bluuebunny/crossref_metadata_2025_split huggingface dataset:
Can physical activity mitigate the effects of aging in middle-aged women?
Authors: Owens J F , Matthews K A , Wing R R , Kuller L H 
Published: June 2012

BACKGROUND
Aging is associated with an increased risk of women dying from coronary heart disease as well as from all causes combined. Alterations in the major biological risk factors for early coronary heart disease and all-cause mortality are frequently seen in aging.

METHODS AND RESULTS
The present investigation tested the hypothesis that high levels of physical activity could protect against age-associated changes in biological risk factor levels. In the Healthy Women Study, 507 women were evaluated at study entry and 3 years later. Weekly physical activity level was measured at each examination via the Paffenbarger Physical Activity Questionnaire. During the 3-year period, women increased significantly in weight, blood pressure, levels of total and low-density lipoprotein cholesterol, triglycerides, and insulin and decreased significantly in levels of total high-density lipoprotein cholesterol (HDL-C) and HDL2-C.

CONCLUSIONS
Consistent with the study hypothesis, women who reported higher levels of activity at baseline had less weight gain over time. Furthermore, women who increased their activity during the 3-year interval had the smallest increases in weight and tended to have the smallest decreases in total HDL-C and HDL2-C. The changes in lipids due to activity were largely independent of changes in body weight.
Patients with evidence of coronary endothelial dysfunction as assessed by acetylcholine infusion demonstrate marked increase in sensitivity to constrictor effects of catecholamines.
Authors: Vita J A , Treasure C B , Yeung A C , Vekshtein V I , Fantasia G M , Fish R D , Ganz P , Selwyn A P 
Published: June 2012

BACKGROUND
Studies in patients undergoing cardiac catheterization have demonstrated that normal coronary arteries dilate and atherosclerotic arteries constrict in response to exercise and the cold pressor test, but the mechanisms are unknown. These vasomotor responses are mirrored by the vasomotor response to the endothelium-dependent agent acetylcholine. Exercise and the cold pressor test are associated with adrenergic stimulation and increased circulating catecholamines. The present study tested the hypothesis that coronary arteries with intact endothelial function are relatively resistant to the constrictor effects of catecholamines, whereas arteries with loss of endothelial function have increased sensitivity to catecholamine-induced constriction.

METHODS AND RESULTS
The vasomotor function of the coronary endothelium was assessed by serial acetylcholine infusions (final concentration, 10(-8) to 10(-6) M) in 30 segments in 15 patients with minimal or no evidence of coronary atherosclerosis. The acetylcholine responses were related to the vasomotor response to intracoronary phenylephrine infusion (final concentration, 10(-9) to 10(-6) M) in the same segments. In the group of 18 segments that constricted to acetylcholine, there was a constrictor response to phenylephrine at an approximately 100-fold lower concentration than the group of 12 segments that did not constrict to acetylcholine.

CONCLUSIONS
These results suggest that the endothelial dysfunction that characterizes early and late atherosclerosis is associated with a marked increase in sensitivity to the constrictor effects of catecholamines. This finding may explain the constrictor responses of atherosclerotic coronary arteries to exercise and the cold pressor test. In stenotic coronary arteries this mechanism may play a role in the production of myocardial ischemia.
Divergent kinetics of 201Tl and 99mTc-SESTAMIBI in cultured chick ventricular myocytes during ATP depletion.
Authors: Piwnica-Worms D , Chiu M L , Kronauge J F 
Published: June 2012

BACKGROUND
Thallous chloride (201Tl) and hexakis(2-methoxyisobutyl isonitrile) technetium (I) (99mTc-SESTAMIBI) are myocardial perfusion imaging agents with biological properties that also reflect tissue viability. Initial myocellular uptake rates of 201Tl reflect activity of Na,K-ATPase, whereas those of 99mTc-SESTAMIBI reflect mean plasma membrane potential.

METHODS AND RESULTS
To better understand the mechanistic responses of these tracers to myocellular injury, cultured chick embryo cardiac myocytes were metabolically inhibited in iodoacetate (1 mM) and rotenone (10 microM) for up to 2 hours, and initial uptake rates of each agent were determined at successive intervals along with correlative cellular contents of ATP, sodium, and potassium and lactate dehydrogenase release. ATP content fell from 30.5 +/- 1.4 to 2.7 +/- 0.9 nmol.(mg protein)-1 within 2 minutes, whereas sodium and potassium contents ran down their thermodynamic gradients more slowly (t 1/2 approximately 60 minutes). Modestly severe cell injury was produced at 2 hours as estimated by lactate dehydrogenase release (18% of total). Initial uptake rates of 201Tl declined from 6.9 +/- 0.8 to 4.0 +/- 0.4 fmol.(mg protein)-1.(nMo)-1.(min)-1 by 20 minutes and remained depressed and ouabain (100 microM)-insensitive at 30 +/- 13% of control. Conversely, initial uptake rates of 99mTc-SESTAMIBI increased from 10.6 +/- 0.8 to 15.0 +/- 0.6 fmol.(mg protein)-1.(nMo)-1.(min)-1 within 10 minutes, remained elevated for 40-60 minutes, and later declined to low values. Injury-induced enhancement of initial uptake rates of 99mTc-SESTAMIBI were insensitive to ouabain (100 microM), carbonyl cyanide-m-chlorophenyl hydrazone (5 microM), and valinomycin (1 microgram/ml) but were significantly inhibited by 130 mM Ko buffer, Ba2+ (1 mM), glybenclamide (100 microM), and quinacrine (10 microM).

CONCLUSIONS
Uptake rates of 201Tl monotonically decline, correlating with Na-K pump inhibition from ATP depletion. Conversely, uptake rates of 99mTc-SESTAMIBI at first increase above control for 40-60 minutes, indicating a mean plasma membrane hyperpolarization possibly resulting from opening of ATP-sensitive and arachidonic acid-activated potassium channels, before declining to low values with more severe cell injury. Correlative non-flow-dependent relations between 201Tl and 99mTc-SESTAMIBI contain information regarding the degree of myocellular injury.
Sex differences in the determinants of left ventricular mass in childhood. The Medical College of Virginia Twin Study.
Authors: Goble M M , Mosteller M , Moskowitz W B , Schieken R M 
Published: June 2012

BACKGROUND
Left ventricular (LV) hypertrophy is a predictor of cardiovascular events in adults and has been observed in children and adolescents with hypertension. We wanted to establish the determinants of LV mass in normotensive preadolescent children. Our objectives were 1) to produce a simplified and generalizable model of the clinical variables that determine normal cardiac growth during childhood and 2) to understand better why males have an increased LV mass relative to females, even as children.

METHODS AND RESULTS
In a group of 243 eleven-year-old children, we analyzed anthropometric, hemodynamic, and echocardiographic data to define which variables were predictors of echocardiographically determined LV mass. Stepwise regression was used to predict LV mass overall, by sex, and by body size (body mass index). Overall, LV mass was directly related to weight, male sex, and systolic and diastolic blood pressure and inversely related to resting heart rate and skin-fold thicknesses. Systolic blood pressure was a determinant in boys but not in girls. Heart rate was a weak inverse correlate in both sexes. When the data were analyzed by body mass index quartile, weight was the sole predictor of LV mass in the largest children.

CONCLUSIONS
We conclude that in normotensive preadolescent children, 1) weight, but not pondersity, is a strong predictor of LV mass; 2) body fat is negatively associated with LV mass; 3) boys have an increased LV mass relative to girls; and 4) boys and girls have similar anthropometric determinants and may have different hemodynamic determinants. Our data suggest that body size, and in particular lean body mass, explains much of the variability in cardiac growth seen in children. The influence of hemodynamic variables seems to be more limited. Our findings are of general interest because, although hypertensive heart disease is well described, the early developmental stages are not well understood.
Platelet-dependent thrombin generation after in vitro fibrinolytic treatment.
Authors: Aronson D L , Chang P , Kessler C M 
Published: June 2012

BACKGROUND
Fibrinolytic therapy is associated with frequent rethrombosis. There is evidence of both increased coagulation and platelet activation.

METHODS AND RESULTS
Platelet-rich plasma (PRP) or washed platelets were incubated with the fibrinolytic agents urokinase, recombinant tissue-type plasminogen activator (rt-PA), or plasmin at concentrations consistent with those in the plasma of patients treated for myocardial infarction. All of the fibrinolytic agents induced a more rapid generation of thrombin and decreased the clotting times of non-contact-activated PRP than in untreated PRP. This effect was not blocked by the inclusion of thrombin inhibitors during the fibrinolytic treatment. Washed platelets derived from rt-PA-treated PRP induced more rapid thrombin generation when resuspended in untreated plasma or treated plasma. Washed platelets were treated with plasmin, rt-PA, and urokinase and added to platelet-poor plasma. Platelets treated with either plasmin or rt-PA increased the ability of washed platelets to support thrombin generation, but urokinase was without significant effect.

CONCLUSIONS
These results indicate not only that plasmin can cause increased platelet support of prothrombin activation but also that rt-PA in the absence of plasminogen can have a direct effect on the platelet, which increases thrombin generation.
Quantitative assessment of coronary artery stenosis by intravascular Doppler catheter technique. Application of the continuity equation.
Authors: Nakatani S , Yamagishi M , Tamai J , Takaki H , Haze K , Miyatake K 
Published: June 2012

BACKGROUND
Quantitative assessment of coronary artery stenoses plays a central role in clinical decision making. According to the continuity equation, the ratio of the time-velocity integral of prestenotic to stenotic flow velocities represents the ratio of the cross-sectional area of the stenotic to prestenotic segments. However, no data exist regarding the application of this method to clinical assessment of human coronary artery diseases. Therefore, we attempted to determine the severity of coronary artery stenoses by applying the continuity equation to the coronary circulation.

METHODS AND RESULTS
Nineteen patients with a stenosis of the proximal left anterior descending coronary artery (LAD) and one patient with a stenosis in an aortocoronary bypass graft to the LAD were studied. Coronary flow velocities at the prestenotic and stenotic segments were measured with an end-mounted Doppler catheter (3F, 20 MHz), and the time-velocity integral ratio was calculated. Percent area stenosis was calculated as (1-time-velocity integral ratio) x 100. In three patients with severe stenosis (greater than 90% in area stenosis), velocity at the stenosis could not be determined because of aliasing of Doppler signals, and in four, Doppler signals at the stenosis were not measurable because of technical difficulties. The stenotic flow velocity was successfully recorded in 13 patients (65%) with mild to moderate stenosis. The diastolic peak flow velocity at the stenosis was 90 +/- 36 cm/sec (mean +/- SD), and was significantly greater than the velocity at the prestenotic segment, 48 +/- 18 cm/sec (p less than 0.01). Percent area stenosis determined by Doppler continuity equation correlated closely with that by biplane coronary angiography (r = 0.83, y = 0.92x-0.45, p less than 0.01).

CONCLUSIONS
Application of the continuity equation to Doppler catheter measurement of coronary flow velocity can be used to successfully compute the severity of coronary stenoses. This may be a useful alternative method to estimate functional severity of coronary artery disease, although further technical developments will be necessary to improve the sensitivity.
Relation between ventricular repolarization duration and cardiac cycle length during 24-hour Holter recordings. Findings in normal patients and patients with long QT syndrome.
Authors: Merri M , Moss A J , Benhorin J , Locati E H , Alberti M , Badilini F 
Published: June 2012

BACKGROUND
The interval from the R wave to the maximum amplitude of the T wave (RTm) contains the heart rate dependency of ventricular repolarization.

METHODS AND RESULTS
A computer algorithm was developed to quantify the RTm and preceding RR intervals for each of more than 50,000 beats on 24-hour ambulatory electrocardiographic (Holter) recordings to evaluate the dynamic relation between repolarization duration and cycle length. The relation of RTm to the preceding RR interval (RTm/RR slope) was determined by the best-fit linear regression equation between these two parameters. Eleven normal subjects and 16 patients with long QT syndrome (LQTS) were investigated. Six of the normal subjects had Holter recordings obtained before and after beta-blocker therapy. beta-Blockers were associated with a significant (p = 0.005) reduction in the RTm/RR slope from 0.13 +/- 0.02 to 0.10 +/- 0.02. The mean value of the RTm/RR slope was significantly (p = 0.003) larger in the LQTS patients (0.21 +/- 0.08) than in normal subjects (0.14 +/- 0.03).

CONCLUSIONS
These findings indicate that 1) quantification of the dynamic relation between ventricular repolarization and RR cycle length can be obtained on a large number of Holter-recorded heart beats; 2) beta-blockers reduce the RTm/RR slope in normal patients; and 3) LQTS patients have an exaggerated delay in repolarization at long RR cycle lengths.
Synchronized repolarization after defibrillation shocks. A possible component of the defibrillation process demonstrated by optical recordings in rabbit heart.
Authors: Dillon S M 
Published: June 2012

BACKGROUND
It is currently believed that defibrillation shocks act primarily by stimulating excitable myocardium to abolish wave fronts. Recent studies have shown that shocks applied during pacing not only stimulate excitable myocardium but also prolong the depolarization and refractoriness of myocardium already in a depolarized state. This study investigates the effects of shocks on fibrillation action potentials.

METHODS AND RESULTS
Recordings of membrane action potentials free of shock artifact were obtained using the voltage-sensitive dye WW781 during defibrillation of isolated rabbit hearts. These records showed that the shocks caused an additional phase of depolarization beginning with an initial rapid depolarization of the optical signal followed by a slow phase of repolarization. This occurred throughout all phases of the fibrillation action potential from just after completion of the upstroke to a time of near maximal repolarization. Defibrillation shocks, however, had the additional effect of causing the myocardium to repolarize at a constant time after the shock regardless of its prior electrical activity--the constant repolarization time response. This effect was not dependent on the presence of D600 (methoxyverapamil) or continuous coronary perfusion. It was accompanied by a similar constancy in the return of myocardial excitability. Recordings taken from multiple adjacent recording sites also showed a constant repolarization time among them.

CONCLUSIONS
A simple model of reentry is used to illustrate how the constant repolarization response, in addition to wave front termination and refractoriness extension, could play a role in the successful termination of fibrillation by electrical shock.
Basic structure-function relations of the epicardial coronary vascular tree. Basis of quantitative coronary arteriography for diffuse coronary artery disease.
Authors: Seiler C , Kirkeeide R L , Gould K L 
Published: June 2012

BACKGROUND
Quantitative coronary arteriography has been validated for stenotic segments of coronary arteries. However, it does not currently account for diffuse coronary artery disease, because the normal size of the coronary artery for its distal myocardial bed size is not known and cannot be measured directly with diffuse involvement of the artery.

METHODS AND RESULTS
From clinical coronary arteriograms of 12 patients without coronary artery disease (group 1) and in 17 patients with coronary artery disease (group 2), we determined by quantitative coronary arteriography 1) the relations among measured coronary artery cross-sectional lumen area, summed distal branch lengths, and regional myocardial mass distal to each point in each coronary artery; 2) the ratio of coronary artery lumen area between parent and daughter vessels at 50 bifurcations; and 3) which of three different theoretical physical principles could underlie the tree structure of the human coronary artery system, by comparing the coronary artery size, branch lengths, regional mass, and relations between parent-to-daughter lumen area ratios with those for the different theoretical physical principles to test which principle best fit the observed data and therefore which principle most probably characterizes the human coronary artery tree structure. The results showed that 1) there is a close correlation between the lumen area of a coronary artery at each point along its length and the corresponding summed distal branch lengths and regional myocardial mass in patients without and with coronary artery disease; 2) measured coronary artery lumen area in patients with coronary artery disease is diffusely 30-50% too small for distal myocardial bed size compared with normal subjects; and 3) the observed relations among coronary artery size, distal summed lengths, myocardial bed size, and parent-to-daughter size ratios are not consistent with the theoretical principle of constant mean blood flow velocity in the coronary circulation but are consistent with the principles of minimum viscous energy loss and of limited/adaptive vascular wall shear stress characterized by a 2/3 power law relating coronary artery lumen area to distal summed branch lengths and regional mass or parent-to-daughter branching ratios.

CONCLUSIONS
These observations provide a basis for quantifying diffuse coronary artery disease on clinical arteriograms.
Spectral analysis of signal-averaged electrocardiograms in patients with idiopathic ventricular tachycardia of left ventricular origin.
Authors: Kinoshita O , Kamakura S , Ohe T , Yutani C , Matsuhisa M , Aihara N , Takaki H , Kurita T , Shimomura K 
Published: June 2012

BACKGROUND
The signal-averaged ECG has been used to detect late potentials, and it is considered a noninvasive marker for areas of slow conduction requisite for reentrant arrhythmia. Late potentials are not usually found in patients with idiopathic ventricular tachycardia (VT); nevertheless, fragmented electrograms are often recorded in those patients during endocardial mapping. The purpose of this study was to investigate the spectral content of the signal-averaged ECGs with use of fast Fourier transform analysis (FFT) in patients with idiopathic VT of left ventricular origin.

METHODS AND RESULTS
Signal-averaged ECGs were recorded in 12 patients with idiopathic VT originating from the left ventricle (group 1) and 25 age-matched normal volunteers (group 2). Frequency analysis with FFT was performed with a Blackman-Harris window in a segment length of 120 msec from 40 msec before the end of the QRS complex, and the frequency spectrum was displayed in a three-dimensional graph. Area ratio 1 (area of 20-50 Hz/area of 10-50 Hz) and area ratio 2 (area of 40-100 Hz/area of 0-40 Hz) were calculated in all subjects. Late potentials defined by the time domain were negative in all subjects. The area ratios of group 1 were significantly higher than those of group 2. High-frequency components in the three-dimensional graph were confined within the QRS complex.

CONCLUSIONS
These results suggest that frequency analysis of signal-averaged ECGs with FFT is an available method for detecting the high-frequency component within the QRS complex in some patients with idiopathic VT of left ventricular origin.
Regular physical exercise and low-fat diet. Effects on progression of coronary artery disease.
Authors: Schuler G , Hambrecht R , Schlierf G , Niebauer J , Hauer K , Neumann J , Hoberg E , Drinkmann A , Bacher F , Grunze M 
Published: June 2012

BACKGROUND
Significant regression of coronary and femoral atherosclerotic lesions has been documented by angiographic studies using aggressive lipid-lowering treatment. This study tested the applicability and effects of intensive physical exercise and low-fat diet on coronary morphology and myocardial perfusion in nonselected patients with stable angina pectoris.

METHODS AND RESULTS
Patients were recruited after routine coronary angiography for stable angina pectoris; they were randomized to an intervention group (n = 56) and a control group on "usual care" (n = 57). Treatment comprised intensive physical exercise in group training sessions (minimum, 2 hr/wk), daily home exercise periods (20 min/d), and low-fat, low-cholesterol diet (American Heart Association recommendation, phase 3). No lipid-lowering agents were prescribed. After 12 months of participation, repeat coronary angiography was performed; relative and minimal diameter reductions of coronary lesions were measured by digital image processing. Change in myocardial perfusion was assessed by 201Tl scintigraphy. In patients participating in the intervention group, body weight decreased by 5% (p less than 0.001), total cholesterol by 10% (p less than 0.001), and triglycerides by 24% (p less than 0.001); high density lipoproteins increased by 3% (p = NS). Physical work capacity improved by 23% (p less than 0.0001), and myocardial oxygen consumption, as estimated from maximal rate-pressure product, by 10% (p less than 0.05). Stress-induced myocardial ischemia decreased concurrently, indicating improvement of myocardial perfusion. Based on minimal lesion diameter, progression of coronary lesions was noted in nine patients (23%), no change in 18 patients (45%), and regression in 13 patients (32%). In the control group, metabolic and hemodynamic variables remained essentially unchanged, whereas progression of coronary lesions was noted in 25 patients (48%), no change in 18 patients (35%), and regression in nine patients (17%). These changes were significantly different from the intervention group (p less than 0.05).

CONCLUSIONS
In patients participating in regular physical exercise and low-fat diet, coronary artery disease progresses at a slower pace compared with a control group on usual care.