bluuebunny/crossref_metadata_2025 huggingface dataset:
Coronary vasodilator reserve in ischemic myocardium of the exercising dog.
Authors: Laxson D D , Dai X Z , Homans D C , Bache R J
Published: June 2012

BACKGROUND

Previous work has reported that coronary vasodilator reserve may persist in myocardium rendered ischemic by hypoperfusion. This study investigated the presence and extent of residual coronary vasomotor tone in myocardial regions made acutely ischemic by a flow-limiting coronary stenosis during exercise.

METHODS AND RESULTS

Studies were done in chronically instrumented dogs undergoing treadmill exercise in the presence of a coronary stenosis that decreased distal left circumflex coronary artery perfusion pressure to approximately 40 mm Hg. Measurements of myocardial blood flow were made with radioactive microspheres during exercise (6.5 km/hr, 6% grade) before and during intracoronary infusion of the potent coronary vasodilator adenosine (40 micrograms/kg/min). Distal coronary perfusion pressure was held equal before and during intracoronary adenosine infusion (43 +/- 5 versus 42 +/- 5 mm Hg) by adjusting the hydraulic coronary occluder. During exercise in the presence of a coronary stenosis, myocardial blood flow (milliliter per minute per gram) was significantly reduced in all layers of the ischemic posterior region compared with the nonischemic anterior region. During intracoronary adenosine infusion, with no change in coronary perfusion pressure, myocardial blood flow was significantly increased compared with preadenosine flows for both the subendocardial layer flow (1.03 +/- 0.74 versus 0.66 +/- 0.50; p less than 0.05) and mean transmural flow (1.54 +/- 0.59 versus 1.16 +/- 0.36; p less than 0.05). In the presence of a coronary stenosis, regional myocardial segment shortening in the ischemic region during exercise fell significantly to 49 +/- 8% of shortening in the absence of a coronary stenosis but improved modestly during adenosine infusion (65 +/- 7 versus 49 +/- 8%; p less than 0.05).

CONCLUSIONS

These results indicate that adenosine-responsive coronary vasodilator reserve persists during exercise-induced myocardial ischemia and suggest that residual microvascular vasoconstrictor tone may affect the extent of myocardial hypoperfusion occurring consequent to a flow-limiting coronary stenosis.
Influence of the Coanda effect on color Doppler jet area and color encoding. In vitro studies using color Doppler flow mapping.
Authors: Chao K , Moises V A , Shandas R , Elkadi T , Sahn D J , Weintraub R
Published: June 2012

We studied surface adherence and its effects on color Doppler jet areas and color encoding in an in vitro model with a noncompliant receiving chamber into which a steady flow jet was directed parallel to either a straight or a curved surface adjacent to and 4 mm away from the inflow orifice (1.50 mm2) with the control condition being a free jet matched for flow rates and driving pressures. Jets were imaged perpendicular to the plane of the surface, the plane in which most clinical images of jet-surface interactions are obtained. Ten different flow rates ranging from 0.13 to 0.30 l/min were used. Surface-adherent jet areas were smaller than control jets for every driving pressure-volume combination (paired t test, p less than 0.01). Computer analysis of color Doppler images showed more green and blue (reverse flow) pixels on the surface side of the adherent jets than the control jets (p less than 0.05), suggesting that viscous energy loss and flow deceleration and reversal play a role in the jet-surface interaction. Analysis of variance demonstrated that linear regression slopes of flow rate versus jet area for surface jets were lower (slopes, 11-21 cm2/l/min; r = 0.95-0.97) than those for the control (slope, 33 cm2/l/min; r = 0.97) (p less than 0.0001). Surface adherence (Coanda effect) influences jet size and color encoding, causing smaller color Doppler jet areas and greater variance and reverse velocity encoding.
Nitroglycerin-induced coronary vasodilation in cardiac transplant recipients. Evaluation with in vivo intracoronary ultrasound.
Authors: Pinto F J , St Goar F G , Fischell T A , Stadius M L , Valantine H A , Alderman E L , Popp R L
Published: June 2012

BACKGROUND

Coronary artery vasomotion is altered after cardiac transplantation. The impact of accelerated transplant coronary atherosclerosis and myocardial rejection on vasomotion is not well understood. Intravascular ultrasound is a new imaging method with the ability to study real-time changes in coronary artery dimensions.

METHODS AND RESULTS

Epicardial coronary artery response to nitroglycerin was studied in 32 cardiac transplant recipients (age, 47 +/- 11 years) 3 weeks to 10 years after transplantation with intracoronary ultrasound. Cross-sectional luminal area and diameter were measured at a fixed position in the left anterior descending artery immediately before and every 30 seconds for 5 minutes after 0.4 mg of sublingual nitroglycerin. Cross-sectional area increased from a baseline of 13.1 +/- 3.9 mm2 to 15.8 +/- 3.9 mm2 at maximal vasodilation; luminal diameter increased from 4.0 +/- 0.6 mm to 4.5 +/- 0.6 mm. This increase reached statistical significance (p less than 0.001) at 1.5 minutes after administration of nitroglycerin; mean maximum increase occurred at 4.5 minutes (24% for cross-sectional area and 11% for luminal diameter). Patients with biopsy-proven mild or moderate concurrent rejection had a significantly blunted vasodilatory response versus the nonrejection group (9% versus 27% for cross-sectional area, p less than 0.04), although a vasodilatory effect was still present. Nitroglycerin response was well preserved in patients up to 10 years after transplantation; however, there was a trend toward a decreased response in patients studied immediately after transplantation (21% versus 29%, p = 0.37). Coronary intimal thickness, as measured by ultrasound, had no impact on the vasodilatory response (R = 0.23, p = 0.34).

CONCLUSIONS

Vasodilatory response to nitroglycerin in cardiac transplant recipients is attenuated during episodes of cardiac rejection. This response is preserved in long-term survivors and is independent of the degree of intimal thickening. Intravascular ultrasound provides a new method to document real-time epicardial coronary vasomotion.
Signal transduction by G proteins in cardiac tissues.
Authors: Fleming J W , Wisler P L , Watanabe A M
Published: June 2012

The role of G proteins in mediating the responses of the heart to circulating catecholamines and to the influences of the autonomic nervous system is of special interest to cardiologists. It is evident that G proteins are essential links in the cascade of biochemical events that ensure when neurotransmitters and hormones interact with receptors on myocardial cells. It is likely [corrected] that dysfunction of G proteins plays a role in cardiovascular pathophysiology. With current methodologies, especially molecular biological and recombinant DNA techniques, and with transgenic animal models that can relate physiological function and specific gene dosage, some cardiovascular diseases may be traced to G protein-related defects.
Pharmacokinetics of tissue-type plasminogen activator during acute myocardial infarction in men. Effect of a prostacyclin analogue.
Authors: Kerins D M , Roy L , Kunitada S , Adedoyin A , FitzGerald G A , Fitzgerald D J
Published: June 2012

BACKGROUND

Coronary reocclusion complicates the thrombolytic therapy of acute myocardial infarction despite the routine use of aspirin. This is consistent with experimental studies demonstrating that multiple agonists, in addition to thromboxane A2, mediate the platelet activation underlying reocclusion. Consequently, a more potent antiplatelet therapy with a broader spectrum of activity than aspirin may be required in this setting. Prostacyclin and its more stable analogue, iloprost, inhibit platelet aggregation to all known agonists and exert an additional effect over aspirin alone. Experiments in animal models have demonstrated, however, that iloprost increases the clearance of tissue-type plasminogen activator (t-PA) and impairs thrombolysis in vivo. This study examines whether a similar interaction occurs in humans.

METHODS AND RESULTS

Twelve patients with acute myocardial infarction received t-PA intravenously, 60 mg in the first hour and a maintenance infusion of 13.3 mg/hr for 3 hours. Patients were assigned in a double-blind fashion to iloprost (2 ng/kg/min) or placebo following the initial 90 minutes of the maintenance infusion of t-PA. Iloprost decreased mean arterial blood pressure (-10 +/- 2.9 mm Hg, p less than 0.05) but did not alter heart rate. Steady-state plasma iloprost concentration was 591 +/- 64 pmol/l. At this concentration, iloprost markedly inhibited platelet aggregation in vitro, particularly in the presence of aspirin. Steady-state clearance of t-PA was unchanged by iloprost (454 +/- 65 versus 443 +/- 136 ml/min in controls, p = NS). Furthermore, neither elimination kinetics nor plasma protein binding of t-PA was altered by iloprost.

CONCLUSIONS

At plasma levels that exert a potent antiplatelet effect, iloprost did not alter the pharmacokinetics of t-PA in men. Prostacyclin analogues may prove useful as an adjunct to plasminogen activators, particularly in patients at high risk for thrombotic reocclusion.
Migratory activity of human smooth muscle cells cultivated from coronary and peripheral primary and restenotic lesions removed by percutaneous atherectomy.
Authors: Bauriedel G , Windstetter U , DeMaio S J , Kandolf R , Höfling B
Published: June 2012

BACKGROUND

The successful cultivation of human smooth muscle cells (SMC) from coronary and peripheral atherosclerotic lesions removed by percutaneous directional atherectomy is described.

METHODS AND RESULTS

Sixty-seven patients in whom plaque material was obtained compose the study population. A total of 73 lesions from both coronary (n = 38) and peripheral (n = 35) arteries of primary (n = 50) and restenotic origin (n = 23) were studied. Successful cultivation was significantly (p less than 0.001) dependent on the quantity of plaque material submitted. Fifty-five percent of patients in whom atherectomy specimens were removed from coronary lesions yielded an adequate SMC population in comparison to 89% of those from peripheral arteries (p less than 0.01). Cultivation was not dependent on the age and sex of patients, lesion origin, risk factors, medications, or incidence of unstable angina. In an attempt to quantify SMC activity, migratory velocity was measured with a computer-assisted motion analysis system. SMC migratory velocity was found to be significantly (p less than 0.001) greater in restenotic than in primary plaque material. This finding was confirmed for both coronary and peripheral lesions.

CONCLUSIONS

Our data suggest that elevated SMC migratory activity may be an important mechanism in the development of restenotic lesions.
A low-sodium diet corrects the defect in beta-adrenergic response in older subjects.
Authors: Feldman R D
Published: June 2012

BACKGROUND

One of the prominent cardiovascular abnormalities in the elderly is reduced beta-adrenoceptor responsiveness. Because dietary sodium restriction corrects the defect in vascular and lymphocyte beta-adrenoceptor responsiveness in hypertensive subjects, we postulated an analogous effect in the elderly. Thus, vascular and lymphocyte beta-adrenergic responsiveness were studied in 10 older normotensive subjects (age, 56 +/- 2 years) on either a 400- or 10-meq/day sodium diet.

METHODS AND RESULTS

In older subjects fed a high-sodium diet, maximal isoproterenol-mediated vasodilation was depressed compared with a group of normotensive younger subjects studied previously. When they were fed a low-sodium diet, however, maximal isoproterenol-mediated vasodilation in the elderly was increased significantly. Lymphocyte adenylyl cyclase sensitivity to isoproterenol was comparably increased. Blood pressure was significantly reduced on a low-sodium diet, and mean arterial pressure was significantly inversely correlated with the extent of isoproterenol-mediated vasodilation.

CONCLUSIONS

These studies indicate that a low-sodium diet corrects the defect in both vascular and lymphocyte beta-adrenergic responsiveness with aging. This suggests an important role for dietary modification in the adrenergic regulation of vascular tone in the elderly.
Evidence of genetic heterogeneity in five kindreds with familial hypertrophic cardiomyopathy.
Authors: Epstein N D , Fananapazir L , Lin H J , Mulvihill J , White R , Lalouel J M , Lifton R P , Nienhuis A W , Leppert M
Published: June 2012

BACKGROUND

Recently, two families with hypertrophic cardiomyopathy have been shown to have mutations in the cardiac beta-myosin heavy chain gene (beta-MHC) located on the long arm of chromosome 14.

METHODS AND RESULTS

We have performed linkage analysis of five newly ascertained pedigrees with more than 50 chromosomal markers detecting polymorphisms. Our findings confirm the linkage to beta-MHC gene locus on chromosome 14 in one family (LOD score, 4.50) and suggest linkage to the same gene in another kindred. Chromosome 14 markers were not linked to the disease gene in the other three kindreds, however, and a test for genetic heterogeneity was statistically significant. Moreover, markers for the beta-MHC gene identified affected individuals who were recombinants with respect to this gene and the disease phenotype in these three kindreds.

CONCLUSIONS

These results provide conclusive evidence that hypertrophic cardiomyopathy in separate families is caused by mutations in disease genes at two or more locations in the genome.
Imaging the rejecting heart. In vivo detection of major histocompatibility complex class II antigen induction.
Authors: Isobe M , Narula J , Southern J F , Strauss H W , Khaw B A , Haber E
Published: June 2012

BACKGROUND

Mice with abdominal heterotopic heart transplants were studied to determine whether scintigraphic detection of an increase in major histocompatibility complex (MHC) class II antigen expression could be used as a noninvasive method for diagnosing early rejection.

METHODS AND RESULTS

Allografts from C3H/He (H2k) donors were transplanted into BALB/c (H2d) recipients (n = 18). Two of the 18 allografted mice were treated with cyclosporine (15 mg/kg/day), and two isografted mice served as controls. Each mouse was injected intravenously with 100 microCi of 111In-labeled anti-MHC class II monoclonal antibodies (10-2-16 and 14-4-4S) 24 hours before scintigraphy. After imaging, the mice were killed for tissue counting and histopathology. Radiotracer uptake in the grafts reflected the severity of rejection as determined by histopathological criteria. The percent injected dose per gram of tissue in excised grafts was 4.8 +/- 1.8 (mean +/- SD) for normal grafts (n = 8), 11.1 +/- 9.7 for grafts with grade IA rejection (n = 3, NS), 18.0 +/- 3.8 for grafts with grade IIIA rejection (n = 4, p less than 0.001 versus normal), 18.7 +/- 3.2 for grafts with grade IIIB rejection (n = 3, p less than 0.001 versus normal), and 22.6 +/- 5.4 for grafts with severe rejection (grade IV) (n = 3, p less than 0.001 versus normal). Rejecting allografts with lymphocyte infiltration but without significant myocyte necrosis could be identified by this scintigraphic method. In the BALB/c donor-C57BL/6 (H2b, IE-) recipient combination, rejecting allografts were visualized by 14-4-4S (anti-IEk,d,p,r) antibody but not by 10-2-16 (anti-IAk,r,s,f) antibody. This difference shows that class II antigens induced on donor hearts are solely responsible for the antibody uptake in positive scintigrams of rejecting allografts.

CONCLUSIONS

We conclude that 111In-labeled anti-MHC class II antigen antibody imaging is a sensitive and noninvasive method for detecting cardiac allograft rejection.
Adenosine causes bradycardia in pacing-induced cardiac failure.
Authors: Belloni F L , Wang J , Hintze T H
Published: June 2012

BACKGROUND

In normal, conscious dogs, systemic injection of adenosine causes arterial hypotension and a baroreceptor reflex tachycardia mediated in part by withdrawal of vagal tone from the sinoatrial node. After vagal section or muscarinic receptor blockade, however, adenosine injection causes bradycardia via a direct sinoatrial node inhibition. Because cardiac failure is marked by a loss of vagal tone, we hypothesized that adenosine injection in dogs with failing hearts would reduce heart rate.

METHODS AND RESULTS

Mongrel dogs were instrumented with indwelling catheters, manometers, and ventricular pacing electrodes. After the dogs had recovered from the surgery, the ventricles were paced continuously at 210 beats per minute for 3 weeks, followed by pacing at 240 beats per minute for an additional week. This regimen caused mild ventricular and more striking atrial hypertrophy and a gradual onset of physiological and clinical signs of congestive heart failure. Adenosine injections that caused large tachycardias before the pacing regimen began caused progressively smaller increments in heart rate during the first 2 weeks of pacing. After 3 and 4 weeks, adenosine injections caused overt reductions in heart rate despite the concomitant arterial depressor response.

CONCLUSIONS

We conclude that the loss of vagal tone associated with the development of cardiac failure unmasks the direct negative chronotropic effect of exogenous adenosine on the sinoatrial node.
Immediate and long-term outcome of percutaneous mitral valvotomy in patients 65 years and older.
Authors: Tuzcu E M , Block P C , Griffin B P , Newell J B , Palacios I F
Published: June 2012

BACKGROUND

We analyzed the immediate and long-term outcome of percutaneous balloon mitral valvotomy (PMV) in 99 patients who were greater than or equal to 65 years of age (81 women and 18 men; mean +/- SEM age, 72 +/- 0.5 years).

METHODS AND RESULTS

There were 84 patients in New York Heart Association (NYHA) class III or IV; 26 patients had previous surgical commissurotomy; 64 had one or more comorbidities; 73 had fluoroscopically visible mitral valve (MV) calcification; and 63 had echocardiographic score greater than 8 (mean +/- SEM score, 9.2 +/- 0.2). There were three procedural deaths, all occurring in our early experience. Pericardial tamponade occurred in five patients, thromboembolism in three, and transient atrioventricular block in one. After PMV, MV area was greater than or equal to 1 cm2 in 86 patients and greater than or equal to 1.5 cm2 in 56. A successful outcome (defined as MV area greater than or equal to 1.5 cm2 without a greater than or equal to 2-grade increase in mitral regurgitation and without left-to-right shunt with a pulmonary-to-systemic flow ratio of greater than or equal to 1.5:1) was achieved in 46 patients. The best multivariate predictor of success was the combination of echocardiographic score, NYHA functional class, and inverse of MV area. Mean follow-up was 16 +/- 1 months. Actuarial survival (79 +/- 7% versus 62 +/- 10%, p = 0.04), survival without MV replacement (71 +/- 8% versus 41 +/- 8%, p = 0.002), and survival without MV replacement and NYHA class III or IV (54 +/- 12% versus 38 +/- 8%, p = 0.01) at 3 years were significantly better in the successful group of 46 patients than in the unsuccessful group of 53 patients. Low echocardiographic score was the only independent predictor of survival. Lack of MV calcification and low NYHA class, low mean left atrial pressure, and low pulmonary artery pressure were the independent predictors of event-free survival.

CONCLUSIONS

PMV can be performed safely in selected patients greater than or equal to 65 years old with good immediate and long-term results. In addition to clinical examination, echocardiographic evaluation of the mitral valve and fluoroscopic screening for valvular calcification are the most important steps in patient selection for successful outcome.
Intracoronary ultrasound in cardiac transplant recipients. In vivo evidence of "angiographically silent" intimal thickening.
Authors: St Goar F G , Pinto F J , Alderman E L , Valantine H A , Schroeder J S , Gao S Z , Stinson E B , Popp R L
Published: June 2012

BACKGROUND

Accelerated coronary atherosclerosis is a major factor limiting allograft longevity in cardiac transplant recipients. Histopathology studies have demonstrated the insensitivity of coronary angiography for detecting early atheromatous disease in this patient population. Intracoronary ultrasound is a new imaging technique that provides characterization of vessel wall morphology. The purpose of this study was to compare in vivo intracoronary ultrasound with angiography in cardiac transplant recipients.

METHODS AND RESULTS

The left anterior descending coronary artery was studied with intracoronary ultrasound in 80 cardiac transplant recipients at the time of routine screening coronary angiography 2 weeks to 13 years after transplantation. A mean and index of intimal thickening were obtained at four coronary sites. Intimal proliferation was classified as minimal, mild, moderate, or severe according to thickness and degree of vessel circumference involved. Twenty patients were studied within 1 month of transplantation and had no angiographic evidence of coronary disease. An intimal layer was visualized by ultrasound in only 13 of these 20 presumably normal hearts. The 60 patients studied 1 year or more after transplantation all had at least minimal intimal thickening. Twenty-one patients (35%) showed minimal or mild, 17 (28%) moderate, and 21 (35%) severe thickening. Forty-two of these 60 patients had angiographically normal coronary arteries, 21 (50%) of whom had either moderate or severe thickening. All 18 patients with angiographic evidence of coronary disease had moderate or severe intimal thickening, but there was no statistically significant difference in intimal thickness or index when compared with the patients with moderate or severe proliferation and normal angiograms (thickness, 0.53 +/- 0.35 mm versus 0.64 +/- 0.30 mm, p = NS; index, 0.28 +/- 0.10 versus 0.34 +/- 0.10, p = NS).

CONCLUSIONS

The majority of patients 1 or more years after cardiac transplantation have ultrasound evidence of intimal thickening not apparent by angiography. Intracoronary ultrasound offers early detection and quantitation of transplant coronary disease and provides characterization of vessel wall morphology, which may prove to be a prognostic marker of disease.
Nitroprusside and regional vascular capacitance in patients with severe congestive heart failure.
Authors: Risöe C , Simonsen S , Rootwelt K , Sire S , Smiseth O A
Published: June 2012

BACKGROUND

This study investigates the effects of sodium nitroprusside on regional vascular capacitance in eight patients with severe congestive heart failure (New York Heart Association class IV) and pulmonary hypertension.

METHODS AND RESULTS

Regional relative blood volumes in the splanchnic and pulmonary region were determined by equilibrium blood pool scintigraphy. Hepatic venous wedge pressure and the mean of pulmonary artery and pulmonary capillary wedge pressure were used to represent the distending pressures of the splanchnic and pulmonary capacitance vessels, respectively. The dose of sodium nitroprusside was increased stepwise until systolic pulmonary artery pressure decreased below 50 mm Hg. This caused reductions in mean aortic pressure from 89 +/- 5 to 66 +/- 3 mm Hg (p less than 0.005), in pulmonary capillary wedge pressure from 31 +/- 1 to 16 +/- 2 mm Hg (p less than 0.001), and in hepatic venous wedge pressure from 10.0 +/- 1.0 to 5.9 +/- 0.6 mm Hg (p less than 0.005). Intestinal blood volume increased by 26 +/- 7% (p less than 0.005), whereas hepatic blood volume decreased by 9 +/- 3% (p less than 0.02). Pulmonary blood volume was unchanged. Analysis of intestinal and pulmonary vascular pressure-volume relations showed larger or equal blood volumes contained at lower distending pressures, indicating that sodium nitroprusside reduced smooth muscle tone of the capacitance vessels in these regions. The reduction of hepatic blood volume was compatible with passive expulsion of blood subsequent to reduced venous pressure. There was no change in the count rate from the spleen.

CONCLUSIONS

Nitroprusside reduced venous pressure in patients with congestive heart failure by active relaxation of intestinal and pulmonary capacitance vessels. Hepatic vascular volume was probably reduced by a passive mechanism.
Selective stimulation of parasympathetic nerve fibers to the human sinoatrial node.
Authors: Carlson M D , Geha A S , Hsu J , Martin P J , Levy M N , Jacobs G , Waldo A L
Published: June 2012

BACKGROUND

In animals, parasympathetic nerve fibers that innervate the sinoatrial node can be selectively stimulated to increase atrial cycle length. These nerve fibers course through an epicardial fat pad at the margin of the right superior pulmonary vein, the superior vena cava, and the right atrium. We hypothesized that similar nerves exist and can be selectively stimulated in humans.

METHODS AND RESULTS

Microscopic examination of fat pads excised from the margin of the right superior pulmonary vein, the superior vena cava, and the right atrium during two human autopsies revealed the presence of nerve fibers and ganglia. We electrically stimulated this epicardial fat pad in 16 patients during cardiac surgery. The fat pads were stimulated with continuous-pulse trains for 15 seconds via a hand-held bipolar electrode using constant current (10-15 mA), constant pulse width (0.02-0.05 msec), and at 6.6, 10, 20, 25, and 30 Hz. The mean atrial cycle length +/- 1 SEM increased from 734 +/- 34 msec at baseline to a maximum of 823 +/- 61 msec at 6.6 Hz, 1,167 +/- 125 msec at 10 Hz, 1,734 +/- 281 msec at 20 Hz, 2,993 +/- 661 msec at 25 Hz, and 2,461 +/- 668 msec at 30 Hz during nerve stimulation. Linear regression analysis showed that the response of atrial cycle length to sinoatrial parasympathetic nerve stimulation was frequency dependent. The maximum response and complete decay of the response occurred within 4-8 seconds of initiation or termination of sinoatrial parasympathetic nerve stimulation. Atrioventricular conduction time and the PR interval did not change during sinoatrial parasympathetic nerve stimulation, even when the atria were paced at the baseline heart rate.

CONCLUSIONS

Electrical stimulation of parasympathetic nerve fibers in a fat pad near the sinoatrial node increased atrial cycle length without affecting atrioventricular nodal conduction. This is the first study in which such nerve fibers that innervate the sinoatrial node have been selectively stimulated in humans.
Radiofrequency catheter ablation of accessory atrioventricular connections in 250 patients. Abbreviated therapeutic approach to Wolff-Parkinson-White syndrome.
Authors: Calkins H , Langberg J , Sousa J , el-Atassi R , Leon A , Kou W , Kalbfleisch S , Morady F
Published: June 2012

BACKGROUND

The purpose of this study was to report the results and complications of radiofrequency catheter ablation of accessory atrioventricular (AV) connections by using an abbreviated approach aimed at minimizing the duration of the procedure.

METHODS AND RESULTS

Two hundred fifty consecutive patients with the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardia involving a concealed accessory AV connection underwent catheter ablation with the use of radiofrequency current. In 179 of the 250 patients, catheter ablation was performed at the time of an initial electrophysiology test. Two hundred thirty-five patients had one accessory AV connection and 15 patients had two or more. One hundred eighty-three accessory AV connections were manifest and 84 were concealed. One hundred sixty-one were were located in the free wall of the left ventricle, 47 were in the right free wall, 44 were posteroseptal, 10 were anteroseptal, and five were intermediate test, and the ablation procedure was recorded for each patient, as was the total duration of fluoroscopy. A follow-up electrophysiology test was performed 2-3 months after the ablation procedure. Ninety-four percent of patients had all accessory AV connections successfully ablated and remained free of symptomatic tachycardia during a mean follow-up of 10 +/- 4 months. Two hundred nineteen patients (88%) had all accessory AV connections ablated during the initial attempt at catheter ablation. Mean duration of the entire procedure was 134 +/- 75 minutes. Procedure duration was longest in patients with multiple accessory AV connections, shortest in patients with intermediate septal accessory AV connections, and similar in all other locations. A nonfatal complication occurred in nine patients (4%).

CONCLUSIONS

The results of this study indicate that catheter ablation of accessory AV connections with radiofrequency current can be performed safely and expeditiously in a majority of patients and confirm in a large series the feasibility of catheter ablation at the time of an initial diagnostic electrophysiology test. This abbreviated therapeutic approach avoids the need for electropharmacological testing, long-term antiarrhythmic drug therapy, and surgical therapy in the majority of patients with the Wolff-Parkinson-White syndrome or with symptomatic tachycardias involving accessory AV connections.
Randomized trial of subcutaneous low-molecular-weight heparin CY 216 (Fraxiparine) compared with intravenous unfractionated heparin in the curative treatment of submassive pulmonary embolism. A dose-ranging study.
Authors: Théry C , Simonneau G , Meyer G , Hélénon O , Bridey F , Armagnac C , d'Azemar P , Coquart J P
Published: June 2012

BACKGROUND

We compared the efficacy and safety of different dosages of a low-molecular-weight heparin, CY 216 D (Fraxiparine), in the treatment of submassive pulmonary embolism with unfractionated heparin in a prospective, randomized, dose-finding study.

METHODS AND RESULTS

The primary outcome was the evolution of pulmonary vascular obstruction. We enrolled 101 patients. Four patient groups were formed: standard heparin by continuous intravenous infusion (group 1) and Fraxiparine subcutaneously 400, 600, and 900 anti-Xa Institute Choay units/kg, respectively (groups 2, 3, and 4). Inclusions were stopped prematurely in groups 3 and 4 because of the incidence of major bleedings. At day 8, the improvement of the pulmonary vascular obstruction and the major bleedings were similar in groups 1 and 2.

CONCLUSIONS

The Fraxiparine dosage of 400 anti-Xa Institute Choay units/kg is as effective and safe as unfractionated heparin in the treatment of submassive pulmonary embolism.
Development and determinants of dynamic obstruction to left ventricular outflow in young patients with hypertrophic cardiomyopathy.
Authors: Panza J A , Maris T J , Maron B J
Published: June 2012

BACKGROUND

To study the development of dynamic subaortic obstruction in young patients with hypertrophic cardiomyopathy (HCM), serial echocardiograms were retrospectively analyzed in a group of 26 consecutive children with this disease who showed no evidence of dynamic outflow obstruction at their initial evaluation (age, 11 +/- 3 years).

METHODS AND RESULTS

After a follow-up of 3-12 years (mean, 7 +/- 3 years), seven of the 26 patients (27%) developed echocardiographic evidence of subaortic obstruction, i.e., marked systolic anterior motion (SAM) of the mitral valve with mitral-septal apposition and increased left ventricular outflow tract systolic velocities (3.8 +/- 0.3 m/sec; range, 3.1-4.5). Patients who developed SAM had smaller transverse dimension of the left ventricular outflow tract and more anteriorly displaced mitral valve when initially evaluated than did patients without development of SAM (outflow tract dimension, 19.1 +/- 4 versus 24.6 +/- 4 mm; mitral valve position index, 1.07 +/- 0.2 versus 0.73 +/- 0.3; each p less than 0.02). In patients with development of SAM, the already reduced outflow tract dimension decreased further during follow-up, and the mitral valve became even more anteriorly displaced within the left ventricular cavity. These developmental alterations in outflow tract size were associated with increases in left ventricular wall thickness, particularly of the basal anterior septum (11.0 +/- 8 mm; 72 +/- 33%) compared with control patients with HCM who did not develop SAM (3.0 +/- 3 mm; 17 +/- 10%; p less than 0.05).

CONCLUSIONS

Development of subaortic obstruction in young patients with HCM results from a process of dynamic remodeling of left ventricular geometry over several years and is characterized by progressive narrowing of the outflow tract with anterior displacement of the mitral valve and disproportionate thickening of the basal anterior ventricular septum.
Cardiac potential and potential gradient fields generated by single, combined, and sequential shocks during ventricular defibrillation.
Authors: Wharton J M , Wolf P D , Smith W M , Chen P S , Frazier D W , Yabe S , Danieley N , Ideker R E
Published: June 2012

BACKGROUND

Potential gradient field determination may be a helpful means of describing the effects of defibrillation shocks; however, potential gradient field requirements for defibrillation with different electrode configurations have not been established.

METHODS AND RESULTS

To evaluate the field requirements for defibrillation, potential fields during defibrillation shocks and the following ventricular activations were recorded with 74 epicardial electrodes in 12 open-chest dogs with the use of a computerized mapping system. Shock electrodes (2.64 cm2) were attached to the lateral right atrium (R), lateral left ventricular base (L), and left ventricular apex (V). Four electrode configurations were tested: single shocks of 14-msec duration given to two single anode-single cathode configurations, R:V and L:V, and to one dual anode-single cathode configuration, (R+L):V; and sequential 7-msec shocks separated by 1 msec given to R:V and L:V (R:V----L:V). Defibrillation threshold (DFT) current was significantly lower for R:V----L:V than for the other configurations and markedly higher for L:V. Despite these differences, the minimum potential gradients measured at DFT were not significantly different (approximately 6-7 V/cm for each electrode configuration). Potential gradient fields generated by the electrode configurations were markedly uneven, with a 15-27-fold change from lowest to highest gradient, with the greatest decrease in gradient occurring near the shock electrodes. Although gradient fields varied with the electrode configuration, all configurations produced weak fields along the right ventricular base. Early sites of epicardial activation after all unsuccessful shocks occurred in areas in which the field was weak; 87% occurred at sites with gradients less than 15 V/cm. Ventricular tachycardia originating in high gradient areas near shock electrodes followed 11 of 67 successful shocks.

CONCLUSIONS

These data suggest that 1) defibrillation fields created by small epicardial electrodes are very uneven; 2) achievement of a certain minimum potential gradient over both ventricles is necessary for ventricular defibrillation; 3) the difference in shock strengths required to achieve this minimum gradient over both ventricles may explain the differences in DFTs for various electrode configurations; and 4) high gradient areas in the uneven fields can induce ectopic activation after successful shocks.
Cilazapril and early atherosclerotic changes after balloon injury of porcine carotid arteries.
Authors: Lam J Y , Lacoste L , Bourassa M G
Published: June 2012

BACKGROUND

Cilazapril, a converting enzyme inhibitor, has been shown to significantly decrease the extent of intimal smooth muscle cell proliferation after arterial injury in a normotensive rat model.

METHODS AND RESULTS

To assess the influence of cilazapril on myofibrotic changes after balloon injury, control (n = 7) or cilazapril-treated (n = 9) (20 mg/kg b.i.d.) normal 3-month-old pigs underwent dilatation angioplasty of the right, and deendothelialization of the left common carotid artery. Carotid arteries isolated at 4 weeks were examined morphometrically with a computerized digitizer after in situ glutaraldehyde fixation. Both in the deendothelialized and dilated arteries, the surface area in square millimeters of the neointima and media were similar in the treated and control animals; therefore, the ratio of neointima to media was again not different. The neointimal changes included a combination of proliferative changes as well as organization of mural thrombus and were equally well distributed in the two groups of animals. At the time that the animals were killed, blood pressure (38.2 +/- 2.1 versus 56.8 +/- 4.8 mm Hg, p = 0.003) and plasma angiotensin converting enzyme activity (5.6 +/- 4.1 versus 182.3 +/- 70.4, p = 0.02) were lower in treated than in control pigs, but aortic media thrombogenicity (as assessed in an ex vivo perfusion flow chamber) and serum lipids were not different between groups.

CONCLUSIONS

In pigs, cilazapril did not alter the development of myofibrotic changes after mild or severe balloon injury despite plasma angiotensin converting enzyme activity inhibition.
Clinical experience with a tiered-therapy, multiprogrammable antiarrhythmia device.
Authors: Bardy G H , Troutman C , Poole J E , Kudenchuk P J , Dolack G L , Johnson G , Hofer B
Published: June 2012

BACKGROUND

The purpose of this report is to describe our initial experience with a tiered-therapy, variable detection criteria, multiprogrammable antiarrhythmia device capable of antitachycardia pacing, cardioversion, and defibrillation in 50 cardiac arrest survivors.

METHODS AND RESULTS

An epicardial lead system was used in 35 patients. A transvenous lead system was used in 15 patients. The index arrhythmia leading to device implantation was ventricular fibrillation (VF) in 23 patients, ventricular tachycardia (VT) in 21 patients, and both VT and VF in six patients. Postoperatively, all 50 patients benefited from the additional functions available in the new device compared with a device capable only of high-energy termination of arrhythmias using a simple rate detection algorithm. Total patient survival over a mean follow-up period of 15 +/- 5 months was 96%, with no patient succumbing to sudden arrhythmic death, cardiac death, or surgical death. Nine patients (18%) avoided the need for a bradycardia pacemaker because of the device's backup bradycardia pacing function. A programmable tachycardia cycle length stability algorithm prevented inappropriate device intervention into atrial fibrillation in 11 patients (22%). Detection schema flexibility, antitachycardia pacing capabilities, and low-energy cardioversion options allowed the elimination or avoidance of antiarrhythmic drugs in 41 patients (82%). Device data storage facilitated troubleshooting and reprogramming of detection algorithms and therapeutic schema in all 50 patients. Finally, the ability to perform noninvasive programmed electrical stimulation obviated the need for invasive cardiac catheterization in 35 of 35 patients who required electrophysiological testing after device implantation.

CONCLUSIONS

These findings indicate that a multiprogrammable antiarrhythmia device can provide a substantial advance in the treatment of patients with disabling or life-threatening ventricular arrhythmias by minimizing the use of painful shocks, reducing the need for antiarrhythmic drugs, lowering the incidence of inappropriate shocks, facilitating electrophysiological evaluation, and obviating the need for dual-device therapy.
Retrograde nontransseptal balloon mitral valvuloplasty. Immediate results and long-term follow-up.
Authors: Stefanadis C , Stratos C , Pitsavos C , Kallikazaros I , Triposkiadis F , Trikas A , Vlachopoulos C , Gavaliatsis I , Toutouzas P
Published: June 2012

BACKGROUND

Percutaneous retrograde nontransseptal balloon mitral valvuloplasty is a new technique developed in our institution for opening a stenotic mitral valve. This technique is based on a new, externally steerable cardiac catheter that enters the left atrium retrogradely via the left ventricle.

METHODS AND RESULTS

The technique was used in 86 consecutive patients (18 men and 68 women; mean age, 51 +/- 11 years). Dilatation of the stenotic mitral valve was achieved in 85 of the 86 patients. After the procedure, mitral valve area increased from 0.92 +/- 0.22 to 2.14 +/- 0.54 cm2 and transmitral gradient decreased from 16 +/- 6 to 5 +/- 2 mm Hg. Major complications, such as cardiac performation, embolic events, or death, were not encountered. Severe mitral regurgitation (greater than 2+) developed in three patients (3.5%). In two patients (2.4%), there was major injury of the femoral artery. The maintenance of the initial improvement was similar to that found in studies that used transseptal techniques. The restenosis rate during the 2-year follow-up was 15.4%.

CONCLUSIONS

The immediate and long-term findings of this study indicate that retrograde percutaneous nontransseptal balloon mitral valvuloplasty is an effective and safe procedure with an acceptable major complication rate. Moreover, this new technique has the advantage that it does not involve puncture and dilatation of the interatrial septum, although it may occasionally lead to arterial damage. Further studies will show whether it may really be considered as an alternative method or method of choice for percutaneous balloon mitral valvuloplasty.
Relation between recovery sequence estimated from body surface potentials and T wave shape in patients with negative T waves and normal subjects.
Authors: Yamaki M , Kubota I , Endo T , Hosoya Y , Ikeda K , Tomoike H
Published: June 2012

BACKGROUND

Advances in analytical methods of the epicardial electrical potentials allowed us to demonstrate spatial distributions of local recovery. Because local recovery will be reflected in events on body surface ECG mapping, abnormalities in recovery sequence that may be responsible for the origin of negative T waves can be detected from body surface potentials.

METHODS AND RESULTS

Eighty-seven unipolar ECGs were recorded simultaneously from the entire thorax in patients having negative T waves on left anterior precordial leads and in normal subjects. These included 40 patients with anterior myocardial infarction (MI), 21 patients with left ventricular hypertrophy (LVH), and 44 male volunteers. We measured Tmax time, defined as the instant of maximal first derivative of the T wave as the index of local recovery (Wyatt's method). Parameters related to T wave potentials were positive T wave amplitude, negative T wave amplitude, and T integral. Significant correlations were observed between the Tmax time and each of the T wave potentials. The T wave potentials were dependent on Tmax times. In the anterior MI, the late Tmax times were located on the upper left anterior chest and early Tmax times on the lower right lateral chest. In the LVH, the area showing a delayed recovery was displaced in a left downward direction compared with anterior MI.

CONCLUSIONS

Body surface Tmax time distributions clearly separate two negative T wave groups, i.e., anterior MI and LVH. Appearance of the negative T waves correlates well with the presence of the area with delayed Tmax time on the spatial distribution.
Normal ultrasonic myocardial reflectivity in athletes with increased left ventricular mass. A tissue characterization study.
Authors: Lattanzi F , Di Bello V , Picano E , Caputo M T , Talarico L , Di Muro C , Landini L , Santoro G , Giusti C , Distante A
Published: June 2012

BACKGROUND

Ultrasonic integrated backscatter of myocardial walls is directly related to the morphometrically evaluated collagen content. The integrated backscatter is also increased in hypertrophic cardiomyopathy, probably because of fiber disarray. The purpose of this study was to investigate myocardial tissue reflectivity in subjects with physiological hypertrophy caused by intense physical training and to assess the relation between the acoustic properties of myocardial tissue and left ventricular wall thickness assessed by conventional two-dimensional echocardiography.

METHODS AND RESULTS

Twenty-four young male athletes (14 professional cyclists and 10 weight lifters, all in full agonistic activity) were studied together with 10 normal age-matched controls with sedentary life. By means of a commercially available two-dimensional echocardiograph, standard measurements were obtained according to the recommendations of the American Society of Echocardiography. With a prototype implemented in our Institute, an on-line radiofrequency analysis of ultrasound signals was also performed to obtain quantitative operator-independent measurements of the integrated backscatter of the myocardial walls. The integrated values of the radiofrequency signal were normalized for the pericardial interface and expressed in percent integrated backscatter (%IB). Compared with control subjects, athletes showed greater thickness values of septum (controls, 9 +/- 1; cyclists, 14 +/- 2; weight lifters, 15 +/- 1 mm, mean +/- SD; p less than 0.01) and posterior wall (9 +/- 1, 12 +/- 2, and 12 +/- 1 mm, respectively; p less than 0.01) but similar values of %IB for both septum (23 +/- 4%, 21 +/- 7%, and 23 +/- 8%, p = NS) and posterior wall (10 +/- 2%, 9 +/- 2%, and 11 +/- 2%, p = NS). In athletes, no correlation was found between septal and posterior wall thickness and the corresponding regional myocardial reflectivity (r = 0.23, p = NS and r = 0.01, p = NS, respectively). Furthermore, we compared the quantitative ultrasonic data between two subsets of 10 athletes and 10 patients with hypertrophic cardiomyopathy and similar degrees of septal thickness (16 +/- 1 versus 17 +/- 1 mm, respectively, p = NS). Septal and posterior wall %IB results were significantly higher in patients with hypertrophic cardiomyopathy (53 +/- 13% and 36 +/- 9%, respectively) than in athletes (21 +/- 7% and 10 +/- 3%, respectively; p less than 0.01 for both).

CONCLUSIONS

We conclude that 1) endurance athletes show a normal pattern of quantitatively assessed ultrasonic backscatter despite of a marked left ventricular hypertrophy and 2) athletes and patients with hypertrophic cardiomyopathy and similar degrees of myocardial wall thickness can be differentiated on the basis of quantitative analysis of backscattered signal.
Gene expression and atrial natriuretic factor processing and secretion in cultured AT-1 cardiac myocytes.
Authors: Lanson N A , Glembotski C C , Steinhelper M E , Field L J , Claycomb W C
Published: June 2012

BACKGROUND

Studies were carried out to characterize several biochemical features of cultured AT-1 cells.

METHODS AND RESULTS

These cells were obtained from a transplantable atrial cardiomyocyte tumor lineage. Reverse transcriptase-polymerase chain reaction-based analyses demonstrated that the pattern of gene expression of cultured AT-1 cells was similar to that of adult atrial myocytes. AT-1 cells expressed atrial natriuretic factor (ANF), alpha-cardiac myosin heavy chain, alpha-cardiac actin, and connexin43. Radioimmunoassays verified that the cells synthesized, stored, and secreted ANF. Through size-exclusion, reversed-phase, and carboxymethyl-ion-exchange high-performance liquid chromatography, it was shown that cultured AT-1 cells stored ANF as pro-ANF (ANF-[1-126]), which was cosecretionally processed quantitatively to ANF-(1-98) and the bioactive 28-amino-acid ANF-(99-126). In addition, cultured AT-1 cells secreted ANF at almost a sixfold greater rate in response to endothelin-1, a potent secretagogue of ANF. KCl, metenkephalinamide, isoproterenol, phenylephrine, and 12-O-tetradecanoyl-phorbol-13-acetate also stimulated ANF release.

CONCLUSIONS

These studies, in combination with previous findings, demonstrated that cultured AT-1 cells, while maintaining the ability to proliferate, have retained functional, biochemical, and ultrastructural features that are characteristic of adult atrial myocytes.