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PubMed1996

Distribution of cAMP-activated chloride current and CFTR mRNA in the guinea pig heart.

Guinea pig ventricular myocytes exhibit a Cl(-)-selective current regulated by the cAMP-dependent pathway. We have investigated the distribution of cAMP-activated Cl- channel current density and cystic fibrosis transmembrane-conductance regulator (CFTR) mRNA in three regions of the guinea pig heart: the atrium, and the epicardium and endocardium of the free wall of the left ventricle. The regional differences in the Cl- current density were investigated in enzymatically isolated myocytes using the whole-cell patch-clamp technique. Forskolin (1 mumol/L) activated Cl(-)-selective currents in all ventricular myocytes and 21% of atrial myocytes examined. The conductance density, estimated as the outward chord conductance normalized to cell capacitance, was greatest in epicardial myocytes (79.8 +/- 8.4 pS/pF, n = 21) and significantly lower in endocardial (59.8 +/- 9.5 pS/pF, n = 22) and atrial (10.9 +/- 5.0 pS/pF, n = 38) myocytes. The regional differences in CFTR mRNA expression levels were investigated by competitive reverse-transcribed polymerase chain reaction. The regional distribution of the mRNA levels was similar to that of the Cl- conductance density, ie, highest in the epicardium (23230 +/- 1840 molecules/microgram total RNA, n = 3), significantly lower in endocardium (10610 +/- 780 molecules/microgram total RNA, n = 3), and lowest in atrium (1450 +/- 290 molecules/microgram total RNA, n = 3). The data indicate that regional differences in CFTR mRNA expression in the guinea pig heart are responsible, at least in part, for the regional differences in cAMP-activated Cl- current density.

Animals↗
PubMed1998

Purkinje-muscle reentry as a mechanism of polymorphic ventricular arrhythmias in a 3-dimensional model of the ventricles.

Multiple electrode mapping of the ventricles during complex tachyarrhythmias has revealed focal subendocardial activation whose mechanism remains unexplained. We hypothesized that reentry involving the Purkinje-muscle junctions (PMJs) may be a mechanism for such focal excitations. We have constructed an anatomically appropriate computerized 3-dimensional model of the mammalian ventricles that includes the Purkinje conduction system and 214 PMJs distributed throughout the endocardium. Isochronal maps during normal excitation, as well as during right or left bundle branch block, resembled experimental measurements and compared well with isochronal maps of propagation in the human heart. Activity observed at both sides of a PMJ in the model showed that propagation from Purkinje fibers to muscle was slower than in the opposite direction. Under these realistic and normal conditions, the evolution of reentrant activity involving muscle and the Purkinje network was simulated. The reentry pattern was independent of the initiation site. It evolved with drifting epicardial breakthroughs and transformed on the endocardium from focal activity to figure-of-8 reentry. In addition, the ECG amplitude undulated during the evolution, and decrease in the cycle period, apparent wavelength, and propagation velocity were observed. Finally, the reentry was terminated if the Purkinje system was disconnected from the muscle before it reached a relative steady state. The simulation results suggest the following: (1) Epicardial breakthroughs and endocardial focal activity may originate at the PMJs. (2) The ECG amplitude may decrease as the reentry stabilizes and the excitation wavelength decreases. (3) The Purkinje system may have a double role in the evolution of reentry: first, it is essential to the reentry at the initial stage; second, it may lead to the establishment of intramyocardial reentry, at which time the Purkinje system becomes irrelevant.

Action Potentials↗
PubMed2002

Mitochondrial preference for short chain fatty acid oxidation during coronary artery constriction.

BACKGROUND: Reduced fatty acid oxidation in hypoperfused myocardium is believed to result from impaired oxidation in mitochondria. This study suggests another mechanism, that oxidative capacity exceeds regulated entry of long chain fatty acid (LCFA). The ability of myocardium to oxidize fatty acids and metabolize glucose during stenosis was examined in open chest, anesthetized pigs. METHODS AND RESULTS: The left anterior descending (LAD) coronary artery was infused for 40 minutes (5 mL/min LAD) with [2-(13)C] butyrate (4 mmol/L), a short chain fatty acid (SCFA), plus [2-(13)C] glucose (10 mmol/L) in either nonischemic controls (n=4) or at the end of 5 hours of LAD flow reduction (40%, n=7). With LAD constriction, left ventricular wall thickening fell 45+/-8% (P<0.01). Despite glycolytic production of lactate and alanine, hypoperfused myocardium preferentially oxidized SCFA over endogenous LCFA. SCFA accounted for 63+/-4% (mean+/-SEM) of carbon units entering oxidation in both ischemic epicardium and endocardium versus only 38+/-4% and 40+/-6% in respective samples from normal myocardium (P<0.002). Unexpectedly, SCFA contributions were elevated in both endocardium and epicardium despite preserved epicardial blood flow versus a 58+/-9% drop in endocardial flow (P<0.05). No significant oxidation of glucose was evident, indicating that unlabeled fuels were primarily LCFA. CONCLUSIONS: Because SCFA bypass LCFA transport into mitochondria, during LAD constriction, mitochondrial capacity to oxidize fatty acid exceeds LCFA entry for oxidation. Importantly, metabolic changes were disassociated from transmural tissue perfusion. These findings suggest that signals other than oxygen availability regulate fatty acid use during hypoperfusion.

Animals↗
PubMed1984

Effect of nitroglycerin on regional myocardial blood flow following an experimental coronary spasm.

This study was designed to evaluate the effect of nitroglycerin (30 micrograms given as an i.v. bolus) on regional distribution of myocardial blood flow in conscious dogs, following an acute coronary occlusion similar to a coronary spasm. The left anterior descending (LAD) coronary artery was acutely occluded with a balloon cuff occluder. The distribution of blood flow between the endocardium and the epicardium of both the normal and ischemic area of the left ventricle was determined by means of the radioactive microsphere technique. Acute occlusion of the left anterior descending coronary artery produced a significant decrease of blood flow reaching the area irrigated by this artery; this decrease was of a lesser magnitude after administration of nitroglycerin. In addition, ischemia produced a disproportionate decrease in endocardial blood flow. This decrement was also of a lesser magnitude following administration of nitroglycerin. Blood perfusion to the non-ischemic myocardium was not altered. These results indicate that an intravenous bolus of nitroglycerin, given after a brief coronary occlusion simulating a coronary spasm, increases blood flow to the ischemic myocardium, induces a favorable redistribution of blood flow toward the ischemic endocardium and does not produce any decrement of blood perfusion to the non-ischemic myocardium.

Animals↗
PubMed2004

Antiarrhythmic and proarrhythmic properties of QT-prolonging antianginal drugs.

In recent years there has been a major reorientation of drug therapy for cardiac arrhythmias, its changing role, and above all, a radical change in the class of arrhythmia drugs because of their impact on mortality. The decline in the use of sodium-channel blockers has led to an ex panding use of beta-blockers and simple or complex class III agents for controlling cardiac arrhythmias. Success with these agents in the context of their side effects has spurred the development of compounds with simpler ion-channel blocking properties that have less complex adverse reactions. The resulting so-called pure class III agents, such as dofetilide or ibutilide, were found to have antifibrillatory effects in atrial fibrillation and flutter and in ventricular tachyarrhythmias. Such agents are effective and have diversity, but they have come into therapeutics with a price: the sometimes-fatal torsades de pointes. The drug amiodarone, a complex compound that was synthesized as an antianginal agent, has been an exception in this regard. Its therapeutic use is associated with a negligibly low incidence of torsades de pointes, even though the drug produces significant bradycardia and QT lengthening to 500 to 700 msec. Recent electrophysiologic studies suggest that this paradox is likely due to the differential block of ion channels in endocardium, epicardium, midmyocardial (M) cells, and Purkinje fibers in the ventricular myocardium. There is also clinical evidence suggesting that amiodarone reduces the "torsadogenic" effects of pure class III agents. Ranolazine was also synthesized for the development of antianginal properties that stem from a partial inhibition of fatty acid oxidation; it too has been found to have electrophysioloigic properties. These are somewhat similar to those of amiodarone on ion channels in endocardium, epicardium, M cells, and Purkinje fibers in the ventricular myocardium, but the drug does not prolong the QT interval to the same extent as amiodarone does. Thus, the drug produces modest increases in repolarization as judged by its effects on the action potential duration (APD) without the potential for the development of torsades de pointes. By virtue of its suppressant action on early afterdepolarizations and triggered activity in Purkinje fibers and M cells, the drug appears to have a powerful potential for reducing the torsadogenic proclivity of conventional class III antiarrhythmic compounds. The rationale for the therapeutic niche for amiodarone, and especially in the case of ranolazine, in the prevention of drug-induced torsades de pointes is discussed.

Angina Pectoris↗
PubMed2005

Tbx20 is essential for cardiac chamber differentiation and repression of Tbx2.

Tbx20, a member of the T-box family of transcriptional regulators, shows evolutionary conserved expression in the developing heart. In the mouse, Tbx20 is expressed in the cardiac crescent, then in the endocardium and myocardium of the linear and looped heart tube before it is restricted to the atrioventricular canal and outflow tract in the multi-chambered heart. Here, we show that Tbx20 is required for progression from the linear heart tube to a multi-chambered heart. Mice carrying a targeted mutation of Tbx20 show early embryonic lethality due to hemodynamic failure. A linear heart tube with normal anteroposterior patterning is established in the mutant. The tube does not elongate, indicating a defect in recruitment of mesenchyme from the secondary heart field, even though markers of the secondary heart field are not affected. Furthermore, dorsoventral patterning of the tube, formation of working myocardium, looping, and further differentiation and morphogenesis fail. Instead, Tbx2, Bmp2 and vinexin alpha (Sh3d4), genes normally restricted to regions of primary myocardium and lining endocardium, are ectopically expressed in the linear heart tube of Tbx20 mutant embryos. Because Tbx2 is both necessary and sufficient to repress chamber differentiation (Christoffels et al., 2004a; Harrelson et al., 2004), Tbx20 may ensure progression to a multi-chambered heart by repressing Tbx2 in the myocardial precursor cells of the linear heart tube destined to form the chambers.

Animals↗
PubMed1992

Interactions between retinoids and TGF beta s in mouse morphogenesis.

Using immunocytochemical methods we describe the distribution of different TGF beta isoforms and the effects of excess retinoic acid on their expression during early mouse embryogenesis (8 1/2 - 10 1/2 days of development). In normal embryos at 9 days, intracellular TGF beta 1 is expressed most intensely in neuroepithelium and cardiac myocardium whereas extracellular TGF beta 1 is expressed in mesenchymal cells and in the endocardium of the heart. At later stages, intracellular TGF beta 1 becomes very restricted to the myocardium and to a limited number of head mesenchymal cells; extracellular TGF beta 1 continues to be expressed widely in cells of mesenchymal origin, particularly in head and trunk mesenchyme, and also in endocardium. TGF beta 2 is widely expressed at all stages investigated while TGF beta 3 is not expressed strongly in any tissue at the stages examined. Exposure of early neural plate stage embryos to retinoic acid caused reduced expression of TGF beta 1 and TGF beta 2 proteins but had no effect on TGF beta 3. Intracellular TGF beta 1 expression was reduced in all tissues except in the myocardium, while extracellular TGF beta 1 was specifically reduced in neuroepithelium and cranial neural crest cells at early stages. TGF beta 2 was reduced in all embryonic tissues. The down-regulation of intracellular TGF beta 1 was observed up to 48 hours after initial exposure to retinoic acid while some down-regulation of TGF beta 2 was still seen up to 60 hours after initial exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

In vivo induction of cardiac Purkinje fiber differentiation by coexpression of preproendothelin-1 and endothelin converting enzyme-1.

The rhythmic heart beat is coordinated by electrical impulses transmitted from Purkinje fibers of the cardiac conduction system. During embryogenesis, the impulse-conducting cells differentiate from cardiac myocytes in direct association with the developing endocardium and coronary arteries, but not with the venous system. This conversion of myocytes into Purkinje fibers requires a paracrine interaction with blood vessels in vivo, and can be induced in vitro by exposing embryonic myocytes to endothelin-1 (ET-1), an endothelial cell-associated paracrine factor. These results suggest that an endothelial cell-derived signal is capable of inducing juxtaposed myocytes to differentiate into Purkinje fibers. It remains unexplained how Purkinje fiber recruitment is restricted to subendocardial and periarterial sites but not those juxtaposed to veins. Here we show that while the ET-receptor is expressed throughout the embryonic myocardium, introduction of the ET-1 precursor (preproET-1) in the embryonic myocardium is not sufficient to induce myocytes to differentiate into conducting cells. ET converting enzyme-1 (ECE-1), however, is expressed preferentially in endothelial cells of the endocardium and coronary arteries where Purkinje fiber recruitment takes place. Retroviral-mediated coexpression of both preproET-1 and ECE-1 in the embryonic myocardium induces myocytes to express Purkinje fiber markers ectopically and precociously. These results suggest that expression of ECE-1 plays a key role in defining an active site of ET signaling in the heart, thereby determining the timing and location of Purkinje fiber differentiation within the embryonic myocardium.

Animals↗
PubMed1998

Morphometric and biochemical characteristics of ventricular hypertrophy in male rainbow trout (Oncorhynchus mykiss).

We examined the morphometric and biochemical effects of ventricular hypertrophy in male rainbow trout (Oncorhynchus mykiss) during sexual maturation. Our investigation focused on characterizing the growth of ventricular layers, on cardiomyocyte dimensions (length, cross-sectional area and cell volume) and on the activities of enzymes involved in intermediary metabolism. Relative ventricle mass (100 x ventricle mass/body mass) increased by as much as 2.4-fold during sexual maturation [as defined by an increasing gonadosomatic index (100 x gonad mass/body mass)], and this resulted in an increased proportion of epicardium relative to endocardium. Ventricular enlargement was associated with increased length (+31 %) and transverse cross-sectional area (+83 %) of cardiomyocytes, which resulted in an expansion of up to 2.2-fold in mean myocyte volume (from 1233 to 2751 micron3). These results indicate that sexual maturation induces ventricular enlargement through myocyte hypertrophy. Cell length and cross-sectional area were similar in both myocardial layers, and myocytes were elliptical rather than circular in transverse cross section. Ventricular hypertrophy did not alter transverse cell shape, perhaps reflecting the maintenance of short diffusion distances for small molecules as cells hypertrophy. Myocyte hypertrophy could not account entirely for the sevenfold range of ventricle masses from different-sized fish, indicating that myocyte hyperplasia contributes substantially to ventricular growth as trout grow. Measurements of the maximal activities of metabolic enzymes demonstrated that ventricular hypertrophy was associated with (1) higher epicardial but not endocardial activities of citrate synthase (by 23 %) and beta-hydroxyacyl-CoA dehydrogenase (by 20 %); (2) lower activities of hexokinase (by 50 %) in both layers, and (3) no change in lactate dehydrogenase or pyruvate kinase activities, which were also similar between layers. These results suggest that the energetic needs of the hypertrophied trout ventricle may be met through increased reliance on fatty acid oxidation, particularly by the endocardium, but decreased reliance on glucose as a metabolic fuel in both layers.

Animals↗
PubMed1999

Expression of extracellular matrix components fibronectin and laminin in the human fetal heart.

It has been well documented that the extracellular matrix components fibronectin and laminin promote or regulate morphogenesis of the myocardial cells in mammalian heart. However, their chronological change of expression (or localization) in the human heart remains elusive. In this study, fibronectin and laminin in the left ventricle of forty-two human fetuses aged from 8 to 26 weeks gestation and left ventricular tissues obtained from a 2-week old infant and two adults were investigated by Western blot analyses and indirect immunofluorescence technique with monoclonal antibodies. In the fetal heart, fibronectins were present along the endocardium, epicardium, and linings of larger blood vessels. In 14-16 weeks gestation, fibronectin immunofluorescence became stronger but not evenly dispersed in the interstitium. After 24 weeks gestation, they were strongly positive only in the relatively larger blood vessels, as well as those in the infant and adult cardiac tissues. Laminins were strongly positive along the endocardium and basement membrane of the myocardial cells and fibroblasts during fetal life. After birth, laminins formed fine fibrillar network along the basement membrane in association with the transverse tubules of myocardial cell; these morphological characteristics remained in the adult cardiac tissues. These results indicate that fibronectin expression is relatively constant during fetal life but decreases after birth; in contrast, laminin expression is not age-dependent and constant throughout the life.

Adult↗
PubMed2003

Novel approach to the quantitation of regional left ventricular systolic and diastolic function using tissue Doppler imaging to create a myocardial velocity profile and gradient.

The myocardial velocity profile (MVP) and gradient (MVG) between the endocardium and epicardium of the left ventricular (LV) wall measured by color-coded tissue Doppler imaging (TDI) are new indices for evaluating regional LV myocardial function. However, accurate recording and measurement of the MVP is difficult using conventional methodology because of the stochastic nature of the ultrasound signal; that is, the effect of speckled noise. The aim of this study was to validate the accuracy and establish the validity of a newly developed method for measuring the MVP and MVG using 10 clinically normal controls and 10 patients with a hypertensive hypertrophied LV posterior wall. A non-isotropic, averaging algorithm was developed that was capable of obtaining a stable MVP (averaged MVP). Averaged MVP was recorded using parasternal, LV short-axis, color-coded TDI, placing regions of interest along the LV posterior wall with the reference point for angle-correction being at the center of LV contraction. The velocity from epicardium to endocardium within the region of interest was automatically angle-corrected to calculate the velocity component radially relative to the LV cavity and was spatially averaged along the circumference within the region of interest. Inter- and intraobserber variabilities of measurements were lower in the averaged MVP and MVG than in the conventional MVP and MVG. The correlation coefficients of the linear regression lines of systolic and early diastolic MVPs in the LV posterior wall were higher in all controls and hypertensive patients with the averaged method than with the conventional TDI procedures. The mean peak systolic and early diastolic MVGs were lower in the hypertensive group than in the controls. In conclusion, the newly developed averaged MVP provides a stable and reproducible index for the quantitative assessment of regional LV myocardial function.

Adult↗
PubMed2000

Time course of left ventricular remodeling after myocardial infarction: a two-dimensional echocardiographic study.

In order to forecast the clinical course of acute myocardial infarction (MI), the time course of the functional changes of the left ventricular myocardium that result in remodeling was evaluated with two-dimensional echocardiography (2DE). The study group comprised 45 patients with anterior MI treated with successful percutaneous transluminal coronary angioplasty. 2DE studies were performed on days 1, 3, 7 and 14; months 1 and 3 and 1 year after MI, and the following parameters were recorded: (1) infarcted wall thickness, (2) traced length of the endocardium and of the epicardium on end-diastolic apical long axis images, and (3) wall motion score (total of asynergy scores of 16 segments of left ventricle (LV); normal: 0, hypokinesis: 1, akinesis: 2, dyskinesis: 3). According to the peak creatine kinase (CK) level, patients were classified into L group (CK > or =8000 U/L, n=16), M group (8000> CK > or =4000, n=13) and S group (CK <4000, n=16). The following results were obtained. (1) There was progressive thinning of the infarcted myocardium up to 1 month after (1 day: 9.3+/-1.7, 14 days: 6.3+/-1.7 vs 1 month: 5.9+/-1.8 mm, p<0.05; vs 1 year: 5.9+/-1.9 mm, NS). (2) Dilatation of the LV cavity occurred shortly after MI and continued up to 14 days (endocardium at 14 days: 176.8+/-13.6 vs 1 day: 164.1+/-11.4 mm, p<0.01; vs 1 year: 176.3+/-12.7 mm, NS). (3) The wall motion score improved rapidly by 14 days, and continued to improve gradually to 1 year (1 day: 12.2+/-3.4, 14 days: 6.8+/-4.0, 1 year: 4.6+/-3.1). (4) The expansion ratio (endocardial length at 14 days/1 day) was significantly greater in the L group than in the S group (p<0.05). Comparing the groups, the LV cavity of the L group remained dilated up to 14 days, whereas that of the S and M groups was dilated up to 7 days (L group 14 days: 179.3+/-11.9 vs 1 day: 156.9+/-9.2mm, p<0.01; vs 1 year: 180.0+/-14.1 mm, NS) (S group 7 days: 171.7+/-13.6 vs 1 day: 161.5+/-7.2 mm, p<0.01; vs 1 year: 172.7+/-14.4 mm, NS) (M group 7 days: 170.5+/-10.5 vs 1 day: 157.7+/-14.5 mm, p<0.05; vs 1 year: 177.08+/-9.6 mm, NS). Serial 2DE on days 1 and 14 after MI were useful for evaluating the course of LV remodeling and to forecast cardiac function in the chronic phase of MI. Determining the length of hospital stay on the basis of infarction size is justified.

Aged↗
PubMed2001

Left ventricular epicardial outflow tract tachycardia: a new distinct subgroup of outflow tract tachycardia.

The present study investigated the incidence and ECG characteristics of ventricular tachycardias (VTs) originating from the left ventricular (LV) epicardium. Thirty-one consecutive patients with VT or premature ventricular contraction originating from the outflow tract (OT-VT) underwent catheter ablation. Twenty-one OT-VTs were ablated from the endocardium in the right ventricular (RV) OT and 3 were ablated from the endocardium in the LVOT. In the remaining 7 patients, 4 (13%) OT-VTs were LV epicardial in origin, and 1 of these was ablated from the left sinus of Valsalva. The ECG characteristics of OT-VT of epicardial origin included prominent tall R-waves in the inferior leads, an R-wave in V1 and an S-wave in V2, precordial R-wave transition in V2-4, a deep QS-wave in aVL, and no S-wave in V6. In addition, there was an atypical left bundle branch block morphology with an inferior axis. These findings were observed during pacing from several sites in the LV epicardium. Furthermore, pacing from the left sinus of Valsalva caused a relatively tall R in V1, deep S-wave in V2 and a tall R-wave with a shallow S-wave in V3, as well as tall R-waves in the inferior leads, which represented intermediate characteristics between RV endocardial OT-VT and LV endocardial OT-VT. In conclusion, OT-VT originating from the LV epicardium is not uncommon and has characteristic ECG findings. Some of them can be ablated from the left sinus of Valsalva.

Adult↗
PubMed1983

Cardiac ultrastructure in primary restrictive cardiomyopathy.

A five-year clinical follow-up and the results of myocardial biopsies are described in a patient with primary restrictive cardiomyopathy. Histologic examination of a right ventricular endomyocardial biopsy taken early in the course of the illness was not contributory. Histologic examination of a left ventricular endomyocardial biopsy five years later showed hypertrophy and disarray of myocytes, thickening of the endocardium, and interstitial fibrosis. Connective tissue was compact and regularly oriented in the endocardium, but tangled and irregularly oriented in the interstitium. It is concluded that the irregular network of collagen fibrils and elastic fibers limits diastolic relaxation and prevents ventricular dilatation; that the coexisting hypertrophy results from an attempt to maintain normal pump function; and that the myocyte disarray is a consequence of abnormal mechanical forces generated under conditions of severe fibrosis.

Biopsy↗
PubMed2007

Large mural vegetation attached to the left ventricular outflow tract: a case report.

We describe an unusual case of staphylococcal endocarditis with vegetation attached to the left ventricular outflow endocardium in a patient with chronic severe aortic regurgitation that was diagnosed by transthoracic echocardiography. There was no involvement of aortic valve endocardium confirmed by transthoracic echocardiography, transesophageal echocardiography, and macroscopically in the operation. This report confirms that chronic endocardial trauma may provide a fertile nidus for the development of bacterial vegetation.

Adult↗
PubMed1974

Case report. Fetal cardiac failure resulting from endocardial fibroelastosis.

An autopsy was performed on a female stillborn infant with generalized edema associated with ascites. On gross examination of the heart the pulmonary trunk was atretic from its origin of the heart to the bifurcation. The ductus arteriosus was abnormally wide. The right ventricle was hypoplastic and its endocardium was diffusely thickened. The inner surface of right ventricle appeared pale, obscuring the identification of trabeculae corneae and papillary muscles. At the posterior wall there was an extremely thin lesion where no apparnet cardiac muscle was contained. The tricuspid orifice was stenotic and the valve was hypoplactic. The right atrium was markedly enlarged and its wall was thickened. The foramen avale had patency of the valvular competent type. Atrial septal defect (ASD) was not present. The left ventricle was remarkably dilated with markedly thick wall. Ventricular septal defect (VSD) was present immediately beneath the right coronary cusp of the aortic valve. Light microscopic examination of the right ventricle revealed a marked increase of collagen and elastic fibers with extensive deposits of calcium not only in the endocardium but also in the deep portion of myocardium. Fibroelastosis appeared particularly prominent in the subendocardial layer. The muscle fibers surrounded by these penetrating fibers and deposits of calcium showed degeneration. The entire myocardial layer of the specific area in the right ventricle where the wall was paper-thin was fully replaced by fibers and calcium. Inflammatory cell infiltration was found only at some places of the pericardium. The left ventricular wall also showed fibroelastosis, although the degree of involvement was much less as compared to that seen in the right ventricle. There were no significant pathological changes in both atria.

Adult↗
PubMed1977

Instantaneous assessments of left ventricular dimensions by ultrasonic analogue conversion system. I. An experimental study.

A new time-to-voltage analogue converter of ultrasound echo was made. The converter samples the echoes from the septal endocardium and the endocardium of the posterior wall of the left ventricle. The converter also enables automatic calculates left ventricular minor axis, volume, and work. In fixed human hearts, the left ventricular minor axis and volume calculated by the converter were close to the actual ones. In anesthetized dogs, left ventricular minor axis, volume, ejection fraction and stroke work calculated by the converter were close to those calculated by cineventriculography. The results indicate applicability of the ultrasonic analogue converter for instantaneous assessments of left ventricular dimensions and function.

Analog-Digital Conversion↗
PubMed1997

Use of the body surface recovery time for detection of coronary artery disease.

We explored the relationship between body surface recovery time (RT), the interval between the QRS onset and the time of maximum derivative in the T-wave on a 16 precordial lead system electrocardiogram (ECG), and monophasic action potential (MAP) duration of the left ventricular endocardium in 9 patients in whom electrophysiologic testing was indicated. The usefulness of RT measurement on body surface ECG for the detection of coronary artery disease was evaluated in 98 patients who had chest pain. The RT located in the right clavicular or upper sternal area showed a very high positive correlation (r = 0.91, p < 0.001) with MAP duration from the left ventricular endocardium and showed specific shortening in patients with one-vessel disease of the left anterior descending coronary artery. With a criterion of the RT located in the right clavicular or upper sternal area corrected by Bazett's formula < 380 msec1/2, a sensitivity of 81% and a specificity of 80% were achieved for detection of one-vessel disease of the left anterior descending coronary artery.

Action Potentials↗