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Results for “Heart Septum”

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At least 19 recordsLinked to original sources
PubMed1977

De subitaneis mortibus. XXIV. Ruptured interventricular septum and heart block.

Five patients with acute posterior myocardial infarction developed varying degrees of atrioventricular (A-V) block prior to rupture of their interventricular septums (IVS). In three of these five the times of septal rupture coincided with the resumption of conduced synus rhythm. During the period of A-V block, the only stable escape rhythm appeared to originate in the A-V junctional region, and in two patients early in their course there was evidence of enhanced A-V junctional automaticity. Although the A-V node contained extensive infarction in all five hearts, its distal part, and the entire His bundle and proximal branches appeared to be spared. The anatomical pattern of dissection within the ruptured IVS was similar in three hearts, extending upward to the crest of the IVS and penetrating into the interatrial septum in two of these. Multiple major coronary narrowing were present in all five hearts, especially of a dominating right coronary artery; recent thrombosis was present in the right coronary artery in four of the five cases. The A-V node artery was markedly narrowed by focal fibromuscular dysplasia in three hearts, compounding the ischemia for the A-V node and eliminating one important source of collateral circulation to the interventricular septum.

Aged↗
PubMedDate not supplied

Effect of avian basal forebrain lesions, including septum, on heart rate conditioning.

The possible involvement of basal telencephalic structures in visually conditioned heart rate change (established by pairing light and foot-shock) was studied in 156 pigeons by evaluating conditioning performance following lesions of the septum or lobus parolfactorius. Extensive destruction of the septal complex had no effect on either the orienting response or the development of the conditioned response. Lesions of the lobus parolfactorius did not affect the orienting response or overall conditioned response levels, but it did slightly prolong the latency of the conditioned heart rate change. It is concluded that the septum, despite its being cardioactive, is not involved in conditioned heart rate change and that the lobus parolfactorius participates minimally. Thus, of the principal limbic structures of the avian telencephalon, only the amygdalar homologue appears critical in this defensive conditioning task [3].

Animals↗
PubMed1979

[Sequence of the spread of excitation in bird heart ventricles].

Intramural multipolar technique revealed primary sites of excitation in the subendocardium of central areas of border line of the apical and middle thirds of the bird heart septum. From the zone of primary depolarization the excitation wave spread on the subendocardium of ventricles. A number of sites of negativity were observed over the epicardium. The main mass of myocardium of free walls and the lower two thirds of the septum are activated by means of myocardium of free walls and the lower two thirds of the septum are activated by means of multifocal depolarization. The base third of the septum is the last to be activated. These features of the excitation of bird myocardium can be accounted for by the special character of distribution of the Purkinje fibers in the muscles of myocardium ventricles.

Animals↗
PubMed1979

The normal anatomy of the atrial septum in the human heart.

The atrial septum is a blade-shaped structure with a concave anterior margin that reflects the curve of the ascending aorta, a convex posterior margin, and an inferior margin along the mitral annulus. The fossa ovalis comprises an average of 28 per cent of the total septal area, or 43 mm.2 in infants and 240 mm.2 in adults. The channel that persists between the fossa ovalis and the muscular atrial septum is patent except at the limbus, providing a useful explanation for the success of blunt transseptal atrial catheterization and right-to-left shunts in individuals with elevated right atrial pressure.

Adolescent↗
PubMed1976

The development of the septum primum relative to atrial septation in the mouse heart.

The septum primum in the mouse originates as a thickened primordium with a straight rather than a sickle-shaped ventral border. It is covered on its ventral border by anterior cushion material which is continuous over the roof of the atrium with the principal anterior cushion mass. A process of cavitation thins the septum primum and precedes actual fenestration. This process shifts the membranous septum to the left thereby providing room for the septum secundum to overlap on the right side. The septum primum cannot contact the posterior cushion until closure of the sinus venosus gutter which is described. The closure of the interatrial foramen, later the foramen primum, is accomplished by cell growth of the anterior cushion material. The ventral thick border of the septum primum contributes to the ventral limbus and the caudal thickened boundary of the fossa ovalis with some contribution from the left venous valve. These boundaries as well as the membranous portion of the interatrial septum are derived from the same primordium, namely the septum primum.

Animals↗
PubMed1976

The hemodynamic simulation of mitral regurgitation in ventricular septal defect after myocardial infarction.

The development of a ventricular septal defect (VSD) following myocardial infarction is an uncommon complication which clinically can be confused with mitral insufficiency due to infarction of a papillary muscle. The clinical and hemodynamic records of six patients with documented acute VSD secondary to myocardial infarction were analyzed to determine which descriptors would be of value in clinically separating these two entities. All six of our patients had a right heart catheterization showing an oxygen step-up consistent with a VSD, and five had a large pulmonary wedge V wave suggesting concomitant mitral insufficiency. The echocardiogram showed only nonspecific chamber enlargement. Since these patients were being considered for open heart surgery to close the VSD, left and right cardiac catheterization including selective coronary arteriography was done. Despite large V waves being present in the pulmonary wedge and/or left atrial pressure tracing in five of the six patients, no mitral insufficiency was present on the left ventricular cineangiograms. It is concluded that a large pulmonary wedge and/or left atrial V wave does not necessarily indicate mitral insufficiency. Since both a VSD and mitral insufficiency are surgically correctable, patients who develop new holosystolic murmurs following myocardial infarction should have complete right and left heart catheterizations with LV angiography for accurate diagnosis if surgical correction of the lesion is contemplated.

Acute Disease↗
PubMed1979

Chronic oral vasodilator therapy to control heart failure in postinfarction ventricular septal defect.

This report describes a 70-year-old woman with biventricular failure following an anteroseptal infarction complicated by interventricular septal rupture. Treatment with nitroprusside followed by oral hydralazine eliminated the failure and reduced the shunt from 2.75 to 1 to 1.7 to 1. She is asymptomatic post-discharge. Chronic medical therapy including oral vasodilators may be an acceptable alternative to surgery in a small minority of patients with this complication of myocardial infarction.

Administration, Oral↗