bluuebunny/crossref_metadata_2025 huggingface dataset:
Methods of measurement of myocardial blood flow in patients: a critical review.
Authors: Marcus M L , Wilson R F , White C W
Published: June 2011

During the past decade, major progress has been made in the evolution of technology directed toward the accurate measurement of regional myocardial perfusion in patients. The deficiencies of some of the older methods (thermodilution and gas clearance) are better appreciated and improved approaches (Doppler catheters, positron-emission tomography, and digital subtraction angiography) have been developed. The new approaches should play a major role in research and for most applications the older methods will gradually be replaced. Efforts to bring these new methods to community hospitals and practicing cardiologists should be stimulated. Doppler catheters, positron-emission tomography, and digital-subtraction angiography are commercially available and Doppler catheters and digital-subtraction angiography could be easily incorporated into routine cardiac catheterization procedures. The Doppler catheter is the most inexpensive and probably the simplest to apply. In our opinion, routine measurements of coronary flow reserve will significantly improve the care of patients with coronary obstructive disease and other diseases that impair myocardial perfusion. If coronary reserve measurements are used frequently, patient selection for coronary angioplasty and bypass surgery will no longer depend entirely on visual assessment of percent diameter stenosis, a very poor criterion in many situations. Also, patients with chest pain syndromes, normal coronary vessels, and impaired coronary reserve will be identified and perhaps some effective treatment for this condition will be devised.(ABSTRACT TRUNCATED AT 250 WORDS)
Time course of regression of left ventricular hypertrophy in hypertensive patients treated with atenolol.
Authors: Dunn F G , Ventura H O , Messerli F H , Kobrin I , Frohlich E D
Published: June 2011

Regression of left ventricular hypertrophy occurs with a number of antihypertensive drugs, but the time course of this regression has not been defined clearly. We obtained echocardiograms at baseline and serially (on seven occasions) during a 1 year treatment period with the beta-adrenergic receptor inhibitor atenolol in 12 patients with previously untreated essential hypertension. To ensure control of blood pressure in all patients throughout the study, it was necessary to add a thiazide diuretic to the therapy of five patients. Baseline blood pressure was 155/100 mm Hg and fell to 136/84 mm Hg; there was a 20% reduction in heart rate. Posterior and septal wall thicknesses were reduced from 1.16 +/- 0.03 to 1.06 +/- 0.02 cm (p less than .05) and from 1.28 +/- 0.07 to 1.18 +/- 0.06 cm (p less than .05), respectively; this reduction became significant initially at 4 weeks. Left ventricular mass decreased from 144 +/- 9 to 127 +/- 7 g/m2 (p less than .05) and this fall first became statistically significant at 6 months. Significant reduction in electrocardiographic voltages was also seen at 6 months. Therefore, regression of left ventricular hypertrophy with atenolol-induced blood pressure control occurred as early as 4 weeks after starting therapy and was maintained thereafter without apparent compromise of left ventricular systolic function.
Two-dimensional and pulsed Doppler echocardiography in the postoperative evaluation of total anomalous pulmonary venous connection.
Authors: Smallhorn J F , Burrows P , Wilson G , Coles J , Gilday D L , Freedom R M
Published: June 2011

The role of combined two-dimensional and pulsed Doppler echocardiography in the postoperative assessment of patients with total anomalous pulmonary venous connection was evaluated. Twenty-two cases with a median age of 9.5 weeks at the initial examination were evaluated. Serial ultrasound examinations were performed throughout the study period. The ultrasound results were compared with chest radiographs obtained during the same period. Of the 22 patients, 16 had normal pulmonary venous flow profiles characterized by low-velocity laminar flow. Of this group 12 had persistent radiographic postoperative pulmonary edema that cleared in all by 4 months. Six patients with pulmonary venous obstruction were identified, the diagnosis being confirmed at catheterization or autopsy. The venous flow pattern in this group was uniformly high velocity and turbulent. It was possible to localize the site of obstruction in each case. Although pulmonary edema was present in each patient, the chest radiograph did not provide reliable information as to the exact site of obstruction. Combined two-dimensional and Doppler echocardiography is a useful adjunct in the postoperative evaluation of patients with total anomalous pulmonary venous connection.
The hemodynamic effects of sotalol and quinidine: analysis by use of rest and exercise gated radionuclide angiography.
Authors: Mahmarian J J , Verani M S , Hohmann T , Hill R , Thornton B C , Bolli R , Young J B , Roberts R , Pratt C M
Published: June 2011

This placebo-controlled, double-blind trial compared the hemodynamic effects of sotalol and quinidine with the use of rest and exercise gated radionuclide angiography. Patients had frequent ventricular premature depolarizations (greater than or equal to 30 VPDs/hour) and depressed cardiac function (mean ejection fraction 43 +/- 15%). Resting left ventricular ejection fraction and stroke volume index increased (p less than .002, p less than .001, respectively) during sotalol therapy, associated with a concomitant fall in heart rate (p less than .001). Quinidine also increased mean left ventricular ejection fraction, but less so than did sotalol (p less than .05). Quinidine significantly decreased left ventricular end-diastolic (p less than .05) and end-systolic (p less than .002) volumes, but had no effect on stroke volume index or heart rate. Neither drug affected cardiac index. Quinidine resulted in no symptomatic deterioration in left ventricular function or serious arrhythmia aggravation. In contrast, five patients on sotalol developed either decompensated congestive heart failure (two patients), arrhythmia aggravation (two patients), or hypotension associated with bradyarrhythmia (one patient). These patients had a unique hemodynamic profile that can be used to identify patients likely to have a poor outcome on sotalol. This profile reflected a lack of cardiac reserve, characterized by an inability to increase stroke volume and cardiac output with supine bicycle exercise.
Frequency-dependent effects of amiodarone on atrioventricular nodal function and slow-channel action potentials: evidence for calcium channel-blocking activity.
Authors: Nattel S , Talajic M , Quantz M , DeRoode M
Published: June 2011

The purpose of these experiments was to determine the frequency dependence of the effects of amiodarone and its active desethyl metabolite on slow-channel tissues. Intravenous amiodarone and desethylamiodarone (10 or 25 mg/kg) increased atrioventricular conduction time (AVCT) and refractory period (AVERP) in open-chest, chloralose-anesthetized dogs. Drug effects on AVCT and AVERP were greatly augmented by increasing atrial stimulation frequency. The frequency dependence of drug effects was quantified by studying the response of atrioventricular (AV) conduction to changes in coupling interval. Under control conditions, premature atrial stimulation increased AVCT with a time constant of 70 msec. In the presence of amiodarone and desethylamiodarone, a biexponential relationship between AVCT and coupling interval was observed. One component had a time constant similar to control, and a slower component with a time constant of about 1 sec appeared. Slow-channel action potentials produced in canine cardiac false tendons by elevated potassium (25 mM) and isoproterenol in vitro showed interval-dependent changes in Vmax with a time constant averaging 74 msec in the absence of amiodarone. In the presence of amiodarone, a slower recovery phase of Vmax with a time constant averaging 0.94 sec was observed. These results indicate that amiodarone and its metabolite produce heart rate-dependent changes in AV nodal function in vivo and suggest use-dependent calcium-channel blockade as a mechanism of this action. Amiodarone's rate-related effects on slow-channel properties should produce selective depression of supraventricular tachyarrhythmias involving rapid activation of the AV node.
Attenuation of dysfunction in the postischemic 'stunned' myocardium by dimethylthiourea.
Authors: Bolli R , Zhu W X , Hartley C J , Michael L H , Repine J E , Hess M L , Kukreja R C , Roberts R
Published: June 2011

The mechanism for the prolonged contractile dysfunction observed in myocardium reperfused after reversible regional ischemia ("stunned" myocardium) is unclear. Recent studies suggest that myocardial stunning may be mediated by oxygen-derived free radicals, but the precise molecular species involved remain unknown. Thus we explored the role of the highly cytotoxic hydroxyl radical in regional postischemic dysfunction by using dimethylthiourea (DMTU), an effective and highly permeable hydroxyl radical scavenger. Open-chest dogs undergoing a 15 min occlusion of the left anterior descending coronary artery followed by 4 hr of reperfusion received either DMTU (0.5 g/kg iv over 45 min starting 30 min before occlusion, n = 14) or saline (n = 15). Control and treated dogs were comparable with respect to variables that may affect postischemic dysfunction, including heart rate, aortic pressure, left atrial pressure, arterial blood gases and hemoglobin concentration, size of the occluded bed (determined by postmortem perfusion), and collateral blood flow (determined by radioactive microspheres). Regional myocardial function was assessed by measuring wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions and similar degrees of dyskinesis during ischemia. After reperfusion, however, wall thickening (expressed as percent of baseline) was considerably greater in treated as compared with control dogs: 53 +/- 9% (mean +/- SEM) vs 9 +/- 14% (p less than .03) at 1 hr, 55 +/- 9% vs 23 +/- 13% (p less than .05) at 2 hr, 60 +/- 9% vs 28 +/- 14% (p less than .05) at 3 hr, and 67 +/- 5% vs 36 +/- 13% (p less than .05) at 4 hr. Thus DMTU produced a significant and sustained improvement in recovery of contractile function. In concentrations greater than the plasma levels attained in vivo, DMTU did not scavenge either hydrogen peroxide or superoxide anion in vitro. These results suggest that the myocardial dysfunction occurring after a brief episode of regional ischemia is mediated in part by the hydroxyl radical.
Lipoproteins and the pathogenesis of atherosclerosis.
Authors: Steinberg D
Published: June 2011

It is now clear that hypercholesterolemia can, in some instances, be a necessary and sufficient cause of premature atherosclerosis. This has been best established in patients with familial hypercholesterolemia, a deficiency of the low-density lipoprotein receptor. Although hypercholesterolemia is not the only cause of atherosclerosis, a large body of evidence has identified it as a determining cause in many cases. This article reviews current hypotheses regarding the mechanisms by which hypercholesterolemia accelerates atherogenesis. The role of the foam cell is discussed in detail because it is a characteristic feature of the earliest lesion, the so-called fatty streak. Once thought to derive exclusively from smooth muscle cells, the foam cell is now known to originate in large part from monocytes that enter the artery wall and alter their properties to become tissue macrophages. Recent studies of the biology of the macrophage-derived foam cell are providing new insights into the mechanisms by which it enters the arterial wall and interacts with various classes of native and modified lipoproteins. As our understanding of the biology of the foam cell and its precursors grows, it may become possible to intervene and slow the progress of atherosclerosis by new modalities that might act synergistically with measures to control plasma cholesterol levels.
Prospective evaluation of a sequential pacing and high-energy bidirectional shock algorithm for transvenous cardioversion in patients with ventricular tachycardia.
Authors: Lindsay B D , Saksena S , Rothbart S T , Wasty N , Pantopoulos D
Published: June 2011

Rapid ventricular pacing alone or in combination with low- or intermediate-energy shocks has limited efficacy in cardioverting rapid ventricular tachycardia (VT) when delivered through two transvenous catheter electrodes. This prospective study determined the efficacy and safety of an algorithm that used a sequence of rapid ventricular pacing (RVP) and intermediate-energy (5 and 15 J) and high-energy (25J) single, bidirectional shocks delivered by two transvenous catheter electrodes in conjunction with a cutaneous electrode in patients with sustained VT. The bidirectional shock was simultaneously delivered over two electrical vectors via a common right ventricular apical cathode and tow anodes consisting of the superior vena caval catheter electrode and cutaneous patch. The electrical therapy delivered was determined by the cycle length of VT. Slow VT (cycle length greater than 300 msec) was sequentially treated by RVP followed by incremental bidirectional shocks of 5, 15, and 25 J. Rapid VT (cycle length less than 300 msec) was treated with no incremental bidirectional shocks of 15 and 25 J. VT was reinduced to determine reproducibility of the algorithm for episodes that were successfully terminated. For patients in whom the primary algorithm failed, a second algorithm was used that excluded 5 and 15 J shocks and went directly to a 25 J shock. VT was reinduced twice and the secondary algorithm was evaluated. Thus, reproducibility of termination of VT with the primary and secondary algorithm was examined. Fifty episodes of slow VT and 40 episodes of rapid VT were induced in 22 patients (mean left ventricular ejection fraction 31 +/- 14%). Six patients had rapid VT, nine patients had slow VT, and seven patients had both.(ABSTRACT TRUNCATED AT 250 WORDS)
Alterations in transmural blood flow and body surface ST segment abnormalities produced by ischemia in the circumflex and left anterior descending coronary arterial beds of the dog.
Authors: Mirvis D M , Ramanathan K B
Published: June 2011

Previous studies have documented a quantitative relation between alterations in transmural myocardial blood flow and body surface electrocardiographic distributions during rapid atrial pacing after chronic occlusion of the left circumflex coronary artery (LCx). Because other studies have described functional differences between the left anterior descending (LAD) and the LCx perfusion beds, we tested the hypothesis that these two territories exhibit quantitative differences in their responses to demand-dependent myocardial ischemia. To do so, 25 sedated dogs were studied 3 weeks after implantation of an ameroid constrictor around the proximal LCx (15 dogs, group I) or the LAD (group II). Oxygen demand was increased by rapid atrial pacing at rates of 90 to 210 beats/min, myocardial blood flow was measured by serial injections of radiolabeled microspheres, and the electrocardiographic consequences were evaluated by isopotential body surface mapping. Endocardial flows and the endocardial/epicardial flow ratio fell to significantly lower levels during atrial pacing in the ischemic LAD bed than in the LCx perfusion zone. Electrocardiographic patterns indicative of subendocardial ischemia also developed with lesser abnormalities in endocardial/epicardial ratios as determined by logistic regression models, in the LAD than in the LCx bed. Thus the LAD bed is more susceptible to ischemia than the LCx region because of differences in collateral blood flow patterns. In addition, the intensity of the surface electrocardiographic potentials during ischemia was significantly greater, as measured by linear regression, after LAD than after LCx obstruction. These data thus demonstrate significant differences between the two cardiac regions as electrocardiographic potential sources during ischemia.
Effect of angioplasty-induced endothelial denudation compared with medial injury on regional coronary blood flow.
Authors: Bates E R , McGillem M J , Beals T F , DeBoe S F , Mikelson J K , Mancini G B , Vogel R A
Published: June 2011

To determine the effect of angioplasty-induced arterial injury on regional coronary blood flow, resting and postocclusion reactive hyperemic flows were measured in the left anterior descending (LAD) and circumflex (LCx) coronary arteries of 32 dogs after one of four interventions in the LAD with a balloon angioplasty catheter: group A, no injury; group B, endothelial denudation; group C, medial injury; group D, pretreatment with 325 mg of aspirin 2 hr before medial injury. Resting flows did not change in any group. In group C, hyperemic flow decreased in both the LAD and LCx by 15% to 20% (p less than .001) over 30 to 90 min, suggesting that a circulating substance changed coronary resistance. Histologic and ultrastructural studies of the LADs demonstrated an intact endothelial cell layer in group A, endothelial disruption with a few adherent platelets in group B, medial injury with a dense layer of adherent platelets in group C, and medial injury with a few adherent platelets in group D. Thus endothelial denudation results in relatively mild platelet deposition and no change in resting or hyperemic coronary blood flow. In contrast, medial injury results in relatively marked platelet deposition and a significant decrease in hyperemic flow, both of which are prevented by platelet inhibition with aspirin.
Predictors of efficacy of amiodarone and characteristics of recurrence of arrhythmia in patients with sustained ventricular tachycardia and coronary artery disease.
Authors: Zhu J , Haines D E , Lerman B B , DiMarco J P
Published: June 2011

The value of serial electropharmacologic testing during long-term oral amiodarone therapy for prediction of long-term drug efficacy as well as characteristics of arrhythmia recurrence is controversial. One-hundred four consecutive patients with coronary artery disease and sustained ventricular tachyarrhythmias (VT) underwent initial electrophysiologic (EP) evaluation in the drug-free state and again after an amiodarone loading period of 25 +/- 14 days (mean +/- SD). Twenty-six patients (25%) had no inducible ventricular tachyarrhythmia during therapy with amiodarone (VT control group), whereas arrhythmia inducibility persisted in the remaining 78 patients (VT noncontrol group). During 17.4 +/- 13.7 months of follow-up, two patients in the VT control group either had VT recurrence or died suddenly compared with 21 VT recurrences and eight sudden cardiac deaths in the VT noncontrol group (actuarial event rates at 36 months of 0.11 and 0.56, respectively, p = .0065). The cycle lengths of recurrent VT in these 21 patients in the VT noncontrol group were compared with those observed at final EP testing. A significant linear correlation was demonstrated (r = .76, p = .0001). Subgroup analysis of patients in the VT noncontrol group showed no EP predictors of outcome, including cycle length of induced VT. However, patients dying suddenly during the follow-up period had a higher prevalence of new or worsening congestive heart failure (75%) compared with patients with VT recurrence (19%) or those with no arrhythmic event (29%) (p less than .02).2off
Time course of resolution of pulmonary hypertension and right ventricular remodeling after orthotopic cardiac transplantation.
Authors: Bhatia S J , Kirshenbaum J M , Shemin R J , Cohn L H , Collins J J , Di Sesa V J , Young P J , Mudge G H , Sutton M G
Published: June 2011

Most patients with severe congestive heart failure have secondary pulmonary hypertension (PHT). Elevation of pulmonary vascular resistance (PVR) to greater than 480 dynes.sec.cm-5 (6 Wood units) is currently the principle hemodynamic contraindication to orthotopic cardiac transplantation. We performed serial two-dimensional Doppler echocardiographic examinations and right heart catheterizations in 24 recipients (21 men, 14-58 years old) of orthotopic cardiac transplants to determine the time course of resolution of PHT and the concomitant remodeling of the donor right ventricle. Right and left heart filling pressures declined in parallel and reached the upper normal range at 2 weeks after the transplant procedure and remained unchanged at 1 year follow-up. Mean pulmonary arterial pressure (mm Hg) decreased from 38 +/- 9 preoperatively to 22 +/- 5 at 2 weeks and was 19 +/- 5 at 1 year after the transplantation procedure. At 1 year after surgery, PVR had decreased from 202 +/- 89 dynes.sec.cm-5 preoperatively to 99 +/- 36 dynes.sec.cm-5 (p less than .001), while cardiac output increased from 3.7 +/- 1.2 to 6.3 +/- 1.5 liters/min (p less than .001). Echocardiographic analysis showed that transplant recipients had an enlarged right ventricle on day 1 after surgery, and a volume overload contraction pattern and tricuspid regurgitation was present in the majority. This increase in right ventricular size was maintained at 1 year follow-up while the incidence of tricuspid regurgitation decreased. We conclude that there is rapid resolution of moderately elevated pulmonary arterial pressures after cardiac transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
Early and late results of intracoronary arterial stenting after coronary angioplasty in dogs.
Authors: Roubin G S , Robinson K A , King S B , Gianturco C , Black A J , Brown J E , Siegel R J , Douglas J S
Published: June 2011

Intimal dissection with acute closure represents the major complication associated with percutaneous transluminal coronary angioplasty (PTCA). Intracoronary stent devices offer the possibility of treatment for this sequela. We developed a balloon catheter-mounted, flexible coil stent for use in such cases. To determine the utility of this device and its immediate and long-term influence on arterial patency, 39 mongrel dogs had the stent placed after PTCA of the left circumflex or left anterior descending coronary arteries. Thirteen animals were treated before and after the procedure with warfarin. In this group there were three early deaths associated with stent thrombosis. Twenty-six animals were subsequently treated before and after with aspirin and dipyridamole. There were no early thrombotic events associated with stent placement in these animals. Late arteriographic examination revealed patent vessels in all dogs. Diameter stenosis for warfarin-treated dogs was 8 +/- 5% (mean +/- SD) at 2 months (n = 9), 6 +/- 4% at 6 months (n = 5), and 11 +/- 7% at 12 months (n = 3). Diameter stenosis for aspirin/dipyridamole-treated dogs was 9 +/- 3% at 2 months (n = 8), 8 +/- 5% at 6 months (n = 12), and 5% at 12 months (n = 1). Light and scanning electron microscopic analyses of stented arteries demonstrated incorporation of the stent wires into the arterial wall. Early findings included mild thrombosis localized to areas of wire entrenchment followed by rapid regrowth of endothelial and/or pseudoendothelial cells over trenches, exposed wires, and elastica.(ABSTRACT TRUNCATED AT 250 WORDS)
Reduction of reperfusion injury in the canine preparation by intracoronary adenosine: importance of the endothelium and the no-reflow phenomenon.
Authors: Olafsson B , Forman M B , Puett D W , Pou A , Cates C U , Friesinger G C , Virmani R
Published: June 2011

We hypothesized that the endogenous coronary vasodilator adenosine may reduce infarct size by progressively increasing reflow in a preparation of coronary occlusion-reperfusion. After 90 min of proximal left anterior descending artery occlusion, 20 dogs were randomized to blood reperfusion with (n = 10) or without (n = 10) adenosine into the proximal left anterior descending vessel at 3.75 mg/min for 60 min after reperfusion. Regional myocardial blood flow was determined serially with microspheres and regional ventricular function was assessed by a computerized radial shortening method. At 24 hr, the area at risk was defined in vivo with monastral blue dye and area of necrosis was determined after incubation of left ventricular slices in triphenyltetrazolium chloride. Hemodynamic variables were similar in the two groups during the experimental protocol. Infarct size was significantly reduced in treated animals, both when expressed as a percentage of the area at risk (9.9 +/- 2.8% vs 40.9 +/- 6.6%, p less than .001) and as a percentage of the left ventricle (4.6 +/- 1.3% vs 18.0 +/- 3.4%, p = .002). This was associated with significant improvement in radial shortening in the ischemic zone 24 hr after reperfusion (10.1 +/- 2.5 vs -2.8 +/- 2.2%, p less than .01). Regional myocardial blood flow was significantly increased in endocardial and epicardial regions from the lateral ischemic zone 1 hr after reperfusion in adenosine-treated animals. Light microscopy demonstrated decreased neutrophil infiltration in the ischemic zone and electron microscopy showed relative preservation of endothelial structure in the subendocardium with reduced neutrophil and red cell stagnation of capillaries in the treated group. These findings suggest that intracoronary administration of adenosine after reperfusion significantly reduces infarct size and improves regional ventricular function in the ischemic zone in the canine preparation.
Prediction of complex atrioventricular conduction rhythms in humans with use of the atrioventricular nodal recovery curve.
Authors: Shrier A , Dubarsky H , Rosengarten M , Guevara M R , Nattel S , Glass L
Published: June 2011

Theoretical considerations indicate that complex patterns of atrioventricular conduction produced by rapid atrial stimulation can be predicted from changes in atrioventricular conduction produced by premature stimulation of the atrium. The purpose of this study was to evaluate the validity of this theoretical approach in seven patients undergoing electrophysiologic investigation. The atrioventricular nodal recovery curve was determined at two different basic cycle lengths. Subsequently, periodic atrial stimulation was delivered for 30 sec periods over a range of frequencies giving 11, Wenckebach, reverse Wenckebach, and 21 rhythms. The recovery curve data was then used to compute the response to periodic stimulation by an iterative technique. The conduction patterns actually seen during periodic atrial stimulation showed close agreement with the computed patterns. This work thus provides a unified explanation for the appearance of Wenckebach, reverse Wenckebach, alternating Wenckebach, and high grade block rhythms.
Cardiac fatigue after prolonged exercise.
Authors: Douglas P S , O'Toole M L , Hiller W D , Hackney K , Reichek N
Published: June 2011

To determine the effects of prolonged exercise on systolic and diastolic left ventricular function, we studied 21 athletes before, at the finish (within 11 +/- 5 min), and during recovery (28 +/- 9 hr) after the Hawaii Ironman Triathlon (2.4 mile swim, 112 mile bike, 26.2 mile run). Two-dimensionally guided M mode echocardiograms were digitized for wall thickness, cavity dimension, fractional shortening, and peak rates of cavity enlargement and wall thinning. Pulsed Doppler left ventricular inflow recordings were analyzed for peak early and late velocities and their ratio. Left ventricular diastolic dimension was reduced at race finish (5.4 +/- 0.6 to 5.1 +/- 0.6 cm) and remained reduced after 1 day of recovery (5.2 +/- 0.6 cm, p less than .05). Fractional shortening fell at race finish (39 +/- 5% to 35 +/- 5%), although systolic blood pressure was unchanged, and rose to 40 +/- 4% after recovery (p less than .05). The return to prerace shortening values after recovery occurred despite continued reduction in diastolic size. Peak circumferential shortening did not change significantly. Individual reductions in fractional shortening were correlated with increases in systolic cavity size (r = -.64, p less than .01), but not with decreases in diastolic size. The stress-shortening relationship was displaced downward at race finish, but returned toward baseline after 1 day of recovery, despite a persistent reduction in cavity size. This suggests that the decrease in shortening was due to impaired contractility as well as altered preload.(ABSTRACT TRUNCATED AT 250 WORDS)
Detection and localization of coronary artery disease with body surface mapping in patients with normal electrocardiograms.
Authors: Green L S , Lux R L , Haws C W
Published: June 2011

Patients with clinically significant coronary artery disease often have normal resting electrocardiograms. Clinical and experimental studies have shown that body surface potential maps provide improved recognition of some disease states and more regionally selective information than standard electrocardiograms. Body surface maps were recorded at rest from 41 symptomatic patients with angiographically documented coronary artery disease and normal electrocardiograms. Patient maps were statistically compared with maps recorded from 644 normal subjects with the use of previously reported data representation technique. By this technique, maps from patients with symptomatic coronary artery disease and normal electrocardiograms were separated from maps of normal subjects with a sensitivity and specificity greater than 94%. The majority of discriminating information was present in the QRS interval. Fifteen of the 41 symptomatic patients had documented single-vessel coronary disease and their maps were separately compared with normal maps. Average maps from each of three patient groups with single-vessel disease contained abnormal patterns during the QRS interval that were unique to the vessel affected. In comparison with a average map from normal subjects, the average map from the group with left anterior descending coronary disease showed lower potentials over the anterior and inferolateral thorax during the early to mid QRS interval, the average map from the circumflex disease group showed decreased potentials around the entire inferior thorax in the mid to late QRS interval, and the average map from the right coronary disease group showed decreased potentials over the right anterior thorax during the mid to late QRS interval.(ABSTRACT TRUNCATED AT 250 WORDS)
Prehospital trial of emergency transcutaneous cardiac pacing.
Authors: Hedges J R , Syverud S A , Dalsey W C , Feero S , Easter R , Shultz B
Published: June 2011

A prospective alternate-day controlled trial of prehospital transcutaneous cardiac pacing (PACE) of hemodynamically significant bradycardia and asystole was undertaken. All patients had a Glasgow coma scale score of 12 or less. Patients in the control group (n = 101) received standard advanced cardiac life support (ACLS) care. Patients in the pacing group (n = 101) were to receive PACE in addition to standard ACLS treatment; 89 patients were actually paced. The two groups were comparable in terms of age, sex, presenting rhythm, and mean times to cardiopulmonary resuscitation (CPR) and ACLS. For the 144 patients in whom the time of arrest could be estimated, the mean times to CPR and ACLS were 5.3 +/- 4.0 and 10.9 +/- 7.1 min, respectively. For the 65 paced patients in whom the time of arrest could be estimated, the mean time from arrest to pacing was 21.8 +/- 8.8 min (range 2 to 43). Multivariate analysis of outcome variables (presentation to emergency department with a pulse, admission to the hospital, and discharge from the hospital) revealed that an initial rhythm of ventricular tachycardia or fibrillation and a short time to ACLS were correlated with a favorable outcome (p less than .05; logistic regression analysis). A short time to PACE was associated with admission to the hospital (p = .20; logistic regression analysis). The use of a stand-alone transcutaneous pacing device in the prehospital arrest setting was associated with generally long times until pacing and did not appreciably improve outcome. Use of PACE in patients demonstrating prehospital bradycardia without neurologic impairment remains to be evaluated.
Laser probe ablation of normal and atherosclerotic human aorta in vitro: a first thermographic and histologic analysis.
Authors: Welch A J , Bradley A B , Torres J H , Motamedi M , Ghidoni J J , Pearce J A , Hussein H , O'Rourke R A
Published: June 2011

The metal-tipped optical fiber or "laser probe" has been extensively studied in animal preparations in vivo and in human clinical trials of revascularization. The aim of this study was to evaluate the thermal characteristics of laser probe tissue ablation and to contrast the vascular tissue response to exposure to the laser probe and bare optical fiber. A 2 mm laser probe was heated with up to 4 W of argon-ion laser irradiation and applied to six postmortem strips of human nonatherosclerotic aorta as well as to five atherosclerotic aortic specimens. Surface temperature maps of the laser probe and of the vascular tissue in air were obtained via 8 to 12 micron thermographic imaging. Laser probe temperature was additionally monitored via thermocouples. Two strips each of normal and diseased aorta were irradiated directly with the bare optical fiber. Thus a total of 43 laser probe application sites and 19 bare fiberoptic laser irradiation sites on a total of 15 aortic strips were analyzed both thermographically and histologically. Based on measured temperature rises and histologic findings, the following observations were made: (1) The laser probe heats initially at its tip and attains a uniform surface temperature distribution within 5 sec. The steady-state temperature attained by the probe is inversely related to the thermal conductivity of the surrounding media. In all media studied, probe temperature increases linearly with applied laser energy. (2) Tissue ablation starts at temperatures greater than 100 degrees C, and ablation temperatures typically exceed 180 degrees C. Adventitial temperatures during laser probe application may reach 70 degrees C. Tissue ablation is enhanced both by greater laser energy deposition in the probe and by higher force at which the probe is applied to tissue. (3) Ablation of fibrofatty atheromata is more extensive than of nonatherosclerotic aortic tissue. This may be due to the lower thermal conductivity of atheromatous tissue. (4) In contrast to direct argon-ion laser ablation of aortic tissue, laser probe-mediated ablation occurs in a controlled fashion, is not associated with extensive subintimal dissections, and allows uniform conduction of heat to tissue as reflected by essentially "isothermal" injury lines.
Coronary perfusion during acute myocardial infarction with a combined therapy of coronary angioplasty and high-dose intravenous streptokinase.
Authors: Stack R S , O'Connor C M , Mark D B , Hinohara T , Phillips H R , Lee M M , Ramirez N M , O'Callaghan W G , Simonton C A , Carlson E B
Published: June 2011

Two hundred and sixteen patients with acute myocardial infarction were treated with immediate infusion of high-dose (1.5 million units) intravenous streptokinase followed by emergency coronary angioplasty. The infarct lesion was crossed and dilated in 99% and persistent coronary perfusion after the procedure was achieved in 90% (including 3% with significant residual stenosis). Total in-hospital mortality was 12%. Multivariable analysis showed a higher hospital mortality with cardiogenic shock (41% vs 5% without shock), older age, lower left ventricular ejection fraction, and female sex. Final patency of the infarct-related vessel was determined by follow-up in-hospital cardiac catheterization. Coronary reocclusion occurred in 11% (symptomatic in 7%, treated with emergency angioplasty or bypass surgery; silent in 4%, treated medically). Of the surviving patients with successful initial establishment of infarct vessel patency, 94% were discharged from the hospital with an open infarct artery or a bypass graft to the infarct vessel. There was significant improvement in both ejection fraction (44% to 49%; p less than .0001) and regional wall motion in the infarct zone (-3.0 SD to -2.4 SD; p less than .0001) among patients with persistent coronary perfusion and insignificant residual stenosis at the time of the follow-up cardiac catheterization. Thus, a treatment strategy for acute myocardial infarction that includes immediate administration of streptokinase followed by emergency coronary angioplasty, and coronary bypass surgery when necessary, results in a high rate of early and sustained patency of the infarct-related vessel.
Low-fat diet and regular, supervised physical exercise in patients with symptomatic coronary artery disease: reduction of stress-induced myocardial ischemia.
Authors: Schuler G , Schlierf G , Wirth A , Mautner H P , Scheurlen H , Thumm M , Roth H , Schwarz F , Kohlmeier M , Mehmel H C
Published: June 2011

The effects of physical exercise and normalization of serum lipoproteins on stress-induced myocardial ischemia were studied in 18 patients with coronary artery disease, stable angina pectoris, and mild hypercholesterolemia (total serum cholesterol 242 +/- 32 mg/dl). These patients underwent a combined regimen of low-fat/low-cholesterol diet and regular, supervised physical exercise at high intensity for 12 months. At 1 year serum lipoproteins has been lowered to ideal levels (serum cholesterol 202 +/- 31 mg/dl, low-density lipoproteins 130 +/- 30 mg/dl, very low-density lipoproteins 22 +/- 15 mg/dl, serum triglycerides 105 [69 to 304] mg/dl) and physical work capacity was improved by 21% (p less than .01). No significant effect was noted on high-density lipoproteins, probably as a result of the low-fat/high-carbohydrate diet. Stress-induced myocardial ischemia, as assessed by thallium-201 scintigraphy, was decreased by 54% (p less than .05) despite higher myocardial oxygen consumption. Eighteen patients matched for age and severity of coronary artery disease served as a control group and "usual medical care" was rendered by their private physicians. No significant changes with respect to serum lipoproteins, physical work capacity, maximal rate-pressure product, or stress-induced myocardial ischemia were observed in this group. These data indicate that regular physical exercise at high intensity, lowered body weight, and normalization of serum lipoproteins may alleviate compromised myocardial perfusion during stress.
Expired carbon dioxide: a noninvasive monitor of cardiopulmonary resuscitation.
Authors: Gudipati C V , Weil M H , Bisera J , Deshmukh H G , Rackow E C
Published: June 2011

End-tidal CO2 concentration (ETCO2) may serve as a simple noninvasive measurement of the blood flow generated by precordial compression during cardiopulmonary resuscitation (CPR). In a mechanically ventilated porcine preparation of ventricular fibrillation, onset of fibrillation was associated with a rapid decrease in ETCO2 from 4.0 +/- 0.2% to less than 0.7 +/- 0.2%. With precordial compression, it increased to 1.9 +/- 0.3%. Animals that were successfully defibrillated after 12 min of CPR demonstrated an immediate increase in ETCO2. The ETCO2 increased from 1.9 +/- 0.3% to 4.9 +/- 0.3% over an interval of between 30 and 60 sec. These changes in ETCO2 were closely related to proportionally similar decreases and increases in cardiac output (CO), and a close correlation between ETCO2 and CO was demonstrated (r = .92). A similar highly significant correlation between ETCO2 and CO was also demonstrated during open-chest cardiac massage (r = .95). ETCO2 therefore serves as a noninvasive measure of pulmonary blood flow and therefore CO. In 17 successfully resuscitated animals. ETCO2 during precordial compression averaged 1.7 +/- 0.2%, whereas it was only 0.5 +/- 0.1% in five animals in whom resuscitation procedures were unsuccessful (p less than .001). Accordingly, ETCO2 prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation.
Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test.
Authors: Nabel E G , Ganz P , Gordon J B , Alexander R W , Selwyn A P
Published: June 2011

Increased vascular constriction has been observed at the site of atherosclerotic lesions, suggesting an association between atherosclerosis and altered vascular tone. While atherosclerosis may increase sensitivity to exogenous vasoconstrictors, little is known about the response of normal and atherosclerotic coronary arteries to an exogenous stimulus that excites the sympathetic nervous system. Therefore, we studied the response to cold pressor test (CPT) using quantitative angiography and Doppler flow velocity measurements in eight patients with angiographically normal coronary arteries (group I), nine patients with mild coronary atherosclerosis (less than 50% diameter narrowing) (group II), and 13 patients with advanced coronary stenoses (greater than 50% diameter narrowing) (group III). In 31 segments of angiographically smooth arteries in group I, the CPT produced vasodilation from a control mean diameter of 2.68 +/- 0.09 (mean +/- SE) to 2.99 +/- 0.09 mm at peak CPT (p less than 0.001), a 12 +/- 1% increase in diameter. In group II, 27 irregular segments constricted to peak CPT from a mean control diameter of 1.82 +/- 0.12 to 1.66 +/- 0.12 mm (p less than .001), a 9 +/- 1% decrease, while 10 smooth segments dilated from a mean control diameter of 1.98 +/- 0.11 mm to 2.34 +/- 0.15 mm (p less than .01), a 19 +/- 2% increase in diameter. Likewise, in group III, the 17 stenotic segments constricted from 1.16 +/- 0.09 to 0.89 +/- 0.09 mm (p less than .001), a 24 +/- 6% decrease; the irregular segments also constricted from 2.44 +/- 0.11 to 2.22 +/- 0.12 mm (p = .002), a 10 +/- 2% decrease. In contrast, two smooth segments dilated from 2.98 to 3.23 mm (mean), an 8% increase in diameter. Coronary blood flow increased 65 +/- 4% (mean) during CPT in group I, it increased 15 +/- 6% in group II, and it decreased 39 +/- 8% in group III. The vasodilator response in four normal patients was partly inhibited by the administration of intracoronary propranolol (17 +/- 3% increase during control, 10 +/- 2% increase after propranolol, 41% less dilation; p = .002). We conclude that the response of normal coronary arteries to the CPT test is dilation, in part related to beta-adrenoreceptor stimulation and possibly flow-mediated endothelial dilation or alpha 2-adrenergic activity. The paradoxical vasoconstrictor response induced by atherosclerosis may represent altered catecholamine sensitivity and/or a defect in endothelial vasodilator function. The presence of atherosclerosis impairs vasodilator responses and thus may contribute to the pathogenesis of myocardial ischemia.
Changes in myocardial repolarization in patients undergoing balloon valvuloplasty for congenital pulmonary stenosis: evidence for contraction-excitation feedback in humans.
Authors: Levine J H , Guarnieri T , Kadish A H , White R I , Calkins H , Kan J S
Published: June 2011

Alterations in ventricular loading conditions lead to changes in action potential duration and arrhythmias via contraction-excitation feedback; a decrease in load leads to prolongation of repolarization. To determine whether changes in right ventricular load alter ventricular repolarization in man, the corrected QT interval, a measure of overall ventricular repolarization, was measured in 32 patients before and after valvuloplasty for pulmonary stenosis. Right ventricular systolic pressure decreased (82.5 +/- 30.7 to 40.5 +/- 9.5 mm Hg, p less than .001) and the QTc increased concurrently (409.1 +/- 24.3 to 440.7 +/- 28.0 msec, p less than .001) after successful valvuloplasty. The increase in QTc was most marked for those patients with a greater than 30 mm Hg decrease in right ventricular pressure (40.0 +/- 23.3 vs 16.3 +/- 21.3 msec, p = .006). In a subset of seven patients in whom monophasic action potentials were recorded, monophasic action potential duration, a measure of local repolarization, was prolonged (230.0 +/- 24.3 vs 216.9 +/- 21.9, p less than .001) after successful valvuloplasty, confirming that the QTc prolongation reflected changes in local ventricular repolarization. In addition, during nine acute right ventricular outflow tract occlusions in a subset of six patients, monophasic action potential duration shortened (206.6 +/- 17.6 vs 221.7 +/- 20.9 msec, p less than .01) and early afterdepolarizations developed consistent with contraction-excitation feedback. These data suggest that, in humans, changes in mechanical load are associated with changes in ventricular repolarization consistent with contraction-excitation feedback.
Treatment of torsade de pointes with magnesium sulfate.
Authors: Tzivoni D , Banai S , Schuger C , Benhorin J , Keren A , Gottlieb S , Stern S
Published: June 2011

Twelve consecutive patients who developed torsade de pointes (polymorphous ventricular tachycardia with marked QT prolongation, TdP) over a 4 year period were treated with intravenous injections of magnesium sulfate. In nine of the patients a single bolus of 2 g completely abolished the TdP within 1 to 5 min, and in three others complete abolition of the TdP was achieved after a second bolus was given 5 to 15 min later. Nine of the patients also received continuous infusion of MgSO4 (3 to 20 mg/min) for 7 to 48 hr until the QT interval was below 0.50 sec. In nine of the 12 patients the TdP was induced by antiarrhythmic agents. The QT interval preceding TdP ranged from 0.54 to 0.72 sec. After the MgSO4 bolus, which prevented the recurrence of TdP, no significant changes were observed in the QT interval. There were no side effects of this treatment. In eight of the 12 patients potassium levels before the TdP were below 3.5 meq/liter; magnesium levels were available in eight patients before TdP, and were normal in all. Five additional patients with polymorphous ventricular tachycardia but normal QT intervals (non-TdP patients) received two to three boluses of MgSO4. This treatment was ineffective in all, but they responded to conventional antiarrhythmic therapy. Thus, MgSO4 is a very effective and safe treatment for TdP, and its application is rapid and simple. Its use is therefore recommended as the first line of therapy for TdP.