bluuebunny/crossref_metadata_2025 huggingface dataset:
A new two-dimensional echocardiographic technique for evaluating right ventricular size and performance in patients with obstructive lung disease.
Authors: Starling M R , Crawford M H , Sorensen S G , O'Rourke R A
Published: June 2011

To compare two-dimensional (2-D) echocardiographic estimates of right ventricular size and performance to similar determinations from equilibrium radionuclide angiography (RNA) before and after isosorbide dinitrate, we evaluated 19 patients with severe chronic obstructive pulmonary disease. The end-diastolic and end-systolic volumes estimated from subcostal 2-D echocardiographic views of the right ventricle correlated with the RNA end-diastolic and end-systolic counts (r = 0.76 and 0.82, respectively). The 2-D echocardiographic and RNA right ventricular ejection fraction (EF) estimates also correlated (r = 0.80), and the average right ventricular EF measures of 42 +/- 11% and 40 +/- 12%, respectively, did not differ significantly. Nitrate administration produced a significant increase in heart rate (99 +/- 11 to 108 +/- 14 beats/min, p less than 0.001) and a decrease in systolic arterial pressure (139 +/- 23 to 120 +/- 22 mm Hg, p less than 0.001). Nitrates also significantly decreased the average 2-D echocardiographic end-diastolic and end-systolic volumes (22 +/- 16% and 18 +/- 12%, p less than 0.001), as well as RNA end-diastolic and end-systolic counts (33 +/- 17% and 32 +/- 22%, p less than 0.001), but did not significantly decrease the average right ventricular EF values (4 +/- 12% and 4 +/- 24%, respectively). Nevertheless, after isosorbide dinitrate, the 2-D echocardiographic right ventricular end-diastolic and end-systolic volume estimates continued to correlate with the corresponding RNA count measures (r = 0.76 and 0.79, respectively), as did the 2-D echocardiographic and RNA right ventricular EF values (r = 0.75). We conclude that 2-D echocardiographic evaluation of right ventricular size and performance is feasible in selected patients with chronic obstructive pulmonary disease, and that 2-D echocardiographic measures of right ventricular size and performance compare favorably with similar determinations by RNA at rest and after nitrate administration.
Postural changes in pulmonary blood flow in pulmonary hypertension: a noninvasive technique using ventilation-perfusion scans.
Authors: Horn M , Hooper W , Brach B , Ashburn W , Moser K
Published: June 2011

To determine whether postural changes in ratio of upper to lower (U:L) zone pulmonary blood flow reflect pulmonary arterial pressures, we used pulmonary perfusion photoscintigraphy to study 12 normal subjects and 10 patients with precapillary pulmonary hypertension (eight classified as "primary" and two as thromboembolic). All patients underwent right-heart catheterization and measurement of pulmonary arterial systolic, diastolic, mean and capillary (wedge) pressures. The distribution of perfusion was then assessed in the supine and erect positions after i.v. injection of technetium-99m-labeled, macroaggregated albumin. Perfusion distribution was corrected for lung volume by xenon-133 equilibrium ventilation scans. In normal subjects, the U:L lung zone perfusion ratio decreased by 70.7 +/- 12.2% with the change in position. The patient group differed (p less than 0.0001) from normal subjects in that there was only a 19 +/- 17.4% shift of U:L ratio with the postural change. The mean pulmonary arterial pressure in the patient groups was 50 +/- 24.2 mm Hg. The postural change in U:L zone ratio correlated significantly with the mean pulmonary arterial pressure (r = -0.84, p less than 0.01) pulmonary arterial systolic (r = -0.83, p less than 0.01) and diastolic pressures (r = -0.72, p less than 0.05) and with the pulmonary vascular resistance (r = -0.74, p less than 0.02). No correlation was found with other hemodynamic, spirometric or blood gas data. We conclude that the postural shift in U:L ratio warrants further exploration as a noninvasive approach for detecting and quantifying pulmonary hypertension.
The tricuspid valve annulus: study of size and motion in normal subjects and in patients with tricuspid regurgitation.
Authors: Tei C , Pilgrim J P , Shah P M , Ormiston J A , Wong M
Published: June 2011

The tricuspid valve leaflets and their annular attachments were recorded by two-dimensional echocardiography from a view of the right ventricular inflow tract obtained by placing the transducer at an intermediate position between the left ventricular apex and the left lower sternal border. The transducer was rotated, and recordings were made at 30 degrees rotational intervals around the circumference of the tricuspid valve annulus. The cyclical pattern of variations in tricuspid annular size was studied with 12 measurements made during the cardiac cycle in five normal subjects. Annular areas and circumferences were measured. The overall motion pattern was similar to that reported in normal mitral valve annular study. Subsequently, in 16 normal subjects and 18 patients with tricuspid regurgitation, the maximum and minimum tricuspid annular sizes and their percent reduction were measured. The mean maximum annular circumference and area were 11.9 +/- 0.9 cm (mean +/- SD) and 11.3 +/- 1.8 cm2 in normal subjects. They were significantly greater in tricuspid regurgitation (14.0 +/- 0.7 cm and 15.8 +/- 1.8 cm2, respectively). The mean minimum annular sizes were much larger in tricuspid regurgitation (12.5 +/- 0.6 cm and 13.0 +/- 1.4 cm2) than in normal subjects (9.6 +/- 0.9 cm, 7.6 +/- 1.4 cm2). Thus, the percent reduction of annular circumference and area were significantly decreased in tricuspid regurgitation. For anatomic correlations, measurements of the tricuspid annular circumference were made at autopsy in 18 hearts without underlying valvular disease. The annular circumference was measured in the fresh and fixed states. The measurement in the fresh state was 13.5 +/- 0.8 cm and in the fixed state was 12.0 +/- 0.8 cm. The values measured in the fixed hearts were more similar to measurements obtained by echocardiography in a group of normal subjects. Thus, tricuspid annular reconstruction by the new two-dimensional echocardiographic method provides additional information about normal and abnormal size and function of the tricuspid valve annulus.
Precordial ST-segment depression during acute inferior myocardial infarction: clinical, scintigraphic and angiographic correlations.
Authors: Gibson R S , Crampton R S , Watson D D , Taylor G J , Carabello B A , Holt N D , Beller G A
Published: June 2011

The cause and associated pathophysiology of precordial ST-segment depression (ST decreases) during acute inferior myocardial infarction (IMI) are controversial. To investigate this problem, electrocardiographic findings in 48 consecutive patients with acute IMI were prospectively compared with results of coronary angiography, submaximal exercise thallium-201 (201TI) scintigraphy and multigated blood pool imaging, all obtained 2 weeks after IMI, and with clinical follow-up at 3 months. Patients were classified according to the admission ECG obtained 3.3 +/- 3.1 hours after the onset of chest pain. Twenty-one patients (group A) had no or less than 1.0 mm ST decreases, and 27 (group B) had greater than or equal to 1.0 mm ST decreases in two or more precordial (V1-6) leads. Patients in group B had more prolonged chest pain after admission to the coronary care unit than those in group A (2.8 +/- 3.0 vs 1.2 +/- 1.1 hours, p less than 0.03), greater summed ST-segment elevation in leads II, III, aVF (6.7 +/- 4.7 vs 3.3 +/- 4.5 mm, p less than 0.02), higher plasma peak creatine kinase levels (1133 +/- 781 vs 653 +/- 482 IU/l, p less than 0.01), a higher prevalence of "true posterior" infarction by ECG criteria (26% vs 5%, p less than 0.05), a lower radionuclide ejection fraction (46 +/- 9% vs 54 +/- 6%, p less than 0.001), more extensive infarct-related asynergy (p less than 0.001) and 201TI perfusion abnormalities (p less than 0.01), more complications during hospitalization (p less than 0.03), and more cardiac events at 3 months (p less than 0.02). There were no significant differences between group A and group B in the extent of underlying coronary disease, prevalence of left anterior descending coronary artery disease, exercise-induced ST decreases or angina, and 201TI defects or wall motion abnormalities in anterior or septal segments. Thus, patients with acute IMI who have associated precordial ST decreases have greater global and regional left ventricular dysfunction due to more extensive inferior or inferoposterior wall infarction, rather than concomitant anteroseptal ischemic injury.
Enhanced detection of the evolution of tissue changes after acute myocardial infarction using color-encoded two-dimensional echocardiography.
Authors: Parisi A F , Nieminen M , O'Boyle J E , Moynihan P F , Khuri S F , Kloner R A , Folland E D , Schoen F J
Published: June 2011

Acute myocardial infarction was produced in 26 dogs by ligation of the left anterior descending coronary artery. Two-dimensional echocardiograms (2-D echoes) were performed through the chest wall before and serially after coronary ligation. The dogs were then killed in four groups at the following intervals: 24-48 hours, 1-2 weeks, 3 weeks and 6-8 weeks. Each 2-D echo was processed through a video quantizer, which encoded echo amplitudes progressively into eight regions of color. The myocardium was graded with respect to color composition in regions that showed any abnormally contracting segment (ACS). The ACS exhibited a progressive increase in echo intensity that became maximal 6-8 weeks after coronary ligation. Histopathologic and histochemical studies verified that these increases in echo amplitude correlated with the evolution of healing and myocardial scar formation. At 6-8 weeks, the mean collagen content of infarcted myocardium had increased by a factor of 4; concurrently, ACS echo amplitude had increased two- to threefold. These observations suggest that color-encoded 2-D echo promotes facile perception of serial changes in tissue characteristics that result from acute myocardial infarction.
Radionuclide ventriculography for assessment of absolute right and left ventricular volumes in children.
Authors: Parrish M D , Graham T P , Born M L , Jones J P , Boucek R J , Partain C L
Published: June 2011

We determined absolute right and left ventricular volumes and cardiac output from the equilibrium radionuclide angiogram in 26 children, ages 3 months to 18 years, with diverse types of heart disease. We validated these results by comparing them with left ventricular (20 patients) and right ventricular (16 patients) cineangiographic volumes and cardiac output. Radionuclide volumes and cardiac outputs were determined in two ways: by a geometric method (area-length for left ventricle, Simpson's rule for right ventricle) and by a count-based method (correcting ventricular regional counts for frame duration, acquisition time, venous blood counts and attenuation). Both methods for estimating left ventricular end-diastolic volume compared favorably with cineangiography (correlation coefficients greater than 0.90). The count-based method also correlated well for the right ventricle. End-systolic measurements were not possible. Count-based assessment of cardiac output also correlated well with cineangiographic values. We conclude that right and left ventricular volumes and cardiac output can be reliably measured in children with equilibrium radionuclide ventriculography.
Fluid dynamics of aortic stenosis: subvalvular gradients without subvalvular obstruction.
Authors: Bird J J , Murgo J P , Pasipoularides A
Published: June 2011

Analysis of a tapering, pulsatile flow field predicts that substantial subvalvular pressure gradients exist in patients with valvular aortic stenosis (AS) without invoking a second anatomic site of obstruction. Using a catheter with two laterally mounted micromanometers, we examined the left ventricle in 11 patients with AS, mean age 64 +/- 11 years (+/- SD); the mean valve area was 1.0 +/- 0.3 cm2. Simultaneous measurements were made in (1) the left ventricular (LV) chamber and the LV outflow tract (LVOT) and (2) the LVOT and ascending aorta (AO). No patient had anatomic evidence of a subvalvular obstruction, but large subvalvular gradients were present in all. The average peak LV-LVOT and LV-AO gradients were 41 +/- 17 mm Hg and 58 +/- 23 mm Hg, respectively. Flow velocity was electromagnetically derived in two patients. The LV-LVOT gradient was associated with an increased flow velocity in the LVOT. This study suggests that large subvalvular gradients are present in AS and help overcome blood's inertia to convective and local accelerations in the tapering subvalvular flow field.
Mechanism of paradoxic pulse in bronchial asthma.
Authors: Jardin F , Farcot J C , Boisante L , Prost J F , Gueret P , Bourdarias J P
Published: June 2011

To elucidate the mechanism of paradoxic pulse in severe bronchial asthma, we performed hemodynamic studies and measured esophageal pressure in nine patients who had status asthmaticus and clinical paradoxic pulse. Two-dimensional echocardiography allowed simultaneous assessment of cyclic changes in right- and left-heart size throughout the respiratory cycle. Esophageal pressure varied from a markedly negative level during inspiration (-24.4 +/- 6.5 cm H2O) to a positive level during expiration (7.6 +/- 6.0 cm H2O). Competition between right- and left-heart chambers for pericardial space during inspiration was suggested by the reduced left ventricular cross-sectional area at end-systole (-24%, p less than 0.01) and end-diastole (-32%, p less than 0.01), the leftward septal shift, and the increased right ventricular internal diameter at end-systole (42%, p less than 0.01) and end-diastole (40%, p less than 0.001). Competition for filling, however, could not entirely account for the paradoxic pulse, for systemic and pulmonary pulse pressures were almost (within one cardiac cycle) in phase: both were minimal at inspiration and maximal at expiration. The increase in impedance to right ventricular ejection is another major factor reducing left ventricular preload at inspiration. This reduction in preload was shown to be the predominant mechanism for the decrease in left ventricular stroke output at inspiration.
Huge chronic pericardial effusion caused by Toxoplasma gondii.
Authors: Sagristá-Sauleda J , Permanyer-Miralda G , Juste-Sánchez C , de Buen-Sánchez M L , Pujadas-Capmany R , Arcalís-Arce L , Soler-Soler J
Published: June 2011

Two patients who had a huge pericardial effusion of at least 9 and 14 years' duration caused by cardiac toxoplasmosis are reported. Toxoplasma gondii were seen in the pericardial fluid, and serologic evidence also demonstrated the activity of the infection. These cases illustrate both the need to exclude toxoplasmosis in chronic pericardial effusion of unknown cause and the possibility of seeing toxoplasma in the pericardial fluid of patients with active toxoplasmic pericarditis. Moreover, in endemic areas, cardiac toxoplasmosis may not be an exceptional cause of chronic pericardial effusion.
Two-dimensional echocardiographic analysis of segmental left ventricular wall motion before and after coronary artery bypass surgery.
Authors: Rubenson D S , Tucker C R , London E , Miller D C , Stinson E B , Popp R L
Published: June 2011

Twenty patients with coronary artery disease were studied with two-dimensional echocardiography the day before saphenous vein bypass graft surgery. Serial studies were obtained 7.4 +/- 2.5 (+/- SD) and 43.4 +/- 13.1 days postoperatively to qualitatively assess the effect of bypass surgery on regional wall motion. Changes in segmental wall motion were assessed semiquantitatively by assigning a segmental wall motion score to each of nine echocardiographically defined segments. Preoperatively, 18% of the segments moved abnormally. The mean overall segmental wall motion score did not change significantly, as shown by comparing the postoperative studies with the preoperative study. However, there was a significant worsening in the septal motion (apical and basal) and a significant improvement in posterior wall motion (apical and basal) after bypass surgery. Anterior and lateral wall motion were not significantly changed. Nonseptal segments that were normal preoperatively usually remained normal; abnormal nonseptal segments usually improved or were unchanged by surgery. The motion of septal segments, however, generally worsened postoperatively whether they were normal or abnormal preoperatively. We conclude that segmental wall motion assessed by two-dimensional echocardiography may improve after revascularization surgery, but the interventricular septum shows impaired motion. This effect of coronary artery bypass on wall motion is better demonstrated relatively late after operation than early in the postoperative course, as has been done in some previous studies.
The effect of aortic valve replacement on survival.
Authors: Schwarz F , Baumann P , Manthey J , Hoffmann M , Schuler G , Mehmel H C , Schmitz W , Kübler W
Published: June 2011

We retrospectively studied 252 operated and 47 unoperated patients with isolated aortic valve disease. Aortic valve replacement (AVR) was recommended to all patients based on clinical and hemodynamic data. Preoperative hemodynamic and angiographic data were similar in operated and unoperated cohorts. Seventy-one percent of patients received a Björk-Shiley prosthesis. Operative mortality was 7% for the entire surgical series. For patients with predominant aortic stenosis (AS), survival at 3 years was 87% in operated and 21% in unoperated patients (p less than 0.001). For patients with predominant aortic insufficiency (AI), the 5-year survival rate was 86% in operated and 87% in unoperated patients (NS). AVR improved long-term survival in patients with AS who had normal or impaired left ventricular (LV) function. In patients with AI and normal LV function, survival was not improved after AVR, but those with LV dysfunction who were operated on tended to survive longer (NS). Long-term survival of unoperated patients with AI was better than that in unoperated patients with AS. We conclude that AVR improves long-term survival in patients with AS who were normal or abnormal LV function, and that AVR does not change long-term survival in patients with AI, although those with LV dysfunction tended to survive longer.
Radionuclide angiographic assessment of global and segmental left ventricular function at rest and during exercise after coronary artery bypass graft surgery.
Authors: Lim Y L , Kalff V , Kelly M J , Mason P J , Currie P J , Harper R W , Anderson S T , Federman J , Stirling G R , Pitt A
Published: June 2011

Left ventricular ejection fraction (LVEF) was measured by radionuclide angiography at rest and during supine bicycle exercise before and 3 months after coronary artery bypass graft surgery (CABG) in 20 patients with chronic stable angina. The right anterior oblique gated first-pass technique was used to assess LVEF response to maximal exercise (Wmax), while the left anterior oblique equilibrium-gated technique was used to assess LVEF and relative LV volume changes during graded submaximal exercise. Mean LVEF was unchanged at rest after CABG by both the first-pass (60 +/- 12% vs 60 +/- 12%) and equilibrium-gated (61 +/- 13% vs 62 +/- 13%) measurements. At Wmax, mean first-pass LVEF was significantly higher postoperatively than preoperatively (63 +/- 17% vs 53 +/- 17%; p less than 0.01) with a higher Wmax (750 +/- 182 vs 590 +/- 202 kpm/min; p less than 0.001) and higher rate-pressure product (302 +/- 59 vs 222 +/- 57 units; p less than 0.001). Similarly, equilibrium-gated LVEF levels during graded exercise, using stepwise regression analysis, were significantly higher postoperatively than preoperatively (p less than 0.001); at the highest graded work load, they averaged 63 +/- 19% postoperatively and 53 +/- 17% preoperatively, with higher work loads (500 +/- 190 vs 417 +/- 155; p less than 0.05) and higher rate-pressure products (271 +/- 55 vs 207 +/- 53; p less than 0.001). The increase in exercise LVEF after surgery was due to a marked decrease in the ratio, relative to resting values, of counts-based end-systolic volumes during submaximal exercise (preoperatively 1.91 +/- 1.04; postoperatively 1.14 +/- 0.46; p less than 0.01). The five subjects in whom LVEF decreased significantly during exercise postoperatively all had one or more blocked or stenosed grafts. This study documents, by two independent radionuclide techniques, an improved LVEF during exercise at an increased maximal work capacity and rate-pressure product 3 months after successful CABG.
Effects of acebutolol on myocardial infarct extension: a randomized electrocardiographic, enzymatic and angiographic study.
Authors: Azancot I , Lorente P , Georgiopoulos G , Beaufils P , Masquet C , Baudouy Y , Slama R
Published: June 2011

The effect of acebutolol (1 mg/kg i.v. during the first 2 days followed by a daily oral dose of 600 mg for 3 weeks) was studied in a randomized trial involving 26 patients seen within 24 hours after the onset of uncomplicated anterior transmural myocardial infarction (TMI). Myocardial ischemia and necrosis were evaluated by precordial maps recorded daily for 9 days. Left ventricular pump function and dyssynergy were quantitatively measured on 30 degrees right anterior oblique cineangiograms. Angiography was performed, using the postextrasystolic potentiation technique, within the first 24 hours after TMI and was repeated 1 month later. The basal and postextrasystolic beats from the initial angiography were computerized and compared with those from the final angiogram. MB-CK serum level was measured from blood samples drawn every 3 hours for the first 72 hours. Fourteen patients selected at random received acebutolol within the first 24 hours; 12 subjects were untreated and served as controls. During the 1-month study, no other drugs were administered. Treated patients showed a significant reduction in capillary wedge pressure, extent of hypokinesis and ST-segment elevation; no significant differences were observed in the control group. However, the predictability based on the angiographic data was the same in both groups, and beta blockade did not alter this predictability significantly. Furthermore, no significant difference was found during the final evaluation for treated compared with control patients for any single variable or set of variables. The incidence of infarct extension was not decreased, but only significantly delayed in treated patients. The high variability of the measurements, probably related to the high variability of the pathophysiologic factors, may account for the failure to demonstrate the efficacy of acebutolol.
The stunned myocardium: prolonged, postischemic ventricular dysfunction.
Authors: Braunwald E , Kloner R A
Published: June 2011

Myocardial ischemia has, for many decades, been viewed as an all-or-none process that causes myocardial necrosis when prolonged and severe, but whose effects are transient when it is brief or mild. In view of the evidence that the ischemic process may "hit, run and stun," perhaps our thinking about the consequences of myocardial ischemia should be expanded. According to this formulation, an ischemic insult not of sufficient severity of duration to produce myocardial necrosis may acutely affect myocardial repolarization and cause angina (hit); but these changes wane rapidly (run), when the balance between myocardial oxygen supply and demand has been reestablished. However, the ischemia may interfere with normal myocardial function, biochemical processes and ultrastructure for prolonged periods (stun). The severity and duration of these postischemic changes depend on the length and intensity of the ischemia, as well as on the condition of the myocardium at the onset of the ischemic episode. Furthermore, it is likely that when the myocardium is repeatedly stunned, it may exhibit chronic postischemic left ventricular dysfunction, an ill-defined condition. If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardial perfusion by surgical treatment.
Electrophysiologic effects of disopyramide in patients with atrioventricular nodal dysfunction.
Authors: Wilkinson P R , Desai J , Hollister J , Gonzalez R , Abbott J A , Scheinman M M
Published: June 2011

Seventeen patients with first-degree or Mobitz I atrioventricular (AV) block and narrow QRS complexes underwent electrophysiologic drug testing before and after i.v. administration of disopyramide. Disopyramide did not significantly change the mean sinus cycle length (895 +/- 131 vs 877 +/- 119 msec), mean maximal sinus node recovery time (1134 +/- 160 vs 1133 +/- 13 msec), mean atrial effective refractory period (314 +/- 72 vs 307 +/- 54 msec), mean AV nodal conduction time (187 +/- 79 vs 180 +/- 73 msec) or the mean paced cycle length at which AV nodal Wenckebach conduction occurred (545 +/- 144 vs 497 +/- 130 msec) after disopyramide. The mean AV nodal effective refractory period decreased significantly (from 535 +/- 137 to 521 +/- 122 msec), and both infranodal conduction time and the paced ventricular cycle length producing ventriculoatrial block increased significantly (from 56 +/- 12 to 63 +/- 13 msec and from 625 +/- 158 to 655 +/- 157 msec, respectively). We conclude that i.v. disopyramide administered in a dose resulting in therapeutic blood levels showed no adverse effects on AV nodal conduction in patients with AV nodal dysfunction. In contrast, i.v. disopyramide depressed retrograde AV conduction.
The microcirculation of the human heart: end-capillary loops with discrete perfusion fields.
Authors: Factor S M , Okun E M , Minase T , Kirk E S
Published: June 2011

We studied 10 autopsied human hearts by perfusing colored Microfil into separate coronary arteries to define organization of capillaries at the borders between two perfusion fields. Sections of "cleared" myocardium were examined with epiillumination at the grossly identified borders of Microfil perfusion. In two- and three-color-injected hearts, the capillaries were arrayed in a pattern of arcades and loops without connections between separately perfused capillary beds. In hearts perfused through only one coronary artery, the capillaries were organized into tufted loops at the border. These findings contrast with the microcirculatory pattern in canine skeletal muscle and brain, in which heterologous capillaries are focally interconnected. We conclude that the human microcirculation is composed of end-capillary loops that supply discrete perfusion fields. This pattern of unconnected heterologous capillary beds suggest that there is no obvious anatomic arrangement of the microcirculation that could account for a significant ischemic lateral border zone in human myocardial infarctions.
Renin-angiotensin system inhibition in acute myocardial infarction in dogs. Effects on systemic hemodynamics, myocardial blood flow, segmental myocardial function and infarct size.
Authors: Liang C S , Gavras H , Black J , Sherman L G , Hood W B
Published: June 2011

Acute left anterior descending coronary artery occlusion was produced in 21 conscious, chronically instrumented dogs. Forty minutes after coronary occlusion, nine dogs were given i.v. teprotide, 25 micrograms/kg/min, followed by oral doses of captopril, 10 mg/kg every 8 hours for 24 hours. The remaining 12 dogs served as saline-infused controls. In all dogs, acute coronary occlusion increased plasma renin activity and peripheral vascular resistance and reduced cardiac output, but did not change mean aortic blood pressure significantly. Teprotide significantly (p less than 0.05) decreased peripheral vascular resistance (from 3804 +/- 1158 to 2876 +/- 816 dy-sec-cm-5) (+/- SD) and mean aortic pressure (from 117 +/- 12 to 107 +/- 15 mm Hg), and increased cardiac output (from 2.63 +/- 0.67 to 3.12 +/- 0.74 l/min). Teprotide also produced a relative increase in flow to the renal and splanchnic circulations compared with the saline-treated controls. There were, however, no differences in segmental systolic shortening, blood flow in the normal or ischemic myocardium, or infarct size. These results indicate that the renin-angiotensin system may play an important role in dogs with acute coronary occlusion and that blockade of this system lowers systemic blood pressure and improves cardiac output. However, direct effects of renin-angiotensin system blockade on the myocardium are lacking; there were no changes in myocardial blood flow, myocardial mechanics or infarct size.
Possible involvement of an endogenous opioid in the antihypertensive effect of clonidine in patients with essential hypertension.
Authors: Farsang C , Kapocsi J , Juhasz I , Kunos G
Published: June 2011

The effect of naloxone on the hypotensive and bradycardiac action of clonidine was studied in 27 hospitalized patients with uncomplicated mild-to-moderate essential hypertension. In a double-blind, crossover study, clonidine, 0.3 mg/day orally for 3 days, significantly reduced systolic and diastolic blood pressure and heart rate, whereas placebo was ineffective. Naloxone, 0.4 mg given intravenously on the third day of clonidine treatment, caused a rapid increase in blood pressure and heart rate in 14 patients (reacting group), but was ineffective in the remaining 13 patients (nonreacting group). Naloxone given during the placebo period was ineffective in all patients. Both the clonidine-induced hypotension and the rebound increase in blood pressure after cessation of clonidine were significantly greater in the reacting than in the nonreacting group. These observations suggest that release of an endogenous opioid contributes to the antihypertensive action of clonidine; this mechanism may be also involved in the discontinuation syndrome after cessation of clonidine.
Transcutaneous angioplasty of experimental aortic coarctation.
Authors: Lock J E , Niemi T , Burke B A , Einzig S , Castaneda-Zuniga W R
Published: June 2011

A dilatable form of juxtaductal aortic coarctation was surgically created in 29 newborn lambs. Of the 17 long-term survivors, four lambs served as controls and 13 underwent transcutaneous balloon dilation angioplasty with either polyvinylchloride or polyethylene catheters after 7--10 weeks of recovery. During growth before dilation, there was little change in the systolic gradient across the coarctation (36.6-35.3 mm Hg) despite an increase in animal weight from 3.8 to 19.3 kg. This systolic gradient remained constant in undilated lambs throughout a 6-month follow-up. Dilation produced an immediate 65% increase in the diameter of the coarctation and a 68% decrease in the systolic gradient across the coarctation site. Successful dilation required very high (6--8 atmospheres) dilating pressures. This gradient relief persisted throughout a follow-up of up to 1 year. Although no late sequelae could be attributed to the angioplasty, one lamb suffered an anterior aortic tear (associated with a difficult postdilation wire passage across the dilation site), which resulted in fatal intrathoracic hemorrhage. Cross pathologic inspection demonstrated intimal and medial tears in successfully dilated lambs in the first 3 days after dilation; on late pathologic examination, the intima appeared completely healed, without evidence of aneurysm or accelerated atheroma formation, within 2 months. These results, in conjunction with previous human in vitro studies, support the hypothesis that human aortic coarctation may be a dilatable lesion, although the safe limits and optimal protocols for dilating human coarctations are not known.
Effects of propranolol therapy on platelet release and prostaglandin generation in patients with coronary heart disease.
Authors: Mehta J , Mehta P
Published: June 2011

Suppression of platelet function is thought to be a mechanism of propranolol's beneficial action in angina pectoris. To study the effects of propranolol on platelets, we measured plasma beta thromboglobulin and plasma thromboxane B2 (TXB2, stable metabolite of TXA2) levels by radioimmunoassay as indexes of platelet alpha-granule and TXA2 release, respectively. Platelet TXA2 generation in vitro in response to arachidonate and thrombin was also quantitated. Twenty-nine patients with coronary disease -- 15 not taking propranolol (group A) and 14 taking propranolol (group B) -- and 15 normal subjects were studied. Plasma beta-thromboglobulin levels were increased in group A and B patients (mean 63 +/- 8 and 96 +/- 14 ng/ml, respectively) compared with normal subjects (mean 46 +/- 6 ng/ml). Plasma TXB2 levels were similar in group A and B patients and in normal subjects (mean 148 +/- 41, 149 +/- 36 and 216 +/- 39 pg/ml). Arachidonate-induced platelet TXA2 generation was significantly higher in group A patients than in normal subjects (725 +/- 393 vs 82 +/- 25 pg TXB2/10(8) platelets, p less than 0.001). In contrast, platelets from group B patients had very low TXA2 generation (mean 21 +/- 18 pg) compared with platelets from group A patients or normal subjects (p less than 0.001). Similar results were obtained using thrombin. These data show that propranolol therapy does not affect platelet-released beta thromboglobulin or TXA2 at rest, but significantly reduces the capability of platelets to generate TXA2 in vitro. Reduction in platelet TXA2 generation may be an important mechanism of action of propranolol in patients with coronary artery disease.
Acute coronary artery occlusion during percutaneous transluminal coronary angioplasty: reopening by intracoronary streptokinase before emergency coronary artery surgery to prevent myocardial infarction.
Authors: Schofer J , Krebber H J , Bleifeld W , Mathey D G
Published: June 2011

Percutaneous transluminal coronary angioplasty (PTCA) was complicated by acute coronary artery occlusion associated with ST elevation and severe chest pain in three patients. Within 10 minutes, the occluded artery was reopened by an intracoronary (i.c.) infusion of streptokinase, resulting in the disappearance of chest pain and normalization of ST segments. To keep the artery patent, i.c. streptokinase had to be continued until emergency bypass surgery was performed. In two patients, no myocardial infarction occurred, as shown by a normal postoperative left ventricular angiogram. ECG and thallium-201 scintigram. In the other patient, who was admitted with an inferior infarction and underwent PTCA after i.c. lysis, no infarct extension was observed. These results show that i.c. streptokinase rapidly opens an acute coronary artery occlusion complicating PTCA, preventing myocardial infarction.
A scanning and transmission electron microscopic study of an infected endocardial pacemaker lead.
Authors: Marrie T J , Nelligan J , Costerton J W
Published: June 2011

We studied the pacemaker lead that had been removed from a patient who suffered three sequential episodes of Staphylococcus aureus bacteremia. This organism was recovered from the surface of the lead. Scanning electron microscopy showed differential colonization of the pacemaker lead. The metal tip, the inner surface and the internal wires were covered with a heavy biofilm of bacteria. The outer silastic surface had no biofilm adherent to it; instead, well-spaced bacterial cells were seen. These observations illustrate why infection of implantable devices persists despite intensive antibiotic chemotherapy.
Aneurysmal coronary artery disease.
Authors: Swaye P S , Fisher L D , Litwin P , Vignola P A , Judkins M P , Kemp H G , Mudd J G , Gosselin A J
Published: June 2011

To examine the clinical and historical features and the natural history of aneurysmal coronary disease, we reviewed the registry data of the Coronary Artery Surgery Study (CASS). Nine hundred seventy-eight patients, representing 4.9% of the total registry population, were identified as having aneurysmal disease. No significant differences were noted between aneurysmal and nonaneurysmal coronary disease patients when features such as hypertension, diabetes, lipid abnormalities, family history, cigarette consumption, incidence of documented myocardial infarction, presence and severity of angina, and presence of peripheral vascular disease were examined. In addition, no difference in 5-year medical survival was noted between these two groups. These findings suggest that aneurysmal coronary disease does not represent a distinct clinical entity but is, rather, a variant of coronary atherosclerosis.
Effect of intravenous aminophylline on plasma levels of catecholamines and related cardiovascular and metabolic responses in man.
Authors: Vestal R E , Eiriksson C E , Musser B , Ozaki L K , Halter J B
Published: June 2011

Theophylline is thought to act by inhibiting the activity of phosphodiesterase, with a resultant increase in intracellular cyclic AMP. However, this concept is largely based on in vitro studies using concentrations of theophylline which greatly exceed therapeutic plasma concentrations. To investigate the relationship of the cardiovascular and metabolic effects of theophylline to activation of the sympathetic nervous system, i.v. aminophylline was administered to six healthy males under basal conditions. Each subject received four infusions. Mean theophylline concentrations (+/- SEM) of 4.5 +/- 0.2, 10.0 +/- 0.5, 14.0 +/- 0.5 and 20.0 +/- 1.2 micrograms/ml were achieved. Plasma epinephrine increased 262% (from 29 +/- 4 to 105 +/- 14 pg/ml, p less than 0.01) and plasma norepinephrine increased 64% (from 190 +/- 18 to 312 +/- 51 pg/ml, p less than 0.05) during the high-dose infusion. The increases in circulating catecholamines were dose-related (p less than 0.001 by analysis of variance). Dose-related increases in heart rate, systolic blood pressure, plasma glucose, free fatty acids and insulin were also observed (p less than 0.001 by analysis of variance). Although the duration of total electromechanical systole (QS2) and left ventricular ejection time adjusted for heart rate fell during the aminophylline infusions, this positive inotropic response was not influenced by dose, except possibly the high dose. Echocardiographic ejection fraction was not changed by the aminophylline infusions. We conclude that the acute cardiovascular and metabolic effects of theophylline may be mediated in part by stimulation of the sympathetic nervous system.
Ventricular and pulmonary artery volumes in patients with absent pulmonary valve. Factors affecting the natural course.
Authors: Hiraishi S , Bargeron L M , Isabel-Jones J B , Emmanouilides G C , Friedman W F , Jarmakani J M
Published: June 2011

Right and left ventricular (RV and LV) volumes were determined in 19 patients with absent pulmonary valve syndrome using Simpson's rule and area-length methods. The volume of the proximal right pulmonary artery (RPAV) was calculated at maximal and minimal size using the area-length method. Patient groups included four newborns who responded to medical management (group 1A), seven critically ill newborns who died (group 1B), four infants ages 1-10 months (group 2) and four children ages 2-8 years (group 3). The RV end-diastolic volume in groups 1B and 2 was significantly greater than that in groups 1A and 3. The RV ejection fraction in groups 1B and 2 was significantly less than that in normal patients and groups 1A and 3. Maximal RPAV correlated well with RV stroke volume and end-diastolic volume. The maximal RPAV in group 1B was significantly greater than that in groups 1A and 3. Pulmonary arterial compliance was greater than normal in all groups, and the compliance in group 1B was more than two times that in the other groups. We conclude that the increased right pulmonary artery compliance and pulmonary regurgitation in patients with absent pulmonary valve contribute to bronchial obstruction and right-heart failure and are the causes of the high morbidity and mortality in these patients. The management should be directed to the alleviation of bronchial obstruction and right-heart failure.
Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs.
Authors: Koehler R C , Chandra N , Guerci A D , Tsitlik J , Traystman R J , Rogers M C , Weisfeldt M L
Published: June 2011

Recent studies have demonstrated that for the same chest compression force during mechanical cardiopulmonary resuscitation (CPR), the carotid artery-to-jugular vein pressure gradient and carotid blood flow are increased when the phasic rise of intrathoracic pressure is enhanced by abdominal binding and simultaneous ventilation at high airway pressure with each chest compression (SCV). The objective of the present study was to assess whether cerebral blood flow is also enhanced, since it is known that fluctuations in intrathoracic pressure are transmitted to the intracranial space and affect intracranial pressure (ICP). In two series of pentobarbital-anesthetized dogs, one of two CPR techniques was initiated immediately after inducing ventricular fibrillation. Brain blood flow was measured by the radiolabeled microsphere technique immediately before cardiac arrest and at 1 and 3 minutes after commencing CPR. Evidence of adequate mixing of spheres and lack of sedimentation under these low-flow conditions was verified by correlation with brain venous outflow, comparison of the arterial concentration-time profile of spheres and a nonsedimentary marker (thallium-201 in solution), and use of multiple arterial sampling sites. During SCV CPR with abdominal binding, mean carotid artery pressure (60 +/- 3 mm Hg) was higher than that during conventional CPR (25 +/- 2 mm HG). Pulsations of ICP occurred that were in phase with chest compression and greater than jugular venous pressure. Mean ICP was higher during SCV (46 +/- 2 mm Hg) than conventional CPR (20 +/- 2 mm Hg). However, the net brain perfusion pressure gradient (carotid artery pressure - ICP) was greater with SCV (14 +/- 3 mm Hg) than with conventional CPR (5 +/- 0.4 mm Hg). Cerebral blood flow was significantly greater during SCV CPR (32 +/- 7% of prearrest cerebral flow) than during conventional CPR (3 +/- 2%). We conclude that SCV CPR combined with abdominal binding substantially improved brain perfusion by enhancing cerebral perfusion pressure in this experimental model.
Prognosis of patients with acute pulmonary edema and normal ejection fraction after acute myocardial infarction.
Authors: Warnowicz M A , Parker H , Cheitlin M D
Published: June 2011

To assess the prognostic importance of resting left ventricular function in survivors of acute myocardial infarction with pulmonary edema, we retrospectively identified 39 consecutive patients who presented with acute pulmonary edema and myocardial infarction. Sixteen patients had radionuclide ejection fractions 10 +/- 2 days postinfarction of greater than 0.45 (group A, mean 0.55 +/- 0.06), and 23 patients had ejection fractions less than or equal to 0.45 (group B, 0.32 +/- 0.06). There were no significant differences between the two groups for age or sex, but group A patients had a significantly greater incidence of first myocardial infarction predominantly inferior in location. The calculated stroke work index during the acute event was significantly greater in group A than in group B (33.4 +/- 2.4 vs 23.4 +/- 2.0) (p less than 0.05). During a follow-up of 9 +/- 3 months, mortality was not significantly different between the two groups: Four (25%) died in group A and seven (30%) died in group B. In addition, eight patients (50%) in group A were hospitalized for recurrent angina, new myocardial infarction or recurrent pulmonary edema, compared with 11 (48%) in group B (NS). Three deaths in group A were preceded by infarction of the anterior wall of the left ventricle, confirmed at autopsy, and two nonfatal infarctions were anterior by electrocardiography. Four patients in group A had coronary arteriography performed during the follow-up period because of unstable angina, and all had significant (greater than or equal to 70% stenosis) three-vessel disease and two had left main coronary artery disease. Therefore, the predischarge ejection fraction did not predict prognosis for this group of patients. Patients with acute pulmonary edema in the course of myocardial infarction form a high-risk group despite good resting left ventricular function at discharge. They have a significant incidence of recurrent myocardial infarction and death and, because they have good residual left ventricular function, are excellent candidates for surgical intervention.
Anatomic validation of left ventricular mass estimates from clinical two-dimensional echocardiography: initial results.
Authors: Reichek N , Helak J , Plappert T , Sutton M S , Weber K T
Published: June 2011

We performed a prospective anatomic validation study to determine the accuracy of left ventricular (LV) mass estimates from clinical two-dimensional echocardiographic (2-D echo) studies. In 21 subjects, antemortem 2-D echo LV mass determinations were compared with anatomic LV weight by postmortem chamber dissection. Major cardiac diagnoses included anatomic LV aneurysm in four, status post aneurysmectomy in one, transmural myocardial infarction in seven, congestive cardiomyopathy in five, rheumatic mitral disease in two, chronic severe mitral or aortic regurgitation in three, amyloid heart in two, and normal heart in three. Marked right-heart dilatation was present in 11 patients and LV thrombus in four. Regression equations derived in vitro for each 2-D echo instrument were used to correct LV mass estimates based on a short-axis, area-length method: uncorrected LV mass = 1.055 x k x 5/6 (AtLt - AcLc) + b, where At = total short-axis LV image area at the high papillary muscle level, Lc = endocardial LV length, k = an instrument-specific regression slope and b = an instrument-specific intercept. LV mass by 2-D echo correlated extremely well with actual LV weight (r = 0.93 slope = 0.85, SEE = 31 g, range 77-454 g). In contrast, M-mode echocardiographic LV mass estimates were less reliable (r = 0.86, SEE = 59 g) in these markedly distorted hearts. These 2-D echo LV mass results compare favorably with reported results from biplane angiography and M-mode echocardiography in more symmetric hearts. Thus, regression-corrected 2-D echo may be the method of choice for determining LV mass in man.
Echocardiographic tissue characterization and range-gated Doppler ultrasound for the diagnosis of pulmonary embolism.
Authors: Sagar K B , Rhyne T L , Greenfield L J
Published: June 2011

We evaluated reflection and absorption indexes of ultrasound as well as Doppler estimates of intrapulmonary blood flow for diagnosing pulmonary embolism. The pulmonary reflection coefficient (PRC), coefficient of tissue attenuation (alpha R) and range-gated blood Doppler signals were studied in 25 patients with pulmonary embolism, 19 with pneumonia, nine with atelectasis, 20 with congestive heart failure, 20 with chronic obstructive lung disease and 10 normal subjects. The PRC was significantly diminished in pulmonary embolism, pneumonia and atelectasis, but was not altered by underlying chronic obstructive lung disease or congestive heart failure. The alpha R in pulmonary embolism was 1.03 +/- 0.04 db/MHz cm, significantly lower than that for pneumonia, 1.48 +/- 0.03 db/MHz cm (p less than 0.001), but not significantly different from that for atelectasis, 0.95 +/- 0.05 db/MHz cm. Doppler signals indicating blood flow in the affected area of lung were present in only two of 25 patients with pulmonary embolism, compared with seven of nine with atelectasis and 17 of 19 with pneumonia. The combined use of PRC, alpha R and blood Doppler signals correctly diagnosed pulmonary embolism in 23 of 25 patients. Thus, ultrasound offers a reliable noninvasive method for diagnosis of pulmonary embolism.