic shock

Characterisation of Myocardial Injury via T1 Mapping in Early Reperfused Myocardial Infarction and its Relationship with Global and Regional Diastolic Dysfunction.

Cardiovascular magnetic resonance (CMR) advances in imaging techniques, permits the ability to accurately characterise tissue injury post myocardial infarction. Pre-contrast T1 mapping enables this through measurement of pre-contrast T1 relaxation times. We investigate the relationship between T1 characterisation of myocardial injury with global and regional diastolic function. Revascularised acute myocardial infarction patients with normal left ventricular (LV) systolic function on TTE were assessed by 1.5T CMR. Acute regional diastolic wall motion abnormalities, global diastolic function measurements, acute segmental damage fraction with LGE and mean segmental pre-contrast T1 values were assessed on matching short axis slices. Forty-four patients were analysed. Mean LVEF was 62.1±9.4%. No difference between NSTEMI (22/44) and STEMI in mean pre-contrast T1 values of infarcted (1025.0±109.2 vs 1011.0±81.6ms, p=0.70), adjacent (948.3±45.3 vs 941.1±46.6ms, p=0.70) and remote (888.8±52.8 vs 881.2±54.5ms, p=0.66) segments was detected. There was no correlation between pre-contrast T1 of infarcted segments with global diastolic dysfunction (E/A, r2=0.216, p=0.06; S/D, r2=0.243, p=0.053; E/E', r2=0.240, p=0.072), but there was significantly positive, moderate correlation with circumferential diastolic strain rate, (r2=0.579, p<0.01) with excellent agreement and reproducibility. Cardiac magnetic resonance evaluation of pre-contrast T1 values revealed no difference between NSTEMI and STEMI patients in terms of tissue characterisation post-myocardial infarction. However, pre-contrast T1 of infarcted tissue is significantly correlated with regional diastolic circumferential strain rate.

Left ventricular diastolic dysfunction in type 2 diabetes patients: a novel 2D strain analysis based on cardiac magnetic resonance imaging

Objective: This study was to develop a strain analysis method to evaluate the left ventricular (LV) functions in type 2 diabetic patients with an asymptomatic LV diastolic dysfunction. Methods: Two groups (10 asymptomatic type 2 diabetic subjects and 10 control ones) were considered. All of the subjects had normal ejection fraction values but impaired diastolic functions assessed by the transmitral blood flow velocity. For each subject, based on cardiac MRI, global indexes including LV volume, LV myocardial mass, cardiac index (CI), and transmitral peak velocity, were measured, and regional indexes (i.e., LV deformation, strain and strain rate) were calculated through an image-registration technology. Results: Most of the global indexes did not differentiate between the two groups, except for the CI, LV myocardial mass and transmitral peak velocity. While for the regional indexes, the global LV diastolic dysfunction of the diabetic indicated an increased strain (0.08 ± 0.044 vs. −0.031 ± 0.077, p = 0.001) and a reduced strain rate (1.834 ± 0.909 vs. 3.791 ± 2.394, p = 0.033) compared to the controls, moreover, the local LV diastolic dysfunction reflected by the strain and strain rate varied, and the degree of dysfunction gradually decreased from the basal level to the apical level. Conclusions: The results showed that the strain and strain rates are effective to capture the subtle alterations of the LV functions, and the proposed method can be used to estimate the LV myocardial function based on cardiac MRI.

Left Ventricular Torsional Parameters in Patients With Non-Ischemic Dilated Cardiomyopathy

Background: Velocity vector imaging (VVI) is a new echocardiography method to assess myocardial deformation in two dimensions. Objectives: In this study, we used VVI to evaluate left ventricular (LV) main torsional parameters in non-ischemic dilated cardiomyopathy (DCM) patients in compared with normal subjects. Patients and Methods: Twenty-six DCM patients and Twenty-four normal subjects were assessed. Echocardiographic images of the short axis apical and basal views of LV were processed by VVI software to measure peak rotation degrees and also peak rotation rates in systole. LV twist was well-defined as the net difference between apical and basal rotation values and also LV torsion was considered as LV twist divided by left ventricular diastolic longitudinal length. In addition, peak untwisting value and untwisting rate were measured in diastole too. Results: LV twist value (5.54 ± 1.94° in DCM VS. 11.5 ± 2.45° in control group) and also LV torsion (0.71 ± 0.28°/cm in DCM VS. 1.53 ± 0.42°/cm in control group) were significantly decreased in DCM patients compared with normal group (P < 0.001 for both); also, the twisting rate was notably lower in DCM vs. control (38.68 ± 14.43°/s in DCM vs. 75.88 ± 17.25°/s in control; P < 0.001) and also untwisting rate (36.28 ± 13.48°/s in DCM vs. -73.79 ± 24.45°/s in control; P < 0.001), However normalization of these times for systolic duration or LV length creates different values. Conclusions: LV twist, torsion and untwist and also rate of them are significantly impaired in DCM and this impairment is well-related to LV global systolic and diastolic dysfunction. VVI is a new noninvasive technique that can be used to evaluate LV torsional parameters.