bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of direct angioplasty for treatment of patients with acute myocardial infarction in hospitals with and without on-site cardiac surgery. The Myocardial Infarction, Triage, and Intervention Project Investigators.
Authors: Weaver W D , Litwin P E , Martin J S 
Published: June 2012

BACKGROUND
In the Myocardial Infarction, Triage, and Intervention (MITI) registry of acute myocardial infarction, 441 (12%) of 3750 patients had direct angioplasty as initial treatment. Approximately half (233) were performed in hospitals with no on-site surgery.

METHODS AND RESULTS
Procedure success rates, use of emergent surgery, and factors influencing outcome were compared in both angioplasty groups as well as with 653 patients treated with thrombolytic therapy in the same hospitals. There was no difference in baseline characteristics between patient groups treated by angioplasty in the two types of hospitals. Patency was established in 88% of patients. Only 1.4% underwent emergent surgery. Overall, survival was 93% but was significantly worse after a failed procedure in all ECG and hemodynamic subsets as well as in those with prior bypass surgery. In a multivariate analysis, age, initial heart rate, blood pressure, and prior bypass surgery but not type of hospital were predictive of survival. Survival rates were similar, but there tended to be fewer strokes (0.6% versus 2.1%, P = .12), shorter hospital stays (7.0 versus 8.1 days, P < .001), and less recurrent ischemia (20% versus 30%, P = .009) in patients treated by angioplasty compared with thrombolysis. Readmission and reinfarction rates were similar for both treatments.

CONCLUSIONS
Observations from this community registry suggest that mortality after direct angioplasty is low and the use of emergent surgery is infrequent. Outcome in this registry study was dependent on initial hemodynamic findings and infarct location but not on the presence of on-site surgery. Compared with thrombolytic therapy, the incidence of complications was the same or lower, but this needs confirmation in randomized trials.
Intracoronary albunex. Its effects on left ventricular hemodynamics, function, and coronary sinus flow in humans.
Authors: Ten Cate F J , Widimsky P , Cornel J H , Waldstein D J , Serruys P W , Waaler A 
Published: June 2012

BACKGROUND
Albunex is a recently developed ultrasonic contrast agent made from sonicated human serum albumin. The effects on left ventricular hemodynamics, function, and coronary sinus flow of intracoronary Albunex in humans have not been reported.

METHODS AND RESULTS
Eighteen patients with known or suspected coronary artery disease were examined at the time of coronary arteriography with simultaneous two-dimensional echocardiography and left ventricular catheter-tip manometry. Intracoronary injections of Albunex into the left main coronary artery were performed, as were injections of 5% human serum albumin and iohexol, a widely used angiographic contrast agent. Mean coronary sinus flow was determined before and after injections of iohexol and 2 mL of Albunex. Injection of 1 mL of Albunex induced no changes in any of the measured hemodynamic parameters (heart rate, peak left ventricular [LV] systolic pressure, LV end-diastolic pressure, positive or negative LV dP/dt, or time constant of relaxation) or echocardiographic determinants of LV function (regional wall motion and global ejection fraction). Injection of 2 mL or more of Albunex caused small, transient (less than 30 seconds) changes in measures of isovolumic relaxation (negative LV dP/dt; 95% confidence interval: mean, -2.41 [-4.3, -0.52] and tau 1; confidence interval mean, 3.52; [1.48, 5.58]) but not in functional measures. Intracoronary injection of 5% human serum albumin had no effect. Iohexol induced small but significant changes in both systolic and diastolic parameters, which lasted beyond 30 seconds after injection. Mean coronary sinus blood flow increased.

CONCLUSIONS
The effects of Albunex on hemodynamics, left ventricular function, and coronary sinus blood flow compare favorably with iohexol. Albunex can be considered to be an essentially inert contrast agent if used in patients with stable coronary artery disease.
Use of inhaled nitric oxide and acetylcholine in the evaluation of pulmonary hypertension and endothelial function after cardiopulmonary bypass.
Authors: Wessel D L , Adatia I , Giglia T M , Thompson J E , Kulik T J 
Published: June 2012

BACKGROUND
Increased pulmonary vascular resistance is common in congenital heart disease and is exacerbated by cardiopulmonary bypass (CPB). We investigated whether CPB is responsible for pulmonary endothelial dysfunction and contributes to postoperative pulmonary hypertension.

METHODS AND RESULTS
We infused the endothelium-dependent vasodilator acetylcholine (ACH) into the pulmonary circulation of pulmonary hypertensive children with congenital heart disease either before (n = 12) or after (n = 22) surgical repair on CPB. The dose response to ACH (10(-9) to 10(-6) M) was recorded for all hemodynamic variables. Nine additional postoperative patients were studied with ACH followed by inhalation of 80 ppm nitric oxide, an endothelium-independent smooth muscle relaxant. Plasma levels of cyclic GMP (cGMP) were measured before and after ACH and nitric oxide administration. Pulmonary vasodilation with 10(-6) M ACH was seen in all preoperative patients but was markedly attenuated in postoperative patients. Baseline pulmonary vascular resistance (5.6 +/- 1.0 U x m2) fell 46 +/- 5% in preoperative patients but declined only 11 +/- 4% from baseline (5.8 +/- 0.9 U x m2) in postoperative patients (P < .002). However, inhalation of 80 ppm nitric oxide after ACH infusion in postoperative patients lowered pulmonary vascular resistance by 33 +/- 4% (P < .0002 compared with postoperative ACH response) with minimal effects on the systemic circulation. This finding suggests that the capacity for smooth muscle relaxation and pulmonary vasodilation was present in postoperative patients but could not be induced by ACH. Plasma levels of cGMP in postoperative patients were unchanged after acetylcholine infusion but rose more than threefold during pulmonary vasodilation with nitric oxide (P < .0001). This finding is consistent with the purported role of cGMP as the second messenger effecting smooth muscle relaxation in this process.

CONCLUSIONS
CPB may be responsible for postoperative dysfunction of the pulmonary endothelial cell and may contribute to postoperative pulmonary hypertension in children. Inhaled nitric oxide is a potent pulmonary vasodilator after CPB with minimal systemic circulatory effects. It may have important diagnostic and therapeutic applications in patients with congenital heart disease.
Relation of plasma levels and composition of apolipoprotein B-containing lipoproteins to angiographically defined coronary artery disease in young patients with myocardial infarction.
Authors: Tornvall P , Båvenholm P , Landou C , de Faire U , Hamsten A 
Published: June 2012

BACKGROUND
Hypertriglyceridemia is a common metabolic disturbance in men < 45 years old with myocardial infarction. To further investigate the relation between triglyceride-rich lipoproteins and severity of coronary atherosclerosis in this subset of postinfarction patients, apolipoprotein B-containing lipoproteins of 64 consecutive patients were subfractionated in connection with coronary angiography.

METHODS AND RESULTS
Density-gradient ultracentrifugation of plasma and coronary angiography were performed 4 to 6 months after the myocardial infarction. Global coronary atherosclerosis and the number and severity of distinct stenoses were evaluated by semiquantitative analysis of 15 proximal coronary segments. The majority of the patients (60%) were hypertriglyceridemic and had higher coronary scores than normotriglyceridemic patients. Of the major plasma lipoproteins, triglycerides and cholesterol in the low-density lipoprotein (LDL) fraction were associated with global coronary atherosclerosis, whereas LDL triglycerides and high-density lipoprotein (HDL) cholesterol correlated directly and inversely, respectively, with the coronary stenosis score. Plasma apolipoprotein B correlated with both coronary scores. The plasma concentrations of lipid and protein in the very-low-density lipoprotein (VLDL) subfractions (VLDL1 through VLDL3) and intermediate-density lipoprotein (IDL) did not correlate with either of the coronary scores, whereas the concentration of triglycerides in dense LDL (density > 1.040 kg/L) was strongly associated with both coronary scores. Compositional analysis of the smallest VLDL particles (VLDL3) and IDL revealed a correlation between the number of cholesteryl ester molecules in small VLDL and global coronary atherosclerosis in hypertriglyceridemic patients.

CONCLUSIONS
Global coronary atherosclerosis and distinct stenoses in young postinfarction patients are associated with the number of apolipoprotein B-containing particles in plasma and the concentration of LDL triglyceride. Specifically, dense triglyceride-rich LDL particles and, in hypertriglyceridemic patients, small cholesteryl ester-rich VLDL particles relate to coronary artery disease severity.
Transition from compensated hypertrophy to intrinsic myocardial dysfunction during development of left ventricular pressure-overload hypertrophy in conscious sheep. Systolic dysfunction precedes diastolic dysfunction.
Authors: Aoyagi T , Fujii A M , Flanagan M F , Arnold L W , Brathwaite K W , Colan S D , Mirsky I 
Published: June 2012

BACKGROUND
Patients with aortic stenosis have a period of compensated left ventricular hypertrophy but may eventually develop congestive heart failure. Previous experimental studies showed either normal myocardial contractility in mild short-term pressure overload or myocardial dysfunction with severe pressure overload. Transition from compensated left ventricular hypertrophy to myocardial dysfunction has not been experimentally demonstrated in an adult large animal. Controversial issues in pressure-overload hypertrophy include whether the left ventricular dysfunction is due to insufficient hypertrophy (afterload mismatch) or to intrinsic myocardial dysfunction and whether diastolic dysfunction precedes systolic dysfunction.

METHODS AND RESULTS
We induced left ventricular hypertrophy (41% increase in left ventricular to body weight ratio) by gradually tightening a hydraulic constrictor around the ascending aorta in 9 chronically instrumented conscious sheep. Afterload (end-systolic stress) elevation remained constant (approximately 33% greater than baseline) by adjustment of the aortic constrictor over 6 weeks, gradually increasing left ventricular pressure (from 117 +/- 6 to 163 +/- 5 mm Hg) as hypertrophy developed. Four sets (baseline, 2 weeks, 4 weeks, and 6 weeks) of serial hemodynamic studies were performed in each animal with beta-blockade, first with and then without aortic constriction to mechanically match loading conditions. Stepwise methoxamine infusion was performed to obtain load-independent assessment of myocardial contractility. Midwall shortening (P < .05) and shortening rate (P < .05) at mechanically matched loading conditions showed that myocardial dysfunction developed between the fourth and the sixth week. Shortening-preload-afterload (P < .05) and shortening rate-preload-afterload (P < .05) relations, load-independent contractility indices based on the systolic myocardial stiffness concept, also revealed depressed myocardial contractility at the sixth week. Time constant of left ventricular isovolumic relaxation and diastolic myocardial stiffness constant did not change over the 6 weeks.

CONCLUSIONS
Transition from normal myocardial contractility to myocardial dysfunction was demonstrated. This transition occurred even when the elevation of afterload remained constant as hypertrophy incompletely adapted to increasing left ventricular pressure. Systolic dysfunction preceded diastolic dysfunction in this model.
Heterogeneous transmural distribution of beta-adrenergic receptor subtypes in failing human hearts.
Authors: Beau S L , Tolley T K , Saffitz J E 
Published: June 2012

BACKGROUND
Downregulation of myocardial beta-adrenergic receptor density does not occur in a spatially uniform distribution in patients with congestive heart failure. Rather, it results primarily from loss of receptors in the subendocardium. In patients with dilated cardiomyopathy, beta 1-receptors have been found to be downregulated selectively. These observations suggest that considerable transmural heterogeneity in the distribution of beta-adrenergic receptor subtypes exists in the failing human heart. The present study was designed to test this hypothesis.

METHODS AND RESULTS
We used quantitative autoradiography of radioligand binding sites to measure the distribution of beta-adrenergic receptor subtypes in transmural sections of left ventricular myocardium obtained from cardiac transplant patients with ischemic (n = 13) and idiopathic dilated (n = 12) cardiomyopathy and from 4 subjects with no history of cognitive heart failure. Analysis of radioligand binding isotherms revealed a significant reduction in total beta-adrenergic receptor density in hearts of patients with ischemic and idiopathic cardiomyopathy (20.3 +/- 1.9 and 18.2 +/- 2.0 fmol/mg protein, respectively, versus 40.0 +/- 11.4 in control subjects; P < .01 for both). Loss of the beta 1-subtype accounted for 86% of the total reduction in beta-receptor density in failing hearts. Despite the significant decreases in overall tissue receptor content, the densities of total beta-receptors and beta-receptor subtypes in subepicardial myocytes were equivalent in failing and control hearts. However, in contrast to control hearts, in which the transmural distribution of total and beta 1-receptors was uniform (endocardial: epicardial receptor density ratios, 0.97 +/- 0.14 and 1.0 +/- 0.2, respectively), hearts of patients with ischemic and idiopathic dilated cardiomyopathy had significantly lower total beta-receptor and beta 1-receptor densities in the subendocardium (ratios, 0.66 +/- 0.06 and 0.46 +/- 0.09 for total and beta 1-receptors, respectively, in ischemic cardiomyopathy and 0.60 +/- 0.08 and 0.52 +/- 0.11 in dilated cardiomyopathy; P < .001 for all values compared with a ratio of 1). Thus, beta 1: beta 2 receptor density ratios were markedly decreased in the subendocardium of ischemic and idiopathic dilated left ventricles compared with control hearts.

CONCLUSIONS
A significant transmural gradient in the density of myocardial beta 1-adrenergic receptors exists in the hearts of patients with ischemic and dilated cardiomyopathy, resulting in a markedly altered beta 1: beta 2 receptor density ratio in the subendocardium.
Prognosis after the onset of coronary heart disease. An investigation of differences in outcome between the sexes according to initial coronary disease presentation.
Authors: Murabito J M , Evans J C , Larson M G , Levy D 
Published: June 2012

BACKGROUND
Differences exist between men and women in prognosis after the onset of coronary heart disease (CHD).

METHODS AND RESULTS
All Framingham Heart Study subjects with the onset of clinically apparent coronary disease from 1951 through 1986 were studied to compare prognosis in men and women according to CHD presentation. Coronary disease presentations included angina, coronary insufficiency (unstable angina), recognized myocardial infarction, unrecognized myocardial infarction, and coronary death. Less than 1% of subjects were lost to follow-up for overall mortality. Cox modeling was used to examine the sex differences in outcome for each coronary presentation. New nonfatal coronary disease developed in 750 men (mean age, 63 years) and 583 women (mean age, 67 years). After onset of angina, men were at greater risk than women for myocardial infarction (hazards ratio [HR], 2.20; 95% confidence interval [CI], 1.45 to 3.34) and coronary death (HR, 2.11; 95% CI, 1.32 to 3.36) after adjustment for age and coronary disease risk factors. After a recognized myocardial infarction, there was a trend toward greater risk for overall mortality in women than men after adjustment for age and risk factors (HR, 0.75; 95% CI, 0.53 to 1.08). In contrast, after an unrecognized myocardial infarction, men were at increased risk for death compared with women (HR, 2.01; 95% CI, 1.28 to 3.15).

CONCLUSIONS
Women fare at least as poorly as men after recognized myocardial infarction, whereas women have a more favorable outlook than men after the onset of angina or unrecognized myocardial infarction. The favorable outcome in women after angina and unrecognized myocardial infarction is due, in part, to greater misclassification of these coronary events in women than in men.
Characterization of spatial patterns of flow within the reperfused myocardium by myocardial contrast echocardiography. Implications in determining extent of myocardial salvage.
Authors: Villanueva F S , Glasheen W P , Sklenar J , Kaul S 
Published: June 2012

BACKGROUND
Since myocardial blood flow changes dynamically after reperfusion and since both hyperemia and impairment in microvascular function exist within the acutely reperfused bed, we sought to investigate the role of myocardial contrast echocardiography (MCE) in (1) defining the temporal variability in perfusion patterns after reflow and relating these to microsphere-derived blood flow; (2) differentiating viable from infarcted tissue during different periods of reflow; and (3) defining spatial perfusion patterns within the infarct bed in response to exogenously induced maximal vasodilation and relating these to infarct size and extent of myocardial salvage.

METHODS AND RESULTS
Twenty-one dogs with 3 hours of left anterior descending coronary artery occlusion and 2 to 3 hours of reflow were studied. MCE was performed at 15 and 45 minutes and 2 and 3 hours after reflow. It was also performed at either 2 or 3 hours after reflow in the presence of 0.56 mg/kg of dipyridamole. Radiolabeled microsphere-derived blood flow was measured at 15 minutes and 2 and 3 hours after reflow and during dipyridamole effect. Infarct size was measured at the end of the experiment by use of triphenyl tetrazolium chloride. MCE data were processed with color-coding schemes that highlighted differences in myocardial videointensities in proportion to the concentration of microbubbles within the microvasculature. There was significant variability in MCE-defined perfusion patterns after reflow, with contrast defects noted mainly within the endocardium. There were fair and significant (P < .05) correlation (r = -.73 to r = -.55) between MCE defect size and normalized endocardial blood flow. Except at 15 minutes after reflow, there was poor correlation (r = .31 to r = .51) between MCE defect and infarct sizes. Even at 15 minutes after reflow, MCE defect size underestimated infarct size by 50%. In comparison, in the presence of dipyridamole, MCE defect size correlated strongly (r = .87, P < .001) with infarct size and reasonably well with normalized transmural blood flow (r = -.62, P = .04). Moreover, the topography of the MCE perfusion defect reflected the topography of the infarct.

CONCLUSIONS
MCE revealed striking temporal heterogeneity in the spatial distribution of myocardial perfusion during postischemia reflow and either significantly underestimated or did not correlate with infarct size during reperfusion. Because of abnormalities in coronary vascular reserve specific to infarcted tissue, MCE in conjunction with intravenous dipyridamole depicted, in vivo, the actual topography of the infarct with remarkable accuracy.
Ventricular fusion during resetting and entrainment of orthodromic supraventricular tachycardia involving septal accessory pathways. Implications for the differential diagnosis with atrioventricular nodal reentry.
Authors: Ormaetxe J M , Almendral J , Arenal A , Martínez-Alday J D , Pastor A , Villacastín J P , Delcán J L 
Published: June 2012

BACKGROUND
Ventricular fusion during transient entrainment of orthodromic atrioventricular reciprocating tachycardias (OAVRT) was originally found to be absent and recently observed only with left ventricular stimulation. However, previous studies were restricted to cases with a left free wall accessory pathway. The hypothesis of the present study was that fusion is likely during resetting and entrainment of OAVRT with right ventricular stimulation if the accessory pathway is septally located, since its insertion is relatively close to the stimulation site. This phenomenon can help in the differential diagnosis with atrioventricular nodal reentry (AVNR).

METHODS AND RESULTS
We performed programmed right ventricular stimulation during regular inducible supraventricular tachycardia with concentric atrial activation in 44 patients--20 with OAVRT and 24 with AVNR. Fusion in the ECG morphology of extrastimuli producing resetting was observed in 19 of 19 OAVRT but in 0 of 11 AVNR reset (P < .001). Transient entrainment was demonstrated in all 31 cases undergoing rapid ventricular pacing (14 OAVRT and 17 AVNR). Entrainment with fusion occurred in 13 of 14 OAVRT and in 0 of 17 AVNR (P < .001). Fusion was critically dependent on the coupling intervals or pacing rates, sometimes having a narrow window for its observation.

CONCLUSIONS
The relative proximity (conduction time) among pacing site, site of entrance to a reentrant circuit, and site of exit from the circuit to the paced chamber are critical for the occurrence of fusion during resetting and/or entrainment. The presence or absence of fusion during these phenomena can help in the differential diagnosis of certain supraventricular tachycardias.