bluuebunny/crossref_metadata_2025 huggingface dataset:
Precision of measurements of right and left ventricular volume by cine computed tomography.
Authors: Reiter S J , Rumberger J A , Feiring A J , Stanford W , Marcus M L
Published: June 2011

Precise determination of left and right ventricular stroke volumes is limited with conventional imaging techniques. We determined whether right and left ventricular stroke volumes could be precisely measured with cine computed tomography (CT). Cine CT enables simultaneous imaging of the right and left ventricles at an 8 mm slice thickness with a maximal scanning rate of 17 frames/sec (50 msec acquisition intervals). In eight dogs, true right ventricular and left ventricular stroke volumes were determined by dividing thermodilution cardiac output by heart rate and/or with the use of an aortic electromagnetic flow probe implanted over a long term. After at least 5 sec of suspended respiration, cine CT images were acquired during central venous injection of a nonionic contrast agent. Multiple perturbations in stroke volume were induced in each dog by the administration of dobutamine, sodium pentobarbital, or sodium nitroprusside or by coronary artery occlusion. Right and left ventricular stroke volumes were obtained by Simpson's reconstruction of end-diastolic and end-systolic short-axis tomograms from apex to base. The cine CT left ventricular stroke volume (range 11 to 45 ml) correlated highly with the true left ventricular stroke volume (r = .99, slope = 1.01, y intercept = -0.2 ml, SEE = 1.5 ml, n = 25). The cine CT right ventricular stroke volume (range 11 to 34 ml) also correlated highly with the true right ventricular stroke volume (r = .98, slope = 0.9, y intercept = 2.2 ml, SEE = 1.7 ml, n = 15). In 12 studies, the mean difference between nearly simultaneous right and left ventricular stroke volumes by cine CT was 1.1 ml (range 0.1 to 3.2 ml). Calculation of right and left ventricular stroke volumes from data from cine CT were highly reproducible. Intraobserver variability in measurements of right ventricular stroke volume (r = 1.0, slope = 0.99, y intercept = 0.19 ml) and left ventricular stroke volume (r = 1.0, slope = 1.02, y intercept = -0.21 ml) was minimal. Interobserver variability in measurements of right ventricular stroke volume (r = .98, slope = 0.90, y intercept = 1.66 ml) and left ventricular stroke volume (r = .99, slope = 0.97, y intercept = -0.02 ml) was likewise minimal. Thus, precise and highly reproducible measurements of right and left ventricular stroke volumes can be obtained with cine CT.
Iodine 123-phenylpentadecanoic acid myocardial scintigraphy: usefulness in the identification of myocardial ischemia.
Authors: Kennedy P L , Corbett J R , Kulkarni P V , Wolfe C L , Jansen D E , Hansen C L , Buja L M , Parkey R W , Willerson J T
Published: June 2011

In this study, we tested the hypothesis that myocardial ischemia induced by exercise in patients is associated with diminished metabolism and/or delayed clearance of an intravenously injected fatty acid, iodine 123-labeled phenylpentadecanoic acid (IPPA). Fifteen normal volunteers and 18 patients with significant coronary heart disease (CHD) received IPPA during exercise. In the patients with CHD, radionuclide ventriculograms were also obtained during exercise. The normal volunteers had relatively uniform initial left ventricular segmental IPPA activity after exercise and uniform IPPA clearance in the interval from 4 to 20 min immediately after exercise. In contrast, the patients with CHD had increased initial left ventricular segmental IPPA activity (63%, p less than .001) and delayed IPPA clearance (44%, p less than .01) in segments supplied by significantly narrowed coronary arteries. Based on analysis with the mean values +/- 1 SD for initial IPPA activity, clearance, or both in normal volunteers, the sensitivity and specificity of exercise IPPA scintigraphy for detecting CHD were 89% and 67%, respectively; when +/- 2 SD differences from the mean values in the normal volunteers were considered, the sensitivity and specificity were 72% and 100%, respectively. Among the total of 27 noninfarcted left ventricular segments supplied by significantly narrowed coronary arteries in the study patients, 26 (96%) had an abnormality (mean +/- 1 SD) of either initial IPPA activity or clearance compared with corresponding segments in the normal volunteers and/or with other left ventricular segments in the same image that were not supplied by significantly narrowed coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
Histologic evidence for small-vessel coronary artery disease in patients with angina pectoris and patent large coronary arteries.
Authors: Mosseri M , Yarom R , Gotsman M S , Hasin Y
Published: June 2011

We studied six patients who suffered from angina pectoris but had angiographically patent major coronary arteries. Two of the patients suffered also from congestive heart failure. Three patients had supraventricular tachyarrhythmias. Three patients had conduction disturbances. During coronary angiography the patients had significantly reduced flow velocity of angiographic contrast medium compared with that in a control group. Echocardiographic and Doppler flow studies showed a tendency for symmetrical thickening of the left ventricular wall, enlargement of the right ventricle, and reduced compliance of both ventricles. Right ventricular endomyocardial biopsy revealed pathologic small coronary arteries with fibromuscular hyperplasia, hypertrophy of the media, myointimal proliferation, and endothelial degeneration. Capillaries had swollen endothelial cells encroaching on the lumen. Myocardial hypertrophy, lipofuscin deposition, and patchy fibrosis were also observed. These cases show that small-vessel coronary artery disease can cause classic angina pectoris. The diagnosis can be suspected when the coronary angiogram shows large patent arteries with slow flow of the angiographic contrast medium and it can be confirmed by endomyocardial biopsy.
Impaired responsiveness of the ventricular sensory receptor in hypertensive patients with left ventricular hypertrophy.
Authors: Trimarco B , De Luca N , Ricciardelli B , Cuocolo A , De Simone A , Volpe M , Mele A F , Condorelli M
Published: June 2011

We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = -29.9, for patients with hypertension = -40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by -40 mm Hg LBNP in normal subjects (+107 +/- 5 vs +129 +/- 15 mm Hg/ml/sec, p less than .05) but not in patients with hypertension. Consequently, the slope of the delta CVP/delta FVR regression was reduced in normal subjects (-20.6, p less than .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of -10 and -40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to -40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.
Arterial-venous relationships in the human left ventricular myocardium: anatomic basis for countercurrent regulation of blood flow.
Authors: Hutchins G M , Moore G W , Hatton E V
Published: June 2011

The mechanism by which myocardial blood flow varies in response to metabolic demand is obscure. One hypothesis is a countercurrent regulation of arterial caliber by diffusible substances carried in venous blood. To study the anatomic basis for blood flow regulation, we performed combined arterial and venous injections in 20 human hearts and studied left ventricular intramyocardial vessels with radiography, 100 micron thick sections, and reconstructions of serial histologic sections. Penetrating arteries lie in interstitial spaces and are closely related to accompanying veins. These interstitial veins partially surround and are indented by branch arteries. A second system of veins lies within muscle fascicles between interstitial spaces and is not related to arteries. The isolated veins have collateral connections with interstitial veins and join them in the subepicardium. This vascular anatomy could allow arterial caliber to be regulated by diffusible substances carried in the interstitial veins. Arterial dilatation might prolong this effect by partial obstruction of interstitial veins, with the isolated venous system providing an alternative pathway for venous drainage and washout. The study shows that a vascular arrangement is present in human left ventricular myocardium that could provide a countercurrent regulation of blood flow with diffusible substances carried in venous blood.
Evidence for a direct renal stimulating effect of prostaglandin E2 on renin release in patients with congestive heart failure.
Authors: Olivari M T , Levine T B , Cohn J N
Published: June 2011

The reduced responsiveness of the renin-angiotensin system to hemodynamic changes in patients with congestive heart failure (CHF) could be due to a defect of the juxtaglomerular apparatus. To test this hypothesis, the responses to viprostol, an analog of prostaglandin E2 (PGE2) that is known to stimulate both the macula densa and the juxtaglomerular cells, and to nitroprusside were compared in patients with CHF. An average fall in mean arterial pressure (MAP) of 6 mm Hg with viprostol was associated with a fivefold increase in plasma renin activity (PRA) from 11.4 +/- 6.4 to 47.9 +/- 31.0 ng/ml/hr; in contrast PRA did not change with nitroprusside, despite a significant decrease in preload and an average decrease in MAP of 16 mm Hg. These data demonstrate that the renin-angiotensin system could be activated by PGE2 in patients with CHF, this activation is not related to the global hemodynamic changes induced by PGE2, and the previously reported unresponsiveness of the renin-angiotensin system in patients with CHF cannot be attributed to a defective response of the juxtaglomerular apparatus.
Resting angina with fixed coronary artery stenosis: nocturnal decline in ischemic threshold.
Authors: Figueras J , Cinca J , Balda F , Moya A , Rius J
Published: June 2011

Atrial pacing was performed in 16 patients with angina at rest and significant coronary artery stenosis (greater than 70%) over 2 consecutive days in the morning (10 A.M. to 1 P.M.), in the afternoon (4 to 7 P.M.), and at night (12 midnight to 3 A.M.) to assess possible circadian variations of their ischemic threshold. Overall, the incidence of resting angina was highest at night. All pacing results were positive (greater than or equal to 1.0 mm ST segment shift) and tended to be reproducible in nine patients, whereas some or all were negative in seven. Among all positive results, ischemic thresholds at night were significantly lower than those in the morning and in the afternoon (125 +/- 3 vs 138 +/- 3 and 139 +/- 2 beats/min, mean +/- SEM; p less than .005). In nine patients, 19 pacing tests produced ST segment elevation, of which 13 were performed at night (68%). We conclude that patients with resting angina and severe coronary stenosis often exhibit a nocturnal decline in their ischemic threshold, which seems to facilitate development of transmural ischemia during atrial pacing.
Mapping of body surface potentials in patients with the idiopathic long QT syndrome.
Authors: De Ambroggi L , Bertoni T , Locati E , Stramba-Badiale M , Schwartz P J
Published: June 2011

Body surface potential maps were recorded from 140 chest leads in 25 patients affected by the idiopathic long QT syndrome (LQTS) and in 25 healthy control subjects matched for age and sex. Potential time integrals of the QRST and ST-T intervals were calculated at each lead point and displayed as isointegral (ISOI) maps. The main abnormalities noted on the QRST and ST-T ISOI maps were one area of negative values larger than normal in the right anterior and inferior thorax and a complex multipeak distribution of the integral values. At least one abnormality was present in 19 (76%) of the patients with LQTS and four (16%) of the control subjects (p less than .001). Each ISOI map was also represented as a weighted sum of nine fundamental components (eigenvectors) to detect and quantitate the nondipolar content. The percent contribution of the nondipolar eigenvectors (all eigenvectors beyond the third) was significantly higher in the LQTS group than in the control group (p less than .005). Specifically, an abnormally high nondipolar content on the QRST ISOI maps was observed much more frequently for patients with LQTS than for control subjects (nine or 36% vs one or 4%), and this was also true on the ST-T ISOI maps (14 or 56% vs one or 4%). No correlation was found between the major abnormalities on body surface maps and syncopal episodes. However, the high prevalence (76%) of these alterations among the patients with LQTS and their infrequent occurrence in the control population strongly suggests that they may be useful markers for the diagnosis of atypical cases. The prominent electronegative area on the anterior thorax can be related to delayed repolarization of a portion of the anterior wall of the heart. This finding is in agreement with the hypothesis that lower than normal right cardiac sympathetic activity is the main pathogenetic mechanism of LQTS. Multipeak distribution and high nondipolar content suggest regional electrical disparities in the ventricular recovery process. This may in part account for the high susceptibility of patients with LQTS to malignant arrhythmias.
The immediate effects of iohexol on coronary blood flow and myocardial function in vivo.
Authors: Friedman H Z , DeBoe S F , McGillem M J , Mancini G B
Published: June 2011

Radiographic techniques used to quantify coronary blood flow all require bolus injection of contrast material, which markedly alters the flow being measured. Newer nonionic contrast agents have been shown to have fewer adverse hemodynamic, inotropic, and rheologic effects compared with ionic media and it has been suggested that they might not substantially affect coronary blood flow. Six dogs were instrumented with electromagnetic flow probes and subendocardial ultrasonic crystals. Intracoronary injections of iohexol (300 mg/ml iodine) were administered to establish a relationship between the dose and rate of contrast injection and the effect on flow and regional myocardial function. Two and 4 ml volumes of iohexol were injected at 3 ml/sec; 4 ml volumes were administered at 1 and 4 ml/sec. The 2 and 4 ml volumes decreased coronary flow by a mean of 31% (p less than .01) and 77% (p less than .001). The 4 ml injection at 1 and 4 ml/sec 77% (p less than .001) and 69% (p less than .001). The magnitude of the fall in flow was directly related to the dose, and the rate at which the flow nadir was attained was directly related to the rate of injection. Decrements in fractional shortening were temporally delayed by several beats compared with the flow changes and showed mean decrements of 19% to 29%. The effects on regional myocardial function were independent of contrast volume. However, the degree of dysfunction was more profound with slower infusion rates, suggesting that prolongation of contrast-induced ischemia was a major modulating factor.(ABSTRACT TRUNCATED AT 250 WORDS)
Reduction in experimental infarct size by recombinant human superoxide dismutase: insights into the pathophysiology of reperfusion injury.
Authors: Ambrosio G , Becker L C , Hutchins G M , Weisman H F , Weisfeldt M L
Published: June 2011

To determine the importance of reperfusion injury and the ability of the free-radical scavenger recombinant human superoxide dismutase (h-SOD) to prevent it, open-chest dogs underwent 90 min of proximal circumflex coronary artery occlusion, and only at the moment of reperfusion received either h-SOD (400,000 IU bolus into the left atrium followed by a 300,000 IU iv infusion over 1 hr) or saline. After 48 hr the surviving animals were killed and measurements were made of the risk region (by postmortem angiography) and infarct size (by gross pathology). All measurements were made by investigators blinded to treatment given, and the code was broken only at the end of the study. Hemodynamic variables and collateral flow during ischemia were similar in the two groups. Infarct size in control animals (n = 8) averaged 22.4 +/- 3.1% of the left ventricle and 52.2 +/- 7.1% of the risk region, compared with 13.3 +/- 0.8% of the left ventricle and 33.6 +/- 2.1% of the risk region in h-SOD-treated dogs (n = 8) (p less than .05). Infarcts in treated animals were not only smaller, but also exhibited a distinctive "patchiness," suggesting protection along vascular distributions. Furthermore, analysis of the relationship between infarct size and collateral flow measured during ischemia in the two groups indicated that protection by h-SOD was greatest in animals with the lowest collateral flows. This study supports the concept that reperfusion of ischemic myocardium results in a separate component of cell damage, presumably linked to the generation of oxygen free radicals on reflow. Since the h-SOD preventable reperfusion component of injury was most pronounced in hearts with the most severe ischemia, scavenging of oxygen radicals at the time of reflow may offer a novel and particularly promising therapeutic approach for the protection of ischemic myocardium.
Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction.
Authors: Cannon R O , Schenke W H , Leon M B , Rosing D R , Urqhart J , Epstein S E
Published: June 2011

Patients with anginal chest pain despite angiographically normal coronary arteries and left ventricles may have abnormalities of coronary flow reserve. Twenty-five patients were found to have limited flow reserve during rapid atrial pacing after administration of 0.15 to 0.30 mg iv ergonovine, associated with precipitation of chest pain and hemodynamic and metabolic evidence of myocardial ischemia. No significant narrowing occurred in epicardial coronary artery luminal diameter. An additional 15 patients had no chest pain during pacing; because they developed significantly higher great cardiac vein flow and lower coronary resistance they were considered to have normal vasodilator reserve. After administration of dipyridamole (0.5 to 0.75 mg/kg iv), the lowest absolute levels to which coronary resistance fell (0.79 +/- 0.23 vs 0.47 +/- 0.12 mm Hg X min/ml; p less than .001) and the maximal absolute levels to which great cardiac vein flow rose (134 +/- 34 vs 202 +/- 45 ml/min; p less than .001) were impaired in the 25 patients with ergonovine-induced flow limitation compared with the 15 patients without flow limitation after ergonovine. In addition, 18 of the 25 patients with limited flow reserve after dipyridamole experienced chest pain despite an increase in coronary flow. In these patients, dipyridamole-induced increased flow across small prearteriolar coronary arteries, which were narrowed because of abnormal tonus or sensitivity to vasoconstrictor stimuli, could have resulted in a transmural redistribution of blood flow away from the subendocardium, precipitating subendocardial ischemia. These studies suggest that patients with anginal chest pain despite normal epicardial coronary arteries may have exaggerated coronary responses to vasoconstrictor stimuli, which can result in myocardial ischemia during stress, as well as attenuated responses to coronary vasodilator stimuli.
Treatment of canine pulmonary hypertension: effects of norepinephrine and isoproterenol on pulmonary vascular pressure-flow characteristics.
Authors: Ducas J , Duval D , Dasilva H , Boiteau P , Prewitt R M
Published: June 2011

Pulmonary vascular flow resistive properties may be described by mean pulmonary arterial pressure (PAP)-cardiac output (CO) plots. The slope of the PAP-CO relationship defines the incremental resistance and the extrapolated pressure intercept defines the effective outflow pressure. We investigated effects of norepinephrine (11 dogs) and isoproterenol (seven dogs) on the pulmonary vascular PAP-CO relationship in a model of pulmonary hypertension produced by injection of autologous blood clots. Multiple PAP-CO coordinates were obtained with and without drug infusion. CO was varied by opening systemic arteriovenous fistulas. PAP-CO relationships were well described by a linear equation (mean r value .964 +/- .032). Isoproterenol increased mean CO by 61% (p less than .01), and calculated pulmonary vascular resistance (PVR) decreased by 31% (p less than .05), corresponding to a 35% decrease (5.1 +/- 2.0 to 3.3 +/- 0.9 mm Hg X liter X min-1; p less than .01) incremental resistance. In the first seven dogs to receive norepinephrine, despite a 25% increase in blood pressure (p less than .01) no significant effects on CO, PAP, PVR, or PAP-CO relationship were observed. In the next four dogs, norepinephrine was infused at a lower dose to increase blood pressure 50% and a higher dose to ensure an increase in CO. In both conditions, calculated PVR fell (p less than .05) compared with that before norepinephrine. However, measured incremental resistance and effective outflow pressure did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
A new intracavitary probe for detecting the site of origin of ectopic ventricular beats during one cardiac cycle.
Authors: Taccardi B , Arisi G , Macchi E , Baruffi S , Spaggiari S
Published: June 2011

An olive-shaped probe (25 X 12 mm) with 41 evenly distributed recording electrodes on its surface was introduced into the left ventricles of seven open-chest dogs via the left atrium. In two other dogs a cylindrical probe (40 X 3 mm) was used. Electrical stimuli were delivered at 66 endocardial, midwall, or epicardial sites in the left and right ventricular walls and the septum. Mechanical stimuli were also applied at various epicardial sites. On-line mapping of equipotential contour lines on the surface of the probe invariably revealed a clear-cut potential minimum on the electrode that faced the pacing site. Time of appearance of potential minimum was 3 to 5 msec after endocardial stimuli, 10 to 25 msec for midwall and epicardial pacing, and 30 msec or more for right ventricular stimulation. Simultaneous stimulation at two sites 1.2 cm apart gave rise to two separate minima on the maps. "Pseudoisochrones" derived from electrograms recorded by the new probe were slightly less accurate in indicating the site of origin of extrasystoles. We conclude that equipotential and "isochrone" contour maps recorded from an array of semidirect electrodes, regularly distributed on the surface of an intraventricular probe, provide information on the site of origin (location and intramural depth) of ectopic paced beats in a normal dog heart.
The association of postural changes in systolic blood pressure and mortality in persons with hypertension: the Hypertension Detection and Follow-up Program experience.
Authors: Davis B R , Langford H G , Blaufox M D , Curb J D , Polk B F , Shulman N B
Published: June 2011

Participants in the Hypertension Detection and Follow-up Program (HDFP) were classified on the basis of baseline standing minus sitting systolic blood pressure into four groups (less than or equal to -20 [group 1], -19 to 0 [group 2], 1 to 20 [group 3], and greater than 20 mm Hg [group 4]) to study 5 year mortality. Group 1, 3.3% of the total, contained those participants who had postural hypotension. The 5 year total and age-adjusted mortality rates for these groups were significantly different (p less than .04), with group 1 having the highest rates. To account for the possible confounding effects of certain baseline risk factors--age, sex, race, prior antihypertensive treatment, randomization group, diabetes, end-organ damage, sitting diastolic and systolic blood pressures, pulse, hematocrit, smoking status, and relative weight (percent of ideal weight)--in assessing group differences in mortality rates, a multiple logistic model was used. Relative weight proved to be a confounding factor for the association of drop in postural systolic blood pressure with mortality. However, there is an interaction between history of diabetes and postural change in systolic blood pressure. Thus, postural hypotension may indicate a poor prognosis in diabetic hypertensive patients.
Evaluation of left ventricular function during upright exercise: correlation of exercise Doppler with postexercise two-dimensional echocardiographic results.
Authors: Mehdirad A A , Williams G A , Labovitz A J , Bryg R J , Chaitman B R
Published: June 2011

The relationship of regional and global left ventricular function to aortic flow dynamics during exercise was determined in 14 normal subjects and 14 patients with coronary artery disease. Doppler and two-dimensional echocardiographic studies were performed before, during, and immediately after an exercise test by the Bruce protocol. Two-dimensional echocardiography was used to determine the ejection fraction and new wall motion abnormalities. The peak ejection velocity, stroke index, and cardiac index were calculated from the pulsed Doppler tracing. In normal subjects the ejection fraction increased significantly (p less than .001) from rest (0.51 +/- 0.07) to peak exercise (0.61 +/- 0.07), while the response in coronary patients was blunted (0.49 +/- 0.11 vs 0.48 +/- 0.16). Similarly, the change in peak ejection velocity throughout exercise in normal subjects (from 0.71 +/- 0.12 to 1.50 +/- 0.35 m/sec) was significantly (p less than .01) greater than that in patients with coronary artery disease (from 0.61 +/- 0.13 to 0.90 +/- 0.29 m/sec). There was a good correlation between the percent change in peak ejection velocity and the percent change in ejection fraction from rest to peak exercise in the entire study group (rs = .64) and in the patients with coronary artery disease (rs = .84). These preliminary data suggest that exercise-induced changes in Doppler echocardiographic variables may offer a potential adjunct in the evaluation of patients with ischemic heart disease.
A randomized, placebo-controlled trial of intravenous recombinant tissue-type plasminogen activator and emergency coronary angioplasty in patients with acute myocardial infarction.
Authors: Topol E J , O'Neill W W , Langburd A B , Walton J A , Bourdillon P D , Bates E R , Grines C L , Schork A M , Kline E , Pitt B
Published: June 2011

To determine the role of tissue-type plasminogen activator (t-PA) and immediate percutaneous transluminal coronary angioplasty (PTCA) in treating patients with evolving transmural myocardial infarction, 50 patients received t-PA (1.25 mg/kg iv over 3 hrs) or placebo according to 3:1 double-blind randomization 3.8 +/- 1.1 hr after onset of symptoms. At emergency coronary arteriography, patency of the infarct-related vessel was demonstrated in 32 of 38 (84%) patients receiving t-PA vs two of 12 (17%) receiving placebo (p less than .001). Of the 32 patients with recanalization after t-PA, 28 had a residual stenosis of at least 50% and underwent randomization a second time to immediate (n = 15) or no PTCA (n = 13). Immediate PTCA of the infarct-related vessel was successful in all 15 patients, with reduction of the residual diameter stenosis from 80.8 +/- 8.2% to 32.5 +/- 15.6% (p less than .001). The incidence of postinfarction angina (greater than or equal to 20 min of chest discomfort and reversible electrocardiographic changes) and reinfarction (documented by recurrent creatine kinase isoenzyme elevation) was reduced in the patients receiving t-PA and PTCA (2/15) compared with that in patients receiving t-PA alone (7/13; p = .006). At 1 week there was no difference in patency of the infarct-related vessel (12/15 t-PA and PTCA vs 9/13 t-PA only) or in global ventricular functional change between the two groups (0.5 +/- 10.4 SD/chord for t-PA and PTCA vs -2.1 +/- 8.2 SD/chord for t-PA only).(ABSTRACT TRUNCATED AT 250 WORDS)
Automated quantitative coronary arteriography: morphologic and physiologic validation in vivo of a rapid digital angiographic method.
Authors: Mancini G B , Simon S B , McGillem M J , LeFree M T , Friedman H Z , Vogel R A
Published: June 2011

Quantitative coronary arteriography has been shown to be useful in assessing the extent of coronary disease, its functional significance, and its response to therapeutic interventions. Most current methods rely either on hand-drawn arterial contours or automatic edge-detection algorithms applied to 35 mm cineangiograms. To assess the performance in vivo of a new, fully automatic, rapid coronary quantitation program, dogs were instrumented with precision-drilled, plastic cylinders to create intraluminal stenoses in the left anterior descending and/or circumflex arteries, as well as with high-fidelity micromanometers and electromagnetic flow probes. Stenosis diameters ranged from 0.83 to 1.83 mm. Biplane, on-line, digital coronary angiograms and cineangiograms were recorded during standard selective coronary arteriography in the closed-chest preparation. The on-line digital images were analyzed in nonsubtracted and subtracted modes. Cineangiograms were digitized to allow coronary quantitation by the same computer program. There was an excellent correlation between known and measured minimal diameter stenoses (r = .87 to .98, SEE = 0.09 to 0.24 mm). Interobserver and intraobserver variability analysis showed high reproducibility (r = .90 to .97, SEE = 0.12 to 0.23 mm). The best results in both analyses were achieved by nonsubtracted digital imaging and the worst by cineradiography. Measures of percent diameter stenosis, percent area stenosis (geometric and videometric), and absolute minimal cross-sectional area (geometric and videometric) were all significantly correlated with independent measures of actual coronary flow reserve. This study provides direct anatomic and physiologic validation in vivo of a new and rapid coronary quantitation method suitable for analysis of both digital angiograms and cineangiograms.
Digital subtraction angiographic imaging of coronary flow reserve.
Authors: Cusma J T , Toggart E J , Folts J D , Peppler W W , Hangiandreou N J , Lee C S , Mistretta C A
Published: June 2011

Recent studies have demonstrated that subjective assessment of the severity of coronary artery stenoses results in poor interobserver concordance and poor correlation with physiologic significance as determined by Doppler measurements of coronary flow reserve. Use of the coronary flow reserve as an integrated measure of the effect of stenosis geometry has been emphasized within the context of quantitative cinemetric analysis. The comparison of two parametric digital subtraction angiographic flow images obtained before and after hyperemic intervention has led to calculation of flow reserve values that correlate well with electromagnetic flowmeter data in dogs. By means of a similar model relating blood flow and image variables, single flow ratio images have been formed. These parametric images provide a two-dimensional display of the ratio of hyperemic flow to baseline flow. Linear temporal interpolation of data from a sequence of cardiac phase-matched subtraction images is used to improve the resolution of the displayed flow ratios. Summation of flow variables measured within the perfusion bed was used to calculate a value for the overall coronary flow reserve and to characterize the significance of isolated lesions in an open-chest canine preparation. A linear regression calculation relating parametric image flow ratio values to electromagnetic flowmeter measurements resulted in a linear fit of y = .96x - 0.19 with a correlation coefficient of .90. The direct visual representation of flow ratio distribution provided by the parametric imaging method may aid in the interpretation of multiple complex lesions as well as of single lesions.
Effects of intracoronary infusion of arterial blood or Fluosol-DA 20% on regional myocardial metabolism and function during brief coronary artery occlusions.
Authors: Tokioka H , Miyazaki A , Fung P , Rajagopalan R E , Kar S , Meerbaum S , Corday E , Drury J K
Published: June 2011

Effects of intracoronary infusion (50 ml/min) of arterial blood, oxygenated or unoxygenated Fluosol, or Plasmalyte A on hemodynamics, electrocardiogram, regional myocardial function, and lactate metabolism were studied in six closed-chest dogs during 2 min occlusions of the left anterior descending coronary artery followed by 10 min of reperfusion. Normal hemodynamics were maintained with infusion of arterial blood and oxygenated Fluosol, whereas unoxygenated Fluosol and Plasmalyte A resulted in hemodynamic deterioration similar to that noted with no treatment. Ischemic zone systolic fractional area change, an index of systolic function measured by two-dimensional echocardiography, remained normal during the occlusion supplemented with intracoronary arterial blood (49 +/- 7%), was moderately hypokinetic with oxygenated Fluosol (31 +/- 10%), and became severely hypokinetic with unoxygenated Fluosol (14 +/- 14%), with Plasmalyte A (2 +/- 13%), and in the absence of treatment (5 +/- 9%). Only infusion of arterial blood resulted in no ST segment elevation or lactate production. Thus intracoronary infusion of arterial blood during brief coronary occlusion maintained normal myocardial function and aerobic metabolism. Infusion of oxygenated Fluosol resulted in amelioration of the decline in regional function after coronary occlusion, but not complete protection.
Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension.
Authors: Fujita T , Ando K , Noda H , Ito Y , Sato Y
Published: June 2011

Recent studies showed that taurine, a sulphonic amino acid, could decrease blood pressure and increase sympathoadrenal tone in DoCA-salt-treated hypertensive rats. To determine whether taurine exerts its antihypertensive action in man in a similar fashion, we studied the effect of oral administration of taurine (6 g for 7 days) on blood pressure and plasma catecholamines in 19 young patients with borderline hypertension in a double-blind, placebo-controlled fashion. Systolic blood pressure in the 10 patients who were treated with taurine decreased by 9.0 +/- 2.9 mm Hg (mean +/- SE; p less than .05 by paired t test), compared with a 2.7 +/- 2.3 mm Hg decrease (NS) in the nine patients treated with placebo and diastolic blood pressure in the taurine-treated patients decreased by 4.1 +/- 1.7 mm Hg (p less than .05) compared with 1.2 +/- 3.0 mm Hg (NS) in the placebo-treated subjects. In the patients receiving taurine plasma epinephrine (E) decreased significantly, with a negligible decrease in plasma norepinephrine (NE). The effect of taurine on plasma catecholamines and the response of plasma E after the stimulation with glucagon was also studied in 12 borderline hypertensive and nine age-matched normotensive subjects. Basal plasma E was significantly higher in borderline hypertensive than in normal subjects, but basal plasma NE did not differ in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Diagnosis of coronary artery anatomy by two-dimensional echocardiography in patients with transposition of the great arteries.
Authors: Pasquini L , Sanders S P , Parness I A , Colan S D
Published: June 2011

With the increasing popularity of the Jatene procedure for the treatment of common or D-transposition of the great arteries (D-TGA), the preoperative definition of coronary artery anatomy in D-TGA has assumed great importance. Consequently, the reliability of two-dimensional echocardiography for determining the coronary artery anatomy was studied in 32 infants with D-TGA. Surgical observation of the coronary anatomy was used to assess the accuracy of the echocardiographic diagnosis. The coronary arteries were visualized in 29 of 32 patients (90%), predominantly with the use of parasternal and apical views. In the three remaining patients visualization of the coronary arteries was inadequate to allow determination of their anatomy. The coronary artery anatomy was correctly predicted in 25 of the 29 patients in whom the coronary arteries were visualized. The anatomic patterns included usual coronary anatomy for D-TGA (n = 16), left circumflex coronary from the right coronary artery (n = 6), single right coronary artery (n = 1), single left coronary artery (n = 1), and inverted origin of the coronary arteries (n = 1). The errors in the remaining four patients were (1) false-negative diagnosis of origin of the left circumflex coronary from the right coronary artery (n = 1); (2) false-positive diagnosis of origin of the left circumflex coronary from the right coronary artery (n = 1), and (3) diagnosis of origin of the left circumflex coronary from the right coronary artery when the correct diagnosis was single right coronary artery (n = 2).(ABSTRACT TRUNCATED AT 250 WORDS)
Transcatheter umbrella closure of congenital heart defects.
Authors: Lock J E , Cockerham J T , Keane J F , Finley J P , Wakely P E , Fellows K E
Published: June 2011

Between October 1984 and September 1986, we attempted transcatheter umbrella closure, using the Rashkind PDA occluder, of 12 congenital or postoperative cardiovascular defects (other than patent ductus arteriosus [PDA]) in 11 patients. In each, we used the umbrella for closure because the defect was too short and/or too large to close with conventional transcatheter methods. The defects included three post-Glenn venous communications (superior vena cava-right atrium, n = 2; azygos vein to inferior vena cava), four congenital "interatrial defects" producing cyanosis ("coronary sinus" septal defect, left superior vena cava to left atrium, patent foramen ovale, left inferior vena cava to left atrium), and five non-PDA systemic-to-pulmonary arterial communications (two congenital and three postoperative). Ten of 12 defects were embolized successfully; nine had complete or subtotal closure, and one was partially closed. The first attempted closure resulted in embolization of a 12 mm device to a lower-lobe pulmonary artery, without clinical sequelae. No other complications occurred. Clinical improvement was most dramatic in those patients whose cyanosis was relieved and less obvious when pulmonary blood flow was reduced. The Rashkind umbrella device, originally designed for closure of PDA, considerably expands the list of congenital or operative defects that can be closed nonsurgically.
Automaticity, triggered activity, and responses to adrenergic stimulation in cat subendocardial Purkinje fibers after healing of myocardial infarction.
Authors: Kimura S , Bassett A L , Kohya T , Kozlovskis P L , Myerburg R J
Published: June 2011

We studied automaticity, triggered activity, and responses to alpha- and beta-adrenergic stimulation in subendocardial Purkinje fibers overlying healed infarct scars (infarct preparation) and from remote normal zones (noninfarct preparation) of cat left ventricles. The preparations were studied 2 to 4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex arteries. Subendocardial Purkinje fibers from corresponding areas of normal hearts served as control samples (control preparation). Transmembrane action potential characteristics and rates of automaticity (spontaneous phase 4 depolarization) did not differ among control, noninfarct, and infarct preparations. However, overdrive at cycle lengths of less than 400 msec suppressed automaticity to a greater degree in Purkinje fibers of infarct preparations than those of control and noninfarct preparations. Changes in automatic rate during superfusion with isoproterenol (10(-10)M to 10(-6)M) were not different among the three groups of preparations, but exposure to phenylephrine (10(-9)M to 10(-5)M) in the presence of 5 X 10(-7)M propranolol reduced the automatic rate to a greater degree in Purkinje fibers of infarct preparations than those of control or noninfarct preparations. Triggered activity arising from delayed afterdepolarizations was recorded in 10 of 29 infarct preparations (34%), but not in 12 control and 10 noninfarct preparations. These afterpotentials were augmented by increasing extracellular Ca++ concentration, 10(-7)M isoproterenol, and 10(-5)M phenylephrine in the presence of 5 X 10(-7)M propranolol. We conclude that Purkinje fibers overlying healed infarct scars have altered physiology of spontaneous automaticity, enhanced responses to alpha-adrenergic interventions, and a tendency to triggered activity, and that both alpha- and beta-adrenergic effects may result in worsening of arrhythmias by augmentation of afterpotentials in healed myocardial infarction.
Elimination of exercise-induced regional myocardial dysfunction by a bradycardiac agent in dogs with chronic coronary stenosis.
Authors: Guth B D , Heusch G , Seitelberger R , Ross J
Published: June 2011

We have previously demonstrated that the beneficial effect of cardioselective beta-blockade on exercise-induced ischemia is due entirely to negative chronotropism. Therefore we studied the effect of a new bradycardiac agent (UL-FS 49) in 10 dogs with chronic coronary artery stenosis produced by an ameroid constrictor. Regional myocardial function (sonomicrometers, wall thickness) and blood flow (microspheres) were measured during a control treadmill exercise bout and an identical run 3 hr later after the administration of UL-FS 49 (1.0 mg/kg iv). In the control run, heart rate increased from 114 +/- 20 to 230 +/- 19 beats/min and systolic wall thickening (%WT) in the poststenotic myocardium decreased from 23.3 +/- 5.2% at rest to 9.3 +/- 5.0%, a 60% reduction. Subendocardial blood flow in the ischemic area decreased from 1.04 +/- 0.30 to 0.55 +/- 0.40 ml/min/g, blood flow per beat decreased from 9.1 X 10(-3) to 2.5 X 10(-3) ml/g, and mean transmural flow failed to increase (1.06 +/- 0.30 vs 1.08 +/- 0.39 ml/min/g). During exercise with UL-FS 49, heart rate increased from 89 +/- 10 to only 139 +/- 10 beats/min. End-diastolic left ventricular pressure was increased compared with that during the control run (35.7 +/- 3.0 vs 28.9 +/- 5.5 mm Hg) but left ventricular peak systolic pressure and dP/dt were unchanged. %WT in the ischemic zone did not change significantly during exercise with UL-FS 49 (23.3 +/- 7.9% at rest, 21.5 +/- 8.4% during the run), and in the nonischemic zone it increased to the same extent as during the control run.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of the pericardium on the diastolic left coronary pressure-flow relationship in the isolated dog heart.
Authors: Watanabe J , Maruyama Y , Satoh S , Keitoku M , Takishima T
Published: June 2011

We studied the effects of the pericardium on diastolic left coronary pressure-flow relationships in heart-blocked and isolated canine preparations. In these preparations, the left and right coronary arteries were dilated with adenosine and perfused by means of a pressurized arterial reservoir. The diastolic left heart pressure (LHP) was controlled by the height of a reservoir connected to the left atrium and left ventricle. The right atrial and ventricular pressure i.e., coronary outflow pressure, was kept constant at 0 mm Hg. Before and after pericardiectomy, diastolic coronary pressure-flow relationships were obtained at three values of LHP (0, 15, and 30 mm Hg) with driving pressure decreasing (2 mm Hg/sec or less) from approximately 60 mm Hg to the actual zero-flow pressure (Pf = 0) during a single long diastole induced by cessation of ventricular pacing. The slopes of the coronary pressure-flow relationships were approximated by a linear regression analysis in which the correlation coefficients were greater than .98 in all cases. Before pericardiectomy, with LHP increasing from 0 to 15 and 30 mm Hg, the value of Pf = 0 significantly increased from 7 +/- 1 to 16 +/- 1 (p less than .01) and 28 +/- 2 mm Hg (p less than .01), respectively. After pericardiectomy, it increased from 7 +/- 1 to 14 +/- 1 (p less than .01) and 17 +/- 2 mm Hg (p less than .01), respectively. When LHP was at 0 and 15 mm Hg, the pericardiectomy had no effect on the value of Pf = 0.(ABSTRACT TRUNCATED AT 250 WORDS)
Prophylactic antiarrhythmic therapy of high-risk survivors of myocardial infarction: lower mortality at 1 month but not at 1 year.
Authors: Gottlieb S H , Achuff S C , Mellits E D , Gerstenblith G , Baughman K L , Becker L , Chandra N C , Henley S , Humphries J O , Heck C
Published: June 2011

To determine whether prophylactic antiarrhythmic therapy influences mortality in high-risk patients after acute myocardial infarction, 143 such patients were randomized in a double-blind individually dose-adjusted, placebo-controlled trial an average of 14 +/- 7 days after myocardial infarction and followed for 1 year. Patients were judged to be at high risk on the basis of (1) ejection fraction less than 40% (n = 60), (2) arrhythmias of Lown class 3 or higher (n = 26), or (3) both (n = 57). Aprindine was chosen because of its long half-life, few side effects, and antiarrhythmic efficacy. Baseline characteristics in the treatment arms did not differ. Holter-detected arrhythmias were reduced in aprindine-treated patients at 3 months (p less than .001) and at 1 year (p less than .001). One patient was lost to follow-up; in the remaining patients 1 year mortality was 20% (28/142; 12 aprindine and 16 placebo). There was no significant difference between the two study arms in overall mortality and sudden death. However, among those who died, median duration of survival was longer in aprindine-treated patients (86 vs 21.5 days) (p = .04). Although antiarrhythmic treatment with aprindine of high-risk patients after myocardial infarction does not affect 1 year survival, mortality appears to be delayed; thus there may be a role for short-term treatment before more definitive therapy such as surgery.
Reduction in infarct size and enhanced recovery of systolic function after coronary thrombolysis with tissue-type plasminogen activator combined with beta-adrenergic blockade with metoprolol.
Authors: Van de Werf F , Vanhaecke J , Jang I K , Flameng W , Collen D , De Geest H
Published: June 2011

The effect of beta-adrenergic blockade on the salvage and functional recovery of reperfused myocardium was investigated in anesthetized dogs. Immediately after thrombotic occlusion of the left anterior descending coronary artery, the cardioselective beta-blocking agent metoprolol was given intravenously at a dose of 0.5 mg/kg infused over 10 min. One hour after the onset of occlusion, recanalization was initiated by intravenous infusion of recombinant human tissue-type plasminogen activator (rt-PA, 10 micrograms/kg/min for 30 min). Anatomic infarct size expressed as percent of the left ventricular mass (I/LV), global ejection fraction, and mean systolic shortening of the segmental radii (SS) of the infarcted area were measured either after 24 hr or 1 week in six groups of six dogs each: group I (rt-PA + metoprolol, evaluated at 24 hr), group II (rt-PA + metoprolol, evaluated at 1 week, group III (rt-PA alone, evaluated at 24 hr), group IV (rt-PA alone, evaluated at 1 week), group V (persistent occlusion, evaluated at 24 hr), and group VI (persistent occlusion, evaluated at 1 week). The smallest infarcts were found in reperfused dogs given metoprolol, but the differences from dogs receiving rt-PA alone were not statistically significant (I/LV, expressed as mean +/- SEM: 5.5 +/- 0.9% in group I, 6.7 +/- 1.9% in group II, 15.4 +/- 5.0% in group III, 11.4 +/- 3.5% in group IV, 23.6 +/- 2.5% in group V, and 26.9 +/- 2.3% in group VI).(ABSTRACT TRUNCATED AT 250 WORDS)