bluuebunny/crossref_metadata_2025_split huggingface dataset:
Double-Outlet Right Ventricle with Pulmonic Stenosis
Authors: GOMES MANUEL M. R. , WEIDMAN WILLIAM H. , MCGOON DWIGHT C. , DANIELSON GORDON K. 
Published: June 2012

The results of complete repair of double-outlet right ventricle with pulmonic stenosis in 22 Mayo Clinic patients were analyzed. The overall mortality rate was 32%. Since 1960, the mortality rate has been reduced to 16%. Anomalies of the distribution of the right coronary artery, a second ventricular septal defect of the atrioventricular canal type, and significant residual pulmonic stenosis were associated with a higher mortality rate. The difficulties in the diagnosis of this uncommon condition are emphasized.
Complete repair is best carried out after the patient is 4 years old. A systemic-to-pulmonary arterial shunt is the procedure of choice for those who are younger than this. In the occasional patient with anomalous distribution of the right coronary artery which precludes adequate relief of the pulmonic stenosis, use of an aortic homograft from the right ventricle to the pulmonary artery should be considered.
Postextrasystolic Ventricular Pressure Responses
Authors: BECK W. , CHESLER E. , SCHRIRE V. 
Published: June 2012

The peak postextrasystolic ventricular pressure was examined in tracings obtained during routine catheterization of the right and left ventricles in 252 cases. The invariable response in the apparently "normal" left ventricle was a fall or no change in peak systolic pressure, whereas in the obstructed left ventricle, the failed left ventricle, the severely volume-overloaded left ventricle, and in mitral stenosis the more usual pattern was a rise in postextrasystolic ventricular pressure. On the right side the usual response both in the normal and abnormal was a rise in postextrasystolic pressures. Significant exceptions were found when the right ventricle ejected against the aortic impedance and in constrictive pericarditis.
In the intact circulation the outflow impedance and its rate of decline during the compensatory pause would appear to be the major determinant of the postextrasystolic pressure response. There is some evidence that alterations in the extent and time course of ventricular filling may be a factor, but the effects of variations in the degree of postextrasystolic potentiation based on variations in the prematurity of the extrasystole, which can so easily be demonstrated under controlled conditions, appear to be largely obscured except when fixed outflow obstruction is present. The only practical value of this observation may be the ability to recognize an "abnormal" left ventricle when the postextrasystolic beat shows a higher peak ventricular pressure and to recognize a right ventricle in free communication with the aorta when the peak right ventricular postextrasystolic pressure fails to rise. Conversely, a lower peak left ventricular systolic pressure following a premature beat should not be misinterpreted as being due to a failure of postextrasystolic potentiation and augmentation, as it is in fact a normal phenomenon.
Clinical, Surgical, and Pathologic Correlation in Patients with Acute Myocardial Infarction and Pump Failure
Authors: BOLOOKI HOOSHANG , LEMBERG LOUIS , GHAHRAMANI ALI , ECONOMIDES CHRIS , CALDWELL THOMAS , JUDE JAMES R. , Boccabella Kathleen 
Published: June 2012

A review was made of the entire hospital course of 20 patients aged 44 to 79 years who suddenly developed clinically intractable left-heart pump failure as a result of acute myocardial infarction. They were divided into three groups according to their presenting circulatory state. Thirteen patients were in cardiac arrest (group I), four had cardiogenic shock due to myocardial rupture (group II), and three had severe intractable left-heart failure (group III). Preoperative partial or complete cardiac catheterization was possible in six patients.
Surgical treatment using cardiopulmonary bypass was selectively undertaken as a mode of therapy in 11 of the 20 cases. In 10, the area of infarction was delineated and was resected. Pathologically, the infarcts were from 1 to 14 days old, and in 19 of 20 cases involved the anterior wall. The specimens weighed 25 to 83 g. One patient, who was discharged, had infarctectomy and double coronary vein bypass graft. One patient lived for 3 weeks after infarctectomy and pulmonary embolectomy. Two others survived after surgery for 2 and 36 hours, respectively.
The results of this prospective study suggest that identification of patients possibly amenable to successful treatment of medically irreversible pump failure by surgical means will require earlier recognition of the high-risk group and intensive hemodynamic and radiographic evaluation of the extent of the disease process.
Natural Course of Peripartum Cardiomyopathy
Authors: DEMAKIS JOHN G. , RAHIMTOOLA SHAHBUDIN H. , SUTTON GEORGE C. , MEADOWS W. ROBERT , SZANTO PAUL B. , TOBIN JOHN R. , GUNNAR ROLF M. 
Published: June 2012

Twenty-seven patients presented in the puerperium with cardiomegaly, abnormal `ECG, and congestive cardiac failure and were considered to have peripartum cardiomyopathy (PPCM). The incidence of PPCM was significantly higher in women over 30 years of age, in women in their third or subsequent pregnancy, and in the presence of twins or toxemia. Within 6 months, 14 patients had normal sized hearts (group A), and 13 patients maintained cardiomegaly (group B).
The 14 patients in group A have been followed for 3 to 21 years (average 10.7 years). Two have died of unrelated causes. Of the remaining 12, eight are functional class I and four are functional class II. Eight patients had 21 subsequent pregnancies, with no permanent deterioration of cardiac function. Of 13 patients in group B, 11 (85%) have died of congestive cardiac failure. Their average survival was 4.7 years; six of 11 were dead in 3 years. Their clinical course was punctuated by repeated admissions for congestive cardiac failure. Six had pulmonary emboli, one had a systemic embolus, and three of six patients with subsequent pregnancies deteriorated in the puerperium. Of the two surviving patients, one is functional class I and the other is functional class II.
Therefore, in those patients in whom cardiomegaly persisted, the prognosis was poor, and subsequent pregnancies were likely to lead to permanent deterioration. In those in whom the heart size returned to normal the prognosis was excellent.
Mobitz Type II Block without Bundle-Branch Block
Authors: ROSEN KENNETH M. , LOEB HENRY S. , GUNNAR ROLF M. , RAHIMTOOLA SHAHBUDIN H. 
Published: June 2012

His bundle (H) electrograms were recorded in three patients with Mobitz type II block and narrow QRS. Block was secondary to digitalis intoxication in one patient. In the second patient, who had first-degree A-V block, type II block occurred with atrial pacing at a slightly increased heart rate. In the third patient, who had corrected transposition of the great vessels, type II block occurred spontaneously. In two additional patients, block simulating type II block was noted. In one, block of single P waves occurred with carotid massage. In the other, Wenckebach periods with small increments in P-R (and P-H) intervals resembled episodes of type II block. In all five patients, block was proximal to H, suggesting the A-V node as the site of block. The conduction defects in these patients were not progressive; none of the patients needed a pacemaker.
Although these mechanisms were identified in patients with narrow QRS complexes, they could occur with bundle-branch block suggesting an erroneous diagnosis of bilateral bundle-branch disease. It is concluded that His bundle recording is helpful in delineating these benign forms of block. The site of block may be a more important determinant of prognosis than the type of block.
Serum Cardiac Glycoside Assay Based upon Displacement of
3
H-Ouabain from Na-K ATPase
Authors: BROOKER GARY , JELLIFFE ROGER W. , Cochran Victoria , Sauer Sabine 
Published: June 2012

An assay of serum digoxin and other cardiac glycosides by displacement of
3
H-ouabain from Na-K ATPase is described. It is rapidly set up by any laboratory with a liquid scintillation counter. It can also assay digitalis leaf, digitoxin, and gitalin (Gitaligin), and has uncovered unsuspected administration of them.

The assay takes less than 1 hour. No quench correction of counts is required. One technician can assay 30 samples/day with results that afternoon. No interfering compounds have been found in over 1,800 assays. It is unaffected by lung scans.
Incidence of toxicity from digoxin is 10%, 25%, and 50% at serum levels of 1.4, 2.0, and 2.9 ng/ml, respectively. Toxic levels of digitalis and digitoxin are usually over 40 ng/ml.
Serum digoxin levels are also highly correlated with computed total-body concentrations of digoxin, obtained from data of dosage, route of administration, and the patient's weight and renal function.
Physicians may now select a serum digoxin level and computed total-body concentration of digoxin which are associated with an incidence of arrhythmias which they feel is reasonable for the urgency of each patient's clinical situation. These selected serum levels are associated with specific loading and maintenance dosage regimens, individualized to that patient's body weight, renal function, and route of digoxin administration.
Eccentric Ventricular Hypertrophy in Familial and Sporadic Instances of 46 XX, XY Turner Phenotype
Authors: EHLERS KATHRYN H. , ENGLE MARY ALLEN , LEVIN AARON R. , DEELY WILLIAM J. 
Published: June 2012

This study of individuals with familial and sporadically occurring 46 XX or XY Turner phenotype documented a wide range of right- and left-sided cardiovascular abnormalities and a previously unreported eccentric hypertrophy of the left ventricle.

A mother and five of her seven children had abnormal cardiovascular findings. Five had an abnormal electrocardiogram with frontal ÂQRS of -60° to ±180° and rS or rsr' in V
1
and rS, qrS, or qRS in V
5
. Catheterization demonstrated the following anomalies: coarctation of the aorta in three, valvular aortic stenosis in one, pulmonary valvular insufficiency with atrial septal defect in one, and pulmonary arterial branch stenosis in one child. All six had a similar abnormality of the left ventricle on angiocardiography. During systole and also in diastole the cavity was encroached on in its superolateral and posteroinferior aspects. Septal hypertrophy altered right ventricular contour in two.

A similarly abnormal electrocardiogram and left ventricle were found in four unrelated individuals with the XX, XY Turner phenotype. Three had pulmonary stenosis; in two there was an associated septal defect. The fourth, with no associated cardiac defect, died in heart failure at 5 months of age. At necropsy she had marked eccentric biventricular hypertrophy, chiefly involving the left ventricle so that the chamber was reduced to a slitlike cavity. The hypertrophied septum bulged into the right ventricular outflow tract.
A number of cardiovascular anomalies occur in familial and sporadic instances of this syndrome; eccentric ventricular hypertrophy recognizable by an electrocardiographic abnormality seems to be a distinctive cardiac lesion in the XX, XY Turner phenotype. Except for the unusual and, we believe, characteristic ECG, there was no clinical clue on physical examination or cardiac series of chest roentgenograms to suggest the presence of eccentric left ventricular hypertrophy. We recommend that selective left ventricular angiocardiography be performed when patients with the Turner phenotype undergo diagnostic cardiac catheterization, especially when the frontal ÂQRS is superiorly directed.
Site of Heart Block as Defined by His Bundle Recording
Authors: ROSEN KENNETH M. , RAHIMTOOLA SHAHBUDIN H. , GUNNAR ROLF M. , LEV MAURICE 
Published: June 2012

His bundle electrograms were recorded in three patients with heart block who subsequently died. Serial sections of the conduction system were performed. Two patients had complete block distal to H with wide QRS and P-H intervals of 135 and 100 msec, respectively (normal 80-140 msec). Postmortem (PM) revealed relatively insignificant A-V nodal lesions and major destructive lesions of both bundle branches. The third patient had block proximal to H with left bundle-branch block and H-V prolongation. PM revealed amyloidosis of the A-V nodal approaches and fatty infiltration of the A-V node and His bundle. There were also fibroelastic lesions, with total disruption of the left and moderate involvement of the right bundle branch.
The first patient also had sinus pauses as well as delay between what was felt to be posterior internodal tract depolarization and the P wave. PM also revealed arteriolosclerosis, mononuclear cell infiltration, and fibroelastosis of the SA nodal approaches.
Block distal to H appeared to reflect total disruption of both bundle branches. Normal P-H intervals appeared to correlate with relatively insignificant A-V nodal lesions. Block proximal to H with bundle-branch block and H-V prolongation reflected multiple conduction lesions. SA block appeared to reflect involvement of the SA nodal approaches.
Abnormalities of Ventricular Motion Induced by Atrial Pacing in Coronary Artery Disease
Authors: PASTERNAC ANDRE , GORLIN RICHARD , SONNENBLICK EDMUND H. , HAFT JACOB I. , KEMP HARVEY G. 
Published: June 2012

In order to study left ventricular performance and motion under ischemic stress, incremental atrial pacing was performed in 10 patients with angiographically proven coronary artery disease until angina pectoris or segmental S-T depression appeared. Single-plane left ventricular cineangiograms were obtained in both the resting and the transiently ischemic state induced by pacing.
Abnormal motion appeared with pacing in two of three patients with normal contraction at rest; in one of them, gross dyskinesis of the cardiac apex was noted. Seven patients had abnormal contraction at rest; six showed an increase in either the severity or the topographic distribution of abnormality, while one showed no change.
Left ventricular end-diastolic pressure and cardiac index were not altered significantly despite changes in the pattern of contraction. Left ventricular end-diastolic volume decreased irrespective of the development of asynergy, but ejection fraction decreased markedly in those patients in whom asynergy was induced de novo or increased.
Thus left ventriculography during pacing-induced ischemia may reveal segmental or generalized abnormalities of contraction not necessarily reflected in the usual hemodynamic parameters of function. Moreover, asynergy induced by pacing is associated with a decreased ejection fraction.
Percutaneous Myocardial Biopsy of the Left Ventricle
Authors: SHIREY EARL K. , HAWK WILLIAM A. , MUKERJI DEVOBROTO , EFFLER DONALD B. 
Published: June 2012

A thin-walled Silverman needle has been used for 254 percutaneous punch biopsies of the left ventricle in 198 patients with closed chests at the Cleveland Clinic. The technic is described. The biopsy specimens were adequate for diagnosis in 192 patients. In all but three patients (who had lupus erythematosus, scleroderma, and chronic glomerulonephritis with congestive heart failure) cardiac catheterization and selective cardioangiographic studies were performed. There was angiographic evidence of primary myocardial disease, coronary atherosclerosis, or both, or rheumatic valvular disease in 175 patients. Cardiac catheterization and angiographic studies demonstrated no evidence of organic heart disease in 20 patients.
Cardiac tamponade was a complication of myocardial biopsy in eight patients. Post-pericardiotomy syndrome occurred in four patients and ventricular fibrillation in one patient.
Myocardium with no pathologic diagnosis and interstitial fibrosis or myocardial hypertrophy or both were the light microscopic findings in 165 patients. Representative sections of the biopsy in 27 patients demonstrated small-vessel disease, basophilic degeneration, focal interstitial myocarditis, amyloidosis, Aschoff's nodules, or vacuolar degeneration. The current experience suggests that myocardial biopsy combined with selective cardioangiography is of experimental value, improves the accuracy of diagnosis, and plays a role in the management of some patients.
Analysis of Left Ventricular Wall Motion by Reflected Ultrasound
Authors: MCDONALD IAN G. , FEIGENBAUM HARVEY , CHANG SONIA 
Published: June 2012

Ultrasound echocardiograms from the septal and posterior left ventricular walls were displayed with a simultaneously recorded electrocardiogram, phonocardiogram, and indirect carotid pulse. These echoes differed in both amplitude and waveform. The contour of the posterior wall echo resembled an inverted ventricular volume curve, while the septal echo was of smaller amplitude and had a characteristic notched appearance. Most of the movement of the left ventricular walls relative to the ultrasound transducer was attributable to systolic contraction and diastolic expansion of the cavity. However, superimposed on this motion due to change in cavity size was movement of the left ventricle as a whole, first anteriorly toward the ultrasound transducer during late systole then posteriorly away from it at the beginning of left ventricular relaxation. These movements added to the amplitude of posterior wall motion but subtracted from the motion of the septum and were responsible for the notch in the waveform of this echo. Attachment superiorly to the aortic root might also have limited septal motion which was less near the base than nearer the apex of the left ventricle.
The internal left ventricular dimension measured by ultrasound was standardized by using the mitral valve as a landmark and by recording the motion of the left side of the interventricular septum and endocardial surface of the posterior left ventricular wall simultaneously. This measurement was reproducible. In normal subjects, the ultrasonic dimension measured 4.40 ± 0.28 cm at the beginning of systole and shortened by 35.5 ± 3.9% at a rate of 1.22 ± 0.31 lengths/sec. By contrast, the average figures for six patients with primary myocardial disease were 6.96 ± 0.43 cm, 14.9 ± 4.2%, and 0.64 ± 0.11 lengths/sec. Calculation of such indices of left ventricular size and of rate and extent of myocardial shortening should be useful in the detection of impaired myocardial function and in following its progress.
Echocardiography in the Diagnosis of Congenital Mitral Stenosis and in Evaluation of the Results of Mitral Valvotomy
Authors: LUNDSTRÖM NILS-RUNE 
Published: June 2012

Seven patients with congenital mitral stenosis have been investigated with echocardiography using reflected ultrasound. In all cases the mitral stenosis was combined with other cardiovascular malformations. The results are compared with those obtained at clinical investigation, cardiac catheterization, and operation and/or autopsy. It is concluded that the method is of definite value in diagnosing congenital mitral stenosis, even when this is combined with other cardiovascular malformations. The method is also found to be of value in assessing the severity of mitral stenosis.
Three patients have been investigated after mitral valvotomy. It is concluded that the findings at echocardiographic examination agree quite well with the clinical findings and with the results of postoperative cardiac catheterization in the evaluation of the result of mitral valvotomy.
Baroreceptor Activity in Normotensive and Hypertensive Uremic Patients
Authors: LAZARUS J. M. , HAMPERS C. L. , LOWRIE E. G. , MERRILL J. P. 
Published: June 2012

Baroreceptor activity and postural blood volume changes were evaluated in four normotensive and nine hypertensive uremic patients before and after bilateral nephrectomy. Baroreceptor activity, reflected by the slope of linear regression of R-R interval with drug-induced systolic blood pressure elevation, was significantly lower in hypertensive than in normotensive patients. Six of nine patients had normal blood pressure following bilateral nephrectomy; however, the mean slopes of all nine patients, irrespective of postnephrectomy blood pressure, approached that of normotensive uremic patients. The slopes of both normotensive and hypertensive patients, before and after bilateral nephrectomy, were significantly less than normal controls. Similar results were found in lowering blood pressure with amyl nitrite.
Depressed baroreceptor activity is suggested to be secondary to neuropathy of the autonomic nervous system, chronic hypertension, heart disease, and anemia. It is speculated that this reduced baroreceptor sensitivity may accentuate the postural symptoms primarly induced by volume reduction on hemodialysis. There is no evidence in this study that depressed baroreceptor activity, as opposed to a reset baroreceptor, is a cause of hypertension in patients with chronic renal failure.
Abnormal Motion of the Interventricular Septum in Right Ventricular Volume Overload
Authors: KERBER RICHARD E. , DIPPEL WILLIAM F. , ABBOUD FRANCOIS M. 
Published: June 2012

Abnormal systolic motion of the interventricular septum has previously been noted using echocardiography in patients with atrial septal defect and has been ascribed to right ventricular volume overload. To evaluate the mechanism responsible for this abnormality, right ventricular volume overload was created in open-chest dogs by pumping blood from the left atrium to the right atrium. In seven of eight dogs changes in interventricular septum motion were produced acutely at shunt flow as low as 500 cc/min. When the shunt was decreased or stopped, interventricular septum motion returned to normal. Shunts producing left ventricular volume overload (aorta to left atrium and right atrium to left atrium) caused no change in interventricular septum motion. Clinical observations showed that six of seven patients with partial anomalous pulmonary venous connection and no atrial septal defect displayed abnormal interventricular septum motion on echocardiography. Twenty-one patients undergoing surgery for atrial septal defect were studied before and after operation. Sixteen of the 21 had abnormal interventricular septum motion preoperatively; the abnormal interventricular septum motion returned to normal in only one of the 16 patients during a postoperative follow-up period of up to one year. Three patients were studied only postoperatively up to six years after closure of atrial septal defect; all three retained abnormal interventricular septum motion.
Since the abnornal motion of the interventricular septum seen in patients with atrial septal defect can be produced and reversed acutely by creating a left-to-right atrial shunt in an experimental model, this abnormality must indeed be related to right ventricular volume overload. However, failure of interventricular septum motion to revert to normal following surgical correction in patients with atrial septal defect suggests that additional factors are involved in the persistence of this abnormal motion.