Myocardial dysfunction identified by three-dimensional speckle tracking echocardiography in type 2 diabetes patients relates to complications of microangiopathy.

BACKGROUND: The clinical effect of diabetic microangiopathy on left ventricular (LV) function is still uncertain. The purpose of this study was to assess the relation between diabetic microvascular complications and comprehensive myocardial deformation measurements using three-dimensional (3D) speckle tracking echocardiography. METHODS: Seventy-seven asymptomatic patients with type 2 diabetes mellitus (DM) and 35 age-matched healthy control subjects underwent 3D echocardiography. Patients with coronary artery disease or LV ejection fraction <50% were excluded. Presence of proliferative retinopathy, microalbuminuria as nephropathy, and decreased coefficient of variation of R-R intervals (CVRR) <3% as cardiac autonomic neuropathy were defined as diabetic microvascular complications. RESULTS: LV ejection fraction, LV mass index, and global radial strain did not differ between control and DM patients. However, global longitudinal and circumferential strain and endocardial area change ratio were lower in patients with DM than in the controls (-12.0±3.0% vs. -16.2±1.9%, -27.7±7.1% vs. 32.2±5.7%, -37.6±7.6% vs. 44.0±6.2%, respectively, p<0.001). In DM patients, longitudinal strain is related to CVRR (R=0.58, p<0.001), retinopathy stage, and nephropathy stage. CONCLUSIONS: Diabetic microangiopathy and its accumulated effects significantly related to subclinical LV dysfunction are characterized by impaired longitudinal shortening.

Subendocardial Systolic Dysfunction in Asymptomatic Normotensive Diabetic Patients.

BACKGROUND: It remains uncertain whether diabetes itself causes specific echocardiographic features of myocardial morphology and function in the absence of hypertension or ischemic heart disease. The purpose of the present study was to determine the characteristics of pure diabetic cardiomyopathy-related echocardiographic morphology and function using layer-by-layer evaluation with myocardial strain echocardiography. METHODS AND RESULTS: We enrolled 104 patients with poorly controlled type 2 diabetes mellitus (mean HbA1c level, 10%) with (n=74) or without (n=40) hypertension and 24 age- and sex-matched healthy volunteers. Patients with coronary artery stenosis or structural heart disease were excluded. Myocardial layer-specific strain was analyzed by speckle tracking echocardiography. Compared with the healthy control group, the normotensive diabetes group showed no significant difference in ejection fraction, left ventricular mass index, diastolic properties, left atrial volume index, or B-type natriuretic protein (BNP) level, but global longitudinal strain and subendocardial radial strain were significantly deteriorated. The deterioration of longitudinal strain correlated with body mass index (R=0.49, P<0.01) and blood pressure (R=0.36, P<0.01) in the normotensive diabetes group. CONCLUSIONS: Deterioration of left ventricular longitudinal shortening accompanied by decreased subendocardial wall thickening are the characteristic functional abnormalities of diabetic cardiomyopathy in patients without hypertrophy, diastolic dysfunction, or elevated BNP. Obesity and blood pressure may also play important roles in this strain abnormality in asymptomatic patients with type 2 diabetes.

Application of 3-dimensional speckle tracking imaging to the assessment of right ventricular regional deformation.

BACKGROUND: The aim of this study was to carry out 3-dimensional speckle tracking imaging (3DSTI) of the right ventricle (RV) and evaluate RV regional wall deformation. METHODS AND RESULTS: 3DSTI of the RV was performed in 35 normal subjects, 8 patients with arrhythmogenic right ventricular cardiomyopathy, and 8 patients with pulmonary arterial hypertension. Peak systolic area change ratio and regional contraction timing relative to global systolic time (time to peak strain/time to end-systole×100) were measured in each segment. Good-quality images were acquired of the inflow segment in 87%, apex in 87%, outflow in 57%, and septum in 94% of the 35 normal subjects. In normal subjects, peak systolic area change ratio of the inflow anterior wall was -41±14%; inflow inferior wall, -35±9%; apical anterior wall, -41±10%; apical inferior wall, -31±11%; outflow, -31±9%; and septum wall, -36±11%. Contraction timing of the apical anterior wall and septum wall were earlier than those of other segments. In patients with RV dysfunction, 3DSTI indicated low peak systolic area change ratio in the damaged area. CONCLUSIONS: RV 3DSTI indicated segmental heterogeneity in magnitude and timing of RV contraction. 3DSTI may be a promising modality for providing precise quantitative information on complex RV wall motion.

Transmural compensation of myocardial deformation to preserve left ventricular ejection performance in chronic aortic regurgitation.

BACKGROUND: In patients with chronic aortic regurgitation (AR), systolic wall stress and volume overload affects left ventricular (LV) systolic function and remodeling. The aim of this study was to assess transmural rearrangements of myocardial deformation to preserve LV ejection performances using speckle-tracking echocardiography in patients with chronic AR. METHODS: Ninety patients with AR were enrolled. On LV short-axis images, total, inner, and outer radial strain and circumferential strain at the inner, mid, and outer layers were calculated. On apical four-chamber images, endocardial longitudinal strain was calculated. End-systolic wall stresses were calculated using previous methods. RESULTS: AR severities were classified as moderate in 31 patients, severe and preserved LV ejection fraction (LVEF) (≥50%) in 42 patients, and severe and reduced LVEF (<50%) in 17 patients. Longitudinal strain was decreased even in the moderate AR group, despite normal end-systolic wall stress. Inner radial strain progressively decreased with increasing end-systolic wall stress, whereas outer radial strain in the moderate and severe AR and preserved LVEF groups was higher than in the control group. Consequently, total radial strain was preserved even in the severe AR and preserved LVEF groups with increased end-systolic wall stress. Similarly, despite reduced inner circumferential strain, outer circumferential strain was higher in the severe AR and preserved LVEF group than in the control group. All strain parameters were lower in the severe AR and reduced LVEF group with dramatically increased end-systolic wall stress than in other groups. CONCLUSIONS: Transmural strain analysis revealed that subendocardial dysfunction accompanied by increased wall thickening at the subepicardium may be a compensatory mechanism of wall thickening to preserve LVEF in patients with chronic AR.

Effects of linear ablation at the isthmus between the tricuspid annulus and inferior vena cava for atrial flutter on autonomic nervous activity: analysis of heart rate variability.

Heart rate is largely affected by the autonomic nervous system. However, little is known about the anatomic pathway of autonomic nerve fibers innervating the sinus node. The present study: (1) evaluates the effects of cavotricuspid isthmus ablation for common atrial flutter (AFL) on autonomic nervous function by using heart rate variability analysis, and (2) investigates the distribution of autonomic nerve pathways innervating the sinus node. Twelve patients with paroxysmal common atrial flutter who maintained sinus rhythm both before and after radiofrequency ablation were selected for the study. Holter ambulatory recordings were performed before and after (2.3 +/- 1.0 days) radiofrequency ablation of cavotricuspid isthmus. Heart rate and time domain (SDANN, rMSSD, pNN50) and frequency domain (low frequency (LF), high frequency (HF), LF/HF) analysis of heart rate variability were compared before and after ablation. Mean heart rate did not change significantly after ablation (59 +/- 6 vs 61 +/- 9 beats/min); parasympathetic indices of heart rate variability (SDANN, rMSSD, pNN50, HF) did not change significantly (110 +/- 37 vs 117 +/- 20 ms; 32 +/- 21 vs 28 +/- 9 ms; 4.8 +/- 0.9 vs 4.7 +/- 0.71n(ms2)); and sympathetic indices of heart rate variability (LF/HF) did not change significantly (1.1 +/- 0.2 vs 1.2 +/- 0.1). Cavotricuspid isthmus ablation for atrial flutter did not significantly change heart rate and heart rate variability because parasympathetic and sympathetic fibers innervating the sinus node are scarce in this region.

Atrial components contributing to pseudo r' deflection in lead V1 in slow/fast atrioventricular nodal reentrant tachycardia: analysis of the atrial activation sequence by basket catheter isochronal mapping.

Electrocardiographic recognition of the P' wave during tachycardia is very useful in the diagnosis of supraventricular tachycardias. In slow/fast (S/F) atrioventricular nodal reentrant tachycardia (AVNRT), no discrete P' waves are observed on ECG and pseudo r' deflection in lead V1 (pseudo r') is commonly recognized. However, the atrial components that contribute to the genesis of pseudo r' in lead V1 have not been described and this study aimed to clarify them by analysis of the whole activation sequence of the right atrium using Basket catheter isochronal mapping. The study group comprised 48 patients with AVNRT. Pseudo r' was defined as an upward deflection in the terminal portion of the QRS complex during tachycardia that was not recognized during sinus rhythm and it occurred in 45 patients (94%). During S/F AVNRT, the retrograde atrial activation was earliest on His bundle electrogram, followed by the coronary sinus ostium, distal coronary sinus and high right atrium. Only the high lateral aspect of the right atrium was activated after the end of the QRS complex. The interval between the onset of QRS in multiple surface ECG leads and the atrial activities on high right atrium was similar to the V-r' interval in lead V1 (111+/-20ms, 117+/-11 ms) and correlated with the V-r' interval (r=0.56). Pseudo r' deflection in lead V1 is a highly sensitive indicator of S/F AVNRT, and appears to result from the activation of the superolateral aspect of the right atrium.