bluuebunny/crossref_metadata_2025 huggingface dataset:
Treatment of viral myocarditis with ribavirin in an animal preparation.
Authors: Matsumori A , Wang H , Abelmann W H , Crumpacker C S
Published: June 2011

The therapeutic effects of ribavirin, a broad-spectrum, antiviral agent, on experimental myocarditis caused by encephalomyocarditis (EMC) virus were investigated. Four-week-old DBA/2 mice were inoculated with 10 plaque-forming units (pfu) of EMC virus. Ribavirin in a dose of 100 (group 1, n = 20), 200 (group 2, n = 10), or 400 mg/kg/day (group 3, n = 10) was administered subcutaneously on days 0 to 12 after virus inoculation, and animals were observed for 12 days. Control animals were injected with saline (n = 20). Mice treated with ribavirin survived longer than controls (mean survival 6.7 days for group 1, 7.4 days for group 2, 7.7 days for group 3, and 5.2 days for control; p less than .005). Myocardial virus titers on days 6 to 8 were significantly lower in group 2 (3.24 +/- 0.49 log10pfu/mg; p less than .005) and in group 3 (1.70 +/- 0.65 log10 pfu/mg; p less than .001) compared with controls (4.09 +/- 0.57 log10 pfu/mg). The incidence of gross myocardial lesions was significantly lower in group 1 (13/20, 65%), group 2 (2/10, 20%), and group 3 (0/20, 0%) compared with controls (20/20, 100%) (p less than .05). Histologic examination showed extensive myocardial necrosis and cellular infiltration in untreated groups; there was less infiltration in groups 2 and 3 (p less than .01) and less severe necrosis in group 3 (p less than .01). Thus ribavirin effectively inhibited myocardial virus replication and reduced the inflammatory response and myocardial damage in an experimental preparation of viral myocarditis.
Effects of altered site of electrical activation on myocardial performance during inotropic stimulation.
Authors: Heyndrickx G R , Vilaine J P , Knight D R , Vatner S F
Published: June 2011

The effects of altering the site of electrical activation on responses to isoproterenol (ISO) and treadmill exercise were examined in mongrel dogs instrumented for long-term measurement of left ventricular pressure, left ventricular dP/dt, coronary blood flow, cardiac output, left ventricular diameters, and mean arterial pressure and O2 content in the coronary sinus and aorta. During spontaneous rhythm, 0.2 micrograms/kg/min ISO increased heart rate by 90 +/- 7 beats/min, left ventricular dP/dt by 2479 +/- 301 mm Hg/sec, cardiac output by 3.5 +/- 0.9 liters/min, coronary blood flow by 30.4 +/- 3.9 ml/min, and myocardial oxygen consumption (MVO2) by 3.91 +/- 0.84 ml/min. During right atrial pacing at 193 +/- 7 beats/min, the effects of ISO were not different from the effects during spontaneous rhythm, with the exception of a lesser increase in coronary blood flow and lesser reductions in coronary resistance and left ventricular end-diastolic diameter and pressure. During right ventricular pacing at an identical rate, ISO increased left ventricular dP/dt (1140 +/- 158 mm Hg/sec) and cardiac output (2.2 +/- 0.5 liters/min) significantly less (p less than .025) than during either sinus rhythm or right atrial pacing, while MVO2 rose to a higher value. During right ventricular pacing the changes in mean arterial pressure and left ventricular end-diastolic diameters with ISO were not significantly different from those during right atrial pacing. Treadmill exercise induced significantly smaller (p less than .025) increases in left ventricular dP/dt during right ventricular pacing as compared with during either right atrial pacing or sinus rhythm, while MVO2 rose to a higher value.(ABSTRACT TRUNCATED AT 250 WORDS)
Impaired inotropic responses to alpha-adrenergic stimulation in experimental left ventricular hypertrophy.
Authors: Fouad F M , Shimamatsu K , Hanna M M , Khairallah P A , Tarazi R C
Published: June 2011

We have previously reported that left ventricular hypertrophy in two-kidney, one-clip renal hypertensive rats (2K-1C RHRs) was associated with diminished inotropic responsiveness to isoproterenol and glucagon, suggesting an alteration in the receptor-adenylate cyclase cascade. The present study was performed to investigate the hypothesis that in these same hearts, inotropic responses to alpha-adrenergic stimuli could be enhanced as a compensatory mechanism. alpha-Adrenergic stimulation was achieved by graded phenylephrine infusion (1.02 to 41.2 microM/min) in the presence of propranolol (10(-7) M). The inotropic response was evaluated in the isovolumetric isolated rat heart (Langendorff preparation) paced at 260 beats/min. Results showed a significantly reduced inotropic response to alpha 1-adrenergic stimulation in 2K-1C RHR hearts irrespective of perfusion pressure (50 or 80 mm Hg [PP50 or PP80]) (+427.5 +/- 62.1 vs +1236 +/- 216.4 mm Hg X sec-1 at PP50, p less than .01 and +339 +/- 98.3 vs +1440 +/- 254 mg Hg X sec-1 at PP80, p less than .001) even when comparison was made at equivalent myocardial flow rates (RHR hearts perfused at 80 mm Hg vs control hearts perfused at 50 mm Hg). Quantitative assessment of number of alpha 1-adrenergic receptors (3H-prazosin binding) showed a significant decrease compared with that in age-matched sham-operated normotensive control rats (45 +/- 2.5 vs 64 +/- 1.7 fmol/mg protein, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of coronary artery reperfusion on regional myocardial blood flow and function in conscious baboons.
Authors: Heyndrickx G R , Amano J , Patrick T A , Manders W T , Rogers G G , Rosendorff C , Vatner S F
Published: June 2011

The effects of coronary artery reperfusion initiated 1 hr and 3 hr after coronary artery occlusion were evaluated on measurements of overall and regional left ventricular function and on regional myocardial blood flow. These experiments were conducted in conscious baboons 2 to 3 weeks after recovery from instrumentation with a solid state left ventricular pressure gauge, aortic and left atrial catheters, a hydraulic occluder around the mid left anterior descending coronary artery, and pairs of ultrasonic transducers implanted in the endocardium of the left ventricular free wall or across the free wall to measure endocardial segment shortening and wall thickening, respectively. Coronary artery occlusion induced similar effects in both groups. At 1 hr after occlusion, the ischemic zone was characterized by severe and equal reductions in both endocardial (-97 +/- 1%) and epicardial (-95 +/- 4%) blood flows and complete loss of regional systolic function, which was replaced by paradoxical wall motion. Reperfusion initiated after 1 hr of ischemia was associated with a marked transient increase in endocardial (+386 +/- 51%) and epicardial (+544 +/- 79%) blood flows. During the subsequent 4 weeks, segment shortening and wall thickening tended to improve. However, at 4 weeks after reperfusion, segment shortening was still depressed by 45 +/- 12% and wall thickening by 58 +/- 14%. In contrast, reperfusion initiated after 3 hr of ischemia was not associated with a significant hyperemic response, and systolic segment shortening and wall thickening did not recover during the subsequent 4 week period.(ABSTRACT TRUNCATED AT 250 WORDS)
Reduction of infarct size with intracoronary perfluorochemical in a canine preparation of reperfusion.
Authors: Forman M B , Bingham S , Kopelman H A , Wehr C , Sandler M P , Kolodgie F , Vaughn W K , Friesinger G C , Virmani R
Published: June 2011

The effect of low-dose (15 ml/kg) intracoronary perfluorochemical (Fluosol-DA) on infarct size, regional myocardial blood flow, and ventricular function was studied in 20 anesthetized closed-chest dogs subjected to 11/2 hr of proximal left anterior descending occlusion. In this preparation reperfusion was simulated with fibrinolytic therapy. The animals were randomly assigned one of two treatment groups and given 15 ml/kg of either oxygenated intracoronary perfluorochemical (n = 9) or saline (n = 11). Contrast ventriculograms were obtained at baseline, 1 hr after occlusion, and at 24 hr after reperfusion and were analyzed with a radial fractional shortening method. Regional myocardial blood flow was measured with radioactive microspheres. At 24 hr the area at risk was defined in vivo with monastryl blue staining and the area of necrosis was estimated after incubation of left ventricular slices with triphenyltetrazolium chloride. No significant changes were noted in heart rate, blood pressure, pulmonary capillary wedge pressure, or dP/dt during the experimental protocol. Infarct size was significantly reduced (p less than .02) in the perfluorochemical-treated group, both when expressed as a percentage of the total left ventricular mass (7.9 +/- 1.7% vs 14.7 +/- 2.5%) and as a percentage of the area at risk (20.1 +/- 5.0% vs 46.8 +/- 8.5%). This was associated with significant improvement in fractional shortening in the jeopardized zone at 24 hr after reperfusion. Although endocardial blood flow was significantly greater in the central ischemic zone and lateral region at risk immediately after reperfusion in the perfluorochemical-treated group, no difference was found 1 hr after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Fibrinopeptide A: a marker of acute coronary thrombosis.
Authors: Eisenberg P R , Sherman L A , Schectman K , Perez J , Sobel B E , Jaffe A S
Published: June 2011

To determine whether coronary thrombosis in vivo is reflected by elevations in levels of fibrinopeptide A (FPA) in plasma, we sequentially characterized plasma FPA levels associated with evolving infarction in patients admitted to the cardiac care unit early after the onset of symptoms, in patients with transmural infarction admitted later, and in patients with nontransmural infarction. Studies were also performed in patients in whom the diagnosis of infarction was suspected but subsequently excluded. FPA values were significantly higher in patients with transmural infarction (42.3 +/- 11.2 ng/ml [mean +/- SEM], n = 53) compared with those in patients with nontransmural infarction (4.8 +/- 1.6 ng/ml, n = 17) or with those in patients in whom infarction was subsequently excluded as a diagnosis (3.5 +/- 0.6 ng/ml, n = 17, p less than .01 for both). Elevations in FPA level were greatest in patients with transmural infarction from whom samples were obtained soon after the onset of symptoms. Thus, in 39 patients from samples were obtained within 10 hr after the onset of symptoms, FPA levels were significantly higher than in 14 patients from whom samples were obtained initially more than 10 hr after the onset of symptoms (55.5 +/- 14.7 vs 4.9 +/- 1.4 ng/ml, p less than .01). In 30 of the 39 patients with evolving transmural infarction from whom samples were obtained within the first 10 hr after the onset of symptoms, the level of FPA was greater than 8 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
External noninvasive temporary cardiac pacing: clinical trials.
Authors: Zoll P M , Zoll R H , Falk R H , Clinton J E , Eitel D R , Antman E M
Published: June 2011

An external cardiac pacemaker-monitor has been developed that provides safe, effective noninvasive ventricular stimulation that is well tolerated in conscious patients and allows clear recognition of electrocardiographic response. The noninvasive temporary pacemaker (NTP) has now been applied in 134 patients in five hospitals. Stimulation was tolerated well in 73 of 82 conscious patients, and nine found it intolerable. The NTP was effective in evoking electrocardiographic responses in 105 patients; the 29 failures were in the presence of prolonged hypoxia or severe discomfort. The NTP was clinically useful in 82 patients: 43 of 86 were resuscitated from emergency or expected arrest, 38 of 40 were maintained in standby readiness for up to 1 month but did not require stimulation, and one of eight patients with tachycardia obtained some clinical benefit. The NTP was especially useful in 25 patients with complications or contraindications to endocardial pacing and in 57 patients in whom insertion of an endocardial electrode was avoided.
Coronary flow regulation in patients with ischemic heart disease: release of purines and prostacyclin and the effect of inhibitors of prostaglandin formation.
Authors: Edlund A , Berglund B , van Dorne D , Kaijser L , Nowak J , Patrono C , Sollevi A , Wennmalm A
Published: June 2011

The present investigation was undertaken to study cardiac release of adenosine and prostacyclin (prostaglandin [PG] I2) in patients with ischemic heart disease (IHD), and to assess coronary vascular resistance before and after inhibition of synthesis in such patients. In 48 patients with IHD, arterial and coronary sinus blood samples were taken at rest, during atrial pacing to angina, and after pacing. Levels of purines were determined by high-performance liquid chromatography and the PGI2 metabolite 6-keto-PGF1 alpha was measured with radioimmunoassay. Coronary sinus blood flow was determined with retrograde continuous thermodilution before and after oral administration of indomethacin, aspirin, naproxen, or ibuprofen. Atrial pacing induced myocardial ischemia, as evidenced by typical chest pain and arrested lactate extraction. Adenosine was extracted at rest, but during ischemia there was a significant release of its metabolite hypoxanthine, indicating increased myocardial breakdown of high-energy adenine nucleotides. Arterial and coronary sinus concentrations of 6-keto-PGF1 alpha were low and no significant differences between them were found. After administration of the PG-synthesis inhibitor indomethacin, coronary vascular resistance was elevated, as was the cardiac oxygen extraction. The three other PG-synthesis inhibitors (aspirin, naproxen, and ibuprofen) did not, however, induce any change in coronary vascular resistance or in the cardiac extraction of oxygen. On the basis of these data we suggest that in patients with IHD cardiac ischemia results in increased myocardial production and release of purines, cardiac ischemia does not elicit any detectable increase in coronary production of prostacyclin, and the increased coronary resistance induced by indomethacin does not reflect the involvement of locally formed PG in the maintenance of coronary flow, but is rather a direct effect of the drug.
Continuous-wave Doppler echocardiographic assessment of severity of calcific aortic stenosis: a simultaneous Doppler-catheter correlative study in 100 adult patients.
Authors: Currie P J , Seward J B , Reeder G S , Vlietstra R E , Bresnahan D R , Bresnahan J F , Smith H C , Hagler D J , Tajik A J
Published: June 2011

Studies of the correlation of aortic valve gradient determined by continuous-wave Doppler echocardiography and that determined at catheterization have, to date, involved young patients and nonsimultaneous measurements. We therefore obtained simultaneous Doppler echocardiographic and catheter measurements of pressure gradient in 100 consecutive adults (mean age 69, range 50 to 89 years). In 63 patients pressure measurements were obtained with dual-catheter techniques and in 37 they were obtained by withdrawal of the catheter from the left ventricle to the ascending aorta. Forty-six of these patients also underwent an outpatient Doppler study 7 days or less before catheterization. The simultaneous pressure waveforms and Doppler spectral velocity profiles were digitized at 10 msec intervals and maximum, mean, and instantaneous gradients (mm Hg) were derived for each. The correlation between the Doppler-determined gradient and the simultaneously measured maximum catheter gradient was r = .92 (SEE = 15 mm Hg), that between the Doppler-determined and mean catheter gradient was r = .93 (SEE = 10 mm Hg), and that between the Doppler and peak-to-peak catheter gradient was r = .91 (SEE = 14). The correlation between the nonsimultaneously Doppler-determined gradient and the maximum gradient measured by catheter was not as strong (r = .79, SEE = 24). The continuous-wave Doppler echocardiographic velocity profile represents the instantaneous transaortic pressure gradient throughout the cardiac cycle. The best correlation with continuous-wave Doppler-determined gradient was obtained with maximum and mean gradients measured by catheter. Continuous-wave Doppler echocardiography can be used to reliably predict the pressure gradient in adults with calcific aortic stenosis.
Dissociation between epicardial and transmural function during acute myocardial ischemia.
Authors: Gallagher K P , Stirling M C , Choy M , Szpunar C A , Gerren R A , Botham M J , Lemmer J H
Published: June 2011

The relationship between epicardial and transmural function (measured with sonomicrometers) was examined in 13 anesthetized open-chest dogs. Systolic wall thickening was used as a standard of integrated transmural function to compare with epicardial function measured as segment shortening parallel to surface fibers. Three levels of coronary inflow restriction were produced by using decrements in systolic wall thickening as an index of changes in the transmural distribution of myocardial blood flow (microspheres) in myocardium perfused by the left anterior descending artery (anterior-apical group, n = 7) or circumflex artery (posterior-basal group, n = 6). Levels 1 and 2 were characterized by reductions in systolic wall thickening of 35% and 80%, respectively, and marked decreases in deep myocardial blood flow. In the subepicardium, myocardial blood flow was minimally affected at levels 1 and 2 and there was no change in posterior-basal epicardial segment shortening, but anterior segment shortening decreased significantly (by 21% and 37%, respectively). At level 3 myocardial blood flow was reduced transmurally, producing systolic wall thinning and marked epicardial dysfunction in both groups. Parallel epicardial segment shortening underestimated the extent of transmural dysfunction in both groups at levels 1 and 2 but the degree of underestimation was greatest in the posterior-basal group. Anterior-apical segment shortening was impaired at levels 1 and 2, whereas posterior-basal segment shortening was unaffected, suggesting that significant regional variability exists in the epicardial response to nontransmural ischemia.
Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical ablation of the accessory pathway.
Authors: Sharma A D , Klein G J , Guiraudon G M , Milstein S
Published: June 2011

The effect of surgical ablation of ablation of atrioventricular accessory pathways on the incidence of atrial fibrillation in patients with Wolff-Parkinson-White syndrome was examined and the results of preoperative electrophysiologic testing were studied to determine factors predictive of outcome. Among 50 consecutive surgical cases, 19 patients were identified with a past history of at least one episode of spontaneous atrial fibrillation documented by electrocardiogram before surgery. The mean number of episodes of atrial fibrillation was 1.97/patient/year during a mean symptomatic period of 6.9 years before surgery. These patients were compared with 19 consecutive patients undergoing surgery during the same time period who had a history of only reciprocating tachycardia. Patients with atrial fibrillation had a significantly shorter antegrade accessory pathway effective refractory period (270 +/- 39 vs 330 +/- 107 msec; p less than .05) and much faster ventricular rates during induced atrial fibrillation (shortest RR interval 219 +/- 73 vs 294 +/- 60 msec, p less than .005; average RR interval 324 +/- 109 vs 405 +/- 127 msec, p less than .01). Patients with atrial fibrillation also had longer PA intervals (47 +/- 13 vs 37 +/- 7 msec; p less than .02). At preoperative electrophysiologic testing, 18 patients with atrial fibrillation had atrial fibrillation induced and 14 sustained the arrhythmia for longer than 10 min. In contrast, atrial fibrillation, although induced in 14 of 19 patients with reciprocating tachycardia, was not sustained in any. Thus electrophysiologic testing suggested that both accessory pathway properties and atrial vulnerability may predispose to atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
A comparison of the thrombolytic and hemorrhagic effects of tissue-type plasminogen activator and streptokinase in rabbits.
Authors: Agnelli G , Buchanan M R , Fernandez F , Boneu B , Van Ryn J , Hirsh J , Collen D
Published: June 2011

Tissue-type plasminogen activator (t-PA) is a promising thrombolytic agent because it can produce thrombolysis without inducing a plasma proteolytic state. It is uncertain if this potentially important feature renders t-PA less hemorrhagic than other plasminogen activators. We have compared the hemorrhagic and thrombolytic effects of t-PA and streptokinase in rabbits. Streptokinase, 4000 U/kg/hr over 4 hr, failed to produce significant thrombolysis and 8000 U/kg/hr streptokinase over 4 hr produced only 28 +/- 6% thrombolysis. Both streptokinase regimens were associated with a plasmin-mediated plasma proteolytic state and both streptokinase regimens produced a significant increase in hemorrhage that was evident within 15 min of beginning the infusion and was progressive over the 4 hr of drug administration. In contrast, t-PA in a dose of 7500 U/kg/hr produced 35 +/- 6% thrombolysis, but it did not produce a plasmin-mediated plasma proteolytic state or a significant increase in hemorrhage over the 4 hr of infusion. t-PA in a dose of 15,000 U/kg/hr produced 85 +/- 4% thrombolysis but was associated with a plasmin-mediated proteolytic state and produced significant bleeding which, in contrast to streptokinase-induced bleeding, was delayed in onset. Therefore, t-PA induced less hemorrhage than streptokinase at doses that produced more effective thrombolysis. Bleeding with both thrombolytic agents was associated with a plasmin-mediated proteolytic state.
The effects of premature stimulation of the His bundle on epicardial activation and body surface late potentials in dogs susceptible to sustained ventricular tachyarrhythmias.
Authors: Spear J F , Richards D A , Blake G J , Simson M B , Moore E N
Published: June 2011

Experiments were performed on 20 anesthetized dogs to determine the effects of premature stimulation of the His bundle on epicardial conduction and late potentials recorded on the body surface. Fifteen dogs underwent occlusion of the left anterior descending coronary for 2 hr followed by reperfusion, and five that did not undergo operation served as controls. Animals were studied 2 to 52 weeks after the induction of infarction, and four animals with infarction and four control animals exhibited no sustained arrhythmias in response to programmed ventricular extrastimulation. Five dogs with infarction and one control dog had ventricular fibrillation while the six remaining dogs had inducible sustained ventricular tachycardia. All animals with ventricular tachycardia had late potentials in the terminal portion of the signal-averaged body surface QRS complexes during sinus rhythm and QRS durations in the animals were 64 msec or greater. The voltage in the last 20 msec of the QRS complex was 13.5 microV or less and the duration of late activity below 30 microV was 18.2 msec or more. These values did not overlap values in animals with no inducible arrhythmias. Ventricular fibrillation was a nonspecific end point in these experiments and values overlapped those in animals with no arrhythmias and those with ventricular tachycardia. All animals with infarction and late potentials associated with their QRS complexes also had delayed and prolonged epicardial electrograms that extended into the time of the late potentials recorded from 45 standard sites in the infarcted regions. A single premature beat evoked by His bundle pacing (coupling interval of 192 to 270 msec) had no significant effect on late potentials or their relationship to epicardial activation in the area of infarct. However, changes in the durations of electrograms in response to premature beats were different in animals with infarction and ventricular tachycardia than in those with ventricular fibrillation. In animals with ventricular tachycardia, electrograms at 15 of 210 sites increased in duration by more than 10 msec while those at 61 of 210 sites decreased in duration. In animals with ventricular fibrillation, electrograms at 40 of 207 sites were of increased duration while those at 26 of 207 decreased. The decreases in duration were usually due to components of fractionated electrograms "dropping out" and likely represent local conduction block near the recording electrode.(ABSTRACT TRUNCATED AT 400 WORDS)
Collateral conductance changes during a brief coronary occlusion in awake dogs.
Authors: Brazzamano S , Fedor J M , Rembert J C , Greenfield J C
Published: June 2011

Function of the coronary collateral circulation during the course of a single abrupt coronary occlusion was evaluated in awake dogs instrumented over the long term. Studies were performed approximately 2 weeks after collateral development had been stimulated in the dogs by partial stenosis of the proximal left circumflex coronary artery. The pressure drop from the central aorta to the distal circumflex coronary artery was measured continuously. Under control conditions and at 30 sec and 4 min of a single abrupt complete circumflex occlusion, myocardial blood flow was determined by a radioactive microsphere technique. Coronary collateral conductance was calculated as mean collateral blood flow divided by the mean drop in pressure. The following was noted in dogs that developed collateral vessels: during the coronary occlusion, mean distal circumflex coronary pressure increased from 42 +/- 9 to 49 +/- 10 mm Hg (p less than or equal to .01); mean collateral flow increased from 0.78 +/- 0.30 to 0.84 +/- 0.33 ml/min/g (p less than or equal to .05); the endocardial/epicardial flow ratio increased from 0.77 +/- 0.36 to 1.04 +/- 0.25 (p less than or equal to .01); and the coronary collateral conductance increased significantly from 0.017 +/- 0.017 to 0.021 +/- 0.021 (ml/min/g)/mm Hg (p less than or equal to .005). These data suggest that during a brief occlusion of a major coronary artery, immature coronary collateral channels do not reach maximal function immediately after the occlusion. Rather, coronary collateral conductance increases with time and may be associated with improved transmural perfusion of the myocardium.
Characteristics of vascular hydraulic load in patients with heart failure.
Authors: Laskey W K , Kussmaul W G , Martin J L , Kleaveland J P , Hirshfeld J W , Shroff S
Published: June 2011

Aortic input impedance and hydraulic power were derived from simultaneous catheter recordings of ascending aortic pressure and velocity in eight normal subjects and 11 age-matched subjects with clinical heart failure secondary to idiopathic congestive cardiomyopathy. Resting data revealed the characteristic depression of cardiac output and elevation of systemic vascular resistance in patients with heart failure. The pulsatile component of vascular hydraulic load, characteristic impedance (Zc), was similar in both groups (Zc normal: 85 +/- 30 dyne-sec-cm-5; Zc cardiomyopathy: 93 +/- 33 dyne-sec-cm-5). The oscillatory fraction of aortic input power in patients with heart failure (14 +/- 4%) was also similar to that of normal subjects (11 +/- 2%). The transition from rest to exercise in patients with heart failure was marked by a decrease in the steady component of arterial hydraulic load, although characteristic impedance did not change. A similar qualitative response occurred in normal subjects, although the systemic vascular resistance during exercise remained above normal in patients with heart failure. The modulus of the first harmonic of impedance significantly decreased during exercise in normal subjects but did not change significantly in patients with heart failure. Furthermore, the modulus of the first harmonic of the reflection coefficient decreased significantly during exercise in normal subjects but did not change in patients with heart failure in spite of systemic vasodilation. Exercise appears to impose no additional increase in vascular hydraulic load on the ejecting left ventricle. The similar aortic characteristic impedances in patients with heart failure and in normal subjects, at rest and during exercise, are consistent with a constant oscillatory fraction of input power.
Local changes in myosin types in diseased human atrial myocardium: a quantitative immunofluorescence study.
Authors: Bouvagnet P , Léger J , Dechesne C A , Dureau G , Anoal M , Léger J J
Published: June 2011

Two monoclonal antibody groups were prepared from adult human atrial and ventricular myosin heavy chains. Using these two groups, we were able to identify two myosin variants in human atria and to classify human atrial fibers into alpha-, mixed, or beta-fibers according to the reactivity of the two monoclonal antibody groups to alpha- and beta-myosin heavy chains of normal young and hypothyroid rat ventricles, respectively. The alpha-fiber percentage of the left atria in two normal human hearts was 15% higher than in the right atria. The auricles contained two to three times more alpha-fibers than beta-fibers, whereas the proportion was reversed in the crista terminalis. The mean fiber diameter of the alpha- and beta-fibers was 13.6 +/- 3 micron. A complete alpha- to beta-fiber transition was observed in all atrial regions of two hearts with severe ventricular myocardial infarction; a moderate alpha- to beta-fiber transition was observed only in the left atria of two hearts with primary congestive cardiomyopathy. The mean diameters of the two fiber types were significantly increased in all diseased hearts (19 +/- 3.8 micron). We hypothesize that pressure overload and increased wall tension successively induce an enlargement of the fiber diameter and an alpha- to beta-myosin transition.
Left ventricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiography: quantitative assessment of aneurysm size in relation to clinical course.
Authors: Matsumoto M , Watanabe F , Goto A , Hamano Y , Yasui K , Minamino T , Abe H , Kamada T
Published: June 2011

A retrospective study was performed to elucidate the process of left ventricular aneurysm formation and its influence on left ventricular enlargement based on serial two-dimensional echocardiographic observations from 150 consecutive patients with first acute anterior myocardial infarction. Echocardiograms were available and interpretable through the entire period of observation in 68 patients. Because of early death in 13 patients, echocardiograms of 55 patients, 22 with and 33 without aneurysm, were analyzed from 1 to 28 days after infarction. Patients with aneurysms were separated into two groups with large (group 1, 11 patients) and small aneurysms (group 2, 11 patients) on the basis of ratios of aneurysm to overall left ventricular circumferential length [Lcf-LV(RAO)] and area [Area-LV(RAO)], i.e., Lcf(An/LV)-RAO and Area(An/LV)-RAO, respectively, in the right anterior oblique equivalent view at the time of aneurysm formation, with reference to Forrester's subset. Group 1 consisted of patients with Lcf(An/LV)-RAO of 0.4 or greater or Area(An/LV)RAO of 0.3 or greater while group 2 included patients with Lcf(An/LV)-RAO less than 0.4 or Area(An/LV)-RAO less than 0.3. In the test for time trend in these groups with a one-way analysis of variance, Lcf-LV in RAO equivalent and apical four-chamber views and Area-LV in apical four-chamber view effectively separated group 1 from groups 2 and 3 (without aneurysm) with significance (p less than .005, p less than .01, and p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Quantification of myocardial infarction: a comparison of single photon-emission computed tomography with pyrophosphate to serial plasma MB-creatine kinase measurements.
Authors: Jansen D E , Corbett J R , Wolfe C L , Lewis S E , Gabliani G , Filipchuk N , Redish G , Parkey R W , Buja L M , Jaffe A S
Published: June 2011

Single photon-emission computed tomography (SPECT) with 99mTc-pyrophosphate (PPi) has been shown to estimate size of myocardial infarction accurately in animals. We tested the hypothesis that SPECT with 99mTc-PPi and blood pool subtraction can provide prompt and accurate estimates of size of myocardial infarction in patients. SPECT estimates are potentially available early after the onset of infarction and should correlate with estimates of infarct size calculated from serial measurements of plasma MB-creatine kinase (CK) activity. Thirty-three patients with acute myocardial infarction and 16 control patients without acute myocardial infarction were studied. Eleven of the patients had transmural anterior myocardial infarction, 16 had transmural inferior myocardial infarction, and six had nontransmural myocardial infarction. SPECT was performed with a commercially available rotating gamma camera. Identical projection images of the distribution of 99mTc-PPi and the ungated cardiac blood pool were acquired sequentially over 180 degrees. Reconstructed sections were color coded and superimposed for purposes of localization of infarct. Areas of increased PPi uptake within myocardial infarcts were thresholded at 65% of peak activity. The blood pool was thresholded at 50% and subtracted to determine the endocardial border for the left ventricle. Myocardial infarcts ranged in size from 1 to 126 gram equivalents (geq) MB-CK. The correlation of MB-CK estimates of size of infarct with size determined by SPECT (both in geq) was good (r = .89 with a regression line of y = 13.1 + 1.5x).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of cyclooxygenase inhibition on vasomotion of proximal coronary arteries with endothelial damage.
Authors: Lane G E , Bove A A
Published: June 2011

Vasomotion of the proximal branches of the left coronary artery was studied in an intact anesthetized canine preparation after injury to the endothelium of the left anterior descending branch of the left coronary artery (LAD) with a balloon angioplasty catheter. The dimensions of the left coronary artery were examined by quantitative angiography and LAD flow was measured by determining intracoronary 133Xe washout. Thirty minutes after endothelial damage alone dimensions of the LAD remained unchanged. In five dogs continued observation for a total of 120 min revealed no significant change in dimensions of the LAD. In another group of five dogs, after the administration of 5 mg/kg indomethacin there was a progressive reduction in cross-sectional area of the LAD by 60, 90, and 105 min (37%, 42%, and 50%, respectively, p less than .05). No significant change in the dimensions of the undamaged left circumflex artery was noted after the administration of indomethacin. The effect of another cyclooxygenase inhibitor (4 mg/kg meclofenamate) on endothelial damage to the LAD in an additional four dogs was also examined. Again significant reduction of the cross-sectional area of the LAD was seen at 60 and 120 min (40% and 44%, respectively, p less than .05). Heart rate and blood pressure were unchanged throughout the experiment in control and indomethacin-treated dogs. Mean blood pressure rose slightly after administration of meclofenamate (from 80 +/- 5 to 98 +/- 7 at 120 min, p less than .05). These data indicate that the combination of endothelial injury and cyclooxygenase inhibition with indomethacin or meclofenamate results in proximal coronary artery vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
Abnormal distribution of pulmonary blood flow after the Glenn shunt or Fontan procedure: risk of development of arteriovenous fistulae.
Authors: Cloutier A , Ash J M , Smallhorn J F , Williams W G , Trusler G A , Rowe R D , Rabinovitch M
Published: June 2011

Since the Fontan procedure results in low pulsatile pulmonary blood flow similar to that seen in patients with a Glenn shunt, it may also be associated with abnormal distribution of flow to the lower lung lobes and with the development of pulmonary arteriovenous fistulae (PAVF). In 12 patients 0.8 to 4.5 years after Fontan procedure and in 20 patients 0.2 to 18 years after receipt of Glenn shunts we assessed ventilation (with 133Xe) and perfusion (after a peripheral injection of 99mTc-macroaggregated albumin) to compare upper to lower lobe distribution of blood flow with that in a control group. The presence of PAVF was assessed by radionuclide activity in kidneys and the brain and by a two-dimensional echocardiographic contrast study. A decreased upper/lower lobe perfusion ratio was noted in 13 of 20 patients with Glenn shunts (65%) and correlated with the time after surgery (p less than .05). Despite the shorter follow-up period, two of 12 (16%) patients who had undergone the Fontan procedure also had a decreased upper/lower lobe perfusion ratio, and one of these developed right heart failure. Brain and kidney radionuclide counts above control values were observed in all patients with Glenn shunts and in 11 of 12 patients who had the Fontan operation. However, in only five of 20 (25%) patients with Glenn shunts were PAVF confirmed by the two-dimensional echocardiographic contrast study. Three of the five patients with PAVF had Glenn shunts of long duration.(ABSTRACT TRUNCATED AT 250 WORDS)
Programmed ventricular stimulation in survivors of an acute myocardial infarction.
Authors: Roy D , Marchand E , Théroux P , Waters D D , Pelletier G B , Bourassa M G
Published: June 2011

The prognostic significance of programmed ventricular stimulation and its usefulness in relation to other forms of invasive and noninvasive testing was evaluated in 150 survivors of acute myocardial infarction. Ventricular tachyarrhythmias of 6 beats or more were induced in 35 (23%) patients. No significant differences existed between patients with inducible ventricular tachyarrhythmias and those without inducible ventricular tachycardia with respect to occurrence of spontaneous ventricular arrhythmias in the acute and early recovery phase of infarction or predischarge exercise-induced ischemia or arrhythmias, severity of coronary artery disease, or degree of left ventricular dysfunction. A higher incidence of inferior myocardial infarction was observed in patients with inducible ventricular tachycardia when compared with those without inducible ventricular tachycardia (66% vs 41%, p less than .01). During a mean follow-up of 10 +/- 5 months (range 2 to 19), there were two sudden deaths, three nonsudden deaths, and two additional patients developed sustained ventricular tachyarrhythmias. There was no significant difference between patients with and those without inducible ventricular tachyarrhythmias with respect to the occurrence of these events. In this study population, a lower mean ejection fraction (p less than .01), the presence of a ventricular aneurysm (p less than .05), and exercise-induced ventricular premature contractions (p less than .05) were predictors of sudden death and of spontaneous ventricular tachycardia. Thus, the findings of this study do not support the hypothesis that the induction of ventricular tachyarrhythmias in patients recovering from acute myocardial infarction identifies a group at high risk for sudden cardiac death.
Change in ventricular cavity size: differential effects on QRS and T wave amplitude.
Authors: Feldman T , Childers R W , Borow K M , Lang R M , Neumann A
Published: June 2011

Although many factors have been reported to change the R wave amplitude of the electrocardiogram (ECG), few observations have been made of the associated changes in T wave amplitude. We hypothesized that changes in R and T wave amplitude should parallel each other. To test this hypothesis, R and T wave amplitudes were measured in 15 normal subjects during increased and decreased left ventricular dimensions induced by infusion of methoxamine and by Valsalva maneuver, respectively, as well as during changes in the proximity of the left ventricle to the chest wall (i.e., shift in patient position from supine to left lateral position). Simultaneous nine-lead ECGs and two-dimensional-guided M mode echocardiograms of the left ventricle were recorded at rest and under each experimental condition. R wave amplitude increased as the left ventricular lateral wall moved closer to the V5 and V6 electrodes. Alterations in R wave amplitude seen with changes in left ventricular chamber size were primarily caused by radial movement of the left ventricle in relation to the chest wall. Proximity of the left ventricle to the chest wall was therefore a major determinant of R wave amplitude. In contrast, T wave amplitude varied directly with alterations in left ventricular chamber size but was unaffected by changes in proximity to the recording electrode on the chest wall. Left ventricular chamber size, and possibly the associated alteration in endocardial-to-epicardial surface area ratio, appeared to be the major determinants of T wave amplitude.
Are right and left ventricular ejection fractions equal? Ejection fractions in normal subjects and in patients with first acute myocardial infarction.
Authors: Marving J , Høilund-Carlsen P F , Chraemmer-Jørgensen B , Gadsbøll N
Published: June 2011

Right and left ventricular ejection fractions (RVEF and LVEF) were determined by radionuclide imaging in 37 normal subjects and 37 patients by means of (1) the traditional way of calculating ejection fraction from first-pass time-activity curves of each ventricle generated from a single fixed ventricular region of interest, (2) dual first-pass time-activity curves generated from the end-diastolic and end-systolic regions, respectively, and (3) the multigated equilibrium method, also applying separate regions in end-diastole and end-systole for each ventricle. Values for RVEF measured by method 2 were significantly higher than values obtained by methods 1 and 3. In normal subjects, the values for RVEF measured by method 2 were equal to the values for LVEF determined by either this method or the equilibrium technique. Methods 1 and 3 had a tendency for underestimation of RVEF, probably because of inclusion of right atrial activity into the right ventricular region of interest. Methods 2 and 3 were applied to measure RVEF and LVEF, respectively, in 153 patients in the second week after first acute myocardial infarction. Among these, 25% had normal ejection fractions, 47% had a decrease in only LVEF, 8% a decrease in only RVEF, and 20% a decrease in both RVEF and LVEF.
The accuracy of Doppler ultrasound measurement of pressure gradients across irregular, dual, and tunnellike obstructions to blood flow.
Authors: Teirstein P S , Yock P G , Popp R L
Published: June 2011

The accuracy of Doppler-estimated pressure gradients in the setting of irregular, multiple, and tunnellike stenoses was investigated. An in vitro model of the left ventricular outflow tract was designed to allow pulsatile flow of red cells in saline across valve orifices from 0.01 to 2.5 cm2. Simultaneous pressure gradients were estimated by both Doppler and direct-pressure manometer techniques. Gradients obtained by the two methods correlated well for valve areas in the range of clinical stenoses at pressure gradients of 10 to 150 mm Hg (r = .97 to .99). Model valves were constructed with a large orifice (0.75 to 1.25 cm2) placed beside a small orifice (0.02 to 0.25 cm2) in the same outflow tract. A distinct jet was recorded when the Doppler transducer was aligned with each orifice. Doppler-estimated gradients for each pair of large and small orifices were identical and correlated well with those measured by manometer (r = .97 to .99). Irregularly shaped orifices also provided good correlation between the two methods (r = .98 to .99). Pulsatile flow was generated through long tunnellike obstructions with cross-sectional areas varying from 0.06 to 1.25 cm2. Tunnel length varied from 0.1 to 4 cm. Tunnel areas above 0.25 cm2 gave good Doppler-to-manometer correspondence at all tunnel lengths. Doppler underestimated manometer-determined values in the 0.25 cm2 tunnel by 8% at 3 cm and by 15% at 4 cm. In the 0.06 cm2 tunnel, Doppler underestimated manometer gradients by 12%, 15%, 32%, and 42% at lengths of 1, 2, 3, and 4 cm, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Patterns of myoglobin release after reperfusion of injured myocardium.
Authors: Ellis A K , Little T , Zaki Masud A R , Klocke F J
Published: June 2011

Myoglobin is an intracardiac protein that is released into the blood after myocardial injury and is then cleared rapidly by the kidneys. This study was undertaken to determine whether successful reperfusion of damaged myocardium could be assessed by examination of blood myoglobin concentration-time patterns. After release of a 2 hr occlusion of the mid left anterior descending coronary artery in 11 dogs that had been instrumented over the long term, immunoreactive arterial plasma concentration of myoglobin, [Mb], rose rapidly to a peak within 25 +/- 2(SEM) min (range 20 to 40). Individual peaks were three to 165 times the myoglobin levels immediately before release of the occlusion. Myoglobin was cleared rapidly from plasma, falling to one-half its peak level 38 +/- 3 min after the peak. Similarly well-defined peaks in [Mb] were evident in plasma from the great cardiac vein (GCV), with a mean time to peak of 16 +/- 2 min and a magnitude of two to 177 times prerelease values. In contrast, arterial and GCV creatine kinase activity-time curves showed less defined peaks and they occurred later and with more variability (60 to 330 min after reperfusion). In nine patients with acute infarction, successful coronary artery reopening was also accompanied by a sharp four- to sixteenfold rise in plasma [Mb] within 1 to 2 hr. Elevations in plasma creatine kinase were slower and more prolonged, peaking at 2 to 18 hr.(ABSTRACT TRUNCATED AT 250 WORDS)
The superiority of maximum fiber elastance over maximum stress-volume ratio as an index of contractile state.
Authors: Wisenbaugh T , Yu G , Evans J
Published: June 2011

The end-systolic pressure-volume relationship has been used as a load-independent measure of ventricular pump performance. Since comparisons of load between ventricles of different size and thickness may be more accurately made with measurements of wall stress than with those of pressure, the end-systolic stress-volume relationship at one or more levels of end-systolic stress has been used to estimate contractile function in hypertrophied ventricles. Linear regression of end-systolic stress against end-systolic volume for differently loaded beats has a slope termed maximum fiber elastance (fiber Emax) and a volume intercept termed Vo; the maximum stress-volume ratio (MSVR) for a single beat is an approximation of fiber Emax but assumes Vo = 0. However, the influence of preload, afterload, and inotropic state on these indexes has not been examined. We therefore studied the stress-volume relationship in seven open-chest dogs instrumented with ultrasonic crystals and micromanometers. Postextrasystolic potentiation (PESP) increased both the MSVR (5.7 +/- 1.83 vs 4.85 +/- 1.43 at control, p less than .05) and fiber Emax (13.93 +/- 3.24 vs 9.24 +/- 2.15 at control; p less than .05). Augmentation of preload by infusion of dextran, with the use of nitroprusside to maintain afterload relatively constant, did not significantly influence either the MSVR or fiber Emax. Vo was not significantly influenced by PESP, but was shifted to higher values by augmentation of preload (17.5 +/- 14.8 vs 13.9 +/- 11.1 ml at control; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)