LV systolic function

imaging in the assessment of LV systolic function by ejection fraction. Though VVI employs a complex multi-step algorithm, it is practically easy to use and involves only obtaining a good quality image and tracing the endocardial border of the region of interest. The advantage is that the border is then automatically tracked through successive cycles and hence cardiac motion may be delineated with greater accuracy. Measurement of global and regional EF by VVI was found to be simple and feasible enough to be used in routine clinical practice.

Previous studies have evaluated the relationship between plasma BNP concentrations and echocardio- graphic measures of disease severity, as well as clinical outcomes for speci fi c valve lesions including aortic sten- osis (AS), aortic regurgitation (AR), mitral regurgitation and mitral stenosis (MS). 5 9 17 18 However, each aortic and mitral valve lesion causes different cardiac pressure and volume loads, and it is unclear whether the mechanism of BNP release and clinical implications of elevated plasma BNP concentrations are dependent on valve lesion type. These previous studies did not dir- ectly compare patients with different valve lesions, which result in different volume and pressure loads on the heart. The aim of this study was to identify both common and valve lesion-speci fi c factors associated with higher plasma BNP concentrations in patients with pre- served LV systolic function, who have isolated AS, AR, mitral regurgitation (MR) or MS, and to assess suitability of BNP for identifying patients with severe valvular heart disease (VHD) across different valve lesions.

On day 1 a total of 47 echocardiographic examinations were available for analysis, since 3 examinations were lost during the installation of a new offline storing and analysis system. Results on day 1 showed that MAPSE was signifi- cantly lower in non-survivors (median 8 [IQR 7.5-11] mm) than in survivors (median 11 [IQR 8.9-13] mm) of 28-day mortality (p= 0.028). No other echocardiograohic parameter showed any significant difference (Table 1). In 14 (30%) patients ejection fraction was preserved (LVEF ≥ 55%) and in 33 patients (70%) impaired (LVEF ≤ 50%) with no significant difference in mortality between these two groups. Six patients had severely reduced LV systolic function (LVEF < 30%). MAPSE was 11 [11–12.8] mm in patients with preserved EF and 9 [7.3-12.3] mm in those with reduced EF (p= 0.069). MAPSE correlated signifi- cantly with LVEF, é, E/é and hsTnT whereas LVEF did not correlate significantly with markers of LV diastolic func- tion, filling pressure or cardiac biomarkers (Table 2). MAPSE showed a negative correlation with age (r=−0.411, p=0.003) but was not associated with previous hyper- tension or cardiac disease. LV diastolic dysfunction (é < 8 cm/s) showed a significant negative association with MAPSE (p= 0.047) whereas there was none with LVEF.

Our study had several limitations. Firstly, a larger sam- ple size of AL-CA patients is required for further investi- gation, with an emphasis on myocardial perfusion. Secondly, our present study did not evaluate whether the interstitial myocardial fibrosis detected by LGE or quantified by T1 blood-pool gadolinium kinetics or T1 mapping on CMR could affect coronary microvascular dysfunction, which are valuable for differential diagnosis and the prediction of outcomes in CA patients [39–41]. The association between LGE, and T1 blood-pool gado- linium kinetics or T1 mapping, and first-perfusion im- aging on CMR in CA patients will be investigated in our future study. Thirdly, resting/exercise electrocardiogram, echocardiography and laboratory examination was per- formed to exclude coronary heart disease, however, not all AL-CA subjects received coronary angiography in our study, which could help to scientifically prove that ischemia is caused by microvascular dysfunction. Finally, patients with LVEF < 50 % were defined as exhibiting im- paired systolic function in our study. However, LVEF re- flects the global LV systolic function and is less sensitive in assessing the regional systolic function. In addition, CA patients has smaller cavity sizes (reduced LVEDV) due to increased wall thickness could result in a com- parative decrease in EF compared with normal controls, EF may be >50 % in patients with small cavity size result from concentric “hypertrophy”, thus may not accurate to evaluated the systolic function and may consequently mis-classifying some patients with truly impaired systolic function into the normal systolic function group. Dan Liu et al. previously reported that longitudinal Table 6 ROC analysis of first-pass perfusion for detecting microvascular dysfunction between AL-CA patients with impaired systolic function and normal controls

The main finding of our study was that despite no difference in LV systolic function between patients with HFpEF and controls, the former had clear evidence for increased LV wall thickness and overall cavity mass, compromised long axis amplitude and velocities as well as worse diastolic function in the form of higher E/A, E/e’ and dyssynchrony as shown by high Tei index and longer t-IVT. LA volumes were also larger and its emptying fraction lower than controls. In addition, patients with MetS had worse LA structure and reservoir function compared to non-MetS. Finally, age, LA diameter and MetS were the only independent predictors of NYHA class in this HFpEF population. Data interpretation

The present study demonstrates that 88% of asympto- matic or mildly symptomatic carriers of LMNA muta- tions causing cardiomyopathy had typical myocardial fibrosis, predominantly in the mid-myocardium of the basal septum. This was observed in all individuals with an AV conduction defect. The pattern of enhancement was typically linear and less than 50% of the area of the segment. Enhancement was associated with wall motion abnormalities at LV basal segments, where the degree of enhancement had a significant correlation with decreased motion. Minor systolic dysfunction without ventricular dilatation, preserved systolic function with mild LV dilatation or systolic dysfunction with mild dilatation of LV, or of both ventricles, was observed in 69% of LMNA mutation carriers. In our patients as an early marker of the disease longitudinal LV systolic function was decreased in nine patients when compared to normal values [13]. In addition, we found that LV EF as well as percentage of myocardial fibrosis correlated significantly with abnormal MAD.

Hypertensive cardiomyopathy can present in neo- nates with nonspecific symptoms and systemic hyper- tension. Because hypertension in infants is sometimes ignored or misinterpreted as agitation, echocardiography can provide critical markers of the disease. Important findings that should lead to this diagnosis include de- pressed LV systolic function without chamber dilation, elevated LV mass, diastolic dysfunction with significant LA dilation, and aortomegaly with Doppler evidence of increased systemic vascular resistance. These findings should result in rapid recognition of the pathophysio- logic condition and should direct appropriate additional

(6 ALL, 12 AML) demonstrated no significant difference from controls in LV systolic function parameters includ- ing LV ejection fraction, similar to what was observed in our patient at initial echocardiography [18]. However, LV diastolic dysfunction has been observed in 38 percent of leukemic patients, independent of age and heart rate. It is likely that cardiac compromise in our patient was due to a combination of restrictive cardiomyopathy due to leuke- mic infiltration, concomitant anemia, cardiac dilatation, conduction blocks and myocardial necrosis. Myocardial necrosis was most likely due to a combination of, a) ischemic damage secondary to anemia and prolonged hypotension and b) extensive leukemic infiltration. Mark- edly rapid decrease in ejection fraction from 66% to 33% also suggests the role of ischemia, since leukemic infiltra- tion is not expected to cause this degree of systolic dys- function over a 24-hour period.

Background: Femoral dP/dt max (maximum rate of the arterial pressure increase during systole) measured by pulse contour analysis has been proposed as a surrogate of left ventricular (LV) dP/dt max and as an estimator of LV systolic function. However, femoral dP/dt max may be influenced by LV loading conditions. In this study, we evaluated the impact of variations of LV systolic function, preload and afterload on femoral dP/dt max in critically ill patients with cardiovascular failure to ascertain its reliability as a marker of LV systolic function.

The proposed mechanisms for LAE in obese patients are illustrated in Figure 1. Obesity causes an increase in total blood volume and cardiac output and is associated with elevated cardiac filling pressures. This hypercircu- lation leads to LV dilatation or can cause compensatory LVH and diastolic dysfunction. The LV dilatation can lead to increased wall stress which can lead to secondary or eccentric hypertrophy of the left ventricle. Presence of chronically elevated wall stress can lead to LV systolic dysfunction which in the presence of increased cardiac work load (exceeding the compensatory hypertrophy) can result in LAE. The strong association of LV wall thickness, LV chamber size and LV systolic function with LAE in our study suggests that LAE likely resulted from the effects of obesity on LV geometry.

Our finding of more than 50% of patients with LV diastolic dysfunction in the present cohort was not unexpected, since LV diastolic dysfunction is considered to be resistant to medical treatment and prevalent in diabetic patients [5,16]. The pathogenesis of LV diastolic function is not known in detail, but a contribution of increased afterload, e.g. due to augmented arterial stiff- ness and microvascular disease, reduced myocardial per- fusion, and increased myocardial stiffness associated with extracellular matrix alterations, fibrosis and meta- bolic derangements have been suggested [33]. Interest- ingly, LV diastolic dysfunction was not related to LV mass or carotid compliance in patients with or without significant CAD, but a strong association with glycaemic control (HbA1c levels) was found. This finding is in accordance with the hypothesis that hyperglycaemia can induce increased myocardial stiffness, e.g. by extracellu- lar advanced glycation products leading to myocardial fibrosis [33]. No patients had restrictive LV diastolic dysfunction and only 4 patients had E/e ’ > 15 which would indicate severely increased LV filling pressures and is considered to be pathognomonic for diastolic heart failure in the presence of heart failure symptoms and normal LV systolic function [27]. The prevalence of moderate-severe LA dilatation was also low and particu- lar severely abnormal LA volume ( ≥ 40 ml/m 2 ) was only observed in 5 patients. A recent study reported LA distension ( > 32 ml/m 2 ) in almost one third of patients with a lower CV risk profile compared to our study cohort [16]. These observations add to the notion that intensive multifactorial treatment may reduce the detri- mental cardiac consequences of diabetes and hereby potentially delay clinical heart failure and reduce CV mortality. However, as stated above the true clinical impact of the presence of echocardiographic abnormal- ities in our present cohort of aggressively treated patients will be examined by planned prospective fol- low-up.

LVSD is defined as a left ventricular ejection fraction less than 50%. [1] The patients with heart disease are classified according to normal or abnormal LV systolic function. [1] Angiotensin converting enzyme inhibitors(ACEi) and β-blockers have been found to improve exercise tolerance and symptoms (usually assessed by the NYHA functional class) in patients with heart failure due to LVSD as well as to significantly prolong survival and reduce hospitalization rates. [2,3]

In patients with heart failure, plasma BNP levels are inversely related to LV systolic function [17]. In contrast, in our study population we did not find any correlation between BNP levels and systolic LV function as evaluated by echocardiographic ejection fraction. This finding is not surprising, since in the study group, which represents con- secutive patients admitted to our Center, the prevalence of LV systolic dysfunction is rather low (only 3 patients had a LVEF <40%). Although our population was not selected, this might not represent the whole spectrum of post car- diac surgery patients.

Left ventricular hypertrophy (LVH) is a common imag- ing finding in daily clinical practice. LVH can be detected in athletes following long-term exercise training, in hypertensive and aortic stenosis patients due to persis- tent pressure overload, in hypertrophic cardiomyopathy patients, and in patients with systemic diseases such as amyloidosis, Fabry disease, Friedreich’s ataxia. Echo- cardiography plays an important role on detecting LVH and underlying causes in current clinical practice [1, 2]. Nowadays, speckle tracking imaging (STI) technique is used to quantify global and regional myocardial defor- mation [3]. Its clinical application has been intensively studied in patients with various cardiovascular disorders over the last decade [4]. STI-based automated function imaging (AFI) is a user friendly advancement to evaluate left ventricular (LV) systolic function and regional pat- terns based on regional LV longitudinal strain values [5]. The result of AFI is usually presented as a bull’s eye plot

We studied nine male patients, mean age 74 years, (range 58-79 years), with severe coronary artery disease (eight with three-vessel and one with two-vessel disease) and severely symptomatic (CCS angina functional class II-III). Except for one patient who had dynpnea, the rest suffered from daily angina. Eight of the patients underwent later coronary bypass grafting (CABG) and one patient with earlier CABG underwent percutanous coronary interven- tion. All patients had normal global LV systolic function at rest except for one patient who had mildly depressed global LV systolic function (LV ejection fraction ≈ 45%). Three patients had a history of myocardial infarction, three had a history of systemic arterial hypertension, three had a history of paroxysmal atrial fibrillation, three had a mild form of chronic renal failure, and none had a history of diabetes mellitus. All patients were treated with aspirin, beta-blockers, long acting nitrates and calcium channel blockers and seven with either angiotensine converting enzyme inhibitors or angiotensine II receptors blockers. Standard echocardiography

Sixty patients were enrolled in the study. Patients were divided into two groups with LVH (n = 30) and without LVH (control group, n = 30). LVH was defined as an LV mass index (LVMI) >96 g/m 2 for women and >114 g/m 2 for men. The causative of patients with LVH was essen- tial hypertension with the exception of chronic renal fail- ure, idiopathic hypertrophic cardiomyopathy, amyloidosis. Patients with myocardial infarction, atrial fibrillation, valvular disorders, and any other structural heart disease were excluded. Patients with poor echocardiographic image quality in the apical 2-chamber and 4-chamber views were also excluded. LV function was measured using conventional echocardiography, tissue Doppler imaging (TDI), and 2D-STE. LV systolic function was assessed by EF, midwall FS, midwall EF, and longitudinal strain. Sys- tolic function was compared between the two groups and the relationships of LVMI with LV systolic parameters, in- cluding midwall EF, were investigated. Ethical review board approval from our hospital was obtained.

Background and Objective : Wilson’s disease is a genetic disorder of copper metabolism that affects liver and other organs including heart. In early stages of myocardial affection, the left ventricle (LV) appears apparently normal when evaluated by traditional two-dimensional (2D) echocardiography. The aim of this study was to detect subclinical LV dysfunction in children with Wilson’s disease using 2D speckle tracking echocardiography. Patients and Methods : Twenty children with Wilson’s disease were compared with age- and sex-matched 20 healthy children. All subjects were evaluated by tradi- tional 2D echocardiography and speckle tracking echocardiography. Results : There were no significant differences between patients and controls regarding conventional echo parameters except for lower E mitral flow and E' annular septal peak velocity in patient group. The regional peak longitudinal strain of apical 4 chamber view was −17.8% ± 4.2% in patients and −20.1% ± 2.3 % in control subjects (P = 0.043), and for apical 2 chambers view, it was −20.1% ± 3.6% in patients and −22.6% ± 3.4% in control subjects (P = 0.034) and it was −18% ± 3.5% in patients and −20.5% ± 3.2% in control subjects (P = 0.025) in apical long axis view. The global peak longitudinal strain was also lower in patients than control group (18.3% ± 3.2%, and 20.85% ± 2.4%) respectively (P = 0.014). There were no significant differences between both groups re- garding circumferential and radial strains (P > 0.05). Conclusions : Despite apparently normal LV systolic function, the children with Wilson’s disease demonstrated significantly lower peak longitudinal strain as an indicator for early affection of LV systolic function.

Copyright © 2012 Piercarlo Ballo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Management of patients with peripartum cardiomyopathy (PPCM) is still a major clinical problem, as only half of them or slightly more show complete recovery of left ventricular (LV) function despite conventional evidence-based treatment for heart failure. Recent observations suggested that bromocriptine might favor recovery of LV systolic function in patients with PPCM. However, no evidence exists regarding its effect on LV diastolic dysfunction, which is commonly observed in these patients. Tissue Doppler (TD) is an echocardiographic technique that provides unique information on LV diastolic performance. We report the case of a 37-year-old white woman with heart failure (NYHA class II), moderate LV systolic dysfunction (ejection fraction 35%), and severe LV diastolic dysfunction secondary to PPCM, who showed no improvement after 2 weeks of treatment with ramipril, bisoprolol, and furosemide. At 6-week followup after addition of bromocriptine, despite persistence of LV systolic dysfunction, normalization of LV diastolic function was shown by TD, together with improvement in functional status (NYHA I). At 18-month followup, the improvement in LV diastolic function was maintained, and normalization of systolic function was observed. This paper might support the clinical utility of bromocriptine in patients with PPCM by suggesting a potential benefit on LV diastolic dysfunction.

sult from the fact none of the previous researchers specified the efficacy of upgrade CRT according to initial pre-PPM LV systolic function. In other words, patients with preserved pre- PPM LVEF (PiCM upgrade) and those with reduced pre-PPM LVEF (non-PiCM upgrade) were all incorporated into the same group, increasing the heterogeneity of the upgrade group. On the contrary, we made an extra effort to break down the up- grade CRT group into the PiCM and non-PiCM upgrade sub- groups; we investigated LVEF prior to PPM implantation and the presence of other causes of LVSD by a comprehensive re- view of patient medical records, including clinical information, echocardiography, ECG and other imaging and laboratory findings. We hypothesized that patients with PiCM would be better CRT responders than those in the other CRT groups, because, by definition, most of them had non-ischemic sub- strate and LBBB pattern, which are well-known predictors for favorable CRT response. 18-21 PiCM patients have other favor-

Figure 1 In vivo alterations in right and left ventricular glucose metabolism and function. Relative change in systolic function of RV (tricuspid annulus systolic plane excursion; TAPSE) (A) and LV (fractional shortening) (B) and metabolic rate of glucose utilisation (MRglu) measured under hy- perinsulinaemic euglycemic clamp conditions for RV (C) and LV (D) of ZL rats (white bars) and ZDF rats (black bars). Data are expressed as mean ± SEM, n = 4-9, * p < 0.05 vs. ZL rats. Relationship of RV systolic function (TAPSE) with LV systolic function (fractional shortening) (E; r = 0.86, p < 0.05, n = 11) and RV MRglu with LV MRglu (F; r = 0.74, p <0.05, n = 10).