Persistence of the left superior caval vein: can it potentiate obstructive lesions of the left ventricle?

1999 ◽  
Vol 9 (3) ◽  
pp. 285-290 ◽  
Author(s):  
Gabriella Agnoletti ◽  
Francesco Annecchino ◽  
Laura Preda ◽  
Adele Borghi
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
Subaortic Stenosis ◽  
Left Heart ◽  
Caval Vein ◽  
Superior Caval Vein ◽  
High Incidence ◽  
Left And Right ◽  
The Right ◽  
Left Heart Syndrome

AbstractRecent evidence has suggested that persistence of the left superior caval vein is associated with a high incidence of obstructive lesions of the left heart. To shed more light on this issue 1085 patients with congenital heart disease were studied retrospectively, with the aim of estimating the prevalence of a persistent left superior caval vein and its associated anomalies, focusing attention on obstructive lesions in the left and right ventricles. Patients with isomerism of the atrial appendages, or hypoplastic left heart syndrome, were excluded. A persisting left superior caval vein was present in 57 patients (5.2%). The overall incidence of obstructive lesions of the left heart was higher in patients with than in those without a persistent left superior caval vein (31.6 versus 7.8%,p< 0.001). Relative hypoplasia of the left ventricle was also higher in patients with persistent left superior caval vein (14 versus 0.8%,p< 0.001). The obstructive lesions found in the left heart, compared with the number in those without a left caval vein, were: mitral stenosis, 5.2 versus 0.7%; subaortic stenosis, 5.3 versus 0.9%; aortic coarctation, 17.5 versus 5.8% (p< 0.01); all of these in association, 3.5 versus 0.4%. In contrast, the incidence of obstructive lesions of the right heart was similar in the two groups of patients. It is concluded that persistence of the left superior caval vein can perturb the normal development of the left ventricle, being strongly associated with obstructions to left ventricular inflow and outflow.

Totally anomalous pulmonary venous connection through the right lung and via a “Scimitar” vein to the inferior caval vein

1993 ◽  
Vol 3 (1) ◽  
pp. 85-87
Author(s):  
Rakesh Dua ◽  
Christine McTigue ◽  
James.L Wilkinson
Keyword(s):  
Pulmonary Vein ◽  
Pulmonary Veins ◽  
Left Lung ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Caval Vein ◽  
Inferior Caval Vein ◽  
The Right ◽  
Left Heart Syndrome ◽  
Anomalous Pulmonary Venous Connection

AbstractWe report a case of totally anomalous pulmonary venous connection in which the two pulmonary veins from the left lung joined to form a common vein which then passed across the midline into a hypoplastic right lung and, after receiving small veins from the right lung, passed inferiorly, exiting the lung below the hilum as a “scimitar” vein and terminating in the inferior caval vein. A separate pulmonary vein from the right lung passed inferiorly independently and joined the “scimitar” vein before it entered the inferior caval vein. There was an associated hypoplastic left heart syndrome.

Preparation for repeated study of left ventricular function in the conscious dog

1975 ◽  
Vol 38 (5) ◽  
pp. 934-936 ◽  
Author(s):  
J. Beazell ◽  
D. Garner ◽  
M. M. Laks
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Function ◽  
Left Ventricular ◽  
Atrial Septum ◽  
Right Atrial ◽  
Left Heart ◽  
Significant Morbidity ◽  
Conscious Dog ◽  
Transseptal Catheterization ◽  
The Right

A method is presented for a relatively simple nontraumatic chronic left heart catheter preparation for the study of left ventricular hemodynamics in the conscious dog. In 30 dogs an 8 Fr Cordis catheter was modified and implanted into the left ventricle via the right atrial septum. Transseptal catheterization was performed without significant morbidity and mortality. Left ventricular cineangiograms and pressures and cardiac outputs have been repeatedly performed on fully conscious dogs with no apparent discomfort displayed by the dog.

Dimensional analysis of right and left ventricles during positive-pressure ventilation in dogs

1982 ◽  
Vol 242 (4) ◽  
pp. H549-H556 ◽  
Author(s):  
S. S. Cassidy ◽  
J. H. Mitchell ◽  
R. L. Johnson
Keyword(s):  
Left Ventricle ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Left Ventricular Volumes ◽  
Ventricular Volumes ◽  
End Diastolic Volume ◽  
Left And Right ◽  
The Right ◽  
Ventricular Dimensions

Our purpose was to determine the effects of controlled ventilation with positive end-expired pressure (PEEP) on ventricular dimensions and to relate changes in shape to changes in stroke volume and left ventricular volumes. Left and right ventricular dimensions were measured using biplane cinefluorography of dogs with radiopaque markers implanted in their hearts, and left ventricular volumes were derived from left ventricular dimensions by assuming that the left ventricle conformed to the shape of a nonprolate ellipsoid. As PEEP increased from 0 to 5, 10, and 15 cmH2O, stroke volume fell 36%, and all three left ventricular end-diastolic dimensions fell, with apex-base falling 5%, anterior-posterior falling 7%, and septal-lateral falling nearly twice as much, 12%. This resulted in a 11.3 cm3 fall in left ventricular end-diastolic volume. The right ventricular end-diastolic dimensions changed in opposite directions with respect to each other as the level and PEEP was raised to 15 cmH2O; one axis fell 3.2 mm, and the midpoint of the right ventricular free wall moved outward by 1.7 mm. Thus the fall in cardiac output (and stroke volume) during PEEP was associated with a fall in left ventricular end-diastolic volume and a change both left and right ventricular configurations. It is not known whether the left ventricular septal-lateral narrowing is the consequence of lateral wall compression by the lungs or encroachment on the left ventricle by the septum.

Parasympathetic control of the heart. I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles

2004 ◽  
Vol 96 (6) ◽  
pp. 2265-2272 ◽  
Author(s):  
Tannis A. Johnson ◽  
Alrich L. Gray ◽  
Jean-Marie Lauenstein ◽  
Stephen S. Newton ◽  
V. John Massari
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Anterior Surface ◽  
Ventricular Performance ◽  
Neuronal Marker ◽  
Left And Right ◽  
Intracardiac Ganglia ◽  
The Right

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 ± 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.

Measurement of left and right ventricular volume from implanted radiopaque markers

1981 ◽  
Vol 240 (6) ◽  
pp. H896-H900
Author(s):  
W. P. Santamore ◽  
R. Carey ◽  
D. Goodrich ◽  
A. A. Bove
Keyword(s):  
Standard Deviation ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Volumes ◽  
Radiopaque Markers ◽  
Left And Right ◽  
The Right

To better understand biventricular mechanics, an algorithm was developed to simultaneously calculate right and left ventricular volumes from randomly placed subendocardial radiopaque markers. Mathematically, the ventricle is represented as a stack of circular discs. The radius R of each disc is calculated as the distance from the subendocardial radiopaque marker to a computer generated base-to-apex line, and the height H of each disc is determined by the projected distance between radiopaque markers along the base-to-apex line. Accordingly, the volume (V) is calculated as V = pi . sigma Hi . Ri2. The validity of this algorithm was tested on 10 canine left ventricular casts, on 10 human right ventricular casts, and in five experiments. For the left ventricle, the regression line between the casts (VT) and calculated (VC) volumes was VC = 0.55 VT + 6.6, with r = 0.95, standard error of estimate (Sy) = 1.9 ml, and the standard deviation of percent error = 12.6%. For the right ventricle, VC = 1.75 VT = 42.5, with r = 0.86, Sy = 16.2 ml, and the standard deviation of percent error = 24.8%. In five animal experiments, radiopaque markers were implanted into the endocardium of the left and right ventricles and comparisons were made between angiographic- and marker-determined ventricular volumes. For the five experiments, the mean correlation coefficient, relating the marker volumes to the angiographic volumes, were 0.92 +/- 0.01 for the left ventricle and 0.89 +/- 0.02 for the right ventricle. The results, which are similar to other volume-determination methods, indicate that this method can be applied to determine right and left ventricular volume. Once implanted, fluoroscopy of these markers provides a noninvasive means of calculating ventricular volume.

Left ventricular failure induced by myocardial infarction. II. Tissue morphometry

1985 ◽  
Vol 248 (6) ◽  
pp. H883-H889 ◽  
Author(s):  
P. Anversa ◽  
A. V. Loud ◽  
V. Levicky ◽  
G. Guideri
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Volume Fraction ◽  
Volume Ratio ◽  
Left Ventricular ◽  
Tissue Growth ◽  
Left And Right ◽  
The Right ◽  
And Diffusion

Three days after myocardial infarction involving 57% of the left ventricle in rats, the viable tissue of the left ventricle expanded 29%, whereas myocardial hypertrophy in the right ventricle was 19%. To determine whether tissue oxygenation in the hypertrophied ventricles was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities and the diffusion distance for O2. The volume fraction of capillary lumen and the luminal surface of capillaries, related to O2 availability and diffusion, were altered by -21 and -19%, respectively, in the left ventricle and by -23 and -20%, respectively, in the right ventricle. The path length for O2 transport was found to be increased by 12 and 15% in the left and right ventricle, respectively. In contrast, myocyte mass expanded in proportion to tissue growth in the left ventricle and exceeded tissue growth by 5% in the right ventricle. Myocyte mitochondria and myofibrils both grew in proportion to the cells, so that their volume ratio was not changed in either ventricle. The relatively inadequate adaptation of the capillary vasculature suggests that hypertrophy after severe myocardial infarction may initially leave the heart more vulnerable to additional ischemic episodes.

scholarly journals Hemodynamic Support Using Percutaneous Transfemoral Impella 5.0 and Impella RP for Refractory Cardiogenic Shock

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Pratik K. Dalal ◽  
Amy Mertens ◽  
Dinesh Shah ◽  
Ivan Hanson
Keyword(s):  
Left Ventricle ◽  
Pulmonary Artery ◽  
Cardiogenic Shock ◽  
Ventricular Function ◽  
Standard Of Care ◽  
Left Ventricular ◽  
Biventricular Failure ◽  
Ventricular Support ◽  
The Right ◽  
Flow Pump

Acute myocardial infarction (AMI) resulting in cardiogenic shock continues to be a substantial source of morbidity and mortality despite advances in recognition and treatment. Prior to the advent of percutaneous and more durable left ventricular support devices, prompt revascularization with the addition of vasopressors and inotropes were the standard of care in the management of this critical population. Recent published studies have shown that in addition to prompt revascularization, unloading of the left ventricle with the placement of the Impella percutaneous axillary flow pump can lead to improvement in mortality. Parameters such as the cardiac power output (CPO) and pulmonary artery pulsatility index (PAPi), obtained through pulmonary artery catheterization, can help ascertain the productivity of right and left ventricular function. Utilization of these parameters can provide the information necessary to escalate support to the right ventricle with the insertion of an Impella RP or the left ventricle with the insertion of larger devices, which provide more forward flow. Herein, we present a case of AMI complicated by cardiogenic shock resulting in biventricular failure treated with the percutaneous insertion of an Impella RP and Impella 5.0 utilizing invasive markers of left and right ventricular function to guide the management and escalation of care.

Total anomalous pulmonary venous connection mimicking hypoplastic left heart syndrome

2021 ◽  
pp. 1-3
Author(s):  
Ryohei Matsuoka ◽  
Jun Muneuchi ◽  
Yoshie Ochiai
Keyword(s):  
Left Ventricle ◽  
Systemic Circulation ◽  
Z Score ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Transverse Arch ◽  
Anomalous Pulmonary Vein ◽  
Pulmonary Arterial ◽  
Left Heart Syndrome ◽  
Anomalous Pulmonary Venous Connection

Abstract A newborn with supracardiac total anomalous pulmonary venous connection vein presented the small left ventricle with z score of −7.5, retrograde blood supply in the transverse arch, and the dutcus-dependent systemic circulation. The patient underwent the repair of the anomalous pulmonary vein and bilateral pulmonary arterial banding soon after the birth and then transcatheter pulmonary arterial debanding at the age of 10 months because of an appropriate growth of the left ventricle.

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