Rural Research Network to engage rural and minority community members in translational research.

Background: To address the high prevalence of health disparities and lack of research opportunities among rural and minority communities, the University of Arkansas for Medical Sciences (UAMS) developed the Rural Research Network in January 2020. Aim: The aim of this report is to describe our process and progress in developing a rural research network. The Rural Research Network provides a platform to expand research participation opportunities to rural Arkansans, many of whom are older adults, low-income individuals, and underrepresented minority populations. Methods: The Rural Research Network leverages existing UAMS Regional Programs family medicine residency clinics within an academic medical center. Results: Since the inception of the Rural Research Network, research infrastructure and processes have been built within the regional sites. Twelve diverse studies have been implemented with recruitment and data collection from 9248 participants, and 32 manuscripts have been published with residents and faculty from the regional sites. Most studies were able to recruit Black/African American participants at or above a representative sample. Conclusions: As the Rural Research Network matures, the types of research will expand in parallel with the health priorities of Arkansas. Relevance to Patients: The Rural Research Network demonstrates how Cancer Institutes and sites funded by a Clinical and Translational Science Award can collaborate to expand research capacity and increase opportunities for research among rural and minority communities.

Left atrial invasion by lung carcinoma through a pulmonary vein.

We describe a rare case of small-cell lung carcinoma invading the left atrium through a pulmonary vein. Echocardiography was particularly useful in this case in assessing the intracavitary extension of the tumor and the outcome of therapy. Echocardiography is a low-cost, easy imaging tool, complementary to radiological techniques and useful in evaluating thoracic tumors involving the cardiovascular structures.

Long-term evaluation of patients with apical hypertrophic cardiomyopathy. Correlation between quantitative echocardiographic assessment of apical hypertrophy and clinical-electrocardiographic findings.

Apical hypertrophic cardiomyopathy (AHCM) is characterized by primary hypertrophy localized exclusively in the apex of the left ventricle. Previous studies have indicated that AHCM results in a unique combination of cross-sectional echocardiographic (CSE) and ECG findings ('giant' T wave inversion and high R wave voltage in the precordial leads). The aims of this study were: (1) to assess the degree of AHCM in a quantitative fashion (2) to evaluate the possible relationship between apical hypertrophy, quantitatively determined, and ECG findings in patients with AHCM (3) to verify the changes in echocardiographic and ECG parameters over time (4) to define the relationship between the severity of AHCM and the clinical course of such patients. Eleven selected patients with AHCM were studied for an average 6 year follow-up period; there were seven men and four women (age from 18 to 62 years, mean 49). Apical hypertrophy was assessed quantitatively by determining the muscle cross-sectional area in the apical region, which was considered an index of myocardial mass. From the end-diastolic apical four chamber view, endocardial and epicardial contours were digitized in order to obtain the total muscle cross-sectional area of the left ventricle. The walls of the left ventricle were then divided into three regions (basal, intermediate, apical). The final value of each cross-sectional muscle area was obtained from the mean measurements of four independent and blinded observers. In AHCM the apical muscle cross-sectional area (AMA) ranged from 10.3 to 17.9 cm2, mean 13.2 +/- 2.6 cm2.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of atrial fibrillation on pulmonary venous flow patterns: transoesophageal pulsed Doppler echocardiographic study.

The effect of atrial fibrillation on pulmonary venous flow patterns is still not well known. Twenty-four patients in atrial fibrillation and 21 patients in sinus rhythm were studied by transoesophageal echocardiography. In ninety-five percent (20/21) of sinus rhythm patients, the early systolic wave due to atrial relaxation or reverse wave due to atrial contraction could be distinguished on pulsed Doppler tracings by transoesophageal echocardiography. However, there was no early systolic wave and/or reverse at the end of diastole in any atrial fibrillation patients. In atrial fibrillation patients without mitral regurgitation (n = 14), the onset of systolic flow was delayed (165 +/- 38 vs 50 +/- 46 ms, P < 0.05), and systolic peak velocities, time-velocity integrals and systolic fractions were reduced (31 +/- 13 vs 54 +/- 17 cm.s-1, P < 0.05; 5 +/- 2 vs 13 +/- 6 cm, P < 0.05 and 36 +/- 8 vs 61 +/- 15%, P < 0.05, respectively) as compared to those in sinus rhythm. Significant mitral regurgitation (n = 10) reduced systolic velocity parameters considerably in atrial fibrillation patients but the diastolic flow parameters were not significantly different between sinus rhythm and atrial fibrillation patients. Stepwise multiple regression analysis identified atrial fibrillation as an important independent predictor for changes in systolic flow parameters. The R-R interval is also an important factor for diastolic flow parameters. Thus, the present study demonstrates that atrial fibrillation significantly modifies pulmonary venous flow pattern and is an important factor for systolic flow parameters. Significant mitral regurgitation can further modify systolic flow pattern in atrial fibrillation patients.

Echocardiographic prediction of the final event in patients dying of acute myocardial infarction.

From an autopsy series of 346 patients who died of acute myocardial infarction, we selected 36 cases for whom echocardiographic data preceding death were available: 17 cases died from a rupture of the left ventricular free wall (group A) and 19 from pump failure (group B). Our aim was to investigate whether any echocardiographic parameter could predict the final event. The total wall motion score, regional wall motion score index and percent of abnormally contracting myocardium were calculated. Diastolic and systolic volumes, ejection fraction and the eccentricity index, as a rough indicator of the left ventricular shape, were also estimated. Interventricular septum and posterior wall thicknesses were also measured. All measured parameters were similar in both groups except posterior wall thickness. Even though an unavoidable selection bias is present in our series, we failed to identify any echocardiographic predictor of the final event in this patient group.

Usefulness of transesophageal echocardiography in evaluation of paracardiac neoplastic masses.

Mediastinal paracardiac tumors may cause both cardiovascular complications and problems in differential diagnosis of cardiac diseases. Transesophageal echocardiography (TEE) may give an additional new window to mediastinal neoplasms, but only a few studies have been reported. TEE was performed in 70 patients with paracardiac neoplastic masses. The procedure was indicated to solve particular clinical problems in 20 patients, and as a prospective study on 50 unselected patients with mediastinal neoplasms. Twenty-three patients underwent follow-up studies; a total of 101 echocardiograms were recorded. The procedure was tolerated well or very well by most patients, and provided additional anatomic or hemodynamic data in every patient in group a and in 45 of 50 in group b. The additional data were relevant for clinical management in 14 of 20 patients in group a, and in 3 of 45 in group b. Based on the results of this study, TEE is useful in association with other radiologic techniques in patients with paracardiac neoplasms. As an imaging technique, it may represent a reliable alternative to computed tomography whenever the latter is not feasible.

Familial dilated cardiomyopathy: a transverse and longitudinal clinical and echocardiographic study.

The familial occurrence of hypertrophic cardiomyopathy is well known; familial dilated cardiomyopathy has so far received less attention. Ten families with two or more members affected by dilated cardiomyopathy were studied by echocardiography. In 3 out of 10 families, a transverse study extended to even apparently healthy subjects was carried out, which included a total of 45 subjects. In 19 out of the 45, dilated cardiomyopathy (either symptomatic or asymptomatic) was diagnosed at echocardiography. Three more relatives, already dead of the disease, were identified through hospital records. A clinical and echocardiographic longitudinal study, lasting up to 11 years, was carried out in 5 of the 10 families. During the follow-up, 8 out of 19 patients who, at first examination were affected by dilated cardiomyopathy, died, one improved, 3 remained in stable condition and 7 were lost at follow-up. One of two patients who presented echocardiographic findings suggestive of border-line dilated cardiomyopathy returned to normality and the other developed dilated cardiomyopathy. The clinical and echocardiographic findings in our patients, and in their relatives, suggest the possibility that idiopathic dilated cardiomyopathy may be a multifactorial disease in which genetic factors might play a variable role.

Quantification of mitral regurgitation: comparison between transthoracic and transesophageal color Doppler flow mapping.

We reviewed transthoracic (TTE) and transesophageal (TEE) echocardiograms of 100 consecutive patients: 63 male, 37 female, mean age 50 years (range 16-83 years), 32 with neoplastic disease, 18 aortic disease, 28 mitral valve disease, and 22 with other diseases. Absence or presence of mitral regurgitation (defined as mild, moderate, or severe) was assessed. TEE showed mild mitral regurgitation in 26 patients where TTE was negative. The overall estimate of regurgitant lesion severity was concordant at TEE and TTE in 64% of cases. The overall estimate of regurgitant lesion severity was also greater by one grade in 1% of cases at TTE, and in 35% of cases at TEE. Maximal digitized jet areas were 3.60 +/- 6.35 cm 2 at TTE and 3.04 +/- 3.79 cm 2 at TEE (P = NS). Correlation was r = 0.69 (TEE = 0.41 TTE + 1.55; P less than 0.001). TEE yielded a higher prevalence of mitral regurgitation than TTE with a trend toward greater overall estimate of mitral regurgitation at the semi-quantitative analysis. TTE and TEE showed similar mean results at the quantitative assessment of maximal jet areas. However, a highly significant random variability was observed in quantifying mitral regurgitation at TEE.

[Color Doppler identification of early diastolic turbulence in the left atrium in patients with mitral valve insufficiency: persistence of regurgitation or inertia phenomenon?]. / Turbolenza protodiastolica in atrio sinistro al color Doppler in pazienti con insufficienza mitralica: persistenza del rigurgito o fenomeno inerziale?

Color Doppler flow mapping represents the most recent non invasive diagnostic tool for the visualization of intracardiac blood flow. By using the color Doppler flow mapping technique, two independent observers identified the persistence of turbulence in early diastole inside the left atrium in a selected group of 8 patients (3 F and 5 M) with mitral insufficiency. All the patients had moderate or severe mitral insufficiency, due to dilated cardiomyopathy and/or ischemic cardiomyopathy and/or valvular disease. The persistence of early diastolic turbulence inside the left atrium was documented and confirmed by using 30 degrees color sector images, which show the highest possible frame rate. The frame by frame analysis facilitated the identification of two simultaneous flow velocities during early diastole, after the mitral valve was open. The first flow was anterograde and was coded as a red signal; it flowed from the mitral valve into the left ventricle and represented early diastolic left ventricular filling. The second flow was retrograde, and was coded as a blue mosaic signal, due to turbulent aliased jet, extending from the mitral valve into the left atrium, away from the transducer. The interpretation of these two dimensional color Doppler findings is uncertain. We believe, however, that these turbulent velocity signals which persist in early diastole and flow from the mitral valve into the left atrium are probably caused by inertial blood flow due to the impact of regurgitant mitral jets during the previous systole.

[Apical hypertrophic cardiomyopathy: variability of bidimensional echocardiographic and electrocardiographic expression]. / Cardiomiopatia ipertrofica apicale: variabilità di espressione ecocardiografica bidimensionale ed elettrocardiografica.

Apical hypertrophic cardiomyopathy is characterized by primary hypertrophy of the myocardium which is localized exclusively at the apex of the left ventricle. Previous studies have indicated that apical hypertrophic cardiomyopathy is characterized by a unique combination of cross-sectional echocardiographic and ECG findings ("giant" T wave inversion and high R wave voltage in the precordial leads). The aim of this study was to evaluate the possible relation between apical hypertrophy, quantitatively defined by cross-sectional echocardiography, and ECG findings in patients with apical hypertrophic cardiomyopathy. We studied 13 pts with apical hypertrophic cardiomyopathy, 10 men and 3 women (aged between 11 and 73 years, mean age 47). Apical hypertrophy was assessed quantitatively by determinating the muscle cross-sectional area in the apical region. From the end-diastolic apical 4 chamber view, endocardial and epicardial contours were digitized in order to obtain the muscle cross-sectional area of the left ventricle. The walls of the left ventricle were then divided into 3 regions (basal, mid-ventricular, apical). Final values of planimetered muscle areas are given as the average of the calculations obtained blindly and independently by 4 observers. The comparison between cross-sectional echocardiographic and electrocardiographic findings showed that patients with giant T wave inversion (T wave greater than 10 mm) and high R wave voltages (R greater than wave 25 mm) had a more severe degree of apical hypertrophy. However there was no complete agreement between cross-sectional echocardiographic and electrocardiographic findings. This study in fact demonstrates a wide variation in the degree of severity of apical hypertrophy among patients with apical hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)