bluuebunny/crossref_metadata_2025 huggingface dataset:
Morphometric analysis of the composition of atherosclerotic plaques in the four major epicardial coronary arteries in acute myocardial infarction and in sudden coronary death.
Authors: Kragel A H , Reddy S G , Wittes J T , Roberts W C
Published: June 2011

We studied at necropsy atherosclerotic plaque composition in the four major (right, left main, left anterior descending, and left circumflex) epicardial coronary arteries in 15 patients who died of consequences of an acute myocardial infarction (AMI) and in 12 patients with sudden coronary death (SCD) without AMI. The coronary epicardial arteries were sectioned at 5-mm intervals, and a Movat-stained section of each segment of artery was prepared and analyzed using a computerized morphometry system. Within the AMI group and within the SCD group, there were no differences in plaque composition among any of the four major epicardial coronary arteries. Within both groups, plaque morphology varied as a function of cross-sectional-area narrowing of the segments. In both groups, the amount of dense relatively acellular fibrous tissue, calcified tissue, and pultaceous debris (amorphous debris containing cholesterol clefts, presumably rich in extracellular lipid) increased in a linear fashion with increasing degrees of cross-sectional-area narrowing of the segments, and the amount of cellular fibrous tissue decreased linearly. In the AMI group, the percentage of plaque consisting of pultaceous debris and of cellular fibrous tissue separated significantly narrowed (greater than 75% cross-sectional area) segments from less narrowed (less than 75%) segments. A comparison of the AMI group to the SCD group showed significant differences. The percentage of plaque consisting of pultaceous debris (16% in the AMI group and 7% in the SCD group), of cellular fibrous tissue (11% vs. 18%), and of heavily calcified tissue (8% vs. 16%) were significantly different in the severely narrowed segments in the AMI and SCD groups. When all arteries containing thrombi were deleted from the analysis, there were no significant changes in the results. Occlusive coronary thrombi were present in 13 of the 15 AMI patients and in one of the 12 SCD patients. Thus, the frequency of coronary thrombi and plaque composition differ in patients with AMI and in those with SCD without AMI.
Biochemical basis for the difference between normal and atherosclerotic arterial fluorescence.
Authors: Laifer L I , O'Brien K M , Stetz M L , Gindi G R , Garrand T J , Deckelbaum L I
Published: June 2011

The observation that laser-induced fluorescence (LIF) spectra of atherosclerotic and normal artery are different has been proposed as the basis for guiding a "smart" laser angioplasty system. The purpose of this study was to investigate the causes of this difference in LIF. Helium-cadmium laser-induced (325 nm) fluorescence was recorded from pure samples of known constituents of normal and atherosclerotic artery including collagen, elastin, calcium, cholesterol, and glycosaminoglycans. Similarities between the LIF spectra of atherosclerotic plaque and collagen and normal aorta and elastin were noted. LIF spectroscopy was then performed on specimens of atherosclerotic aortic plaque (n = 9) and normal aorta (n = 13) and on their extracted lipid, collagen, and elastin. Lipid extraction did not significantly alter atherosclerotic plaque or normal aortic LIF, suggesting a minor contribution of lipid to arterial LIF. The LIF spectra of normal aorta wall was similar to the spectra of the extracted elastin, whereas the LIF spectra of atherosclerotic aortic plaque was similar to the spectra of the extracted collagen. These observations are consistent with the reported relative collagen-to-elastin content ratio of 0.5 for normal arterial wall and 7.3 for atherosclerotic plaque. A classification algorithm was developed to discriminate normal and atherosclerotic aortic spectra based on an elastin and collagen spectral decomposition. A discriminant score was formed by the difference of elastin and collagen (E-C) coefficients and used to classify 182 aortic fluorescence spectra. The mean E-C value was +0.83 +/- 0.04 for normal and -0.48 +/- 0.07 for atherosclerotic aorta (p less than 0.001). Classification accuracy was 92%.(ABSTRACT TRUNCATED AT 250 WORDS)
Relation of left ventricular filling dynamics to alterations in load and compliance in patients with and without pressure-overload hypertrophy.
Authors: Wisenbaugh T , Harlamert E , DeMaria A N
Published: June 2011

A large atrial contribution to left ventricular (LV) filling (%A) in patients with LV hypertrophy has been assumed by some to indicate abnormal LV compliance. We tested this assumption by examining the influence of short- and long-term changes in load on compliance and filling dynamics using nitroprusside to decrease load in 11 patients with severe aortic stenosis (AS) and ergonovine to increase load in nine normal subjects. LV angiographic volume was analyzed frame-by-frame simultaneous with micromanometer pressure recordings. Operative LV chamber compliance (dV/VdP) and a time constant for isovolumic relaxation rate were computed using three-constant exponential equations fit to the data. Compared with normal subjects, resting left ventricular end-diastolic pressure was increased and dV/VdP was reduced in AS, but %A was not different. %A was inversely related to left ventricular end-diastolic pressure (r = -0.48, p = 0.02) and positively correlated with dV/VdP (r = 0.90, p less than 0.001) within the AS group. Nitroprusside infusion reduced LV peak systolic pressure by 11%, end-diastolic pressure by 38%, and end-diastolic volume by 12% (p less than or equal to 0.004 for each) and tended to increase dV/VdP by 26% (p = 0.23). These alterations in load resulted in a 21% decrease (-16 ml) in the early filling volume (p less than 0.05) and variable increases (mean, +7 ml; p = NS) in the late atrial filling volume and in the percent atrial contribution to ventricular filling (26 +/- 19% to 35 +/- 25% for the AS group, p = NS) that were related to changes in compliance.(ABSTRACT TRUNCATED AT 250 WORDS)
Role of adenosine in pathogenesis of anginal pain.
Authors: Crea F , Pupita G , Galassi A R , el-Tamimi H , Kaski J C , Davies G , Maseri A
Published: June 2011

The intravenous infusion of adenosine provokes anginalike chest pain. To establish its origin, an intracoronary infusion of increasing adenosine concentrations was given in 22 patients with stable angina pectoris. During adenosine infusion, 20 patients had chest pain without electrocardiographic signs of ischemia. They all reported that the chest pain was similar to their usual anginal pain. In 10 of the 22 patients adenosine was also infused into the right atrium, but it never produced symptoms at the doses that had provoked chest pain during intracoronary infusion. In seven other patients, the intracoronary adenosine infusion was repeated after intravenous administration of aminophylline, an antagonist of adenosine P1-receptors. Aminophylline decreased the severity of adenosine-induced chest pain (assessed with a visual analog scale) from 42 +/- 22 to 23 +/- 17 mm (p less than 0.002). In the remaining five of the 22 patients, monitoring of blood oxygen saturation in the coronary sinus during intracoronary adenosine administration showed that maximum coronary vasodilation was achieved at doses lower than those responsible for chest pain. A single-blind, placebo-controlled, randomized trial of the effect of aminophylline on exercise-induced chest pain was also performed in 20 other patients with stable angina. Aminophylline, compared with placebo, decreased the severity of chest pain at peak exercise from 67 +/- 21 to 51 +/- 23 mm (p less than 0.02), despite the achievement of a similar degree of ST-segment depression. Finally, the effect of intravenous adenosine was compared in 10 patients with predominantly painful myocardial ischemia and in 10 patients with predominantly silent ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Ventricular reentry around a fixed barrier. Resetting with advancement in an in vitro model.
Authors: Bernstein R C , Frame L H
Published: June 2011

We studied an in vitro model of reentrant tachycardia in a ring of ventricular endocardial tissue surrounding the canine mitral and aortic valves to understand how the response of a reentrant tachycardia to premature impulses can provide insight into the underlying tachycardia mechanism, circuit characteristics, and nature of the central barrier. Reproducible regular reentrant tachycardias (cycle length range, 177-450 msec) were induced with programmed stimulation in 19 intact preparations studied at 34-38 degrees C. Tachycardias were sustained and stable until terminated by programmed stimulation in 95% of preparations. Reentry was reliably reinitiated during experiments lasting 2-15 hours. Data supporting reentry as the mechanism of these tachycardias included sequential activation around the ring that spanned the cycle length of the tachycardia, unidirectional block during initiation of the reentrant rhythm, and termination of the tachycardia after interruption of the circuit. Tachycardias in 13 preparations were systematically reset by premature stimuli. During reentry, each of these preparations had full recovery of excitability by the end of their excitable gap as evidenced by a flat portion along their resetting response curve (eight of 13) or by lack of faster conduction velocity during the second poststimulus beat after premature impulses that produced a long return cycle (13 of 13). From analysis of the conduction of premature impulses and their return cycles, we reached several conclusions useful for interpreting resetting response curves when the reentrant circuit is not fully accessible for study. The duration of a flat portion of the resetting response curve indicated the duration of the shortest fully recovered excitable gap in the reentrant circuit. The window of reset of the tachycardia reflected only the local excitable gap at the site of stimulation and did not define the shortest excitable gap within the circuit. The extent of advancement of the tachycardia provided a lower-limit estimate of the shortest excitable gap in the reentrant circuit. Advancement of a tachycardia in time by premature stimuli indicated advancement at each point in the circuit. Finally, for tachycardias advanced by premature impulses, the length of the reentrant path cannot be determined by the recovery of a refractory barrier.
Transvenous atrial septal defect occlusion in piglets with a "buttoned" double-disk device.
Authors: Sideris E B , Sideris S E , Fowlkes J P , Ehly R L , Smith J E , Gulde R E
Published: June 2011

The feasibility and safety of transvenous closure of atrial septal defects by a new device was tested in 20 piglets, in which atrial septal defects were created by foramen ovale dilatation with angioplasty balloons. The device was small enough to be introduced in a 7F or 8F sheath, and it measured 20-25 mm. It has no hooks and consists of a foam occluder from the left atrium and a counter-occluder from the right atrium, buttoned independently. The animals were observed by angiography and color flow mapping, and they were electively killed at various intervals up to 2 months after occlusion. The device was not thrombogenic and had endothelialized by 2-3 weeks. All atrial defects were found to be completely occluded. Complications occurred only with the first three prototype devices, including counter-occluder detachment, right atrial perforation, and need for double occlusion and pulmonary artery embolization. No such complications occurred in the last 17 experiments because of modifications of the device and operator experience. These observations showed the feasibility of occlusion of moderate-size atrial septal defects in piglets by a new device introduced through a small sheath. The method appears promising for potential human application.
Exercise capacity for survivors of cardiac transplantation or sustained medical therapy for stable heart failure.
Authors: Stevenson L W , Sietsema K , Tillisch J H , Lem V , Walden J , Kobashigawa J A , Moriguchi J
Published: June 2011

Cardiac transplantation is predicted to improve survival for patients with severe symptoms of heart failure and ejection fraction of 20% or less, but the exercise capacity after cardiac transplantation is less than normal. Patients responding to vasodilators and diuretics have progressive improvement in exercise capacity despite low ejection fraction. We hypothesized that among patients currently considered appropriate for transplantation who could nonetheless subsequently be stabilized on medical therapy tailored to hemodynamic goals, survivors after 6 months of sustained medical therapy would demonstrate exercise capacity comparable to that of survivors of transplantation. Of 146 patients referred, 118 (81%) were discharged on tailored therapy without transplantation, and 88 (60%) were stable for at least 1 month. Stability after discharge was more likely in patients with lower right atrial pressures and better renal function on therapy. Of the 88 stable patients, 45 patients were listed for transplant, and 43 were ineligible or unwilling. From these patients, 42 survivors for more than 6 months follow-up after cardiac transplantation or tailoring of medical therapy underwent exercise testing. Baseline functional and hemodynamic status and left ventricular ejection fraction (15 +/- 4%) were not different between the transplant and sustained medical survivor groups at the time of initial evaluation. After 14 +/- 6 months, left ventricular ejection fraction had increased to 62 +/- 7% after transplantation (p less than 0.01) and only 22 +/- 9% after sustained medical therapy (p less than 0.05). However, there were no significant differences in the maximum workload, oxygen uptake, anaerobic threshold, or maximum oxygen pulse between survivors of cardiac transplantation and survivors on sustained medical therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Influence of coronary occlusion during PTCA on end-systolic and end-diastolic pressure-volume relations in humans.
Authors: Kass D A , Midei M , Brinker J , Maughan W L
Published: June 2011

The influence of acute coronary occlusion on systolic and diastolic left ventricular pressure-volume relations was studied in 10 patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Pressure-volume relations were obtained by conductance catheter and micromanometer techniques and with volume load altered by transient inferior vena caval occlusion. End-systolic and end-diastolic pressure-volume relations were obtained at baseline, during 60-90 seconds of ischemia, and at return to baseline after angioplasty balloon deflation. Coronary occlusion significantly altered systolic and diastolic chamber function. Systolic dysfunction was characterized by a reproducible rightward shift of the end-systolic pressure-volume relation (+25.4 +/- 18.4 ml) that was greater for proximal left anterior descending and circumflex coronary artery occlusions (+41 ml) than for distal or right coronary artery occlusions (+15.4 ml, p less than 0.05). Occlusion also lowered chamber systolic function indexes, such as the end-systolic pressure-volume relation slope (from 4.2 to 2.8 mm Hg/ml) and preload recruitable stroke work (from 97 to 78.6 mm Hg). All systolic (and diastolic) changes were resolved with successful angioplasty. Diastolic abnormalities during angioplasty were characterized by prolonged pressure relaxation and an upward shift of the resting diastolic pressure-volume data and by an apparent increase in chamber elastic stiffness. However, when end-diastolic data from multiple beats during inferior vena caval occlusion were compared, control and ischemic end-diastolic pressure-volume relations displayed little or no difference. Thus, elevations in resting diastolic pressure-volume relations and apparent increase in chamber elastic stiffness during coronary occlusion in humans appear dominated by altered right ventricular or pericardial loading. These data indicate that pressure-volume analysis is useful in assessing the functional significance of coronary lesions and reperfusion.
Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure.
Authors: Sullivan M J , Green H J , Cobb F R
Published: June 2011

Recent studies in patients with long-term heart failure have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise. The present study provides an analysis of substrate and enzyme content, fiber typing, and capillarization in skeletal muscle biopsy samples obtained at rest from the vastus lateralis in 11 patients with long-term heart failure (left ventricular ejection fraction, 21 +/- 8%) and nine normal subjects. Patients demonstrated a reduced peak exercise oxygen consumption (13.0 +/- 3.3 ml/kg/min) when compared with normals (30.2 +/- 8.6 ml/kg/min, p less than 0.001) and had an accelerated rise in blood lactate levels during exercise. In mixed fiber skeletal muscle, total phosphorylase and glycolytic enzyme activities were not different in the two groups, whereas mitochondrial enzymes involved in terminal oxidation were decreased in patients as compared with normal subjects as indicated by reductions in succinate dehydrogenase (51 +/- 15 vs. 81 +/- 17 microM/g protein/min, p less than 0.001) and citrate synthetase (26 +/- 7 vs. 43 +/- 20 microM/g protein/min, p less than 0.05). 3-Hydroxyacyl-CoA-dehydrogenase, an important enzyme mediating beta-oxidation of fatty acids, was also reduced in patients as compared with normals (18 +/- 7 vs. 27 +/- 10 microM/g protein/min, p less than 0.05). There was no difference in high-energy phosphagens or lactate concentration of mixed muscle in the two groups, whereas glycogen content was decreased in patients (262 +/- 29 vs. 298 +/- 35 microM glucosyl units/kg dry wt, p = 0.01). Patients demonstrated a reduced percentage of slow twitch type I fibers (36 +/- 7% vs. 52 +/- 22%, p less than 0.05) and had a higher percentage of type IIb fast twitch fibers (24 +/- 9% vs. 11 +/- 12%, p = 0.02), which were smaller than the type IIb fibers seen in normal subjects (p less than 0.05). In patients, the number of capillaries per fiber was decreased for type I and type IIa fibers (both, p less than 0.03), but the ratio of capillaries to cross-sectional fiber area was not different for the two groups. These data demonstrate major alterations in skeletal muscle histology and biochemistry in patients with long-term heart failure, including fiber atrophy, a decrease in percentage of composition of type I fibers, and an increase in type IIb fibers accompanied by a decrease in oxidative enzyme capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
Behavior of right and left ventricles during episodes of variant angina in relation to the site of coronary vasospasm.
Authors: Neglia D , Parodi O , Marzullo P , Sambuceti G , Marcassa C , Michelassi C , L'Abbate A
Published: June 2011

The effects of single-vessel coronary occlusion on simultaneously evaluated right (RV) and left ventricular (LV) performance were assessed and compared with LV perfusion patterns in 25 patients with variant angina. Coronary spasm involved the right coronary artery in 15 patients (group 1) and the left anterior descending coronary artery in 10 patients (group 2). Biventricular function was assessed by radionuclide angiography under basal conditions, during spontaneous or ergonovine-induced ischemia, and after resolution of the ischemic attack. Myocardial perfusion was assessed by thallium 201 scintigraphy in 21 patients of this series during superimposable ischemic episodes. In group 1, ischemia caused RV (14 of 15 patients) and LV (13 of 15 patients) regional dysfunction with significant reduction in RV and LV ejection fractions. The interventricular spetum was involved in six of 15 patients, causing a more pronounced LV impairment. In group 2, all patients showed septal dyssynergies associated with a reduction of LV ejection fraction; absent or trivial RV involvement was observed. In both groups, LV perfusion defects were present in all patients with LV wall motion abnormalities during ischemia, matching the site of regional dyssynergies. Thus, in a group of patients with variant angina and single-vessel disease, transient occlusion of the right coronary artery directly caused RV and LV impairment; in these patients, the extent of LV but not RV dysfunction appeared related to the presence of septal ischemia. Vasospasm of the left anterior descending coronary artery consistently caused LV dysfunction not associated with secondary effects on RV systolic function.
Importance of preexcited QRS morphology during induced atrial fibrillation to the diagnosis and localization of multiple accessory pathways.
Authors: Fananapazir L , German L D , Gallagher J J , Lowe J E , Prystowsky E N
Published: June 2011

The present investigation evaluates the ability of several electrocardiographic (ECG) and electrophysiologic methods to identify multiple accessory pathways in 47 patients in whom the presence and sites of multiple accessory pathways were confirmed intraoperatively. To establish ECG features that suggested the presence of multiple accessory pathways in these patients, we initially studied the 12-lead ECG during maximal preexcitation in 101 patients with single accessory pathways. Distinctive 12-lead ECG patterns were noted for six defined anatomic areas around the right and left atrioventricular groove. Multiple preexcited QRS morphologies, each typical for a separate accessory pathway, and atypical preexcited QRS morphologies were recorded during atrial fibrillation in 31 of 47 (66%) patients with multiple accessory pathways. By comparison, the ECG during sinus rhythm and rapid atrial pacing identified 14 (32%) and 26 (55%) of the patients, respectively. In 12 (26%) patients in whom evidence for multiple accessory pathways was absent from endocardial mapping data, atrial fibrillation provided the diagnosis. In five (11%) patients, atrial fibrillation was the only method that demonstrated the presence of multiple accessory pathways. A combination of ECG findings during atrial fibrillation and rapid atrial pacing plus endocardial mapping data identified 43 (91%) of the patients with multiple accessory pathways. There were two unique fusion patterns on the 12-lead ECG that were characteristic of specific multiple accessory pathway combinations.(ABSTRACT TRUNCATED AT 250 WORDS)
Simultaneous conductance catheter and dimension assessment of left ventricle volume in the intact animal.
Authors: Applegate R J , Cheng C P , Little W C
Published: June 2011

We compared left ventricle (LV) volume (V) simultaneously measured using the conductance catheter (VM) with volume calculated from three LV dimensions (VD) determined ultrasonically from endocardial crystals. Seven adult mongrel dogs (20-30 kg) were anesthetized and instrumented to measure micromanometer LV pressure and V. Three pairs of crystals were placed orthogonally in subendocardial positions and a conductance catheter was placed in the LV retrograde across the aortic valve. Under steady-state conditions, over the range of a single cardiac cycle, the relation between VM and VD was well described by a straight line. There was an excellent correlation of conductance and dimension volumes with r equal to 0.97 +/- 0.04 and SEE 0.8 +/- 0.5 ml. The gain (1/alpha) and parallel conductance volume (alpha VC) were constant. At lower volumes obtained during bicaval occlusion, however, the relation between VM and VD was curvilinear. 1/alpha and alpha VC both decreased as LVV fell. Thus, determination of absolute volume using the conductance catheter depended on the conditions under which the data were obtained. Under steady-state conditions, alpha VC calculated by both the saline method (mean +/- SD, 50 +/- 15 ml) and by regression of VM and VD, (45 +/- 21 ml) were similar. Consequently, absolute LV end-diastolic volumes and end-systolic volumes by the conductance and dimension methods were similar (53 +/- 14 ml and 38 +/- 14 ml vs. 56 +/- 17 ml and 44 +/- 16 ml, respectively, p = NS). When volume decreased during bicaval occlusion, there was a progressively greater decrease in VM as compared with VD. The absolute slope (EES) of the end-systolic pressure-volume relation (ESPVR) was consistently higher by the dimension method, group average, 16.3 +/- 7.6, than by the catheter, 8.5 +/- 5.9, p less than 0.05. The direction and magnitude of the change in EES at different inotropic states (autonomic blockade; dobutamine), however, was similarly measured by both the conductance catheter and dimension method. We conclude that the gain and offset of the conductance catheter are relatively constant at steady state but vary when volume is reduced by caval occlusion. Thus, the conductance catheter accurately measures absolute volumes at steady state but can underestimate the slope and position of the ESPVR when it is determined by caval occlusion. The conductance catheter does, however, accurately measure the directions and magnitude of change in contractile state.
Catheter ablation of the atrial myocardium in human type I atrial flutter.
Authors: Saoudi N , Atallah G , Kirkorian G , Touboul P
Published: June 2011

To avoid atrioventricular node-His bundle ablation, catheter ablation of the atrial myocardium was attempted in eight patients with drug refractory type I atrial flutter. In seven of eight patients, a zone of prolongation and fragmentation of the endocardial electrogram was found in the low posterior part of the right atrium. Entrainment of the atrial flutter by high right atrial pacing was accompanied by local recording of second-degree regional block in several atrial sectors but never in the low septal area. We, therefore, hypothesized that the latter represented the critical slow conduction zone of the reentrant flutter circuit. One or two cathodal DC shocks were locally delivered without immediate or late complications. One single ablation attempt was performed in five patients, whereas three patients underwent a second attempt because of early flutter recurrence. Patients were initially discharged without (and after a second session with) antiarrhythmic drugs. After a mean follow-up of 15.5 months (range, 10-23 months), five patients are free of arrhythmias without antiarrhythmic drug therapy. Two patients did not experience atrial arrhythmias while on a drug regimen that was previously found to be ineffective, and a third patient had flutter recurrences. This study suggests that patients with type I atrial flutter referred for atrioventricular node-His bundle ablation may be successfully managed by delivering the ablative shock directly on the atrial arrhythmia substrate.
Improving the predictive ability of the signal-averaged electrocardiogram with a linear logistic model incorporating clinical variables.
Authors: Vatterott P J , Bailey K R , Hammill S C
Published: June 2011

To improve the predictive accuracy of the signal-averaged electrocardiogram, we created a linear logistic model for predicting ventricular tachycardia during electrophysiologic testing. This signal-averaged electrocardiographic model was created from data obtained from 214 patients undergoing electrophysiologic testing (70 had ventricular tachycardia during electrophysiologic testing) by using stepwise logistic regression to rank eight clinical and nine signal-averaged electrocardiographic variables. The best predictors were ejection fraction, history of infarction, ventricular ectopic pairs or nonsustained ventricular tachycardia on Holter monitoring, QRS duration after 25-Hz filtering, and root mean square voltage of the terminal 40 msec of the QRS complex after 40- and 80-Hz filtering. Cross validation (a statistical technique that can be used to accurately evaluate how a predictive model will perform on a prospective patient population) was used to validate the model. After cross validation, the model's sensitivity was 91% and specificity was 59% for predicting ventricular tachycardia during electrophysiologic testing. This model compared favorably with established 25-Hz late-potential criteria (QRS duration of more than 110 msec and root mean square voltage of less than 25 microV of the terminal 40 msec of the QRS complex; sensitivity, 64%; specificity, 85%) and with established 40-Hz late-potential criteria (QRS duration of more than 114 msec or root mean square voltage of less than 20 microV of the terminal 40 msec of the QRS complex or duration of the low-amplitude signal less than 40 microV at the terminal QRS complex that is greater than 38 msec; sensitivity, 84%; specificity, 54%).(ABSTRACT TRUNCATED AT 250 WORDS)
Paradoxical narrowing of atherosclerotic coronary arteries induced by increases in heart rate.
Authors: Nabel E G , Selwyn A P , Ganz P
Published: June 2011

Vasodilation in normal and vasoconstriction in atherosclerotic coronary arteries have been observed in response to complex stimuli such as exercise and the cold pressor test. To study a single parameter that changes during these activities, and to better understand the pathophysiology of ischemia associated with increases in heart rate, we studied coronary vasomotion and blood flow response to increasing heart rate alone, produced by atrial pacing, with quantitative angiographic and Doppler flow-velocity measurements in 15 patients. In five patients with angiographically smooth coronary arteries (group 1), tachycardia produced progressive dilation of the epicardial artery with increases in cross-sectional area (CSA) of +15.5 +/- 3.4%, +22.4 +/- 2.1%, +28.5 +/- 3.3%, and +30.6 +/- 2.2% at 90, 110, 130, and 150 beats/min, respectively. In contrast, in five patients with mild angiographic narrowings (group 2), coronary segments failed to dilate with progressive tachycardia (-6.3 +/- 2.0%, -8.3 +/- 2.0%, -12.5 +/- 2.0%, and -11.4% at 90, 110, 130, and 150 beats/min, respectively), and progressive loss of luminal area was observed in five patients with severe angiographic narrowings (group 3) (-34.4 +/- 3.4%, -49.6 +/- 2.2%, -59.2%, and -72.8% at 90, 110, 130, and 150 beats/min, respectively). Coronary blood flow increased significantly with tachycardia in group 1 (+44.5 +/- 10.2%, +86.0 +/- 24.6%, +105.8 +/- 29.3%, and +137.5 +/- 46.0%), increased slightly in group 2 (+7.8 +/- 3.2%, +9.4 +/- 4.4%, +8.4 +/- 3.9%, and +10.0%), and decreased significantly in group 3 (-31.8 +/- 6%, -42.6 +/- 10.7%, -61.0%, and -70.0%). We conclude that an isolated increase in heart rate in patients with normal coronary arteries results in a modest increase in flow and vasodilation. In early atherosclerosis, the flow increase is blunted and dilation is replaced with paradoxical loss in luminal size. In patients with stenoses, further loss in luminal size occurs accompanied by a decrease in coronary blood flow. Thus, increasing heart rate alone in the setting of coronary stenoses could produce myocardial ischemia by a reduction in coronary supply, as well as by an increase in oxygen demand.
Comparative hemodynamic effects of procainamide, tocainide, and encainide in severe chronic heart failure.
Authors: Gottlieb S S , Kukin M L , Medina N , Yushak M , Packer M
Published: June 2011

Many of the newer antiarrhythmic agents are said to cause minimal myocardial depression, but their hemodynamic effects have not been invasively evaluated and compared in patients with severe chronic heart failure. In a randomized, crossover study, the hemodynamic responses to single oral doses of procainamide (750 mg), tocainide (600 mg), and encainide (50 mg) given to 21 patients with severe chronic heart failure were compared. Cardiac performance decreased with all three drugs, but the magnitude of deterioration differed among the three agents. Stroke volume index decreased with procainamide (-5 +/- 1 ml/m2, p less than 0.001), tocainide (-7 +/- 1 ml/m2, p less than 0.001), and encainide (-8 +/- 1 ml/m2, p less than 0.001), but the decline was significantly greater with encainide than with procainamide (p less than 0.05). Similarly, left ventricular filling pressure increased with tocainide and encainide (+4 +/- 1 and +5 +/- 2 mm Hg, respectively; both p less than 0.05), but not with procainamide; the increase was significantly greater with tocainide and encainide than with procainamide (p less than 0.001). These deleterious hemodynamic effects were accompanied by worsening symptoms of heart failure in six patients with encainide and seven patients with tocainide but in only two patients with procainamide. Serum levels for all drugs were in the therapeutic range. In conclusion, although the three type I antiarrhythmic agents tested may all adversely affect left ventricular function in patients with heart failure, encainide and tocainide are more likely than procainamide to cause hemodynamic and clinical deterioration.
Wide-range load shift of combined aortic valvuloplasty-arterial vasodilation slows isovolumic relaxation of the hypertrophied left ventricle.
Authors: Paulus W J , Heyndrickx G R , Buyl P , Goethals M A , Andries E
Published: June 2011

To assess the effects of left ventricular (LV) load on isovolumic relaxation rate of the hypertrophied LV, wide range LV load shifts were imposed by the sequential use of balloon aortic valvuloplasty (BAV) and arterial vasodilation in 14 patients with severe sclerocalcific aortic stenosis (aortic valve area, 0.45 +/- 0.16 cm2). Micromanometer tip-catheter LV pressure recordings (n = 14) and simultaneous LV angiograms (n = 9) were obtained before BAV, during nitroprusside infusion (NIT) before BAV, 48 hours after BAV, and 48 hours after BAV during NIT. LV peak systolic pressure (LVPSP) decreased from 237 +/- 33 mm Hg before BAV to 200 +/- 33 mm Hg (p less than 0.01) during NIT before BAV, to 201 +/- 27 mm Hg (p less than 0.01) after BAV and to 165 +/- 26 mm Hg (p less than 0.01) during NIT after BAV.LV end-systolic volume (LVESV) decreased from 55 +/- 34 ml before BAV to 25 +/- 23 ml (p less than 0.01) during NIT before BAV, to 30 +/- 32 ml (p less than 0.025) after BAV and to 15 +/- 12 ml (p less than 0.025) during NIT after BAV. LV end-systolic wall stress (LVESs) decreased from 90 +/- 30.10(3) dyne/cm2 before BAV to 41 +/- 13.10(3) dyne/cm2 (p less than 0.01) during NIT before BAV, to 55 +/- 16.10(3) dyne/cm2 (p less than 0.025) after BAV and to 26 +/- 6.10(3) dyne/cm2 (p less than 0.01) during NIT after BAV. Only after sequential BAV-NIT was the time of LV electromechanical systole (LVEST), which marked the onset of the LV isovolumic relaxation period, significantly reduced (from 419 +/- 26 msec before BAV to 363 +/- 28 msec after BAV-NIT [p less than 0.01]). The time constants of LV pressure decay with zero or nonzero asymptote pressure (TO and TPB) remained unchanged after BAV and during NIT before BAV. At the lowest LVPSP, LVESV, and LVESs after sequential BAV-NIT, both TO and TPB significantly prolonged from 35.7 +/- 6.3 to 46.7 +/- 12.6 msec (p less than 0.025) and from 46.6 +/- 12.5 to 73.2 +/- 23.3 msec (p less than 0.01). Phase-plane plots (LV dP/dt vs. LVP) of the LV pressure (P) signal during isovolumic relaxation were constructed for the four different loading states by matching corresponding LVP and LV dP/dt points. For a given LVP value, the corresponding LV dP/dt values on the phase plane plots were comparable before BAV, during NIT before BAV, and after BAV. The corresponding LV dP/dt value was higher during NIT after BAV, impling a slower relaxation rate at the same LVP after sequential BAV-NIT. A shift in the control of isovolumic LV relaxation kinetics from myofilamentary detachment to myoplasmic calcium removal, which proceeds slower in hypertrophied myocardium, could explain the observed slowing of LV isovolumic relaxation after drastic LV unloading of sequential BAV-NIT.
Intravenous thrombolytic therapy with a combination of single-chain urokinase-type plasminogen activator and recombinant tissue-type plasminogen activator in acute myocardial infarction.
Authors: Bode C , Schuler G , Nordt T , Schönermark S , Baumann H , Richardt G , Dietz R , Gurewich V , Kübler W
Published: June 2011

The effects of simultaneous intravenous infusions of 12 mg recombinant tissue-type plasminogen activator (rt-PA) over 30 minutes and 48 mg single-chain urokinase-type plasminogen activator (scuPA) over 40 minutes were studied in 38 patients with acute myocardial infarction. Coronary arterial patency was assessed angiographically 60 minutes and 90 minutes after initiation of treatment. Patency was achieved in 19 of 31 patients (61.3%) (95% confidence limits, 42-78%) at 60 minutes and in 27 of 33 patients (81.8%) (95% confidence limits, 65-93%) at 90 minutes. Nonspecific plasminogen activation was monitored by measuring relevant plasma parameters. At 60 minutes and 120 minutes, the fibrinogen concentration decreased slightly to 82.8 +/- 24.3% and 91.2 +/- 17.4% of the preinfusion level, and the plasminogen concentration to 66.3 +/- 15.2% and 65.3 +/- 13.4%, respectively. A greater consumption of alpha 2-antiplasmin was observed, which decreased to 30.7 +/- 22.8% and 32.2 +/- 21.2% of the preinfusion level at 60 and 120 minutes, respectively. No bleeding necessitating transfusion was observed. Two patients (5.3%) died during hospitalization. The findings suggest that the combined intravenous infusion of rt-PA and scuPA at appropriate doses induces highly effective coronary thrombolysis equal to the best results obtained with either rt-PA or scuPA alone. This efficacy is coupled with high specificity. Thus, the data support the potential use of combinations of rt-PA and scuPA in place of monotherapy.
111In platelet imaging of left ventricular thrombi. Predictive value for systemic emboli.
Authors: Stratton J R , Ritchie J L
Published: June 2011

To determine whether a positive indium 111 platelet image for a left ventricular thrombus, which indicates ongoing thrombogenic activity, predicts an increased risk of systemic embolization, we compared the embolic rate in 34 patients with positive 111In platelet images with that in 69 patients with negative images during a mean follow-up of 38 +/- 31 (+/- SD) months after platelet imaging. The positive and negative image groups were similar with respect to age (59 +/- 11 vs. 62 +/- 10 years), prevalence of previous infarction (94% vs. 78%, p less than 0.05), time from last infarction (28 +/- 51 vs. 33 +/- 47 months), ejection fraction (29 +/- 14 vs. 33 +/- 14), long-term or paroxysmal atrial fibrillation (15% vs. 26%), warfarin therapy during follow-up (26% vs. 20%), platelet-inhibitory therapy during follow-up (50% vs. 33%), injected 111In dose (330 +/- 92 vs. 344 +/- 118 microCi), and latest imaging time (greater than or equal to 48 hours in all patients). During follow-up, embolic events occurred in 21% (seven of 34) of patients with positive platelet images for left ventricular thrombi as compared with 3% (two of 69) of patients with negative images (p = 0.002). By actuarial methods, at 42 months after platelet imaging, only 86% of patients with positive images were embolus free as compared with 98% of patients with negative images (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of intravenous propranolol on coronary vasomotion at rest and during dynamic exercise in patients with coronary artery disease.
Authors: Bortone A S , Hess O M , Gaglione A , Suter T , Nonogi H , Grimm J , Krayenbuehl H P
Published: June 2011

Coronary vasomotion was studied at rest and during bicycle exercise with biplane quantitative coronary arteriography in 28 patients with coronary artery disease. Patients were divided into two groups; the first 18 patients served as controls (group 1), and the next 10 patients were treated with propranolol 0.1 mg/kg, which was infused intravenously before exercise (group 2). Luminal area of a normal and a stenotic vessel segment was determined at rest, during supine bicycle exercise, and 5 minutes after sublingual administration of 1.6 mg nitroglycerin after exercise. In group 1, the normal vessel showed vasodilation (+16%, p less than 0.001) during exercise, whereas the stenotic vessel segment showed vasoconstriction (-31%, p less than 0.001). After sublingual administration of nitroglycerin, there was coronary vasodilation of both normal (+36%, p less than 0.001 vs. rest) and stenotic (+20%, p less than 0.001) vessel segments. Patients with angina pectoris during supine exercise (n = 10) had significantly (p less than 0.05) more vasoconstriction (-36%) than patients without angina (-23%). In group 2, intravenous administration of propranolol at rest was associated with a decrease in luminal area of both normal (-24%, p less than 0.001) and stenotic (-43%, p less than 0.001) vessel segments; however, during subsequent exercise, both normal (-2%, p = NS vs. rest) and stenotic (-3%, p = NS vs. rest) vessel segments dilated when compared with the measurements after propranolol. Administration of nitroglycerin further increased luminal area of both vessel segments (normal segment, +23%, p less than 0.001; stenotic segment, +46%, p less than 0.001 vs. rest). It is concluded that dynamic exercise in patients with coronary artery disease is associated with coronary vasodilation of the normal and vasoconstriction of the stenotic coronary arteries. Patients with exercise-induced angina had significantly more stenosis vasoconstriction than patients without angina although minimal luminal area at rest was similar. Intravenous administration of propranolol is accompanied by a significant decrease in coronary luminal area of both normal and stenotic vessel segments at rest, which is overridden by dynamic exercise and sublingual nitroglycerin. The reduction in myocardial oxygen consumption and the prevention of exercise-induced stenosis vasoconstriction might explain the beneficial effect of beta-blocker treatment in most patients with coronary artery disease.
Transvenous defibrillation in humans via the coronary sinus.
Authors: Bardy G H , Allen M D , Mehra R , Johnson G , Feldman S , Greene H L , Ivey T D
Published: June 2011

A consistently effective transvenous defibrillation system for use in automatic defibrillators could significantly alter the approach to patients at risk of sudden death. Transvenous defibrillation systems that use a right ventricular (RV) electrode only or an RV electrode in combination with a chest patch are relatively inefficient at applying current to the posterolateral left ventricle. An RV electrode combined with a coronary sinus (CS) electrode, however, may improve current distribution to the posterolateral left ventricle. The purpose of this investigation, therefore, was to evaluate the effectiveness and safety of a specially designed transvenous lead system with a CS electrode capable of current delivery to this relatively inaccessible region of the heart. In 20 survivors of cardiac arrest, we determined defibrillation efficacy immediately before defibrillator surgery for monophasic pulses delivered between an RV catheter electrode and a CS catheter electrode system and compared these findings with an RV catheter electrode-thoracic patch defibrillation system. Subsequently, we referenced the efficacy of both transvenous systems to an epicardial patch electrode system at the time of defibrillator implantation. The mean delivered-energy defibrillation threshold for the CS-RV electrode system was 17.5 +/- 7.9 J, which was substantially lower than the RV electrode-thoracic patch system (25.6 +/- 11.4 J, p = 0.0016 [46% more]). Defibrillation threshold voltage was 529 +/- 123 V for the CS-RV electrode system and 647 +/- 164 V (22% more) for the RV electrode-thoracic patch system (p = 0.0013).(ABSTRACT TRUNCATED AT 250 WORDS)
Mean transit time for the assessment of myocardial perfusion by videodensitometry.
Authors: Pijls N H , Uijen G J , Hoevelaken A , Arts T , Aengevaeren W R , Bos H S , Fast J H , van Leeuwen K L , van der Werf T
Published: June 2011

The intrinsic limitations of coronary arteriography to predict the physiological effects of coronary obstructions are well known. Therefore, more direct assessments of the functional significance of coronary stenoses are becoming increasingly important. Study of contrast passage by electrocardiogram-triggered digital radiography has been proposed as a way of assessing changes in myocardial perfusion. The main problems in this approach are the limited time for motionless image acquisition, the potential alteration of vascular volume between different states, and the changing flow pattern induced by contrast agents. This has led to empiric substitution of mean transit time (Tmn) by other time parameters and to representation of vascular volume by maximal contrast intensity (Dmax). To avoid these problems, intact dogs were studied during almost motionless image acquisition of 20-25 consecutive paced heart beats obtained with synchronous radiographic pulses. In this way, unequivocal and reproducible determination of Tmn was possible. Constant and maximal vascular volume was created by continuous infusion of dipyridamole, and it was proved that coronary flow in this model was not influenced by contrast injections. Flow in the circumflex artery was measured by a ring mounted and calibrated Doppler probe. In each dog, flow in the circumflex artery was varied by a balloon occluder in 12 small steps (range, 0-174 +/- 42 ml/min). Inverse appearance time (1/Tapp), Dmax, Dmax/Tapp, inverse time of maximal intensity (1/Tmax), and 1/Tmn were calculated and the relations of these parameters to measured flow were investigated. Tmn proved to be the most reliable parameter for this purpose (r = 0.97 +/- 0.02; mean +/- SD), followed by Tmax (r = 0.93 +/- 0.04). Dmax failed to represent vascular volume but, in fact, showed a moderate correlation with flow (r = 0.78 +/- 0.22), as did Tapp (r = 0.64 +/- 0.18, 0.75 +/- 0.27, and 0.59 +/- 0.26 for the three definitions of Tapp used in this study). Dmax/Tapp correlated better with flow than either component separately. Our results indicate that the mean transit time calculated by videodensitometry can be used to accurately assess changes in myocardial perfusion strictly according to the original principles of indicator dilution theory.