bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of age and aerobic capacity on arterial stiffness in healthy adults.
Authors: Vaitkevicius P V , Fleg J L , Engel J H , O'Connor F C , Wright J G , Lakatta L E , Yin F C , Lakatta E G 
Published: June 2012

BACKGROUND
It has been well established that arterial stiffness, manifest as an increase in arterial pulse wave velocity or late systolic amplification of the carotid artery pressure pulse, increases with age. However, the populations studied in prior investigations were not rigorously screened to exclude clinical hypertension, occult coronary disease, or diabetes. Furthermore, it is unknown whether exercise capacity or chronic physical endurance training affects the age-associated increase in arterial stiffness.

METHODS AND RESULTS
Carotid arterial pressure pulse augmentation index (AGI), using applanation tonometry, and aortic pulse wave velocity (APWV) were measured in 146 male and female volunteers 21 to 96 years old from the Baltimore Longitudinal Study of Aging, who were rigorously screened to exclude clinical and occult cardiovascular disease. Aerobic capacity was determined in all individuals by measurement of maximal oxygen consumption (VO2max) during treadmill exercise. In this healthy, largely sedentary cohort, the arterial stiffness indexes AGI and APWV increased approximately fivefold and twofold, respectively, across the age span in both men and women, despite only a 14% increase in systolic blood pressure (SBP). These age-associated increases in AGI and APWV were of a similar magnitude to those in prior studies of less rigorously screened populations. Both AGI and APWV varied inversely with VO2max, and this relationship, at least for AGI, was independent of age. In endurance trained male athletes, 54 to 75 years old (VO2max = 44 +/- 3 mL.kg-1.min-1), the arterial stiffness indexes were significantly reduced relative to their sedentary age peers (AGI, 36% lower; APWV, 26% lower) despite similar blood pressures.

CONCLUSIONS
Even in normotensive, rigorously screened volunteers in whom SBP increased an average of only 14% between ages 20 and 90 years, major age-associated increases of arterial stiffness occur. Higher physical conditioning status, indexed by VO2max, was associated with reduced arterial stiffness, both within this predominantly sedentary population and in endurance trained older men relative to their less active age peers. These findings suggest that interventions to improve aerobic capacity may mitigate the stiffening of the arterial tree that accompanies normative aging.
Prognosis of myocardial infarctions involving more than 40% of the left ventricle after acute reperfusion therapy.
Authors: McCallister B D , Christian T F , Gersh B J , Gibbons R J 
Published: June 2012

BACKGROUND
Prior studies based on autopsy data suggest that infarction of more than 40% of the left ventricle necessitates cardiogenic shock and death.

METHODS AND RESULTS
Technetium-99m Sestamibi tomography was used prospectively to measure infarct size at discharge in 166 patients with acute myocardial infarction. Patients with previous myocardial infarction or revascularization were excluded from the trial. Sixteen patients were identified with final infarct sizes > 40% of the left ventricle despite acute reperfusion therapy. These 16 patients (13 men) had a mean age of 63 +/- 10 years; 44% had a previous history of angina. Ten patients had emergent coronary angioplasty only (mean time to percutaneous transluminal coronary angioplasty [PTCA], 6.0 +/- 3.0 hours); 6 had thrombolysis (mean time to tissue plasminogen activator, 4.0 +/- 1.5 hours), of which 2 had rescue PTCA (5 and 3 hours from onset of pain). Of 15 patients who had angiograms after therapy, 15 had open infarct-related arteries. The left anterior descending artery was the infarct-related artery in 14 (9 proximal and 5 distal lesions). Half the patients had only single-vessel disease. Infarct size measured 50 +/- 7% of the left ventricle (range, 42% to 68%). Ejection fraction by radionuclide angiogram was 0.33 +/- 0.09 and 0.38 +/- 0.07 at discharge and 6 weeks, respectively. Hospital complications included shock (1 patient), pulmonary edema (2), angina (3), symptomatic nonsustained ventricular tachycardia (1), transient complete heart block (2), and transient bifascicular block (1). At follow-up (13 +/- 9 months), the patient with shock had died, but the remaining 15 patients were asymptomatic (1 had late PTCA for angina).

CONCLUSIONS
In the interventional and thrombolytic era, patients with large residual myocardial infarctions can survive without heart failure.
Residual flow to the infarct zone as a determinant of infarct size after direct angioplasty.
Authors: Clements I P , Christian T F , Higano S T , Gibbons R J , Gersh B J 
Published: June 2012

BACKGROUND
In acute myocardial infarction, residual flow to the infarct zone either through antegrade flow in the infarct-related coronary artery or collateral flow from the non-infarct-related arteries is often present before reperfusion therapy. The purpose of this study was to assess the influence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before successful direct angioplasty on infarct size and myocardial salvage in patients with acute evolving myocardial infarction.

METHODS AND RESULTS
Sixty patients with acute evolving myocardial infarction underwent direct successful angioplasty without prior thrombolytic therapy. The myocardium at risk of infarction, the final infarct size, and myocardial salvage were measured by tomographic perfusion imaging with 99mTc sestamibi. Antegrade flow in the infarct-related artery before intervention was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study group classification. Collateral flow to the infarct zone before angioplasty was also graded (0 through 3, 0 being no collateral flow). The presence of even minimal antegrade flow before angioplasty (TIMI grade 1) in the infarct-related artery compared with absent flow was associated with a significant reduction in final infarct size (9 +/- 17% versus 23 +/- 19% of left ventricle, P = .02) and a significant increase in myocardial salvage (23 +/- 16% versus 14 +/- 13% of left ventricle, P = .05) after angioplasty. When antegrade flow in the infarct-related artery was absent before angioplasty, the presence of collateral flow before angioplasty resulted in a significantly smaller final infarct size (P = .01) and more myocardial salvage (P = .05) after angioplasty. Both antegrade infarct-related artery flow and collateral flow to the infarct zone had significant independent ability to predict infarct size after angioplasty. When collateral grade and TIMI grade were added to provide an estimate of residual flow, a model including residual flow, myocardium at risk, and the interaction of residual flow and infarct site explained 83% of the variability in infarct size after angioplasty.

CONCLUSIONS
The presence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before direct angioplasty in acute evolving infarction results in a smaller infarct size after direct successful angioplasty.
Predicting early and intermediate-term outcome of coronary angioplasty in the elderly.
Authors: Thompson R C , Holmes D R , Gersh B J , Bailey K R 
Published: June 2012

BACKGROUND
Although the technical success rate of coronary angioplasty in the elderly in high, very old patients have increased risk of procedure-related death and late recurrence of severe angina. We proposed to determine baseline variables that predict early and intermediate-term failure of percutaneous transluminal coronary angioplasty (PTCA) in patients more than 65 so we could effectively stratify risk.

METHODS AND RESULTS
We studied 982 patients at least 65 years old who had urgent or elective PTCA (1980 through 1990). Follow-up (mean, 25 months) was obtained for all patients. Multiple baseline variables were analyzed with univariate and multivariate logistic regression to select independent ones to fit predictive models for in-hospital death or myocardial infarction (overall rate, 6.3%), total in-hospital adverse outcome (overall rate, 18.7%), cumulative survival free of myocardial infarction (overall rate, 15% at 3 years), and cumulative survival free of late nonfatal myocardial infarction, bypass surgery, repeat PTCA, or recurrent severe angina (overall rate, 47% at 3 years). The most heavily weighted parameter in the probability regression equation for each end point was the number of diseased coronary artery segments with at least 70% stenosis. Advanced age was less important. The number of concomitant medical illnesses was predictive of late outcome but not early in-hospital events. Lowest risk quintile versus highest risk quintile event rate was 2.9% versus 14% for acute myocardial infarction or death and 17.2% versus 29% for cumulative in-hospital events. For posthospital events at 3 years' follow-up, lowest risk quintile death or myocardial infarction rate was 4% versus 33% for highest risk quintile. For cumulative late adverse events at 3 years, the event rate was 28% versus 63% for the highest risk quintile.

CONCLUSIONS
These results stratify patients at high and low risk of early and intermediate-term success after PTCA and identify elderly patients in whom PTCA is most appropriate.
Effects of flecainide on ectopic atrial automaticity and conduction.
Authors: Windle J R , Witt R C , Rozanski G J 
Published: June 2012

BACKGROUND
Previous studies have shown that class Ic antiarrhythmic agents are effective in suppressing ectopic atrial rhythms and accessory pathway conduction.

METHODS AND RESULTS
To explore the potential mechanisms for their effectiveness, we investigated the concentration-dependent effects of the Ic agent flecainide acetate (0.5 to 10 micrograms/mL) on atrial ectopic automaticity and exit conduction in isolated rabbit tricuspid valves. This experimental model consists of three major cell types as defined anatomically and by intracellular recordings: pacemaker, transitional, and working atrial muscle. Simultaneous recordings from these cell types before and during flecainide superfusion (n = 7) showed that the drug produced a slight, concentration-dependent slowing of pacemaker-transitional conduction but elicited third-degree transitional-working atrial muscle block in six of seven preparations at 10 micrograms/mL. Flecainide caused a significant dose-dependent reduction in the initial phase of diastolic depolarization of pacemaker cells but produced only a small, biphasic change in spontaneous pacemaker cycle length. It also caused a significant prolongation in action potential duration in pacemaker and transitional cells and reduction in upstroke velocity in atrial cells. Of note in four additional preparations, flecainide caused a concentration-dependent upward shift in the strength-duration curve for atrial fibers.

CONCLUSIONS
These data suggest that flecainide has little direct effect on ectopic atrial automaticity but rather causes exit conduction slowing and block between transitional and atrial muscle fibers. The mechanism for the induction of block is likely due to a decrease in atrial excitability creating a greater electrical load on generated impulses.
Differentiation between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation using RR interval scattergram.
Authors: Suyama A C , Sunagawa K , Sugimachi M , Anan T , Egashira K , Takeshita A 
Published: June 2012

BACKGROUND
Differentiation between aberrant ventricular conduction and ventricular ectopy during atrial fibrillation (AF) is of etiologic, prognostic, and therapeutic importance. We developed a noninvasive technique to diagnose aberrant ventricular conduction and ventricular ectopy in AF.

METHODS AND RESULTS
We studied the Holter ECGs of 34 patients with paroxysmal AF and 62 patients with chronic AF. In all the patients, frequent wide QRS complexes were observed, and 32 patients were shown by electrophysiological examination to have ventricular ectopies or aberrant ventricular conductions. We obtained the RR interval scattergrams by plotting sequential pairs of RR intervals. Each point has the (n)th RR interval as its x value and the (n + 1)th RR interval as its y value. The irregularity of the RR intervals in AF resulted in widely scattered points delineated by the envelope along the axes. The y value of the envelope along the x axis indicates the shortest coupling interval to the preceding RR interval. Therefore, this curve defines the functional refractory period of atrioventricular conduction. The scattergram of the RR interval pairs immediately preceding the aberrant conduction (coupling points of aberrant conduction) specifically distributed along the envelope. In contrast, the coupling points of ventricular ectopies showed different distributions that had no relation to the envelope. That is, it included three typical patterns, ie, linear distribution below the envelope, linear distribution partially overlapped in the area of normal AF conduction, and chaotic distribution in the AF area. None of the scattergrams of ventricular ectopies showed curvilinear distribution along the envelope as aberrant conduction did. The specific distribution of the aberrant conduction on the RR interval scattergram suggested that aberrant conduction in AF could result from the difference of refractory periods between the AV node and bundle branch block.

CONCLUSIONS
We conclude that the RR interval scattergram makes it possible to differentiate between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation, and thus, it is a useful noninvasive clinical tool.
Short-term synchronized retroperfusion before reperfusion reduces infarct size after prolonged ischemia in dogs.
Authors: Wakida Y , Nordlander R , Kobayashi S , Kar S , Haendchen R , Corday E 
Published: June 2012

BACKGROUND
Previous studies have demonstrated that synchronized coronary venous retroperfusion (SRP) can restore blood flow to the ischemic myocardium, resulting in infarct size reduction and improvement of the left ventricular function. Despite the nutritive blood flow achieved by SRP being relatively limited, SRP has been shown to improve washout of by-products from the ischemic myocardium. The aim of this study was to investigate whether short-term SRP immediately prior to reperfusion would attenuate the deteriorative phenomena following reperfusion.

METHODS AND RESULTS
Closed-chest anesthetized dogs underwent 3 hours of left anterior descending coronary artery (LAD) occlusion. The dogs were then randomized into two groups: (1) control group (n = 9), in which the occlusion was immediately followed by 3-hour reperfusion; or (2) SRP group (n = 9), in which SRP was started 3 hours after occlusion and maintained for 30 minutes with sustained occlusion followed by 2.5-hour reperfusion with simultaneous discontinuation of SRP. There were no statistical differences between the groups in global hemodynamics and degree of ischemia measured by radiolabeled microspheres. Myocardial infarct size (triphenyltetrazolium method) expressed as percentage of risk area was significantly smaller in the SRP group (24 +/- 7%, mean +/- SEM) than in the control group (54 +/- 9%). The extent of myocardial hemorrhage expressed as percentage of infarct size was also significantly reduced in the SRP group (3 +/- 2%) compared with the control group (24 +/- 6%). The increase in end-diastolic wall thickness in the ischemic area after reperfusion assessed by two-dimensional echocardiography was significantly less in the SRP group. Blood flow measurements after reperfusion demonstrated the occurrence of no-reflow phenomenon only in the control group. Histological examination revealed extensive myocardial hemorrhages only in the control group, which extended into the nonnecrotic myocardium in four of nine hearts and extensive contraction band necrosis compared with the SRP group.

CONCLUSIONS
Short-term SRP prior to reperfusion can reduce infarct size, myocardial hemorrhage, wall swelling, and no-reflow phenomenon. The mechanism of this beneficial effect is not clear but might be due to gradual reperfusion and washout of by-products from the ischemic myocardium before fully oxygenated arterial blood reperfusion.
Late reperfusion for acute myocardial infarction limits the dilatation of left ventricle without the reduction of infarct size.
Authors: Hirayama A , Adachi T , Asada S , Mishima M , Nanto S , Kusuoka H , Yamamoto K , Matsumura Y , Hori M , Inoue M 
Published: June 2012

BACKGROUND
While previous clinical studies have shown a possible beneficial effect of the reperfusion performed at a relatively late phase of acute myocardial infarction ("late reperfusion") in preventing left ventricular enlargement, the mechanism has not been clarified.

METHODS AND RESULTS
Of 89 patients with an initial anterior myocardial infarction, reperfusion was successful in 69. These 69 were divided into three groups according to the time required to achieve reperfusion after the onset of symptoms: early-reperfused (< 3 hours from the onset to reperfusion; n = 22), intermediate-reperfused (3 to 6 hours from the onset to reperfusion; n = 28), and late-reperfused (> 6 hours from the onset to reperfusion; n = 19). The 20 patients whose infarct-related artery were occluded in the acute phase as well as 1 month later was classified as nonreperfused. Infarct size, evaluated as defect volume by 201Tl single-photon emission computed tomography 1 month after the onset, was 1593 +/- 652 units (mean +/- SD) in the late-reperfused group, significantly larger (P < .05) than that of the intermediate-reperfused (1066 +/- 546 U) or the early-reperfused groups (372 +/- 453 U) but not different from that of the nonreperfused group (1736 +/- 562 U). Wall motion abnormality index as well as global ejection fraction evaluated by left ventriculography 1 month after the onset showed that late reperfusion did not preserve the left ventricular wall motion and function. These results indicate that the earlier reperfusion decreased the size of the infarction and preserved left ventricular function, whereas late reperfusion (> 6 hours after onset) did not limit infarct size or preserve left ventricular function. In contrast, the end-diastolic volume index did not differ significantly among the early-reperfused (50 +/- 15 mL/m2), intermediate-reperfused (54 +/- 14 mL/m2), and late-reperfused (53 +/- 19 mL/m2) groups; those were significantly smaller than that of the nonreperfused group (68 +/- 12 mL/m2; P < .05). Left ventriculographic data obtained in both the acute and chronic phase in 39 patients showed that left ventricular volumes increased significantly during the course of myocardial infarction only in the nonreperfused group.

CONCLUSIONS
Late reperfusion appeared to prevent ventricular dilatation acute myocardial infarction independent of the limitation of infarct size.
Effects of adenosine on rate-dependent atrioventricular nodal function. Potential roles in tachycardia termination and physiological regulation.
Authors: Nayebpour M , Billette J , Amellal F , Nattel S 
Published: June 2012

BACKGROUND
Adenosine is well known to depress atrioventricular (AV) nodal conduction, but the potential interactions between adenosine and functional AV nodal properties have not been explored. The purpose of the present study was to determine (1) whether exogenous adenosine modifies the rate-dependent properties of the AV node, (2) to what extent such changes underlie the actions of adenosine in an in vitro model of AV reentrant tachycardia (AVRT), and (3) the potential role of endogenous adenosine in rate-induced AV nodal responses.

METHODS AND RESULTS
The functional properties of AV nodal recovery (defining the conduction delay of a single premature activation), facilitation (effect of short cycles on subsequent nodal recovery), and fatigue (slowly developing AV nodal delay at a rapid rate) were studied selectively in isolated, superfused rabbit and guinea pig cardiac preparations. Exogenous adenosine increased AV nodal fatigue and attenuated facilitation, resulting in tachycardia-dependent increases in AH interval and AV nodal effective refractory period (AVERP). In experimental AVRT, adenosine caused greater increases in tachycardia cycle length (T) and AVERP as tachycardia rate increased. AVRT was sustained when AVERP/T was < 1, and adenosine suppressed AVRT by increasing the slope of the AVERP/T versus tachycardia rate relation, causing the critical ratio of 1 to be attained at slower rates. A mathematical model incorporating quantitative descriptors of recovery, facilitation, and fatigue accounted for changes in AH interval, AVERP, tachycardia cycle length, and AVERP/T under control conditions and in the presence of adenosine. In the absence of exogenous adenosine, 8-phenyltheophylline (10 mumol/L), an adenosine receptor antagonist, did not alter recovery or facilitation but significantly reduced rate-related fatigue (by 31 +/- 8%, mean +/- SEM, P < .05, in rabbit hearts; 46 +/- 5%, P < .01, in guinea pig hearts). Combined inhibition of adenosine deaminase (with erythro-9-[2-hydroxy-3-nonyl]-adenine hydrochloride, 5 mumol/L) and adenosine uptake (with dipyridamole, 1 mumol/L) increased fatigue in the absence of exogenous adenosine by 57 +/- 20% (P < .05).

CONCLUSIONS
We conclude that (1) exogenously administered adenosine increases AV nodal fatigue and reduces facilitation, without altering AV nodal recovery; (2) these changes cause rate-dependent AV nodal depression, which plays a role in adenosine's actions on experimental AVRT; and (3) endogenous adenosine receptor activation plays a role in physiological AV nodal fatigue. Adenosine's ability to terminate reentrant supraventricular tachycardia may be due, at least in part, to its ability to enhance the physiological conduction slowing that results from sustained increases in AV nodal activation rate.
Platelet activation during coronary angioplasty in humans.
Authors: Gasperetti C M , Gonias S L , Gimple L W , Powers E R 
Published: June 2012

BACKGROUND
Previous studies have indicated that balloon angioplasty is associated with local platelet activation. In addition, different contrast media have different effects on thrombus formation during angioplasty in humans. We hypothesized that coronary angioplasty in humans is associated with activation of platelets to specific platelet agonists and that this activation may be differently modified by different angiographic contrast agents.

METHODS AND RESULTS
We studied 25 patients referred for angioplasty of the left anterior descending or circumflex coronary arteries. All patients were pretreated with aspirin and received heparin. Blood samples for assessment of platelet aggregation to serotonin, ADP, epinephrine, and collagen were obtained from the coronary sinus before any contrast injection, after initial diagnostic contrast injections, and after three balloon inflations. Patients were randomized to receive iopamidol, diatrizoate, or ioxaglate. Contrast alone was not associated with altered platelet aggregation. However, balloon angioplasty was consistently associated with increased platelet aggregation to serotonin but not to ADP, epinephrine, or collagen. These effects were similar with the three contrast agents studied except that the use of iopamidol was associated with increased platelet responsiveness to all concentrations of ADP after balloon dilation.

CONCLUSIONS
Coronary angioplasty in humans was associated with increased platelet aggregation in blood drawn from the coronary sinus. This effect was primarily seen when serotonin was used as an agonist.