bluuebunny/crossref_metadata_2025 huggingface dataset:
Delayed afterdepolarizations and triggered activity induced in feline Purkinje fibers by alpha-adrenergic stimulation in the presence of elevated calcium levels.
Authors: Kimura S , Cameron J S , Kozlovskis P L , Bassett A L , Myerburg R J
Published: June 2011

We studied the ability of alpha-adrenergic stimulation to induce delayed afterdepolarizations and triggered activity in Purkinje fibers from cat hearts in the presence of an elevated Ca++ concentration. Delayed afterdepolarizations could not be induced at drive cycle lengths of 200 to 500 msec in the presence of extracellular Ca++ concentrations of 2.7 to 8.1 mM. However, the addition of 10(-5)M phenylephrine in the presence of 5 X 10(-7)M propranolol elicited delayed afterdepolarizations in eight of 10 preparations at a Ca++ concentration of 8.1 mM; nondrive-triggered action potentials were recorded from three of the preparations. These afterpotentials were completely suppressed by 5 X 10(-7)M prazosin or 10(-6)M phentolamine. In the presence of 5 X 10(-7)M propranolol, 10(-5)M phenylephrine prolonged action potential duration and this effect was suppressed by 5 X 10(-7)M prazosin. Methoxamine, at a concentration of 5 X 10(-6)M, was also observed to potentiate delayed afterdepolarizations in all of three preparations studied. These results demonstrate that alpha-adrenergic stimulation can induce afterpotentials in the presence of elevated Ca++ levels in cat hearts. Stimulation of alpha-adrenoceptors may be responsible for arrhythmias under Ca++-loaded conditions such as ischemia and coronary reperfusion.
Clinical pharmacology in patients with evolving myocardial infarction of tissue-type plasminogen activator produced by recombinant DNA technology.
Authors: Tiefenbrunn A J , Robinson A K , Kurnik P B , Ludbrook P A , Sobel B E
Published: June 2011

This study was performed to characterize selected pharmacologic properties and effects on the fibrinolytic system of tissue-type plasminogen activator synthesized by recombinant DNA technology (rt-PA) in 12 patients treated for coronary thrombosis. rt-PA was infused parenterally (by the intracoronary route in four patients and intravenously in eight) in doses of 8.3, 12.5, or 16.7 micrograms/kg/min for 30 to 60 min, yielding a total dosage of 20 to 40 mg/patient. The drug induced coronary thrombolysis in 10 of the 12 patients treated (83%), including six of the eight given rt-PA intravenously. No bleeding complications were encountered. Serial blood samples were obtained before, during, and after infusion of rt-PA and analyzed for t-PA antigen (i.e., immunoassayable rt-PA protein), functional fibrinolytic activity attributable to rt-PA, fibrinogen, plasminogen, alpha 2-antiplasmin, fibrinogen degradation products, prothrombin time, activated partial thromboplastin time, and protamine-corrected thrombin time. Pretreatment plasma t-PA antigen levels averaged 16.5 +/- 5(SD) ng/ml. Peak plasma values were generally proportional to dose, averaging 3330 +/- 1201 ng/ml. Approximately 90% of peak level was reached in 30 min, with a plateau at peak reached within 40 min. Functional t-PA activity increased monotonically in a comparable fashion. Curves for disappearance of both t-PA antigen and functional activity from plasma were monoexponential for at least two half-lives (r = .99 for both) and were concordant. The observed half-lives were similar, averaging 8.3 and 9.1 min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
The long QT syndrome: a prospective international study.
Authors: Moss A J , Schwartz P J , Crampton R S , Locati E , Carleen E
Published: June 2011

During the past 4 years 196 patients with the idiopathic long QT syndrome were enrolled in a prospective international study conducted to obtain a better understanding of the clinical course of this unusual repolarization disorder. The mean patient age was 24 years, 64% were female, and 88% had family members with QT prolongation. During an average follow-up of 26 months per patient, four patients died suddenly (1.3% per year) and 27 patients had one or more syncopal episodes (8.6% per year). Multivariate analysis identified congenital deafness, history of syncope, female gender, and a documented episode of torsades de pointes or ventricular fibrillation as independent risk factors for postenrollment syncope or sudden death. Two types of treatment (left stellate ganglionectomy and beta-blocker therapy) were associated with a significant reduction in the occurrence of cardiac events during follow-up.
Nitrates and endothelial prostacyclin production: studies in vitro.
Authors: De Caterina R , Dorso C R , Tack-Goldman K , Weksler B B
Published: June 2011

The hypothesis that nitrates evoke prostacyclin production by vascular endothelium has been reevaluated on cultured umbilical vein endothelial cells and in vascular fragments, both obtained from humans. Endothelial cell monolayers (passages 1 and 2) were washed free of culture medium and exposed for 3 to 5 min to buffer or nitroglycerin (NTG), isosorbide dinitrate (ISDN), or isosorbide-5-mononitrate (ISMN) over a range of concentrations (10(-9)M to 10(-6)M) encompassing those usually attained in vivo, with or without 25 microM sodium arachidonate. Basal prostacyclin production, measured by radioimmunoassay of the stable metabolite 6-keto-PGF1 alpha, depended on cell density in the endothelial monolayer (being higher in preconfluent cultures) and on incubation time. Basal prostacyclin, however, was not altered by incubation with NTG (3.3 +/- 2.0 pg/1000 cells without drug vs 3.9 +/- 3.8 pg/1000 cells with drug, mean +/- SD), ISDN (3.1 +/- 1.9 vs 3.1 +/- 2.2), or ISMN (2.0 +/- 0.9 vs 2.3 +/- 1.5) at 10(-7)M (all differences NS). Also, long-term incubation (2, 6, and 24 hr) with ISDN and ISMN did not alter prostacyclin production over control. Over a 30-fold increase (p less than .001) in prostacyclin production was obtained with arachidonate stimulation, but incubation with nitrates did not significantly modify the stimulated production. Saphenous vein, mesenteric artery, and atrial appendage fragments incubated at 37 degrees C for 20 min in a shaking water bath with a control buffer produced 27.8 +/- 13.9, 189.7 +/- 75.2, and 662.3 +/- 390.6 pg 6-keto-PGF1 alpha/mg tissue, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Heritability of cardiac size: an echocardiographic and electrocardiographic study of monozygotic and dizygotic twins.
Authors: Adams T D , Yanowitz F G , Fisher A G , Ridges J D , Nelson A G , Hagan A D , Williams R R , Hunt S C
Published: June 2011

Because of the uncertainty as to the extent to which cardiac size is determined by exercise training vs genetic endowment, this study investigated familial (genetic plus common family environment) vs nonfamilial influences on cardiac size. College-age monozygotic twins (group 1, 31 sets), dizygotic twins (group 2, 10 sets), siblings of like sex (group 3, six sets), and nonrelated subjects (group 4, 15 sets) underwent echocardiographic and electrocardiographic tests, measurement of maximum oxygen uptake (VO2max), and evaluation of pulmonary and body composition; mean intrapair differences of the four groups were compared. Mean intrapair differences in cardiac size varied as much for subjects in group 1 as for those in groups 2 and 3. However, subjects in groups 1, 2, and 3 had less variation (p less than .05) than those in group 4. After the initial testing, 14 pairs of monozygotic twins, five sets of dizygotic twins, and six sets of siblings underwent 14 weeks of exercise training (both members participated) and all tests were repeated. After exercise training, subjects in group 1 still had as much intrapair variability in cardiac size as those in groups 2 and 3. The data suggest cultural familial influences are more important in determining cardiac size than nonfamilial influences or even genetic influences alone.
Evaluation of energy metabolism in skeletal muscle of patients with heart failure with gated phosphorus-31 nuclear magnetic resonance.
Authors: Wilson J R , Fink L , Maris J , Ferraro N , Power-Vanwart J , Eleff S , Chance B
Published: June 2011

Exertional fatigue is a major limiting symptom in patients with heart failure. To investigate the metabolic basis of this fatigue, we used gated nuclear magnetic resonance spectroscopy to compare inorganic phosphate (Pi), phosphocreatine (PCr) and pH levels, and fatigue (1 to 4+) during mild forearm exercise in eight normal men and nine men with heart failure. Wrist flexion every 5 sec for 7 min was performed at 1, 2, and 3 J (average power output = 0.2, 0.4, and 0.6 W). In both groups linear relationships were noted between power output and Pi/PCr; the slope of this relationship was used to compare PCr depletion patterns. At rest both groups had similar Pi/PCr ratios (normal subjects 0.12 +/- 0.06, those with heart failure 0.15 +/- 0.03) and pH (normal subjects 7.04 +/- 0.13, those with heart failure 7.10 +/- 0.11). In normal subjects exercise resulted in a progressive increase in Pi/PCr (slope = 1.17 +/- 0.20 Pi/PCr units/W), a reduction in pH only at 0.6 W (0.2 W: 7.03 +/- 0.10, 0.4 W: 7.01 +/- 0.10, 0.6 W: 6.88 +/- 16) and moderate fatigue (0.2 W: 0 +/- 0, 0.4 W: 1.3 +/- 0.5, 0.6 W: 1.9 +/- 0.6). In patients with heart failure exercise resulted in significantly greater fatigue at all workloads (0.2 W: 1.0 +/- 0.5, 0.4 W: 1.9 +/- 0.6, 0.6 W: 2.9 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)
Electrophysiologic testing in patients with the long QT syndrome.
Authors: Bhandari A K , Shapiro W A , Morady F , Shen E N , Mason J , Scheinman M M
Published: June 2011

Electrophysiologic studies were performed in 15 patients with syncope and/or cardiac arrest who had the long QT syndrome and 11 control subjects who had normal QT intervals. The syndrome was familial in five patients and idiopathic in 10. All patients had a prolonged QT (546 +/- 68 msec, mean +/- SD) and corrected QT (550 +/- 51 msec). Incremental atrial pacing at cycle lengths of 600 to 400 msec resulted in shortening of the QT interval, but there was no significant difference in the magnitude or percent of shortening of the QT interval between patients with the long QT syndrome and control subjects. Intravenous propranolol did not influence the QT interval measured at fixed atrial-paced cycle lengths in patients with either the familial or idiopathic form of the syndrome. Programmed right and left ventricular stimulation with up to three extrastimuli before and during isoproterenol infusion did not induce sustained ventricular tachycardia or ventricular fibrillation in any of the patients. However, rapid polymorphic nonsustained ventricular tachycardia was induced in six of the 15 patients (40%). Neither the inducibility of nonsustained ventricular tachycardia nor the results of electropharmacologic testing with beta-blockers proved to be of any prognostic value during the mean follow-up period of 28 +/- 17 months. Electrophysiologic studies are of limited value in the diagnosis and treatment of patients with the long QT syndrome.
Slow regional clearance of myocardial thallium-201 in the absence of perfusion defect: contribution to detection of individual coronary artery stenoses and mechanism for occurrence.
Authors: Abdulla A , Maddahi J , Garcia E , Rozanski A , Swan H J , Berman D S
Published: June 2011

As a result of the "spatially relative" nature of perfusion defect analysis of stress-redistribution thallium-201 (201Tl) scintigrams, hypoperfused myocardial segments may not appear as perfusion defects but they may demonstrate a slow washout rate of 201Tl that can be analyzed in a "spatially nonrelative" manner. Quantitative analysis of perfusion defects and slow washout rate of 201Tl was performed on scintigrams from 116 consecutive patients with adequate exercise tests, defined as achievement of 85% or more of age-predicted maximum heart rate or development of angina or ST segment depression. A total of 232 diseased and 116 nondiseased vessels were found in the patients. Additional analysis of slow washout rate significantly (p less than .05) improved sensitivity for detection of disease in the left anterior descending (from 74% to 82%), left circumflex (from 40% to 61%), and right coronary arteries (from 78% to 90%) without significant loss of specificity. This improvement resulted from the additional detection of 32 of 232 (14%) diseased vascular distributions when the isolated slow washout rate of 201Tl was also determined. In nine of these 32, isolated slow washout rate was associated with another region with isolated slow washout rate in the contralateral myocardial segment. Coronary arteriography revealed similar degrees of stenosis in the vessels supplying these segment pairs. In 13 of 32 cases, a perfusion defect and a slow washout rate were found in the contralateral segment.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of aging on arterial distensibility in populations with high and low prevalence of hypertension: comparison between urban and rural communities in China.
Authors: Avolio A P , Deng F Q , Li W Q , Luo Y F , Huang Z D , Xing L F , O'Rourke M F
Published: June 2011

Arterial pulse wave velocity, an established index of arterial distensibility, was measured together with arterial pressure in a group of 524 normal subjects of both sexes 2 months to 94 years old (mean age 45.6 +/- 15.3 years [SD]) in rural Guangzhou, China, an area with known low prevalence of hypertension. Fasting serum lipid levels and overnight Na+ and K+ urinary excretion levels were determined in a subgroup of 104 subjects (ages 8 to 88 years). Comparisons were made with data obtained similarly from normal subjects in urban Beijing, an area with known high prevalence of hypertension. Serum cholesterol levels were similar and low in each group (Guangzhou, 4.34 +/- 0.12 mmol/liter [SE]; BEijing, 4.49 +/- 0.11 mmol/liter). Prevalence of hypertension (WHO criteria) was 4.9% (Guangzhou) and 15.6% (Beijing). In Guangzhou subjects pulse wave velocity was consistently lower in the aorta, arm, and leg, and increased to a lesser degree with age compared with Beijing subjects. Regression equations (x = pulse wave velocity [cm/sec], y = age [years]) were as follows: (1) aorta, Guangzhou: y = 5.1x + 533, r = .552, p less than .05; Beijing: y = 9.2x + 615, r = .673, p less than .001; (2) arm, Guangzhou: y = 0.61x + 817, r = .121, p less than .05; Beijing: y = 4.8x + 998, r = .453, p less than .001; (3) leg, Guangzhou: y = 4.43x + 718, r = .512, p less than .05; Beijing: y = 5.6x + 791, r = .630, p less than .001.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical experience, complications, and survival in 70 patients with the automatic implantable cardioverter/defibrillator.
Authors: Echt D S , Armstrong K , Schmidt P , Oyer P E , Stinson E B , Winkle R A
Published: June 2011

Seventy patients received the automatic implantable defibrillator, five original devices and 72 modified second-generation devices using only bipolar rate sensing and delivering an R wave synchronous cardioverting/defibrillating shock, for either ventricular tachycardia or fibrillation. The primary clinical arrhythmia was sustained ventricular tachycardia in 32 patients, ventricular fibrillation in 20 patients, and both ventricular tachycardia and fibrillation in 18 patients. Before implantation of the device the patients had survived 3.1 +/- 2.3 arrhythmic episodes, including 1.9 +/- 1.7 cardiac arrest, and had received 4.0 +/- 2.1 antiarrhythmic drugs without improvement. Sixty-eight patients ultimately received devices. After a follow-up period of 8.9 +/- 7.7 months (range 1 to 33), 37 patients received a total of 463 discharges. Inability to determine the precise reason for most discharges and the unpleasant nature of the discharges were the major clinical problems encountered. Complications included postoperative death (one patient), lead problems (six patients), inadequate energy requiring explanation (two patients), and pocket infection (one patient. Life-table analysis revealed 6 and 12 month cardiovascular survival of 95.0% and 89.9% and sudden death survival of 98.2%. In our experience, survival with the automatic implantable cardioverter/defibrillator exceeds that with other forms of therapy.
The status of surgery for cardiac arrhythmias.
Authors: Cox J L
Published: June 2011

Successful surgical treatment of all forms of supraventricular tachyarrhythmias is dependent on accurate electrophysiologic guidance. Surgery for WPW syndrome is no longer experimental and should be offered to (1) patients with medically refractory reciprocating tachycardia associated with the syndrome, (2) patients with spontaneous atrial fibrillation who are at risk for sudden death, (3) patients with drug intolerance, and (4) young, otherwise healthy patients with symptoms that warrant more than minimal medical therapy. The current results of surgery for WPW syndrome would seem to lessen the likelihood that a major new method of superior nonpharmacologic treatment will emerge in the near future. Surgery for most other types of supraventricular tachyarrhythmias remains experimental and should be applied only under the most controlled circumstances and after satisfying the most rigid criteria for surgical intervention, the main indication being absolute medical refractoriness. The single exception at the present time is surgery for AV node reentry tachycardia, which appears to be easily cured by the new technique of discrete cryosurgery of the peri-AV nodal region of the lower right atrial septum. In a majority of patients, ventricular tachycardia can be successfully ablated surgically without the use of electrophysiologic mapping to guide the surgeon. If such an approach is taken, however, the surgical treatment of these complex arrhythmias becomes a completely service-oriented exercise. Although delivery of such a service is of undeniable importance, the potential for learning more about these complex and lethal arrhythmias is lost unless each patient is studied as comprehensively as possible.(ABSTRACT TRUNCATED AT 250 WORDS)
Assessment of the performance of electrocardiographic computer programs with the use of a reference data base.
Authors: Willems J L , Arnaud P , van Bemmel J H , Bourdillon P J , Brohet C , Dalla Volta S , Andersen J D , Degani R , Denis B , Demeester M
Published: June 2011

To allow an exchange of measurements and criteria between different electrocardiographic (ECG) computer programs, an international cooperative project has been initiated aimed at standardization of computer-derived ECG measurements. To this end an ECG reference library of 250 ECGs with selected abnormalities was established and a comprehensive reviewing scheme was devised for the visual determination of the onsets and offsets of P, QRS, and T waves. This task was performed by a group of cardiologists on highly amplified, selected complexes from the library of ECGs. With use of a modified Delphi approach, individual outlying point estimates were eliminated in four successive rounds. In this way final referee estimates were obtained that proved to be highly reproducible and precise. This reference data base was used to study measurement results obtained with nine vectorcardiographic and 10 standard 12-lead ECG analysis programs. The medians of program determinations of P, QRS, and T wave onsets and offsets were close to the final referee estimates. However, an important variability could be demonstrated between measurements from individual programs and mean differences from the referee estimates amounted to 10 msec for QRS for certain programs. In addition, the variances of all programs with respect to the referee point estimates were variable. Some programs proved to be more accurate and stable when the data from high- vs low-noise recordings were analyzed. Average Q wave durations calculated from ECGs for which programs agreed on the presence of a Q or QS wave differed by more than 8 msec in several program-to-program comparisons. Such differences may have important consequences with respect to diagnostic performance. Various factors that might explain these differences have been determined. The present study demonstrates that to allow an exchange of results and diagnostic criteria between different ECG computer programs, definitions, minimum wave requirements, and measurement procedures urgently need to be standardized.
Determination of parameters of left ventricular diastolic filling with pulsed Doppler echocardiography: comparison with cineangiography.
Authors: Rokey R , Kuo L C , Zoghbi W A , Limacher M C , Quinones M A
Published: June 2011

To determine the relationship between Doppler-derived flow velocity through the mitral anulus and angiographic parameters of left ventricular filling, 30 patients were studied by two-dimensional echocardiography combined with pulsed Doppler echocardiography followed within 1 hr by left ventricular angiography. The average heart rate for each test was 69 beats/min. Doppler-derived parameters included: early peak diastolic velocity (E) and peak atrial velocity, peak filling rate computed as E X cross-sectional area of the mitral anulus derived from the annular diameter, normalized peak filling rate computed as peak filling rate divided by the left ventricular end-diastolic volume determined by two-dimensional echocardiography, and half filling fraction derived from the time-velocity integral of the Doppler-determined velocity curve. Frame-by-frame left ventricular volumes were obtained throughout diastole from single-plane cineangiograms. A volume-time curve with its derivative was generated by computer processing from which peak filling rate, normalized peak filling rate, and half filling fraction were measured. Morphologically, the Doppler-derived velocity profile resembled the derivative of the angiographic volume curve. In patients with reduced angiographic peak filling rates, early peak diastolic velocity was often decreased less than 45 cm/sec with a relative increase in peak atrial velocity resulting in an early peak diastolic velocity to peak atrial velocity ratio less than 1.0. There were no significant differences in mean values for peak filling rate, normalized peak filling rate, and half filling fraction by Doppler echocardiography vs angiography (296 vs 283 ml/sec, 1.9 vs 2.0 sec-1 and 0.55 vs 0.55, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Coronary pacing during percutaneous transluminal coronary angioplasty.
Authors: Meier B , Rutishauser W
Published: June 2011

To avoid venous puncture, a new concept for standby cardiac pacing during percutaneous transluminal coronary angioplasty (PTCA) and diagnostic cardiac catheterization was developed. It uses an arterial guidewire as a unipolar pacing electrode with the second electrode attached to the skin. The system was tested in 25 coronary arteries of 22 patients undergoing PTCA and in the left ventricles of 10 patients undergoing diagnostic cardiac catheterization. Coronary pacing via the guidewire used for directing the balloon catheter was possible in all patients and in 24 of the 25 coronary arteries attempted. Maximum duration of pacing was 8 min. Threshold currents ranged from 1 to 15 mA (mean 5.7). Left ventricular pacing via the same wires or standard wires used for introduction of diagnostic or guiding catheters was possible in all patients and was maintained for up to 10 min. Threshold currents ranged from 1 to 7 mA (mean 3.9). Neither method for pacing produced adverse effects during these short applications. The setup for coronary pacing also allowed recording of an intracoronary electrocardiogram during PTCA. The presented system provides backup for the rare event of sustained bradycardia during PTCA or diagnostic cardiac catheterization. If applied cautiously, it may safely and reliably replace the standby of a conventional transvenous pacing catheter.
Effects of global ischemia on the diastolic properties of the left ventricle in the conscious dog.
Authors: Visner M S , Arentzen C E , Parrish D G , Larson E V , O'Connor M J , Crumbley A J , Bache R J , Anderson R W
Published: June 2011

The alterations in regional diastolic mechanics that occur during regional myocardial ischemia (creep and increased myocardial stiffness) may be the result of interactions between the ischemic and surrounding nonischemic myocardium rather than the direct result of ischemia. Thus similar changes may not occur when the entire left ventricle is ischemic. Thus similar changes may not occur when the entire left ventricle is ischemic. To investigate this proposition, left ventricular diastolic mechanics were studied in seven chronically instrumented conscious dogs during global left ventricular ischemia. The anterior-posterior, septal-free wall, and base-apex axes of the left ventricle were measured with ultrasonic dimension transducers. Left and right ventricular pressures were measured with micromanometers. Myocardial blood flows were measured with left atrial injections of 15 microns radioactive microspheres. Global left ventricular ischemia was induced by hydraulic constriction of the left main coronary artery, which resulted in a 54% decrease in mean left ventricular subendocardial blood flow. Left ventricular volume, midwall circumference, and midwall circumferential stress were calculated from ellipsoidal shell theory. To construct pressure-strain and stress-strain relationships from diastolic data collected during vena caval occlusions, all measured and calculated dimensions were normalized to Lagrangian strains (fractional extension from unstressed dimension). During ischemia, creep (elongation of unstressed dimension) occurred in each of the three left ventricular axes. The mean unstressed dimension of the anterior-posterior axis increased from 5.39 +/- 0.53 to 5.85 +/- 0.50 cm ( p less than or equal to .05); the septal-free wall unstressed dimension increased from 5.11 +/- 0.53 to 5.72 +/- 0.80 cm (p less than or equal to .05); and the base-apex unstressed dimension increased from 7.04 +/- 0.61 to 7.25 +/- 0.65 cm (p less than or equal to .05). The relationship between diastolic midwall circumferential stress and strain shifted upward and to the left with ischemia, indicating that an increase in intrinsic myocardial stiffness had occurred. As a result of these mechanical alterations, there was a decrease in left ventricular chamber compliance that was manifested by a leftward shift of the diastolic pressure-volume strain relationship. Neither systolic bulging nor dysynchronous systolic shortening occurred in any of the three left ventricular spatial axes during ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
Noninvasive pulsed Doppler echocardiographic detection of the direction of shunt flow in patients with atrial septal defect: usefulness of the right parasternal approach.
Authors: Minagoe S , Tei C , Kisanuki A , Arikawa K , Nakazono Y , Yoshimura H , Kashima T , Tanaka H
Published: June 2011

Noninvasive pulsed Doppler echocardiography combined with two-dimensional echocardiography by the right parasternal approach was performed to detect the shunt flow through the defect in 31 patients with suspected secundum atrial septal defect (ASD). A defect of the interatrial septum was seen on the two-dimensional echocardiograms of 30 of 31 patients. In all the 30 patients, Doppler signals of shunt flow could be recorded by placing the sample volume in the center of the defect on the two-dimensional echocardiogram. Neither a defect nor Doppler signal indicating shunt flow were demonstrated in any of 15 normal control subjects. Cardiac catheterization indicated significant shunt flow in all the 31 patients with suspected ASD. Doppler signals obtained from the center of the defect showed left-to-right and/or right-to-left shunt flow patterns. The direction of the shunt flow was mainly left to right, with its peak in late systole and atrial systole in 28 of 30 patients; mainly right-to-left flow was present in the remaining two patients, who had Eisenmenger's syndrome. The direction of flow as predicted by the Doppler signal was confirmed by the coincidence of direction of flow as seen on the contrast two-dimensional echocardiogram. In 22 patients for whom the measurement of the pulmonary-to-systemic flow ratio by oximetry was believed to be reasonably accurate, the ratio was fairly well correlated with Doppler-determined left-to-right shunt flow velocity (r = .71, SEE = 6.7 cm/sec).(ABSTRACT TRUNCATED AT 250 WORDS)
Production of systolic anterior motion of the mitral valve in dogs.
Authors: Sakurai S , Tanaka H , Yoshimura H , Nakao S , Tahara M
Published: June 2011

Production of an experimental preparation of systolic anterior motion (SAM) of the mitral valve was attempted for the purpose of clarifying its causal factors. Fourteen thoracotomized dogs under pentobarbital anesthesia were administered dobutamine, and the echocardiogram, left ventricular pressure, and aortic pressure of each were simultaneously recorded. In two of the dogs in which SAM was produced, two-dimensional echocardiograms were also obtained. Although SAM was absent in all 14 dogs before the administration of dobutamine, it appeared in nine of them after the drug was given. In seven of these dogs, the magnitude of SAM and outflow pressure gradient varied in a dose-dependent manner. No signs of asymmetric septal hypertrophy were observed in any of these dogs. SAM tended to occur even when there was no reduction in preejection period when narrowing of the left ventricular outflow tract was observed. On the two-dimensional echocardiograms, the position of coaptation of the mitral valve was shifted closer to the base of the anterior leaflet in the presence of dobutamine-induced SAM than before the drug was administered. Although the left ventricular cavity became narrow, it was not completely obliterated. This study demonstrates that experimental preparations of SAM can be produced by the administration of dobutamine with a relatively high success rate in normal dogs, and that experimental SAM is accompanied by an outflow tract pressure gradient.
Failure of the xanthine oxidase inhibitor allopurinol to limit infarct size after ischemia and reperfusion in dogs.
Authors: Reimer K A , Jennings R B
Published: June 2011

During the acute phase of myocardial ischemia, adenine nucleotides are degraded to nucleosides and bases, especially inosine and hypoxanthine. Simultaneously, xanthine dehydrogenase is converted to xanthine oxidase, an enzyme that converts hypoxanthine to xanthine, and xanthine to uric acid, producing a superoxide anion for each molecule of hypoxanthine or xanthine oxidized. To determine if free radicals via this enzymatic source contribute to cell death in myocardial ischemia, we determined whether allopurinol, an inhibitor of xanthine oxidase, could limit infarct size in a reperfusion preparation of myocardial infarction. The circumflex coronary artery of each of 34 dogs was occluded for 40 min, followed by reperfusion for 4 days. Infarct size then was measured by histologic methods and was related to major baseline predictors of infarct size, including anatomic area at risk and collateral blood flow. Infarct size was larger (NS) in the allopurinol (n = 8) than in the control (n = 11) group, a trend that was related to slightly higher (NS) collateral blood flow in the control group. We conclude that allopurinol has no beneficial effect in this preparation of experimental myocardial infarction. The results oppose the hypothesis that free radicals, produced via the xanthine oxidase reaction, are an important contributing factor in myocardial ischemic cell death.
Left ventricular contractility and contractile reserve in humans after cardiac transplantation.
Authors: Borow K M , Neumann A , Arensman F W , Yacoub M H
Published: June 2011

Limited data are available concerning left ventricular contractility and contractile reserve in the chronically denervated, transplanted human heart. This is primarily because of the inability of traditional tests of left ventricular performance to distinguish changes in contractility from alterations in ventricular loading conditions. In this study, load-independent end-systolic indexes of left ventricular contractility were measured by echocardiography and calibrated carotid pulse tracings in 10 patients who had undergone orthotopic cardiac transplant (age 48 +/- 4 years; interval from operation to study 1.2 +/- 0.8 years) and in 10 normal control subjects (age 25 +/- 4 years) matched for donor heart age (25 +/- 6 years). None of the transplant patients had evidence of rejection as determined by endomyocardial biopsy. Baseline left ventricular contractility was assessed over a wide range of afterload generated by infusion of methoxamine. Contractile reserve was measured as the response to an infusion of dobutamine plus methoxamine. Before afterload challenge, baseline left ventricular percent fractional shortening was higher for the transplant patients than for the control subjects (36.5 +/- 5.7% vs 32.1 +/- 2.1%; p less than .05). These differences occurred at a time that end-systolic wall stress (a measure of afterload) was significantly lower for the transplant patients (38 +/- 16 vs 50 +/- 9 g/cm2; p less than .05). When the left ventricular end-systolic pressure-dimension and stress-shortening relationships were determined for the transplant and control subjects, no differences in contractility or contractile reserve were noted. Thus the chronically denervated, transplanted, nonrejecting human left ventricle demonstrates normal contractile characteristics and reserve.
The QRS complex during transient myocardial ischemia: studies in patients with variant angina pectoris and in a canine preparation.
Authors: Barnhill J E , Wikswo J P , Dawson A K , Gundersen S , Robertson R M , Robertson D , Virmani R , Smith R F
Published: June 2011

We made continuous electrocardiographic recordings on magnetic tape during 15 episodes of ischemia in five patients with variant angina to determine the characteristics of the QRS changes. Orthogonal leads were used and the electrocardiograms were analyzed visually and by digital computer. Changes were quantified by subtracting baseline electrocardiograms from those obtained during ischemia. Large changes in the QRS occurred during ischemia but the waveform quickly returned to baseline when the episode subsided. In all patients there was prolongation of the QRS duration and an increase in QRS voltage during the terminal 40 msec of the waveform in the lead(s) showing the most marked ST displacement. The increase in the terminal QRS could be represented by a vector directed toward the ischemic zone. In a given patient the amplitude of ST displacement varied between episodes, presumably because of variation in the intensity of ischemia, but the QRS changes were directionally similar in each episode. In two patients there was also a smaller change involving the initial 40 msec of the QRS that could be represented by a vector directed away from the ischemic zone. To determine the possible mechanism for the electrocardiographic changes, ischemic episodes of 120 to 150 sec were produced in seven dogs and electrocardiographic recording and analysis techniques similar to those used in patients were employed. Myocardial conduction velocity was measured in three directions in the ischemic zone and was correlated with simultaneous electrocardiographic recordings from the body surface. The electrocardiographic changes in the dog preparation were virtually identical to those in the patients and strongly correlated with a fall in myocardial conduction velocity. We conclude that the QRS changes during variant angina result from the altered excitation pattern produced by conduction delay in the ischemic zone. The probable cause for the increase in terminal QRS voltage is delayed (and uncancelled) activation of the ischemic zone.
Spontaneous hemodynamic improvement or stabilization and associated biopsy findings in patients with congestive cardiomyopathy.
Authors: Figulla H R , Rahlf G , Nieger M , Luig H , Kreuzer H
Published: June 2011

The hemodynamic courses of 56 patients with congestive cardiomyopathy (CCM) were investigated. Fourteen patients died within 24 months after diagnosis. The hemodynamic courses of the remaining 42 patients were investigated in subsequent examinations by determination of left ventricular ejection fraction (LVEF), mean pulmonary arterial pressure at maximal workload, and peak systolic pressure/end-systolic volume index. During the study interval of 32.2 +/- 20.0 months the conditions of 20 patients (48%) deteriorated, according to their hemodynamic status, and at least five of these died of terminal heart failure. Surprisingly, the conditions of 22 patients (52%) improved or stabilized. One of these died of leukemia. Seven patients in the latter group with initial LVEFs of 0.30 or less experienced an average increase from 0.22 to 0.51. Retrospectively consideration of age, alcohol intake, exercise capacity, and hemodynamic status were not helpful in predicting the course of the disease. In 38 patients endomyocardial biopsy samples could be obtained at the time of diagnosis. Reduced myofibril volume fraction (less than 60%) had prognostic significance for both hemodynamic deterioration and death (sensitivity 23/24 = 96%), while 14 of 15 patients whose conditions improved or stabilized had a myofibril volume fraction of 60% or more (specificity 14/15 or 93%, p less than .002). A relationship between hemodynamic status and the myofibril volume fraction could not be found. Individual patients with CCM differ significantly with respect to course of the disease. A distinct separation of the patients by means of morphologic criteria is possible. This makes it more likely that the pathogenesis of the disease is not unique.
Immunologic behavior of lymphocytes in experimental viral myocarditis: significance of T lymphocytes in the severity of myocarditis and silent myocarditis in BALB/c-nu/nu mice.
Authors: Kishimoto C , Kuribayashi K , Masuda T , Tomioka N , Kawai C
Published: June 2011

To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I). B cells were demonstrated by staining with fluorescein isothiocyanate (FITC)-labeled rabbit antimouse immunoglobulin (Ig). T cells were demonstrated with rat anti-Thy1.2 monoclonal antibody plus FITC-labeled antimouse Ig. There was a marked decrease in T cells in peripheral blood and a moderate decrease in the cells in the spleen on day 14. There were no significant changes in B cells in peripheral blood or spleen throughout the entire period and T cells accounted for approximately 80% of the cells in the myocardium on days 7 and 14. To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALB/c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction).
Authors: Drexler H , Depenbusch J W , Truog A G , Zelis R , Flaim S F
Published: June 2011

The effects of intravenous infusion of diltiazem on regional blood flow (radioactive microspheres), hemodynamics, and maximum rate of oxygen consumption were evaluated in conscious rats with congestive heart failure caused by large myocardial infarction (n = 10, infarct size 41.8% of left ventricle) and compared with data obtained from rats subjected to sham surgical procedures (n = 9). In both groups data were obtained at rest and during submaximal treadmill exercise during alternate infusion of diltiazem and saline. In the group with heart failure, diltiazem increased stroke volume at rest and during exercise (p less than .05), reduced heart rate (p less than .05), and improved cardiac output during exercise (p less than .05) without increasing left ventricular end-diastolic pressure in any of the animals. Blood flow to renal and splanchnic circulations was reduced in the group with heart failure but was increased by diltiazem to values similar to those observed in sham-operated animals. Although skeletal muscle flow during exercise was significantly increased by the drug, maximal rate of oxygen consumption was not, indicating unchanged oxygen availability within working muscle. Thus diltiazem caused redistribution of blood flow to kidney and gut in animals with myocardial infarction and failure, thereby restoring blood flow to circulatory beds known to be impaired in this setting.
Quantitative analysis of the high-frequency components of the signal-averaged QRS complex in patients with acute myocardial infarction: a prospective study.
Authors: Gomes J A , Mehra R , Barreca P , el-Sherif N , Hariman R , Holtzman R
Published: June 2011

We performed a prospective study of the high-frequency components of the terminal portion of the QRS complex in 50 patients with acute myocardial infarction (AMI) (mean age 63 +/- 10 years) within 3.25 +/- 2.45 days of the acute event. Signal averaging (400 beats) at a filter setting of 80 to 300 Hz was performed and the duration of the low-amplitude signals of less than 40 microV in the terminal portion of the QRS, the root-mean-square (RMS) voltage of the terminal 40 msec of the QRS complex, and the total duration of the signal-averaged QRS vector complex were measured. The low-amplitude signals were abnormally prolonged in 22 of 50 patients (44%); the RMS-V was abnormal (less than 20 microV) in 21 of 50 patients (58%), and the signal-averaged vector complex was abnormal (greater than 120 msec) in 15 of 46 patients (33%) without bundle branch block. There was no significant correlation between any of the signal-averaged parameters and site of AMI or total creatine kinase (CK) and CK-MB values. On the basis of the occurrence of spontaneous ventricular tachycardia in the acute and postcoronary care phase of AMI, the patients were divided into two groups. Group I consisted of 31 patients (62%) who had no documented ventricular tachycardia and group II consisted of 19 patients (38%) who had one or more runs of ventricular tachycardia. Fourteen of the 19 patients in group II (73.6%) had nonsustained ventricular tachycardia and five patients (26.3%) suffered sustained ventricular tachycardia/ventricular fibrillation or sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
Efficacy and safety of transcatheter ablation of posteroseptal accessory pathways.
Authors: Morady F , Scheinman M M , Winston S A , DiCarlo L A , Davis J C , Griffin J C , Ruder M , Abbott J A , Eldar M
Published: June 2011

Eight patients with a posteroseptal accessory pathway and symptomatic atrial fibrillation and/or orthodromic reciprocating tachycardia underwent attempted transcatheter ablation of the accessory pathway. A quadripolar electrode catheter was positioned within the coronary sinus such that the proximal pair of electrodes straddled the os. This proximal pair of electrodes was made electrically common and connected to the cathodal output of a defibrillator. A patch electrode placed over the midthoracic spine was connected to the anodal sink of the defibrillator. Two to three transcatheter shocks were delivered, with a cumulative energy of 600 to 900 J. Immediately after the shocks were delivered, retrograde accessory pathway conduction was absent in each patient. Anterograde conduction through the posteroseptal accessory pathway was absent in six patients. In one patient, retrograde accessory pathway conduction was absent and anterograde conduction was present but was slower than at baseline. In this patient, orthodromic tachycardia was no longer inducible and the ventricular rate during induced atrial fibrillation was 150 beats/min, compared with 220 beats/min before the attempted ablation. He has remained asymptomatic without antiarrhythmic drug therapy for 18 months. In one patient, the transcatheter shocks had no long-term effect on accessory pathway conduction. The shocks delivered at the os of the coronary sinus were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of the combination of diltiazem and atenolol on exercise-induced regional myocardial ischemia in conscious dogs.
Authors: Matsuzaki M , Guth B , Tajimi T , Kemper W S , Ross J
Published: June 2011

The effect of combination therapy with diltiazem and atenolol on the regional myocardial blood flow-function relationship was studied in eight conscious dogs with chronic coronary artery stenosis. An ameroid constrictor and hydraulic occluder were placed around the left circumflex coronary artery, sonomicrometers were implanted for measuring wall thickness in control and ischemic regions, and regional myocardial blood flow was measured with the microsphere method. Eighteen days (average) after surgery, resting regional myocardial function and blood flow were normal, but treadmill exercise induced severe regional myocardial dysfunction in the posterior wall (wall thickening during systole reduced from 25.5% to 2.7%, a 90% reduction). Subendocardial blood flow decreased by 68% from the control standing value, while subepicardial flow increased. An identical exercise bout was performed 3 hr after administration of atenolol (1.0 mg/kg orally) and 15 min after administration of diltiazem (0.3 mg/kg iv). Heart rate during running was significantly lower as were left ventricular peak systolic pressure, end-diastolic pressure, and peak dP/dt. Wall thickening in the control region was not augmented during exercise after atenolol and diltiazem. There was less dysfunction in the ischemic region (35% reduction) and the improved performance was accompanied by a substantial increase in subendocardial perfusion (0.31 +/- 0.14 vs 0.61 +/- 0.30 ml/min/g, a 36% reduction from rest). Epicardial flow was unchanged, and the endocardial/epicardial ratio increased (0.27 +/- 0.13 vs 0.62 +/- 0.29). Recovery time for regional wall thickening also improved. The beneficial effects of the combination of atenolol and diltiazem in a preparation of single-vessel chronic coronary stenosis were shown to be significantly greater than those of either drug alone.