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PubMed1980

[The effects of nitroglycerin on coronary blood flow (author's transl)].

In the healthy myocardium, nitroglycerin (NG) produces vasodilatation by a double mechanism: direct action and reflex action through metabolic autoregulation. It also redistributes coronary blood in a manner which benefits the endocardium. In the ischaemic myocardium, the vasodilator effect of NG has not been conclusively demonstrated, yet there is no doubt that the drug redistributes blood in such a way as to benefit both the endocardium and the ischaemic areas. The mechanisms involved here are multiple (dilatation of the collateral vessels and intramural arteries, reduction of oxygen consumption, etc.) and act synergistically. However, the effects of NG on coronary blood flow cannot by themselves account for the anti-anginal properties of the drug, which are to a great extent directly or indirectly assisted by its peripheral systemic effects.

Animals↗
PubMed1982

Effect of nitroglycerin and aortic occlusion on myocardial blood flow.

To better characterize the cardiac and peripheral effects of nitroglycerin during aortic occlusion, we measured myocardial blood flow in 43 normal and pentobarbital (PB)-depressed dogs (groups I to VII). PB was continuously infused in groups IV to VII to maintain reduced cardiac output and contractility. In groups VI and VII nitroglycerin was administered at 2 micrograms/kg/min. Sequential injections of radioactive microspheres (10 micrometers) and hemodynamic measurements were performed during 2-hour occlusions of the infrarenal aorta. The hearts were divided into endocardium, midmyocardium, and epicardium; total and regional blood flows and the ratio of endocardial to epicardial blood flow (endo/epi) were calculated. The results (mean +/- SEM) were subjected to analysis of variance. Normal dogs that underwent aortic occlusion had predictable increases in peripheral vascular resistance. Coronary vascular resistance fell (P less than 0.05) and endo/epi ratios were maintained above 1. Following PB administration, the myocardial blood flow uniformly fell (1.08 +/- 0.34 to 0.55 +/-0.09 ml/min/gm, P less than 0.001), and the animals not treated with nitroglycerin demonstrated decreased endo/epi ratios (1.11 +/- 0-.07 to 0.83 +/- 0.08, P less than 0.001). Although nitroglycerin did not prevent decreases in total myocardial blood flow, endo/epi ratios were maintained above 1 in treated animals (group VI, 1.04 +/- 0.08; group VII, 1.18 +/- 0.17). Furthermore, the increases in left ventricular end diastolic pressure in the untreated animals were significantly greater than those in animals receiving nitroglycerin (P less than 0.01). Despite severe cardiac depression, nitroglycerin maintained normal transmural distribution favoring the endocardium. Since coronary and peripheral vascular resistances were not altered, this benefit most probably reflects decreased ventricular wall tension secondary to preload reduction.

Anesthesia, Inhalation↗
PubMed1983

Transmural myocardial flow distribution during hypothermia. Effects of coronary inflow restriction.

Hypothermic coronary perfusion and blood cardioplegia have been used clinically to minimize intraoperative myocardial damage. However, pressure-flow characteristics in regions supplied by inflow-limiting collateral coronary arteries have not been investigated during hypothermic conditions. In this study tracer microspheres determined transmural myocardial blood flow distribution during cardiopulmonary bypass in normothermic empty, beating dog hearts (EBH), during hypothermic sanguineous perfusion at 15 degrees C (HP), and after hemodilution of cooled (15 degrees C) hearts to a hematocrit value of 20 vol% (HDL). Animals in Group I (N = 8) had normal hearts. Group II dogs (N = 9) had one region supplied predominantly by narrow collateral vessels (CR) and another nourished by normal coronary arteries (NR). Retrograde circumflex pressures were measured continuously for Group II as an additional index of CR perfusion. Flow characteristics in Group I hearts were always similar to the NR of Group II dogs. With HP, endocardial blood flow in the NR decreased from approximately 0.80 to 0.50 ml/min/gm. Subsequently, following HDL this flow increased to approximately 1.70 ml/min/gm, or over twice control levels. In comparison, flow to CR endocardium decreased even more during HP (0.12 ml/min/gm). Even though control flow levels were reestablished in CR endocardium by adding HDL, an unfavorable endocardial/epicardial ratio persisted. With both HP and HDL, retrograde circumflex pressure never changed from EBH values. These data suggest that a significant endocardial flow defect exists during periods of hypothermic sanguineous perfusion and may become more prevalent in regions subserved by inflow-limiting coronary vessels. Similar flow maldistributions may occur in patients if blood-containing cardioplegic solutions are used and during systemic hypothermia. Significant hemodilution helps minimize these imbalances and permits salutary effects of hypothermia to be delivered more evenly across the ventricular wall.

Animals↗
PubMed1982

Effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium of dogs.

The effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium was studied in 45 dogs in vivo. By recording pairs of local electrograms from the endocardium and epicardium and by stimulating the ventricle close to one of a pair of electrodes, we measured conduction times in the subendocardial layer (Endo 1-2), in the subepicardial layer (Epi 1-2), and from the endocardium to the epicardium (Endo-Epi). We then estimated the effect of lidocaine on each of them. In normal myocardium, lidocaine in a therapeutic dose (serum level 2.5 +/- 0.4 micrograms/ml) did not affect any of the three conduction times, but in a larger dose (serum level 6.5 +/- 0.7 micrograms/ml) it prolonged Endo-Epi significantly (P less than 0.05) and Endo 1-2 and Epi 1-2 slightly. In acutely ischemic myocardium caused by single stage ligation of the left anterior descending coronary artery, lidocaine in a therapeutic dose prolonged Endo 1-2 and Endo-Epi significantly (P less than 0.001) in the early stage after administration but did not affect Epi 1-2 simultaneously. Lidocaine in a larger dose, however, prolonged all three conduction times (P less than 0.001). The data indicate that within normal ventricular myocardium, lidocaine does not influence conduction unless its dose is toxic, and that within acutely ischemic ventricular myocardium, at a therapeutic dose, lidocaine prolongs conduction rapidly, but this effect is produced heterogeneously in the ischemic myocardium and is poor in the subepicardial layer.

Animals↗
PubMed1980

[Infective endocarditis: a complication of idiopathic hypertrophic subaortic stenosis (author's transl)].

The idiopathic hypertrophic subaortic stenosis (IHSS) is thought to be infrequently complicated by infective endocarditis. Because IHSS is a disorder of the myocardium and not endocardium is not generally considered to have increased risk of infective endocarditis. Some Authors found, however, that approximately 5% of patients with IHSS develop bacterial endocarditis, because hemodynamically IHSS is like to valvular diseases. Therefore the incidence of endocarditis in IHSS is the same of valvular diseases. The vegetations can be found on anterior mitral valve leaflet, aortic cusps and subaortic endocardium. Some patients have dental surgery prior to the onset of endocarditis and others are infected with oral streptococci. For these reasons prophylactic antibiotics should be administered to patients with IHSS undergoing dental manipulation and in other settings where the risk of developing bacteremia is high. We describe one case of IHSS complicated with streptococcus viridans endocarditis. Vegetations, determined with echocardiography, were present on anterior mitral valve leaflet, aortic right coronary cusp and interventricular septum. In a review of literature we are been able to find twenty-seven cases of IHSS complicated with endocarditis.

Cardiomyopathy, Hypertrophic↗
PubMed1981

Early differentiation of the heart in mouse embryos.

The differentiation of the heart was examined in mouse embryos, isolated between the afternoons of the eighth and ninth day of gestation, by means of scanning electron microscopy as well as by light microscopy of standard histological material and thin plastic sections. Cavitation within the presumptive pericardial mesoderm commences during the late presomite stage (afternoon of eighth day) and myocardial rudiments are established by thickening of the pericardial lining adjacent to the endoderm near the base of the foregut pocket. At first the thickening lies on the ventral aspect of the pericardial cavity but, as the foregut pocket deepens and the trunk region of the embryo moves en masse caudally and ventrally, it comes to lie on the dorsal wall. A separate layer of cells comprising the primitive endocardium differentiates deep to the myocardial thickening, between the latter and the endoderm. Cavitation of the endocardial tissue occurs bilaterally about the 1-2 somite stage so as to establish bilateral endocardial tubes. These endocardial tubes become enclosed within the myocardial mantle which bulges into the pericardial cavity. A layer of acellular material (the cardiac jelly) appears between the endocardium and myocardium at about this time. At about the 4-somite stage, the endocardial tubes coalesce across the mid-line to establish a single median cardiac tube, and the entire heart rudiment is suspended in the mid-line by a wide dorsal mesocardium. Our observations indicate that, contrary to previous views, at no time during cardiogenesis in the mouse are two distinct heart primordia present which subsequently fuse to form a single median entity. The principal similarities and differences between cardiogenesis in the mouse, and mammals in general, and avians are discussed.

Animals↗
PubMed1981

[Determination of right ventricular volume by subxiphoid two-dimensional echocardiography (author's transl)].

To establish the measurement method of right ventricular (RV) volume by two-dimensional (2-D) echocardiography, a comparative study was performed in respect to the quantitative evaluations of the RV areas or volumes obtained by biplane 2-D echographic and angiographic methods. At first, a preliminary investigation was performed to define the optimum tracing of the endocardial surface on the 2-D echogram by using a fresh mongrel dog heart. It was revealed that the 2-D echographic views of the ventricular surface contained some artifact echoes inside the true echo of the endocardium. As a result, the optimum line for tracing was considered to be in external margin of the echo which seemed to represent the endocardium. This technique was then applied to 10 patients with congenital heart disease who were followed by cardiac catheterization. Ages ranged from 9 months to 5 years with an average of 2 years and 4 months. The RV was imaged by a subxiphoid approach. The RV apex, pulmonary valve (PV) and mid-portion of the tricuspid valve were showed in a frontal view, which allowed to measure the frontal RV area (f). In a sagittal plane, the RV wall and the PV were imaged, and then the lateral area (l) and the RV long axis (d) were measured. From the biplane cineangiography, the frontal RV area (f') lateral area (l'), RV long axis (d') and RV end-diastolic volume (EDV) by arealength method were calculated. The f and l were correlated with the f' (r = 0.90) and with the l' (r = 0.86), respectively. However, the values by the echocardiographic measurement were smaller than those by the cineangiographic ones. The f was also well correlated with the RVEDV (r = 0.94). The f.l/d, considered to represent a variable of echography measurement of the RV volume by area-length method, was well correlated with the RVEDV (r = 0.84). Although there are still some problems related to the imaging technique and sharpness of the echogram, further improvement to establish a echocardiographic measurement of RV volume is expected with the advance of the techniques.

Animals↗
PubMed1980

[Types of pathomorphological changes in the heart caused by cardiostimulating electrodes].

Reaction at the site of pacemaker electrode was examined at post-mortem by morphological and histological means in a group of 18 deceased patients with pacemakers implanted through the endovasal channels. The changes were classified into 5 basic types depending on their nature and rate of incidence: changes in the endocardium (connective tissue bridging of the electrode, and changes in the tricuspid valve) and in the myocardium (electrode penetration, reaction under the tip of the electrode, and no changes). The particular types occurred either independently of each other, in in mutual combination. Electrode fixation to the endocardium by means of connective-tissue organizing wall thrombi was found in 97% of all the cases examined. There was no unambiguous proof of the duration of pacemakers electrode implantation as being directly dependent on the extent of connective tissue bridging of the electrode. There were exceptional cases of malacia or scars in the myocardium under the tip of the electrode in the normal position of the electrode in patients with myocarditis.

Adult↗
PubMed1995

Localized mitochondrial dysfunction in canine myocardial ischemia.

Effects of myocardial ischemia on mitochondrial enzymes and mitochondrial DNA (mtDNA) were examined using the model of Ameroid constriction of canine cardiac vessels. Endocardium supplied by constricted coronary arteries was found to have significantly lower citrate synthase and complex IV activities compared to values obtained from either epicardium supplied by constricted vessels or endocardium supplied by unconstricted coronary arteries. Neither significant differences in mtDNA copy number nor changes in respiratory complexes I, III and V were detected. These results suggest that highly localized, specific mitochondrial enzyme changes result from chronic myocardial ischemia.

Animals↗
PubMed1976

Orientation of the fascicles of the ventricular myocardium.

A new technique was developed to examine the arrangement of the fascicles of the myocardium. Liquid plastic was injected intramurally into the free walls and the septum of more than 300 hearts of mammals and birds. After the plastic hardened, the tissues were digested in alkali, thereby releasing a plastic cast which had been formed in the myocardium. The plastic plates formed in the heart were consistently perpendicular to the surfaces of the epicardium and the endocardium. Related studies have shown that each cluster or clone of muscle fibers is contained in a fibrous connective tissue capsule. The injected plastic is therefore confined to the trabecular (extracapsular) clefts which define the borders of the capsules. The casts show that the capsules containing the muscle fibers are arranged in the planes of great circles of the myocardial spheroid. These capsules are shaped as wedges with acute angles at the endocardium, and with dihedral angles less than 1 degree. Interventricular sulci interrupt and separate the capsules of the right free wall from the left free wall. Septal capsules are separated from but aligned with the long directions of the capsules of the adjacent free walls. These data challenge the currently accepted concept of the bandage-like arrangement of the myocardial fascicles. The significance of our findings with respect to myocardial function is discussed.

Animals↗
PubMed1993

[Tendon of Todaro in the human heart].

The material consists of 50 human hearts without either pathological changes or congenital malformations. Macroscopic and microscopic methods were applied. Histological specimens were stained alternatively with hematoxylin-eosin and according to van Giesson and Masson. In each heart the tendon of Todaro was dissected from its portion situated between the inferior vena cava and coronary sinus up to central part of the membranous septum (Fig. 1). The hearts were divided into 3 groups according to age: fetuses (20 hearts), infants (15) and adults (15) (Table I). In all hearts of fetuses and infants the tendon of Todaro was found to be a well-developed cylindrical structure covered with endocardium. In histologic specimens the tendon was s solid structure well-separated from other tissues (Fig. 3, Fig. 4). In hearts of adults (17-45 years old) the tendon of Todaro was less evident. However, in histological specimens it was present as a compact connective tissue band (Fig. 2). In hearts of subjects older than 50, the endocardium of this area was not elevated and not distinguishable even by palpation. The connective tissue band was formed by rather dissipated fibres, poorly separated from surrounding structures. As a result of our study one may conclude that the tendon of Todaro is present in each human heart. It is well-developed in hearts of fetuses and infants. Later it diminishes gradually becoming almost inconspicuous in old subjects.

Adolescent↗
PubMed1993

[Non-pharmacological treatment of ventricular tachycardia (anti-arrhythmic surgery excluded)].

There has been real change in the treatment of VT in recent years including the promotion of non-medical methods. In the large group of non-responders to medical therapy, only a minority offers possibilities of radical surgical treatment of VT. In the others, two options remain: ablative methods and implantable automatic cardioverter defibrillators. The destruction of foci of tachycardia by catheterisation necessitates prior investigation of the ventricular endocardium with recordings of endocardial electrograms during VT. Criteria defining the zone for ablation are two-fold: either the zone of earliest endocardial depolarisation or the exit zone (generally preceding the tachycardia QRS complexes by 20 to 30 ms). The second is the zone of slow conduction which corresponds to the cardiac substrate in which the tachycardia arises. In the absence of satisfactory mapping, localisation of the ablation target may be performed by stimulating the endocardium at different points with the aim of reproducing the tachycardia QRS complexes. Two types of physical agents have been used for ablation: high energy electric shocks and, at present, radiofrequency currents. Complications of the procedure are rare: thromboembolism, cardiac rupture, cardiogenic shock in patients with initially poor hemodynamic conditions. Prevention of VT is obtained in over half the cases providing complementary antiarrhythmic therapy is prescribed. The other alternative is the implantable automatic defibrillator which is tending to take over the leading role in non-pharmacological treatment of VT. At first, these devices were exclusively defibrillators but nowadays they have anti-tachycardia functions which widen the indications to include subjects with sustained VT even in the absence of cardiac arrest.(ABSTRACT TRUNCATED AT 250 WORDS)

Catheter Ablation↗
PubMed1993

Myocardial distribution of cardioplegic solution after retrograde delivery in patients undergoing cardiac surgical procedures.

The myocardial distribution of both antegrade and retrograde cardioplegia for cardiac surgical intervention, after induction of cardioplegia via the aortic root, was directly assessed and compared in 19 patients by means of contrast echocardiography. Two-dimensional transesophageal echocardiographic images of the short axis of the left ventricle at the level of the papillary muscles were obtained after sonicated Renografin-76 microbubbles were injected into an aortic root and/or transatrial coronary sinus catheter during delivery of cardioplegic solution. Segmental distribution of cardioplegic solution was immediately noted in the myocardium at the time of contrast injections. In 11 of 18 patients (61%) cardioplegic solution was dispersed to all left ventricular myocardial segments after antegrade delivery. In 17 of 19 patients (90%) retrogradely delivered cardioplegic solution (after antegrade induction of cardioplegia in 18 of the 19 patients) was dispersed to all the left ventricular myocardial segments, including the septum. In 2 of the patients, initial lack of retrograde distribution of cardioplegic solution was remedied when the coronary sinus catheter was repositioned and contrast cardioplegic solution was reinjected. Imaging of the right ventricle was possible in only 4 of the 19 patients and revealed that after retrograde delivery, cardioplegic solution had been at least partially distributed to the right ventricle as well. We performed off-line videodensitometric analysis in 9 patients after retrograde delivery of cardioplegic solution. Mean peak pixel-intensity ratio of flow from the endocardium to the epicardium in the left ventricular free wall was 1.46 +/- 0.27, and mean peak pixel-intensity ratio of flow from the left to the right intraventricular septal endocardium was 1.39 +/- 0.33 (p < or = 0.05).

Aged↗
PubMedDate not supplied

Anatomy, histology, and development of the cardiac valvular system in elasmobranchs.

We report here on the anatomy, histology, and development of the three sets of cardiac valves in embryonic and adult elasmobranch fishes. The sinus venosus is the first segment of the heart to receive blood, and a pair of sinoatrial (SA) valves prevent backward flow of blood into the sinus venosus. The SA valves derive from two dorsolateral infoldings of the cardiac wall and consist of a simple endocardium covering transverse sheets rich in collagen. The SA valves are simple flaps of tissue without papillary muscles or chordae tendineae. Blood from the atrium passes the atrioventricular (AV; semilunar) valves, which are attached to papillary muscles in the ventricle by way of the chordae tendineae. A series of rows of conal or pocket valves (CV) in the conus arteriosus, equipped with chordae tendineae but no papillary muscles, prevent blood from reentering the ventricle. Chordae tendineae form in a similar fashion in both chambers. Elevations from the chamber wall emerge as a sheet covered on both surfaces with endocardium and separated by a core of connective tissue. Endocardial cells extend basal projections toward the opposing epithelium through their basal laminae. Basal cell projections make contact to create perforations that enlarge to produce spaces between the nascent chordae. Fibroblasts in the core of the chordae enlarge and strengthen the chordae by producing linear arrays of collagen fibers.

Aging↗
PubMed1996

Effects of afterload on regional left ventricular torsion.

OBJECTIVE: To determine if left ventricular torsion, as measured by magnetic resonance tissue tagging, is afterload dependent in a canine isolated heart model in which neurohumoral responses are absent, and preload is constant. METHODS: In ten isolated, blood perfused, ejecting, canine hearts, three afterloads were studied, while keeping preload constant: low afterload, high afterload (stroke volume reduced by approx. 50% of low afterload), and isovolumic loading (infinite afterload). RESULTS: There were significant effects of afterload on both torsion (P < 0.05) and circumferential shortening (P < 0.0005). Between low and high afterloads, at the anterior region of the endocardium only, where torsion was maximal, there was a significant reduction in torsion (15.1 +/- 2.2 degrees to 7.8 +/- 1.8 degrees, P < 0.05). Between high afterload and isovolumic loading there was no significant change in torsion (7.8 +/- 1.8 degrees to 6.2 +/- 1.5 degrees, P = NS). Circumferential shortening at the anterior endocardium was significantly reduced both between low and high afterload (-0.19 +/- 0.02 to -0.11 +/- 0.02, P < 0.0005), and also between high afterload and isovolumic loading (-0.11 +/- 0.02 to 0.00 +/- 0.02, P < 0.05). Plots of strains with respect to end-systolic volume demonstrated a reduction in both torsion and shortening with afterload-induced increases in end-systolic volume. Torsion, but not circumferential shortening, persisted at isovolumic loading. CONCLUSIONS: Maximal regional torsion of the left ventricle is afterload dependent. The afterload response of torsion appears related to the effects of afterload on end-systolic volume.

Animals↗
PubMed1996

[The architectonics of the lymphatic networks in the sheep heart].

Lymphatic networks of the heart were studied in sheep. Principal scheme of lymphatic networks structural organization in endocardium, myocardium and epicardium of the mammals studied was established to have a series of regularities similar to those in man and animals although possessing specific peculiarities. Lymphomicrocirculatory bed of the heart is composed of interdependent lymphatic networks of endocardium, myocardium and epicardium. Endocardial and epicardial lymphatic networks are plane and single-layered, while myocardial one is spatial. All heart coats lymphatic networks are characterized with local peculiarities (different loop parameters, capillary diameter and density in some areas) which indicates varying drainage and state of metabolism in different heart region.

Aging↗
PubMedDate not supplied

Intravenous basic fibroblast growth factor protects the lung but not mediastinal organs against radiation-induced apoptosis in vivo.

PURPOSE: We evaluated the therapeutic potential of intravenously injected basic fibroblast growth factor against the lethal syndromes associated with irradiation of intrathoracic organs and assessed whether such protection might be associated with inhibition of programmed cell death (apoptosis) in the exposed tissues. MATERIALS AND METHODS: C3H/HeJ and C3H/scid mice received either whole-chest, mediastinal, or bilateral lung irradiation. Human recombinant basic fibroblast growth factor was injected intravenously at doses of 400 ng immediately before and after irradiation, and then at 1 hour and 2 hours later. Time-adjusted survival was calculated from the date of irradiation by the product-limit Kaplan-Meier method. Detection of apoptotic changes in paraffin sections was performed by the DNA terminal transferase nick-end translation method. RESULTS: Basic fibroblast growth factor protected the lungs but not other intrathoracic organs against radiation-induced damage. When radiation was restricted to the lungs, the LD50/180 from radiation pneumonitis was 20.75 Gy and increased to 23.0 Gy in basic fibroblast growth factor-treated mice. When the whole thorax was irradiated, basic fibroblast growth factor partially protected against pneumonitis at the low range of radiation doses (< or = LD50/180), but failed to confer protection at higher doses, nor did it protect against lethal radiation esophagitis. Staining for the presence of apoptotic nuclei revealed time- and radiation dose-dependent development of apoptosis in endothelial cells of the pulmonary capillary network, endocardium, and mesothelial cells of the pleura and pericardium. Although basic fibroblast growth factor inhibited apoptosis in the microvascular endothelium and the endocardium, it had no effect on apoptosis in the serosal mesothelium of the pleura and pericardium. CONCLUSIONS: Intravenous basic fibroblast growth factor protects against the apoptotic microvascular component of early-phase radiation pneumonitis but may have no effect on other elements of the primary damage produced by radiation in the lungs and other intrathoracic organs. Understanding the patterns and temporal evolution of radiation-induced apoptosis and basic fibroblast growth factor-mediated antiapoptotic effects in thoracic organs and tumors may offer opportunities for pharmacologic intervention in the radiotherapeutic management of primary and metastatic lung tumors.

Animals↗
PubMed1997

Left ventricular aneurysms: the endoventricular circular patch plasty.

The endoventricular circular patch plasty (EVCPP) technique was first used by us in 1984 to re-establish a more normal morphology of the left ventricular cavity distorted by post-myocardial infarction scar tissue. This technique includes the placement of a subendocardial circumferential pursestring suture inside the left ventricle around the base of the aneurysm at the junction of scarred and normal endocardium. A patch is then placed at this level to establish a new contour for the left ventricular cavity. Because this patch is placed at the junction of scar and normal endocardium, a substantial portion of the distal ventricular septum is excluded from the left ventricular cavity. The overall hospital mortality in our series of more than 715 cases is approximately 7% and, in the survivors, the ejection fraction is increased an average of 0.10.

Heart Aneurysm↗