bluuebunny/crossref_metadata_2025_split huggingface dataset:
Echocardiographic assessment of mitral valve size in obstructive hypertrophic cardiomyopathy. Anatomic validation from mitral valve specimen.
Authors: Klues H G , Proschan M A , Dollar A L , Spirito P , Roberts W C , Maron B J 
Published: June 2012

BACKGROUND
In patients with hypertrophic cardiomyopathy, obstruction to left ventricular outflow is produced by systolic anterior motion of the mitral valve. In many of these patients, the mitral leaflets are elongated and increased in overall size. Mitral valve size may be responsible, in part, for the presence and magnitude of the outflow gradient and the pattern of systolic anterior motion of the leaflets. It may also influence the effectiveness of ventricular septal myotomy-myectomy in relieving subaortic obstruction. Therefore, the present study was undertaken to determine whether mitral valve dimensions could be assessed in quantitative terms from the echocardiogram in patients with hypertrophic cardiomyopathy.

METHODS AND RESULTS
A group of 37 patients with hypertrophic cardiomyopathy was selected for this study by virtue of having a high-quality transthoracic or intraoperative echocardiogram suitable for certain quantitative measurements from stop-frame images as well as a morphologically intact mitral valve specimen (removed during surgery). Seven measurements of mitral valve dimensions were obtained from the two-dimensional and M-mode echocardiograms. A univariate regression analysis identified the mitral valve opening area as the best single predictor of actual mitral leaflet area measured from the specimen (r2 = .75; r = .87). The linear relation between mitral valve opening area as assessed by two-dimensional echocardiography and actual mitral leaflet area measured from the mitral valve specimen accounted for approximately 75% of the variability in mitral leaflet area. With such statistical models, it was possible to reliably identify from the echocardiogram enlarged mitral valves (> or = 12.0 cm2) in 16 of 19 patients (84%) and normal-sized valves in 15 of 18 patients (83%).

CONCLUSIONS
In a selected group of patients with obstructive hypertrophic cardiomyopathy, a model derived from a regression analysis of quantitative echocardiographic measurements permitted (with good precision) estimation of actual mitral leaflet area and consequently overall mitral valve size and the discrimination of enlarged from normal-sized mitral valves.
Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion.
Authors: Laster S B , Shelton T J , Barzilai B , Goldstein J A 
Published: June 2012

BACKGROUND
Patients with acute ischemic right ventricular dysfunction often develop hemodynamic compromise, yet most manifest spontaneous early clinical improvement and later recovery of global right ventricular performance. This study was designed to delineate the determinants of right ventricular performance following chronic right coronary artery occlusion.

METHODS AND RESULTS
Thrombotic right coronary artery occlusion was induced in 16 closed-chest dogs. Acute occlusion depressed right ventricular free wall motion (motion score, 1.0 +/- 0.0 to 3.4 +/- 0.1*) and global performance (right ventricular fractional area change, 29.2 +/- 1.8% to 2.3 +/- 1.9%*). There was right ventricular dilatation and reversed septal curvature, with elevated and equalized diastolic filling pressures. At 5 days, despite persistent severe right ventricular free wall dysfunction (motion score, 3.4 +/- 0.1 to 2.7 +/- 0.1*), global right ventricular performance improved (fractional area change, 2.3 +/- 1.9% to 17.0 +/- 3.8%*), in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall end-diastolic thickness. At 7 weeks, collateral flow had restored right ventricular free wall perfusion to baseline values. The increased right ventricular free wall thickness had resolved, right ventricular free wall motion was improved (2.7 +/- 0.1 to 1.6 +/- 0.1*), and global right ventricular performance had recovered further (17.0 +/- 3.8 to 20.9 +/- 0.9). Right ventricular dilatation was reduced, septal curvature normalized, and there was resolution of equalized filling pressures. Histopathological analysis demonstrated minimal right ventricular infarction.

CONCLUSIONS
Acute right coronary artery occlusion results in right ventricular free wall dyskinesis and depressed global right ventricular performance. Global right ventricular function improves early, in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall diastolic thickness. Collateral restoration of perfusion facilitates late recovery of right ventricular free wall function (*P < .05).
Pacing-induced dilated cardiomyopathy increases left-to-right ventricular systolic interaction.
Authors: Farrar D J , Woodard J C , Chow E 
Published: June 2012

BACKGROUND
The right ventricle (RV) receives part of its systolic pumping force from the left ventricle through systolic ventricular interaction. The purpose of this study was to determine the effects of dilated cardiomyopathy on left ventricular to right ventricular (LV-to-RV) systolic interaction.

METHODS AND RESULTS
Studies were performed in six normal pigs and in six pigs in which dilated cardiomyopathy resulting in congestive heart failure (CHF) was produced with rapid ventricular pacing at 230 beats per minute for 1 week. In all pigs, we rapidly withdrew blood from the LV apex into a prosthetic ventricle in a single beat, which reduced LV systolic pressure without changing RV or LV end-diastolic pressure, and the resultant instantaneous changes in RV systolic pressure and pulmonary artery flow were determined. The LV-to-RV mean systolic interaction gain was calculated as the change from a normal beat to the instantaneous unloaded beat in mean RV systolic pressure divided by the change in mean LV systolic pressure. Mean systolic pressure gain was approximately 2 1/2 times greater (P < .05) in the CHF animals (0.103 +/- 0.018 mm Hg/mm Hg) than in the normal pigs (0.04- +/- 0.011 mm Hg/mm Hg).

CONCLUSIONS
These data demonstrate that left-to-right ventricular systolic interaction is significantly greater in dilated cardiomyopathy compared with the normal heart, indicating that the contribution of the left ventricle to RV systolic pressure generation has increased. This is consistent with decreased elastance of the interventricular septum resulting in increased coupling between the ventricles.
Peripheral bypass-induced pulmonary and coronary vascular injury. Association with increased levels of tumor necrosis factor.
Authors: Dauber I M , Parsons P E , Welsh C H , Giclas P C , Whitman G J , Wheeler G S , Horwitz L D , Weil J V 
Published: June 2012

BACKGROUND
Although cardiopulmonary bypass is associated with systemic complement activation and neutrophil sequestration, it is unclear whether bypass-induced vascular injury is localized and dependent on organ ischemia. We hypothesized that other factors perhaps related to placement of a bypass circuit or to blood perfusion of a pump-oxygenator system may produce vascular injury caused by systemically circulating mediators. In dogs, we determined whether application of a systemic venoarterial bypass circuit with pump-oxygenator perfusion but without pulmonary or cardiac flow diversion (peripheral bypass) leads to vascular injury. Since several features of the postperfusion syndrome after bypass resemble sequelae of endotoxin exposure, we also measured circulating endotoxin and tumor necrosis factor levels.

METHODS AND RESULTS
Anesthetized dogs underwent 2 hours of exposure to a pump-oxygenator with peripheral venoarterial bypass. We used a double indicator measurement of pulmonary and coronary vascular permeability (protein leak index [PLI]) as indexes of vascular injury. Compared with controls (n = 7), the pulmonary PLI of dogs undergoing bypass (n = 11) increased more than threefold (18.8 +/- 2.3 vs 63.3 +/- 7.6 x 10(-4) min-1; P < .05) and the coronary PLI increased more than twofold (P < .05). The rate of disappearance of intravascular radiolabeled protein increased threefold after bypass (disappearance t1/2, 241 +/- 35 vs 84 +/- 15 minutes, control vs bypass; P < .05), suggesting a generalized increase in vascular permeability. Circulating endotoxin was detectable in blood samples from 8 of 8 bypass animals (range, 0.24 to 4.56 ng/mL) compared with 2 of 5 controls (P < .05). Tumor necrosis factor levels increased significantly with bypass (6.7 +/- 3.8 vs 146.7 +/- 33.6 U/mL, baseline vs bypass; P < .05) and were only slightly and nonsignificantly increased in controls (7.0 +/- 4.4 vs 18.2 +/- 5.9 U/mL; P = NS). Peak tumor necrosis factor but not peak endotoxin levels correlated with pulmonary and with coronary protein leak. As expected, circulating complement (CH50) levels decreased significantly during bypass, reflecting systemic complement activation. However, the levels correlated poorly with the severity of vascular injury.

CONCLUSIONS
We conclude that peripheral pump-oxygenator bypass causes coronary and pulmonary vascular injury that is independent of blood flow diversion and is associated with the appearance of circulating levels of endotoxin and tumor necrosis factor, which may play a role in bypass-induced vascular injury.
Diagnosis of intramural coronary artery in transposition of the great arteries using two-dimensional echocardiography.
Authors: Pasquini L , Parness I A , Colan S D , Wernovsky G , Mayer J E , Sanders S P 
Published: June 2012

BACKGROUND
An intramural coronary is an uncommon but potentially significant risk factor for transfer of the coronary arteries as part of the arterial switch operation for transposition of the great arteries. Preoperative diagnosis is advantageous because it helps prevent accidental injury to the intramural coronary artery during transection of the aortic root and excision of the coronary artery ostium from the aorta. Therefore, we investigated the reliability of two-dimensional echocardiography for detecting an intramural coronary artery in infants with d-transposition of the great arteries.

METHODS AND RESULTS
All infants with d-transposition of the great arteries who underwent echocardiography and primary surgical repair at this institution between January 1987 and June 1992 were identified by search of the cardiology data base. From this group, all patients diagnosed with an intramural coronary artery were identified by review of the echocardiographic, surgical, and autopsy reports. Among 435 infants with transposition, 29 infants were diagnosed as having an intramural coronary artery. In 27 cases, the diagnosis was confirmed at surgery or autopsy, and there were two false-positive echocardiographic diagnoses (specificity, 99.5%). Twenty of the 27 patients with an intramural coronary artery were correctly diagnosed prospectively by echocardiography (sensitivity, 75%), including 17 of 23 patients with an intramural left coronary artery or left anterior descending coronary artery and 3 of 4 patients with an intramural right coronary artery. Two primary diagnostic criteria were identified: a major coronary artery arising from the contralateral septal sinus, near the usually intercoronary commissure, and a course for this vessel within the posterior aortic wall between the great arteries, creating a "double-border" appearance. Retrospective review using these criteria identified 26 of the 27 intramural arteries with no false-positive diagnoses.

CONCLUSIONS
We conclude that coronary echocardiography is a very promising technique for detecting an intramural coronary artery in transposition of the great arteries. Careful prospective application of the identified diagnostic criteria should greatly improve the diagnostic accuracy.
Validation of the proximal flow convergence method. Calculation of orifice area in patients with mitral stenosis.
Authors: Rodriguez L , Thomas J D , Monterroso V , Weyman A E , Harrigan P , Mueller L N , Levine R A 
Published: June 2012

BACKGROUND
It has been proposed recently that measuring the flow convergence region proximal to an orifice by Doppler flow mapping can provide a means of calculating regurgitant flow rate. Although verified in experimental models, this approach is difficult to validate clinically because there is no ideal gold standard for regurgitant flows in patients. However, this method also can be used to derive cardiac output or flow rate proximal to stenotic orifices and therefore to calculate their areas by the continuity equation (area = flow rate/velocity). Applying this method in mitral stenosis would provide a unique way of validating the underlying concept because the predicted areas could be compared with those measured directly by planimetry.

METHODS AND RESULTS
We studied 40 patients with mitral stenosis using imaging and Doppler echocardiography. Doppler color flow recordings of mitral inflow were obtained from the apex, and the radius of the proximal flow convergence region was measured at its peak diastolic value from the orifice to the first color alias along the axis of flow. Flow rate was calculated assuming uniform radial flow convergence toward the orifice, modified by a factor that accounted for the inflow funnel angle formed by the mitral leaflets. Mitral valve area was then calculated as peak flow rate divided by peak velocity by continuous-wave Doppler. The calculated areas agreed well with those from three comparative techniques over a range of 0.5 to 2.2 cm2: 1) cross-sectional area by planimetry (y = 1.08x-0.13, r = .91, SEE = 0.21 cm2); 2) area derived from the Doppler pressure half-time (y = 1.02x-0.14, r = .89, SEE = 0.24 cm2); and 3) area calculated by the Gorlin equation in the 26 patients who underwent catheterization (y = 0.89x + 0.08, r = .86, SEE = 0.24 cm2). Agreement with planimetry was similar for 22 patients with mitral regurgitation and 18 without it (P > .6), as well as for 6 in atrial fibrillation (P > .2).

CONCLUSIONS
These results validate the proximal flow convergence concept in the clinical setting and also demonstrate that it can be extended to orifice area calculation using the continuity equation.
Tone-dependent coronary arterial-venous pressure differences at the cessation of venous outflow during long diastoles.
Authors: Satoh S , Klocke F J , Canty J M 
Published: June 2012

BACKGROUND
The origin and magnitude of the back pressure opposing diastolic coronary inflow remain controversial. The arterial pressure at which coronary inflow stops during a prolonged diastole, ie, "zero-flow pressure," is higher than coronary venous pressure. However, because of capacitive discharge as distending pressure falls, flow at the microcirculatory level exceeds inflow, and coronary outflow ceases later than inflow. If coronary arterial pressure continues to exceed venous pressure at the point of venous flow cessation, zero-flow pressure cannot be an artifact of capacitive discharge.

METHODS AND RESULTS
Coronary inflow and outflow, arterial pressure, and right atrial pressure have been measured during long diastoles in closed-chest dogs chronically instrumented with volumetric flow probes on the great cardiac vein or coronary sinus as well as the circumflex artery. Although venous outflow continued for 1 to 4 seconds after arterial inflow ceased, coronary artery pressure at the point of venous flow cessation (Pfv = 0) always exceeded right atrial pressure (13 +/- 1.3 mm Hg [SEM] vs 6 +/- 0.7 mm Hg, P < .001). When vasomotor tone was augmented using vasopressin, the diastolic pressure-flow relation shifted to the right, with Pfv = 0 increasing to 21 +/- 2.4 mm Hg despite an unchanged right atrial pressure (6 +/- 0.5 mm Hg).

CONCLUSIONS
Transcoronary pressure differences persist when venous outflow stops and are larger when vasomotor tone is augmented. Measurements of zero-flow pressure that exceed venous pressure cannot be considered an artifact of continuing capacitive discharge after the cessation of arterial inflow. Diastolic coronary back pressure exceeds right atrial pressure and is tone dependent.
Combination treatment with captopril and the thyroid hormone analogue 3,5-diiodothyropropionic acid. A new approach to improving left ventricular performance in heart failure.
Authors: Pennock G D , Raya T E , Bahl J J , Goldman S , Morkin E 
Published: June 2012

BACKGROUND
An agent that improves left ventricular (LV) performance by non-cAMP-mediated mechanisms would be valuable in the treatment of chronic heart failure. We have shown earlier that the thyroid hormone analogue 3,5-diiodothyropropionic acid (DITPA) binds to nuclear receptors, alters transcription of T3-responsive genes, and increases +dP/dtmax in hypothyroid rats with substantially less effect on heart rate and metabolism than thyroid hormone, which makes it a selective cardiotonic agent.

METHODS AND RESULTS
To determine whether DITPA might be useful in treating heart failure, we compared chronic treatment with normal saline, captopril (2 g/L), or the combination of DITPA (375 micrograms/100 g) and captopril (2 g/L) in Sprague-Dawley rats beginning 3 weeks after coronary artery ligation. Both DITPA/captopril and captopril treatment decreased LV end-diastolic pressure compared with controls (21 +/- 2 and 26 +/- 2 mm Hg, respectively, vs 34 +/- 3 mm Hg, P < .05 for each). The addition of DITPA to captopril produced a 36% increase in resting cardiac index (P < .05) and shifted the cardiac function curve upward and to the left, indicative of enhanced myocardial performance. Also, DITPA/captopril compared with captopril treatment or control produced an increase in the rate of LV relaxation, as manifested by a decrease in tau, the time constant of LV pressure decline (17.5 +/- 1.0 vs 22.2 +/- 1.7 milliseconds, P < .05) and a larger absolute value for -dP/dtmax (-4561 +/- 361 vs -3346 +/- 232 mm Hg/s, P < .05). These changes occurred without changes in heart rate, LV mass, LV systolic pressure, or peripheral resistance relative to captopril treatment (P > .05).

CONCLUSIONS
The combination of DITPA and captopril improved cardiac output, increased -dP/dtmax, and increased the rate of LV relaxation to a greater extent than captopril treatment in the rat postinfarction model of heart failure. Use of a cardiotonic analogue of thyroid hormone represents a new approach to improving LV performance and may be a useful adjunct to afterload reduction for the treatment of heart failure.
Detailed angiographic analysis of high-speed mechanical rotational atherectomy in human coronary arteries.
Authors: Safian R D , Niazi K A , Strzelecki M , Lichtenberg A , May M A , Juran N , Freed M , Ramos R , Gangadharan V , Grines C L 
Published: June 2012

BACKGROUND
Several types of atherectomy devices have been developed recently for treatment of patients with ischemic heart disease.

METHODS AND RESULTS
Mechanical rotational atherectomy (MRA) using a high-speed rotational burr (Rotablator) was performed on 116 lesions in 104 patients. MRA alone was performed in 27 lesions (23%), and conventional balloon angioplasty (PTCA) was performed after MRA in 89 lesions (77%). Diameter stenosis decreased from 70 +/- 13% before MRA to 54 +/- 23% after MRA, and the final diameter stenosis (after MRA alone or with adjunctive PTCA) was 30 +/- 20% (P < .001). Minimal lumen diameter increased from 1.0 +/- 0.5 mm before MRA to 1.4 +/- 0.7 mm after MRA, and the final minimal lumen diameter was 2.3 +/- 0.7 mm (P < .001). MRA resulted in a decrease in diameter stenosis of 20% or more in 44% of lesions, and the final diameter stenosis (after MRA alone or after PTCA) was less than 50% in 75% of lesions. Considering the small diameter of available burrs, the magnitude of lumen enlargement was equal to 91% of the burr diameter, and only 9% of the burr diameter was "lost" due to elastic recoil or spasm. These angiographic results were obtained despite the presence of complex lesion morphology, including the presence of calcification in 17% of lesions and ostial location in 26% of lesions. Significant angiographic complications included abrupt closure (13 lesions, 11.2%), no reflow (8 lesions, 7%), severe coronary vasospasm (16 lesions, 13.8%), and guide wire fracture (3 lesions, 2.7%). There were no coronary artery perforations. Adjunctive therapy, including salvage PTCA, thrombolytic agents, and vasodilators, was successful in treating angiographic complications in 42 of 49 lesions (86%). Clinical complications included Q-wave myocardial infarction (5 patients, 4.8%), non-Q-wave myocardial infarction (3 patients, 2.9%), femoral vascular injury requiring surgery (3 patients, 2.9%) or blood transfusion (8 patients, 7.7%), abrupt closure requiring emergency bypass graft surgery (2 patients, 1.9%), and in-hospital death (1 patient, 1.0%). Angiographic follow-up (mean follow-up interval, 5.0 +/- 2.0 months) was available in 84% of successfully treated patients and revealed a restenosis rate of 51%, defined as a residual diameter stenosis of more than 50%. There was no significant difference in restenosis rates between de novo lesions (50%) and restenosis (54%) lesions.

CONCLUSIONS
These data suggest that for the treatment of most coronary stenoses, PTCA is required after MRA to achieve satisfactory lumen enlargement or to salvage complications. Angiographic complications appear to be more common after MRA, and salvage PTCA often is required to manage these device-induced complications. The combination of MRA and PTCA does not prevent restenosis.
Restenosis rate after multiple percutaneous transluminal coronary angioplasty procedures at the same site. A quantitative angiographic study in consecutive patients undergoing a third angioplasty procedure for a second restenosis.
Authors: Bauters C , Mc Fadden E P , Lablanche J M , Quandalle P , Bertrand M E 
Published: June 2012

BACKGROUND
Several studies suggest that repeated percutaneous transluminal coronary angioplasty procedures at the same site are associated with a progressively increasing risk of further restenosis and that short time intervals between successive procedures are predictive of future restenosis.

METHODS AND RESULTS
We assessed by quantitative coronary angiography the angiographic probability of restenosis when repeat percutaneous transluminal coronary angioplasty was performed at a site where restenosis had occurred after two previous angioplasty procedures. Of 99 consecutive patients who underwent a third angioplasty procedure, 96 had successful procedures. Uncomplicated failure (residual stenosis > or = 50%) occurred in 3 patients. No major complications occurred. Follow-up angiography was routinely advised; it was performed in 83 patients (86%) with successful procedures. Restenosis (recurrence of > or = 50% stenosis determined by quantitative coronary angiography) occurred in 32 patients (39%). An interval of < 3 months between the second and third angioplasty was strongly associated (P < .005) with the occurrence of further restenosis after a third procedure.

CONCLUSIONS
The angiographic probability of further restenosis after three successive angioplasty procedures at the same site is similar to that reported after a first angioplasty procedure in studies that used a similar definition of restenosis. Patients who undergo a third angioplasty procedure within 3 months of a previous procedure at the same site have a much higher risk of subsequent restenosis. This easily identified subgroup may benefit from an alternative therapeutic approach.