bluuebunny/crossref_metadata_2025 huggingface dataset:
Evaluation of coronary artery anatomy in patients with tetralogy of Fallot by two-dimensional echocardiography.
Authors: Berry J M , Einzig S , Krabill K A , Bass J L
Published: June 2011

A major coronary artery crossing the right ventricular outflow tract in patients with tetralogy of Fallot interferes with a transannular patch, and preoperative detection of this artery is important. We evaluated the ability of two-dimensional echocardiography to define noninvasively the coronary artery anatomy in 37 consecutive patients (age range, 1 day to 18 years; mean age, 40.9 months). The origin and distribution of the right anterior descending and circumflex coronary arteries, as well as any anteriorly coursing vessel, were examined from parasternal views. Complete studies were obtained in 29 (78%) of the 37 patients. Coronary artery anatomy was determined to be normal by echocardiography in 20 (69%) of the 29 patients. An anterior vessel across the right ventricular outflow tract was detected in the remaining nine patients. Six patients had an anterior descending artery from the left main coronary artery (paired anterior descending arteries in three patients, a right anterior descending artery from the left main coronary artery in two patients, and a right coronary-to-pulmonary artery fistula in one patient). Three patients had no anterior descending artery from the left main coronary artery (anterior descending artery from the right main coronary artery in two patients, and anterior descending and circumflex arteries from the right main coronary artery in one patient). Angiography, surgery, or autopsy confirmed the diagnoses in all but the final patient in whom the anterior descending artery arose from the right main coronary artery as observed at surgery, but the circumflex artery was not seen. Accurate evaluation of coronary artery anatomy is possible by echocardiography in the majority of patients with tetralogy of Fallot. Noninvasive identification of a major coronary artery coursing anteriorly can influence the timing of cardiac catheterization and surgery and the need for angiography.
Transcatheter electrical ablation of right bundle branch. A method of treating macroreentrant ventricular tachycardia attributed to bundle branch reentry.
Authors: Tchou P , Jazayeri M , Denker S , Dongas J , Caceres J , Akhtar M
Published: June 2011

The present study describes the clinical and electrophysiological characteristics of sustained bundle branch reentrant ventricular tachycardia treated with electrical ablation of the right bundle branch. Seven patients presented with syncopal episodes, and six of the seven had documented episodes of ventricular tachycardia. All patients had depressed left ventricular ejection fraction with cardiomegaly. Six of the seven had dilated cardiomyopathy in the absence of significant coronary disease. Twelve-lead electrocardiograms in all seven patients during sinus rhythm were remarkably similar; six demonstrated intraventricular conduction defect resembling left bundle branch block, and one showed left anterior fascicular block. All patients showed prolonged His-to-ventricle intervals during sinus rhythm. Sustained ventricular tachycardia (with atrioventricular dissociation) because of bundle branch reentry was induced in all patients during baseline electrophysiological study. The His-to-ventricle intervals during tachycardia were similar to those seen during sinus rhythm. Electrical ablation of the right bundle branch was accomplished in each patient with delivery of two electrical shocks (170-310 J) through electrode catheters. Right bundle branch block developed on their surface electrocardiogram immediately after the ablation. Follow-up electrophysiological studies showed no inducible ventricular tachycardia. Clinical follow-up showed no recurrence of syncope or ventricular tachycardia. From the data presented, the following can be concluded. First, right bundle branch ablation is a safe and promising means of treating ventricular tachycardia because of bundle branch reentry and can obviate the need for antiarrhythmic drug therapy and its frequent undesirable side effects. Second, there are common clinical and electrophysiological characteristics that are frequently seen in patients with this tachycardia, and the recognition of these common characteristics should alert the physician to a bundle branch reentrant mechanism of ventricular tachycardia.
Clinical evaluation versus Doppler echocardiography in the quantitative assessment of valvular heart disease.
Authors: Jaffe W M , Roche A H , Coverdale H A , McAlister H F , Ormiston J A , Greene E R
Published: June 2011

We tested the hypotheses that Doppler echocardiography has a higher accuracy than clinical evaluation in the detection of significant aortic and mitral valvular heart disease and that Doppler echocardiography is highly accurate as compared with cardiac catheterization for the assessment of valvular disease severity. Thus, cardiac catheterization for the assessment of valve lesion severity may be unnecessary in selected patients. We prospectively evaluated 75 consecutive patients, ages 20-74 years (mean, 52 years), with clinically suspected valvular heart disease. Specific clinical and Doppler echocardiographic criteria were used to categorize each valve lesion as absent, insignificant, or significant. Criteria for a significant lesion at cardiac catheterization was an aortic or mitral valve area less than 1.1 or 1.5 cm2, respectively, or equal to or greater than 3+ cm2 aortic or mitral regurgitation at angiography. In all valve lesions, Doppler echocardiography had a higher overall accuracy than clinical evaluation. Increases in accuracies of 28%, 19%, 15%, and 7% occurred for mitral stenosis, aortic stenosis, aortic regurgitation, and mitral regurgitation, respectively, resulting in overall accuracies of 97%, 100%, 95%, and 96%. Clinical evaluation alone made 28 errors (37% of patients and 19% of valve lesions assessed), and 17 of these errors (23% of patients and 12% of valve lesions) would have resulted in inappropriate management. In only four (24%) of these 17 patients, the attending cardiologist would not have proceeded to assess the valve at cardiac catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma atrial natriuretic factor and cyclic GMP in mitral stenosis treated by balloon valvulotomy. Effect of atrial fibrillation.
Authors: Dussaule J C , Vahanian A , Michel P L , Soullier I , Czekalski S , Acar J , Ardaillou R
Published: June 2011

To study the relation between plasma atrial natriuretic factor (ANF) and cardiac pressures, we measured plasma ANF in 24 patients with mitral stenosis 30 minutes before and 20 minutes after balloon mitral valvulotomy. All patients were without physical signs of congestive heart failure. Normal sinus rhythm was present in 15 (group 1), whereas the other nine (group 2) had permanent atrial fibrillation. There were no significant differences between groups for basal mean pressures in right atrium (RA), left atrium (LA), and pulmonary artery (PA). Valvulotomy resulted in a fall in both groups (p less than 0.001) in LA and PA mean pressures, whereas heart rate, cardiac index, and RA and aorta (AO) pressures did not change significantly. Basal ANF was not different in either group in RA (240 +/- 43 vs. 266 +/- 35 pg/ml) or AO (441 +/- 92 vs. 643 +/- 70 pg/ml) but tended to be higher in group 2 in LA (428 +/- 88 vs. 682 +/- 84 pg/ml; p = 0.059) and PA (488 +/- 93 vs. 759 +/- 92 pg/ml; p = 0.057). Plasma ANF was the highest in PA, and about 50% ANF was extracted in the systemic circulation. After valvulotomy, plasma ANF was greater (p less than 0.05) in group 2 (372 +/- 90, 755 +/- 152, 805 +/- 134, and 707 +/- 144 pg/ml) than in group 1 (206 +/- 36, 386 +/- 47, 429 +/- 66, and 421 +/- 49 pg/ml), regardless of the site of blood collection (RA, LA, PA, and AO, respectively). PA ANF was correlated with LA pressure (p less than 0.05) in group 1 before as well as after valvulotomy, whereas there was no such correlation in group 2. Cyclic GMP (cGMP) in LA was correlated (p less than 0.01) with PA ANF in group 1, and LA cGMP (10.0 +/- 1.2 and 9.1 +/- 1.8 pmol/ml in groups 1 and 2, respectively) was higher (p less than 0.05) than PA cGMP (9.1 +/- 1.0 and 8.0 +/- 1.5 pmol/ml in groups 1 and 2, respectively) before valvulotomy, which suggests the presence of ANF receptors in the pulmonary circulation. Taken together, these results indicate that in patients in sinus rhythm with mitral stenosis, there is an increase in ANF secretion depending on LA pressure. ANF secretion is also high in patients with mitral stenosis and atrial fibrillation but does not respond appropriately to changes in LA pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia.
Authors: Davies G J , Bencivelli W , Fragasso G , Chierchia S , Crea F , Crow J , Crean P A , Pratt T , Morgan M , Maseri A
Published: June 2011

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium-99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The maximum increase in end-diastolic volume was slightly greater in painful than in painless episodes, 38 +/- 8.0% versus 28 +/- 12.4%, but no significant difference was observed in the rate of volume change or in the maximum increase of end-systolic volume (133 +/- 50% and 110 +/- 27.3%), stroke volume (-28 +/- 15% and -25 +/- 12.4%), or ejection fraction (-32 +/- 8.7% and -26 +/- 6.0%). Although the maximum end-diastolic volume achieved is greater in painful episodes, this effect cannot be separated from that of duration, and, furthermore, there was no significant difference in end-diastolic volume at the moment chest pain began. Thus, in patients with angina at rest, transient asymptomatic ST segment shifts are consistently associated with large changes in left ventricular volume, similar to those observed during painful episodes. The rate and extent of acute left ventricular dilatation do not appear to be factors directly causing anginal pain.
Evaluation of nonradioactive, colored microspheres for measurement of regional myocardial blood flow in dogs.
Authors: Hale S L , Alker K J , Kloner R A
Published: June 2011

Measurement of regional myocardial blood flow (RMBF) is crucial in experimental studies of myocardial ischemia and reperfusion in dogs. The standard measurement technique uses radioactive microspheres; however, not all institutions are able to dispose of radioactive waste and therefore cannot make use of this method. We tested a new, nonradioactive microsphere, labeled with colors instead of nuclides. Simultaneous blood flow measurements with two nuclide-labeled and two colored microspheres were performed after coronary occlusion in dogs. Both techniques show a within-method correlation of r greater than 0.98. Duplicate variability for paired RMBF values in 80 samples was 8.7 +/- 0.1% when computed with radioactive microspheres and 13.2 +/- 1.8% when computed with colored microspheres. There was a good correlation in the measurement of RMBF between the radioactive- and colored-microsphere methods (r = 0.98). The best-fitting linear regression line was expressed by the formula: Colored-microsphere RMBF = 1.11 (radioactive-microsphere RMBF)-0.02. When measured by colored microspheres, RMBF was approximately 8% higher than when computed with radioactive microspheres for blood flow values of 0-2 ml/min/g. When blood flow was increased pharmacologically to levels of 2-7.5 ml/min/g, colored microspheres yielded blood flow values 39% higher than the values computed by radioactive microspheres. We conclude that the nonradioactive, colored-microsphere method correlates with the radioactive technique, but at high flows, it yields values greater than those obtained with radioactive microspheres.
Prevention of coronary artery reocclusion and reduction in late coronary artery stenosis after thrombolytic therapy in patients with acute myocardial infarction. A randomized study of maintenance infusion of recombinant human tissue-type plasminogen activator.
Authors: Johns J A , Gold H K , Leinbach R C , Yasuda T , Gimple L W , Werner W , Finkelstein D , Newell J , Ziskind A A , Collen D
Published: June 2011

Sixty-eight patients with acute "transmural" myocardial infarction presenting within 6 hours (range, 1.3-5.8 hours) of onset of chest pain were given intravenous recombinant tissue-type plasminogen activator (rt-PA) at a dosage of 1 mg/kg during 90 minutes. Coronary angiography at 90 minutes revealed a patent infarct-related coronary artery in 52 patients (76%). These patients were randomized either to treatment by continuous infusion of heparin alone (27 patients) or to treatment by heparin and a maintenance infusion of rt-PA at a dosage of 0.8 mg/kg during 4 hours (25 patients). Coronary angiography was repeated 60 minutes after the start of the maintenance infusion and again after 8-14 days. Acute symptomatic reocclusion of the infarct-related artery occurred during the 1-hour observation period in five (19%) patients treated with heparin alone but in none of the patients treated with rt-PA (p = 0.05). The measured residual stenosis of the patent infarct-related coronary artery was similar in the heparin-treated and the rt-PA-treated groups at 90 minutes infusion: 66 +/- 14% versus 68 +/- 13% diameter stenosis, respectively (mean +/- SD) and 1.1 +/- 1.1 mm2 versus 0.82 +/- 0.7 mm2 area (p = 0.35). At 8-14 days after infusion, residual stenosis was unchanged in the heparin-treated group, but it improved to 55 +/- 17% (p = 0.001) and 1.6 +/- 1.2 mm2 (p = 0.003) in the rt-PA-treated group. At 90 minutes of infusion, residual intraluminal thrombus was observed in 29 of the 52 patients (56%) with a comparably measured distribution in the two groups (p = 0.43). At 150 minutes, however, the extent of intraluminal thrombus was significantly reduced in the rt-PA-treated group as compared with the heparin-treated group (p = 0.03). In-hospital ischemic events (symptomatic reocclusion, unstable angina, or cardiovascular death) occurred in 12 patients of the heparin-treated group but only in three patients of the rt-PA-treated group (p = 0.03). Fibrinogen levels decreased to 65 +/- 21% of baseline at 90 minutes of rt-PA infusion. During the rt-PA maintenance infusion, fibrinogen fell slightly from 63 +/- 26 to 57 +/- 28% (p = 0.18). This study shows that after successful reperfusion with 1 mg/kg rt-PA during 90 minutes, a maintenance infusion of 0.8 mg/kg rt-PA during 4 hours prevents acute symptomatic coronary artery reocclusion, and it reduces the frequency of ischemic events and the severity of residual coronary artery stenosis at hospital discharge.
New catheter technique for recording left free-wall accessory atrioventricular pathway activation. Identification of pathway fiber orientation.
Authors: Jackman W M , Friday K J , Yeung-Lai-Wah J A , Fitzgerald D M , Beck B , Bowman A J , Stelzer P , Harrison L , Lazzara R
Published: June 2011

The ability to record accessory atrioventricular (AV) pathway activation consistently may be uniquely beneficial in improving pathway localization, identifying anatomic relations, and providing insight into unusual conduction properties. For the purpose of recording left AV accessory pathway activation, an electrode catheter was specially designed for use in the coronary sinus. The orthogonal catheter has three sets of four electrodes spaced evenly around the circumference. Electrograms were recorded at low gain (less than 1 cm/mV) between adjacent electrodes on the same set (interelectrode distance, 1.5 mm, center to center). This provides a recording dipole perpendicular to the atrioventricular groove to enhance recording of accessory pathway activation while minimizing overlapping atrial or ventricular potentials. The orthogonal electrode catheter was used in the electrophysiological study of 48 consecutive patients with 59 left AV accessory pathways. The catheter could be advanced along the coronary sinus beyond the site of earliest retrograde atrial activation in 49 of the 59 accessory pathways. Activation potentials were recorded from 45 of the 49 (92%) accessory pathways accessible to the catheter (5 of 5 anterior, 8 of 8 anterolateral, 15 of 16 lateral, 5 of 5 posterolateral, 5 of 5 posterior, and 7 of 10 posteroseptal). Accessory pathway potentials were validated by dissociating them from both atrial and ventricular activation by programmed-stimulation techniques. During surgery, accessory pathway potentials were identified from orthogonal catheter electrodes in the coronary sinus in 14 of 16 accessory pathways (12 patients). Epicardial mapping confirmed the location of the accessory pathway, and direct pressure over the orthogonal catheter electrode that recorded the accessory pathway potential resulted in transient conduction block in nine of the 14 accessory pathways. Orthogonal electrode maps of the coronary sinus identified an oblique course in 39 of 45 recorded accessory pathways. Thirty-two of 38 left free-wall accessory pathways were oriented with atrial insertion 4-30 mm (median, 14 mm) proximal (posterior) to the ventricular insertion. In the remaining six free-wall accessory pathways, the lateral excursion could not be determined because either only the atrial end of the accessory pathway was recorded or activation of multiple pathway fibers prevented tracking of individual strands. The seven recorded posteroseptal pathways exhibited accessory pathway potentials throughout an 8-18-mm (median, 10 mm) length of the proximal coronary sinus, but fiber orientation was difficult to determine.(ABSTRACT TRUNCATED AT 400 WORDS)
Potentiation of the hemodynamic effects of acutely administered nitroglycerin by methionine.
Authors: Levy W S , Katz R J , Ruffalo R L , Leiboff R H , Wasserman A G
Published: June 2011

It is believed that nitroglycerin causes vasodilatation by interacting with sulfhydryl groups present in vascular smooth muscle. This study was performed to assess whether methionine, an amino acid capable of increasing sulfhydryl availability, would potentiate the hemodynamic effects of nitroglycerin. Nitroglycerin was initially infused in incremental doses from 1 to 50 micrograms/min in all patients to determine the dose required to reduce mean arterial pressure by 10% and pulmonary capillary wedge pressure by 30%. After a washout period, 10 patients received 5 g methionine i.v. and five patients received an equal volume of 5% dextrose in water (control). Nitroglycerin dose titration was then repeated. Methionine alone induced no hemodynamic effects, but after methionine infusion, there was a significant reduction in the nitroglycerin infusion rate required to reach each hemodynamic endpoint (p less than 0.01). In the control group, there was no significant change in responsiveness to nitroglycerin between infusions. Thus, methionine potentiates the hemodynamic effects of acutely administered intravenous nitroglycerin.
Combined influence of ventricular loading and relaxation on the transmitral flow velocity profile in dogs measured by Doppler echocardiography.
Authors: Choong C Y , Abascal V M , Thomas J D , Guerrero J L , McGlew S , Weyman A E
Published: June 2011

The relation of the Doppler transmitral flow velocity profile to left ventricular loading conditions and diastolic properties remains poorly described. We studied seven adult mongrel dogs with an open-chest right heart bypass model in which left atrial pressure, representing preload, was varied by controlling blood flow into the pulmonary artery and left ventricular systolic pressure, representing afterload, was controlled independently by pumping blood into or from the femoral arteries. Heart rate was kept constant by crushing the sinus node and pacing the right atrium. Mitral inflow velocity profiles were measured by pulsed-wave Doppler echocardiography at multiple left atrial and left ventricular systolic pressures. In individual dogs, the peak E-wave velocity increased linearly with increasing left atrial V-wave pressure at constant left ventricular systolic pressure and decreased with increasing left ventricular systolic pressure at constant left atrial pressure. Stepwise multiple linear regression analysis of data pooled from all experimental stages in all dogs identified left atrial V-wave pressure, the time constant of relaxation (TL), and left ventricular systolic pressure, in order of decreasing significance, as predictors of the peak E-wave velocity (n = 82, multiple r = 0.87, p less than 0.0001). Multivariate analysis with the same three factors in individual dogs yielded higher r values (mean r = 0.89; range, 0.85-0.97), suggesting the presence of important interdog differences that were not accounted for by these three factors alone. When the values of codeterminant hemodynamic factors were kept within narrower limits, correlations between peak E-wave velocity and left atrial V-wave pressure (n = 35, multiple r = 0.83, p less than 0.0001), TL (n = 76, multiple r = -0.54, p less than 0.0001) and left ventricular systolic pressure (n = 20, multiple r = -0.59, p less than 0.005) improved substantially. In the pooled data, the relation of the peak E-wave velocity to left atrial V-wave pressure was shifted downward by an increase in TL (reduced relaxation rate), and the relation of the peak E-wave velocity to TL was shifted upward by an increase in left atrial V-wave pressure. Multivariate analysis also selected left atrial V-wave pressure and TL as the two most significant correlates of the velocity-time integral and deceleration rate of the E wave.(ABSTRACT TRUNCATED AT 400 WORDS)
Mechanisms of depressed conduction from long-term amiodarone therapy in canine myocardium.
Authors: Levine J H , Moore E N , Kadish A H , Weisman H F , Balke C W , Hanich R F , Spear J F
Published: June 2011

Amiodarone therapy leads to a significant impairment in myocardial conduction, yet it causes only a modest decrease in the maximum rate of depolarization of the action potential (dV/dT). To determine whether the decrease in dV/dT solely accounts for the impaired myocardial conduction or whether passive membrane properties may also be involved, we studied 21 ventricular epicardial tissues from 14 beagles; six dogs received long-term treatment (3-6 weeks) of amiodarone orally, and the remaining dogs served as controls. Amiodarone therapy was associated with a decrease in conduction velocity (0.41 +/- 0.15 vs. 0.56 +/- 0.05 m/sec; p less than 0.01). There was a trend toward a decrease in dV/dT and a significant decrease in the space constant (0.69 +/- 0.27 vs. 1.05 +/- 0.25 mm; p = 0.01), of which the latter correlated closely with the decrease in conduction velocity measured in the amiodarone-treated tissues (r = 0.85, p less than 0.05). These data indicate that the decrease in myocardial conduction velocity caused by amiodarone is primarily due to effects on overall resistance to passive current flow rather than effects on the inward sodium current.
Competition between lidocaine and one of its metabolites, glycylxylidide, for cardiac sodium channels.
Authors: Bennett P B , Woosley R L , Hondeghem L M
Published: June 2011

The modulated receptor hypothesis states that sodium channels have a specific receptor for antiarrhythmic drugs. Therefore, two agents that block sodium channels by binding to this receptor are expected to compete for occupancy. Glycylxylidide (GX) is a deethylated metabolite of lidocaine that accumulates in patients on lidocaine therapy. In single, voltage-clamped cardiocytes, GX, like lidocaine, blocked cardiac sodium channels in a use-dependent manner. However, its kinetics of recovery from block were markedly different from lidocaine: at potentials between -80 and -100 mV, GX-blocked channels recovered faster and more completely than lidocaine-blocked channels but recovered more slowly at more negative potentials (-120 to -140 mV). If lidocaine and GX compete for a common receptor, then there are conditions in which addition of a "faster" drug to a "slower" drug will produce less block than the slower drug alone. At potentials between -120 and -140 mV, addition of GX (slower drug) to lidocaine always increased the level of block, but addition of lidocaine to GX decreased the block in four of nine experiments and did not increase it in three of nine experiments. Conversely, at potentials between -80 and -100 mV, addition of lidocaine (slower drug) to GX always increased block, whereas addition of GX to lidocaine reduced the level of block in five of 16 experiments and did not increase it in seven of 16 experiments. Thus, upon addition of more blocker, the sodium current increased in 36% of cases or did not decline in 76% of cases. These results can be explained by the modulated receptor hypothesis with two drugs competing for the same receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
Sensitization of reperfused myocardium to subsequent coronary flow reductions. An extension of the concept of myocardial stunning.
Authors: Schröder E S , Sirna S J , Kieso R A , Kerber R E
Published: June 2011

The purpose of the present study was to evaluate the response of briefly ischemic and reperfused myocardium to subsequent moderate reductions of coronary arterial flow. In mongrel dogs, a carotid to left anterior descending coronary shunt was constricted to produce moderate coronary flow reductions (50-60% of control) and to thereby reduce regional systolic thickening (measured by echocardiography or sonomicrometry). First, we demonstrated an abnormal response of reperfused myocardium to subsequent flow reductions. We performed two episodes of coronary shunt stenosis, with an intervening 5-minute complete coronary shunt occlusion followed by 30 minutes of reperfusion. In a control group, the same two shunt stenoses were done, but no intervening shunt occlusion was performed. In the control dogs, repeated coronary shunt stenosis that produced equivalent perfusion reductions also produced equivalent declines in regional wall thickening. In contrast, in the intervention group (animals undergoing the intervening occlusion-reperfusion sequence between two shunt stenoses), the second coronary shunt stenosis produced an exaggerated decline in regional systolic thickening, even though the decline in myocardial perfusion was similar to the first stenosis. Second, we sought to demonstrate the mechanism of the exaggerated decline of the reperfused myocardium to subsequent moderate flow reductions. Again, two groups of animals were studied. Each group underwent two episodes of coronary shunt stenosis with an intervening sequence of 5 minutes of complete shunt occlusion and 30 minutes of reperfusion. In addition, one of the groups received an infusion of the oxygen free radical scavengers superoxide dismutase and catalase during the occlusion-reperfusion sequence. In the superoxide dismutase and catalase-treated animals, the decline in regional systolic function during the postreperfusion shunt stenosis was similar to the preocclusion stenosis. Thus, oxygen free radical scavengers blocked the exaggerated contraction decline in response to the postreperfusion flow reduction. We conclude that briefly ischemic and reperfused myocardium displays an exaggerated response to subsequent coronary arterial flow reductions and that this response is a subtle manifestation of postischemic ventricular dyskinesis, or "stunning." The mechanism is probably oxygen free radical toxicity.
Random exercise stress test in diagnosing effort angina.
Authors: Suyama A , Sunagawa K , Hayashida K , Sugimachi M , Todaka K , Nose Y , Nakamura M
Published: June 2011

To improve the performance of exercise stress testing in the diagnosis of effort angina while minimizing risks of serious complications, we evaluated an impulse response of ST changes, which is a transient ST response resulting from a hypothetical, strenuous-impulselike exercise, without actually imposing the strenuous load. To obtain the impulse response, subjects walked intermittently according to a computer-generated random binary sequence on a treadmill for 20 minutes (with a constant speed of 1.7 mph and a slope of 10%). We used Fourier transform for beat-to-beat changes in ST level and the binary sequence of exercise. We then determined the transfer function by taking the ratio of Fourier transformed ST level to exercise over the frequency range of 0.5 through 5.0 cycles/min. Converting the transfer function to the time domain yielded the impulse response of ST change. The subjects consisted of 49 patients (60 +/- 9 years) with effort angina, 13 patients with atypical chest pain (56 +/- 9 years), and 30 healthy, male volunteers (23 +/- 7 years). In 82 subjects (89%), the ST impulse response showed an initial depression followed by a smooth, gradual restoration toward the preexercise ST level (type I response). The average duration of the initial depression was 8 +/- 3 seconds in the healthy volunteers, whereas it was significantly prolonged to 23 +/- 14 seconds in effort angina (p less than 0.05). The depression in patients with atypical chest pain was not significantly different from that in the healthy volunteers.(ABSTRACT TRUNCATED AT 250 WORDS)
Quantitative analysis of regional systolic function with left ventricular aneurysm.
Authors: Nicolosi A C , Spotnitz H M
Published: June 2011

Left ventricular aneurysm (LVA) remains a poorly understood entity, often resulting in congestive failure that is not consistently improved by standard resection with linear closure. Although other surgical approaches have been proposed, current methods to assess their effect on left ventricular function are not adequate. The purpose of the present study was to quantitatively define regional systolic function in patients with LVA and to assess acute changes in regional function after standard repair. Seven patients underwent resection of an anteroapical LVA. Intraoperative two-dimensional echocardiography was performed off cardiopulmonary bypass immediately before and after resection. In all patients, short-axis views at the papillary muscle (apex) level showed anteroseptal paradox and distorted geometry, whereas at the mitral valve (base), symmetric wall motion and geometry were preserved. Videotaped echo images were divided into octants by a floating axis fitted to internal landmarks. Myocardial area and midwall perimeter were obtained for each octant, and wall thickness was calculated at end diastole (ED), isovolumetric systole (IS), and end systole (ES). Wall thickening (delta t) for each segment was calculated as the percent increase in thickness from ED and averaged for all seven patients. At the apex level before resection, isovolumetric thinning occurred in the aneurysm as well as bordering segments, with delta t ranging from -17 +/- 5% (+/- SEM) in the anteroseptal segment to 12 +/- 6% posterolaterally (p less than 0.05). The isovolumetric bulge was followed by late-systolic thickening, however, with delta t ranging from 13 +/- 7% to 27 +/- 8% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Randomized, double-blinded multicenter study. Comparison of intracoronary single-chain urokinase-type plasminogen activator, pro-urokinase (GE-0943), and intracoronary urokinase in patients with acute myocardial infarction.
Authors: Kambara H , Kawai C , Kajiwara N , Niitani H , Sasayama S , Kanmatsuse K , Kodama K , Sato H , Nobuyoshi M , Nakashima M
Published: June 2011

Coronary recanalization rates and changes in the coagulation and fibrinolysis system were evaluated in a randomized fashion in patients with acute myocardial infarction after intracoronary administration of single-chain urokinase-type plasminogen activator (pro-urokinase: GE-0943) or urokinase. Three groups of patients were studied: group H (n = 50), 6,000 units pro-urokinase i.c.; group L (n = 44), 3,000 units pro-urokinase i.c.; and group U (n = 54), 960,000 IU urokinase i.c. Coronary recanalization rates determined angiographically after 45 minutes of intracoronary infusion averaged 90% in group H, 59% in group L, and 61% in group U. The differences were statistically significant between group H and the latter two groups. Pro-urokinase affected plasma proteins of the fibrinolytic system to a lesser degree than urokinase. Bleeding complications were present in one patient in group L, in none in group H, and in five in group U. Thus, intracoronary administration of 6,000 units pro-urokinase is more effective in coronary thrombolysis and causes less systemic fibrinogenolysis than intracoronary administration of urokinase.
Postextrasystolic potentiation worsens fast filling of the hypertrophied left ventricle in aortic stenosis and hypertrophic cardiomyopathy.
Authors: Paulus W J , Sys S U , Nellens P , Heyndrickx G R , Andries E
Published: June 2011

Impaired left ventricular (LV) filling in aortic stenosis (AS) and in hypertrophic cardiomyopathy (HCM) is caused by slow LV pressure decay, which could be explained by depressed inactivation of hypertrophied myocardium. Postextrasystolic potentiation (PESP), which increases activator calcium, could lead to further deterioration of LV relaxation. The influence of PESP on LV filling dynamics was, therefore, investigated in normal controls and in patients with LV hypertrophy caused by AS or by HCM. LV hemodynamics and LV hemodynamic relaxation indexes were determined during normal sinus rhythm (NSR) and after PESP. LV pressures were recorded by micromanometer tip catheters (controls, n = 10; AS, n = 17; HCM, n = 11). Simultaneous mitral flow Doppler echocardiograms were obtained in patients with LV hypertrophy (AS, n = 8, HCM, n = 5). Despite significant increases of LV dP/dtmax after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (TPB) derived from exponential curve fits with nonzero asymptote pressure remained unaltered after PESP in normal controls, rose from 62 +/- 17 to 74 +/- 21 msec (p less than 0.02) in patients with AS, and rose from 74 +/- 18 to 84 +/- 19 msec (p less than 0.02) in patients with HCM. Early diastolic LV pressure decay was measured by phi (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dtmin to LV minimum diastolic pressure). After PESP, phi remained unaltered in normal controls but decreased in AS from 42.8 +/- 19.1 degrees to 24.0 +/- 28.8 degrees (p less than 0.001) and in HCM from 39.7 +/- 15.4 degrees to 26.9 +/- 15.7 degrees (p less than 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 +/- 48 to 205 +/- 86 msec (p less than 0.001) and in HCM from 168 +/- 40 to 208 +/- 53 msec (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
Hemodynamic and hormonal adaptations to beta-adrenoceptor blockade. A 24-hour study of acebutolol, atenolol, pindolol, and propranolol in hypertensive patients.
Authors: van den Meiracker A H , Man in 't Veld A J , van Eck H J , Boomsma F , Schalekamp M A
Published: June 2011

Comparison of the hemodynamic and hormonal effects of beta-adrenoceptor antagonists with different ancillary properties may help to clarify the antihypertensive mechanism of these drugs. Under strict basal conditions, the effects of acebutolol (400 mg b.i.d.), atenolol (100 mg b.i.d.), pindolol (10 mg b.i.d.), and propranolol (80 mg t.i.d.), were studied for the first 24 hours in 40 hypertensive patients. With pindolol, mean arterial pressure was reduced (p less than 0.05) 1 hour after administration, whereas the cardiac index and the systemic vascular resistance index did not change. With the other three drugs, the fall in mean arterial pressure was delayed 2-3 hours. With these drugs, the fall in mean arterial pressure was preceded by a rise in the resistance index, which compensated for the initial fall in cardiac index. With each drug, the decrements in mean arterial pressure were associated with parallel decrements in the resistance index, and percent changes in mean arterial pressure and the resistance index were always significantly (p less than 0.001) correlated. At the end of the 24-hour period, the four drugs shared an equal antihypertensive effect, which varied 14-17%. This was associated with a return of the cardiac index toward control values by acebutolol, atenolol, and propranolol treatment and a moderately increased cardiac index above pretreatment values (13%, p less than 0.01) with pindolol. The secondary rise in the cardiac index was inversely correlated (p less than 0.001) with the fall in mean arterial pressure with all four drugs. Plasma renin was maximally suppressed 2 hours after treatment, thus before any change in mean arterial pressure had occurred with acebutolol, atenolol, and propranolol. Pretreatment values of active renin and the reduction of mean arterial pressure 24 hours after administration were not correlated in any of the four groups. Despite the "vasodilator" action of the four drugs, plasma norepinephrine did not rise. Our data show that the main hemodynamic change that occurs at the time blood pressure falls after beta-adrenoceptor antagonism is vasodilation. Neither autoregulation of blood flow nor renin suppression can explain this vasodilator action. The absence of an increase in norepinephrine, despite vasodilation, suggests that beta-adrenoceptor antagonism interferes with sympathetic vasoconstrictor nerve activity. This effect may explain the vasodilator and antihypertensive potential of beta-adrenoceptor antagonists.
Inaccuracy of mitral pressure half-time immediately after percutaneous mitral valvotomy. Dependence on transmitral gradient and left atrial and ventricular compliance.
Authors: Thomas J D , Wilkins G T , Choong C Y , Abascal V M , Palacios I F , Block P C , Weyman A E
Published: June 2011

Mitral pressure half-time (T1/2) is widely used as an independent measure of mitral valve area in patients undergoing percutaneous mitral valvotomy. However, fluid dynamics theory predicts T1/2 to be strongly dependent on chamber compliance and the peak transmitral gradient, which are variables that change dramatically with valvotomy. These theoretical predictions were tested in an in vitro model of the left heart where valve area, chamber compliance, and initial gradient were independently adjusted. Measured T1/2 was observed to vary inversely with orifice area and directly with net chamber compliance and the square root of the initial pressure gradient. Theoretical predictions of T1/2 agreed with observed values with r = 0.998. To test this theory in vivo, the hemodynamic tracings of 18 patients undergoing mitral valvotomy were reviewed. Predictions were made for T1/2 assuming dependence only on valve area; these showed some correlations before valvotomy (r = 0.48-0.64, p less than 0.05) but none after valvotomy (r = 0.05-0.28, p = NS). Predictions for T1/2 based on the theoretical derivation (and thus including compliance and pressure in their calculation) were much better: before valvotomy, r = 0.93-0.96, p less than 0.0001; after valvotomy, r = 0.52-0.66, p less than 0.05. These data indicate that T1/2 is not an independent inverse measure of mitral valve area but is also directly proportional to net chamber compliance and the square root of the initial transmitral gradient. These other factors render T1/2 an unreliable measure of mitral valve area in the setting of acute mitral valvotomy.
Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion.
Authors: Takayama M , Norris R M , Brown M A , Armiger L C , Rivers J T , White H D
Published: June 2011

Postsystolic shortening and thickening of ischemic and postischemic myocardium are well-recognized phenomena, but their significance is controversial. To discover whether postsystolic shortening and thickening might represent an active process and to establish their place as possible predictors of functional recovery during and after recovery from ischemia, we examined correlations in severely ischemic dyskinetic myocardial segments in 14 open-chest anesthetized dogs (90 minutes' ischemia, n = 9; 180 minutes' ischemia, n = 5) between the magnitudes of postsystolic shortening and thickening during ischemia and either the magnitudes of systolic shortening and thickening in the same segments before coronary occlusion or the magnitudes of shortening and thickening at 30-60 minutes and at 2-3 weeks after reperfusion. We found positive correlations between preocclusion shortening and postsystolic shortening (r = 0.44, n = 33 myocardial segments; p less than 0.02) and between preocclusion thickening and postsystolic thickening (r = 0.73, n = 13 segments; p less than 0.01), both measured at 5 minutes after onset of ischemia. Strong correlations were found also between postsystolic shortening and thickening measured immediately before reperfusion and systolic shortening and thickening measured after recovery at 2-3 weeks (r = 0.73, n = 28; p less than 0.001 for shortening; r = 0.79, n = 12; p less than 0.01 for thickening). Significant but less-exact correlations were found between postsystolic shortening and thickening measured immediately before reperfusion and early recovery of shortening and thickening at 30-60 minutes after reperfusion (during the "stunned myocardium" period). Postsystolic shortening and thickening persisted early after reperfusion in dogs that had had 90 minutes of ischemia, and this predicted further significant return of function at 2-3 weeks. However, dogs that had had 180 minutes of ischemia did not have postsystolic shortening or thickening during early recovery and showed no further return of function at 2-3 weeks. The magnitudes of postsystolic shortening and thickening immediately before reperfusion were better predictors of late return of function than the histological appearance of the ischemic segments at 2-3 weeks or the magnitude of their blood flow during ischemia (15 +/- 3 micron microspheres). From correlations made immediately before reperfusion with those at functional recovery after reperfusion, we conclude that postsystolic shortening and thickening of dyskinetic myocardial segments are markers of their potential for recovery.(ABSTRACT TRUNCATED AT 400 WORDS)
Long-term serial changes in left ventricular function and reversal of ventricular dilatation after valve replacement for chronic aortic regurgitation.
Authors: Bonow R O , Dodd J T , Maron B J , O'Gara P T , White G G , McIntosh C L , Clark R E , Epstein S E
Published: June 2011

In most patients with aortic regurgitation, valve replacement results in reduction in left ventricular dilatation and an increase in ejection fraction. To determine the relation between serial changes in ventricular dilatation and changes in ejection fraction, we studied 61 patients with chronic severe aortic regurgitation by echocardiography and radionuclide angiography before, 6-8 months after, and 3-7 years after aortic valve replacement. Between preoperative and early postoperative studies, left ventricular end-diastolic dimension decreased (from 75 +/- 6 to 56 +/- 9 mm, p less than 0.001), peak systolic wall stress decreased (from 247 +/- 50 to 163 +/- 42 dynes x 10(3)/cm2), and ejection fraction increased (from 43 +/- 9% to 51 +/- 16%, p less than 0.001). Between early and late postoperative studies, diastolic dimension and peak systolic wall stress did not change, but ejection fraction increased further (to 56 +/- 19%, p less than 0.001). The increase in ejection fraction correlated with magnitude of reduction in diastolic dimension between preoperative and early postoperative studies (r = 0.63), between early and late postoperative studies (r = 0.54), and between preoperative and late postoperative studies (r = 0.69). Late increases in ejection fraction usually represented the continuation of an initial increase occurring early after operation. Thus, short-term and long-term improvement in left ventricular systolic function after operation is related significantly to the early reduction in left ventricular dilatation arising from correction of left ventricular volume overload. Moreover, late improvement in ejection fraction occurs commonly in patients with an early increase in ejection fraction after valve replacement but is unlikely to occur in patients with no change in ejection fraction during the first 6 months after operation.
Improvement in symptoms and left ventricular performance after balloon aortic valvuloplasty in patients with aortic stenosis and depressed left ventricular ejection fraction.
Authors: Safian R D , Warren S E , Berman A D , Diver D J , McKay L L , Come P C , Grossman W , McKay R G
Published: June 2011

The application of balloon aortic valvuloplasty to elderly patients with severe aortic stenosis and a low ventricular ejection fraction is undefined. Balloon aortic valvuloplasty was performed in a subset of 28 patients with low left ventricular ejection fraction (37 +/- 11%), severe aortic stenosis, and a mean age of 79 +/- 5 years. After valvuloplasty, significant increases were seen in aortic valve area (from 0.5 +/- 0.1 to 0.9 +/- 0.2 cm2), aortic systolic pressure (from 120 +/- 12 to 135 +/- 22 mm Hg), and cardiac output (from 4.2 +/- 1.1 to 4.8 +/- 1.6 l/min) (p less than 0.01), and significant decreases were seen in transaortic pressure gradient (from 69 +/- 25 to 35 +/- 15 mm Hg) and pulmonary capillary wedge pressure (from 24 +/- 9 to 20 +/- 7 mm Hg) (p less than 0.01). All patients had symptomatically improved at the time of discharge. Serial radionuclide ventriculography showed an increase in left ventricular ejection fraction from 37 +/- 11% before valvuloplasty to 44 +/- 14% within 48 hours after dilatation and to 49 +/- 13% at 3 months after dilatation. However, there was substantial heterogeneity of response. Thirteen patients (group A) showed progressive increases in left ventricular ejection fraction (from 34 +/- 11% to 49 +/- 15% to 58 +/- 11%, p less than 0.0001), whereas 15 patients (group B) showed no significant change in ejection fraction (from 41 +/- 10% to 40 +/- 13% to 41 +/- 10%, p = NS) over 3 months. There was no difference between these groups with respect to age, extent of coronary artery disease, history of myocardial infarction, and aortic valve area before and after valvuloplasty. However, peak systolic wall stress and left ventricular dimensions were higher in group B compared with group A. In conclusion, balloon aortic valvuloplasty may result in symptomatic improvement in patients with aortic stenosis and depressed left ventricular ejection fraction; some patients develop progressive increases in ejection fraction, whereas others fail to show improvement.