bluuebunny/crossref_metadata_2025 huggingface dataset:
Atrial natriuretic factor potentiates forearm reflex vasoconstriction induced by cardiopulmonary receptor deactivation in man.
Authors: Volpe M , De Luca N , Bigazzi M C , Vecchione F , Lembo G , Condorelli M , Trimarco B
Published: June 2011

Previous evidence suggests that atrial natriuretic factor (ANF) interferes with the autonomic control of circulation. In the present study we investigated whether ANF modulates forearm vasoconstriction reflexly induced by cardiopulmonary receptor unloading in man. For this purpose, the hemodynamic response to -20 mm Hg lower body negative pressure (LBNP) was assessed under control conditions and during the constant infusion of alpha-human ANF (0.5 micrograms/kg bolus followed by 0.05 micrograms/kg/min) in seven normal subjects. ANF infusion resulted in a slight reduction in blood pressure and right atrial pressure, did not modify heart rate or forearm vascular resistance, but significantly potentiated the reflex increase in forearm vascular resistance during LBNP (+25 +/- 9% under control conditions vs +40 +/- 12% during ANF, p less than .05). In an attempt to clarify the mechanisms underlying the enhanced reflex vasoconstriction during infusion of ANF, in five additional subjects we demonstrated that there was a comparable vascular reflex response to LBNP under control conditions and during nitroglycerin infusion at a dose that induced a reduction in atrial pressure comparable to that observed during ANF. Finally, in seven additional subjects we found that ANF infusion did not alter the reflex hemodynamic responses elicited by carotid baroreceptor unloading induced by a +60 mm Hg increase in external neck pressure. We conclude that during the infusion of a pharmacologic dose of ANF the reflex forearm vasoconstriction in response to selective cardiopulmonary receptor unloading is potentiated. This effect does not seem to be related to the hemodynamic actions of the peptide or to interference with the sympathetic control of peripheral circulation.
Myocardial oxygen consumption, oxygen supply/demand heterogeneity, and microvascular patency in regionally stunned myocardium.
Authors: Stahl L D , Weiss H R , Becker L C
Published: June 2011

Although oxygen consumption closely parallels mechanical work in the normal heart, previous studies have found that stunned myocardium may have normal or even increased oxygen consumption despite depressed function. In this study we used microspectrophotometry to measure the oxygen saturations within arteries and veins of less than 100 micron diameter in quick-frozen biopsy samples from normal and regionally stunned myocardium of 10 open-chest anesthetized dogs. Regional myocardial blood flow, measured by radioactive microspheres, was similar in stunned and normal regions, as was mean arteriolar oxygen saturation. However, mean venous oxygen saturation was lower in the stunned region (epicardium 38.0% vs 43.8%, p less than .02; endocardium 36.2% vs 39.5%, p = .12), indicating increased oxygen extraction and consumption, despite a marked reduction in mean systolic segmental shortening from 14.4% to 0.5%. In addition, there was greater vein-to-vein heterogeneity of oxygen saturation in the stunned region, with an excess of veins having low saturations (statistically significant in epicardium, nonsignificant trend in endocardium). Microvascular injections studies with Microfil or drafting ink revealed filling of over 95% of arterioles and 85% of capillaries in the stunned region, similar to the findings in the normal region. Our results are consistent with an inefficient transfer of energy into myocyte contraction or an increased use of energy for noncontractile activities in stunned myocardium. In addition, the finding of increased heterogeneity of oxygen extraction suggests that the injury to stunned myocardium may not be uniform to all contractile elements, but instead may be focally and irregularly distributed.
Effects of lidocaine and procainamide on normal and abnormal intraventricular electrograms during sinus rhythm.
Authors: Schmitt C G , Kadish A H , Marchlinski F E , Miller J M , Buxton A E , Josephson M E
Published: June 2011

The effect of lidocaine (n = 6) and procainamide (n = 12) on electrogram characteristics from electrically normal right ventricular and electrically abnormal left ventricular endocardial sites was determined in 18 patients with prior myocardial infarction. Bipolar electrograms were recorded during sinus rhythm with No. 6F catheters positioned at a left ventricular abnormal site (electrograms fulfilling two of the following criteria: amplitude less than 3 mV, duration greater than 70 msec, or an amplitude to duration ratio less than .046) and normal sites at the right ventricular apex (RVA) and right ventricular outflow tract (RVOT). All electrograms were recorded from the same location before and after intravenous lidocaine or procainamide administered to obtain mean serum concentrations of 4.2 +/- 0.6 and 9.42 +/- 2 micrograms/ml respectively. Lidocaine and procainamide had no significant effect on sinus cycle length or electrogram amplitude. After lidocaine, no significant change in QRS width (112 +/- 23 vs 114 +/- 24 msec), left ventricular electrogram duration (76 +/- 21 vs 78 +/- 15 msec), or right ventricular electrogram duration (RVA 33 +/- 9 vs 33 +/- 10 msec, RVOT 31 +/- 9 vs 33 +/- 11 msec) was noted during sinus rhythm. At a paced cycle length of 600 msec, there was also no change in the paced QRS duration (197 vs 198 msec), the RVA electrogram duration (30 vs 32 msec), the RVOT electrogram duration (49 vs 52 msec), or the left ventricular electrogram duration (102 vs 108 msec).(ABSTRACT TRUNCATED AT 250 WORDS)
Vasodilatation by calcitonin gene-related peptide and by substance P: a comparison of their effects on resistance and capacitance vessels of human forearms.
Authors: McEwan J R , Benjamin N , Larkin S , Fuller R W , Dollery C T , MacIntyre I
Published: June 2011

A comparison has been made of the effects of the potent vasodilating peptide calcitonin gene-related peptide (CGRP) and substance P (SP) on resistance and capacitance vessels of normal subjects. Brachial artery infusion of 1.25 to 10 pmol/min CGRP and of 0.25 to 1.5 pmol/min SP produced maximal increases in forearm blood flow (177 +/- 75% and 198 +/- 50%, respectively), as measured by venous occlusion plethysmography. The vasodilation due to CGRP was prolonged, with a half-life of biological effect of approximately 18 min, while that due to SP was of short duration, with a half-life of biological effect of approximately 15 sec. There was rapid development of tachyphylaxis to the effects of arterial infusion of SP, but not of CGRP, during a prolonged infusion at one dose. CGRP did not alter the diameter of a superficial hand vein, either at rest or when the vein was constricted by a simultaneous infusion of norepinephrine or by the single deep breath reflex. In contrast, SP caused dilatation of veins preconstricted with norepinephrine, although the effect was only transient and dose-response curves could not be constructed. The venoconstrictor response to a single deep breath was abolished by SP. Simultaneous arterial infusion of both peptides produced at least additive, and possibly synergistic, effects on forearm blood flow. We propose that both CGRP and SP have a role in the regulation of vascular smooth muscle tone.
Long-term effects of xamoterol on left ventricular diastolic function and late remodeling: a study in patients with anterior myocardial infarction and single-vessel disease.
Authors: Pouleur H , van Eyll C , Hanet C , Cheron P , Charlier A A , Rousseau M F
Published: June 2011

The purpose of the study was to examine whether the prolonged administration of the beta 1-adrenoceptor partial agonist xamoterol could improve left ventricular diastolic function and affect the global remodeling process of the left ventricle after anterior myocardial infarction. In 22 patients with anterior myocardial infarction and single-vessel disease, left ventricular angiography (+ Millar) was performed under basal conditions 1 to 2 months after the acute myocardial infarction. Eight patients were then treated for 3 months with placebo and 14 were treated with xamoterol (200 mg bid) and a second left ventricular angiographic study was performed. Angiograms were digitized frame by frame to derive the diastolic pressure-volume relationship and to compute wall stress. An index of elastic myocardial stiffness was computed at a constant stress of 30 kdynes/cm2 before and after treatment. To evaluate changes in left ventricular shape, segmental areas in anterior and inferior segments were computed and compared at end-diastole and end-systole. After xamoterol, left ventricular end-diastolic pressure and mean diastolic wall stress decreased (from 24 +/- 5 to 15 +/- 5 mm Hg and from 57 +/- 32 to 38 +/- 22 kdynes/cm2, respectively; both p less than .01 vs baseline and vs placebo). These changes were accompanied by a downward shift in the diastolic pressure-volume relationship and by a decrease in the index of myocardial stiffness from 526 +/- 270 to 371 +/- 194 kdynes/cm2 (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)
Myocardial structure in patients with exercise-induced ischemia.
Authors: Hess O M , Schneider J , Nonogi H , Carroll J D , Schneider K , Turina M , Krayenbuehl H P
Published: June 2011

Myocardial structure of left ventricular segments with recurrent myocardial ischemia was evaluated by morphometry and compared with that of segments with normal blood supply in 15 patients with exercise-induced myocardial ischemia. Left ventricular high-fidelity pressure measurements and simultaneous biplane angiocardiography were performed in patients at rest and during supine bicycle exercise. Left ventricular transmural biopsy samples were obtained during open heart surgery in a normally contracting region and in a region with exercise-induced de novo wall motion abnormalities. Transmural and endocardial and epicardial left ventricular muscle fiber diameter and interstitial nonmuscular tissue were determined by morphometry. Eight patients were restudied 8 months after successful bypass grafting. Heart rate and left ventricular end-diastolic pressure increased significantly preoperatively and postoperatively during exercise. However, left ventricular end-diastolic pressure was significantly higher preoperatively (33 mm Hg) during exercise than postoperatively (19 mm Hg; p less than .01). Left ventricular ejection fraction dropped significantly during exercise (63% vs 54%; p less than .001) before surgery but remained unchanged (64% vs 66%; NS) after revascularization. Regional axis shortening of the normokinetic region increased slightly during exercise pre- and postoperatively, but decreased in the hypokinetic region from 42% at rest to 25% during exercise (p less than .001) before surgery and from 47% at rest to 41% during exercise (p less than .05) after revascularization. Transmural muscle fiber diameter (normal less than or equal to 23 microns) was significantly larger in regions with exercise-induced ischemia (29.3 microns, p less than .025) than in normally contracting regions (27.3 microns). Interstitial nonmuscular tissue (normal less than or equal to 10%) was significantly increased in regions with exercise-induced wall motion abnormalities (19.8%) compared with normally contracting regions (15.5%; p less than .05). In the endocardial half of left ventricular segments with recurrent myocardial ischemia interstitial tissue was significantly increased (23.7%; p less than .01) compared with that in the epicardial half of the same segment (17.5%). It is concluded that structural alterations of the myocardium (muscle fiber hypertrophy and increased interstitial nonmuscular tissue) develop especially in the endocardial layers of the transiently ischemic myocardium with normal function at rest.(ABSTRACT TRUNCATED AT 400 WORDS)
Serum immunoglobulin E response to myocardial infarction.
Authors: Szczeklik A , Sladek K , Szczerba A , Dropinski J
Published: June 2011

Mast cells have been implicated in the pathogenesis of coronary heart disease. They can be activated by immunoglobulin (Ig) E-mediated mechanisms to release powerful mediators affecting local blood flow. We have determined systematically serum IgE concentrations in 100 patients with acute myocardial infarction. There was a consistent pattern of change in serum IgE, characterized by a significant increase on the third and fifth day, peak values on the seventh day, and a gradual decline to initial levels by the end of the third week after infarction. The increase in serum IgE shortly after myocardial infarction was similar to the increase in blood eosinophil count, but was in contrast to serum IgG levels. After infarction, patients with high initial IgE levels (greater than 200 IU/ml) had a greater increase in IgE and less frequent severe complications than those whose initial IgE levels were below 200 IU/ml. In 16 subjects with acute coronary insufficiency without infarction serum IgE levels remained unchanged. It is suggested that in myocardial infarction circulating IgE sensitizes both mast cells of coronary arteries and eosinophils, invading ischemic myocardium; this facilitates release of chemical mediators. Patients with high IgE levels might be protected against complications of infarction because of a favorable ratio of locally released mediators and because of decreased platelet function.
Diagnosis of right ventricular involvement in chronic inferior myocardial infarction by means of body surface QRS changes.
Authors: Yamaki M , Ikeda K , Honma K , Kiriyama N , Tono-oka I , Tsuiki K , Yasui S
Published: June 2011

ST segment elevation in right precordial leads is thought to be good predictor of right ventricular involvement in patients with acute inferior myocardial infarction. This view, however, is rapidly disappearing. Therefore, using QRS changes in body surface potential maps in the chronic phase, we have attempted to differentiate patients with or without right ventricular involvement. Thirty patients with chronic inferior myocardial infarction (2 or more months after onset) were studied, in whom 87 unipolar ECGs and right ventriculograms were recorded. The patients were then divided into three groups depending on the locations of their abnormal QRS potentials (-2SD area) exceeding the normal range (mean -2SD). In group A, the -2SD area was located predominantly on the right inferior chest, in group B on the left inferior chest, and in group N on both the right and left inferior chests equally. The results showed that group A had a lower right ventricular ejection fraction (RVEF) compared with group B (A, 40 +/- 7%; B, 53 +/- 10%; p less than .001), while there was no difference in left ventricular ejection fraction between the two groups (49 +/- 11% and 49 +/- 11%, respectively). Moreover, right ventricular asynergy occurred in 14 of the 18 patients (78%) of group A but in only one of the 10 patients (10%) of group B. Group N was presumed to be intermediate between groups A and B.(ABSTRACT TRUNCATED AT 250 WORDS)
Procainamide infusion test: inability to identify patients with Wolff-Parkinson-White syndrome who are potentially at risk of sudden death.
Authors: Fananapazir L , Packer D L , German L D , Greer G S , Gallagher J J , Pressley J C , Prystowsky E N
Published: June 2011

Persistence of preexcitation in sinus rhythm with procainamide infusion has been reported to occur in patients with a short anterograde accessory pathway effective refractory period (AERPAP) and this test has been proposed as a reliable noninvasive method to identify patients with the Wolff-Parkinson-White syndrome who are at risk of sudden death. However, sudden death correlates best with a shortest preexcited RR interval during atrial fibrillation (SRRPE) of 260 msec or less. We infused 10 to 12 mg/kg procainamide to 56 patients to determine whether persistence or loss of preexcitation in sinus rhythm identified patients with SRRPEs of 260 or less or greater than 260 msec, respectively. Atrial fibrillation was induced in 53 patients. Of these, 32 patients had persistence of preexcitation with procainamide infusion and SRRPE in this group of patients was shorter than that in patients in whom preexcitation was lost (194 +/- 44 vs 235 +/- 55 msec, p less than .05). However, preexcitation persisted after procainamide infusion in only 31 of 46 (67%) patients with SRRPEs of 260 msec or less. Furthermore, 15 of 21 patients who lost preexcitation had SRRPEs of 260 msec or less and two of these patients had a history of ventricular fibrillation. The correlation between AERPAP and SRRPE was studied in a separate group of 79 patients with single accessory pathways. There was a significant (p less than .001) but poor (r = .58) correlation between these two variables. Thus, the procainamide test regarding accessory pathway refractoriness often cannot be extrapolated to SRRPE.(ABSTRACT TRUNCATED AT 250 WORDS)
Recommendations for prevention of bacterial endocarditis: compliance by dental general practitioners.
Authors: Sadowsky D , Kunzel C
Published: June 2011

Telephone interviews were conducted with a national sample of general practice dentists (n = 460). Clinical vignettes were used to test clinicians' knowledge of, and compliance with, the 1984 American Heart Association (AHA) recommendations for prevention of bacterial endocarditis. Analyses of the data document a relatively low level of knowledge of correct indications and regimens for antibiotic prophylaxis to prevent endocarditis. Respondents were unsure, and often incorrect, about the relationship between a variety of cardiac conditions and potential risk for endocarditis. Compliance with the guidelines for proper dosage and timing of antibiotics was also problematic. Those clinicians who had a better understanding of patient risk factors and the principles underlying the AHA recommendations were more likely to follow them, as were practitioners who kept a copy of the recommendations in the office. The findings are significant in view of previous suggestions that use of inappropriate antibiotic regimens may predispose to adverse outcomes.
Does desmopressin acetate reduce blood loss after surgery in patients on cardiopulmonary bypass?
Authors: Rocha E , Llorens R , Páramo J A , Arcas R , Cuesta B , Trenor A M
Published: June 2011

It has been suggested that desmopressin acetate (DDAVP) administration reduces blood loss after cardiac surgery. We have investigated the effect of DDAVP administration in a double-blind, randomized, prospective trial including 100 patients placed on cardiopulmonary bypass during surgery. Fifty patients received 0.3 micrograms/kg DDAVP and 50 patients received a placebo administered in a 50 ml saline solution over 15 min when cardiopulmonary bypass had been concluded. Results showed no significant differences either in total blood loss per square meter (458 +/- 206 ml in the DDAVP group vs 536 +/- 304 ml in the placebo group) or in necessity for red cell transfusions (1642 +/- 705 ml in the DDAVP group vs 1574 +/- 645 ml in the placebo group) in the first 72 hr after surgery. Only intraoperative blood loss per square meter was significantly lower (p less than .02) in the DDAVP group (131 +/- 106 ml) as compared with the placebo group (193 +/- 137 ml). The prolongation of bleeding time and the decrease of factor VIII:C and factor VIII:von Willebrand factor 90 min after treatment were significantly lower (p less than .001) in the DDAVP group as compared with the placebo group. We conclude that the administration of DDAVP in patients placed on cardiopulmonary bypass during surgery does not reduce total blood loss and is only effective in reducing intraoperative bleeding.
Cryosurgical ablation of atrioventricular nodal reentry: histologic localization of the proximal common pathway.
Authors: Holman W L , Hackel D B , Lease J G , Ikeshita M , Cox J L
Published: June 2011

A method using cryosurgery has been previously described to selectively ablate atrioventricular nodal reentry tachycardia while preserving intact atrioventricular conduction. The purpose of the present study was to define the histologic features of the cryolesions in relationship to the specialized conduction system. In 12 adult dogs a series of nine discrete cryolesions was placed along the perimeter of the triangle of Koch while continuously monitoring the His bundle electrogram. All animals survived the operation and maintained intact atrioventricular conduction. At 14 weeks after surgery the hearts were sectioned and examined. In all 12 animals there was a confluent mass of dense fibrous tissue present in the lower atrial septum that was in immediate proximity to but did not involve the atrioventricular node-His bundle. The ablation of perinodal tissue with preservation of the specialized conduction system with the use of this cryosurgical technique was confirmed. It is likely that the cryoablated perinodal tissue represents the proximal common pathway of the circuit for atrioventricular nodal reentry tachycardia.
Magnesium suppression of early afterdepolarizations and ventricular tachyarrhythmias induced by cesium in dogs.
Authors: Bailie D S , Inoue H , Kaseda S , Ben-David J , Zipes D P
Published: June 2011

The mechanism by which magnesium therapy suppresses some ventricular tachyarrhythmias characterized by a prolonged QT interval (e.g., torsades de pointes) is unknown. Since early afterdepolarizations have been proposed as a cause of the long QT syndrome and the related ventricular tachyarrhythmias, we hypothesized that magnesium therapy would suppress both the early afterdepolarizations and the ventricular arrhythmias. The present study was performed to test that hypothesis. Using monophasic action potentials (MAP) recorded with a contact electrode from the right ventricular endocardium to demonstrate early afterdepolarizations, cesium chloride (168 mg/kg iv) was administered before, during, and 1 to 2 hr after discontinuation of a magnesium infusion (1 to 2 mg/kg/min for 20 to 30 min). Before magnesium infusion, cesium induced early afterdepolarizations that were 49.7 +/- 1.6% (mean +/- SE) of the amplitude of the corresponding monophasic action potential. The amplitude of the early afterdepolarization decreased to 31.2 +/- 3.8% of the MAP amplitude during magnesium infusion (p less than .003) and increased to 48.0 +/- 4.0% 1 to 2 hr after termination of the magnesium infusion (p less than .003). Cesium induced sustained monomorphic ventricular tachycardia, torsades de pointes, or ventricular fibrillation in 12 of 13 dogs before magnesium infusion, and in eight of 11 dogs 1 to 2 hr after stopping infusion, but in only three of 13 dogs during magnesium infusion. Cesium prolonged the corrected QT interval from 338 +/- 16 msec (control) to 387 +/- 14 msec before (p less than .003), 356 +/- 12 msec during (p less than .003), and 406 +/- 16 msec after stopping the magnesium infusion (p less than .003).(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of pressure-controlled intermittent coronary sinus occlusion on pacing-induced myocardial ischemia in domestic swine.
Authors: Fedele F A , Capone R J , Most A S , Gewirtz H
Published: June 2011

This study tested the hypothesis that pressure-controlled intermittent coronary sinus occlusion (PICSO) would be useful in ameliorating myocardial ischemia under conditions characterized by preserved, but reduced (relative to demand), myocardial blood flow. Studies were conducted in closed-chest, sedated domestic swine prepared with an artificial stenosis that reduced luminal diameter of the animal's left anterior descending coronary artery by 80%. Measurements of hemodynamics, regional myocardial blood flow, and oxygen, lactate, and nucleoside metabolism were obtained in 10 animals (1) before placement of stenosis, (2) 30 min after insertion of stenosis, (3) after 30 and 60 min of PICSO, and (4) 30 min after discontinuation of PICSO. Two groups of control animals were studied to observe the natural history of metabolic markers of ischemia. Control group I consisted of four animals studied concurrently and subjected to the same protocol except for the fact that PICSO was not applied. Control group II consisted of eight additional animals studied as a group. A specially designed balloon-tipped catheter positioned in the proximal portion of the animal's great cardiac vein was used to provide PICSO. Heart rate was controlled by atrial pacing (rate, 145 beats/min) through the study. After placement of the stenosis, flow in endocardial and transmural layers distal to the stenosis declined significantly (p less than .01) vs control. Application of PICSO failed to increase arterial inflow distal to the stenosis in any myocardial layer. Myocardial aerobic metabolism was adversely affected by stenosis and changed from consumption of lactate, inosine, and hypoxanthine before stenosis to production at 30 min after stenosis. Although PICSO was associated with reduced production and a return toward consumption of lactate, inosine, and hypoxanthine, a similar pattern of changes in lactate, inosine, and hypoxanthine metabolism was observed in control animals over a comparable period of time. In addition, regional myocardial oxygen extraction and consumption were not changed vs poststenosis levels by PICSO. However, in comparison with controls, PICSO did accelerate the rate of resolution of myocardial ischemia as assessed by lactate metabolism. At 30 min of PICSO (or sham) the change vs poststenosis was +33.6 +/- 25.0 mumol/min/100 g in the PICSO but only +6.7 +/- 29.7 in the control group (p = .05). We conclude, therefore, that even though PICSO did not alter the final level of myocardial ischemia under conditions modeled in this study it did accelerate its rate of resolution, an effect that may be beneficial clinically.
Measurement of absolute myocardial blood flow with H215O and dynamic positron-emission tomography. Strategy for quantification in relation to the partial-volume effect.
Authors: Iida H , Kanno I , Takahashi A , Miura S , Murakami M , Takahashi K , Ono Y , Shishido F , Inugami A , Tomura N
Published: June 2011

An in vivo technique was developed for measuring the absolute myocardial blood flow with H215O and dynamic positron-emission tomography. This technique was based on a new model involving the concept of the tissue fraction, which was defined as the fraction of the tissue mass in the volume of the region of interest. The myocardium was imaged dynamically by positron-emission tomography, starting at the time of intravenous bolus injection of H215O. The arterial input function was measured continuously with a beta-ray detector. A separate image after C15O inhalation was also obtained for correction of the H215O radioactivity in the blood. The absolute myocardial blood flow and the tissue fraction were calculated for 15 subjects with a kinetic technique under region-of-interest analysis. These results seem consistent with their coronary angiographic findings. The mean value of the measured absolute myocardial blood flows in normal subjects was 0.95 +/- 0.09 ml/min/g. This technique detected a diffuse decrease of myocardial blood flow in patients with triple-vessel disease.
Criteria for two-staged arterial switch operation for simple transposition of great arteries.
Authors: Nakazawa M , Oyama K , Imai Y , Nojima K , Aotsuka H , Satomi G , Kurosawa H , Takao A
Published: June 2011

We analyzed hemodynamic variables in patients with transposition of the great arteries with intact ventricular septum (simple transposition) after pulmonary artery banding and Blalock-Taussig anastomosis to establish the criteria for two-staged arterial switch operation. The study included 35 patients who underwent the switch operation after banding and anastomosis; two died shortly after surgery, and one died of tachycardia 31 days after the operation. The left-to-right ventricular pressure ratio was above 0.83 in all surviving patients, 0.68 and 0.63 in the two operative deaths, and 0.84 in the other death. In the 32 surviving patients, angiographically determined left ventricular (LV) end-diastolic volume and ejection fraction averaged 147 +/- 46(SD)% of normal and 0.64 +/- 0.12, respectively. We also measured LV mass using angiographic LV semiaxes and end-diastolic LV posterior wall thickness obtained from an echocardiogram. These variables of the patients who died were not different from those of the surviving patients. The wall thickness was greater than 4 mm in the surviving patients, while it was 3.5 mm in the two patients who died early and 5 mm in the patient who died later. From the semiaxes, the wall thickness, and aortic diastolic pressure, all of which were obtained before the anatomic repair, we calculated the predictive LV wall stress. This wall stress would indicate the LV wall stress at the time of aortic valve opening immediately after the arterial switch operation. Predictive wall stress was less than 120 x 10(3) dynes/cm2 in all but one of the surviving patients, whereas it was 151, 153, and 186 x 10(3) dynes/cm2 in the three patients who died.(ABSTRACT TRUNCATED AT 250 WORDS)
Treatment of canine embolic pulmonary hypertension with recombinant tissue plasminogen activator. Efficacy of dosing regimes.
Authors: Shiffman F , Ducas J , Hollett P , Israels E , Greenberg D , Cook R , Prewitt R M
Published: June 2011

We investigated effects of two dosing regimes of recombinant tissue plasminogen activator (rt-PA) and sodium heparin on pulmonary thrombolysis in a canine model of pulmonary hypertension, induced by injection of radioactive blood clots. By continuously counting over both lung fields with a mobile gamma camera, we correlated rate and extent of pulmonary thrombolysis with corresponding pulmonary hemodynamics. Treatment with heparin, over a 3-hour interval, did not result in significant thrombolysis or in a decrease in mean pulmonary artery pressure (PAP). In contrast, rt-PA caused marked pulmonary thrombolysis. While total clot lysis was similar when 1 mg/kg rt-PA was infused over 15 (rt-PA15) or 90 (rt-PA90) minutes (47% and 42%, respectively), rate of lysis during infusion was markedly increased with rt-PA15 (56% vs. 27%/hr, p less than 0.001). Corresponding to the increased rate of thrombolysis with rt-PA15, relative PAP decrease was greater at 15 and 30 minutes. At 4 hours, PAP decreased most with rt-PA90. However, two of the six dogs given rt-PA15 had an increase in PAP and lung radioactivity 1 hour after rt-PA. This was associated with dislodgment of a previously trapped clot. These results suggest that rt-PA may be appropriate therapy for pulmonary embolism and support further studies designed to optimize dosing regimes.
Verapamil and tiapamil in prevention of ventricular fibrillation in pigs with coronary ligation. Comparative effects on left ventricular function.
Authors: Muller C A , Opie L H , Hamm C W , Peisach M , Pineda C A , Thandroyen F T
Published: June 2011

Antiarrhythmic and hemodynamic effects of the calcium channel antagonist verapamil were compared with those of tiapamil, a congener, in open-chest pigs with anterior descending coronary artery ligation. Tiapamil (6 mg/kg i.v.) decreased the incidence of ventricular fibrillation to 4 of 10 versus 22 of 25 in controls (p less than 0.05) and maintained left ventricular dP/dtmax after ligation (predrug value: 2,312 +/- 112 mm Hg/sec; 20 minutes after ligation: 2,139 +/- 229 mm Hg/sec). Tiapamil increased blood flow in the peripheral ischemic zone (24 +/- 3.2% vs. 16.9 +/- 1.6% of preligation value in controls, p less than 0.05) as well as in the peri-ischemic and nonischemic zones (153.9 +/- 12.7% and 186.3 +/- 17.1%, respectively; both p less than 0.0001 vs. 97.9 +/- 5% and 91.3 +/- 4.7% in controls). Verapamil (0.6 mg/kg i.v.) decreased the incidence of ventricular fibrillation to 0 of 7 versus 22 of 25 in controls (p less than 0.005); left ventricular dP/dtmax decreased from 2,062 +/- 144 to 1,060 +/- 168 mm Hg/sec (p less than 0.0001). Verapamil did not change blood flow in the peripheral, peri-ischemic, or nonischemic zones. Thus, tiapamil, and not verapamil, decreased ischemic ventricular fibrillation while maintaining left ventricular mechanical function. Verapamil congeners warrant further evaluation as antiarrhythmic agents in acute myocardial ischemia.
Effects of lower-body negative pressure on sympathetic nerve responses to static exercise in humans. Microneurographic evidence against cardiac baroreflex modulation of the exercise pressor reflex.
Authors: Scherrer U , Vissing S F , Victor R G
Published: June 2011

Although previous studies in both animals and humans have suggested that cardiac baroreceptors modulate reflex sympathetic vasoconstriction during exercise, more recent studies in conscious animals have not supported this view. To further test this concept in humans, we measured sympathetic nerve discharge with intraneural microelectrodes while we used static handgrip to activate the exercise pressor reflex and nonhypotensive lower-body negative pressure (LBNP) to selectively unload the cardiac baroreflex. In nine healthy subjects, we measured blood pressure, heart rate, central venous pressure, and muscle sympathetic nerve activity (MSNA) from the peroneal nerve (resting leg) during 2 minutes of static handgrip at 20% and 30% of maximal voluntary contraction (MVC) alone and in combination with LBNP at -5 mm Hg. Handgrip alone (exercise reflex) at 20% and 30% MVC caused graded increases in MSNA. LBNP alone (cardiac reflex) did not alter blood pressure or heart rate but decreased central venous pressure by 2.5 +/- 0.1 mm Hg (mean +/- SEM, p less than 0.05) and increased MSNA by 92 +/- 22% over the control value. Most important, handgrip performed during LBNP (interaction of reflexes) caused increases in MSNA that were comparable with the increases during handgrip alone: +114 +/- 32% versus +175 +/- 89% at 20% MVC and +328 +/- 101% versus +431 +/- 110% at 30% MVC (handgrip plus LBNP vs. handgrip alone, p greater than 0.1). Pressor and heart rate responses to handgrip also were unaffected by LBNP. In five additional experiments, comparable findings were obtained when the LBNP was superimposed on handgrip rather than handgrip being superimposed on LBNP. In conclusion, this study provides direct evidence in humans that nonhypotensive LBNP does not augment muscle sympathetic outflow during static handgrip and challenges the concept of an important interaction between cardiac baroreceptor and exercise pressor reflexes during this form of exercise.
Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.
Authors: Brown K A , Ditchey R V
Published: June 2011

This study was undertaken to determine 1) whether a combined radionuclide-hemodynamic technique could define the right ventricular end-systolic pressure-volume relation (RV ESPVR) in the clinical setting, 2) whether the human RV ESPVR defined by maximal elastance is linear and responsive to inotropic interventions, and 3) whether more easily measured modifications of the ESPVR are reliable substitutes as an index of RV function. Eight patients with normal RV function were studied with simultaneous micromanometer RV pressure measurements and radionuclide ventriculography to construct RV pressure-volume loops. Data were collected at baseline and after at least two alterations in loading conditions with nitroglycerin, phenylephrine, or saline. End systole was defined by maximal elastance (E(t) = P(t)/[V(t) - V0]). Data were also obtained during administration of dobutamine in four patients and after atrial pacing tachycardia in one patient. The RV ESPVR defined by maximal elastance was highly linear (r = 0.988-0.999) throughout the range of pressures and volumes tested. Furthermore, the linear correlations were significantly higher (p less than 0.005), and the linear regression standard error of the estimate (SEE) was significantly lower (p less than 0.005) for the RV ESPVR defined by maximal elastance compared with modifications of the ESPVR with the ratio of pulmonary artery-dicrotic notch pressure or RV peak pressure to end-ejection volume. Dobutamine or atrial pacing tachycardia produced a leftward shift of the entire RV pressure-volume loop, and in each patient (five of five), the point of maximal elastance fell outside the 95% confidence interval defined by the baseline ESPVR. However, because of the larger SEE, the leftward shift with modifications of the ESPVR was not statistically significant in any patient by the pulmonary artery-dicrotic notch pressure: end-ejection volume ratio and was significant in only one of five patients by the RV peak pressure: end-ejection volume ratio (p less than 0.03). Therefore, it appears that the steady-state RV ESPVR defined by maximal elastance in patients with normal RV function is responsive to alterations in inotropic state and is more sensitive to alterations in RV function than the frequently used, more easily measured modifications of the RV ESPVR.
Spontaneous variability of simple and complex ventricular premature contractions during long time intervals in patients with severe organic heart disease.
Authors: Schmidt G , Ulm K , Barthel P , Goedel-Meinen L , Jahns G , Baedeker W
Published: June 2011

Calculations of the spontaneous variability of ventricular arrhythmias are usually based upon the results of Holter electrocardiograms recorded either successively or separated by a short time interval. Only recently was it shown that the variability of ventricular premature contractions increases with longer intervals. This study was undertaken to investigate the variability of simple and complex ventricular arrhythmias over long periods to derive efficacy criteria for long-term antiarrhythmic therapy. In a prospective study, the influence of the length of the time interval on spontaneous variability was investigated in 100 patients with coronary artery disease or idiopathic dilated cardiomyopathy and untreated ventricular arrhythmia Lown grade IV. Patient follow-up was carried out for 260 +/- 387 days. In each of the 498 ambulatory Holter tapes, the mean hourly arrhythmia count (AC) of ventricular premature contractions, couplets, and salvos was verified. The variability of arrhythmia counts between two Holter electrocardiograms was defined as the logarithm of the ratio of (ACday 2 + 0.01) to (ACday 1 + 0.01). The 95% intervals for these ratios were calculated as +/- 2 SD, considering the fact that all mean values did not differ significantly from zero. The lower limit of these intervals refers to the reduction that is required for assuming drug efficacy, whereas the upper limit refers to an aggravation. The 95% intervals were calculated for each of four ranges of control intervals (0-6, 7-89, 90-364, and greater than or equal to 365 days). They increased significantly with longer control intervals.(ABSTRACT TRUNCATED AT 250 WORDS)
Ischemic heart disease mortality in Hispanics, American Indians, and non-Hispanic whites in New Mexico, 1958-1982.
Authors: Becker T M , Wiggins C , Key C R , Samet J M
Published: June 2011

To describe trends in mortality from ischemic heart disease in New Mexico's Hispanic, American Indian, and non-Hispanic white populations, we used vital records data collected from 1958 through 1982. We calculated age-adjusted and age-specific mortality rates for ischemic heart disease for each of the state's principal ethnic groups. Death certificate data were used in combination with population estimates based on the censuses of 1960, 1970, and 1980. Age-adjusted mortality rates for ischemic heart disease among Hispanics, American Indians, and non-Hispanic white men were consistent with nationwide patterns of rising mortality rates during the 1960s followed by declining rates. Mortality rates from ischemic heart disease in all three ethnic groups in New Mexico were lower than national rates for whites. Rates for Hispanics in New Mexico were lower than for non-Hispanic whites; rates for American Indians were the lowest among the three groups. These data support previous observations that Hispanics and American Indians in the Southwest are at decreased risk for mortality from ischemic heart disease in comparison with U.S. whites.
Lack of involvement of thromboxane A2 in postischemic recovery of stunned canine myocardium.
Authors: Farber N E , Pieper G M , Gross G J
Published: June 2011

Modification of the thromboxane: prostacyclin ratio alters the severity of reperfusion arrhythmias and postischemic damage in long-term, irreversibly injured myocardium. In this study, the effects of the thromboxane synthetase inhibitor dazmegrel and the thromboxane receptor antagonist BM 13.505 on myocardial postischemic functional recovery and preservation of tissue adenine nucleotides was examined after a 15-minute episode of ischemia followed by 3 hours of reperfusion (myocardial stunning). Dazmegrel (3 or 8 mg/kg) or BM 13.505 (10 mg/kg) was given 15 minutes before coronary occlusion and compared with a control group in barbital-anesthetized dogs. Regional segment shortening (percent segment shortening, sonomicrometry), regional myocardial blood flow (microspheres), and coronary venous eicosanoid and high-energy phosphate levels (biopsies after 3 hours of reperfusion) were measured. Areas at risk, regional myocardial blood flow, and regional segment shortening during coronary occlusion were similar in all groups. Dazmegrel (3 mg/kg) attenuated the decrease in endocardial and midmyocardial adenosine 5'-triphosphate, and both doses significantly improved regional segment shortening during reperfusion. Coronary venous thromboxane levels were significantly decreased throughout the experiment in both dazmegrel-treated groups, and thromboxane levels were significantly elevated in the control group 3 hours after reperfusion. Prostacyclin, measured in the form of its main metabolite, 6-keto-prostaglandin F1 alpha, did not change significantly in the control group throughout the experiment, but it was markedly increased in dazmegrel groups throughout reperfusion, particularly in the dazmegrel group receiving 3 mg/kg. BM 13.505 exerted no beneficial effects on postischemic function or metabolism. In conclusion, after a reversible ischemic insult, postischemic recovery of function and metabolic status was not enhanced by preocclusion treatment with a thromboxane receptor blocker, and thus, the beneficial effects of thromboxane synthesis inhibition on postischemic abnormalities was not due to a reduction in thromboxane but was the result of endoperoxide shunting and a subsequent increase in prostacyclin. Therefore, thromboxane does not appear to be an important mediator of reversible ischemia-reperfusion damage.
No reflow and extent of infarction during maximal vasodilation in the porcine heart.
Authors: Johnson W B , Malone S A , Pantely G A , Anselone C G , Bristow J D
Published: June 2011

To explore the relation between myocardial and vascular injury in the generation of the no-reflow phenomenon, the pressure-flow relation during maximal vasodilation after coronary artery reperfusion was studied in the open-chest porcine model. During both endogenous and maximal vasodilation with intracoronary adenosine, pressure-flow (P/Q) plots were constructed before and after 20-minute (n = 9) or 40-minute (n = 17) circumflex artery occlusions. Decreases in circumflex vascular bed conductance were represented by downward shifts in P/Q plot regression lines. No significant change occurred in P/Q line slope or pressure at zero flow 30 minutes after release of the 20-minute occlusion, and no infarction was found. After release of the 40-minute occlusion, a small but insignificant decrease in P/Q line slope occurred during endogenous vasodilation. However, during maximal vasodilation, a significant (p less than 0.01) decrease in P/Q line slope was present during reperfusion compared with preocclusion corresponding to a decrease in vasodilatory reserve (P/Q line slope = 1.52 +/- 0.14 ml/min/mm Hg preocclusion vs. 1.03 +/- 0.13 at 15 minutes reperfusion). Pretreatment with aspirin did not prevent this decrease in vascular conductance during maximal vasodilation. Total circumflex, as well as subendocardial, midmyocardial, and subepicardial blood flows, was measured with radioactive microspheres. There was a good correlation between the extent of infarction measured by triphenyltetrazolium chloride staining and the decrease in vascular conductance during maximal vasodilation for all three myocardial layers as well as for the total circumflex vascular bed. Hence, the degree of no-reflow correlates closely with the extent of infarction during maximal vasodilation (but not during endogenous vasodilation) and is not altered by aspirin therapy.
Endogenous sex hormones and cardiovascular disease in men. A prospective population-based study.
Authors: Barrett-Connor E , Khaw K T
Published: June 2011

Plasma obtained and frozen in 1972-1974 from 1,009 white men (40-79 years old) who have been followed for 12 years was examined for endogenous sex hormone levels according to prevalent or subsequent cardiovascular disease. In these older men, no sex hormone measured (testosterone, androstenedione, estrone, or estradiol) was significantly associated with known cardiovascular disease at baseline or with subsequent cardiovascular mortality or ischemic heart disease morbidity or mortality. Sex hormone-binding globulin levels were also similar by disease status. Analyses of hormone:sex hormone-binding globulin ratios or of estrogen:androgen ratios showed a similar lack of association with cardiovascular disease. Testosterone levels were significantly inversely associated with levels of blood pressure, fasting plasma glucose, and triglyceride and body mass index. In contrast, the only significant estrogen risk factor associations were positive correlations of estrone with total plasma cholesterol, triglyceride, and glucose. These data do not support a causal role for elevated endogenous estrogen levels and heart disease.
Intra-arterial stenting in the atherosclerotic rabbit.
Authors: Robinson K A , Roubin G S , Siegel R J , Black A J , Apkarian R P , King S B
Published: June 2011

The major problem associated with percutaneous transluminal coronary angioplasty is recurrence of the stenotic lesion. Balloon catheter-mounted intracoronary stent devices may reduce restenosis by improving luminal morphology and flow characteristics. This study assessed the effects of a stainless steel wire, interdigitating coil stent on restenosis in the atherosclerotic rabbit model. Fifteen cholesterol-fed rabbits with preexisting iliac arterial lesions induced by balloon deendothelialization were instrumented in one iliac artery with a 2.0-mm diameter stent after balloon dilatation; the contralateral iliac lesion was treated by dilatation only to serve as a control. The animals were given heparin with aspirin (60 mg) and aspirin every 3rd day until death. Arteriography was repeated 4 weeks after stenting, just before death. Tissue sections from stented and control arterial segments were analyzed morphometrically. Stented arteries had a significantly larger luminal diameter at restudy, whether measured by arteriography (1.38 +/- 0.19 vs. 0.94 +/- 0.35 mm, p less than 0.01) or from tissue sections (1.26 +/- 0.18 vs. 0.81 +/- 0.30 mm, p = 0.0001). Wall thickness of the stented segment was slightly, but significantly, less than the control segment (436 +/- 143 vs. 532 +/- 221 microns, p less than 0.05). Scanning electron microscopy of five stented atherosclerotic rabbit aortas revealed regeneration of a nonthrombogenic, confluent, flow-directed endothelium by 4 weeks after placement. Intra-arterial stenting may be of benefit in the prevention of restenosis by the preservation of a larger functional lumen and by a decrease in the neointimal hyperplastic response to arterial injury.