bluuebunny/crossref_metadata_2025 huggingface dataset:
Alteration of left ventricular endocardial function by intracavitary high-power ultrasound interacts with volume, inotropic state, and alpha 1-adrenergic stimulation.
Authors: De Hert S G , Gillebert T C , Brutsaert D L
Published: June 2012

BACKGROUND

High-power intracavitary ultrasound abbreviates left ventricular (LV) ejection duration, thereby decreasing mechanical LV performance, presumably by selective impairment of endocardial endothelial function.

METHODS AND RESULTS

Effects of ultrasound were evaluated in the ejecting LV of anesthetized, open-chest dogs under different conditions of LV volume and contractile state and after mild selective alpha 1-adrenergic stimulation. LV pressures, left atrial pressures, and regional segment lengths were measured in anterior and posterior midwall. A cylindrical ultrasound probe (0.9 MHz, 25 W) mounted on a catheter was inserted into the LV cavity through the apex and was activated for 4 minutes in each condition. In protocol A (n = 7), LV volume was altered with caval vein occlusion and intravenous dextran infusion. The ultrasound probe was activated at low (4.1 +/- 0.9 mm Hg), mid (10.6 +/- 1.5 mm Hg), and high (17.9 +/- 1.8 mm Hg) LV end-diastolic pressure (EDP). Effects of ultrasound were less pronounced at higher EDP. For example, the time interval from end-diastole to peak (-)dP/dt decreased by 7.5 +/- 2.3% at low, 4.4 +/- 2.2% at mid, and 1.9 +/- 1.6% at high LVEDP (p < 0.001). In protocol B (n = 7), LV inotropic state was altered by slow intravenous infusion of low-dose calcium. The ultrasound probe was activated before and after calcium. Effects of ultrasound were less pronounced after calcium. Time from end-diastole to peak (-)dP/dt decreased by 8.4 +/- 3.1% at baseline and by 3.5 +/- 2.1% after calcium (p < 0.001). In protocol C (n = 7), activation of the ultrasound probe was performed at baseline and after mild selective alpha 1-adrenergic stimulation (propranolol plus phenylephrine). Effects of ultrasound were similar at baseline and after propranolol but increased after phenylephrine. Time from end-diastole to peak (-)dP/dt decreased by 5.2 +/- 2.4% at baseline, by 5.3 +/- 1.9% after propranolol, and by 8.9 +/- 3.2% after phenylephrine (p < 0.05).

CONCLUSIONS

Effects of intracavitary ultrasound, which are presumably mediated through modulation of endocardial endothelial function, were more important at low volume, lower calcium, and under mild selective alpha 1-adrenergic stimulation.
Development of the pharyngeal arch system related to the pulmonary and bronchial vessels in the avian embryo. With a concept on systemic-pulmonary collateral artery formation.
Authors: DeRuiter M C , Gittenberger-de Groot A C , Poelmann R E , VanIperen L , Mentink M M
Published: June 2012

BACKGROUND

The literature is ambiguous as to the question of the developmental background of systemic-pulmonary collateral arteries. These are found in combination with various congenital heart malformations such as pulmonary atresia. From a clinical point of view, it is of interest to know whether we are dealing with the persistence of transient embryological vessels such as ventral segmental arteries or parts of pharyngeal arch arteries or with the prenatal or postnatal recruitment of the bronchial vasculature that normally supplies the lung. This study of the embryology of the extrapulmonary and intrapulmonary vasculature aims at a better understanding of the variations in origin, course, branching pattern, and histology of collateral arteries.

METHODS AND RESULTS

Serial sections of quail embryos ranging between stage HH11 and stage HH28 were incubated with a monoclonal antibody (alpha MB1) against endothelial cells and their precursors. Additional series of chick embryos were injected with india ink to study the lumenized vascular patterns. A splanchnic plexus consisting of endothelial cells and precursors is present around the foregut before the lung buds develop. This plexus expands and gives rise to the pharyngeal arch arteries, the ventral pharyngeal veins, the pulmonary vessels, and the bronchial vessels, including the intrapulmonary vessel network. During two subsequent periods, the splanchnic plexus is transiently connected to the systemic arteries and veins. The bronchial arteries and veins develop in the second period from these transient vessels. The expansion and extension of the splanchnic plexus to many organs during the formation of the bronchial vessels explains the varying course and branching pattern of the bronchial vasculature.

CONCLUSIONS

These results show that we are not dealing with two or more individual vascular systems that contribute to the developing vessels of the lungs but with one vascular plexus that normally gives rise to the pulmonary and bronchial vasculature but has the potential to give rise to other systemic-pulmonary connections.
Analysis of coronary angioplasty practice in the United States with an insurance-claims data base.
Authors: Topol E J , Ellis S G , Cosgrove D M , Bates E R , Muller D W , Schork N J , Schork M A , Loop F D
Published: June 2012

BACKGROUND

Coronary angioplasty is frequently performed in the United States, with more than 300,000 procedures in 1990. Despite the high rate of use of the procedure, there have been few studies addressing practice patterns.

METHODS AND RESULTS

From a private insurance claims data base of 5.4 million individuals, a total of 2,101 patients who underwent coronary angioplasty during 1988-1989 were identified. Using their 4,578 hospital admission records and 87,578 outpatient claim records, with an average follow-up of 332 +/- 182 days, we compared patients' outcomes and charges according to whether they had an exercise stress test before the procedure, by sex, by region of the country, and by whether the angioplasty was performed in an institution with a training program. Only 29% of the study cohort had exercise testing before angioplasty; patients in the West (p = 0.001), those undergoing multivessel angioplasty (p = 0.00001), and those whose procedures were performed at sites with training programs (p = 0.04) were more likely to have a screening test, whereas women (p = 0.008) and those with a recent myocardial infarction (p = 0.00001) were less likely to have a screening test. The average length of stay for patients without myocardial infarction as a primary diagnosis was 5.6 days, with a total hospital charge of $15,027. In follow-up, 15.1% had coronary artery bypass surgery and 15% had at least one additional angioplasty procedure; the average follow-up charges were $4,879. Charges varied according to sex, region of the country, and academic status of the angioplasty institution. Certain outcomes showed variation by region of the country and academic status of the angioplasty institution.

CONCLUSIONS

The relative lack of an objective definition of myocardial ischemia and the marked variability of use of procedures according to geographic region suggest the need for further implementation of established guidelines.
Dobutamine stress echocardiography for assessment of perioperative cardiac risk in patients undergoing major vascular surgery.
Authors: Poldermans D , Fioretti P M , Forster T , Thomson I R , Boersma E , el-Said E M , du Bois N A , Roelandt J R , van Urk H
Published: June 2012

BACKGROUND

The purpose of this study was to determine the predictive value of dobutamine stress echocardiography for perioperative cardiac events in patients scheduled for elective major noncardiac vascular surgery.

METHODS AND RESULTS

Patients (n = 136; mean age, 68 years) unable to exercise underwent a dobutamine stress test before surgery (incremental dobutamine infusion [10-40 micrograms.kg-1.min-1] continued with atropine [0.25-1 mg i.v.] if necessary to achieve 85% of the age-predicted maximal heart rate without symptoms or signs of ischemia). The clinical risk profile was evaluated by Detsky's modification of Goldman's risk factor analysis. Echocardiographic images were evaluated by two observers blinded to the clinical data of the patients, and results of the test were not used for clinical decision making. Technically adequate images were obtained in 134 of 136 patients, one major complication occurred (ventricular fibrillation), and three tests were discontinued prematurely because of side effects. Finally, data from 131 patients were analyzed with univariate and multivariate methods. The dobutamine stress test was positive (new or worsened wall motion abnormality) in 35 of 131 patients. In the postoperative period, five patients died of myocardial infarction, nine patients had unstable angina, and one patient developed pulmonary edema. All patients with cardiac complications (15 patients) had a positive dobutamine stress test. No cardiac events occurred in patients with negative tests. Five patients with a technically inadequate or prematurely stopped test were operated on without complications. By multivariate analysis (logistic regression), only age > 70 years and new wall motion abnormalities during the dobutamine test were significant predictors of perioperative cardiac events.

CONCLUSIONS

Dobutamine stress echocardiography is a feasible, safe, and useful method for identifying patients at high or low risk of perioperative cardiac events. The test yields additional information, beyond that provided by clinical variables, in patients who are scheduled for major noncardiac vascular surgery.
Action potential alternans and irregular dynamics in quinidine-intoxicated ventricular muscle cells. Implications for ventricular proarrhythmia.
Authors: Karagueuzian H S , Khan S S , Hong K , Kobayashi Y , Denton T , Mandel W J , Diamond G A
Published: June 2012

BACKGROUND

Cardiac cells display rate-dependent beat-to-beat variations in action-potential duration (APD), action potential amplitude (APA), and excitability during periodic stimulation. We hypothesized that quinidine causes a marked increase in the variability of APD, APA, and excitability of ventricular cells isolated from quinidine-toxic, arrhythmic ventricles.

METHODS AND RESULTS

Action potentials were recorded from right ventricular endocardial tissues (2 x 1 cm, < 2 mm thick) isolated from dogs in which ventricular tachycardia and ventricular fibrillation (VT/VF) were induced with intravenous quinidine (80-100 mg/kg) over a 5-hour period in vivo (n = 7). As the basic cycle length (BCL) of stimulation was progressively shortened, rate-dependent variations in APD and APA occurred. The initial dynamic change was alternans of APD and APA that could be either in or out of phase between two cells. The magnitude of alternans was a function of the BCL and the strength of the stimulation current. At critically short BCLs, irregular APD and APA behavior emerged in the quinidine-intoxicated cells. In control cells (n = 16) isolated from three nontreated dogs, APD and APA remained constant at all BCLs tested (2,000-300 msec). Quinidine increased the slope of the APD restitution curve compared with control. The observed quinidine APD restitution curve was fitted with a biexponential equation, and computer simulation using the fitted restitution curve reproduced the aperiodic APD seen in the quinidine toxic cells during periodic stimulation. Thus, the observed irregular APD behavior was predictable from the restitution curve.

CONCLUSIONS

Quinidine toxicity increases the temporal and spatial variability of APD and APA in the ventricle that may promote the initiation of reentrant VT/VF in vivo. The slope of the APD restitution curve provides a method to quantitate inhomogeneities in repolarization time and could be a useful marker for proarrhythmia.
Decreased proportion of type I myofibers in skeletal muscle of dogs with chronic heart failure.
Authors: Sabbah H N , Hansen-Smith F , Sharov V G , Kono T , Lesch M , Gengo P J , Steffen R P , Levine T B , Goldstein S
Published: June 2012

BACKGROUND

Whether biochemical and histological abnormalities of skeletal muscle (SM) develop in patients with chronic heart failure (HF) remains controversial. In the present study, dogs with chronic HF were used to examine potential alterations of SM fiber type, fiber size, number of capillaries per fiber (C/F), beta-adrenergic receptor density (Bmax), and fiber ultrastructural integrity.

METHODS AND RESULTS

HF was produced in 17 dogs by sequential intracoronary microembolizations. Biopsies of the lateral head of the triceps muscle were used in all studies. Type I and type II fibers were differentiated by myofibrillar ATPase (pH 9.4 or 4.2). Bmax was assessed by radioligand binding and SM ultrastructure by transmission electron microscopy. Comparisons were made with biopsies obtained from nine control dogs. The percentage of SM type I fibers was reduced in HF dogs compared with control dogs (19 +/- 2% versus 32 +/- 5%) (p < 0.001), whereas the percentage of SM type II fibers was increased (81 +/- 2% versus 68 +/- 5%) (p < 0.001). The change in fiber type composition was not associated with a preferential atrophy or hypertrophy of either fiber type. There was no difference in SM Bmax (198.9 +/- 14.3 versus 186.8 +/- 17.3 fmol/mg protein) or in C/F (5.37 +/- 0.26 versus 5.84 +/- 0.21) between HF dogs and control dogs. No ultrastructural abnormalities were present in SM fibers of HF dogs.

CONCLUSIONS

In dogs with HF, there is a decrease in the relative composition of the slow-twitch type I SM fibers and an increase in fast-twitch type II fibers. The shift in fiber type composition is not associated with preferential atrophy of either fiber type or with a reduction in C/F, beta-adrenergic receptor density, or structural abnormalities of the myofibers.
Lipid lowering and plaque regression. New insights into prevention of plaque disruption and clinical events in coronary disease.
Authors: Brown B G , Zhao X Q , Sacco D E , Albers J J
Published: June 2012

The consensus of evidence from angiographic trials demonstrates both coronary artery and clinical benefits from lowering of lipids by a variety of regimens. The findings of reduced arterial disease progression and increased regression have been convincing but, at best, modest in their magnitude. For example, among those treated intensively in FATS, the mean improvement in proximal stenosis severity per patient was < 1% stenosis, and only 12% of all lesions showed convincing regression. In view of these modest arterial benefits, the associated reductions in cardiovascular events have been surprisingly great. For example, coronary events were reduced 75% in FATS; this was entirely a result of a 93% reduction in the likelihood that a mildly or moderately diseased arterial segment would experience substantial progression to a severe lesion at the time of a clinical event. We believe that the magnitude of the clinical benefit is best explained in terms of this observation, according to the following lines of reasoning. Clinical events most commonly spring from lesions that are initially of mild or moderate severity and then abruptly undergo a disruptive transformation to a severe culprit lesion. The process of plaque fissuring, leading to plaque disruption and thrombosis, triggers most clinical coronary events. Fissuring is predicted by a large accumulation of core lipid in the plaque and by a high density of lipid-laden macrophages in its thinned fibrous cap. Lesions with these characteristics constitute only 10-20% of the overall lesion population but account for 80-90% of the acute clinical events. In the experimental setting, normalization of an atherogenic lipid profile substantially decreases the number of lipid-laden intimal macrophages (foam cells) and depletes cholesterol from the core lipid pool. In the clinical setting, intensive lipid lowering virtually halts the progression of mild and moderate lesions to clinical events. Thus, the reduction in clinical events observed in these trials appears to be best explained by the relation of the lipid and foam cell content of the plaque to its likelihood of fissuring and by the effects of lipid-lowering therapy on these "high-risk" features of plaque morphology. The composite of data presented here supports the hypothesis that lipid-lowering therapy selectively depletes (regresses) that relatively small but dangerous subgroup of fatty lesions containing a large lipid core and dense clusters of intimal macrophages. By doing so, these lesions are effectively stabilized and clinical event rate is accordingly decreased.
Myocardial infarct size can be estimated from serial plasma myoglobin measurements within 4 hours of reperfusion.
Authors: Yamashita T , Abe S , Arima S , Nomoto K , Miyata M , Maruyama I , Toda H , Okino H , Atsuchi Y , Tahara M
Published: June 2012

BACKGROUND

An early estimation of infarct size is useful for the appropriate early treatment of patients with acute myocardial infarction. We evaluated how early and how accurately infarct size could be estimated from serial plasma myoglobin (Mb) measurements in patients with successful reperfusion.

METHODS AND RESULTS

We measured plasma Mb and creatine kinase (CK) in 35 patients in whom reperfusion therapy was successfully performed. Blood samples were collected at 15-minute intervals for 2 hours after reperfusion, at 30-minute intervals for the subsequent 2 hours, and at 3-6-hour intervals until 52 hours after reperfusion. Plasma Mb was measured by a newly developed turbidimetric latex agglutination assay. Total Mb and CK release (sigma Mb, sigma CK) were calculated with a one-compartment model. The mean chord motion in the most hypokinetic 50% of the infarct-related artery territory was calculated from follow-up ventriculograms as an index of the severity of regional hypokinesis. There were significant correlations between sigma Mb and sigma CK (r = 0.89), between log sigma Mb and the severity of regional hypokinesis (r = -0.85), and between log sigma CK and the severity of regional hypokinesis (r = -0.74). The time required for the cumulative Mb release curves to reach a plateau was 64 +/- 28 minutes. An additional 53 +/- 14 minutes was required to calculate the disappearance rate constant of Mb, and 15 minutes was necessary for the assay. Therefore, the total time required for sigma Mb to be available was 132 +/- 40 minutes, significantly shorter than the time required for sigma CK, 24.3 +/- 9.1 hours (p < 0.001). The infarct size could be estimated from the sigma Mb in 34 of 35 patients within 4 hours of reperfusion.

CONCLUSIONS

Infarct size can be estimated accurately 4 hours after reperfusion by calculating the sigma Mb in patients with successful reperfusion.
Angiopeptin inhibits intimal hyperplasia after angioplasty in porcine coronary arteries.
Authors: Santoian E D , Schneider J E , Gravanis M B , Foegh M , Tarazona N , Cipolla G D , King S B
Published: June 2012

BACKGROUND

Restenosis is mediated by uncontrolled neointimal growth at the site of coronary angioplasty. Angiopeptin is an octapeptide analogue of somatostatin that has been shown to decrease the experimental intimal hyperplasia associated with vascular injury in rats and rabbits. The study purpose was to determine if angiopeptin inhibits the development of intimal hyperplasia in normolipemic swine coronary arteries after overstretch-balloon injury.

METHODS AND RESULTS

Overstretch-balloon injury was performed in normolipemic swine coronary arteries using a 3.5-mm angioplasty balloon. Treated animals received angiopeptin (50 micrograms/kg) 1 hour before and at the time of balloon injury. Angiopeptin was administered at 100 (micrograms/kg)/day SQ in two divided doses for 14 days. Animals were killed at 14 and 28 days (2 weeks after cessation of angiopeptin) after balloon injury. Treatment animals were compared with control animals receiving balloon injury alone. Angiopeptin significantly limited the experimental intimal hyperplasia estimated by the maximal intimal thickness and residual lumen (lumen area/lumen area+intimal area) compared with controls.

CONCLUSIONS

Angiopeptin inhibits the development of intimal hyperplasia in swine coronary arteries after balloon injury. The beneficial effect was detectable 2 weeks after cessation of angiopeptin therapy.
Regional wall motion analysis predicts survival and functional outcome after subendocardial resection in patients with prior anterior myocardial infarction.
Authors: Nath S , Haines D E , Kron I L , Barber M J , DiMarco J P
Published: June 2012

BACKGROUND

Subendocardial resection is an established surgical technique for the treatment of ventricular tachycardia associated with prior myocardial infarction. Preoperative factors predictive of survival and functional outcome after surgery have not been completely characterized. We hypothesized that a quantitative assessment of regional wall motion would be a sensitive predictor of both survival and functional outcome after subendocardial resection. This was retrospectively tested in a group of 80 patients with prior anterior myocardial infarction who had undergone subendocardial resection for sustained ventricular tachycardia at out institution.

METHODS AND RESULTS

Centerline chord motion analysis was used to derive a wall motion score from the preoperative contrast right anterior oblique ventriculogram. Multivariate analysis revealed wall motion score to be a significant independent predictor of both long-term survival (p < 0.01) and New York Heart Association (NYHA) functional class I or II status at 6 months (p < 0.01) and at 24 months (p < 0.001) after surgery. Patients with a wall motion score of > 16%, compared with patients with a wall motion score of < or = 16%, had a better 5-year actuarial survival (74% versus 45%, p = 0.02) and were more likely to be NYHA class I or II at 6 months (87% versus 58%, p < 0.01) and at 24 months (82% versus 34%, p < 0.0001) after subendocardial resection.

CONCLUSIONS

A wall motion score derived from centerline chord motion analysis is a sensitive predictor of survival and functional outcome after subendocardial resection. Patients with a wall motion score of > 16% have an excellent prognosis after subendocardial resection. In contrast, patients with a wall motion score of < or = 16% have a poorer outcome and should be considered candidates only if other forms of therapy have failed or are unavailable.
Demonstration of functional border zone with myocardial contrast echocardiography in human hearts. Simultaneous analysis of myocardial perfusion and wall motion abnormalities.
Authors: Nanto S , Masuyama T , Lim Y J , Hori M , Kodama K , Kamada T
Published: June 2012

BACKGROUND

Although the presence of a functional border zone (FBZ), defined as the nonischemic but asynergic myocardium adjacent to the ischemic area, has been demonstrated in animal hearts, it is not known whether this zone exists in humans.

METHODS AND RESULTS

Myocardial contrast echocardiography (MCE) was performed before and during balloon inflation in the area of coronary stenosis by injecting contrast medium through the guiding catheter in 13 patients with effort angina who underwent successful coronary angioplasty. The area showing MCE defect during balloon inflation was determined with reference to the preangioplasty MCE and was regarded as an ischemic area. The size of the FBZ was assessed by measuring the length of the endocardium that showed asynergy in the echo-enhanced (nonischemic) area. The FBZ measured was 13 +/- 4 mm in the short-axis view (n = 5) and 16 +/- 9 mm in the long-axis view (n = 8).

CONCLUSIONS

Nonischemic contractile dysfunction exists even in human hearts. The presence of an FBZ may limit the use of wall motion analysis in assessing the risk or ischemic area in patients with myocardial infarction. MCE appears to be a unique technique for assessing the risk or ischemic area.
Bamiphylline improves exercise-induced myocardial ischemia through a novel mechanism of action.
Authors: Gaspardone A , Crea F , Iamele M , Tomai F , Versaci F , Pellegrino A , Chiariello L , Gioffré P A
Published: June 2012

BACKGROUND

In patients with stable angina pectoris aminophylline, a nonselective antagonist of adenosine receptors, markedly improves exercise capacity. To establish the role played by A1 adenosine receptors in the anti-ischemic action of aminophylline, the effects of bamiphylline, a selective A1 antagonist, on exercise-induced ischemia were investigated in patients with stable angina pectoris.

METHODS AND RESULTS

In a single-blind, placebo-controlled, randomized cross-over trial in 18 patients, oral administration of 1200 mg bamiphylline increased both the time to 1-mm ST segment depression (from 524 +/- 177 to 664 +/- 192 seconds, P < .01) and the rate-pressure product at 1-mm ST segment depression (from 159 +/- 31 to 190 +/- 34 beats per minute per mm Hg/10(2) (P < .001). End-diastolic and end-systolic left ventricular volumes, left ventricular ejection fraction, and systolic septal and posterior wall thickening investigated by two-dimensional echocardiography in 12 of the 18 patients were not affected by oral administration of bamiphylline (124 +/- 22 versus 125 +/- 20 mL, P = NS; 49 +/- 12 versus 50 +/- 13 mL, P = NS; 60 +/- 8% versus 58 +/- 7%, P = NS; 35 +/- 6% versus 36 +/- 7%, P = NS; 32 +/- 6% versus 33 +/- 6%, P = NS, respectively). In 7 of the 18 patients, the intravenous infusion of bamiphylline (5 mg/kg in 15 minutes) during cardiac catheterization did not produce any significant change of heart rate (76 +/- 10 versus 75 +/- 13 beats per minute, P = NS), mean right atrial pressure (3.8 +/- 1.7 versus 3.7 +/- 1.7 mm Hg, P = NS), mean aortic pressure (102 +/- 12 versus 99 +/- 10 mm Hg, P = NS), or left ventricular end-diastolic pressure (14 +/- 3 versus 14 +/- 4 mm Hg, P = NS) compared with baseline. Furthermore, after intravenous infusion of bamiphylline, the diameter of seven proximal and distal normal segments and of seven stenotic segments were similar to those measured at baseline (3.1 +/- 0.5 versus 3.1 +/- 0.5 mm, P = NS; 1.6 +/- 0.2 versus 1.7 +/- 0.2 mm, P = NS; 1.6 +/- 0.5 versus 1.6 +/- 0.5 mm, P = NS, respectively).

CONCLUSIONS

In patients with stable angina pectoris, oral administration of bamiphylline improves exercise capacity. Its anti-ischemic action does not appear to be mediated by systemic hemodynamic effects or by stenosis dilation. Therefore, the improvement of myocardial ischemia caused by bamiphylline is probably due to redistribution of coronary blood flow toward the underperfused subendocardium. This novel anti-ischemic action would appear to be mediated by antagonism of A1 receptors.
A simplified, single-lead unipolar transvenous cardioversion-defibrillation system.
Authors: Bardy G H , Johnson G , Poole J E , Dolack G L , Kudenchuk P J , Kelso D , Mitchell R , Mehra R , Hofer B
Published: June 2012

BACKGROUND

Transvenous implantable cardioverter-defibrillators provide significant advantages in the treatment of patients with life-threatening ventricular arrhythmias. However, present technology requires considerable electrophysiology expertise, multiple incisions, and long operative times for successful implementation.

METHODS AND RESULTS

In this study, we present a prototype of a new, easy-to-insert unipolar transvenous defibrillation system that has the reliability of epicardial defibrillation but the ease of pacemaker insertion. This system incorporates a single anodal right ventricular defibrillation electrode using a 65% tilt biphasic pulse delivered to a 108-cm2 surface area pulse generator titanium alloy shell as an active cathode placed in a left infraclavicular pocket. Testing of this system was performed before implantation of a standard nonthoracotomy-transvenous defibrillation system in 40 consecutive patients with a history of ventricular tachycardia or fibrillation. The simplified unipolar single-lead system resulted in a defibrillation threshold of 9.3 +/- 6.0 J with 37 of 40 patients (93%) having a defibrillation threshold of less than 20 J. Moreover, the unipolar defibrillation system was efficiently used requiring only 3.4 +/- 0.8 ventricular fibrillation inductions to measure the defibrillation threshold and 100 +/- 28 minutes to implement.

CONCLUSIONS

This new unipolar transvenous defibrillation system is as simple to insert as a pacemaker, requires few ventricular fibrillation inductions, demands less technical expertise, and provides defibrillation at energy levels comparable to that reported with epicardial lead systems. It should substantially reduce the morbidity, time, and cost of defibrillator implantation.
Echocardiographic assessment of mitral valve size in obstructive hypertrophic cardiomyopathy. Anatomic validation from mitral valve specimen.
Authors: Klues H G , Proschan M A , Dollar A L , Spirito P , Roberts W C , Maron B J
Published: June 2012

BACKGROUND

In patients with hypertrophic cardiomyopathy, obstruction to left ventricular outflow is produced by systolic anterior motion of the mitral valve. In many of these patients, the mitral leaflets are elongated and increased in overall size. Mitral valve size may be responsible, in part, for the presence and magnitude of the outflow gradient and the pattern of systolic anterior motion of the leaflets. It may also influence the effectiveness of ventricular septal myotomy-myectomy in relieving subaortic obstruction. Therefore, the present study was undertaken to determine whether mitral valve dimensions could be assessed in quantitative terms from the echocardiogram in patients with hypertrophic cardiomyopathy.

METHODS AND RESULTS

A group of 37 patients with hypertrophic cardiomyopathy was selected for this study by virtue of having a high-quality transthoracic or intraoperative echocardiogram suitable for certain quantitative measurements from stop-frame images as well as a morphologically intact mitral valve specimen (removed during surgery). Seven measurements of mitral valve dimensions were obtained from the two-dimensional and M-mode echocardiograms. A univariate regression analysis identified the mitral valve opening area as the best single predictor of actual mitral leaflet area measured from the specimen (r2 = .75; r = .87). The linear relation between mitral valve opening area as assessed by two-dimensional echocardiography and actual mitral leaflet area measured from the mitral valve specimen accounted for approximately 75% of the variability in mitral leaflet area. With such statistical models, it was possible to reliably identify from the echocardiogram enlarged mitral valves (> or = 12.0 cm2) in 16 of 19 patients (84%) and normal-sized valves in 15 of 18 patients (83%).

CONCLUSIONS

In a selected group of patients with obstructive hypertrophic cardiomyopathy, a model derived from a regression analysis of quantitative echocardiographic measurements permitted (with good precision) estimation of actual mitral leaflet area and consequently overall mitral valve size and the discrimination of enlarged from normal-sized mitral valves.
Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion.
Authors: Laster S B , Shelton T J , Barzilai B , Goldstein J A
Published: June 2012

BACKGROUND

Patients with acute ischemic right ventricular dysfunction often develop hemodynamic compromise, yet most manifest spontaneous early clinical improvement and later recovery of global right ventricular performance. This study was designed to delineate the determinants of right ventricular performance following chronic right coronary artery occlusion.

METHODS AND RESULTS

Thrombotic right coronary artery occlusion was induced in 16 closed-chest dogs. Acute occlusion depressed right ventricular free wall motion (motion score, 1.0 +/- 0.0 to 3.4 +/- 0.1*) and global performance (right ventricular fractional area change, 29.2 +/- 1.8% to 2.3 +/- 1.9%*). There was right ventricular dilatation and reversed septal curvature, with elevated and equalized diastolic filling pressures. At 5 days, despite persistent severe right ventricular free wall dysfunction (motion score, 3.4 +/- 0.1 to 2.7 +/- 0.1*), global right ventricular performance improved (fractional area change, 2.3 +/- 1.9% to 17.0 +/- 3.8%*), in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall end-diastolic thickness. At 7 weeks, collateral flow had restored right ventricular free wall perfusion to baseline values. The increased right ventricular free wall thickness had resolved, right ventricular free wall motion was improved (2.7 +/- 0.1 to 1.6 +/- 0.1*), and global right ventricular performance had recovered further (17.0 +/- 3.8 to 20.9 +/- 0.9). Right ventricular dilatation was reduced, septal curvature normalized, and there was resolution of equalized filling pressures. Histopathological analysis demonstrated minimal right ventricular infarction.

CONCLUSIONS

Acute right coronary artery occlusion results in right ventricular free wall dyskinesis and depressed global right ventricular performance. Global right ventricular function improves early, in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall diastolic thickness. Collateral restoration of perfusion facilitates late recovery of right ventricular free wall function (*P < .05).
Pacing-induced dilated cardiomyopathy increases left-to-right ventricular systolic interaction.
Authors: Farrar D J , Woodard J C , Chow E
Published: June 2012

BACKGROUND

The right ventricle (RV) receives part of its systolic pumping force from the left ventricle through systolic ventricular interaction. The purpose of this study was to determine the effects of dilated cardiomyopathy on left ventricular to right ventricular (LV-to-RV) systolic interaction.

METHODS AND RESULTS

Studies were performed in six normal pigs and in six pigs in which dilated cardiomyopathy resulting in congestive heart failure (CHF) was produced with rapid ventricular pacing at 230 beats per minute for 1 week. In all pigs, we rapidly withdrew blood from the LV apex into a prosthetic ventricle in a single beat, which reduced LV systolic pressure without changing RV or LV end-diastolic pressure, and the resultant instantaneous changes in RV systolic pressure and pulmonary artery flow were determined. The LV-to-RV mean systolic interaction gain was calculated as the change from a normal beat to the instantaneous unloaded beat in mean RV systolic pressure divided by the change in mean LV systolic pressure. Mean systolic pressure gain was approximately 2 1/2 times greater (P < .05) in the CHF animals (0.103 +/- 0.018 mm Hg/mm Hg) than in the normal pigs (0.04- +/- 0.011 mm Hg/mm Hg).

CONCLUSIONS

These data demonstrate that left-to-right ventricular systolic interaction is significantly greater in dilated cardiomyopathy compared with the normal heart, indicating that the contribution of the left ventricle to RV systolic pressure generation has increased. This is consistent with decreased elastance of the interventricular septum resulting in increased coupling between the ventricles.
Peripheral bypass-induced pulmonary and coronary vascular injury. Association with increased levels of tumor necrosis factor.
Authors: Dauber I M , Parsons P E , Welsh C H , Giclas P C , Whitman G J , Wheeler G S , Horwitz L D , Weil J V
Published: June 2012

BACKGROUND

Although cardiopulmonary bypass is associated with systemic complement activation and neutrophil sequestration, it is unclear whether bypass-induced vascular injury is localized and dependent on organ ischemia. We hypothesized that other factors perhaps related to placement of a bypass circuit or to blood perfusion of a pump-oxygenator system may produce vascular injury caused by systemically circulating mediators. In dogs, we determined whether application of a systemic venoarterial bypass circuit with pump-oxygenator perfusion but without pulmonary or cardiac flow diversion (peripheral bypass) leads to vascular injury. Since several features of the postperfusion syndrome after bypass resemble sequelae of endotoxin exposure, we also measured circulating endotoxin and tumor necrosis factor levels.

METHODS AND RESULTS

Anesthetized dogs underwent 2 hours of exposure to a pump-oxygenator with peripheral venoarterial bypass. We used a double indicator measurement of pulmonary and coronary vascular permeability (protein leak index [PLI]) as indexes of vascular injury. Compared with controls (n = 7), the pulmonary PLI of dogs undergoing bypass (n = 11) increased more than threefold (18.8 +/- 2.3 vs 63.3 +/- 7.6 x 10(-4) min-1; P < .05) and the coronary PLI increased more than twofold (P < .05). The rate of disappearance of intravascular radiolabeled protein increased threefold after bypass (disappearance t1/2, 241 +/- 35 vs 84 +/- 15 minutes, control vs bypass; P < .05), suggesting a generalized increase in vascular permeability. Circulating endotoxin was detectable in blood samples from 8 of 8 bypass animals (range, 0.24 to 4.56 ng/mL) compared with 2 of 5 controls (P < .05). Tumor necrosis factor levels increased significantly with bypass (6.7 +/- 3.8 vs 146.7 +/- 33.6 U/mL, baseline vs bypass; P < .05) and were only slightly and nonsignificantly increased in controls (7.0 +/- 4.4 vs 18.2 +/- 5.9 U/mL; P = NS). Peak tumor necrosis factor but not peak endotoxin levels correlated with pulmonary and with coronary protein leak. As expected, circulating complement (CH50) levels decreased significantly during bypass, reflecting systemic complement activation. However, the levels correlated poorly with the severity of vascular injury.

CONCLUSIONS

We conclude that peripheral pump-oxygenator bypass causes coronary and pulmonary vascular injury that is independent of blood flow diversion and is associated with the appearance of circulating levels of endotoxin and tumor necrosis factor, which may play a role in bypass-induced vascular injury.
Diagnosis of intramural coronary artery in transposition of the great arteries using two-dimensional echocardiography.
Authors: Pasquini L , Parness I A , Colan S D , Wernovsky G , Mayer J E , Sanders S P
Published: June 2012

BACKGROUND

An intramural coronary is an uncommon but potentially significant risk factor for transfer of the coronary arteries as part of the arterial switch operation for transposition of the great arteries. Preoperative diagnosis is advantageous because it helps prevent accidental injury to the intramural coronary artery during transection of the aortic root and excision of the coronary artery ostium from the aorta. Therefore, we investigated the reliability of two-dimensional echocardiography for detecting an intramural coronary artery in infants with d-transposition of the great arteries.

METHODS AND RESULTS

All infants with d-transposition of the great arteries who underwent echocardiography and primary surgical repair at this institution between January 1987 and June 1992 were identified by search of the cardiology data base. From this group, all patients diagnosed with an intramural coronary artery were identified by review of the echocardiographic, surgical, and autopsy reports. Among 435 infants with transposition, 29 infants were diagnosed as having an intramural coronary artery. In 27 cases, the diagnosis was confirmed at surgery or autopsy, and there were two false-positive echocardiographic diagnoses (specificity, 99.5%). Twenty of the 27 patients with an intramural coronary artery were correctly diagnosed prospectively by echocardiography (sensitivity, 75%), including 17 of 23 patients with an intramural left coronary artery or left anterior descending coronary artery and 3 of 4 patients with an intramural right coronary artery. Two primary diagnostic criteria were identified: a major coronary artery arising from the contralateral septal sinus, near the usually intercoronary commissure, and a course for this vessel within the posterior aortic wall between the great arteries, creating a "double-border" appearance. Retrospective review using these criteria identified 26 of the 27 intramural arteries with no false-positive diagnoses.

CONCLUSIONS

We conclude that coronary echocardiography is a very promising technique for detecting an intramural coronary artery in transposition of the great arteries. Careful prospective application of the identified diagnostic criteria should greatly improve the diagnostic accuracy.
Validation of the proximal flow convergence method. Calculation of orifice area in patients with mitral stenosis.
Authors: Rodriguez L , Thomas J D , Monterroso V , Weyman A E , Harrigan P , Mueller L N , Levine R A
Published: June 2012

BACKGROUND

It has been proposed recently that measuring the flow convergence region proximal to an orifice by Doppler flow mapping can provide a means of calculating regurgitant flow rate. Although verified in experimental models, this approach is difficult to validate clinically because there is no ideal gold standard for regurgitant flows in patients. However, this method also can be used to derive cardiac output or flow rate proximal to stenotic orifices and therefore to calculate their areas by the continuity equation (area = flow rate/velocity). Applying this method in mitral stenosis would provide a unique way of validating the underlying concept because the predicted areas could be compared with those measured directly by planimetry.

METHODS AND RESULTS

We studied 40 patients with mitral stenosis using imaging and Doppler echocardiography. Doppler color flow recordings of mitral inflow were obtained from the apex, and the radius of the proximal flow convergence region was measured at its peak diastolic value from the orifice to the first color alias along the axis of flow. Flow rate was calculated assuming uniform radial flow convergence toward the orifice, modified by a factor that accounted for the inflow funnel angle formed by the mitral leaflets. Mitral valve area was then calculated as peak flow rate divided by peak velocity by continuous-wave Doppler. The calculated areas agreed well with those from three comparative techniques over a range of 0.5 to 2.2 cm2: 1) cross-sectional area by planimetry (y = 1.08x-0.13, r = .91, SEE = 0.21 cm2); 2) area derived from the Doppler pressure half-time (y = 1.02x-0.14, r = .89, SEE = 0.24 cm2); and 3) area calculated by the Gorlin equation in the 26 patients who underwent catheterization (y = 0.89x + 0.08, r = .86, SEE = 0.24 cm2). Agreement with planimetry was similar for 22 patients with mitral regurgitation and 18 without it (P > .6), as well as for 6 in atrial fibrillation (P > .2).

CONCLUSIONS

These results validate the proximal flow convergence concept in the clinical setting and also demonstrate that it can be extended to orifice area calculation using the continuity equation.
Tone-dependent coronary arterial-venous pressure differences at the cessation of venous outflow during long diastoles.
Authors: Satoh S , Klocke F J , Canty J M
Published: June 2012

BACKGROUND

The origin and magnitude of the back pressure opposing diastolic coronary inflow remain controversial. The arterial pressure at which coronary inflow stops during a prolonged diastole, ie, "zero-flow pressure," is higher than coronary venous pressure. However, because of capacitive discharge as distending pressure falls, flow at the microcirculatory level exceeds inflow, and coronary outflow ceases later than inflow. If coronary arterial pressure continues to exceed venous pressure at the point of venous flow cessation, zero-flow pressure cannot be an artifact of capacitive discharge.

METHODS AND RESULTS

Coronary inflow and outflow, arterial pressure, and right atrial pressure have been measured during long diastoles in closed-chest dogs chronically instrumented with volumetric flow probes on the great cardiac vein or coronary sinus as well as the circumflex artery. Although venous outflow continued for 1 to 4 seconds after arterial inflow ceased, coronary artery pressure at the point of venous flow cessation (Pfv = 0) always exceeded right atrial pressure (13 +/- 1.3 mm Hg [SEM] vs 6 +/- 0.7 mm Hg, P < .001). When vasomotor tone was augmented using vasopressin, the diastolic pressure-flow relation shifted to the right, with Pfv = 0 increasing to 21 +/- 2.4 mm Hg despite an unchanged right atrial pressure (6 +/- 0.5 mm Hg).

CONCLUSIONS

Transcoronary pressure differences persist when venous outflow stops and are larger when vasomotor tone is augmented. Measurements of zero-flow pressure that exceed venous pressure cannot be considered an artifact of continuing capacitive discharge after the cessation of arterial inflow. Diastolic coronary back pressure exceeds right atrial pressure and is tone dependent.
Combination treatment with captopril and the thyroid hormone analogue 3,5-diiodothyropropionic acid. A new approach to improving left ventricular performance in heart failure.
Authors: Pennock G D , Raya T E , Bahl J J , Goldman S , Morkin E
Published: June 2012

BACKGROUND

An agent that improves left ventricular (LV) performance by non-cAMP-mediated mechanisms would be valuable in the treatment of chronic heart failure. We have shown earlier that the thyroid hormone analogue 3,5-diiodothyropropionic acid (DITPA) binds to nuclear receptors, alters transcription of T3-responsive genes, and increases +dP/dtmax in hypothyroid rats with substantially less effect on heart rate and metabolism than thyroid hormone, which makes it a selective cardiotonic agent.

METHODS AND RESULTS

To determine whether DITPA might be useful in treating heart failure, we compared chronic treatment with normal saline, captopril (2 g/L), or the combination of DITPA (375 micrograms/100 g) and captopril (2 g/L) in Sprague-Dawley rats beginning 3 weeks after coronary artery ligation. Both DITPA/captopril and captopril treatment decreased LV end-diastolic pressure compared with controls (21 +/- 2 and 26 +/- 2 mm Hg, respectively, vs 34 +/- 3 mm Hg, P < .05 for each). The addition of DITPA to captopril produced a 36% increase in resting cardiac index (P < .05) and shifted the cardiac function curve upward and to the left, indicative of enhanced myocardial performance. Also, DITPA/captopril compared with captopril treatment or control produced an increase in the rate of LV relaxation, as manifested by a decrease in tau, the time constant of LV pressure decline (17.5 +/- 1.0 vs 22.2 +/- 1.7 milliseconds, P < .05) and a larger absolute value for -dP/dtmax (-4561 +/- 361 vs -3346 +/- 232 mm Hg/s, P < .05). These changes occurred without changes in heart rate, LV mass, LV systolic pressure, or peripheral resistance relative to captopril treatment (P > .05).

CONCLUSIONS

The combination of DITPA and captopril improved cardiac output, increased -dP/dtmax, and increased the rate of LV relaxation to a greater extent than captopril treatment in the rat postinfarction model of heart failure. Use of a cardiotonic analogue of thyroid hormone represents a new approach to improving LV performance and may be a useful adjunct to afterload reduction for the treatment of heart failure.