Citations

Background— Recurrent functional mitral regurgitation (MR) has been reported after mitral valve repair with annuloplasty in patients with dilated cardiomyopathy, but the mechanism is not understood completely. The authors sought to identify abnormalities of the mitral valve and left ventricle that are associated with recurrent MR after mitral annuloplasty. Method and Results— In 104 patients with idiopathic dilated cardiomyopathy who underwent annuloplasty for functional MR, basal mitral anterior leaflet angle, distal mitral anterior leaflet angle (ALA tip ), posterior leaflet angle, coaptation depth, tenting area, mitral annular dimensions, left ventricular volumes, and MR severity were quantified by echocardiography before surgery and at 6-month intervals after it. Compared with patients without MR recurrence (n=79), patients with recurrent MR (defined as ≥2+) (n=25) had greater ALA tip ( P <0.001) and basal mitral anterior leaflet angle ( P <0.001), greater coaptation depth and tenting area ( P <0.001), larger left ventricular volumes ( P <0.001), and worse left ventricular ejection fraction ( P <0.05) but similar mitral annular dimensions and postoperative exaggeration in posterior leaflet angle. Multivariable analysis identified postoperative ALA tip as the major determinant of postoperative MR. Receiver operator characteristic curves identified preoperative ALA tip as the best predictor of MR recurrence (area under curve, 0.98). For ALA tip >25°, the sensitivity, specificity, and positive and negative predictive values in predicting recurrent MR were 88%, 94%, 82%, and 93%, respectively. Three distinct patterns of anterior leaflet tethering (minimal, basal, and distal) with an increasing risk of recurrent MR were identified. Conclusions— Posterior leaflet tethering is invariable after mitral annuloplasty, rendering postoperative mitral competence highly dependent on distal anterior leaflet mobility.

Background— Primary amyloidosis has a poor prognosis as a result of frequent cardiac involvement. We recently reported a high prevalence of intracardiac thrombus in cardiac amyloid patients at autopsy. However, neither the prevalence nor the effect of anticoagulation on intracardiac thrombus has been evaluated antemortem. Methods and Results— We studied all transthoracic and transesophageal echocardiograms of cardiac amyloid patients at the Mayo Clinic. The prevalence of intracardiac thrombosis, clinical and transthoracic/transesophageal echocardiographic risks for intracardiac thrombosis, and effect of anticoagulation were investigated. We identified 156 patients with cardiac amyloidosis who underwent transesophageal echocardiograms. Amyloidosis was the primary type (AL) in 80; other types occurred in 76 patients, including 56 with the wild transthyretin type, 17 with the mutant transthyretin type, and 3 with the secondary type. Fifth-eight intracardiac thrombi were identified in 42 patients (27%). AL amyloid had more frequent intracardiac thrombus than the other types (35% versus 18%; P =0.02), although the AL patients were younger and had less atrial fibrillation. Multivariate analysis showed that atrial fibrillation, poor left ventricular diastolic function, and lower left atrial appendage emptying velocity were independently associated with increased risk for intracardiac thrombosis, whereas anticoagulation was associated with a significantly decreased risk (odds ratio, 0.09; 95% CI, 0.01 to 0.51; P <0.006). Conclusions— Intracardiac thrombosis occurs frequently in cardiac amyloid patients, especially in the AL type and in those with atrial fibrillation. Risk for thrombosis increased if left ventricular diastolic dysfunction and atrial mechanical dysfunction were present. Anticoagulation therapy appears protective. Timely screening in high-risk patients may allow early detection of intracardiac thrombus. Anticoagulation should be carefully considered.

Object The pathophysiology of myocardial dysfunction after subarachnoid hemorrhage (SAH) remains unclear. Using myocardial real-time perfusion contrast echocardiography (RTP-CE), the authors evaluated microvascular function in patients with acute SAH. Methods Over a 15-month period, 10 patients with acute SAH and evidence of cardiac dysfunction were prospectively enrolled. The authors performed RTP-CE within 48 hours of SAH diagnosis. Wall motion and myocardial perfusion were evaluated in 16 left ventricle segments. Qualitative and quantitative RTP-CE analyses were conducted to compare patients with and without regional wall motion abnormalities (RWMAs). Follow-up RTP-CE at a mean of 53.7 ± 43 days was undertaken in patients with baseline RWMAs. Results Ten patients with SAH and evidence of cardiac dysfunction were prospectively enrolled. There were 3 men and 7 women whose mean age was 63.5 ± 10.1 years. The authors documented evidence of RWMAs in 6 patients. Normal perfusion was demonstrated by RTP-CE in all patients at baseline and follow-up, despite the presence of RWMAs. Compared with patients presenting with normal wall motion, in patients with RWMAs there was a trend for higher quantitative RTP-CE parameters, suggesting hyperemia with mean myocardial blood flow velocity (β, s−1) of 1.08 ± 0.61 (95% CI 0–2.61) compared with 1.62 ± 0.64 (95% CI 0.94–2.29) and myocardial blood flow (A × β, dB/s) of 0.99 ± 0.41 (95% CI 0–2.0) versus 1.63 ± 0.86 (95% CI 0.72–2.53). Follow-up RTP-CE was feasible in 3 patients with RWMAs. Regional systolic function was restored in those who completed follow-up. Conclusions The authors found that RTP-CE readily evaluates microvascular function in patients with SAH. Wall motion and perfusion dissociation were observed. Quantitative RTP-CE showed a trend for microvascular hyperemia in patients with RWMAs, suggesting that post-SAH myocardial dysfunction could occur in the absence of microvascular dysfunction.

Background— Papillary muscle rupture (PMR) is an infrequent but catastrophic complication of acute myocardial infarction (MI). Although always considered, surgical treatment is often denied because of high operative mortality. Moreover, the effects of surgery for PMR on long-term outcome, particularly compared with expected outcome after MI, are undefined. Methods and Results— Fifty-four consecutive patients (age, 70±8 years; 74% male) underwent mitral surgery for post-MI PMR from January 1980 through December 2000. Severe presentation (cardiogenic shock, pulmonary edema, or cardiac arrest) was noted in 91% preoperatively. Performance of coronary artery bypass graft was associated with lower operative mortality (odds ratio, 0.18; 95% CI, 0.04 to 0.83; P =0.011), whereas there was a trend for lower mortality after surgery after 1990 (odds ratio, 0.28; 95% CI, 0.06 to 1.3). Thus, operative mortality (overall, 18.5%) decreased from 67% up to 1990 without coronary artery bypass graft to 8.7% after 1990 with coronary artery bypass graft. Overall 5-year survival was 65±7%, and survival free of congestive heart failure was 52±7%. Five-year survival of 30-day operative survivors was 79±4%, identical ( P =0.24) to that of matched controls with MI (similar age, sex, ejection fraction, MI location, and MI year). Survival free of congestive heart failure was similar in PMR cases and MI controls (10-year survival, 28±8% versus 36±6%; P =0.46). Conclusions— Surgery for post-MI PMR involves a notable operative mortality, but there are recent trends for lower operative risk, particularly with associated coronary artery bypass graft. Long term after surgery, outcome is restored to that of similar MI without PMR. These encouraging observations emphasize the importance of prompt diagnosis and aggressive therapeutic approach for patients incurring PMR after MI.

Background— Various dyssynchrony indexes derived from tissue velocity and strain imaging have been proposed to predict the effectiveness of cardiac resynchronization therapy (CRT). We sought to compare the effect of CRT on dyssynchrony indexes derived by tissue velocity and strain and to determine which baseline intraventricular dyssynchrony parameters correlate with improvement in left ventricular volume after CRT. Methods and Results— Echocardiography with tissue Doppler imaging was performed in 45 patients with systolic heart failure at baseline, 1 day after CRT, and a median of 6 months after CRT. We calculated septal–lateral delay and anteroseptal–posterior delay and standard deviation of time to peak systolic velocity in the 12 basal and mid-left ventricular segments (Tv-SD). The standard deviation for time to peak strain in the 12 basal and mid-left ventricular segments (Tε-SD) was calculated as a strain-derived dyssynchrony index. None of the tissue velocity–derived dyssynchrony indexes improved after CRT (septal–lateral delay, P =0.39; anteroseptal–posterior delay, P =0.46; Tv-SD, P =0.30), whereas Tε-SD decreased significantly after CRT ( P <0.001). Improvement in Tε-SD 1 day after CRT correlated with the reduction in end-systolic volume at follow-up ( r =0.66; P <0.001). Baseline Tε-SD demonstrated significant correlation with the reduction of end-systolic volume at follow-up ( r =0.57; P <0.001); however, baseline tissue velocity–derived dyssynchrony indexes failed to predict the effect of CRT. Conclusions— The strain-derived dyssynchrony index is a better measurement than the tissue velocity dyssynchrony index for monitoring changes in mechanical dyssynchrony after CRT and for predicting reduction in left ventricular volume after CRT.

Background— Several echocardiographic dyssynchrony indexes have been proposed to identify responders to cardiac resynchronization therapy using tissue velocity and strain. The present study aimed to compare tissue velocity–derived and strain-derived dyssynchrony indexes in patients with or without systolic dysfunction and left bundle-branch block. Methods and Results— Tissue Doppler imaging was performed in 120 subjects divided into 4 groups: group 1 (n=40), normal subjects; group 2 (n=20), normal left ventricular ejection fraction and left bundle-branch block; group 3 (n=20), left ventricular ejection fraction <35% and normal conduction; and group 4 (n=40), left ventricular ejection fraction <35% and left bundle-branch block. Dyssynchrony indexes based on time to peak tissue velocity (septal-lateral delay, anteroseptal-posterior delay, and SD in time to peak systolic velocity in the 12 left ventricular segments) and strain (SD of time to peak strain in 12 segments) were measured. The SD in time to peak systolic velocity in the 12 left ventricular segments was greater in group 4 (54 ms; 25th and 75th percentiles, 46 to 64 ms) than group 1 (44 ms; 25th and 75th percentiles, 28 to 53 ms; P =0.006), but there was a considerable overlap of all tissue velocity–derived indexes among 4 groups, with 40% to 68% of group 1 having values proposed for predicting the responders of cardiac resynchronization therapy. The SD of time to peak strain in 12 segments distinguished these groups with much less overlap ( P <0.01 for all pairwise comparisons). Conclusions— A substantial proportion of normal subjects have tissue velocity–derived dyssynchrony indexes higher than the cutoff value proposed for predicting beneficial effect of cardiac resynchronization therapy. Strain-derived timing index appears to be more specific for dyssynchrony in patients with systolic dysfunction and left bundle-branch block. Identifying an optimal tissue velocity– or strain-derived dyssynchrony index requires a large prospective clinical trial.