bluuebunny/crossref_metadata_2025 huggingface dataset:
Spontaneous changes in left ventricular function over the first 24 hours of acute myocardial infarction: implications for evaluating early therapeutic interventions.
Authors: Wackers F J , Berger H J , Weinberg M A , Zaret B L
Published: June 2011

The spontaneous changes in left ventricular ejection fraction (LVEF) during the first 24 hours of a first transmural infarction were assessed in 34 patients by serial gated cardiac blood pool imaging. Major therapeutic interventions with a view to limit infarct size were not used. Four determinations of LVEF were performed. Study 1 was performed as soon as possible after admission to the hospital. Studies 2 and 3 were performed 2 and 4 hours, respectively, after study 1. Twenty-four patients (70%) had study 1 within 6 hours after the onset of acute chest pain and 10 had it 6-12 hours after the onset of chest pain. Study 4 was performed 24 hours after the onset of chest pain. Compared with study 1, 19 of 34 patients (56%) had spontaneous changes in LVEF in at least one of the subsequent studies, exceeding the expected variability in stable patients. The changes ranged from a 32% increase to 14% absolute decrease. LVEF improved in 11 patients and deteriorated in eight. These spontaneous changes in left ventricular performance indicate that a single assessment of LVEF during the early hours of transmural myocardial infarction may not properly characterize cardiac performance in an individual patient and may not be the most appropriate reference against which to compare subsequent evolution of left ventricular function. These data may have implications for studies of the effects of early therapeutic interventions on LVEF.
Evaluation of tricuspid regurgitation by pulsed Doppler and two-dimensional echocardiography.
Authors: Miyatake K , Okamoto M , Kinoshita N , Ohta M , Kozuka T , Sakakibara H , Nimura Y
Published: June 2011

We analyzed tricuspid regurgitation noninvasively using ultrasonic pulsed Doppler and two-dimensional echocardiography in 66 patients in whom tricuspid regurgitation was suspected from routine clinical evaluation. All of the patients also underwent right ventriculography. Ten healthy subjects served as controls. In 62 of 66 patients, the study was adequately performed. In 58 of 62 patients, pansystolic abnormal Doppler signals were detected in the right atrial cavity, and were interpreted to indicate tricuspid regurgitant flow. Two-dimensional echocardiograms in the parasternal four-chamber view demonstrated that the region in which the abnormal Doppler signals were detected was spindle-shaped and extended from the tricuspid orifice toward the right atrial posterior wall parallel to the interatrial septum. The severity of regurgitation was graded on a four-point scale, based on the distance reached by the abnormal signals from the tricuspid orifice toward the posterior wall. For comparison, the right ventriculograms were evaluated on a four-point scale similar to the Sellers classification of mitral regurgitation. The grades by the two methods matched exactly in 36 cases, differed by one level in 23 and by two levels in three. Thus, the two methods showed a good correspondence. Similar results were obtained for the grading based on the area covered by the abnormal signals. We conclude that noninvasive grading of tricuspid regurgitation by ultrasonic pulsed Doppler and two-dimensional echocardiography is practicable.
"Sawfish" systolic narrowing of the left anterior descending coronary artery: an angiographic sign of hypertrophic cardiomyopathy.
Authors: Brugada P , Bär F W , de Zwaan C , Roy D , Green M , Wellens H J
Published: June 2011

The morphologic characteristics at coronary arteriography of systolic narrowing of the left anterior descending coronary artery (LAD) were evaluated in 14 patients. Six patients had systolic narrowing of the LAD not associated with other cardiac abnormalities (group A) and eight patients had systolic narrowing of the LAD associated with hypertrophic cardiomyopathy (group B). Patients in group A showed a smooth and progressive constriction of the vessel up to the point of maximal stenosis, giving it a "rat-tail" appearance. There was no systolic narrowing of septal branches or of other epicardial vessels in this group. In patients of group B, systolic narrowing of the LAD had a "saw-fish" appearance. Seven patients had systolic narrowing of the septal branches, and five had systolic narrowing of other epicardial vessels. These data indicate that systolic narrowing of the LAD in patients with hypertrophic cardiomyopathy differs angiographically from systolic narrowing due to an intramural course of a part of the vessel (as in group A patients). We postulate that in patients with hypertropic cardiomyopathy, fiber hypertrophy and disarray in the vicinity of the coronary vessels is responsible for the morphology and the widespread distribution of systolic narrowing.
Congenital aneurysms of the left atrium: recognition by cross-sectional echocardiography.
Authors: Foale R A , Gibson T C , Guyer D E , Gillam L , King M E , Weyman A E
Published: June 2011

The two-dimensional echocardiographic features of three patients with congenital aneurysms of the left atrium are described. The aneurysm arose from the left atrial appendage in two patients and from the posterior left atrial wall in one. The aneurysms were characterized by their origin from an otherwise normal left atrium, a well-defined neck, their position within the pericardial space, and distortion of the left ventricular free wall by the aneurysmal body. The differentiation of these structures from other abnormalities of the left atrium are also discussed. Two-dimensional echocardiography is a safe and reliable method for diagnosing congenital aneurysm of the left atrium, and such studies should be considered in any patient with an otherwise unexplained abnormality on the chest radiograph.
Antibiotic prophylaxis of subacute bacterial endocarditis for adult patients by dentists in Dade County, Florida.
Authors: Hashway T , Stone L J
Published: June 2011

To determine compliance with 1977 American Heart Association (AHA) recommendations for antibiotic prophylaxis (AbP) of subacute bacterial endocarditis (SBE), we mailed a questionnaire to 1019 licensed dentists from Dade County, Florida. Of the 614 practicing dentists who responded, 97.7% believe that AbP prevents SBE and 94.2% always obtain a cardiac history from new patients. AbP is given to patients with known rheumatic or other valvular heart disease by 98.9% of responders and to patients with known prosthetic heart valves by 81.5%. The majority of dentists prescribe the antibiotics recommended by the AHA, but the dosage, route, frequency and duration of therapy are usually not according to AHA guidelines. AbP completely consistent with these guidelines is prescribed by 15.4% of dentists for patients with heart disease and by only 6.7% of dentists for patients with prosthetic heart valves. The AHA recommends parenteral AbP for most patients with prosthetic heart valves, but approximately 80% of dentists use only oral agents for these patients. We conclude that most dental patients predisposed to SBE receive AbP, but not in accordance with AHA guidelines. The widest deviation occurs among patients with prosthetic heart valves.
Percutaneous transluminal coronary angioplasty immediately after intracoronary streptolysis of transmural myocardial infarction.
Authors: Meyer J , Merx W , Schmitz H , Erbel R , Kiesslich T , Dörr R , Lambertz H , Bethge C , Krebs W , Bardos P , Minale C , Messmer B J , Effert S
Published: June 2011

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 21 patients with acute myocardial infarction (AMI) treated by intracoronary infusion of streptokinase within 8 hours after the onset of symptoms. Streptolysis therapy began a mean of 3.6 +/- 1.2 hours (+/- SD) after the onset of symptoms. The vessel was occluded in 14 patients and highly stenosed in seven. After the infusion of 67,300 +/- 63,200 IU of streptokinase over 26.1 +/- 21.5 minutes, patency of the occluded vessels was reached. PTCA as performed 20-60 minutes after the end of streptokinase treatment in 19 patients and 24 and 31 hours after treatment in two patients. The dilation was successful in 17 patients (81%). The degree of vessel obstruction was reduced from 90.2 +/- 7.3% to 58.6 +/- 19.5% (area method) and from 71.4 +/- 12.4% to 39.2 +/- 19.7% (diameter method). The improvement was 31.5 +/- 18.4% and 32.2 +/- 19.3%, respectively. No reocclusion was induced by PTCA. Twenty patients were discharged. One died during hospitalization; at autopsy, the treated vessel was still patent. During the follow-up period, two reinfarctions and one asymptomatic reocclusion occurred. The clinical findings during the hospital course and the follow-up period were compared with those of a control group of 18 patients with AMI and comparable coronary stenoses who were treated only with streptokinase infusion. Four of these patients had a reinfarction during the hospital course, and three died during the follow-up period. PTCA can be performed safely and successfully immediately after intracoronary infusion of streptokinase in patients with AMI. By reducing the subtotal stenosis, this treatment contributes to the reperfusion of the ischemic myocardium, diminishes the risk of a reocclusion and seems to improve the prognosis.
Relations between myocardial blood flow and postextrasystolic potentiation in epicardial and endocardial left ventricular regions early after coronary occlusion in dogs.
Authors: Crozatier B
Published: June 2011

Postextrasystolic potentiation was studied during control and 5 minutes after coronary occlusion in epicardial regions of 12 open-chest dogs. Segmental behavior evaluated with ultrasonic crystals was correlated with regional myocardial blood flow (MBF) measured with radioactive microspheres. A similar correlation was found between the percentage of systolic shortening in postextrasystolic beats and MBF in epicardial (r = 0.64) and endocardial (r = 0.97) regions, although the scatter was much larger in the epicardium. The correlation was similar when segmental function was expressed as the area of the pressure-segment length loop. Three types of segments were described; completely ischemic segments (transmural MBF less than 5% of control), in which end-systolic length was larger than end-diastolic length after postextrasystolic potentiation; severely ischemic segments (5% less than or equal to transmural MBF less than 25% of control), in which the ischemic bulge during control beats was replaced by active shortening after premature ventricular complexes; and marginal segments (25% less than or equal to transmural MBF less than 100% of control), in which depressed shortening was enhanced close to control after a premature ventricular complex. These data reconcile conflicting studies, which did not consider similar degrees of ischemia and show a rapid loss of postextrasystolic potentiation in completely ischemic segments.
The natural history of left ventricular hypertrophy in hypertrophic cardiomyopathy: an electrocardiographic study.
Authors: McKenna W J , Borggrefe M , England D , Deanfield J , Oakley C M , Goodwin J F
Published: June 2011

The natural history of electrocardiographic left ventricular hypertrophy was assessed in relation to clinical features, treatment with propranolol and prognosis in 100 patients with hypertrophic cardiomyopathy who were followed 5--20 years (mean 8 years). Seventy-one patients received propranolol, 120--800 mg/day (mean 240 mg). At diagnosis, the voltage measurement from SV1 + RV5 was 37 +/- 20 mm, the R wave in aVL was 12 +/- 6 mm and the mean frontal plane voltage was 15 +/- 10 mm. After 5 years, these values were increased to 43 +/- 22 mm (p less than 0.0002), 14 +/- 6 mm (p less than 0.003) and 17 +/- 10 mm (p less than 0.01), respectively. Neither a left ventricular outflow tract gradient nor propranolol treatment influenced these voltage changes. Twenty patients had an increase of more than 10 mm in SV1 + RV5, which was associated with exertional chest pain (p less than 0.006) and death (p less than 0.02). Four patients had a decrease of more than 10 mm in SV1 + RV5. Two of these received high-dose propranolol, one 720 mg/day for 12 years and another 800 mg/day for 12 years. No other patient received more than 480 mg of propranolol daily. In hypertrophic cardiomyopathy there is electrocardiographic evidence of progressive hypertrophy, which is associated with poor prognosis and is not influenced by treatment with propranolol in moderate dosage. Regression of hypertrophy is rare and may be related to long-term treatment with high-dose propranolol.
Digoxin-quinidine interaction in patients with chronic renal failure.
Authors: Fenster P E , Hager W D , Perrier D , Powell J R , Graves P E , Michael U F
Published: June 2011

We evaluated the effect of quinidine on digoxin pharmacokinetic in six patients with severe renal failure. Quinidine reduced the total body clearance of digoxin from 1.87 to 1.06 l/hour (p less than 0.001), and prolonged the digoxin half-life of elimination from 5.20 to 9.61 days (p less than 0.01). The digoxin volume of distribution was unchanged. Renal clearance of digoxin was negligible; thus, the decrease in total body clearance was due to a decrease in the nonrenal clearance of digoxin. The mean trough serum concentrations of quinidine ranged from 1.0 to 3.0 micrograms/ml. We conclude that in patients with chronic renal failure, the dose of digoxin should be decreased by 50% if quinidine therapy is initiated.
Echocardiographic identification of right-sided cardiac intracavitary thromboembolus in massive pulmonary embolism.
Authors: Starkey I R , de Bono D P
Published: June 2011

In a patient with clinical features of massive pulmonary embolism, two-dimensional echocardiography demonstrated an echo-dense mass moving freely across the tricuspid valve between the right atrium and right ventricle. This mass was also visualized at angiography, which in addition confirmed extensive pulmonary embolism. At autopsy, the mass was found to be a coiled thrombus, one end of which had become wedged in a probe-patent foramen ovale. In another patient, bedside echocardiographic demonstration of thrombus in the right ventricular outflow tract was followed by immediate and successful embolectomy.
Clinical and echocardiographic features of pulmonary valve endocarditis.
Authors: Nakamura K , Satomi G , Sakai T , Ando M , Hashimoto A , Koyanagi H , Hirosawa K , Takao A
Published: June 2011

We studied the clinical and echocardiographic features of eight patients with infective pulmonary valve endocarditis. In two patients, the vegetation was limited to the pulmonary valve; in the six other patients, infective lesions were also present on the mitral or aortic valves. None of the patients were addicted to narcotics. Seven of the eight patients had underlying congenital heart disease. In six patients the organism responsible for the infective endocarditis was Streptococcus viridans. Two-dimensional echocardiography performed using a wide-angle sector scanner was more useful than M-mode echocardiography for evaluating patients with pulmonary valve endocarditis.
Impaired function of salvaged myocardium: two-dimensional echocardiographic quantification of regional wall thickening in the open-chest dog.
Authors: Blumenthal D S , Becker L C , Bulkley B H , Hutchins G M , Weisfeldt M L , Weiss J L
Published: June 2011

This study was designed to examine the functional properties of myocardium subjected to acute coronary occlusion but surviving the ischemic insult. Ten conscious mongrel dogs underwent mild-circumflex coronary occlusion and were treated for 6 hours with prostacyclin, 540 ng/kg/min, and ibuprofen, 110 micrograms/kg/min, or dipyridamole (7-9.7 micrograms/kg/min). At 7 days, each dog was anesthetized, the chest was opened, and cross-sectional two-dimensional echocardiograms were obtained through the middle of the occluded vascular bed. A computer-aided contouring system was used to assess percent systolic thickening in 16 equally spaced segments around the left ventricle. Metal markers sewn to the epicardium permitted precise regional correlation of histology, percent systolic thickening, and flow, as measured by radioactive microspheres. Necrosis was minimal, averaging only 2.2 +/- 0.8% (+/- SEM) of the left ventricular ring corresponding to the echocardiographic cross section. Percent systolic thickening was 28.6 +/- 4.7 in the nonischemic anterior wall, but was reduced to -4.5 +/- 3.1 in the occluded bed (p less than 0.01). In individual echo segments, percent systolic thickening correlated with local flow (r = 0.69, p less than 0.001), but was still depressed even when flow was normal. In six segments within the occluded bed that had normal histology and flow, percent systolic thickening was 52% less than that in the nonischemic region (p less than 0.02). Thus, coronary artery occlusion combined with drug treatment results in myocardium that, although histologically normal and supplied by normal myocardial blood flow, remains functionally abnormal 7 days after occlusion.
The response to procainamide during electrophysiologic study for sustained ventricular tachyarrhythmias predicts the response to other medications.
Authors: Waxman H L , Buxton A E , Sadowski L M , Josephson M E
Published: June 2011

We evaluated 126 patients with inducible sustained ventricular tachyarrhythmias to assess whether the response to procainamide during electrophysiologic study could predict responses to other conventional antiarrhythmic agents and combinations of agents. Thirty of 42 patients in whom tachycardia was not inducible after the administration of procainamide and 69 of 84 patients in whom ventricular tachycardia was inducible after procainamide underwent serial electrophysiologic studies. Forty-three of 67 antiarrhythmic regimens (64%) tested in the patients in whom ventricular tachycardia could not be induced after procainamide prevented induction of ventricular tachycardia, compared with 10 of 145 regimens (7%) tested in the patients in whom ventricular tachycardia could be induced after procainamide. Sixty of the 69 patients in whom ventricular tachycardia remained inducible after procainamide had ventricular tachycardia induced on all other conventional antiarrhythmic regimens tested. By comparison, of the 30 patients in whom ventricular tachycardia became noninducible after procainamide, 25 had no ventricular tachycardia inducible on at least one other antiarrhythmic regimen tested. Thus, the response to procainamide accurately predicted the response to other conventional antiarrhythmic agents during electrophysiologic study.
Mechanism of relief of pacing induced angina with oral verapamil: reduced oxygen demand.
Authors: Rouleau J L , Chatterjee K , Ports T A , Doyle M B , Hiramatsu B , Parmley W W
Published: June 2011

To evaluate the influence of oral verapamil (80 and 120 mg) on angina threshold, coronary blood flow, myocardial oxygen consumption and left ventricular function, we subjected 13 patients with effort angina and fixed obstructive coronary artery disease to atrial pacing at progressively higher heart rates. After 120 mg of verapamil, the time to onset of angina and the heart rate at the onset of ST-segment depression increased by 18% (p less than 0.005) and 10% (p less than 0.001), respectively, without any change in the angina threshold (rate-pressure product at the onset of angina). The rate-pressure product, coronary blood flow and myocardial oxygen consumption were lower at rest and at pre-angina heart rates but not when the angina threshold was reached. Thus, the beneficial effect of verapamil was primarily due to decreased myocardial oxygen demand rather than to increased coronary blood flow. The decreased demand resulted from a lower arterial pressure at each pacing rate. In these patients without heart failure, left ventricular pump function did not deteriorate. This beneficial response was less with 80 mg of oral verapamil. These findings suggest that oral verapamil has a potential role in the management of patients with effort angina due to fixed obstructive coronary artery disease.
Regional blood flow during cardiopulmonary resuscitation in dogs using simultaneous and nonsimultaneous compression and ventilation.
Authors: Luce J M , Ross B K , O'Quin R J , Culver B H , Sivarajan M , Amory D W , Niskanen R A , Alferness C A , Kirk W L , Pierson L B , Butler J
Published: June 2011

We studied regional blood flow (QR) using radiolabeled microspheres and measured hemodynamic variables in 20 anesthetized dogs in normal sinus rhythm and during ventricular fibrillation treated with cardiopulmonary resuscitation (CPR). Nonsimultaneous compression and ventilation CPR (NSCV-CPR) was performed in seven dogs with a pneumatic piston that gave 50 chest compressions/min with an open airway with 10 ventilations at an airway pressure of 33 mm Hg interposed between each fifth and sixth compression. Simultaneous compression and ventilation (SCV-CPR) was performed in seven dogs with the piston and in six other dogs with a circumferential pneumatic vest. Both devices gave 30 compressions/min simultaneously with 30 ventilations that elevated airway pressure to 80 mm Hg., The abdomen was bound during SCV-CPR. Regional blood flow (mean +/- SD) to the cerebral hemispheres, cardiac ventricles, and kidneys, expressed as ml/min/100 g tissue, was 3.1 +/- 4.0, 3.4 +/- 3.3 and 1.5 +/- 1.5, respectively, during NSCV-CPR; 11.5 +/- 5.9, 4.9 +/- 4.7 and 2.7 +/- 2.7 during SCV-CPR (vest); and 16.2 +/- 7.2, 11.0 +/- 4.0 and 20.1 +/- 20.2 during SCV-CPR (piston) (all p less than 0.05 compared with NSCV-CPR). These results indicate that QR to all organs studied is reduced below normal sinus rhythm levels during CPR for ventricular fibrillation, QR to the brain is proportionately greater than QR to the heart and kidneys, and QR to the brain is greater with both forms of SCV-CPR than with NSCV-CPR.
Outcome in one-vessel coronary artery disease.
Authors: Califf R M , Tomabechi Y , Lee K L , Phillips H , Pryor D B , Harrell F E , Harris P J , Peter R H , Behar V S , Kong Y , Rosati R A
Published: June 2011

We analyzed the clinical outcomes in 688 patients with isolated stenosis of one major coronary artery. The survival rate among patients with disease of the right coronary artery (RCA) was higher than that among patients with left anterior descending (LAD) or left circumflex coronary artery (LCA) disease. The survival rate among patients in all three anatomic subgroups exceeded 90% at 5 years. The presence of a lesion proximal to the first septal perforator of the LAD was associated with decreased survival compared with the presence of a more distal lesion. For the entire group of one-vessel disease patients, total ischemic events (death and nonfatal infarction) occurred at similar rates regardless of the anatomic location of the lesion. Left ventricular ejection fraction was the baseline descriptor most strongly associated with survival, and the characteristics of the angina had the strongest relationship with nonfatal myocardial infarction. No differences in survival or total cardiac event rates were found with surgical or nonsurgical therapy. The relief of angina was superior with surgical therapy, although the majority of nonsurgically treated patients had significant relief of angina. The survival rate of patients with one-vessel coronary disease is excellent, and the risk of nonfatal infarction is low. Clinical strategies for the care of these patients must consider the long-term clinical course of one-vessel coronary disease.
Comparative sensitivity of exercise, cold pressor and ergonovine testing in provoking attacks of variant angina in patients with active disease.
Authors: Waters D D , Szlachcic J , Bonan R , Miller D D , Dauwe F , Theroux P
Published: June 2011

Exercise, ergonovine and the cold pressor test have been used to provoke variant angina attacks. The sensitivity of these three tests was compared in 34 hospitalized patients with well documented, active variant angina who had recently undergone coronary arteriography. The three tests were usually performed on three consecutive days, and 28 of the 34 had the three tests within 1 week. Angina was provoked by ergonovine in all 34 patients, by exercise in 17 and by cold pressor test in only five (p less than 0.005). ST elevation developed during the ergonovine test in 32 (94%), during exercise in 10 (29%) and during the cold pressor test in only three (9%). With ergonovine, one patient had only ST depression and one had no ECG changes. During the cold pressor test two patients had pseudonormalization of abnormally negative T waves and 29 had no ECG changes. Exercise induced T-wave pseudonormalization in four patients, ST depression in nine others and no ECG changes in 11. ST elevation was more frequent with ergonovine than with either of the other tests (p less than 0.0001). ST elevation or T-wave pseudonormalization occurred more often with exercise than with cold (p less than 0.05), but both occurred less often than with ergonovine (p less than 0.0001). We conclude that the sensitivity of the ergonovine test is very high in patients with active variant angina and that exercise will provoke angina with ST elevation in about 30% of these cases. In contrast, the sensitivity of the cold pressor test is too low to be of much clinical value in the diagnosis of variant angina.
Analysis of interectopic activation patterns during sustained ventricular tachycardia.
Authors: Brachmann J , Kabell G , Scherlag B , Harrison L , Lazarra R
Published: June 2011

We analyzed the patterns of interectopic continuous electrical activity recorded within interectopic intervals of sustained ventricular tachycardias. These arrhythmias were induced in dogs that were studied 4 days after left anterior descending coronary artery occlusion. Standard ECG leads and electrograms from the His bundle and left ventricular epicardium, both infarct and normal zone, were recorded. In 19 of 24 dogs with transmural myocardial infarction, one to three ventricular paced beats induced sustained ventricular tachycardia, characterized by continuous electrical activity between the initiating and spontaneous ectopic beat and between successive ectopic beats recorded from the epicardium over the infarct zone but not from the normal epicardium. Continuous activity consisted of discrete potentials that were reproduced in each cardiac cycle, suggesting slow conduction within a reentrant circuit. The interectopic activity was divided into three distinct temporal periods, delineated by potentials occurring at the initial portion, the mid-interectopic portion and terminal portion or exit of the slow conduction segment of the presumed reentrant circuit. In some cases, sustained ventricular tachycardia was induced only if an appropriate initial potential was engaged. Spontaneous termination of the sustained ventricular tachycardia was associated with Wenckebach-like block of conduction in the initial or exit potential. Ventricular pacing caused alteration of the interectopic patterns and resulted in cessation of the arrhythmia. Procainamide produced dose-dependent slowing of the ectopic rate due to depression of conduction in the mid-interectopic portion of the continuous electric activity. Inducibility of the sustained ventricular tachycardia was inhibited by decremental conduction in this compartment of the presumed reentry circuit. The present study uses a preparation showing sustained ventricular tachycardia that is stable and regular. Functional analysis of the various portions of the continuous electrical activity during sustained tachycardias allows further insight into the mechanisms of initiation and termination of sustained ventricular tachycardias. The ability to localize the effect of antiarrhythmic drugs on specific portions of a possible reentrant circuit may provide important correlative data for the analysis and interpretation of detailed epicardial mapping studies.
Primary pulmonary artery sarcoma diagnosed noninvasively by two-dimensional echocardiography.
Authors: Wright E C , Wellons H A , Martin R P
Published: June 2011

A 21-year-old white male was evaluated in our echocardiographic laboratory for presumed mitral valvular bacterial endocarditis. Electrocardiographic, physical, and initial two-dimensional echocardiographic findings suggested a left-to-right shunt at the atrial septal level. However, injection of contrast saline solution failed to demonstrate signs of an atrial septal defect. Continuation of the echocardiographic study led to the diagnosis of an unsuspected primary sarcoma of the pulmonary trunk, which was rapidly confirmed by computerized axial tomography. Therapeutic interventions were undertaken. This case highlights the usefulness of two-dimensional echocardiography.
Total disconnection of the right ventricular free wall: surgical treatment of right ventricular tachycardia associated with right ventricular dysplasia.
Authors: Guiraudon G M , Klein G J , Gulamhusein S S , Painvin G A , Del Campo C , Gonzales J C , Ko P T
Published: June 2011

Arrhythmogenic right ventricular dysplasia is a myopathy that affects the right ventricular free wall (RVFW) and gives rise to recurrent reentrant ventricular tachycardia (VT). Because the entire right ventricle is potentially arrhythmogenic, ablating a single site of VT may not eliminate the arrhythmia. We developed an operation to confine any arrhythmic activity arising from the right ventricle to that chamber: total disconnection of the RVFW from the left ventricle. We performed RVFW disconnection in two patients with refractory VT associated with arrhythmogenic right ventricular dysplasia. At least two sites or origin of morphologically distinct VT were identified in the RVFW in each patient. RVFW disconnection was carried out under normothermic cardiopulmonary bypass. An encircling incision was made along the attachment of the RVFW to the aortoventricular unit and the tricuspid annulus; the right coronary artery and its RVFW branches were left intact. Electrical activity of the two chambers became dissociated, and VT arising from the RVFW was confined to that chamber. Postoperatively, there was no clinical evidence of hemodynamic impairment (follow-up 4 months and 3 months). Left ventricular function was unchanged and right ventricular flow was maintained by atrial contraction and motion of the septum toward the RVFW during left ventricular systole. One patient had incessant right ventricular tachycardia confined to the RVFW for 3 weeks. We conclude that RVFW disconnection is feasible and applicable to patients with refractory VT originating in the diffusely diseased RVFW.
Does length or eccentricity of coronary stenoses influence the outcome of transluminal dilatation?
Authors: Meier B , Gruentzig A R , Hollman J , Ischinger T , Bradford J M
Published: June 2011

In 526 patients undergoing a first percutaneous transluminal coronary angioplasty (PTCA) of a single native vessel, we studied the influence of length and eccentricity of the lesion on complications and primary success. Long stenoses (greater than or equal to 5 mm, n = 153) did not differ from short stenoses (less than or equal to 4 mm, n = 265) in terms of overall complications or gain in lumen diameter and distal pressure. Eccentric stenoses (n = 155) showed a lower rate of primary success than concentric stenoses (n = 338) (80% vs 89%, p less than 0.05). Inability to cross the stenosis was the main reason for failure. Stenoses that were long and eccentric (n = 51) had the highest incidence of complications (24%) and stenoses that were short and concentric (n = 177) the lowest (12%, p less than 0.05). However, the average outcome expressed by gain in lumen diameter and distal pressure was equal in both groups and is obviously more dependent on technical factors than on anatomy. Nevertheless, length and, particularly, eccentricity of a lesion constitute risk factors for PTCA. They may be overcome by technical skill and sophisticated equipment, such as steerable catheters.
Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure.
Authors: Fitzpatrick D , Ikram H , Nicholls M G , Espiner E A
Published: June 2011

The hemodynamic, hormonal and electrolyte effects of prenalterol, a synthetic selective beta 1 agonist, were studied in six patients with New York Heart Association functional class II and III heart failure. Prenalterol was infused incrementally at 60, 120 and 240 nmol/min, each rate for 24 hours, producing steady-state plasma prenalterol levels of 52 +/- 3, 121 +/- 6 and 194 +/- 9 nmol/1, respectively (mean +/- SEM). Hemodynamic and hormonal measurements were performed before, during and after prenalterol administration under conditions of constant body posture and a regulated intake of dietary sodium and potassium. Prenalterol induced a statistically significant increase in cardiac index (from 2.6 +/- 0.2 to 3.1 +/- 0.3 1/min/m2), with parallel increases in stroke index (from 28 +/- 2 to 34 +/- 2 ml/beat/m2). Forearm blood flow measurements increased (from 2.9 +/- 0.5 to 4.1 +/- 0.6 ml/min/100 g), while calculated systemic vascular resistance fell, as did pulmonary capillary wedge pressure (from 13.7 +/- 1.6 to 10.5 +/- 1.7 mm Hg). The drug did not alter heart rate, arterial pressure, right heart pressures or the frequency of ventricular premature beats. Prenalterol increased plasma renin activity (from 2.9 +/- 0.8 to 6.6 +/- 1.8 nmol/1/hour), angiotensin II (from 59 +/- 12 to 89 +/- 22 pmol/1), urinary aldosterone excretion (from 41 +/- 10 to 78 +/- 34 nmol/day) and plasma insulin (from 10.6 +/- 2.2 to 19.8 +/- 3.9 mU/1). Circulating catecholamines, cortisol, glucose, glucagon or pancreatic polypeptide did not change. Dose-response studies in five patients showed dose-dependent increments in hemodynamic variables, while hormonal changes plateaued at the second dose level. We conclude that prenalterol infusion augments myocardial contractility, reduces systemic vascular resistance, and stimulates insulin release and the renin-angiotensin-aldosterone system.
Late sudden death after repair of tetralogy of Fallot: a clinicopathologic study.
Authors: Deanfield J E , Ho S Y , Anderson R H , McKenna W J , Allwork S P , Hallidie-Smith K A
Published: June 2011

Retrospective analysis was performed to determine the likely cause of death in six patients who died suddenly 1-9 years after repair of tetralogy of Fallot. The integrity of the atrioventricular conduction system and myocardium was examined in three hearts at necropsy. Two of three patients who complained of palpitation or syncope had frequent premature ventricular complexes on routine ECGs. All the patients had complete right bundle branch block and one had left-axis deviation after repair. Postoperative cardiac catheterization (four patients) showed no residual ventricular septal defects, but right ventricular pressure was elevated in all. At necropsy, the atrioventricular conduction tissue was related to the margin of perimembranous ventricular septal defect in two patients, but was well posterior in one patient with an infundibular muscular defect. Histologic examination showed that in all cases the atrioventricular node, atrioventricular bundle and left bundle branch were undamaged. There was, however, extensive fibrosis of the right ventricular myocardium in the ventriculotomy site (three patients), septum (one patient) and outflow tract (one patient). These clinical and necropsy findings suggest that ventricular arrhythmia rather than atrioventricular block was responsible for sudden death in these patients after repair of tetralogy of Fallot.
The myxomatous mitral valve and sudden death.
Authors: Chesler E , King R A , Edwards J E
Published: June 2011

The clincopathologic features of 14 cases of sudden death attributable to dysrhythmias associated with the myxomatous mitral valve are described. The patients were 14-59 years old (mean 27 +/- 11 years). Eleven were female and three male. Of the seven ECGs available, none showed prolongation of the QT interval, but two showed repolarization abnormalities. The material was classified according to the degree of prolapse in the pathologic specimen. When obvious prolapse was found, the expected auscultatory findings had been documented. In three cases there was minimal prolapse, casting some doubt on the hypothesis that traction on the papillary muscles or diastolic dumping of the leaflets may be implicated in the pathogenesis of the dysrhythmias. In one of the cases with minimal prolapse there was a strong family history of sudden death. Endocardial friction lesions were present in 11 cases, including two of the three with minimal prolapse. In five cases there was a thrombotic lesion in the angle between the posterior leaflet and the left atrial wall containing fibrin and platelets. These abnormalities may be important in the pathogenesis of the ventricular dysrhythmias.
Cardiovascular reflexes stimulated by reperfusion of ischemic myocardium in acute myocardial infarction.
Authors: Wei J Y , Markis J E , Malagold M , Braunwald E
Published: June 2011

Acute myocardial infarction (AMI), especially of the inferior left ventricular wall, where most cardiac receptors with vagal afferents that are stimulated during coronary occlusion are located, is commonly associated with reflex hypotension and sinus bradycardia. To determine whether reperfusion of an acutely ischemic area can activate cardiac reflexes, changes in the heart rate, arterial pressure and rhythm were correlated with the time course and location of intracoronary thrombolytic therapy in 41 patients with AMI. Of the 27 patients with successful reperfusion, 17 developed significant transient bradycardia and hypotension and one became tachycardic and hypertensive at the time of recanalization. Spontaneous reversion of the bradycardia and hypotension occurred definitely in six patients and possibly in more (nine reverted after atropine and two after fluids). A positive correlation existed between the changes in heart rate and blood pressure, in contrast to the usual inverse relationship when baroreceptors are stimulated. Two of the three patients in whom reperfusion was transient also developed hypotension and bradycardia. In contrast, all 11 patients with persistent occlusion demonstrated no reflex cardiovascular changes during intracoronary thrombolytic therapy. Thus, successful reperfusion in AMI stimulates cardioinhibitory and vasodepressor (Bezold-Jarisch) reflexes. These findings raise the possibility that the transient hypotension and bradycardia observed during AMI, particularly inferior MI, may sometimes reflect the occurrence of spontaneous reperfusion of the acutely ischemic myocardium.
The diagnosis of acute, recurrent, deep-vein thrombosis: a diagnostic challenge.
Authors: Hull R D , Carter C J , Jay R M , Ockelford P A , Hirsch J , Turpie A G , Zielinsky A , Gent M , Powers P J
Published: June 2011

Recurrent venous thrombosis presents a diagnostic challenge. Venography, impedance plethysmography and fibrinogen leg scanning all have potential limitations, and their role in this context has not been evaluated. We performed a prospective cohort study evaluating impedance plethysmography and leg scanning, plus venography, using outcome on long-term follow-up as the end point in 270 patients with clinically suspected recurrent deep-vein thrombosis. Anticoagulant treatment was withheld in the 181 patients negative by noninvasive testing and was given in patients positive by impedance plethysmography if leg scanning was positive or if intraluminal filling defects were detected by venography. The validity of this approach was tested by long-term follow-up. Three of 181 patients (1.7%) negative by noninvasive testing had a recurrence, compared with 18 of 89 (20%) with positive findings (p less than 0.001). Our objective diagnostic approach has high clinical utility; an objective rationale for withholding or giving treatment was established in 95% of patients.
Rate-dependent changes in excitability of depressed cardiac Purkinje fibers as a mechanism of intermittent bundle branch block.
Authors: Jalife J , Antzelevitch C , Lamanna V , Moe G K
Published: June 2011

When the heart rate is accelerated, rate-dependent intraventricular block may occur. This block has been attributed to abnormal action potential prolongation in a diseased conducting pathway. Less often, intraventricular block develops during slowing of the heart rate and has been explained in terms of phase 4 depolarization in potentially automatic cells within the diseased fascicle. We tested these hypotheses in isolated bundles of Purkinje fibers placed in a three-chambered tissue bath. In one group of experiments, conditions of localized injury and depressed excitability were mimicked by superfusing the central segment with sucrose solution. Action potentials were initiated in the proximal segment while the slope of phase 4 of cells in the distal end was controlled by intracellular ramps of current of either polarity. In these preparations, phase 4 depolarization facilitated rather than retarded propagation across the depressed segment, even at takeoff potentials as low as -45 mV. In a second group, depressed excitability was induced by exposing the three fiber segments to Tyrode's solution that contained high concentrations of KCl and CaCl2 or isoproterenol (0.1 microgram/ml). Under these conditions, Purkinje fibers did not undergo phase 4 depolarization and did not generate abnormally prolonged action potentials. These preparations showed a biphasic time dependence of conduction during premature stimulation or in response to changes in the basic cycle length. Conduction impairment and block were manifest at either side of an optimal interval or cycle length. Our results suggest that phase 4 depolarization and abnormally prolonged action potentials are not necessary conditions for intermittent block. Both tachycardia and bradycardia-dependent intraventricular conduction abnormalities may be associated with time-dependent variations in the excitability of depolarized conducting fibers as well as in the amplitude of the slow responses generated by these fibers. These alterations can be explained in terms of regulation of slow inward current by the intracellular calcium concentration.
Reduction of the extent of ischemic myocardial injury by neutrophil depletion in the dog.
Authors: Romson J L , Hook B G , Kunkel S L , Abrams G D , Schork M A , Lucchesi B R
Published: June 2011

Accumulation of polymorphonuclear neutrophils during the acute inflammatory response may exacerbate tissue injury through the release of activated oxygen products or proteolytic enzymes or both. To assess the role of neutrophils in acute myocardial infarction, circulating neutrophil levels in dogs were reduced by 77 +/- 2% (mean +/- SEM) by administering rabbit antiserum to dog neutrophils. Acute myocardial infarction was induced in open-chest anesthetized dogs by 90 minutes of left circumflex coronary artery occlusion followed by 6 hours of reperfusion. Dogs treated with neutrophil antiserum (n = 8) developed myocardial infarcts that were an average of 43% smaller than infarcts in dogs treated with nonimmune rabbit serum (n = 7) (27.0 +/- 4.5% vs 47.1% +/- 7.5% of the area at risk, p less than 0.05). In a saline-treated control group (n = 8), infarct size was 48.0 +/- 4.7% of the area at risk, a value not significantly different from that of the nonimmune serum group but significantly greater than that in the neutrophil antiserum dogs (p less than 0.05). There were no major hemodynamic differences between groups. Histopathologic examination revealed that infarcted myocardium from dogs given saline or treated with nonimmune serum had a substantial neutrophilic infiltrate, which was virtually absent in infarcted tissue from dogs treated with neutrophil antiserum. These observations suggest that neutrophil accumulation in response to myocardial ischemia may be responsible for a substantial portion of the irreversible myocardial injury resulting from temporary coronary artery occlusion.
Effect of rate-dependent left bundle branch block on global and regional left ventricular function.
Authors: Bramlet D A , Morris K G , Coleman R E , Albert D , Cobb F R
Published: June 2011

Seven subjects with rate-dependent left bundle branch block (RDLBBB) and 13 subjects with normal conduction (control group) underwent upright bicycle exercise radionuclide angiography to determine the effects of the development of RDLBBB on global and regional left ventricular function. Six of the seven subjects with RDLBBB had atypical chest pain syndromes; none had evidence of cardiac disease based on clinical examination and either normal cardiac catheterization or exercise thallium-201 scintigraphy. Radionuclide angiograms were recorded at rest and immediately before and after RDLBBB in the test group, and at rest and during intermediate and maximal exercise in the control group. The development of RDLBBB was associated with an abrupt decrease in left ventricular ejection fraction (LVEF) in six of seven patients (mean decrease 6 +/- 5%) and no overall increase in LVEF between rest and maximal exercise (65 +/- 9% and 65 +/- 12%, respectively). In contrast, LVEF in the control group was 62 +/- 8% at rest and increased to 72 +/- 8% at intermediate and 78 +/- 7% at maximal exercise. The onset of RDLBBB was associated with the development of asynchronous left ventricular contraction in each patient and hypokinesis in four of seven patients. All patients in the control group had normal wall motion at rest and exercise. These data indicate that the development of RDLBBB is associated with changes in global and regional ventricular function that may be confused with development of left ventricular ischemia during exercise.
Sustained hemodynamic and clinical effects of a new cardiotonic agent, WIN 47203, in patients with severe congestive heart failure.
Authors: Maskin C S , Sinoway L , Chadwick B , Sonnenblick E H , Le Jemtel T H
Published: June 2011

The hemodynamic and clinical effects of WIN 47203, a newly synthesized noncatecholamine, nonglycosidic inotropic agent, were studied in 11 patients with severe chronic congestive heart failure. Intravenous WIN 47203 increased cardiac index from 1.93 +/- 0.36 to 2.87 +/- 0.45 l/min/m2 (p less than 0.001) and reduced pulmonary capillary wedge pressure from 27.0 +/- 8.4 to 16.3 +/- 6.1 mm Hg (p less than 0.001). Mean systemic arterial pressure decreased from 75.2 +/- 6.7 to 72.4 +/- 6.3 mm Hg (p less than 0.01) and systemic vascular resistance from 1591 +/- 397 to 1071 +/- 293 dyn-sec-cm5 (p less than 0.001); heart rate was unchanged. Oral WIN 47203 produced similar hemodynamic improvement. Hemodynamic monitoring of six consecutive doses did not demonstrate evidence for attenuation of effectiveness. Chronic therapy with WIN 47203 produced substantial symptomatic improvement and increased maximal oxygen uptake at 1 week. Patients were further improved after 4 weeks of WIN 47203, and maximal oxygen uptake increased from 9.0 +/- 1.9 to 11.6 +/- 2.5 ml/kg/min (p less than 0.01 vs control). No overt clinical or laboratory manifestations of toxicity were observed. Withdrawal of WIN 47203 in two patients in whom clinical benefit was not sustained resulted in clinical and hemodynamic deterioration, which was reversed by reinstitution of the drug. Therefore, this study demonstrates the acute and sustained cardiotonic efficacy of WIN 47203 in man. If long-term administration remains well tolerated and without side effects, this drug appears to be very promising for treatment of chronic severe congestive heart failure.