Left ventricular mechanical dispersion by tissue Doppler imaging: a novel approach for identifying high-risk individuals with long QT syndrome

Forutsigelse av livstruende hjerterytmeforstyrrelser Hjertespesialist og forsker Kristina Hermann Haugaa har i sin doktorgrad funnet en ny metode som kan brukes til å forutsi hvilke pasienter som kommer til å få alvorlige hjerterytmeforstyrrelser: Ultralyd av hjertet med ny metode kan avsløre hvem som har risiko for hjerterytmeforstyrrelser og hvem som ikke har det. Plutselig hjertedød på grunn av hjerterytmeforstyrrelser er en av de vanligste dødsårsakene i Norge og i den øvrige vestlige verden. Den største risikogruppen er personer som har hatt hjerteinfarkt. Plutselig hjertedød hos yngre skyldes ofte arvelige hjertesykdommer. I avhandlingen “Prediction of cardiac ventricular arrhythmias by echocardiography in patients at risk” undersøker Kristina Haugaa både yngre pasienter med arvelige hjerterytmeforstyrrelser og pasienter som har gjennomgått hjerteinfarkt med den nye metoden for hjerteultralyd. Pasientene ble fulgt i over to år etter hjerteinfarkt. Studiene viser at ujevn hjertekontraksjon er en risikomarkør for å få hjerterytmeforstyrrelser og at den nye metoden vurderer risikoen bedre enn dagens metoder. Med bedre risikovurdering kan man bedre fordele resursene for behandling. Behandlingen innebærer oftest at pasientene i tillegg til medisin får operert inn en automatisk hjertestarter. Den nye metoden som er brukt i avhandlingen vil kunne forbedre utvelgelsen av pasienter med høy risiko for død slik at disse kan utstyres med hjertestarter

Cardiac Mechanical Alterations and Genotype Specific Differences in Subjects With Long QT Syndrome

AbstractObjectivesThis study aimed to explore systolic and diastolic function and to investigate genotype-specific differences in subjects with long QT syndrome (LQTS).BackgroundLQTS is an arrhythmogenic cardiac ion channelopathy that traditionally has been considered a purely electrical disease. The most commonly affected ion channels are the slow potassium channel, IKs (KCNQ1 gene/LQT1), and the rapid potassium channel, IKr (KCNH2 gene/LQT2). Recent reports have indicated mechanical abnormalities in patients with LQTS.MethodsWe included 192 subjects with genotyped LQTS (139 LQT1, 53 LQT2). Healthy persons of similar age and sex as patients served as controls (n = 60). Using echocardiography, we assessed systolic function by left ventricular (LV) ejection fraction (EF), global longitudinal strain (GLS), and contraction duration (16 LV segments). Mechanical dispersion was calculated as standard deviation of contraction duration. Time difference between contraction duration and QT interval from electrocardiography (ECG) was defined as electromechanical time difference. We assessed diastolic function by transmitral filling velocities, early diastolic myocardial velocity (e′), and left atrial volume index (LAVI). Heart rate corrected QT interval (QTc) was assessed from 12-lead ECG.ResultsSystolic function by GLS was reduced in subjects with LQTS compared with healthy controls (−22.1 ± 2.1% vs. −23.0 ± 2.0%, p = 0.01), and GLS was worse in subjects with LQT2 compared with subjects with LQT1 (p = 0.01). Subjects with LQTS had longer contraction duration (426 ± 41 ms vs. 391 ± 36 ms, p < 0.001) and more dispersed contractions (33 ± 14 ms vs. 21 ± 7 ms, p < 0.001) compared with healthy controls. Diastolic function was also reduced in subjects with LQTS compared with healthy controls; e′ was lower (10.7 ± 2.7 cm/s vs. 12.5 ± 2.0 cm/s, p < 0.001), and LAVI was increased (30 ± 8 ml/m2 vs. 26 ± 5 ml/m2, p = 0.01), also when adjusted for age and other possible confounders.ConclusionsSubjects with LQTS had a consistent reduction in both systolic and diastolic function compared with healthy controls. Differences in myocardial function between subjects with LQT1 and subjects with LQT2 may indicate that mechanical alterations in LQTS are genotype specific

Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography

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Mechanical Dispersion Assessed by Myocardial Strain in Patients After Myocardial Infarction for Risk Prediction of Ventricular Arrhythmia

ObjectivesThe aim of this study was to investigate whether myocardial strain echocardiography can predict ventricular arrhythmias in patients after myocardial infarction (MI).BackgroundLeft ventricular (LV) ejection fraction (EF) is insufficient for selecting patients for implantable cardioverter-defibrillator (ICD) therapy after MI. Electrical dispersion in infarcted myocardium facilitates malignant arrhythmia. Myocardial strain by echocardiography can quantify detailed regional and global myocardial function and timing. We hypothesized that electrical abnormalities in patients after MI will lead to LV mechanical dispersion, which can be measured as regional heterogeneity of contraction by myocardial strain.MethodsWe prospectively included 85 post-MI patients, 44 meeting primary and 41 meeting secondary ICD prevention criteria. After 2.3 years (range 0.6 to 5.5 years) of follow-up, 47 patients had no and 38 patients had 1 or more recorded arrhythmias requiring appropriate ICD therapy. Longitudinal strain was measured by speckle tracking echocardiography. The SD of time to maximum myocardial shortening in a 16-segment LV model was calculated as a parameter of mechanical dispersion. Global strain was calculated as average strain in a 16-segment LV model.ResultsThe EF did not differ between ICD patients with and without arrhythmias occurring during follow-up (34 ± 11% vs. 35 ± 9%, p = 0.70). Mechanical dispersion was greater in ICD patients with recorded ventricular arrhythmias compared with those without (85 ± 29 ms vs. 56 ± 13 ms, p < 0.001). By Cox regression, mechanical dispersion was a strong and independent predictor of arrhythmias requiring ICD therapy (hazard ratio: 1.25 per 10-ms increase, 95% confidence interval: 1.1 to 1.4, p < 0.001). In patients with an EF >35%, global strain showed better LV function in those without recorded arrhythmias (−14.0% ± 4.0% vs. −12.0 ± 3.0%, p = 0.05), whereas the EF did not differ (44 ± 8% vs. 41 ± 5%, p = 0.23).ConclusionsMechanical dispersion was more pronounced in post-MI patients with recurrent arrhythmias. Global strain was a marker of arrhythmias in post-MI patients with relatively preserved ventricular function. These novel parameters assessed by myocardial strain may add important information about susceptibility for ventricular arrhythmias after MI

ESC core curriculum for the general cardiologist (2013)

[No abstract available

Evaluation of left ventricular diastolic function: state of the art after 35 years with Doppler assessment

Left ventricular (LV) diastolic function can be evaluated by echocardiographic indices of LV relaxation/restoring forces, diastolic compliance, and filling pressure. By using a combination of indices, diastolic function can be graded and LV filling pressure estimated with high feasibility and good accuracy. Evaluation of diastolic function is of particular importance in patients with unexplained exertional dyspnea or other symptoms or signs of heart failure which cannot be attributed to impaired LV systolic function and to assess filling pressure in patients with heart failure and reduced LV ejection fraction. Furthermore, grading of diastolic dysfunction can be used for risk assessment in asymptomatic subjects and in patients with heart disease

Mechanism of harm from left bundle branch block

The impact of left bundle branch block (LBBB) on cardiac mechanical function ranges from minimal effect in some patients to marked reduction in left ventricular (LV) systolic function in others. It appears that this variability in part reflects differences in anatomical location of the bundle block. In most patients with LBBB and congestive heart failure, however, there is associated cardiac disease such as cardiomyopathies or coronary artery disease which contributes to LV dysfunction. The mechanism of harmful effect of LBBB on cardiac function is in-coordinated ventricular contractions which result in LV contractile inefficiency. Septal contribution to LV systolic function is lost or attenuated and an excessive workload is placed on the LV free wall which responds with remodeling and in some cases it decompensates. The magnitude of the contractile inefficiency depends on the extent of electrical conduction delay and degree of associated heart disease. Another mechanism, which in many patients contributes to cardiac dysfunction in LBBB, is mitral regurgitation due to in-coordinated contractions of the papillary muscles and altered mitral valve function due to LV remodeling. Potentially, reduced LV filling time due to prolonged LV systole may contribute to cardiac dysfunction, but there is limited knowledge about the clinical importance of this mechanism. In LBBB there is typically reduced septal perfusion, probably not as a sign of ischemia, but reflecting physiologic autoregulation of coronary flow in response to reduced septal work that reduces metabolic demand. Future studies should explore how current insights into mechanisms of cardiac mechanical effects of LBBB can be incorporated into decision algorithms for selection of patients for cardiac resynchronization therapy, as well as how to manage patients with LBBB and preserved LV function

A systematic review of diastolic stress tests in heart failure with preserved ejection fraction, with proposals from the EU-FP7 MEDIA study group

Aims: Cardiac function should be assessed during stress in patients with suspected heart failure with preserved ejection fraction (HFPEF), but it is unclear how to define impaired diastolic reserve. Methods and results: We conducted a systematic review to identify which pathophysiological changes serve as appropriate targets for diagnostic imaging. We identified 38 studies of 1111 patients with HFPEF (mean age 65 years), 744 control patients without HFPEF, and 458 healthy subjects. Qualifying EF was >45–55%; diastolic dysfunction at rest was a required criterion in 45% of studies. The initial workload during bicycle exercise (25 studies) varied from 12.5 to 30 W (mean 23.1 ± 4.6), with increments of 10–25 W (mean 19.9 ± 6) and stage duration 1–5 min (mean 2.5 ± 1); targets were submaximal (n = 8) or maximal (n = 17). Other protocols used treadmill exercise, handgrip, dobutamine, lower body negative pressure, nitroprusside, fluid challenge, leg raising, or atrial pacing. Reproducibility of echocardiographic variables during stress and validation against independent reference criteria were assessed in few studies. Change in E/e' was the most frequent measurement, but there is insufficient evidence to establish this or other tests for routine use when evaluating patients with HFPEF. Conclusions: To meet the clinical requirements of performing stress testing in elderly subjects, we propose a ramped exercise protocol on a semi-supine bicycle, starting at 15 W, with increments of 5 W/min to a submaximal target (heart rate 100–110 b.p.m., or symptoms). Measurements during submaximal and recovery stages should include changes from baseline in LV long-axis function and indirect echocardiographic indices of LV diastolic pressure