bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressure-area relations.
Authors: Gorcsan J , Gasior T A , Mandarino W A , Deneault L G , Hattler B G , Pinsky M R 
Published: June 2012

BACKGROUND
Pressure-volume relations have been established as useful measures of left ventricular (LV) performance. Application of these methods to the intraoperative setting have been limited because of difficulties acquiring LV volume data. Transesophageal echocardiographic automated border detection can measure LV cross-sectional area as an index of volume, which can be coupled with pressure data to construct pressure-area loops on-line. The purpose of this study was to evaluate intraoperative LV performance in patients undergoing coronary bypass surgery before and immediately after cardiopulmonary bypass using on-line pressure-area relations.

METHODS AND RESULTS
Studies were attempted in 13 consecutive patients. Simultaneous measures of LV cross-sectional area, LV pressure, and electromagnetic flow probe-derived aortic flow recorded on a computer work station interfaced with the ultrasound system. Pressure-area loops were compared with simultaneous pressure-volume loops constructed from pressure and flow data during inferior vena caval occlusions before and after bypass. Pressure-volume calculations (end-systolic elastance, maximal elastance, and preload-recruitable stroke work) were then applied to pressure-area loops with area substituted for volume data. Changes in stroke force from pressure-area loops were closely correlated with changes in estimates of stroke work from pressure-volume loops for individual patients before bypass (r = .99 +/- .03, SEE = 5 +/- 2%, n = 10) and after bypass (r = .96 +/- .05, SEE = 5 +/- 2%, n = 9). Pressure-area estimates of end-systolic elastance, maximal elastance, and preload-recruitable stroke force decreased significantly from before to after cardiopulmonary bypass in the 7 patients with paired data sets. Load-dependent measures of LV function (stroke volume, cardiac output, and fractional area change) were unchanged after surgery in these same patients.

CONCLUSIONS
Intraoperative pressure-area loops may be acquired and displayed on-line using transesophageal echocardiographic automated border detection and readily analyzed in a manner similar to pressure-volume loops. LV performance was depressed immediately after cardiopulmonary bypass compared with before. On-line pressure-area relations may be clinically useful to assess LV performance in patients undergoing cardiac surgery in whom load and contractility may be expected to vary rapidly.
Serial echocardiographic assessment of left ventricular geometry and function after large myocardial infarction in the rat.
Authors: Litwin S E , Katz S E , Morgan J P , Douglas P S 
Published: June 2012

BACKGROUND
The development of heart failure after acute myocardial infarction (MI) may be related to alterations of left ventricular (LV) structure and function. Pathological LV remodeling may exacerbate systolic and diastolic dysfunction because increased cavity dimensions tend to increase LV wall stress. Unfortunately, many complicating factors have made it difficult to clearly define the time course of LV remodeling after myocardial infarction in patients, and the contribution of structural changes to altered function has not been fully explored.

METHODS AND RESULTS
To determine the type, magnitude, and time course of changes in LV geometry and function, we performed transthoracic Doppler echocardiographic examinations in rats before and 1 and 6 weeks after transmural MI induced by coronary ligation. LV internal diastolic dimension was greater in infarcted than in sham-operated rats at 1 and 6 weeks after MI (9.4 +/- 0.6 versus 8.0 +/- 0.5 and 10.1 +/- 0.9 versus 8.5 +/- 0.9 mm, respectively; P < .05 compared with sham-operated rats). There was significant thinning of the infarcted anterior wall at 1 and 6 weeks (0.99 +/- 0.2 versus 1.33 +/- 0.19 and 0.96 +/- 0.22 versus 1.51 +/- 0.18 mm, P < .05), while the thickness of the noninfarcted posterior wall increased but was not different from normal growth in sham-operated rats. Six weeks after surgery, fractional shortening was impaired (11 +/- 5% versus 35 +/- 5%, P < .05), and systolic thickening of the noninfarcted posterior wall was depressed (38 +/- 9% versus 67 +/- 18%, P < .05) in infarcted rats compared with shams. These changes in structure and systolic function were accompanied by progressive alterations in LV diastolic filling. Peak early filling velocity increased at 1 and 6 weeks in MI rats (91 +/- 9 versus 79 +/- 9 and 100 +/- 14 versus 74 +/- 11 cm/s, P < .05), and the deceleration rate of the early filling wave was more rapid in rats with MI (21.6 +/- 5.0 versus 15.6 +/- 3.1 and 26.1 +/- 9.8 versus 11.2 +/- 2.7 m/s2, P < .05). Late filling velocity was decreased (16 +/- 15 versus 33 +/- 7 and 15 +/- 18 versus 34 +/- 5 cm/s, P < .05), resulting in a marked increase in the ratio of early to late filling. The peak velocity and the velocity-time integral of LV outflow did not change after MI.

CONCLUSIONS
Postinfarction LV remodeling in the rat is characterized by progressive cavity dilatation, inadequate hypertrophy of the surviving myocardium, the gradual development of regional contractile dysfunction in noninfarcted segments, and marked abnormalities of diastolic filling. These changes can be tracked longitudinally with transthoracic echocardiography.
Effect of calcitonin gene-related peptide on coronary microvessels and its role in acute myocardial ischemia.
Authors: Sekiguchi N , Kanatsuka H , Sato K , Wang Y , Akai K , Komaru T , Takishima T 
Published: June 2012

BACKGROUND
Calcitonin gene-related peptide (CGRP) is a potent dilator of epicardial conduit vessels and is released during myocardial ischemia in humans. However, the effect of CGRP on coronary arterial microvessels is still unclear, and it is unknown if CGRP modulates the tone of coronary arterial microvessels during acute myocardial ischemia.

METHODS AND RESULTS
Epimyocardial microvessels were observed through a microscope equipped with a floating objective system in anesthetized open-chest dogs. Heart rate and aortic pressure were maintained at control levels. Flow velocity of the left anterior descending coronary artery (LAD) was measured with a suction-cup Doppler probe. When CGRP was cumulatively infused into the LAD (0.05, 0.5, 5.0, and 50 pmol/kg per minute) or superfused (0.03, 0.3, 3.0, and 30 nmol/L) over the left ventricular surface, arterial control microvessels > 100 microns in diameter dilated dose dependently at dosages of 0.5 to 50 pmol/kg per minute (infused) or 0.3 to 30 nmol/L (superfused), but those < 100 microns dilated only at the highest dose, and those > 100 microns had greater dilation in both groups. Only the highest dose of CGRP (infused) significantly increased coronary flow. The superfusion of CGRP(8-37) (CGRP receptor antagonist, 300 nmol/L) did not affect the control diameters of coronary arterial microvessels but completely abolished CGRP-induced vasodilation at the same doses (infused and superfused). However, 300 nmol/L of CGRP(8-37) did not affect the response of coronary arterial microvessels to the LAD occlusion in any size.

CONCLUSIONS
CGRP preferentially dilates the coronary arterial microvessels > 100 microns in diameter but has only a small effect on those < 100 microns. Endogenous CGRP does not modulate the tone of coronary arterial microvessels during acute myocardial ischemia in beating canine hearts.
Ethinyl estradiol acutely attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women.
Authors: Reis S E , Gloth S T , Blumenthal R S , Resar J R , Zacur H A , Gerstenblith G , Brinker J A 
Published: June 2012

BACKGROUND
Estrogen administration in postmenopausal women is associated with a 50% reduction in the clinical manifestations of coronary artery disease. The mechanisms are not known, although one potential explanation is estrogen-induced modulation of coronary vasoreactivity. Acetylcholine is an endothelium-dependent vasodilator that may be used to assess coronary vasoreactivity and elicits coronary responses that parallel those found with common daily vasomotor stimuli. Therefore, we tested whether estrogen attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women.

METHODS AND RESULTS
Acetylcholine-induced changes in coronary flow, resistance, and cross-sectional area were determined before and 15 minutes after intravenous administration of ethinyl estradiol (EE, 35 micrograms) in 15 postmenopausal women. The influence of estrogen on basal coronary flow, resistance, and epicardial cross-sectional area was also assessed by measuring these parameters before and after EE or placebo administration in 33 women. Estrogen altered basal coronary vasomotor tone in 22 women as manifested by an EE-induced 23.3 +/- 4.5% (mean +/- SEM) increase (P < .01) in coronary flow, a 15.0 +/- 3.2% decrease (P < .01) in resistance, and a 20.0 +/- 6.5% increase (P = .02) in epicardial cross-sectional area. Placebo administration in 11 women did not change these parameters. Estrogen also attenuated abnormal coronary vasomotor responses to acetylcholine. Seven women who exhibited a paradoxical acetylcholine-induced decrease in coronary flow (-33.5 +/- 12.3%, P < .01) and increase in resistance (38.9 +/- 14.1%, P = .05) and seven who had an abnormal acetylcholine-induced decrease in epicardial cross-sectional area (-14.2 +/- 4.4%; P = .04) did not have acetylcholine-induced changes in these parameters after EE administration. Acetylcholine-induced flow, resistance, and cross-sectional area responses before and after EE were significantly different (P < .01, P = .02, and P = .02, respectively). Normal coronary responses to acetylcholine were not affected by EE administration.

CONCLUSIONS
EE attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women. EE also decreases basal coronary vasomotor tone as manifested by increased coronary flow, decreased resistance, and increased epicardial cross-sectional area. These acute effects of estrogen on coronary vasoreactivity may explain, in part, the cardioprotective effects of estrogen in postmenopausal women.
Long-term prognostic importance of patency of the infarct-related coronary artery after thrombolytic therapy for acute myocardial infarction.
Authors: White H D , Cross D B , Elliott J M , Norris R M , Yee T W 
Published: June 2012

BACKGROUND
After thrombolytic therapy, long-term patency of the infarct-related artery may reduce arrhythmias, limit ventricular dilatation, and provide collaterals to another infarct zone if further infarction occurs. However, independent long-term prognostic value of infarct artery patency has not been shown.

METHODS AND RESULTS
We followed 312 patients with first myocardial infarction treated < 4 hours after pain onset with thrombolysis (streptokinase [n = 188] or recombinant tissue-type plasminogen activator [n = 124]). At 28 +/- 11 days, cardiac catheterization was performed. Flow of the infarct-related artery was assessed by the TIMI scoring system, and a scoring system relating coronary stenoses and flow to the amount of myocardium supplied was also used. Follow-up was for 39 +/- 13 months. Cardiac death occurred in 5.8% of patients, and there were two noncardiac deaths. Revascularization was performed in 11.5% of patients. On univariate and multivariate analysis, ventricular function (ejection fraction, P = .006 and .02, or end-systolic volume index, P = .01 and .06) was the most important prognostic factor. Patency of the infarct-related artery measured as TIMI 3 flow was marginally significant on univariate analysis (P = .08) but not on multivariate analysis (P = .2). Patency was an independent prognostic factor in univariate and multivariate analysis when measured as an occlusion score (amount of myocardium supplied by an occluded artery, P = .01 and < .05). When the ejection fraction was > or = 50%, only occluded arteries supplying > 25% of the left ventricle affected prognosis adversely. If the ejection fraction was < 50%, occluded arteries supplying < 25% of myocardium also adversely affected prognosis. Treadmill exercise duration 4 weeks after infarction was the only other prognostic factor identified.

CONCLUSIONS
Ventricular function and infarct-related artery patency are independent prognostic factors after thrombolytic therapy for acute myocardial infarction.
Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril.
Authors: St John Sutton M , Pfeffer M A , Plappert T , Rouleau J L , Moyé L A , Dagenais G R , Lamas G A , Klein M , Sussex B , Goldman S 
Published: June 2012

BACKGROUND
Left ventricular enlargement after myocardial infarction increases the likelihood of an adverse outcome. In an echocardiographic substudy of the Survival and Ventricular Enlargement (SAVE) Trial, we assessed whether captopril would attenuate progressive left ventricular enlargement in patients with left ventricular dysfunction after acute myocardial infarction and, if so, whether this would be associated with improved clinical outcome.

METHODS AND RESULTS
Two-dimensional transthoracic echocardiograms were obtained in 512 patients at a mean of 11.1 +/- 3.2 days after infarction and were repeated at 1 year in 420 survivors. Left ventricular size was assessed as left ventricular cavity areas at end diastole and end systole and left ventricular function as percent change in cavity area from end diastole to end systole. Patients were randomly assigned to placebo or captopril, and the incidence of adverse cardiovascular events consisting of cardiovascular death, heart failure requiring either hospitalization or open-label angiotensin-converting enzyme inhibitor therapy, and recurrent infarction were determined over a follow-up period averaging 3.0 +/- 0.6 years. Irrespective of treatment assignment, baseline left ventricular systolic area and percent change in area were strong predictors of cardiovascular mortality and adverse cardiovascular events. At 1 year, left ventricular end-diastolic and end-systolic areas were larger in the placebo than in the captopril group (P = .038, P = .015, respectively), and percent change in cavity area was greater in the captopril group (P = .005). One hundred eleven of the 420 1-year survivors with 1-year echo measurements (26.4%) experienced a major adverse cardiovascular event, and these patients had more than a threefold greater increase in left ventricular cavity areas than those with an uncomplicated course. Sixty-nine patients with adverse cardiovascular events were in the placebo group compared with 42 patients in the captopril-treated group (a risk reduction of 35%, P = .010).

CONCLUSIONS
Two-dimensional echocardiography provides important and independent prognostic information in patients after infarction. Left ventricular enlargement and function after infarction are associated with the development of adverse cardiac events. Attenuation of ventricular enlargement with captopril in these patients was associated with a reduction in adverse events. This study demonstrates the linkage between attenuation of left ventricular enlargement by captopril after infarction and improved clinical outcome.
Combination antithrombotic therapy in unstable rest angina and non-Q-wave infarction in nonprior aspirin users. Primary end points analysis from the ATACS trial. Antithrombotic Therapy in Acute Coronary Syndromes Research Group.
Authors: Cohen M , Adams P C , Parry G , Xiong J , Chamberlain D , Wieczorek I , Fox K A , Chesebro J H , Strain J , Keller C 
Published: June 2012

BACKGROUND
The purpose of this study was to compare combination antithrombotic therapy with aspirin plus anticoagulation versus aspirin alone, when added to conventional antianginal therapy in patients with unstable rest angina or non-Q-wave myocardial infarction who were nonprior aspirin users.

METHODS AND RESULTS
Two hundred fourteen patients were randomized; 109 were randomized to receive aspirin alone (162.5 mg daily) and 105 to receive a combination of aspirin plus anticoagulation, ie, aspirin 162.5 mg daily plus heparin (activated partial thromboplastin time, two times control) followed by aspirin 162.5 mg daily plus warfarin (international normalized ratio, 2 to 3). Trial therapy was begun by 9.5 +/- 8.8 hours of qualifying pain and was continued for 12 weeks. Primary end points were recurrent angina with ECG changes, myocardial infarction, and/or death. Analysis by intention to treat of primary events at 12 weeks was performed. At 14 days, there was a significant reduction in total ischemic events in the combination group versus aspirin alone (10.5% versus 27%, P = .004). An efficacy analysis of primary events at 12 weeks also revealed a large reduction in total ischemic events in the combination group versus aspirin alone (13% versus 25%, P = .06). Bleeding complications were slightly more common with combination therapy.

CONCLUSIONS
In nonprior aspirin users, combination antithrombotic therapy with aspirin plus anticoagulation significantly reduces recurrent ischemic events in the early phase of unstable angina.
Randomized trial of a GPIIb/IIIa platelet receptor blocker in refractory unstable angina. European Cooperative Study Group.
Authors: Simoons M L , de Boer M J , van den Brand M J , van Miltenburg A J , Hoorntje J C , Heyndrickx G R , van der Wieken L R , de Bono D , Rutsch W , Schaible T F 
Published: June 2012

BACKGROUND
Patients with unstable angina despite intensive medical therapy, ie, refractory angina, are at high risk for developing thrombotic complications: myocardial infarction or coronary occlusion during percutaneous transluminal coronary angioplasty (PTCA). Chimeric 7E3 (c7E3) Fab is an antibody fragment that blocks the platelet glycoprotein (GP) IIb/IIIa receptor and potently inhibits platelet aggregation.

METHODS AND RESULTS
To evaluate whether potent platelet inhibition could reduce these complications, 60 patients with dynamic ST-T changes and recurrent pain despite intensive medical therapy were randomized to c7E3 Fab or placebo. After initial angiography had demonstrated a culprit lesion suitable for PTCA, placebo or c7E3 Fab was administered as 0.25 mg/kg bolus injection followed by 10 micrograms/min for 18 to 24 hours until 1 hour after completion of second angiography and PTCA. During study drug infusion, ischemia occurred in 9 c7E3 Fab and 16 placebo patients (P = .06). During hospital stay, 12 major events occurred in 7 placebo patients (23%), including 1 death, 4 infarcts, and 7 urgent interventions. In the c7E3 Fab group, only 1 event (an infarct) occurred (3%, P = .03). Angiography showed improved TIMI flow in 4 placebo and 6 c7E3 Fab patients and worsening of flow in 3 placebo patients but in none of the c7E3 Fab patients. Quantitative analysis showed significant improvement of the lesion in the patients treated with c7E3 Fab, which was not observed in the placebo group, although the difference between the two treatment groups was not significant. Measurement of platelet function and bleeding time demonstrated > 90% blockade of GPIIb/IIIa receptors, > 90% reduction of ex vivo platelet aggregation to ADP, and a significantly prolonged bleeding time during c7E3 Fab infusion, without excess bleeding.

CONCLUSIONS
Combined therapy with c7E3 Fab, heparin, and aspirin appears safe. These pilot study results support the concept that effective blockade of the platelet GPIIb/IIIa receptors can reduce myocardial infarction and facilitate PTCA in patients with refractory unstable angina.
Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses.
Authors: Cannegieter S C , Rosendaal F R , Briët E 
Published: June 2012

BACKGROUND
Patients with mechanical heart valve prostheses may experience valve thrombosis and subsequent systemic embolism for which they are treated with oral anticoagulant therapy. It is essential to know reliable estimates of the risks and benefits of this therapy in order to answer a number of clinical questions rationally. We sought to obtain more precise estimates of the risks and benefits by combining the data from individual studies by using meta-analysis.

METHODS AND RESULTS
We searched for studies in which the incidences were reported of embolic or bleeding complications in patients with mechanical heart valve prostheses. They were collected from the Medline and Current Contents database and by cross-references between 1970 and 1992. Since most studies vary greatly in many respects, we used a number of inclusion criteria, thus selecting comparable studies of acceptable quality only. The influence of antithrombotic therapy, valve position, and valve type was analyzed by univariate and by multivariate analysis with Poisson regression techniques. Forty-six studies were found, including 13,088 patients studied for 53,647 patient-years. We found an incidence of major embolism in the absence of antithrombotic therapy of 4 per 100 patient-years. With antiplatelet therapy this risk was 2.2 per 100 patient-years, and with coumarin therapy it was reduced to 1 per 100 patient-years. This risk varied with the type and the site of the prosthesis. A prosthesis in mitral position increased the risk almost twice as compared with the aortic position. Tilting disc valves and bileaflet valves showed a lower incidence of major embolism than caged ball valves. An incidence of major bleeding was found in patients treated with coumarin derivatives of 1.4 per 100 patient-years. The incidence of bleeding became significantly higher with the addition of antiplatelet therapy, although this did not decrease the risk of thromboembolism any further.

CONCLUSIONS
These data provide a reference for future studies and give adequate risk estimates for clinical decision making.