bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of renal Na+,K(+)-ATPase in the regulation of sodium excretion under normal conditions and in acute congestive heart failure.
Authors: Lloyd M A , Sandberg S M , Edwards B S 
Published: June 2012

BACKGROUND
Cardiac glycosides have traditionally been used as inotropic agents in the treatment of congestive heart failure (CHF). The renal actions of cardiac glycosides independent of inotropic effects are not characterized. The presence of endogenous digitalis-like factors (EDLFs) with characteristic Na+,K(+)-ATPase activity has been postulated in volume-expanded states such as CHF, and recent studies have demonstrated that at least one EDLF shares structural homology with ouabain. This study was undertaken to evaluate the renal actions of ouabain in normal dogs and those with CHF.

METHODS AND RESULTS
After surgical preparation, normal dogs (n = 6) and dogs in pacing-induced CHF (n = 6) received intrarenal ouabain in sequential doses of 0.167 micrograms/kg/min, 0.334 micrograms/kg/min, and 0.668 micrograms/kg/min. Hemodynamics and renal function were evaluated during the infusion. There was no change in heart rate or mean arterial pressure during the infusion compared with baseline in both groups. Sodium excretion and urine volume significantly increased in both groups. Plasma renin activity, activated by the onset of pacing in the CHF group, was inhibited by the administration of intrarenal ouabain in this group only.

CONCLUSIONS
These studies demonstrate that ouabain has diuretic and natriuretic actions independent of cardiac hemodynamics that are preserved in CHF. Furthermore, intrarenal ouabain suppresses activation of renin in CHF.
ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease.
Authors: Perondi R , Saino A , Tio R A , Pomidossi G , Gregorini L , Alessio P , Morganti A , Zanchetti A , Mancia G 
Published: June 2012

BACKGROUND
In humans, angiotensin converting enzyme (ACE) inhibition attenuates the vasoconstriction induced by sympathetic stimulation in a number of peripheral districts. Whether this is also the case in the coronary circulation is unknown, however.

METHODS AND RESULTS
In nine normotensive patients with angiographically assessed coronary atherosclerosis, we measured the changes in mean arterial pressure (intra-arterial catheter), heart rate, rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between mean arterial pressure and CBF) induced by the cold pressor test (CPT, 2 minutes) and diving (30 seconds), i.e., two stimuli eliciting a sympathetic coronary vasoconstriction. The measurements were performed in the control condition and 30 minutes after captopril 25 mg p.o. In the control condition, CPT caused an increase in mean arterial pressure and heart rate. Despite the increase in RPP (+20.7 +/- 3.2%, p less than 0.01), CBF did not change and CVR increased (+12.2 +/- 4.0%, p less than 0.05). diving caused an increase in mean arterial pressure and a reduction in heart rate. RPP increased (+14.3 +/- 3.5%, p less than 0.01), but despite this increase, there was a reduction in CBF and a marked increase in CVR (+37.3 +/- 7.4%, p less than 0.01). Captopril did not modify the blood pressure and heart rate responses to both stimuli except for a slight accentuation of the bradycardia to diving. Despite the unchanged or only slightly reduced RPP response, the increase in CVR was markedly and significantly attenuated (p less than 0.01).

CONCLUSIONS
ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. This is probably due to removal of the facilitating influence of angiotensin II on sympathetic modulation of coronary vasomotor tone.
A randomized trial of late reperfusion therapy for acute myocardial infarction. Thrombolysis and Angioplasty in Myocardial Infarction-6 Study Group.
Authors: Topol E J , Califf R M , Vandormael M , Grines C L , George B S , Sanz M L , Wall T , O'Brien M , Schwaiger M , Aguirre F V 
Published: June 2012

BACKGROUND
Experimental and observational clinical studies of acute coronary occlusion have suggested that late reperfusion prevents infarct expansion and facilitates myocardial healing. The purpose of this trial was to assess whether infarct vessel patency could be achieved in late-entry patients and what benefit, if any, can be demonstrated.

METHODS AND RESULTS
In a double-blind fashion, 197 patients with 6 to 24 hours of symptoms and ECG ST elevation were randomly assigned to tissue-type plasminogen activator (100 mg over 2 hours) or placebo. Coronary angiography within 24 hours was used to determine infarct vessel patency status. Patients with infarct-related occluded arteries were then eligible for a second randomization to either angioplasty (34 patients) or no angioplasty (37 patients). Ventricular function and cavity size were reassessed at 1 month by gated blood pool scintigraphy and at 6 months by repeat cardiac catheterization. The primary end point, infarct vessel patency, was 65% for plasminogen activator patients compared with 27% in the placebo group (p less than 0.0001). There were no differences between these groups in ejection fraction or infarct zone regional wall motion at 1 or 6 months. At 6 months, infarct vessel patency was 59% in both groups. In the placebo group, there was a significant increase in end-diastolic volume from acute phase of 127 ml to 159 ml at 6-month follow-up (p = 0.006) but no increase in cavity size for the plasminogen activator group patients. Coronary angioplasty was associated with an initial 81% recanalization success and improved ventricular function at 1 month, but by late follow-up no advantage could be demonstrated for this procedure, and there was a 38% spontaneous recanalization rate in the patients assigned to no angioplasty.

CONCLUSIONS
The study demonstrates that it is possible to achieve infarct vessel recanalization in the majority of late-entry patients with either thrombolytic therapy or angioplasty. Thrombolytic intervention had a favorable effect on prevention of cavity dilatation and left ventricular remodeling, but there are no late benefits on systolic function after thrombolysis or coronary angioplasty. The conclusions concerning overall potential benefit of applying late reperfusion therapy will require data from large-scale trials designed to assess mortality reduction.
Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy.
Authors: Haissaguerre M , Gaita F , Fischer B , Commenges D , Montserrat P , d'Ivernois C , Lemetayer P , Warin J F 
Published: June 2012

BACKGROUND
Ablation of the slow pathway has been performed to eliminate atrioventricular (AV) nodal reentrant tachycardia (AVNRT) either by a surgical approach or by using radiofrequency catheter technique guided by retrograde slow pathway activation mapping. From previous experience of midseptal and posteroseptal mapping, we were aware of the existence of peculiar slow potentials in most humans. Postulating their role in AVNRT, we studied these potentials and the effects of radiofrequency energy.

METHODS AND RESULTS
Sixty-four patients (mean age, 48 +/- 19 years) with the usual form of AVNRT were studied. Slow, low-amplitude potentials were recorded when using the anterograde AV conducting system. Slow potentials occupied all (giving a continuum of electrograms) or some of the time between the atrial and ventricular electrograms. Their most specific patterns were their progressive response to increasing atrial rates, which resulted in a dramatic decline in amplitude and slope, a corresponding increase in duration, and a separation from preceding atrial potentials until the disappearance of any consistent activity. Slow potentials were recorded along a vertical band at the mid or posterior part of the septum near the tricuspid annulus. Radiofrequency energy applied at the slow potential site resulted in interruption of induced tachycardia within a few seconds and rendered tachycardia noninducible in all patients. A median of two impulses was delivered to each patient. In 69% of patients, postablation atrial stimulation cannot achieve a long atrial-His interval, which previously was critical for tachycardia induction or maintenance. No patient had AVNRT over a follow-up period of 1-16 months, and all had preserved AV conduction. In all except two patients, the PR interval was unchanged. In 47 patients, long-term electrophysiological studies confirmed the efficacy of ablation and the nonreversibility of results by isoproterenol; however, echo beats remained inducible in 40% of patients.

CONCLUSIONS
An area showing slow potentials is present at the perinodal region in humans. In patients with AVNRT, application of radiofrequency energy renders tachycardia noninducible through the preferential modification of the anterograde slow pathway. With present clinical methods, the exact origin and significance of these physiological potentials cannot be specified.
Thrombolysis in patients with unstable angina improves the angiographic but not the clinical outcome. Results of UNASEM, a multicenter, randomized, placebo-controlled, clinical trial with anistreplase.
Authors: Bär F W , Verheugt F W , Col J , Materne P , Monassier J P , Geslin P G , Metzger J , Raynaud P , Foucault J , de Zwaan C 
Published: June 2012

BACKGROUND
The value of thrombolytic therapy in unstable angina is unclear.

METHODS AND RESULTS
To study this problem, 159 patients were studied in a double-blind, placebo-controlled multicenter trial. Patients without a previous myocardial infarction, with a typical history of unstable angina, and ECG abnormalities indicative of ischemia were included. After baseline angiography, study medication (anistreplase or placebo) was given. Angiography was repeated after 12-28 hours. A significant decrease occurred in diameter stenosis between the first and second angiogram in the anistreplase group compared with the placebo group (11% versus 3%, p = 0.008). This difference was caused by reopening of occluded vessels in the thrombolytic group. However, no beneficial clinical effects of thrombolytic treatment were found. Bleeding complications were significantly higher in patients who received thrombolytic therapy (21 versus seven patients, p = 0.001).

CONCLUSIONS
Thus, angiographic but no clinical improvement after thrombolytic treatment with anistreplase was found in patients with unstable angina with an excess of bleeding complications. Therefore, thrombolytic treatment cannot be recommended in patients diagnosed as having unstable angina until proven otherwise.
Estimation of left ventricular cavity area with an on-line, semiautomated echocardiographic edge detection system.
Authors: Vandenberg B F , Rath L S , Stuhlmuller P , Melton H E , Skorton D J 
Published: June 2012

BACKGROUND
Automated edge detection of endocardial borders in echocardiograms provides objective, reproducible estimation of cavity area; however, most methods have required off-line analysis. A recently developed prototype echocardiographic imaging system permits real-time automated edge detection during imaging and thus, the potential for measurement of cyclic changes in cavity area and the assessment of left ventricular function on-line. Our purpose was to compare measurements of endocardial area manually traced from conventional echocardiograms with those obtained with the real-time automated edge detection system in normal subjects.

METHODS AND RESULTS
Two training sets of images were used to establish optimal methods of gain setting; the settings were then evaluated in a test set of images. In the high-gain training group (n = 8 subjects, 119 images), gain settings were adjusted sufficiently high to display at least 90% of the endocardial border. Manually drawn and real-time area measurements correlated at r = 0.92, but manually drawn areas were underestimated by computer. In the low-gain training group (n = 7 subjects, 104 images), gain settings were adjusted sufficiently low to avoid cavity clutter despite the presence of dropout of endocardial edges. Manually drawn and real-time areas again correlated (r = 0.79), but manually drawn areas were overestimated by computer. In the intermediate-gain test group (n = 7 subjects, 105 images), gain settings were balanced between maximal endocardial definition (greater than or equal to 90%) and minimal cavity clutter (less than or equal to 1 cm2). Manually drawn and real-time areas correlated at r = 0.91 for the group, and r ranged from 0.94 to 0.99 in individual subjects. Interobserver variability was 9.5% for manually traced areas and 10.6% for real-time area measurements.

CONCLUSIONS
Real-time on-line automated edge detection provides accurate estimation of manually drawn cavity areas. Although the method is gain dependent, measurements are reproducible. The system should have clinical application in settings in which measurements of left ventricular function are important.
Myocardial viability in patients with Q wave myocardial infarction and no residual ischemia.
Authors: Montalescot G , Faraggi M , Drobinski G , Messian O , Evans J , Grosgogeat Y , Thomas D 
Published: June 2012

BACKGROUND
Coronary revascularization in patients with persistent angina after myocardial infarction reduces the incidence of recurrent angina pectoris and myocardial infarction and improves left ventricular function. The results of revascularization after a Q wave myocardial infarction when there is no residual ischemia may depend on myocardial viability.

METHODS AND RESULTS
To determine whether there was viable myocardium in the infarct area in the absence of clinical and scintigraphic evidence of myocardial ischemia, 15 asymptomatic patients with a Q wave myocardial infarction, no redistribution on stress 201Tl test, and single-vessel disease (greater than 70% stenosis) with persistent anterograde blood flow were randomized to percutaneous transluminal coronary artery angioplasty (PTCA) or conservative medical treatment. After 2 months of follow-up, mean coronary blood flow measured by Doppler catheter in the infarct-related artery was higher in the PTCA treatment group (33 +/- 6 ml/min, n = 8) than in the conservative treatment group (16 +/- 4 ml/min, n = 7; p less than 0.05 between groups). The 201Tl pathological-to-normal ratios measured on postexercise images did not change in patients treated conservatively during the follow-up period (delta = +1.1 +/- 2.2%; NS from baseline) but increased significantly in patients treated by PTCA (delta = +8.5 +/- 2.3%; p less than 0.01 from baseline; p less than 0.05 between groups). Segmental wall motion improved on left ventricular angiography 2 months after PTCA (delta = +11.5 +/- 2.2%; p less than 0.001 from baseline) significantly more than in the conservative treatment group (delta = +4.1 +/- 1.4%; p less than 0.05 between both groups). Improvements of 201Tl ratios and segmental wall motion indexes correlated significantly (r = 0.73, p = 0.002). The mild improvement of global left ventricular ejection fraction measured in the PTCA treatment group did not differ significantly from changes in the conservative treatment group.

CONCLUSIONS
Successful angioplasty of the stenotic infarct artery in patients with a Q wave myocardial infarction and no residual ischemia improved coronary flow, 201Tl uptake in the infarct area, and regional wall motion. Therefore, myocardial viability may last several weeks, as long as residual blood flow persists in the infarct-related artery. Optimal assessment of viability by imaging techniques should identify patients who are most likely to benefit from revascularization.
Structural remodeling of cardiac myocytes in patients with ischemic cardiomyopathy.
Authors: Gerdes A M , Kellerman S E , Moore J A , Muffly K E , Clark L C , Reaves P Y , Malec K B , McKeown P P , Schocken D D 
Published: June 2012

BACKGROUND
Chronic ischemic heart disease may lead to ventricular dilation and congestive heart failure (ischemic cardiomyopathy [ICM]). The changes in cardiac myocyte shape associated with this dilation, however, are not known.

METHODS AND RESULTS
Left ventricular myocyte dimensions were assessed in cells isolated from explanted human hearts obtained from patients with ICM (n = 6) who were undergoing heart transplantation. Cells were also examined from three nonfailing donor hearts with normal coronary arteries (NCA). Compared with cells from patients with NCA, myocyte length was 40% longer in hearts from patients with ICM (197 +/- 8 versus 141 +/- 9 microns, p less than 0.01), cell width was not significantly different, and cell length/width ratio was 49% greater (11.2 +/- 0.9 versus 7.5 +/- 0.6, p less than 0.01). Sarcomere length was the same in myocytes from both groups. The extent of myocyte lengthening is comparable to the increase in end-diastolic diameter commonly reported in patients with ICM.

CONCLUSIONS
These data suggest that increased myocyte length (an intracellular event), instead of myocyte slippage (an extracellular event), is largely responsible for the chamber dilation in ICM. Furthermore, maladaptive remodeling of myocyte shape (e.g., increased myocyte length/width ratio) may contribute to the elevated wall stress (e.g., increased chamber radius/wall thickness) in ICM.
Effect of balloon angioplasty on femoral artery evaluated with intravascular ultrasound imaging.
Authors: The S H , Gussenhoven E J , Zhong Y , Li W , van Egmond F , Pieterman H , van Urk H , Gerritsen G P , Borst C , Wilson R A 
Published: June 2012

BACKGROUND
Intravascular ultrasound was used to assess the immediate effect of balloon angioplasty on the superficial femoral artery.

METHODS AND RESULTS
In 16 consecutive patients, corresponding ultrasonic cross sections (n = 72) before and after balloon angioplasty were qualitatively and quantitatively analyzed. The qualitative data were compared with angiographic findings. Before intervention, the angiographically demonstrated obstructive lesions were confirmed by intravascular ultrasound. Ultrasound enabled discrimination between soft (n = 43) and hard (n = 29) lesions, as well as between eccentric (n = 57) and concentric (n = 15) lesions. After balloon angioplasty, the presence of a dissection assessed angiographically in 14 patients was confirmed by intravascular ultrasound. Additional morphological information provided by ultrasound included plaque rupture in 14 patients and internal lamina rupture in six patients. Quantitative ultrasound data revealed an increase in free lumen area from 9.7 +/- 4.7 to 18.3 +/- 7.0 mm2 (p less than or equal to 0.01), an increase in minimal lumen diameter from 2.8 +/- 0.7 to 3.6 +/- 1.2 mm (p less than or equal to 0.01), and an increase in media-bounded area from 21.7 +/- 5.4 to 28.3 +/- 5.8 mm2 (p less than or equal to 0.01). The lesion area for the majority of cases (n = 32) remained unchanged (13.0 +/- 4.9 mm2 versus 12.9 +/- 4.6 mm2), or the lesion disappeared partially (from 9.1 +/- 0.9 to 4.3 +/- 1.4 mm2, n = 4, p less than or equal to 0.01) or totally (from 10.1 +/- 4.2 to 0 mm2, n = 6). Stretching of the arterial wall was further evidenced by medial thinning from 0.55 +/- 0.19 to 0.34 +/- 0.11 mm (p less than or equal to 0.01).

CONCLUSIONS
Luminal enlargement by balloon dilatation is achieved primarily by overstretching the arterial wall, with the lesion volume remaining practically unchanged. Overstretching is accompanied almost always by dissection and plaque rupture and occasionally by an internal lamina rupture.
Effects of aging, sex, and physical training on cardiovascular responses to exercise.
Authors: Ogawa T , Spina R J , Martin W H , Kohrt W M , Schechtman K B , Holloszy J O , Ehsani A A 
Published: June 2012

BACKGROUND
The relative contributions of decreases in maximal heart rate, stroke volume, and oxygen extraction and of changes in body weight and composition to the age-related decline in maximal oxygen uptake (VO2max) are unclear and may be influenced by sex and level of physical activity.

METHODS AND RESULTS
To investigate mechanisms by which aging, sex, and physical activity influence VO2max, we quantified VO2, cardiac output, and heart rate during submaximal and maximal treadmill exercise and assessed weight and fat-free mass in healthy younger and older sedentary and endurance exercise-trained men and women. For results expressed in milliliters per kilogram per minute, a three-to-four-decade greater age was associated with a 40-41% lower VO2max in sedentary subjects and a 25-32% lower VO2max in trained individuals (p less than 0.001). A smaller stroke volume accounted for nearly 50% of these age-related differences, and the remainder was explained by a lower maximal heart rate and reduced oxygen extraction (all p less than 0.001). Age-related effects on maximal heart rate and oxygen extraction were attenuated in trained subjects (p less than 0.05). After normalization of VO2max and maximal cardiac output to fat-free mass, age- and training-related differences were reduced by 24-47% but remained significant (p less than 0.05). For trained but not sedentary subjects, maximal cardiac output and stroke volume normalized to fat-free mass were greater in men than in women (p less than 0.05).

CONCLUSIONS
A lower stroke volume, heart rate, and arteriovenous oxygen difference at maximal exercise all contribute to the age-related decline in VO2max. Effects of age and training on VO2max, maximal cardiac output, and stroke volume cannot be fully explained by differences in body composition. In sedentary subjects, however, the sex difference in maximal cardiac output and stroke volume can be accounted for by the greater percentage of body fat in women than in men.
Effective arterial elastance as index of arterial vascular load in humans.
Authors: Kelly R P , Ting C T , Yang T M , Liu C P , Maughan W L , Chang M S , Kass D A 
Published: June 2012

BACKGROUND
This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures.

METHODS AND RESULTS
Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV) = 0.97.Ea(Z) + 0.17; n = 33, r2 = 0.98, SEE = 0.09, p less than 0.0001. Whereas Ea(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated.

CONCLUSIONS
Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.