bluuebunny/crossref_metadata_2025 huggingface dataset:
Kinetics and imaging of indium-11-labeled autologous platelets in experimental myocardial infarction.
Authors: Laws K H , Clanton J A , Starnes V A , Lupinetti F M , Collins J C , Oates J A , Hammon J W
Published: June 2011

The kinetics of accumulation and the external imaging patterns of indium-111-labeled platelets infused in a dog model of left anterior descending coronary artery occlusion with reperfusion were studied. The effects of infarct age and regional residual myocardial blood flow upon platelet accumulation were quantified, and the capacity of indium-111 platelets to image the experimental infarction was evaluated qualitatively. The endocardial accumulation of indium-111 platelets occurred primarily in infarct zones with residual blood flow less than 0.6 times normal and was maximal (24.98 +/- 2.76 times normal) in the lowest blood flow zone (less than 0.1 times normal). Indium-111 platelet accumulation in the epicardium occurred in the regions with blood flow less than 0.6 times normal and was maximal (17.83 +/- 1.20 times normal) in the lowest blood flow zone (less than 0.1 times normal). The maximal endocardial and epicardial platelet accumulation occurred 24 hours after reperfusion and was significantly decreased at 48 hours. In vivo cardiac images revealed discrete areas of increased myocardial radioactivity uptake in the anterior wall of dogs 24 hours after reperfusion. All images 48 hours after reperfusion were negative. Thus, in the experimental setting, indium-111 platelets allow quantification of platelet accumulation after myocardial infarction at a tissue level and provide a noninvasive means of in vivo imaging of reperfused infarcted myocardium.
Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.
Authors: Forman R , Cho S , Factor S M , Kirk E S
Published: June 2011

In this study we quantitated the region of preserved myocardium between a subendocardial myocardial infarct (SEMI) and the endocardium in dogs and determined whether this preserved zone was within the region at risk and whether infarct extension could occur in this region. We also evaluated whether a similar subendocardial region exists in patients with SEMI. A 40-minute temporary occlusion of the left anterior descending coronary artery (LAD) in eight dogs resulted in a 35 +/- 5% transmural infarct with 8 +/- 1% subendocardial preservation as assessed by point-counting of the histologic specimens. In vivo perfusion of coronary vessels with Microfil showed that this preserved subendocardial zone was within the region at risk. The preserved subendocardial zone had significantly fewer cell layers in the dogs ventilated with room air than in dogs ventilated with 100% oxygen (8 +/- 4 vs 19 +/- 4, p less than 0.001), which suggests that diffusion from the ventricular cavity was the mechanism of cell preservation. In contrast, the inspired oxygen concentration did not influence the size of the SEMI. Reocclusion of the LAD for 24 hours in an additional eight dogs, 1 week after a SEMI had been created by a 40-minute temporary occlusion, resulted in both subendocardial and subepicardial extension involving 5 +/- % and 29 +/- 9%, respectively, of the transmural myocardium at the infarct center. Subendocardial infarct extension of a similar dimension to that in dogs ventilated on 100% oxygen was observed in postmortem material from eight patients with infarct extension. The preserved layers of subendocardium presumably receive sufficient nutrients from the ventricular cavity to maintain the viability of this region during temporary, but not permanent, reduction of blood supply from the coronary arteries.
Radionuclide angiographic evaluation of right and left ventricular function during exercise after repair of transposition of the great arteries. Comparison with normal subjects and patients with congenitally corrected transposition.
Authors: Parrish M D , Graham T P , Bender H W , Jones J P , Patton J , Partain C L
Published: June 2011

We assessed the incidence, clinical significance and etiology of ventricular dysfunction after intraatrial repair of d-transposition of the great arteries in 11 patients, mean age 9 +/- 3 years, who had had Mustard operations. We compared the results to 15 patients who were considered to have normal ventricular function, two patients who had Rastelli operations and five patients with congenitally corrected transposition. Gated equilibrium radionuclide angiography with supine exercise stress testing was used to assess these children. We found no significant difference between our patient groups in exercise capacity, heart rate, or blood pressure response to exercise. However, we found a high incidence of right ventricular dysfunction in the patient groups, manifested by an abnormal right ventricular ejection fraction response to dysfunction in the patient groups, manifested by an abnormal right ventricular ejection fraction response to exercise in six of 11 patients with a Mustard repair, both patients with a Rastelli repair and all five with congenitally corrected transposition. In addition, the left ventricular response to exercise was abnormal in 10 of 11 patients who had undergone a Mustard repair, both patients with a Rastelli repair, and two of five patients with congenitally corrected transposition. We conclude that biventricular dysfunction is frequently present after intraatrial repair of d-transposition of the great arteries. Despite this dysfunction, no significant decrease in exercise tolerance is found in childhood.
Echocardiography in chronic aortic insufficiency. Is valve replacement too late when left ventricular end-systolic dimension reaches 55 mm?
Authors: Fioretti P , Roelandt J , Bos R J , Meltzer R S , van Hoogenhuijze D , Serruys P W , Nauta J , Hugenholtz P G
Published: June 2011

To determine whether a ventricular (LV) end-systolic dimension (ESD) greater than or equal to 55 mm and LV left fractional shortening less than 25% are risk factors for aortic valve replacement (AVR) in patients with aortic insufficiency, we analyzed the clinical course and M-mode echocardiograms in 47 consecutive patients who underwent AVR for isolated symptomatic AI. Group 1 patients (n = 27) had a preoperative ESD less than 55 mm (mean 44 mm, range 30-52 mm) and group 2 patients (n = 20) had a preoperative ESD greater than or equal to 55 mm (mean 62 mm, range 55-85 mm). One patient in group 1 and 10 patients in group 2 had left ventricular fractional shortening less than 25%. There were no perioperative or postoperative deaths during an average follow-up of 41 months (range 6-76 months). Five patients had perioperative myocardial infarctions (MIs), three in group 1 and two in group 2. Since myocardial protection with cold potassium cardioplegia was instituted, no patient has suffered a perioperative MI. The average preoperative New York Heart Association functional classification was 2.3 (group 1) and 2.6 (group 2). Postoperatively, it was 1.2 in group 1 and 1.1 in group 2. Thirty-three patients (20 in group 1 and 13 in group 2) had echocardiograms at least 1 year after AVR. Of these, LV-end diastolic dimension decreased fro 67 +/- 6 to 53 +/- 6 mm (mean +/- SD) in group 1 (p less than 0.001) and from 79 +/- 3 to 55 +/- 6 mm in group 2 (p less than 0.001). The LVESD also decreased, but this is difficult to interpret because of frequent postoperative abnormal interventricular septal motion. The LV cross-sectional area, an index of LV mass, decreased in group 1 from 25 +/- 5 to 20 +/- 5 cm2 (p lss than 0.001) and in group 2 from 32 +/- 9 to 20 +/- 5 cm2 (p less than 0.001). Postoperative end-diastolic dimension and cross-sectional area were not significantly different between the two groups. We concluded that in aortic insufficiency, a preoperative ESD greater than or equal to 55 mm does not preclude successful AVR, as judged by long-term survival, symptomatic relief, and normalization of LV dimensions assessed by echocardiography.
Value of two-dimensional echocardiography in detecting tricuspid stenosis.
Authors: Nanna M , Chandraratna P A , Reid C , Nimalasuriya A , Rahimtoola S H
Published: June 2011

We reviewed the M-mode and two-dimensional echocardiograms of 100 consecutive patients with rheumatic heart disease. All were subsequently studied by cardiac catheterization and angiography. In four patients, cardiac catheterization showed tricuspid stenosis (average mean diastolic gradient 6.2 mm Hg), which was confirmed during cardiac surgery. M-mode echocardiography showed a diminished EF slope in 12 patients (mean 26 mm/sec), including the four patients with tricuspid stenosis. Seven of the eight patients without tricuspid stenosis had significant pulmonary hypertension; the reasons for the diminished EF slope in the other patient could not be identified. Tricuspid stenosis was diagnosed in four patients from two-dimensional echocardiograms on the basis of diastolic doming and restricted leaflet motion of the tricuspid valve. These four patients were the same patients in whom tricuspid stenosis was diagnosed by cardiac catheterization. We conclude that two-dimensional echocardiography is useful in the diagnosis of tricuspid stenosis.
Physical training increases ventricular fibrillation thresholds of isolated rat hearts during normoxia, hypoxia and regional ischemia.
Authors: Noakes T D , Higginson L , Opie L H
Published: June 2011

The effect of exercise training on cardiovascular mortality is controversial. The purpose of this study was to determine the effect of a period of treadmill training on the ventricular fibrillation threshold of the isolated rat heart. Trained hearts had higher threshold values during standard, control perfusion conditions, and when exposed to hypoxia, hypoxia plus isoproterenol infusion, or when subjected to coronary artery ligation. Myocardial metabolic studies failed to define the mechanism for the effect of running training. However, in coronary ligated hearts, the content of the arrhythmogenic substance 3',5' cyclic adenosine monophosphate (cyclic AMP) was reduced in the ischemic zone of hearts from trained rats. Cyclic AMP levels were also lower in trained hearts during control perfusions. We conclude that running training increases the resistance of the heart to ventricular fibrillation by mechanisms that are largely unknown, although they may involve cyclic AMP.
Effects of abrupt changes in cycle length on refractoriness of the His-Purkinje system in man.
Authors: Denker S , Shenasa M , Gilbert C J , Akhtar M
Published: June 2011

Abrupt changes in cycle length (CL) occur frequently in the clinical setting of atrial fibrillation. However, the effects of such changes on the His-Purkinje system (HPS) have not previously been considered during aberrant ventricular conduction (VAb). In 12 patients who manifested VAb with atrial premature stimulation (A2) during sinus rhythm, the relative refractory period (RRP) of the HPS was evaluated during a constant atrial CL (method I) and during abrupt changes in the CL (method II), wherein the A2 was coupled to an atrial CL (last A1A1) comparable to method I. This last A1A1 during method II was preceded by a series of constant atrial CLs 100-200 msec longer (method IIA) in 11 of 12 patients, or 109-300 msec shorter (method IIB) in all 12 patients. Although abrupt changes in the atrial CL using method IIA resulted in a longer HH interval (by 0-30 msec; mean 13.2 +/- 9.2 msec) preceding the A2, the RRP-HPS was 5-20 msec shorter (mean 9.3 +/- 5.3 msec) compared with method I in eight patients. The effect of abrupt changes was further evaluated in nine patients using method III, with a constant atrial CL, with a duration equal to the last H1H1 interval of method IIA. The VAb that occurred with method III was not manifested with method IIA in seven of nine patients, and in two patients the RRP-HPS was the same or less. Conversely, method IIB resulted in a shorter HH interval (by 0.110 msec; mean 28.9 +/- 21.1 msec) preceding A2, but in 10 patients, RRP-HPS was 5-40 msec longer (mean 20.7 +/- 10.5 msec) than that of method I and in two, VAb was only manifested using method IIB. Further scanning with method III, derived from the HH interval immediately preceding A2 of method IIB, was performed in seven patients and compared with method IIB. Prolongation in the RRP-HPS was shown using the latter method. The results indicate that abrupt changes in CL influence the functional behavior of the HPS in a manner not anticipated. Such changes may have important implications in determining the occurrence of VAb during atrial fibrillation.
Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.
Authors: Bourdillon P D , Lorell B H , Mirsky I , Paulus W J , Wynne J , Grossman W
Published: June 2011

The left ventricular diastolic pressure-volume relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and M-mode echocardiography before and during angina induced by pacing tachycardia. All patients had two- or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 +/- 3 to 31 +/- 6 mm Hg, p less than 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 +/- 2.1 to 9.2 +/- 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 +/- 37 to 48 +/- 27 mm/sec, p less than 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 +/- 5 to 58 +/- 7 msec, p less than 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (sigma R = -PR). A radial stiffness modulus (ER) was determined by the slope of the PR vs log h plots before and after pacing. Over the same range of residual radial stress (sigma R), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.
Effect of rate on left ventricular volumes and ejection fraction during chronic ventricular pacing.
Authors: Narahara K A , Blettel M L
Published: June 2011

Resting left ventricular (LV) function was evaluated in 22 patients with permanent ventricular pacemakers. LV ejection fraction and volume indexes were determined by gated blood pool scintigraphy at ventricular pacing rates of 50-100 beats/min. In patients with a normal heart size, increases in pacing rates resulted in significant linear decreases in stroke volume index and ejection fraction. However, end-systolic volume index and cardiac index did not change. Patients with cardiomegaly appeared to respond differently. End-diastolic volume index decreased significantly as the pacing rate was increased from 50 to 100 beats/min. Ejection fraction was significantly reduced only at pacing rates of 90 and 100 beats/min. Mean cardiac index was highest at ventricular pacing rates of 70-90 beats/min. Increases in cardiac index, achieved by increasing the pacing rate, were maintained over a 4.3-month follow-up. Patients with underlying sinus rhythm had a 27% increase in cardiac output in association with an increase in ejection fraction from 55% to 62% when sinus rhythm was compared to ventricular pacing at a rate of 60 beats/min. These data suggest that patients with cardiomegaly have a narrow range of optimal pacing rates at rest.
Ventricular septal defect after myocardial infarction: diagnosis by two-dimensional contrast echocardiography.
Authors: Drobac M , Gilbert B , Howard R , Baigrie R , Rakowski H
Published: June 2011

Thirteen patients who had ventricular septal defects (VSDs) after myocardial infarction (MI) underwent two-dimensional echocardiography (2-D echo), with confirmation of the VSD by oximetry. Eight of the patients were male and five were female, ages 51-76 years. Five had anterior and eight inferior MIs. Two-dimensional echocardiography revealed akinesis or dyskinesis of the interventricular septum (IVS) in all 13 patients. In only six could a defect in the IVS be directly visualized. Two-dimensional echocardiographic left ventricular (LV) wall motion abnormalities correlated with ECG and angiographic site of infarction in all patients. Twelve patients had adequate saline contrast studies. Positive LV contrast (microbubbles entering the left ventricle through the VSD) was seen in 11 patients, and negative right ventricular (RV) contrast (washout of the RV bubbles by LV blood crossing the VSD) in five patients; at least one abnormality was present in every patient. The location of the VSD was determined by visualizing a VSD or by the site of the positive LV or negative RV contrast. Oximetry showed VSD shunts of 1.4:1 to 7:1, with no correlation between the degree of negative RV contrast and shunt size. Surgical or pathologic confirmation of VSD was obtained in 12 patients, with agreement of VSD location by 2-D echo in all. Four of the 11 patients who underwent surgical repair died, and two patients died before surgery could be attempted. We conclude tht 2-D echo is a sensitive, rapid and safe technique for diagnosing VSD after MI. Positive LV contrast, with or without negative RV contrast, is more sensitive in the diagnosis and localization of post-MI VSD than direct echocardiographic visualization of the defect.
Two-dimensional echocardiographic diagnosis of left-atrial thrombus in rheumatic heart disease. A clinicopathologic study.
Authors: Shrestha N K , Moreno F L , Narciso F V , Torres L , Calleja H B
Published: June 2011

Two-dimensional echocardiographic studies were performed in 293 patients with rheumatic heart disease who underwent open-heart mitral valve surgery during an 18-month period. Diagnostic confirmation of a left atrial thrombus was based on direct inspection of the left atrium during surgery and histopathologic examination. Two-dimensional echocardiographic recordings were reviewed. Of the 293 patients, 33 had left atrial thrombi by two-dimensional echocardiographic criteria. This diagnosis was confirmed at surgery and histopathologic study in 30 (specificity 98.8%). A thrombus was not found in three patients. In 21 other patients, left atrial thrombi were present but were not detected by two-dimensional echocardiography (sensitivity 58.8%). Ten of these 21 had thrombi in the left atrial cavity. In 11 patients, thrombi were located in the left atrial appendage, all of which were missed by two-dimensional echocardiography. Excluding these 11 left atrial appendage thrombi, the sensitivity of two-dimensional echocardiography for detecting left atrial cavity thrombi was 75.0%.
Alterations in left ventricular three-dimensional dynamic geometry and systolic function during acute right ventricular hypertension in the conscious dog.
Authors: Visner M C , Arentzen C E , O'Connor M J , Larson E V , Anderson R W
Published: June 2011

Fifteen chronically instrumented, conscious dogs were studied to determine whether, in the intact circulation, mechanical interactions dictated by the anatomic contiguity of the two ventricles significantly alter left ventricular (LV) dynamic geometry and systolic function during acute right ventricular (RV) hypertension. The three-dimensional geometry of the left ventricle was monitored with three pairs of ultrasonic dimension transducers; ventricular pressures were measured with micromanometers. Data collected during pulmonary artery constriction (RV pressure 68 +/- 8/7 +/- 4 mm Hg) were compared with control data collected at matched heart rates (RV pressure 32 +/- 8/4 +/- 4 mm Hg). During pulmonary artery constriction, mean calculated LV end-diastolic volumes decreased from 69.2 +/- 20.0 to 56.2 +/- 21.3 cm3 (p less than or equal to 0.05). Mean systolic stroke volume decreased from 20.6 +/- 5.5 to 14.0 +/- 6.3 cm3 (p less than or equal to 0.05). These changes were entirely accounted for by alterations in the behavior of the LV septal-free wall minor axis and rearrangements in LV equatorial geometry. When the pulmonary artery was constricted, elongation of the septal-free wall axis occurred during isovolumic systole and was accompanied by a reciprocal decrease in anterior-posterior dimension. Most of the decrease in septal-free wall dimension occurred during relaxation and early diastole rather than during ejection. Mean septal-free wall end-diastolic dimension decreased from 5.45 +/- 0.69 to 4.90 +/- 0.75 cm (p less than or equal to 0.05). The mean systolic decrease in septal-free wall dimension fell from 0.36 +/- 0.18 to 0.14 +/- 0.22 cm (p less than or equal to 0.05). The end-diastolic dimensions and systolic shortening of the LV anterior-posterior minor axis and base-apex major axis were not significantly altered by pulmonary artery constriction. These findings suggest that during acute RV hypertension, impairment of LV systolic function and rearrangements in LV dynamic geometry are primarily the result of the anatomic contiguity of the two ventricles.
Hemodynamic and neuroendocrine responses to acute and chronic alpha-adrenergic blockade with prazosin and phenoxybenzamine.
Authors: Mulvihill-Wilson J , Gaffney F A , Pettinger W A , Blomqvist C G , Anderson S , Graham R M
Published: June 2011

We investigated the relevance of the selective alpha 1-adrenergic receptor blockade produced by prazosin to its blood pressure-lowering efficacy in man. The hemodynamic and neuroendocrine responses to the acute and chronic oral administration of prazosin and phenoxybenzamine were compared in a randomized, double-blind, placebo-controlled, crossover study of 11 patients with essential hypertension. These responses were also evaluated during lower body negative pressure and dynamic bicycle exercise, which produce potent but diversified activation of the sympathetic nervous system. In the acute studies, arterial blood pressure decreased to similar levels with prazosin or phenoxybenzamine; however, hemodynamic and neuroendocrine responses differed both before and during sympathetic nervous system activation. Prazosin lowered arterial blood pressure by reducing total peripheral resistance (p less than 0.05). In contrast, phenoxybenzamine produced a modest reduction in cardiac output (8%, p less than 0.05) with little change in total peripheral resistance, forearm vascular resistance or forearm blood flow. Additionally, plasma norepinephrine concentration and heart rate rose to significantly higher levels with prazosin (p less than 0.02) than with phenoxybenzamine, a difference that was most evident with lower body negative pressure or dynamic exercise. Baroreceptor control of arterial pressure homeostasis was preserved with both agents, except during marked degrees of cardiovascular stress. With chronic therapy, the circulatory responses adapted to the alpha-adrenergic antagonists, and both drugs produced similar hemodynamic and neuroendocrine profiles. The differences with acute administration may be the result of a more rapid onset of action and a more marked degree of alpha-adrenergic blockage with prazosin than with phenoxybenzamine therapy, rather than to any difference in their alpha 1- and alpha 2-adrenergic receptor blocking properties. Moreover, the findings of the present study suggest that the prejunctional alpha 2-receptor, autoinhibitory to sympathetic neuronal norepinephrine release, is of no functional significance in patients with essential hypertension.
Origin of the third heart sound. I. Studies in dogs.
Authors: Ozawa Y , Smith D , Craige E
Published: June 2011

We studied 13 anesthetized dogs in which a third heart sound (S3) was repeatedly induced by hypoxemia plus fluid overload. A miniature accelerometer with a mass of about 1.1 g was applied at three levels--intact chest wall over cardiac apex, in the pericardium and on the epicardium--to record motion of the structures under observation as well as sound. Intraventricular pressure and sound were monitored using a Millar catheter. Application of two accelerometers simultaneously over the epicardium permitted observation of the chronologic sequence of ventricular wall dynamics in early diastole. The S3 at each level occurred simultaneously with the sudden onset of reduced acceleration, or negative jerk. These dynamic phenomena were maximal at or near the cardiac apex. We conclude that the event that triggers the S3 is a sudden intrinsic limitation of longitudinal expansion of the left ventricular wall.
Hemodynamic effects of verapamil in children and adolescents with hypertrophic cardiomyopathy.
Authors: Spicer R L , Rocchini A P , Crowley D C , Vasiliades J , Rosenthal A
Published: June 2011

The acute hemodynamic effects of verapamil were evaluated in nine children with hypertrophic cardiomyopathy. Verapamil, 0.1 mg/kg, was administered as an i.v. bolus over 2 minutes, followed by a 20-minute continuous infusion of 0.007 mg/kg/min. Hemodynamic measurements were obtained at rest in nine patients and at maximal supine bicycle exercise in seven before and 15 minutes after verapamil. At rest, verapamil increased the mean cardiac output from 3.3 +/- 0.9 to 3.7 +/- 0.9 l/min/m2 (+/- SD) (p less than 0.02) and decreased left ventricular end-diastolic pressure from 19.3 +/- 8.1 to 14.5 +/- 6.9 mm Hg (p less than 0.006). In six patients with resting left ventricular outflow tract obstruction, the systolic pressure gradient decreased from 17.5 +/- 7.2 to 5.2 +/- 4.5 mm Hg (p less than 0.04). Repeat supine bicycle exercise testing after verapamil showed increases in total work performed (1743 +/- 1284 to 3168 +/- 1643 kg-m, p less than 0.006) and maximal cardiac index during exercise (6.5 +/- 1.3 to 7.8 +/- 1.8 l/min/m2, p less than 0.05), and decreases in maximal exercise left ventricular end-diastolic pressure (29.1 +/- 10.1 to 19.3 +/- 10.4 mm Hg, p less than 0.002) and left ventricular systolic outflow tract gradient (31.2 +/- 10.5 to 1.75 +/- 1.7 mm Hg, p less than 0.04). These results suggest that verapamil may be an effective therapeutic agent for the treatment of hypertrophic cardiomyopathy in children.
The effects of reperfusion and retrograde coronary flow bleeding after coronary occlusion on induced electrical instability in the dog.
Authors: Jones-Collins B A , Patterson R E
Published: June 2011

Reperfusion achieved by streptokinase infusion early after myocardial infarction (MI) is now being performed in patients, but the effect on electrical instability of increasing or decreasing perfusion in the region at risk for MI is unknown. Accordingly, 34 dogs were randomized to control (13 dogs), reperfusion (11 dogs) and retrograde bleeding (10 dogs) groups. All dogs underwent coronary artery occlusion (23 of the left anterior descending and 11 of the circumflex artery). In the control dogs, occlusion was permanent. In the reperfused dogs, the occlusion was released at 2 hours. In the retrograde bleeding dogs, retrograde flow bleeding distal to the occlusive tie was continued for 2 hours after coronary occlusion. Four days later, all dogs underwent a standard right ventricular pacing protocol. Induced arrhythmias were scored; ventricular fibrillation was assigned the highest score, followed by sustained ventricular tachycardia, nonsustained ventricular tachycardia and repetitive ventricular response. Arrhythmias provocable later in diastole were assigned higher scores than those provocable early in diastole. Infarct size was not different in the three groups (35%, 28% and 39% of the area at risk in control, reperfusion and retrograde bleeding groups, respectively). However, the electrical instability index was lower in the reperfusion group than in the other two groups (e.g., electrical instability index A at 200 beats/min: p less than 0.005 for reperfusion vs control; p less than 0.01 for reperfusion vs retrograde bleeding). Retrograde bleeding did not alter the electrical instability index from the control state. These results suggest that despite no significant reduction in infarct size, reperfusion after infarction may reduce electrical instability.
Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology.
Authors: Jackman W M , Prystowsky E N , Naccarelli G V , Fineberg N S , Rahilly G T , Heger J J , Zipes D P
Published: June 2011

The syndrome of enhanced atrioventricular nodal (AVN) conduction has been defined arbitrarily by: AH interval during normal sinus rhythm (AH-NSR) less than or equal to 60 msec; shortest right atrial pacing cycle length (PCL) maintaining 1:1 AVN conduction (shortest PCL 1:1) less than or equal to 300 msec; and at the shortest PCL 1:1, an increase in the AH interval from AH-NSR (delta AH) less than or equal to 100 msec. We examined the relationship between AH-NSR, shortest PCL 1:1, and delta AH in 160 consecutively studied patients who did not have accessory AV pathways or second-degree AV block to determine whether a distinct subgroup of patients with unusually rapid AVN conduction properties could be identified. The frequency distribution of each of the variables was unimodal and continuous. Cluster analysis, combining the three variables, failed to reveal a distinct subgroup at the lower end of the spectrum. Sixty-six patients (41%) had AH-NSR less than or equal to 60 msec, 36 (23%) shortest PCL 1:1 less than or equal to 300 msec, 76 (48%) delta AH less than or equal to 100 msec, and 17 (11%) all three criteria. The shape of the AH vs atrial PCL curve was independent of shortest PCL 1:1. Neither delta AH nor the terminal slope of the curve for AH vs atrial PCL (measured over the 20-40 msec before Wenckebach block) was related to AH-NSR or shortest PCL 1:1. We conclude that a subgroup cannot be identified by AH-NSR, shortest PCL 1:1, and delta AH, and that enhanced AVN conduction as previously defined represents simply one end of the continuous spectrum of normal AVN physiology.
Platelet tests and antiplatelet drugs in coronary artery disease.
Authors: de Boer A C , Han P , Turpie A G , Butt R , Gent M , Genton E
Published: June 2011

This study was designed to clarify discrepancies in the literature concerning platelet survival time and beta-thromboglobulin (beta TG) levels in patients with coronary artery disease (CAD) and the effect of platelet-suppressant drugs on these tests. Platelet survival time and plasma beta TG levels were determined in 48 patients with angiographically documented CAD. The effect of sulfinpyrazone or aspirin/dipyridamole on these measurements was investigated in a double-blind, crossover trial that included a placebo phase. In patients with CAD, the mean plasma beta TG concentration was significantly elevated, but the mean platelet survival time was not significantly different from that in controls. Treatment with sulfinpyrazone or aspirin/dipyridamole did not produce changes in platelet survival time or plasma beta TG concentration that were significantly different from the values during the placebo phase. This study demonstrates that compared with the spontaneous variation in platelet survival time or beta TG concentration, there was no measureable effect of sulfinpyrazone or aspirin/dipyridamole on the results of the tests.
Myocardial contrast echocardiography: a reproducible technique of myocardial opacification for identifying regional perfusion deficits.
Authors: Tei C , Sakamaki T , Shah P M , Meerbaum S , Shimoura K , Kondo S , Corday E
Published: June 2011

The effects and reliability of a simple method of contrast two-dimensional echocardiographic delineation of myocardium after intracoronary injections were evaluated in closed-chest dogs. Multiple injections of an agitated saline-Renografin (meglumine diatrizoate) mixture (3:2 ratio, 2-ml bolus) into the left main coronary artery as well as at different sites of the left anterior descending and circumflex coronary arteries were studied in several short-axis and long-axis cross sections of the left ventricle. These contrast injections opacified specific regions of left ventricular myocardium depending on the site of injection. Contrast injection into the left main coronary artery provided a clear, echo-free outline (negative contrast) of underperfused myocardium distal to the coronary occlusion. Reproducibility studies of the extent of involved zones measured in echocardiographic cross sections indicated high intra- and interobserver correlation coefficients (r = 0.97 and 0.97). The effects of the intracoronary injection of contrast material appeared minor and brief. ECG ST-T changes lasted 49.4 +/- 36.7 seconds, aortic systolic pressure was reduced by 7.6 +/- 4.4% for 18.9 +/- 4.8 seconds, and the peak rate of left ventricular pressure rise decreased by 14.3 +/- 2.6%, but returned to control levels within 19.4 +/- 6.1 seconds. The zone of left ventricular asynergy after coronary occlusions was also delineated by cross-sectional echocardiography and corresponded to the contrast-outlined underperfused zone (negative contrast). This new intracoronary echocardiographic technique has only minor hemodynamic consequences and provides reliable quantitation of underperfused and dysfunctioning zones after experimental coronary occlusions. Further investigation and validation of this method may provide useful characterization of the extent and severity of myocardial ischemia and infarction.
Noninvasive Doppler determination of cardiac output in man. Clinical validation.
Authors: Huntsman L L , Stewart D K , Barnes S R , Franklin S B , Colocousis J S , Hessel E A
Published: June 2011

A noninvasive technique for assessing cardiac output (CO) was evaluated by comparing it with thermodilution determinations in patients in the intensive care unit. The new method uses pulsed ultrasound to measure aortic diameter and continuous-wave Doppler ultrasound to obtain aortic blood velocity. An initial study evaluating just the velocity measurement showed that changes of the Doppler index of output (DI) correlated well with those of thermodilution cardiac output (TDCO). Linear regression analysis yielded delta DI = 0.87 delta TDCO + 0.14 (r = 0.83, n = 95). Using a university research instrument these measurements were possible in 54 of 60 patients (90%). A second study using a prototype commercial device incorporated the diameter measurement. Ultrasonic cardiac output (UCO), calculated as the time integral of velocity multiplied by the aortic area, was compared to TDCO. The data, obtained from 45 of 53 patients (85%), are described by the linear regression UCO = 0.95TDCO + 0.38 (r = 0.94, n = 110) over a range of 2-11 l/min. Patients with aortic stenosis, aortic insufficiency or a prosthetic valve have been excluded from the second study due to conditions likely to violate the assumptions upon which the calculation of absolute cardiac output is based. These results indicate that accurate CO can be measured by noninvasive ultrasound in most patients. The technique may be useful for extended CO monitoring in acute care patients and for CO assessment in many other types of patients undergoing diagnostic studies and therapeutic interventions.
Functional significance of collaterals during ameroid-induced coronary stenosis in conscious dogs. Interrelationships among regional shortening, regional flow and grade of coronary stenosis.
Authors: Tomoike H , Inou T , Watanabe K , Mizukami M , Kikuchi Y , Nakamura M
Published: June 2011

We studied the relationships among collateral flow, regional myocardial shortening and the grade of coronary stenosis during ameroid-induced chronic coronary constriction in 22 conscious dogs. A radiolucent ameroid, a Doppler flow probe and a cuff occluder were placed on the left circumflex coronary artery (LCx). Regional myocardial shortening and regional myocardial blood flow were assessed simultaneously using ultrasonic dimension gauges and the tracer microsphere technique, respectively, during temporary occlusion of the LCx. Regional hypokinesia and ischemia were attenuated as a function of time during progressive coronary stenosis. Fifty percent recovery and full recovery of regional shortening during occlusion were observed 19 +/- 3 and 25 +/- 4 days after instrumentation, respectively, when the endocardial blood flow recovered from 0.42 +/- 0.07 ml/min/g at 7 days to 0.56 +/- 0.07 and 0.80 +/- 0.05 ml/min/g, respectively. Greater than 75% coronary stenosis coincided with collateral development, as estimated from regional shortening rate and the appearance of angiographically opacified collaterals. Our study confirms that the development of collateral vessels reduces regional ischemia and hypokinesia induced during abrupt coronary occlusion in a canine model.
Association between coronary heart disease risk factors and physical fitness in healthy adult women.
Authors: Gibbons L W , Blair S N , Cooper K H , Smith M
Published: June 2011

We examined associations between physical fitness and risk factors for coronary heart disease in healthy women ages 18-65 years. Physical fitness was objectively determined by the duration of a maximal treadmill exercise test. Six physical fitness categories (very poor to superior), specific within 10-year age increments, were established. Mean risk factor levels varied across categories, but so did potential confounders such as age and weight. Multiple linear regression modeling was used to control for the effects of age, weight and year of exam on coronary risk factors. After adjustment, physical fitness was independently associated with triglycerides (p less than 0.001), high-density lipoprotein cholesterol (HDL-C) (p less than or equal to 0.001), total cholesterol/HDL-C ratio (p less than or equal to 0.001), blood pressure (p less than or equal to 0.001) and cigarette smoking (p less than or equal to 0.001).
Value and limitations of computed tomography in assessing aortocoronary bypass graft patency.
Authors: Daniel W G , Döhring W , Stender H S , Lichtlen P R
Published: June 2011

To determine the value of nondynamic computed tomography (CT) in assessing aortocoronary bypass graft patency, we studied 67 patients with 125 grafts by CT and by coronary angiography at close time intervals. CT scans were performed before and after one to three (average 1.98 +/- 0.65) 50-ml i.v. bolus injections of contrast material. Eighty-four of 92 grafts patent at angiography were also visualized by CT (sensitivity 91.3%); 29 of 33 grafts closed at angiography were considered to be occluded by CT (specificity 87.9%). Eleven of 13 grafts demonstrating one or more severe obstructions at angiography were considered to be patent by CT. Interobserver disagreement existed in four of 125 grafts (3.2%) and intraobserver variability was 1.6%. Although nondynamic CT allows a correct assessment of graft patency in many cases, it does not provide sufficient information on graft stenosis and function to replace angiography in patients who are symptomatic after surgery.
A new ECG classification system for myocardial infarction based on receiver operating characteristic curve analysis and information theory.
Authors: Abreu-Lima C , Correia D M , Almeida J , Antunes-Lopes M , Cerqueira-Gomes M
Published: June 2011

An optimized three-lead ECG hierarchial decision-tree type of classification system for myocardial infarction is presented. For selection of the best threshold values for each criterion and the best association of features, we developed a procedure based on "receiver operating characteristic" (ROC) curve data analysis and information theory. Optimization was obtained through maximization of information content of the criteria. The classifier is based on nine measurements that can be easily obtained by hand (QX duration, Q/R Y amplitude, R Y amplitude, Q/R Y duration, Q Z amplitude, QRS and T axes in the horizontal plane, Q Z duration and R Z amplitude) and achieved a satisfactory performance in an independent group of patients (true-positive ratio 0.853, false-positive ratio 0.105, average information content 0.308 bits).
Comparison of early thallium-201 scintigraphy and gated blood pool imaging for predicting mortality in patients with acute myocardial infarction.
Authors: Becker L C , Silverman K J , Bulkley B H , Kallman C H , Mellits E D , Weisfeldt M
Published: June 2011

The extent of abnormality in early thallium-201 and gated cardiac blood pool scintigrams has been reported to be useful for predicting mortality in patients with acute myocardial infarction (AMI). To compare the two techniques, 91 patients admitted consecutively with evident or strongly suspected AMI underwent both imaging studies within 15 hours of the onset of symptoms. Patients with pulmonary edema or shock were excluded. AMI developed in 84% of patients, and 6-month mortality for the entire group was 16%. A thallium defect score of 7.0 or greater (corresponding to at least a moderate reduction of activity involving 40% of the left ventricular circumference) identified a subgroup of 14 patients with 64% 6-month mortality rate. Similarly, a left ventricular ejection fraction of 35% or less identified a high-risk subgroup of 10 patients with a 6-month mortality of 60%. Mortality in the remaining patients was 8% for thallium score less than 7 and 11% for ejection fraction greater than 35%. The mortality rate was highest among patients who had concordant high-risk scintigrams (five of six, 83%), lowest in those with concordant low-risk studies (five of 64, 8%) and intermediate in those with discordant results (four of 11, 36%). Of a number of clinical variables, only the appearance of Q waves, peak creatine kinase greater than 1000 IU/I, and history of infarction were significantly associated with mortality. High-risk thallium or blood pool scintigraphic results were significantly more predictive and a thallium score of 7 or greater was more sensitive for detecting nonsurvivors than ejection fraction 35% or less at a similar level of specificity. Stepwise multiple logistic analysis showed that the thallium score was the best predictor of mortality, but that appearance of Q waves and ejection fraction were additive. Using these three variables, 11 patients were calculated to have a 50% or greater chance of dying and eight (73%) actually died, compared with six of 70 (9%) with a calculated chance of death of less than 50%. These results in a prospectively identified and consecutive group of patients support the value of early thallium and blood pool scintigraphy for separating high- and low-risk subgroups of hemodynamically stable infarct patients.
Serum creatine kinase MM isoenzyme sub-bands after acute myocardial infarction in man.
Authors: Morelli R L , Carlson C J , Emilson B , Abendschein D R , Rapaport E
Published: June 2011

Using an isoelectric-focusing (IEF) method developed to quantitate MM isoenzyme-creatine kinase (CK) sub-band activity, we identified a reproducible time-varying pattern of these sub-bands in the serum of eight patients with acute myocardial infarction (MI). Our observations are consistent with the view that MM3-CK (the M2-CK dimer, the pure gene product) is converted intravascularly to MM2-CK, and then to MM1-CK (the M1-CK dimer, the pure postsynthetic sub-band). The MM3-CK reaches a peak first, 16 hours after infarction, followed by MM2-CK, and then by MM1-CK. The MM3-CK is the dominant sub-band in normal myocardium; there is much less MM2-CK and virtually no MM1-CK. The MM3-CK sub-band peak may indicate the time at which enzyme ceases to be released from the injured myocardium. The ratio MM3-CK:MM1-CK rises within 6 hours after onset of chest pain from a baseline of 0.38 and peaks 10 hours after MI. The peak ratio was between 1.1 and 4.2, and the value correlated with the time when total CK activity peaked after MI. The 10-fold change in the MM3:MM1 ratio after MI, as well as the early period at which this ratio peaks (10 hours), makes this an earlier and more sensitive indicator of enzyme release.
Chest wall velocity and the second heart sound. An improved sensor of S2 splitting.
Authors: Smith D , Ozawa Y , Craige E
Published: June 2011

We report a new method of detection of the timing of the aortic and pulmonary valve closure that depends not on the registration of audible vibrations, but rather, on subtle but distinct movements of the chest wall, which are external manifestations of these events. We studied these phenomena in six open-chest dogs and in 69 human subjects. The dog studies show that the two distinct inward movements detected by a motion sensor applied to the epicardium in the vicinity of the right ventricular outflow tract correlate with the timing of the incisural notches of the pressure signals from the great vessels. In humans, these movements are transmitted to the skin surface and can be detected noninvasively. In 48 of the 69 human subjects (70%), these spikes provided a significantly better indication of the timing of semilunar valve closure than did the conventional phonocardiogram.
Plasma norepinephrine concentration and plasma dopamine-beta-hydroxylase activity in patients with congestive heart failure.
Authors: Minami M , Yasuda H , Yamazaki N , Kojima S , Nishijima H , Matsumura N , Togashi H , Koike Y , Saito H
Published: June 2011

The relationship between plasma norepinephrine (NE), epinephrine (E) and dopamine-beta-hydroxylase activity (DBH) was studied in 90 cardiac patients (New York Heart Association [NYHA] classes I-IV), 85 healthy control subjects and 18 competitive skiers. The cardiac patients in NYHA classes III and IV had significantly higher NE (p less than 0.001) and lower DBH (p less than 0.001) levels than the controls, whereas the skiers had significantly lower NE (p less than 0.001) and higher DBH (p less than 0.05) levels than the controls. Seven cardiac patients in whom successful cardiac surgery was performed had decreased NE (p less than 0.001) and increased DBH (p less than 0.02), as well as significantly improved NYHA cardiac status (p less than 0.001). These findings demonstrate an inverse relationship between NE and DBH in a population of athletes, normal subjects and cardiac patients; the same inverse relationship holds for these patients when sequential studies are done after a change in cardiac status.
Low-dose captopril titration in patients with moderate-to-severe hypertension treated with diuretics.
Authors: Thind G S , Mahapatra R K , Johnson A , Coleman R D
Published: June 2011

To study the value of low-dose captopril (6.25 and 12.5 mg) and a diuretic combination, the blood pressure and heart rate of 17 patients with moderate-to-severe hypertension were monitored for 6 hours (hospital) or 3 hours (office) after the single low-dose or larger (25, 50, 100 and 150 mg) captopril dosage. All patients had preserved renal function and were taking an oral diuretic (hydrochlorothiazide or furosemide) for at least 4 weeks. The supine and upright acute blood pressure lowering with 6.25 mg was not different from the larger captopril doses; none produced persistent or profound hypotension. There was no deterioration of renal function, new or persistent increase in proteinuria, neutropenia or agranulocytosis acutely or during 17 +/- 2 weeks of follow-up. Low-dose captopril (6.25 or 12.5 mg three times daily) normalized the supine blood pressure of 35% of these patients acutely. We suggest that in hypertensive patients already taking a diuretic, a lower starting dose of captopril than the recommended 25 mg three times daily may be desirable.