bluuebunny/crossref_metadata_2025_split huggingface dataset:
Energy conversion efficiency in human left ventricle.
Authors: Kameyama T , Asanoi H , Ishizaka S , Yamanishi K , Fujita M , Sasayama S 
Published: June 2012

BACKGROUND
Left ventricular mechanical efficiency is one of the most important measures of left ventricular pump performance. Several clinical studies, however, have shown that mechanical efficiency does not fall substantially as the heart fails. To clarify the insensitivity of mechanical efficiency to the change in pump performance, we analyzed human left ventricular mechanical efficiency, applying the concept of left ventricular systolic pressure-volume area (PVA).

METHODS AND RESULTS
PVA correlates linearly with myocardial oxygen consumption per beat (MVO2): MVO2 = a.PVA+b, and represents the total mechanical energy of contraction. We determined MVO2-PVA relation and external work in 11 patients with different contractile states. We also calculated the energy transfer from MVO2 to PVA (PVA/MVO2 efficiency), that from PVA to external work (work efficiency), and mechanical efficiency (external work/MVO2). Left ventricular pressure-volume loops were constructed by plotting the instantaneous left ventricular pressure against the left ventricular volume at baseline and during pressure loading. The contractile properties of the ventricle were defined by the slope of the end-systolic pressure-volume relation (Ees). Pressure elevation raised external work by 41.4%, PVA by 71.2%, and MVO2 by 54.5%. These changes were associated with a decrease in work efficiency and an increase in PVA/MVO2 efficiency. The opposite directional changes in these two efficiencies rendered the mechanical efficiency constant. The slope, a, of the relation between MVO2 and PVA was relatively constant (2.46 +/- 0.33) over the range of 0.8-8.8 mm Hg/ml of Ees, but the oxygen axis intercept, b, tended to decrease with the reduction in Ees. PVA/MVO2 efficiency correlated inversely (r = -0.66, p less than 0.05) with Ees, whereas work efficiency correlated linearly with Ees (r = 0.91, p less than 0.01).

CONCLUSIONS
Mechanical efficiency is not appreciably affected by changes in loading and inotropic conditions as long as the left ventricular contractility is not severely depressed.
Low high density lipoprotein level is associated with increased restenosis rate after coronary angioplasty.
Authors: Shah P K , Amin J 
Published: June 2012

BACKGROUND
To determine the relation of post-percutaneous transluminal coronary angioplasty (PTCA) restenosis to serum lipid fractions and to circulating levels of endogenous tissue plasminogen activator (t-PA) and its rapid inhibitor (PAI-1), 68 patients with coronary artery disease who underwent a successful PTCA were studied.

METHODS AND RESULTS
During a mean follow-up of 9 months (range, 7-11 months), 28 (41%) patients developed restenosis. A low high density lipoprotein (HDL) cholesterol level was independently and strongly related to both the risk of restenosis (p less than 0.001) and to the time of restenosis (p = 0.03). The mean HDL cholesterol level was 33 +/- 12 mg% in the restenosis group compared with 45 +/- 12 mg% in the nonrestenosis group (p less than 0.001). Restenosis developed in 22 of 34 (64%) patients with an HDL cholesterol less than or equal to 40 mg% compared with six of 34 (17%) patients with an HDL cholesterol greater than 40 mg% (p less than 0.002). The only other variable that was significantly related to restenosis was a low PAI-1 level (p = 0.04).

CONCLUSIONS
The strong relation between a low HDL cholesterol level and the risk of restenosis suggests that lipid fractions could be important in the pathogenesis and prevention of restenosis.
Electrophysiological findings and long-term follow-up of patients with the permanent form of junctional reciprocating tachycardia treated by catheter ablation.
Authors: Chien W W , Cohen T J , Lee M A , Lesh M D , Griffin J C , Schiller N B , Scheinman M M 
Published: June 2012

BACKGROUND
The permanent form of junctional reciprocating tachycardia (PJRT) commonly presents as recurrent drug-refractory, narrow-complex tachycardia. We studied the efficacy and safety of catheter ablation in treating these patients.

METHODS AND RESULTS
Six patients with the diagnosis of PJRT were treated at our institution with direct-current catheter ablation. The study cohort comprised three men and three women with a mean age of 33.8 +/- 4.5 years. The mean time from onset of symptoms to ablation was 129 +/- 44.7 months. All failed multiple drug therapy (mean number of drugs failed was 5.3 +/- 0.5). The left ventricular ejection fractions were calculated by echocardiography and were greater than 60% in all except two patients, whose ejection fractions were 25% and 32%. Symptom duration was significantly longer in those with depressed ejection fraction compared with normal patients (258 versus 64.5 months, p less than 0.01). Electrophysiological findings revealed evidence of an atrioventricular reciprocating tachycardia involving retrograde decremental conduction over an accessory pathway localized to the posteroseptal area. Five patients received two direct-current shocks (250 +/- 16.7 J per shock) via paired electrodes from a catheter positioned just outside the coronary sinus os to a patch placed between the scapulae or on the anterior chest wall. One patient received a single direct-current shock of 300 J. The only complication was the development of complete atrioventricular block in one patient. This patient had previously undergone permanent pacemaker insertion for the sick sinus syndrome. The mean hospital stay after ablation was 2.2 days. Mean peak creatinine phosphokinase after ablation was 352 +/- 58.1 units/l and the MB fraction was 12 +/- 2%. Follow-up echocardiograms or gated nuclear studies showed improvement of ejection fraction in the two patients who presented with depressed ejection fractions. After a mean follow-up of 35.8 +/- 10.3 months, all patients remained free of tachycardia without antiarrhythmic drugs.

CONCLUSIONS
We conclude that catheter ablation by using direct current energy appears to be an effective treatment in patients with PJRT.
Imaging of vascular injury with 99mTc-labeled monoclonal antiplatelet antibody S12. Preliminary experience in human percutaneous transluminal angioplasty.
Authors: Miller D D , Rivera F J , Garcia O J , Palmaz J C , Berger H J , Weisman H F 
Published: June 2012

BACKGROUND
To evaluate the in vivo safety, biodistribution, and diagnostic accuracy of a monoclonal Fab' antibody (S12) that is specific for the platelet membrane glycoprotein (GMP-140) expressed during platelet activation at vascular injury sites, 11 peripheral percutaneous transluminal angioplasty (PTA) patients (age, 61 +/- 8 years) with severe vascular disease had serial 99mTcS12 radionuclide imaging at 5 and 90 minutes, 4-6 hours, and 20-24 hours after a total of 23 angiographically successful PTA procedures. No acute allergic reactions or hematologic toxicity occurred.

METHODS AND RESULTS
The average PTA percent angiographic diameter stenosis (DS) at all 23 sites decreased from 85 +/- 12% to 12 +/- 11%, with a mean before-to-after-PTA change of 73 +/- 14% (p less than 0.01). The mean radionuclide image-derived ratio of 99mTc S12 activity in PTA versus contralateral non-PTA arterial segments for all angioplasty sites was 1.6 +/- 0.5. Vascular 99mTc S12 antibody activity was qualitatively evident in the majority (78%) of PTA sites at 4-6 hours after injection. 99mTc S12 target-to-background (muscle) ratio equaled 2.3 +/- 0.6 at PTA sites. Nine PTA sites (39%) had residual 99mTc S12 activity at 24 hours after injection (mean PTA site-to-contralateral artery ratio, 1.5 +/- 0.4). The mean vascular 99mTc S12 activity ratios in 10 procedurally complicated (defined as extensive dilation [greater than 2 cm] or grade I or greater arterial dissection) and 13 uncomplicated PTA segments were 1.9 +/- 0.5 versus 1.2 +/- 0.1, respectively (p less than 0.01). The associated before-to-after-PTA angiographic improvement was significantly less in procedurally complicated PTA sites (66 +/- 12% versus 80 +/- 12% DS; p less than 0.01).

CONCLUSIONS
99mTc S12 activity is significantly increased at angiographically patent PTA sites that are procedurally complicated and are associated with less significant before-to-after-PTA angiographic improvement. 99mTc S12 monoclonal Fab' antibody imaging permits noninvasive identification of local vascular platelet activation resulting from angioplasty balloon injury in humans.
Pericardial adaptation in severe chronic pulmonary hypertension. An intraoperative transesophageal echocardiographic study.
Authors: Blanchard D G , Dittrich H C 
Published: June 2012

BACKGROUND
The pericardium both limits cardiac distension and accentuates ventricular interdependence. Although this effect appears minimal under normal circumstances, the pericardium markedly restricts acute cardiac enlargement. Animal studies have demonstrated gradual pericardial adaptation and expansion in chronic volume overload and cardiomegaly, but the pericardial response in humans with cardiac hypertrophy and enlargement has not been examined fully. To investigate this further, 14 patients with right ventricular hypertrophy and cardiomegaly secondary to chronic pulmonary thromboembolic disease and severe pulmonary hypertension were studied during pulmonary thromboendarterectomy.

METHODS AND RESULTS
Simultaneous intraoperative transesophageal Doppler echocardiography and direct biventricular hemodynamic measurements were performed at steady state immediately before and after pericardiotomy. All hemodynamic variables showed no significant change before and after pericardiotomy, including heart rate (76 +/- 16 versus 75 +/- 15 beats per minute), mean pulmonary arterial pressure (46.3 +/- 11.1 versus 45.5 +/- 11.7 mm Hg), cardiac index (1.8 +/- 0.5 versus 2.0 +/- 0.6 l/min/m2), left ventricular end-diastolic pressure (5.9 +/- 5.7 versus 7.1 +/- 5.0 mm Hg), and right ventricular end-diastolic pressure (7.9 +/- 6.6 versus 8.0 +/- 6.7 mm Hg). Similarly, there were no significant changes in all Doppler echocardiographic parameters, including right ventricular end-diastolic area (23.2 +/- 5.7 versus 22.6 +/- 5.4 cm2), left ventricular end-diastolic area (15.3 +/- 5.9 versus 15.5 +/- 4.4 cm2), the position of the interventricular septum, and the Doppler-derived mitral inflow measures of diastolic function.

CONCLUSIONS
The pericardium appears to have little influence on the marked cardiac and septal deformations seen in patients with chronic, severe right ventricular pressure overload and cardiomegaly. This study confirms that the human pericardium is capable of adapting over time to changes in cardiac size and geometry.
Reduced left ventricular compliance in human mitral stenosis. Role of reversible internal constraint.
Authors: Liu C P , Ting C T , Yang T M , Chen J W , Chang M S , Maughan W L , Lawrence W , Kass D A 
Published: June 2012

BACKGROUND
The mechanisms of depressed left ventricular (LV) pump performance in human mitral stenosis (MS) remain poorly understood, because reduced filling alone affects many hemodynamic measurements. Therefore, pressure-volume relations were examined in nine subjects with MS and compared with eight age-matched normal controls.

METHODS AND RESULTS
Data were obtained by conductance catheter/micromanometer technique with transient inferior vena cava occlusion used to alter load and generate pressure-volume relations. In a subset of patients (n = 5), data were obtained both acutely and at 3 months (n = 4) after balloon valvuloplasty. MS patients had reduced cardiac output (3.3 +/- 0.9 versus 5.6 +/- 1.7 l/min) and end-diastolic volume (68.0 +/- 6.9 versus 115 +/- 31 ml) versus controls (p less than 0.001), with a mean transvalvular gradient of 14 +/- 6 mm Hg and estimated valve area of 0.6 +/- 0.2 cm2. Systolic function as assessed by the end-systolic pressure-volume relation was virtually the same in MS and control subjects. In contrast, end-diastolic pressure-volume relations in MS were consistently shifted leftward and had an increased slope (lower compliance) at matched pressure ranges (6.5 +/- 3.0 versus 2.2 +/- 0.53 ml/mm Hg at a mean diastolic pressure of 8 mm Hg, p less than 0.001). This change was not a result of reduced LV filling or probably of increased right heart loading. Valvuloplasty acutely returned chamber compliance to near normal, a change that was sustained at 3-month follow-up. Systolic function was little altered at this time.

CONCLUSIONS
These data indicate an impairment of diastolic function in human MS that can be acutely reversed by balloon valvuloplasty. Lowered LV compliance probably results from a functional restriction caused by ventricular attachment to a thickened and immobile valve apparatus.
New redistribution index of nutritive blood flow to skeletal muscle during dynamic exercise.
Authors: Asanoi H , Wada O , Miyagi K , Ishizaka S , Kameyama T , Seto H , Sasayama S 
Published: June 2012

BACKGROUND
Cardiac output is effectively redistributed to working muscle by regional changes in vascular resistance. However, there has been no suitable method to quantify blood flow distribution to large working and nonworking muscles involved in ergometer or treadmill exercise.

METHODS AND RESULTS
To quantify the redistribution of blood flow, we compared thallium activity in a bicycle pedaling leg with that in the contralateral resting leg in 10 normal subjects. The regional thallium activity was expressed as a percentage of the whole-body radioisotope activity. Comparison of thallium activity between legs was performed at rest and at the work rates of anaerobic threshold and peak exercise during one-leg exercise. Thallium distribution of both legs was essentially the same at rest. At the anaerobic threshold, thallium activity increased about threefold to fourfold in the exercising thigh and about twofold in the exercising calf. The thallium distribution in these muscles at peak exercise was the same as at the anaerobic threshold. In the nonexercising calf, thallium distribution during exercise decreased significantly, and it was unchanged in the nonexercising thigh. Consequently, the ratio of thallium activity between the exercising and nonexercising thighs increased from 1.1 +/- 0.1 to 4.0 +/- 0.9 at the anaerobic threshold and to 3.3 +/- 0.6 at peak exercise. Similarly, the ratio between the exercising and nonexercising calves increased from 1.0 +/- 0.0 to 3.8 +/- 1.3 at the anaerobic threshold and to 3.5 +/- 1.0 at peak exercise. The ratios at peak exercise, however, did not differ significantly from those at the anaerobic threshold.

CONCLUSIONS
These findings suggest that the redistribution of blood flow occurs predominantly during mild to moderate exercise; therefore, blood flow in the leg during strenuous exercise would depend primarily upon an increased cardiac output. Thus, the thallium activity ratio of exercising and nonexercising legs reflects the difference in vascular tone of each leg and could provide a noninvasive and quantitative index of blood flow redistribution.
Collagen loss in the stunned myocardium.
Authors: Charney R H , Takahashi S , Zhao M , Sonnenblick E H , Eng C 
Published: June 2012

BACKGROUND
This study was performed to biochemically assess and quantify the previously observed ultrastructural alterations in the collagen matrix of stunned myocardium.

METHODS AND RESULTS
The stunned myocardium was produced in 13 mongrel dogs by a series of 12 coronary artery occlusions of 5 minutes followed by 10-minute reperfusion periods, with a final reperfusion period of 90 minutes. Regional systolic function in the stunned myocardium was 17% of control. Relative end-diastolic length in the stunned region increased up to 8%. There was a nonuniform transmural loss of collagen. Hydroxyproline in the stunned endocardium was not different from control. The stunned midwall and epicardium demonstrated 12.5% (p less than 0.05) and 14.6% (p less than 0.005) decreases, respectively. All transmural layers in the stunned myocardium had significant increases in collagenase activity before procollagenase activation, averaging a 73.6% increase (p less than 0.025). Complete activation of all procollagenase forms with aminophenylmercuric acetate revealed no differences in fully activated collagenase between the stunned and normal regions. The lysosomal enzymes, elastase and cathepsin G, were not different between stunned and normal zone tissue. These results would tend to exclude exogenous sources of protease in the stunned myocardium at the 90-minute final reperfusion time frame. Collagen fibers were isolated from the stunned and normal zone tissue and underwent dansyl chloride reaction. Stunned collagen fibers had 9% greater dansyl labeling, suggesting greater numbers of exposed N-terminal amino acid residues on the fiber and compatible with greater enzymatic cleavage activity on the stunned collagen matrix. Tissue water content was consistently greater in the stunned region compared to the normal: a uniform transmural increase of approximately 1.7%.

CONCLUSIONS
The stunned myocardium is characterized by both systolic dysfunction and diastolic expansion or dilatation. Endogenous procollagenase is activated by the ischemic process leading to degradation of the extracellular matrix. The underlying mechanisms may be relevant in ischemic enlargement of the heart and cardiomyopathy.
Endogenous adenosine blunts beta-adrenoceptor-mediated inotropic response in hypoperfused canine myocardium.
Authors: Sato H , Hori M , Kitakaze M , Takashima S , Inoue M , Kitabatake A , Kamada T 
Published: June 2012

BACKGROUND
Adenosine attenuates beta-adrenoceptor-mediated inotropic responses through GTP-binding protein in vitro. The goal of the present study was to test the hypothesis that endogenous adenosine released from the ischemic myocardium blunts the inotropic response to beta-adrenergic stimulation.

METHODS AND RESULTS
In 45 open-chest dogs, the left anterior descending coronary artery was perfused through an extracorporeal bypass tube from the carotid artery. Coronary perfusion pressure was reduced so that coronary blood flow was decreased to 60% of the basal level by partial occlusion of the bypass tube, and the reduced coronary perfusion pressure was kept constant thereafter. Inotropic responses to isoproterenol were assessed by fractional shortening of the myocardium in the perfused area. After the onset of hypoperfusion, lactate extraction ratio (18.8 +/- 1.2%) and fractional shortening (20.7 +/- 1.1%) were significantly decreased to -8.4 +/- 8.0% and 5.9 +/- 1.5%, respectively, and coronary arteriovenous differences of adenosine were increased from 4.6 +/- 3.6 to 89.4 +/- 10.5 pmol/ml. In the untreated condition, an intravenous infusion of isoproterenol (150 ng/kg/min) augmented fractional shortening from 5.9 +/- 1.5% to 13.6 +/- 0.8%. When adenosine release was attenuated by administration of prazosin (4 micrograms/kg/min i.c.) during hypoperfusion, the response of fractional shortening to isoproterenol (from 5.3 +/- 1.2% to 20.5 +/- 1.4%) was much greater (p less than 0.05) than that in the untreated control condition. Exogenous administration of adenosine significantly attenuated the inotropic response to isoproterenol in the prazosin-treated hearts. In contrast, an adenosine receptor antagonist, 8-phenyltheophylline, also enhanced the inotropic response to isoproterenol. The attenuation of beta-adrenoceptor-mediated inotropic response by adenosine could not be attributed to the inhibition of norepinephrine release from the sympathetic nerve endings, because identical results were observed in the chemically denervated hearts.

CONCLUSIONS
Endogenous adenosine released from the ischemic myocardium attenuates beta-adrenoceptor-mediated inotropic response in the ischemic heart.
Hypolipidemic effect of type Ia antiarrhythmic agents in postinfarction patients.
Authors: Boden W E , Moss A J , Oakes D 
Published: June 2012

BACKGROUND
Elevated levels of cholesterol and apoprotein B (apo B), the essential carrier protein for low density lipoprotein, are major lipid risk factors for premature coronary disease. Antiarrhythmic agents are frequently prescribed to patients with coronary heart disease and associated cardiac arrhythmias. As part of another study, we retrospectively investigated the effect of antiarrhythmic agents on blood lipids.

METHODS AND RESULTS
The study population consisted of 1,567 postinfarction patients on whom we prospectively collected serial blood samples for lipid and apoprotein determinations and recorded the concomitant medications the patients were receiving at three follow-up time periods. The lipids, analyzed at a central core laboratory, included total cholesterol, triglycerides, high density lipoprotein cholesterol (HDL C), and apoproteins A-I (apo A-I), A-II (apo A-II), and apo B. The difference in the group mean lipid values for patients receiving and not receiving type Ia antiarrhythmic agents (quinidine, procainamide, and disopyramide) was evaluated by the two-sample t test, and multiple linear regression analyses were performed to adjust for relevant covariates. Patients using type Ia antiarrhythmic agents at the 30-month postinfarction contact (n = 76) had 8.6% lower cholesterol (p less than 0.003), 22.3% lower triglycerides (p less than 0.0002), 6.2% lower apo A-I (p = 0.02), 10.1% lower apo A-II (p less than 0.001), and 12.7% lower apo B (p less than 0.0001) levels than patients not on these medications (n = 1,491). These lower lipid levels were found after adjustment for age, sex, diabetes, smoking status, concomitant medications, and a variety of clinical factors relating to the severity of the coronary disease process. The HDL C levels were similar in those receiving and not receiving type Ia agents.

CONCLUSIONS
Patients on type Ia antiarrhythmic agents had significantly and meaningfully lower cholesterol, triglyceride, apo A-II, and apo B levels than patients not receiving these agents. The mechanism of this hypolipidemic effect is undefined, but the mechanism may be related to an alteration by these agents of ionic membrane currents at the hepatocyte level.