Citations

Introduction: Accurate stroke volume (SV) calculation is critical for calculating aortic valve area by echocardiography. 2D-Doppler estimation of SV (SV 2D ) assumes uniform blood flow velocities through the left ventricular outflow tract (LVOT). Non-uniform flow through the LVOT, appreciated as spectral broadening of the LVOT Doppler signal, could result in inaccurate SV calculation. Hypothesis: Increased spectral broadening in the LVOT will result in overestimation of SV by the SV 2D method compared to 3D volumetric assessment of SV (SV 3D ). Methods: Fifty-one consecutive patients with aortic stenosis underwent comprehensive 2D-TTE and assessment of SV 3D . Patients with ≥ moderate mitral or aortic regurgitation were excluded. An LVOT pulse-wave Doppler signal with > 0.4 m/s difference between outer and inner edge of velocity spectral display (at time of peak velocity) was considered non-uniform flow (i.e., spectral broadening). Results: Spectral broadening was present in 33% of the cohort. These patients were commonly female with smaller ventricles and higher ejection fraction. Spectral broadening was associated with a significant overestimation of SV on Doppler-based measurements (101±20 ml vs 78±15 mL, SV 2D vs SV 3D , respectively; r=0.83, p<0.0001); such differences were not seen in patients with uniform flow velocities (82±15 vs 79±14 mL, r=0.83, p=0.03). Patient characteristics by spectral broadening are shown in table 1. Conclusion: In aortic stenosis patients with non-uniform flow, Doppler-based methods overestimated SV by 29.5% on average (maximum 64%) when compared to 3D methods. This results in a proportional increase in calculated valve area despite a similar mean gradient between groups. Substituting SV 3D resulted in similar SV, valve area, and mean gradient between uniform and non-uniform groups. When spectral broadening >0.40 cm/s is present, 3D volumetric assessment of SV should be considered for accurate estimation of aortic valve area.

Objective: In patients with aortic stenosis (AS), the development of left ventricular (LV) systolic dysfunction adversely affects the natural history and is associated with poor outcomes following aortic valve replacement. However, the timing and possible reasons for transition from preserved to impaired LV ejection fraction (LVEF) in patients with AS have not been described. The aim of this study was to describe the time course of development of LV dysfunction and associated conditions in patients with severe AS. Methods & Results: Between 1/1/2009 and 12/31/2012, 667 (19%) of 3528 patients with severe AS (aortic valve area (AVA) ≤1 cm2) identified from the Mayo Clinic, Rochester, MN Echocardiographic Laboratory database; had LVEF ≤50%. Of those 667 patients, 263 (39%) had previous echocardiograms (median: 71.6 months, 25 IQR: 36.3, 75:118.2) before the development of severe AS, allowing an assessment of change in LVEF over time. Among these 263 patients, 8 (3%) had dilated cardiomyopathy (DCM), 225 (86%) had ischemic heart disease (IHD), 5 (2%) had other significant valve disease, and 25 (10%) had no concomitant heart disease before the development of severe AS. The evolution of development of reduced LVEF at several time points is shown in the Figure. The initial LVEF was 34±12 % in DCM patients, 51±13% in IHD patients and 61±9 % in AS patients without other heart diseases (p<0.001, ANOVA). Patients with AS alone or AS+DCM/IHD showed a gradual decline in LVEF before AS became severe, and a more rapid decline in LVEF once the AVA reached ≤ 1 cm2. Conclusion: In patients with severe AS, a majority of the patients (86%) with reduced EF had ischemic heart disease. Although there was a gradual decline in LVEF before development of severe AS, the decline was more rapid after AS became severe in almost all patients regardless of associated cardiac condition. More frequent monitoring may be indicated in AS patients especially when AVA reaches 1cm2 and concomitant IHD.

Background: Although dynamic left ventricular outflow tract (LVOT) obstruction is a hallmark for hypertrophic obstructive cardiomyopathy (HOCM), it can occur in other conditions. The aim of this study was to determine underlying conditions and clinical importance of LVOT obstruction in patients without HOCM. Methods: We reviewed the echocardiographic and clinical data of patients who underwent transthoracic echocardiography in Mayo Clinic Rochester from October 2001 to August 2006, and had LVOT peak pressure gradient (PG) > 25mmHg at rest. Results: Of 719 patients identified, 159 (22 %) patients had dynamic LVOT obstruction without HOCM (77 men; mean age, 66.6 ± 12.9 years). Main presenting symptoms were chest pains in 95 (59.7 %), and dyspnea in 46 (28.9 %). LVOT PG was 51 ± 24 mmHg at rest and 68 ± 27 mmHg after provocation. In 114 (71.7 %) patients, early diastolic transmitral inflow velocity (E) and early diastolic mitral annular tissue velocity (Ea) were obtained. Mean E, Ea, and E/Ea were 105 ± 47 cm/s, 6.4 ± 5.7 cm/s, and 18.3 ± 11.0, respectively. Systolic anterior motion of mitral apparatus was observed in 100 (62.9 %) patients. Concentric increase in LV wall thickness or LVH was most common condition present in 57 patients (36%). The cause of LVH was hypertension in 40 (70.1%), aortic stenosis in 8 (14.0%), and chronic renal failure in 4 (7.0%). In these patients, major precipitating factors were hyperdynamic LV systolic function in 54 (94.7%), use of vasodilator in 34 (59.6%) and small LV cavity in 30 (52.6%). Other prominent associated conditions were basal septal hypertrophy, mitral valve repair, cardiac amyloid, and apical ballooning. There were 28 (17.6%) all-cause mortalities during follow up (25 ± 17 months) including malignancy in 6 (21.4 %), sudden cardiac deaths in 4 (14.3 %), congestive heart failure in 3 (10.7 %). Conclusions: Dynamic LVOT obstruction can be found in patients without HOCM. The most common condition to develop dynamic LVOT obstruction without HOCM, is concentric increase in LV wall thickness in the setting of hyperdynamic motion, small LV cavity, and use of vasodilator. Other conditions which predispose patients for dynamic LVOT obstruction are hypovolemia, cardiac amyloidosis, apical ballooning syndrome, and mitral valve repair.

Background: Assessment of coexisting pericardial and myocardial disease in constrictive pericarditis (CP) remains a diagnostic challenge and decision for pericardiectomy depends on the degree of pericardial versus myocardial restraint limiting left ventricular (LV) filling. Early diastolic longitudinal mitral annulus velocity (Ea) can help to differentiate CP from restrictive cardiomyopathy. Recently, acceleration rate of Ea has been shown to be an index of LV myocardial relaxation. We therefore assessed acceleration (Ea-AR) and deceleration (Ea-DR) rate of Ea in patients with CP before and after pericardiectomy. Methods: We retrospectively studied patients (n=42) with surgically confirmed CP who underwent radical pericardiectomy between 2003–2006 at Mayo Clinic Rochester. Ea-AR and Ea-DR slopes were measured before (pre-Echo) and after (post-Echo) pericardiectomy. Patients were divided into primary CP (idiopathic & acute pericarditis with presumed normal myocardial function) and secondary CP (cardiac surgery & chest irradiation with presumed abnormal myocardial function). Results: Ea-AR and Ea-DR changed significantly after pericardiectomy in primary CP patients, however remained similar in secondary CP patients. Diagnostic accuracy of Ea-AR, Ea-DR and Ea to discriminate primary versus secondary CP by ROC analysis was 0.88, 0.80 and 0.81 respectively. Conclusion: Assessment of Ea-AR and Ea-DR in patients with CP is useful to discriminate primary from secondary CP and may help to predict coexistence of myocardial disease: Prepericardiectomy Ea-AR and Ea-DR appear to reflect the interaction of intrinsic myocardial relaxation with enhanced early LV filling. The lack of decrease of Ea-AR and Ea-DR in patients with secondary CP seems to indicate a primarily restrictive component. The significant decrease of Ea-DR in patients with primary CP after pericardiectomy could reflect abolition of a predominant pericardial limitation to LV filling. Early Diastolic Longitudinal Mitral Annulus Motion before and after Pericardiectomy

Backgrounds: Left ventricular torsion (LVtor) is an integral part of systole and untwisting plays an important role in diastole. The aim of this study was to characterize LVtor and untwisting in different grades of diastolic dysfunction. Methods: We studied 135 patients with normal LV EF with various grades of diastolic dysfunction (40 group1:mild,42 group 2:moderate,and 22 group 3:severe dysfunction) and 31 controls with normal diastolic function. Apical and basal short axis rotations were measured by 2D STE. LVtor was defined as net difference between apical and basal rotation. Results: Age, gender, and EF were similar in 3 groups and control. Mitral annulus early diastolic velocity was reduced in all 3 groups (see table ). Peak LVtor was significantly greater in group 1 compared with control, group 2 and group 3. The time from peak LVtor to Mitral valve opening, and to peak early diastolic velocity were significantly delayed in group 1 compared to control (p=0.0030 and 0.0409, respectively). The twisting rate and untwisting rate were found to be highest in group 1. Conclusions: Systolic torsion and diastolic untwisting are significantly increased in patients with mild diastolic dysfunction. In patients with advanced diastolic dysfunction with increased filling pressure, torsion and untwisting are normalized. Hence, vigorous LV torsion appears to be a compensatory mechanism during an early stage of diastolic dysfunction to maintain normal filling in the setting of reduced longitudinal myocardial motion.

Background: Isovolumic contraction time (ICT) and pre-ejection period (PEP) are altered by electrical conduction delay as well as impaired contractility. An abnormal PEP has been used to select patients for cardiac resynchronization therapy (CRT), however, the predictive value of PEP for reverse remodeling (RR) has not been reported. The purpose of this study is to determine the predictive value of ICT and PEP for the RR in a prospective, single center CRT registry. Methods: Prospective registry of all heart failure patients undergoing CRT with echo pre-implant and at 3 and 6 months after implant. PEP was measured from the ECG Q wave onset to the aortic valve opening from the left ventricular outflow tract pulsed-wave Doppler tracing. The timing interval from the QRS onset to mitral valve closure was measured (mitral valve closure time). ICT was calculated as PEP-mitral valve closure time. RR was defined as >15% reduction in end-systolic volume (ESV) measured by biplane Simpson’s method. Death due to cardiac cause and heart transplantation during the 6 month period were considered as a non-response in the receiver-operating characteristics (ROC)analysis. Results: Echocardiography data was available in 83 patients at 3 and 59 patients at 6 month after CRT. RR occurred in 42 patients (51%) at 3 months and in 32 (54%) patients at 6 months By ROC analysis, the area under the curve (AUC) for predicting RR was 0.74 for ICT (p<0.001) and 0.73 for PEP (p=0.001) (See table ). ICT>123 ms yielded a very high specificity of 90–93% to predict responders at 6 month after CRT either in entire population or after excluding the patients with atrial fibrillation. Conclusion: A prolonged ICT is highly specific for predicting reverse remodeling after CRT although it is found in a limited number of patients. A strategy employing a screening ICT measurement may identify patients highly likely to achieve reverse remodeling after CRT, but can not be used to exclude patients for CRT. ROC analysis

Background : Dyssynchrony indexes derived from time to peak systolic velocity and time to peak strain have been reported to predict left ventricular reverse remodeling (RR) after cardiac resynchronization therapy (CRT). The predictive characteristics of these indices have not been validated in a variety of clinical settings. Our objective was to determine the predictive value of strain and tissue velocity derived dyssynchrony indices for RR or clinical response to CRT in a prospective single-center CRT registry. Methods : Prospective registry of all heart failure patients (pts) undergoing CRT with echo before and 3 and 6 months after CRT. Color -coded tissue Doppler imaging in 12 segments was used to calculate the standard deviation of time to peak strain (Tϵ-SD) and time to peak systolic velocity (Tv-SD). RR was defined as a decrease in end systolic volume (ESV; biplane Simpson’s method) ≥15%. Indices were assessed with receiver-operating characteristics (ROC) analysis and the area under the curve (AUC) calculated in all pts and excluding those with atrial fibrillation at implant. Results : To date, of the first 87 patients, 4 died (classified as non-responder); 83 pts had 3 and 59 pts had 6 month echocardiography follow-up. Tϵ-SD (93%) and Tv-SD (98%) were feasible in most pts. RR occurred in 42 pts (51%) at 3 month and 32 patients (54%) at 6 month follow-up. See table . Tϵ-SD was superior to Tv-SD for prediction of RR in all pts and in those without atrial fibrillation. Findings were similar regardless of ischemic (68% of patients) or non-ischemic etiology. Neither baseline Tϵ-SD nor Tv-SD correlated with the improvement in clinical response measured by the change in six minute walk distance or peak VO 2 at 3 or 6 month after CRT (data not shown). Conclusions : In this single center experience, mechanical dyssynchrony measured by strain imaging but not tissue velocity imaging was predictive of RR. Neither index predicted clinical response.

Background: Effect of CRT on the timing of regional myocardial strain is not fully described. We aimed to explore the effect of CRT on the timing of regional myocardial strain using speckle tracking echocardiography (STE). Methods: STE and tissue Doppler imaging were performed in 91 patients before and 6 month after CRT. Time to peak longitudinal strain (Tϵ) from the onset of QRS was measured in 16 segments from three apical views. Time to peak systolic tissue velocity (Tv) was also measured in 12 basal and mid segments. Reverse remodeling was defined as 10% reduction in end-systolic volume. Results: At baseline, Tϵ and Tv demonstrated specific pattern with earlier septal and delayed lateral contraction (Figure ). Tϵ in responders showed significantly earlier timing in mid inferoseptal (p=0.003) and anteroseptal segments (base, P=0.005, mid P=0.007) than in nonresponders, whereas the timing of free wall did not differ between responders and non-responders. After CRT, Tϵ in earlier segments (inferoseptal, anteroseptal and inferior wall) prolonged significantly (p<0.001), whereas other segments did not change timing. Accordingly, SD of Tϵ in 12 segments reduced after CRT (110±46 ms vs. 81±36 ms, p<0.001). Tv did not change in all segments and SD of Tv did not improve after CRT (43±16 vs. 46±16 ms, p=0.20). Conclusions: Simultaneous electrical activation of LV free wall and septum with CRT achieves mechanical synchronization by delaying the timing of earlier contracting segment rather than directly shortening the timing in lateral wall. This could be explained by the increased wall stress on the septum as it contracts simultaneously with the opposing LV free wall. Figure. Change in Regional Timing in Strain and Peak Velocity

Background: Cardiac resynchronization therapy (CRT) improves global systolic function in left ventricle. However, the impact of CRT on regional myocardial function is less clear. The aim of this study, therefore, is to evaluate regional changes in myocardial strain after CRT. Methods: Speckle tracking echocardiography (STE) was performed in 91 patients before and 6 month after CRT. Peak longitudinal strain was measured in 18 segments at base, mid and apex in three apical views. Left ventricular end-systolic volume (ESV) was measured by biplane Simpson’s method and reverse remodeling was defined as 10 % reduction in ESV at 6 month after CRT. Results: Peak strain improved in basal and mid segments of medial walls (basal inferoseptal, anteroseptal and inferior segments, p<0.05, mid inferoseptal and inferior segments: p<0.01) in entire group after CRT, with a greater degree of improvement in CRT responders than in nonresponders (Figure ). There was no significant improvement in free wall strain, with significant reduction in basal inferolateral segment after CRT (P=0.047) in entire group. Nonresponders had significant reduction in strain at the mid anterolateral segment (P=0.004) (Figure ). Strain of the apical segments also did not improve. Conclusions: CRT induces reverse remodeling by enhancing regional myocardial function in the septum, but suppresses the function in the free wall. Lack of reverse remodeling after CRT was characterized by the reduced function in lateral segments without improvement in septal function..

Background: Radiation therapy (RT) to the chest may induce various combined cardiac problems such as constrictive pericarditis (CP), restrictive myocardial disease, and coronary artery disease. Therefore, it was hypothesized that the MRI and transthoracic echocardiographic (TTE) findings in patients with CP may differ according to the history of RT. Methods: A total of 68 patients with CP who performed both TTE and MRI study at Mayo Clinic from 2002 to 2008 were reviewed and divided into two groups according to the history of RT; RT group (group I, n=13, 53.6±9.8 years, 8 males) versus no RT group (group II, n=55, 59.0±14.8, 45 males). Results: The results of TTE study were summarized in table . Early diastolic velocity of septal mitral annulus (E′) and deceleration time (DT) of mitral inflow was significantly lower, and the ratio of early diastolic mitral inflow velocity (E) to E′ is significantly higher in group I than in group II. Left atrial volume index (LAVI) was significantly lower and LA area and left ventricular end-diastolic dimension (LVEDD) was significantly smaller in group I than in group II. Delayed enhancement of pericardium was the only significant finding in MRI and significantly prevalent in group I than in group II (100.0% in group I vs 63.6% in group II, p=0.012). The other MRI findings including pericardial thickness, left ventricular and right ventricular ejection fraction, and the presence of pericardial and pleural effusion were not different between the groups. Conclusion: In CP patients with the history of RT compared to patients without history of RT, E′ and DT was significantly lower, LAVI and LVEDD were smaller, pericardial DE in MRI was invariably found. The lower E′ velocity and decreased chamber size and volumes may be explained by RT induced coexisting myocardial disease. TTE findings of the patients