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Objectives: This study assessed 3-dimensional fusion echocardiography (3DFE), combining several real-time 3-dimensional echocardiography (RT3DE) full volumes from different transducer positions, for improvement in quality and completeness of the reconstructed image., Background: The RT3DE technique has limited image quality and completeness of datasets even with current matrix transducers., Methods: RT3DE datasets were acquired in 32 participants (mean age 33.7 +/- 18.8 years; 27 men, 5 women). The 3DFE technique was also performed on a cardiac phantom. The endocardial border definition of RT3DE and 3DFE segments was graded for quality: good (2), intermediate (1), poor (0), or out of sector. Short-axis and apical images were compared in RT3DE and 3DFE, yielding 2,048 segments. The images were processed to generate 3DFE and then compared with cardiac magnetic resonance., Results: In the heart phantom, fused datasets showed improved contrast to noise ratio from 49.4 +/- 25.1 (single dataset) to 125.4 +/- 25.1 (6 datasets fused together). In subjects, more segments were graded as good quality with 3DFE (805 vs. 435; p < 0.0001) and fewer as intermediate (184 vs. 283; p = 0.017), poor (31 vs. 265; p < 0.0001), or out of sector (4 vs. 41; p < 0.001) compared with the single 3-dimensional dataset. End-diastolic volume (EDV) and end-systolic volume (ESV) obtained from 3-dimensional fused datasets were equivalent to those from single datasets (EDV 118.2 +/- 39 ml vs. 119.7 +/- 43 ml; p = 0.41; ESV 48.1 +/- 30 ml vs. 48.4 +/- 35 ml; p = 0.87; ejection fraction [EF] 61.0 +/- 10% vs. 61.8 +/- 10%; p = 0.44). Bland-Altman analysis showed good 95% limits of agreement for the nonfused datasets (EDV +/-46 ml; ESV +/-36 ml; EF +/-14%) and the fused datasets (EDV +/-45 ml; ESV +/-35 ml; EF +/-16%), when compared with cardiac magnetic resonance., Conclusions: Fusion of full-volume datasets resulted in an improvement in endocardial borders, image quality, and completeness of the datasets., (Copyright 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

We examine the effects of familial longevity and familial mortality on mortality rates for 10 leading causes of death in a Utah Population Database (UPDB) cohort. Familial excess longevity (FEL) and familial standardized mortality ratios (FSMR) were estimated for 666,921 individuals born from 1830 through 1963, who survived to at least age 40. Cox regression analysis shows that familial death and familial longevity have independent effects on cause-specific mortality rates for 10 leading causes of death. A family history of disease increases one's risk of dying from the same cause, whereas a family history of longevity is protective, except in the case of cancer. Families with greater longevity do not die of causes distinct from other members of the cohort, but they die from the same causes at reduced rates. Individuals from longer lived families have lower mortality from most age-related diseases including heart disease, stroke, and diabetes, but not cancer.

The recently developed echocardiographic technology of color kinesis (CK) displays endocardial motion in color layers on a single end-systolic 2-dimensional echocardiographic frame. Previous work using this method is promising for quantitation of regional function, but there is limited experience in patients with severely reduced left ventricular function. Twenty patients (age 59 +/- 10 years) with dilated cardiomyopathy (left ventricular ejection fraction 22 +/- 8%) underwent CK imaging. Endocardial motion was quantitated by measuring the distance of endocardial motion during the systolic interval and also by calculating the endocardial velocity. CK measurements were compared among 4 wall motion grades (i.e., normal, hypokinetic, akinetic, and dyskinetic) assessed by qualitative wall motion scoring. There was a significant overall difference (p < 0.0001) in the mean systolic endocardial inward motion (i.e., contraction) and outward motion (i.e., expansion) among wall motion grades. The mean endocardial outward distance was significantly greater for the dyskinetic segments than for the other grades (p < 0.001). There were also differences in the mean velocity of endocardial motion among the wall motion grades. In the presence of left bundle branch block, there was no difference in the mean endocardial inward distance of the hypokinetic, akinetic, and dyskinetic septal segments. We conclude that in the absence of left bundle branch block, normal, hypokinetic, akinetic, and dyskinetic ventricular wall segments may be distinguished in patients with dilated cardiomyopathy on the basis of endocardial motion measured with CK.

Transesophageal echocardiography (TEE) improves the diagnostic accuracy of transthoracic echocardiography in the identification of potential cardiac sources of embolus. However, there are few studies of the impact of TEE on the medical management of patients with focal cerebral ischemia. The records of 52 consecutive, hospitalized patients undergoing both TEE and transthoracic echocardiography for suspected cardiac source of embolus were reviewed to determine the influence of TEE on the decision to anticoagulate patients. Of 52 patients, 39 had focal cerebral ischemia (transient ischemic attack, n = 9; acute cerebral infarction, n = 30). In 4 of these 39 patients (10%), the TEE results changed the management of anticoagulation. In 19 of 39 patients (49%), the TEE results helped confirm anticoagulation decisions, and in 16 (41%), the results had no effect on anticoagulation decisions, because of overriding clinical information. Ten of the latter 16 patients had TEE evidence for a possible source of an embolus, but were not anticoagulated; 5 of these were poor candidates for long-term anticoagulation, and the others had right-to-left shunting across a patent foramen ovale or an interatrial septal aneurysm. Clinical variables (atrial fibrillation, TEE findings and pre-TEE anticoagulation status) were considered as possible predictors of post-TEE anticoagulation status using logistic regression analysis; the strongest predictor of post-TEE anticoagulation status was pre-TEE anticoagulation status (p < 0.0005). Despite the selection of patients presumed to receive maximal benefit from TEE, this study suggests that TEE findings are not predictive of subsequent anticoagulation management. However, TEE is at least confirmatory of anticoagulation decisions in most cases.

Two-dimensional echocardiography is an excellent technique for detecting left ventricular thrombi, however, acute clot is sometimes difficult to differentiate from adjacent myocardium and intracavitary signals. We hypothesized that quantitative assessment of the acoustic properties of acute left ventricular thrombi using a quantitative backscatter imaging system would permit the differentiation of thrombus from adjacent myocardium and intracavitary echoes. Acute, experimental left ventricular thrombi in seven dogs were evaluated with a quantitative backscatter imaging system that allowed the measurement of relative integrated backscatter and cyclic (i.e., diastolic minus systolic) variation in integrated backscatter. Coronary ligation abolished the cyclic variation in relative backscatter that occurred in normal myocardium. The end-diastolic relative backscatter in the thrombus (16.9 +/- 1.3 dB) was significantly higher than in apical myocardium (13.2 +/- 0.6 dB, p less than 0.05). There was no significant difference in the cyclic variation in relative backscatter among thrombus, ischemic myocardium, or intracavitary blood. Thus, the quantitative assessment of the acoustic properties of left ventricular thrombi can be useful in their detection and in the differentiation from myocardium and intracavitary signals.

Echocardiographic differentiation among intracavitary thrombus, cavity noise, and adjacent myocardium can be difficult. As an initial step toward quantitative thrombus characterization with ultrasound, 11 dogs were studied with an in vivo intracardiac thrombus model to delineate the acoustic properties of acute thrombi. The apical coronary arteries were ligated, and subsequently injections of 5% sodium rescinoleate and 1000 units of thrombin at the endocardium-blood interface created left ventricular mural thrombi. Echocardiographic images were obtained in long- and short-axis views with a digital acquisition system, and a statistical analysis of echo intensities was performed in regions of interest in the thrombus, surrounding ventricular cavity and adjacent myocardium. Statistical measurements used to evaluate echo intensities in each region of interest included mean gray level, standard deviation, skewness, and kurtosis. The results showed that thrombus could be distinguished from myocardium (by mean gray level and standard deviation) only in short-axis views, where regions of interest could be placed at similar depths of field. Mean gray level, standard deviation, and skewness all distinguished thrombus from intracavitary blood regardless of the region of interest placement. The phase of the cardiac cycle at which data were acquired did not alter the results. We conclude that acute intracardiac thrombi can be distinguished from surrounding blood and myocardium with ultrasound tissue characterization techniques that may have the potential for clinical application.

111In-labeled platelet scintigraphy and two-dimensional echocardiography were performed in 40 dogs to determine the ability of the two techniques to detect left atrial appendage thrombi. Thrombi were induced in 33 dogs that were classified into two groups, "acute" or "chronic," according to the time of labeled-platelet injection after thrombus induction. In the acute group (17 dogs), platelets were injected 24 hours after thrombus induction. In the chronic group (16 dogs), platelets were injected 4-8 days after thrombus induction. "Sham" thoracotomies were performed on seven additional control dogs who did not receive thrombin injections. Analog and blood pool-corrected 111In-labeled platelet scintigraphy images were obtained 4-72 hours later. Closed-chest two-dimensional echocardiography was performed before thoracotomy and repeated at the time of scintigraphy. The location and size of each thrombus were verified at autopsy. Two-dimensional echocardiography detected three of 17 acute (mean volume, 1.2 +/- 1.0 cc) and three of 10 chronic (mean volume, 0.4 +/- 0.3 cc; p less than 0.025) left atrial appendage thrombi. 111In-labeled platelet scintigraphy detected all 17 acute thrombi but only two of 10 chronic thrombi. The measured radioactivity levels of the excised thrombi were 1,949 +/- 1,665 cpm/clot/dose in group 1 and 228 +/- 213 cpm/clot/dose in group 2 (p less than 0.005). In this model, 111In-labeled platelet scintigraphy was able to detect acute left atrial appendage thrombi that could not be identified by two-dimensional echocardiography. Both techniques showed poor sensitivity for detection of chronic thrombi. The decline in sensitivity of 111In-labeled platelet scintigraphy for detection of older thrombi is probably due to diminished labeled-platelet incorporation.

The cardiovascular manifestations of the mucopolysaccharidoses (MPS) have not been well characterized. We studied nine children with various forms of MPS, using noninvasive cardiac diagnostic techniques. The echocardiograms of two brothers with Type I H/S MPS showed slow mitral valve early diastolic closure velocities (MVEDC) (18, 29 mm/sec) consistent with mitral stenosis. Each had a soft opening snap, low frequency presystolic murmurs and X-ray evidence of calcific mitral stenosis. Three patients with Type II A MPS had echocardiographic evidence of impaired left ventricular function, suggesting the presence of myocardial damage. One of these had an abnormal electrocardiogram; non had murmurs. No cardiac abnormalities were discovered in two patients with Type III A and IV MPS. One patient with Type VI A MPS had presystolic, holostolic and early diastolic murmurs. A soft opening snap was recorded. The echocardiogram showed a slow MVEDC (18 mm/sec) and a slightly enlarged left atrial dimension (2.2 cm/m2). In summary, noninvasive studies are useful in evaluating patients with MPS. Type I H/S and Type VI A patients may show evidence of valvular deformity, the former associated with mitral valvular calcification and the latter with both aortic and mitral valve involvement. Type II A patients have muscle function abnormalities and Type III A and IV are shown by noninvasive methods to be free of cardiovascular abnormalities.

We reviewed echocardiographic findings in patients aged 15 to 45 years with acute nonhemorrhagic cerebral infarction (NHCI). Among 132 patients with NHCI, 96 (72.7%) had M-mode and two-dimensional echocardiography, including contrast echocardiography with intravenous saline injection when clinically indicated. Echocardiograms were abnormal in 33 patients. Of these, 7 had other conditions that could cause NHCI. Echocardiography corroborated the clinical diagnosis of a cardiogenic source for cerebral infarction in 17 others. The other 9 had no other clues for cardiovascular disease. Potential etiologies of NHCI diagnosed by echocardiography in these 9 cases included: paradoxical embolism, 5 patients; right atrial myxoma, 1; rheumatic mitral valve vegetation, 1; myxomatous mitral valve (marantic endocarditis at postmortem), 1; and left atrial enlargement associated with decreased left ventricular function, 1. Routine echocardiography frequently conveys useful information in patients under age 45 with NHCI. In young patients with cerebral embolism of unknown etiology if routine M-mode and two dimensional echocardiographic studies are normal, contrast echocardiographic studies should be performed to rule out intracardiac shunts and the possibility of paradoxical cerebral embolism.

Protocols used to prepare patients with leukemia for bone marrow transplantation have the potential for cardiac toxicity due to high-dose cyclophosphamide and total-body irradiation. We have reported one regimen, combining cytarabine (5 mg/kg), cyclophosphamide (90 mg/kg), and total-body irradiation (900 cGy), which is relatively effective in the treatment of leukemia. To assess cardiac effects of this treatment regimen, we performed serial echocardiography and radionuclide ventriculography in 28 patients with leukemia (age range, 18-48 years; mean, 31; 21 males) undergoing allogeneic bone marrow transplantation. No significant change in left ventricular fractional minor axis shortening or increase in left ventricular diastolic dimension was seen with weekly echocardiography. At an average of 77 days (range, 28-358) after transplant, repeat radionuclide ventriculography in 17 patients revealed no significant change in resting left ventricular ejection fraction compared to that on admission to the hospital (58% +/- 6.8% vs 56% +/- 8.0% SD; P = not significant). In seven of these 17 patients (41%), resting ejection fraction fell between baseline and discharge (from mean of 60% to 50%). Resting ejection fraction in four of these patients (23% of the entire group) fell into the abnormal range (from mean of 56% to 44%; lowest, 41%). Ten patients also had exercise radionuclide ventriculography and all had normal responses (greater than 5% increase with exercise) pre- and post-transplant. We conclude that this effective bone marrow transplantation regimen has little apparent short-term cardiac toxicity in the majority of patients; since a few patients do exhibit a deterioration in left ventricular function, continued cardiac surveillance is probably indicated in posttransplant patients.