bluuebunny/crossref_metadata_2025 huggingface dataset:
Improved accuracy of echocardiographic endocardial borders by spatiotemporal filtered Fourier reconstruction: description of the method and optimization of filter cutoffs.
Authors: Thomas J D , Hagege A A , Choong C Y , Wilkins G T , Newell J B , Weyman A E
Published: June 2011

The usefulness of digitized echocardiographic borders in quantitative regional left ventricular function analysis has been limited by the wide reported range for normal wall motion with this technique. We postulated that random error in endocardial border positioning is a major cause of this limitation. To test this hypothesis, we traced the endocardial borders field by field from 17 complete echocardiographic cycles in six dogs. These cycles showed a great deal of random movement, with each endocardial point reversing its motion an average of 18.5 times per cardiac cycle. Spatiotemporal Fourier analysis of these sequences demonstrated that most of the valid information on endocardial motion was contained in the first four temporal harmonics and the first seven spatial harmonics and that beyond these points the Fourier transform has the spectral characteristics of noise. Reconstruction of these 17 cycles eliminating all Fourier components above the sixth temporal and eighth spatial harmonics reduced the mean number of endocardial reversals per cycle to 2.3 (p less than .00001). To derive the optimal temporal and spatial cutoffs, we compared reconstructions of each of the 17 cycles with three M mode echocardiograms obtained simultaneously with the cross-sectional images. Fourier cutoffs were varied between two and 20 harmonics and demonstrated that the optimal temporal cutoff was 5.5 harmonics and optimal spatial cutoff 6.9. With optimal filtering, the correlation between ventricular diameter derived from the M mode and from the cross-sectional images was r = .965, compared with .877 for the M mode vs unfiltered cross-sectional data (p less than .0001). We conclude that two-dimensional filtered Fourier reconstruction significantly improves the accuracy of traced echocardiographic borders. This technique should be useful in the postprocessing of endocardial borders extracted by automated edge detection schemes and should also be applicable to cardiac images derived from modalities other than echocardiography.
Quantitative assessment of regional left ventricular function by densitometric analysis of digital-subtraction ventriculograms: correlation with myocardial systolic shortening in dogs.
Authors: Chappuis F , Widmann T , Guth B , Nicod P , Peterson K L
Published: June 2011

Conventional wall motion analysis of contrast ventriculograms assesses only that part of the wall that is tangential to the x-ray beam. To assess regional left ventricular function in three dimensions, a new computerized method based on densitometric analysis of digital subtraction left ventriculograms was developed and validated in nine open-chest dogs instrumented with a circumflex coronary artery occluder and sonomicrometers in the anterior and posterior walls. Each dog underwent digital subtraction ventriculography at baseline and at five levels (I to V) of dysfunction of the inferior wall induced by progressive stenoses of the circumflex coronary artery. The ventriculogram was divided into six segments around the end-diastolic center of gravity. Time-volume curves were obtained by densitometry in the normal anterior and ischemic inferior segments containing the sonomicrometers. From these curves, regional ejection fraction (R-EF), regional peak ejection rate (R-PER), and regional phase (R-PH) and amplitude (R-AMP) of the first Fourier harmonic were derived. From baseline to level V of dysfunction, myocardial systolic shortening determined by sonomicrometry decreased by 124 +/- 34% of control (mean +/- SD; p less than .001) in the ischemic wall, while it increased by 12 +/- 19% (NS) in the normal wall. At the same time, R-EF, R-PER, and R-AMP decreased in the ischemic segment by 65 +/- 12%, 46 +/- 30%, and 45 +/- 15% of control, respectively (all p less than .01), while they remained unchanged or increased in the normal segment. R-PH was delayed by 14 +/- 5% (p less than .01) in the ischemic segment, but remained unchanged in the normal segment, reflecting the asynchrony of regional left ventricular contraction during ischemia. Densitometric indexes of regional function correlated well with sonomicrometric systolic shortening both in normal and ischemic segments, with r values of .84 for R-EF, .80 for R-AMP, .64 for R-PER, and .55 for R-PH (all p less than .0001). Thus, densitometric analysis of digital subtraction left ventriculograms allows three-dimensional assessment of the extent, velocity, and synchrony of regional left ventricular contraction. Densitometric indexes of regional contraction correlate well with direct measurements of myocardial systolic shortening and are useful in quantitating regional left ventricular dysfunction.
Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics.
Authors: Ohe T , Shimomura K , Aihara N , Kamakura S , Matsuhisa M , Sato I , Nakagawa H , Shimizu A
Published: June 2011

Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.
Entrainment of ventricular tachycardia: explanation for surface electrocardiographic phenomena by analysis of electrograms recorded within the tachycardia circuit.
Authors: Almendral J M , Gottlieb C D , Rosenthal M E , Stamato N J , Buxton A E , Marchlinski F E , Miller J M , Josephson M E
Published: June 2011

Transient entrainment was demonstrated during 59 pacing events in 18 episodes of sustained uniform ventricular tachycardia (VT) while recording electrograms from the site of origin of tachycardia (LE-SOO). During entrainment, the morphology of the initial component of the LE-SOO was identical to the morphology observed during the tachycardia in 13 VTs (group I), but in five VTs (group II), the initial component changed at a "critical" paced cycle length. The presence of the proposed surface electrocardiographic criteria for entrainment--fixed fusion and a first postpacing complex without fusion but occurring at the paced cycle length--were integrally dependent on the morphologic changes in the local presystolic electrogram. Fixed fusion of the surface electrocardiogram at one or more paced cycle lengths was detected during entrainment at 35 of 59 paced cycle lengths in 12 of 18 tachycardias, 10 of which were group I and two of which were group II VTs. Fixed fusion demonstrated by analysis of the LE-SOO was observed at one or more pacing cycle lengths in 17 of 18 VTs. In five tachycardias in which surface electrocardiographic fusion was not observed, fixed fusion was evident on analysis of the left ventricular LE-SOO during right ventricular pacing. The first postpacing interval, as measured at the surface electrocardiogram, was consistently equal to the paced cycle length in only one of 18 tachycardias and was greater than the VT cycle length in eight of 17 tachycardias. A pathway with a long conduction time was demonstrated during entrainment. However, in those 12 VTs in patients in whom pacing was performed at more than one cycle length and there was preservation of the LE-SOO morphology, the conduction time between the stimulus and presystolic electrogram remained constant. Thus, no evidence for "atrioventricular nodal-like" decremental conduction was observed over a wide range of pacing cycle lengths. We conclude that: (1) two of the previously proposed criteria for diagnosis of entrainment (fixed fusion on the surface electrocardiogram and a first postpacing interval equal to the paced cycle length) are overly restrictive criteria for definition of "entrainment" of VT, (2) analysis of endocardial recordings from the site of origin of tachycardia during attempted entrainment of VT is useful for documenting the presence of entrainment, and (3) such analysis provides a basis for the understanding of surface electrocardiographic phenomenon associated with entrainment.
Resetting of ventricular tachycardia with electrocardiographic fusion: incidence and significance.
Authors: Rosenthal M E , Stamato N J , Almendral J M , Gottlieb C D , Josephson M E
Published: June 2011

The incidence and significance of fusion of the QRS complex during resetting of sustained ventricular tachycardias (VTs) was determined in 53 VTs induced by programmed stimulation in 46 patients with prior myocardial infarction. All 53 VTs were reset with one or two extrastimuli delivered at the right ventricular apex (RVA); 29 (54.7%) demonstrated fusion of the VT QRS complex coincident with the extrastimulus resetting the VT. Activation time at the RVA during VT (measured from the onset of the VT QRS complex to the first rapid deflection of the RVA electrogram) was longer in VT reset with fusion compared with those without fusion (91 +/- 30 vs 33 +/- 32 msec; p less than .001). A right bundle branch block VT QRS morphology and a rightward and inferior axis were more common in VT reset with electrocardiographic (ECG) fusion. Additionally, the shortest return cycle following the extrastimulus resetting the VT was shorter in VT reset with ECG fusion compared with those without (327 +/- 66 vs 423 +/- 84 msec; p less than .001). Fusion of the endocardial electrogram recorded at the site of VT origin was noted in 11 of 15 VTs that were reset while a recording catheter was positioned at this site, including all eight VTs with evidence of surface ECG fusion and three of seven VTs without fusion. Seventeen VTs were reset from the right ventricular outflow tract as well as the RVA; eight demonstrated QRS fusion at both sites, five from the right ventricular outflow tract only, and four from neither site.(ABSTRACT TRUNCATED AT 250 WORDS)
Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation.
Authors: de Bakker J M , van Capelle F J , Janse M J , Wilde A A , Coronel R , Becker A E , Dingemans K P , van Hemel N M , Hauer R N
Published: June 2011

In this report we describe electrophysiologic and histologic findings in hearts and endocardially resected preparations from patients with sustained ventricular tachycardias in the chronic phase of myocardial infarction. We recorded simultaneously from 64 endocardial sites during tachycardia in 72 patients that were operated on for medically intractable ventricular tachycardias. Two other patients underwent heart transplantation, and mapping was performed on the explanted isolated heart connected to a Langendorff perfusion set-up. During operation 139 tachycardias with different morphologies could be induced. Although the majority of evidence supports the concept of a reentrant mechanism for these tachycardias, we found that 105 tachycardias appeared to arise at a focal area of less than 1.4 cm2. In only three cases macroreentry around the infarction scar could be detected. Of 21 tachycardias in which the "origin" appeared to be focal, earliest subendocardial activation was preceded by discrete electrograms of low amplitude (presystolic activity). In three tachycardias presystolic activity was detected at several sites, permitting reconstruction of its route. Histology of the endocardial resected preparation in one of these cases revealed separate zones of viable myocardial fibers in areas in which presystolic activity was recorded. These zones were located intramurally and subendocardially, supporting the concept that reentry occurred via isolated bundles of surviving myocytes at the border of the infarct and the larger subendocardial muscle mass. Conduction velocity through the isolated tracts was on the order of 25 cm/sec. Similar reentrant pathways were found in the two isolated hearts. Extracellular and intracellular recordings were made from 20 endocardial preparations that were excised from areas in which tachycardia originated. Preparations were superfused in a tissue bath. These experiments showed that action potentials were usually close to normal, but occasionally action potentials with reduced amplitude and slow upstrokes were found. In addition, there were cells that exhibited both fast and slow upstrokes, depending on the direction of the wavefront. Histology of seven resected preparations and the isolated hearts showed subendocardially as well as intramurally located zones of viable myocardium. Fractionation of extracellular electrograms and slow conduction were found in areas where surviving muscle fibers and strands of fibrous tissue were interwoven, and in zones where muscle fibers were oriented in parallel but isolated by strands of connective tissue.(ABSTRACT TRUNCATED AT 400 WORDS)
Mediation of reocclusion by thromboxane A2 and serotonin after thrombolysis with tissue-type plasminogen activator in a canine preparation of coronary thrombosis.
Authors: Golino P , Ashton J H , Glas-Greenwalt P , McNatt J , Buja L M , Willerson J T
Published: June 2011

Human recombinant tissue-type plasminogen activator (rt-PA) has been shown to be an effective and safe agent for coronary thrombolysis in patients with acute myocardial infarction. However, thrombolysis is associated with a high rate of acute reocclusion after discontinuation of rt-PA. The goals of the present study were to assess whether reocclusion after thrombolysis is caused by intracoronary platelet aggregation and to determine the role of thromboxane A2 (TxA2) and serotonin (5HT) in mediating this phenomenon. Accordingly, coronary thrombosis was induced in anesthetized, open-chest dogs by insertion of a copper coil into the left anterior descending coronary artery (LAD). LAD blood flow was monitored throughout the experiment by means of a Doppler flow probe placed proximally to the coil. Thrombolysis was achieved with rt-PA (0.05 mg/kg bolus + micrograms/kg/min infusion) in 23 +/- 3 min. rt-PA was then discontinued and each animal received a bolus of heparin (150 U/kg) every hour. Reperfusion was followed by repeated cycles of gradual occlusions followed by spontaneous restorations of blood flow (cyclic flow variations, CFVs) before a persistent occlusion recurred. In control dogs (n = 6), heparin alone did not prevent CFVs and reocclusion time was 25 +/- 4 min. Administration of an intravenous bolus of 0.2 +/- 0.06 mg/kg SQ29548, a TxA2/prostaglandin H2-receptor antagonist, and an intravenous bolus of 0.2 +/- 0.04 mg/kg ketanserin, a 5HT2-receptor antagonist, completely abolished CFVs in six of six dogs and reocclusion time was greater than 158 +/- 14 min (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias.
Authors: Garan H , McGovern B A , Canzanello V J , McCauley J , Bodvarsson M , Harrington J T , Madias N E , Newell J B , Ruskin J N
Published: June 2011

The effect of potassium ion (K+) depletion on postmyocardial infarction ventricular arrhythmias was investigated in 32 dogs: 12 control animals, 10 animals that ate a diet extremely low in K+ for 15 days, and 10 others that, in addition to dietary K+ deprivation, received 50 mg of hydrochlorothiazide four times. The experimental myocardial infarction was created by proximal left anterior descending coronary artery ligation. In a subgroup of 24 animals selected for relatively uniform size of myocardial infarction (14% to 22% of left ventricular mass), eight animals with mean cumulative K+ balance of -4.01 +/- 2.19 meq/kg developed spontaneous ventricular fibrillation within 4 to 17 min of coronary ligation, whereas 16 animals with a mean cumulative K+ balance of -0.11 +/- 1.82 meq/kg didn't. By univariate analysis cumulative K+ deficit (p = .001) and plasma K+ concentration (p = .039) correlated significantly with spontaneous ventricular fibrillation. Multivariate analysis of the entire population of 32 animals identified cumulative K+ deficit and size of myocardial infarction as the only independent predictors of ventricular fibrillation. Cumulative K+ deficit was also an independent predictor of ventricular fibrillation induced by programmed cardiac stimulation in the conscious state 1 day after myocardial infarction.
Comparative clinical and electrophysiologic effects of adenosine triphosphate and verapamil on paroxysmal reciprocating junctional tachycardia.
Authors: Belhassen B , Glick A , Laniado S
Published: June 2011

The efficacy, electrophysiologic effects, and side effects of adenosine triphosphate (ATP) and verapamil in the short-term management of paroxysmal reciprocating junctional tachycardia (PRJT) were compared in 20 patients. All patients had inducible sustained PRJT during control electrophysiologic study. Fourteen patients had PRJT involving a retrograde accessory pathway, and six patients had atrioventricular (AV) nodal reentrant tachycardia ("slow-fast" type). ATP, which has a very short half-life, was first administered (10 mg iv over 1 sec) during sustained PRJT. If PRJT did not terminate within 2 min, a bolus of 20 mg ATP was given. Verapamil (5 mg iv over 15 sec) was subsequently administered during sustained PRJT, and if the latter did not terminate within 3 min another bolus of 5 mg verapamil was given. The cycle lengths of PRJT before administration of 10 or 20 mg ATP and 5 mg verapamil were similar. The 10 mg dose of ATP terminated PRJT in 17 of the 20 patients, and 20 mg ATP was required to terminate PRJT in the three remaining patients. The 5 mg dose of verapamil terminated PRJT in 15 patients, whereas an additional bolus of 5 mg terminated PRJT in one of the remaining five patients. The overall efficacy of ATP (20/20, 100%) was significantly greater than that of verapamil (16/20, 80%) (p less than .05); however, there was no significant difference between the conversion rate of PRJT after administration of 10 mg ATP (17/20) and 5 mg verapamil (15/20). ATP terminated PRJT more quickly than verapamil (mean 24 sec vs mean 51 sec; p less than .01). Termination of PRJT by either ATP or verapamil was mainly related to a block in the AV node in patients with accessory pathways and to a block in the antegrade slow pathway in patients with AV nodal reentry. Cycle length alternans before termination of tachycardia was observed more frequently after verapamil than after ATP (7/16 vs 1/20; p less than .01). The total incidence of transient second-degree AV nodal block and various cardiac supraventricular and ventricular arrhythmias was higher after termination of PRJT by ATP than after verapamil (17/20 vs 5/16; p less than .001). A higher incidence of transient but frequently uncomfortable noncardiac side effects was observed after ATP. We conclude that ATP (10 to 20 mg) is more effective and more rapid than verapamil (5 or 5 + 5 mg) in terminating PRJT but results in a higher incidence of cardiac and noncardiac side effects.(ABSTRACT TRUNCATED AT 400 WORDS)
Clinical implications of internal mammary artery bypass grafts: the Coronary Artery Surgery Study experience.
Authors: Cameron A , Davis K B , Green G E , Myers W O , Pettinger M
Published: June 2011

From the Coronary Artery Surgery Study Registry, all patients undergoing initial bypass surgery procedures with independent vein grafts were identified. The 950 patients receiving an internal mammary artery bypass graft were compared with the 6027 patients receiving vein graft alone. Improved survival rates with internal mammary artery grafts were noted at hospitals in which these grafts were performed infrequently as well as those in which the internal mammary artery graft was used frequently. The improved survival was noted in patients with normal (p = .004) as well as impaired (p = .004) ventricular function, in men (p = .0001) as well as women (p = .005), in patients over age 65 (p = .01) as well as younger patients (p less than .0001), and in those with (p = .05) or without (p less than .0001) critical stenosis of the left main coronary artery. The internal mammary artery bypass graft was an independent predictor of survival (p = .0004) and reduced the risk of dying by a factor of 0.64. It was concluded that the internal mammary artery graft is the bypass vessel of choice and should not be denied any subgroup.
The effect of coronary angioplasty on coronary flow reserve.
Authors: Wilson R F , Johnson M R , Marcus M L , Aylward P E , Skorton D J , Collins S , White C W
Published: June 2011

To determine the effects of coronary angioplasty on coronary flow reserve (CFR), we studied 32 patients before and immediately after single-vessel coronary angioplasty and 31 patients evaluated late after angioplasty (7.5 +/- 1.2 months, mean +/- SEM). The geometry (percent area stenosis and minimal cross-sectional area) of each lesion was determined by quantitative coronary angiography (Brown/Dodge method) and the integrated optical density was measured by videodensitometry. CFR was measured with a No. 3F coronary Doppler catheter placed immediately proximal to the lesion and a maximally vasodilating dose of intracoronary papaverine. The translesional pressure gradient was obtained in all lesions before and immediately after angioplasty and in 18 of 31 vessels late after angioplasty. CFR immediately after angioplasty returned to normal levels (greater than 3.5 peak/resting velocity ratio) in 14 of 31 patients and was improved, although not normalized, in the remaining 17 patients. CFR immediately after dilation was not significantly correlated with any of the angiographic variables of arterial stenosis nor the resting pressure gradient. Moreover, the pressure gradient and absolute distal coronary pressure at peak hyperemia were not significantly different in vessels with normal and those with abnormal flow reserve immediately after dilation, suggesting that the residual stenosis did not significantly limit hyperemia. Late after angioplasty, however, a significant relationship emerged between CFR and all four indexes of residual arterial stenosis (percent area stenosis r = .70, p less than .01; minimum arterial cross-sectional area r = .70, p less than .01; integrated optical density r = .60, p less than .01; and translesional pressure gradient r = .77, p less than .01). Furthermore, in the absence of restenosis, CFR eventually normalized in all patients. These findings demonstrate that in one-half of patients there is a transient reduction in coronary flow reserve immediately after angioplasty. In the absence of restenosis, coronary flow reserve later normalizes. Consequently, measurements of coronary flow reserve immediately after angioplasty may not reflect the eventual success of the procedure in removing physiologic obstruction to coronary blood flow.
A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion.
Authors: Henthorn R W , Okumura K , Olshansky B , Plumb V J , Hess P G , Waldo A L
Published: June 2011

Prior data pertaining to transient entrainment and associated phenomena have been best explained by pacing capture of a reentrant circuit. On this basis, we hypothesized that rapid pacing from a single site of two different constant pacing rates could constantly capture an appropriately selected bipolar electrogram recording site from one direction with a constant stimulus-to-electrogram interval during pacing at one rate, yet be constantly captured from another direction with a different constant stimulus-to-electrogram interval when pacing at a different constant pacing rate. To test this hypothesis, we studied a group of patients, each with a representative tachycardia (ventricular tachycardia, circus-movement tachycardia involving an atrioventricular bypass pathway, atrial tachycardia, and atrial flutter). For each tachycardia, pacing was performed from a single site for at least two different constant rates faster than the spontaneous rate of the tachycardia. We observed in these patients that a local bipolar recording site was constantly captured from different directions at two different pacing rates without interrupting the tachycardia at pacing termination. The evidence that the same site was captured from a different direction at two different pacing rates was supported by demonstrating a change in conduction time to that site associated with a change in the bipolar electrogram morphology at that site when comparing pacing at each rate. The mean conduction time (stimulus-to-recording site electrogram interval) was 319 +/- 69 msec while pacing at a mean cycle length of 265 +/- 50 msec, yet only 81 +/- 38 msec while pacing at a second mean cycle length of 233 +/- 51 msec, a mean change in conduction time of 238 +/- 56 msec. Remarkably, the faster pacing rate resulted in a shorter conduction time. The fact that the same electrode recording site was activated from different directions without interruption of the spontaneous tachycardia at pacing termination is difficult to explain on any mechanistic basis other than reentry. Also, these changes in conduction time and electrogram morphology occurred in parallel with the demonstration of progressive fusion beats on the electrocardiogram, the latter being an established criterion for transient entrainment.(ABSTRACT TRUNCATED AT 400 WORDS)
Characteristics and outcome of patients in whom reperfusion with intravenous tissue-type plasminogen activator fails: results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I trial.
Authors: Califf R M , Topol E J , George B S , Boswick J M , Lee K L , Stump D , Dillon J , Abbottsmith C , Candela R J , Kereiakes D J
Published: June 2011

To examine the outcome of patients with persistent coronary artery occlusion despite treatment with intravenous tissue-type plasminogen activator (t-PA), the clinical course of 96 patients with persistent occlusion after 90 min of therapy was evaluated. All patients underwent cardiac catheterization 90 min after initiation of intravenous t-PA. Immediate coronary angioplasty (PTCA) was attempted when the infarct-related artery failed to reperfuse unless the vessel was technically unsuitable or the infarct was thought to be small. No baseline differences could be found between these 96 patients and 288 patients who achieved perfusion with the same protocol. Although patients with and without successful perfusion after t-PA had similar clinical courses before cardiac catheterization, those without perfusion had more complications (ventricular fibrillation, severe bradycardia, hypotension) during catheterization. PTCA achieved reperfusion with less than 50% residual stenosis in 73% of the 86 patients in whom it was attempted, while 16% were left with a high-grade (greater than 50%) residual stenosis and PTCA failed in 11%. Mortality was highest in the nine patients with complete PTCA failure (44%), compared with a 6% mortality in the 63 patients with an insignificant residual stenosis after PTCA and a 14% mortality in the 14 patients with reperfusion, but a greater than 50% residual stenosis after PTCA. In 10 patients with small infarcts (six), unsuitable anatomy (two), or "spontaneous" drug induced (but later) opening before contemplated PTCA (two), PTCA was not attempted and no mortality occurred. The in-hospital reocclusion rate after successful PTCA was 29%, despite the use of heparin and antiplatelet agents.(ABSTRACT TRUNCATED AT 250 WORDS)
Coronary arterial thrombolysis with combined infusion of recombinant tissue-type plasminogen activator and urokinase in patients with acute myocardial infarction.
Authors: Topol E J , Califf R M , George B S , Kereiakes D J , Rothbaum D , Candela R J , Abbotsmith C W , Pinkerton C A , Stump D C , Collen D
Published: June 2011

To determine whether tissue-type plasminogen activator (t-PA) and urokinase (UK) act synergistically to achieve coronary thrombolysis, incremental doses of both drugs were infused intravenously over 60 min. In 146 consecutive patients treated 3.0 +/- 1.0 hr from symptom onset, coronary angiography was performed 90 min after the start of the infusion and at 7 days. The groups of patients treated by different dose regimen were as follows: group I, 14 patients treated with t-PA 25 mg and UK 0.5 million U; group II, 20 patients given t-PA 25 mg and UK 1.0 million U; group III, 24 patients given t-PA 1.0 mg/kg and UK 0.5 million U; group IV, 33 patients treated with t-PA 1.0 mg/kg and UK 1.0 million U; and group V, 55 patients given t-PA 1.0 mg/kg and UK 2.0 million U. In groups I and II, patency of the infarct-related vessel at 90 min was only 36% and 42%, respectively. With 1 mg/kg t-PA and increasing doses of UK (groups III to V), patency ranged from 72% to 75% (overall 73%). Repeat catheterization at 7 days demonstrated reocclusion in groups III to V in 10 of 110 (9%). The patency and reocclusion rates in groups III to V were not significantly different from those in our previous study of 386 patients treated with t-PA alone (150 mg over 6 to 8 hr). In that study the patency rate of the infarct-related vessel at 90 min was 75% (p = .66) and reocclusion occurred in 15% (p = .11).(ABSTRACT TRUNCATED AT 250 WORDS)
Distribution of extracellular potassium and its relation to electrophysiologic changes during acute myocardial ischemia in the isolated perfused porcine heart.
Authors: Coronel R , Fiolet J W , Wilms-Schopman F J , Schaapherder A F , Johnson T A , Gettes L S , Janse M J
Published: June 2011

An experimental approach is described to quantitate inhomogeneity in extracellular K concentration ([K+]out) in the presence of ischemia and to relate this inhomogeneity to the electrophysiologic changes. Extracellular potassium concentration and local direct-current electrograms from the same sites were measured in isolated perfused pig hearts with the use of multiple electrodes. Dispersion of [K+]out is described under three conditions: (1) during regional ischemia in the "central zone" and the "borderzone", (2) during global ischemia, and (3) during perfusion of the heart with a high-K perfusate. Inhomogeneity was greatest during regional ischemia, especially in the borderzone, where generally lower concentrations were measured. When during regional ischemia the normal zone was perfused with a high-K perfusate, dispersion in the ischemic borderzone diminished, and higher concentrations than in the central zone were measured. During global ischemia inhomogeneity was slightly larger than during high-K perfusion. Dispersion during the latter was considered due to experimental error. A decrease in [K+]out during regional ischemia after the initial increase was closely correlated with electrical recovery of the electrograms. This decrease occurred earlier in the borderzone than in the central zone. During ischemia [K+]out was not related to the occurrence of monophasic electrograms, which are indicative of the absence of local regenerative responses. For every single electrode position a linear relationship between TQ depression and [K+]out was found, the slope of which varied with the position of the electrode. When all sites were taken together, there was no correlation between TQ depression and [K+]out. We conclude that: (1) inhomogeneity of K+ is largest in the borderzone, (2) potassium flows from the ischemic zone into the normal zone, (3) transient electrical recovery is related to a decrease (after an initial increase) in [K+]out, which is at least partly due to a flow of K+ toward the normal zone, (4) monophasic ("block") electrograms can be recorded from intrinsically excitable tissue, (5) for every single site in the ischemic region there is a linear relationship between local [K+]out and local TQ segment depression, and (6) the degree of TQ depression at a particular site is not a reliable index of the degree of ischemic injury at that site.
Autonomic modulation of ventricular arrhythmia in cesium chloride-induced long QT syndrome.
Authors: Hanich R F , Levine J H , Spear J F , Moore E N
Published: June 2011

To evaluate autonomic influence on arrhythmogenesis in an animal preparation of triggered activity, we gave increasing doses of cesium chloride (0.125 to 5.0 mmol/kg iv) to 24 dogs distributed equally among four protocols of autonomic intervention: control, total denervation, beta-blockade, and left stellate stimulation. All dogs underwent atrioventricular node ablation followed by ventricular pacing. A left ventricular endocardial monophasic action potential (MAP) catheter allowed for detection of "MAP early afterdepolarizations" (mEAD). mEAD amplitude was measured relative to MAP amplitude. Cesium chloride (CsCl) increased both MAP duration (132% after 0.125 mmol/kg to 188% after 1.0 mmol/kg; p less than .001) and mEAD amplitude (20% after 0.125 mmol/kg to 49% after 1.0 mmol/kg; p less than .001) in a dose-dependent fashion. All dogs exhibited ventricular ectopy at roughly equivalent doses (0.88 +/- 0.5 mmol/kg). Cesium's peak effect on MAP characteristics, sinus node automaticity, and systolic blood pressure coincided with the onset of sustained ventricular tachycardia (VT). Whereas control and denervated dogs developed VT after similar doses of CsCl (1.21 +/- 0.1 vs 1.12 +/- 0.14 mmol/kg; p = NS), none of the six beta-blocked dogs developed sustained VT. Conversely, those dogs having undergone stellate stimulation developed VT after smaller doses (0.58 +/- 0.34 mmol/kg; p less than .001) and with earlier onset (12 vs 30 sec; p less than .025). After 0.5 mmol/kg of CsCl, left stellate stimulation augmented relative mEAD amplitude compared with control (51% vs 38%; p less than .001), whereas beta-blockade had little effect (39% vs 38%; p = NS). Autonomic intervention as such can affect the arrhythmogenicity of CsCl and similarly alter MAP characteristics. Furthermore, as beta-blockade can prevent sustained arrhythmia without eliminating mEADs, autonomic tone appears to modulate the expression of mEADs as sustained VT.
Anisotropic conduction and functional dissociation of ischemic tissue during reentrant ventricular tachycardia in canine myocardial infarction.
Authors: Cardinal R , Vermeulen M , Shenasa M , Roberge F , Page P , Hélie F , Savard P
Published: June 2011

We measured the conduction characteristics at the epicardial surface of the left anterior ventricular wall in the in situ canine heart before and 3 to 5 days (n = 9 dogs) after permanent occlusion of the left anterior descending coronary artery (LAD). During ventricular stimulation generating wavefronts conducted along the longitudinal or the transverse fiber direction, 61 unipolar electrograms were recorded with a fine-meshed plaque electrode. Before occlusion, the fastest conduction velocity was consistently found in a direction perpendicular to the nearby LAD segment (longitudinal direction), and the slowest velocity in a direction parallel to the LAD segment (transverse fiber direction). In 3- to 5-day-old infarct preparations, a layer of subepicardial muscle with 1 to 3 mm thickness survived over necrotic tissue. The velocities and directions of fast and of slow conduction measured in ischemic subepicardial muscle were not significantly different from preocclusion values during stimulation at a basic rate, but excitability was found to be depressed in response to premature stimuli. Premature impulses initiated in nonischemic myocardium and conducted into ischemic tissue in the longitudinal or in the transverse directions induced sustained (greater than 100 beats) monomorphic tachycardias during which figure-eight activation patterns were mapped with sock-array electrodes. During these tachycardias, the direction of the common reentrant wavefront of the figure-eight pattern was preferentially oriented along the longitudinal fiber direction, independently of the direction of the initiating impulse. When polymorphic beats were induced, tachycardia terminated spontaneously within 20 beats, or changed to a monomorphic pattern, as described above. In conclusion, the anisotropic organization of surviving subepicardial muscle overlying an infarct provides a spatial constraint that determines a preferential direction of reentrant propagation and may contribute to sustaining monomorphic tachycardia.
Arrested rotation of the outflow tract may explain double-outlet right ventricle.
Authors: Bostrom M P , Hutchins G M
Published: June 2011

In a previous study the possibility that tetralogy of Fallot and transposition of the great arteries may result of embryonic arrests in the normal rotation of the junction of the outflow tract and the great arteries was investigated. The results suggested that the development of other transposition complexes such as double-outlet right ventricle might also be related to arrests in this process of rotation. To further study this question 20 normal hearts and 15 hearts with double-outlet right ventricle obtained at autopsy were studied. The angle of the aortic-to-pulmonary valve axis relative to the inferior surface of the heart, as viewed from apex to base, was measured from postmortem radiographs. For normal hearts the mean angle was 81 +/- 7(SE) degrees. For 13 of the 15 hearts with double-outlet right ventricle the mean angle was 4 +/- 7(SE) degrees. Two hearts with double-outlet right ventricle showed markedly divergent aortic-to-pulmonary valve angles, with a mean of 228 +/- 11(SE) degrees, and were therefore grouped separately. Although direct comparison of hearts and embryos is difficult because of the differences in methods of determining angles, the valve positions in normal hearts was most similar to Carnegie stage 19, as found in an earlier study. The majority of the hearts with double-outlet right ventricle resembled stage 16 embryos. The results of this study, as well as those of the earlier studies, support the hypothesis that a spectrum of cardiac anomalies with anomalous origin of great vessels arises as arrests in the normal rotation of the semilunar valve region during embryogenesis.
Monophasic action potentials at discontinuation of cardiopulmonary bypass: evidence for contraction-excitation feedback in man.
Authors: Taggart P , Sutton P M , Treasure T , Lab M , O'Brien W , Runnalls M , Swanton R H , Emanuel R W
Published: June 2011

Mechanical dysfunction is the strongest predictor of sudden cardiac death due to arrhythmia. Contraction-excitation feedback whereby changes in myocardial length/tension influence the time course of repolarization and excitability would provide a possible mechanism. Such a relationship has been shown in animals but has yet to be demonstrated in man. A useful model for studying this relationship is provided by the process of weaning off cardiopulmonary bypass after routine coronary artery surgery. During this weaning period of approximately 1 min, the heart is converted from being partially empty and flaccid (i.e., a "nonworking" state) to being filled and stretched to support the circulation (i.e., a "working" state). Monophasic action potentials (MAPs) were recorded from the left ventricular epicardium as a measure of repolarization time in 16 patients at discontinuation of cardiopulmonary bypass. Systolic pressure was recorded from the radial artery line. Measurements were made at three stages that related to different dynamic states of the heart: (1) starting to come off bypass ("minimally working"), defined as the time of first appearance of an inflection on the arterial pressure trace indicating the start of left ventricular ejection and valve opening, when arterial pressures represent left ventricular pressure, (2) half off bypass ("partially working"), and (3) off bypass ("wholly working"). During the process of discontinuing bypass MAP duration shortened, while systolic pressure increased. MAP duration at 90% and 60% repolarization (MAP D90, MAP D60) decreased from 288.0 +/- 29.5 msec (mean +/- SEM) and 235.0 +/- 27.9 msec in the minimally working heart to 274.5 +/- 30.2 msec and 224.2 +/- 27.3 msec in the partially working heart (p less than .001), with a subsequent decrease to 261.0 +/- 28.8 and 214.0 +/- 28.7 when the heart was wholly working (p less than .001). Systolic pressure increased from 54.1 +/- 9.3 mm Hg in the minimally working heart to 65.9 +/- 13.8 mm Hg in the partially working heart (p less than .001) and subsequently increased to 75.5 +/- 13.3 mm Hg when the heart was wholly working (p less than .001). Mean heart rates did not change significantly. A strong correlation was obtained between absolute MAP duration and systolic pressure. Regression analysis revealed: MAP D90 vs systolic pressure (p less than .001) and MAP D60 vs systolic pressure (p less than .01).(ABSTRACT TRUNCATED AT 400 WORDS)
Serial changes in left ventricular relaxation and chamber stiffness after large myocardial infarction in rats.
Authors: Raya T E , Gay R G , Lancaster L , Aguirre M , Moffett C , Goldman S
Published: June 2011

To determine the time course of changes in left ventricular diastolic properties after a large myocardial infarction, we serially measured left ventricular relaxation, chamber stiffness, and the ratio of left ventricular cavity to wall volume (V/VW) after coronary artery ligation in rats. Left ventricular relaxation was measured during the occlusion and then both relaxation and chamber stiffness were measured at 3 hr, 24 hr, and 3, 5, and more than 22 days after infarction. Left ventricular pressures and left ventricular dP/dt were recorded with micromanometer-tipped catheters. Left ventricular relaxation was measured by computer digitization of the left ventricular pressure tracings and averaged over 100 to 150 cardiac cycles. Five chamber stiffness constants were calculated from pressure-volume curves that were obtained ex vivo. We found ventricular relaxation prolonged for the first hour after coronary occlusion; relaxation was maximally prolonged at 10 to 15 min after onset of occlusion. After 1 hr relaxation returned to normal. However, by 5 days ventricular relaxation was again prolonged. Left ventricular stiffness constants were increased at 3 and 24 hr, resulting in a shift of the left ventricular pressure-volume relation to the left. At 3 days after coronary artery ligation, all stiffness constants and the pressure-volume relation returned to normal. At more than 22 days the pressure-volume relation was shifted to the right and the stiffness constant for low filling pressures was decreased. V/VW was significantly decreased from 0.603 +/- 0.021 at 3 and 24 hr to 0.379 +/- 0.024 and 0.362 +/- 0.032, respectively. V/VW was significantly increased at more than 22 days (0.921 +/- 0.094).(ABSTRACT TRUNCATED AT 250 WORDS)
Long-term prognosis for patients with variant angina and influential factors.
Authors: Yasue H , Takizawa A , Nagao M , Nishida S , Horie M , Kubota J , Omote S , Takaoka K , Okumura K
Published: June 2011

Two hundred forty-five patients with variant angina were followed for an average of 80.5 months (range, 36-184 months). Survival rate at 1, 3, 5, and 10 years was 98%, 97%, 97%, and 93%, respectively. Survival rate without myocardial infarction at 1, 3, 5, and 10 years was 86%, 85%, 83%, and 81%, respectively. By univarite analysis, ST segment elevation in both the anterior and inferior electrocardiographic leads was the most important factor influencing survival, followed by use of calcium antagonists, left ventricular function, smoking, and alcohol intake. The variables that significantly correlated with survival without myocardial infarction were use of calcium antagonists, left ventricular function, extent and severity of coronary artery disease, coronary artery bypass surgery, and disease activity. Multivariate analysis using the Cox proportional hazards model showed that intake of calcium antagonists, extent and severity of coronary artery disease, and ST segment elevation in both the anterior and inferior leads were significant independent predictors of survival without myocardial infarction. We conclude that long-term prognosis for patients with variant angina is relatively good and that use of calcium antagonists improves it.
Abnormal blood pathways in left ventricular cavity in acute myocardial infarction. Experimental observations with special reference to regional wall motion abnormality and hemostasis.
Authors: Beppu S , Izumi S , Miyatake K , Nagata S , Park Y D , Sakakibara H , Nimura Y
Published: June 2011

To elucidate the mechanism of regional hemostasis in the left ventricular (LV) cavity during myocardial infarction, the blood pathway in LV cavity was examined with contrast echocardiography injected from the left atrium before and after coronary ligation in nine canines. Before coronary ligation, contrast echoes spread over LV cavity with one rush. After ligation, smokelike echoes indicating hemostasis were observed at the apical middle of the LV cavity in five dogs with apical akinesis and at the apical area in four dogs with apical dyskinesis. The contrast echoes did not reach the apex within one diastolic period but turned upward to the outflow tract in the middle of the cavity in all dogs. In the cardiac beats that followed, some contrast echoes spread slowly toward the apex, forming a thin layer along the posterior wall in cases with akinesis but not in cases with dyskinesis. The area separated from the blood pathway developed where the smokelike echoes had been developed. Tachycardia exaggerated the abnormality of blood pathway and widened the contrast echo-free area. The abnormal pathway of the blood in apical myocardial infarction develops hemostasis in the apex. This should be one of the mechanisms of thrombus formation in myocardial infarction.