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PubMed2004

Electrocardiographic recognition of the epicardial origin of ventricular tachycardias.

BACKGROUND: Some ventricular tachycardias (VTs) originating from the epicardium are not suitable for endocardial radiofrequency ablation and require an epicardial approach. The aim of this study was to define the ECG characteristics that may identify an epicardial origin of VTs. METHODS AND RESULTS: We analyzed the 12-lead ECG recordings during epicardial and endocardial left ventricular pacing in 9 patients to verify the hypothesis that the epicardial origin of the ventricular activation widens the initial part of the QRS complex. Then, we analyzed the ECG pattern in 14 VTs successfully ablated from the epicardium after a failed endocardial approach (group A), in 27 VTs successfully ablated from the endocardium (group B), and in 28 additional VTs that could not be ablated from the endocardium (group C). Four distinct intervals of ventricular activation were defined and measured: (1) the pseudodelta wave, (2) the intrinsicoid deflection time in V2, (3) the shortest RS complex, and (4) the QRS complex. VTs from groups A and C showed a significantly longer pseudodelta wave, intrinsicoid deflection time, and RS complex duration compared with VTs of group B. There was no difference between groups A and C. A pseudodelta wave of > or =34 ms has a sensitivity of 83% and a specificity of 95%, an intrinsicoid deflection time of > or =85 ms has a sensitivity of 87% and a specificity of 90%, and an RS complex duration of > or =121 ms has a sensitivity of 76% and a specificity of 85% in identifying an epicardial origin of the VTs. CONCLUSIONS: ECG suggests VTs originating from the epicardium and those with an unsuccessful radiofrequency ablation from the endocardium.

Cardiac Pacing, Artificial↗
PubMed2000

Assessment of nonuniformity of transmural myocardial velocities by color-coded tissue Doppler imaging: characterization of normal, ischemic, and stunned myocardium.

BACKGROUND: Transmural myocardial contractile performance is nonuniform across the different layers of the left ventricular wall. We evaluated the accuracy of color M-mode tissue Doppler imaging (TDI) to assess the transmural distribution of myocardial velocities and to quantify the severity of dysfunction induced by acute ischemia and reperfusion in the inner and outer myocardial layers. METHODS AND RESULTS: Thirteen open-chest dogs underwent 15 minutes of left anterior descending coronary artery occlusion followed by 120 minutes of reperfusion. M-mode TDI was obtained from an epicardial short-axis view. Systolic velocities were calculated within endocardium and epicardium of the anterior and posterior walls. Regional myocardial blood flow was assessed by radioactive microspheres. Segment shortening was measured by sonomicrometry in endocardium and epicardium of both the anterior and posterior walls. At baseline, endocardial velocities were higher than epicardial velocities, resulting in an inner/outer myocardial velocity gradient. Ischemia caused a significant and comparable reduction in endocardial and epicardial systolic velocities in the anterior wall with the disappearance of the velocity gradient. Systolic velocities significantly correlated with segment shortening in both endocardium and epicardium during ischemia and reperfusion. In the first minutes after reflow, endocardial velocities showed a greater improvement than epicardial velocities, and the velocity gradient resumed although to a limited extent, indicative of stunning. CONCLUSIONS: TDI is an accurate method to assess the nonuniformity of transmural velocities and may be a promising new tool for quantifying ischemia-induced regional myocardial dysfunction.

Animals↗
PubMed1978

Echocardiographic features of constrictive pericarditis.

The most characteristic echocardiographic features of 12 patients with constrictive pericarditis were compared with the findings in 10 normal volunteers. Left ventricular posterior wall (LVPW) "flatness" was quantified by measuring the diastolic change in distance from the crystal artifact to the LVPW endocardium. In 11 of 12 patients the net diastolic LVPW endocardial movement was less than 1 mm. In 10 normal volunteers LVPW endocardium moved posteriorly in diastole from 1.5 to 4 mm (mean 2.2 +/- 0.8). Abnormal septal motion was present in five of 12 patients with constriction. Pericardial thickness measured using standard damping techniques for both cnstriction and normal population did not distinguish the two groups. The "flattening" of the left ventricular endocardium as quantified above verifies earlier qualitative observations and was the most consistent finding in this series of patients with constrictive pericarditis.

Aged↗
PubMed1984

Preservation of high-energy phosphates by verapamil in reperfused myocardium.

To determine whether verapamil prevents depletion of adenine nucleotides during and after severe myocardial ischemia, dogs were subjected to 15 min occlusions of the left anterior descending coronary artery followed by 240 min of reperfusion. One hour before occlusion, dogs were randomly assigned to a treatment group (n = 10) to which an infusion of intravenous verapamil was given until the onset of reperfusion or to an untreated saline group (n = 9). Verapamil reduced mean aortic pressure and heart rate. After 15 min of ischemia, endocardial adenosine triphosphate (ATP) level, determined by needle biopsy, decreased in the untreated group from 34.7 +/- 2.0 to 24.4 +/- 2.7 nmol X mg protein-1 (p less than .005 vs preocclusion) and in the verapamil group from 32.8 +/- 1.5 to 30.3 +/- 1.5 nmol X mg protein-1 (NS vs preocclusion). Dogs receiving verapamil had significantly higher ATP levels than untreated animals after 90 and 240 min of reperfusion. In untreated animals the sum of inosine and hypoxanthine levels increased during occlusion from very low levels to 4.6 +/- 1.1 nmol X mg protein-1 in the epicardium and to 6.8 +/- 1.5 nmol X mg protein-1 in the endocardium (p less than .05 compared with preocclusion values). In verapamil-treated dogs inosine and hypoxanthine levels increased to only 1.2 +/- 0.3 (epicardium) and 1.9 +/- 0.6 nmol X mg protein-1 (endocardium) (both NS compared with preocclusion values). After 90 min of reperfusion the sum of ATP, adenosine diphosphate, adenosine monophosphate, inosine, and hypoxanthine levels was decreased in the endocardium by 10.2 nmol X mg protein-1 in the untreated group, but no change was observed in verapamil-treated animals. We conclude that breakdown of ATP to inosine and hypoxanthine during severe ischemia is reduced by verapamil, resulting in higher ATP concentrations during occlusion and reperfusion and decreased washout of the diffusible purines inosine and hypoxanthine during reperfusion.

Adenosine Diphosphate↗
PubMed1987

Monophasic action potential mapping in human subjects with normal electrocardiograms: direct evidence for the genesis of the T wave.

T wave concordance in the normal human electrocardiogram (ECG) generally is explained by assuming opposite directions of ventricular depolarization and repolarization; however, direct experimental evidence for this hypothesis is lacking. We used a contact electrode catheter to record monophasic action potentials (MAPs) from 54 left ventricular endocardial sites during cardiac catheterization (seven patients) and a new contact electrode probe to record MAPs from 23 epicardial sites during cardiac surgery (three patients). All patients had normal left ventricular function and ECGs with concordant T waves. MAP recordings during constant sinus rhythm or right atrial pacing were analyzed for activation time (AT) = earliest QRS deflection to MAP upstroke, action potential duration (APD) = MAP upstroke to 90% repolarization, and repolarization time (RT) = AT plus APD. AT and APD varied by 32 and 64 msec, respectively, over the left ventricular endocardium and by 55 and 73 msec, respectively, over the left ventricular epicardium. On a regional basis, the diaphragmatic and apicoseptal endocardium had the shortest AT and the longest APD, and the anteroapical and posterolateral endocardium had the longest AT and the shortest APD (p less than .05 to less than .0001). RT was less heterogeneous than APD, and no significant transventricular gradients of RT were found. In percent of the simultaneously recorded QT interval, epicardial RT ranged from 70.8 to 87.4 (mean 80.7 +/- 3.9) and endocardial RT ranged from 80 to 97.8 (mean 87.1 +/- 4.4) (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Circumferential myocardial shortening in the normal human left ventricle. Assessment by magnetic resonance imaging using spatial modulation of magnetization.

BACKGROUND: Conventional cardiac imaging methods do not depict true segmental myocardial shortening, since they cannot determine segment length between fixed points in the myocardium. METHODS AND RESULTS: We used electrocardiographically gated magnetic resonance imaging with spatial modulation of magnetization to noninvasively "tag" the myocardium with dark stripes at uniform 7-mm intervals center to center at end diastole. We then determined end-systolic stripe separation and thereby calculated circumferential shortening. When end systole was not reached in the first image series, a second temporally overlapped series starting in late systole was used to determine late-systolic shortening. Septal, anterior, lateral, and inferior segments were assessed at endocardium, midwall, and epicardium on five midventricular short-axis sections each in 10 normal volunteers. A transmural gradient in circumferential shortening was observed, with the percentage of endocardial segment shortening consistently greater than epicardial segment shortening (epicardial, 22 +/- 5%; midwall, 30 +/- 6%; and endocardial, 44 +/- 6%; p less than 0.0001 by analysis of variance). Circumferential shortening varied from apex to base with slices closer to the base of the left ventricle showing less shortening at the midwall (28 +/- 9%) and endocardium (39 +/- 6%) than more apical slices at the midwall (34 +/- 13%) and endocardium (49 +/- 9%) (p less than 0.05 and p less than 0.01, respectively, by analysis of variance). CONCLUSIONS: Transmural and longitudinal heterogeneity of circumferential shortening is present in the normal human left ventricle. Magnetic resonance imaging with spatial modulation of magnetization is a powerful new tool for assessment of circumferential shortening and provides information unobtainable with conventional imaging methods.

Adult↗
PubMed1992

Dissociation between left ventricular untwisting and filling. Accentuation by catecholamines.

BACKGROUND: Efficient early diastolic filling is essential for normal cardiac function. Diastolic suction, as evidenced by a decreasing left ventricular pressure during early filling, could result from restoring forces (the release of potential energy stored during systolic deformation) dependent on myofilament relaxation. Although these restoring forces have been envisioned within individual myofibers, recent studies suggest that gross fiber rearrangement involving the connective tissue network occurs easy in diastole. This may lead to the release of potential energy stored during systole and suction-aided filling. METHODS AND RESULTS: To establish precisely the timing and extent of restoration of the systolic torsional deformation of the left ventricle with respect to early filling at baseline and with enhanced relaxation, we studied untwisting during control conditions and with catecholamine stimulation. Using noninvasive and nondestructive magnetic resonance tagging, torsional deformation of the left ventricle was measured at 20-msec intervals in 10 open-chest, atrially paced dogs, starting at aortic valve closure. Eight equiangular tags intersected the epicardium and endocardium in three short-axis imaging planes (base, mid, and apex). From the intersection points, epicardial and endocardial circumferential chord and arc lengths were measured and angular twist of mid and apical levels with respect to the base (maximal torsion and its reversal, untwisting) was calculated. Echo-Doppler provided timing of aortic valve closure and of mitral valve opening. Zero torsion was defined at end diastole. Torsion at the apical level reversed rapidly between its maximum and the time immediately after mitral valve opening: from 7.0 +/- 5.8 degrees to 3.2 +/- 5.4 degrees and 12.0 +/- 8.5 degrees to 6.9 +/- 7.8 degrees (mean +/- SD, both p less than 0.01) at the epicardium and endocardium, respectively. During the same period, no significant circumferential segment length changes occurred. As expected, after mitral valve opening, filling resulted in significant circumferential segment lengthening, whereas further reversal of torsion was small and nonsignificant. During dobutamine infusion, torsion at end systole was greater and reversal during isovolumic relaxation was much more rapid and greater in extent (p less than 0.01). Torsion reversed from 11.5 +/- 4.3 degrees to 5.7 +/- 4.8 degrees and 17.4 +/- 6.4 degrees to 6.9 +/- 7.7 degrees at epicardium and endocardium. CONCLUSIONS: Untwisting occurs principally during isovolumic relaxation before filling and is markedly enhanced in speed and magnitude by catecholamines. This partial return of the left ventricle to its preejection configuration before mitral valve opening could represent an important mechanism for the release of potential energy stored in elastic elements during the systolic deformation. These myocardial restoring forces would be markedly enhanced by physiological changes consequent to catecholamines such as during exercise, offsetting the concomitant shortening of the filling period.

Animals↗
PubMed1993

Persistent T-wave changes after alteration of the ventricular activation sequence. New insights into cellular mechanisms of 'cardiac memory'.

BACKGROUND: "Cardiac memory" refers to persistent T-wave changes on ECG that follow resumption of sinus rhythm after a period of altered activation sequence. Previous studies demonstrated that cardiac memory in intact dogs was abolished by 4-aminopyridine (4-AP), which blocks both the transient outward potassium current, Ito, and IK. METHODS AND RESULTS: We used standard microelectrode techniques to study the mechanism for cardiac memory in canine ventricular subepicardial and subendocardial slabs measuring 15 x 30 x 1 to 2 mm. Bipolar electrodes were used to stimulate slabs parallel to fiber axis, simulating normal activation, and perpendicular to fiber axis, simulating ventricular pacing. Four 30-minute periods of normal activation at a basic cycle length of 650 milliseconds were interrupted by three 20-minute periods of ventricular pacing at a basic cycle length of 450 milliseconds. We first recorded action potentials differentially from epicardial and endocardial slabs. The stimulation protocol induced changes in the "T" wave of the difference signals that mimicked cardiac memory and that could be explained on the basis of the transmural gradient in repolarization between epicardium and endocardium. This result was not obtainable with slow and rapid pacing from one site only. In subsequent experiments, action potential characteristics of epicardial and endocardial slabs were studied by the same pacing protocol with alternation between simulated normal activation and ventricular pacing. During ventricular pacing, the epicardial phase 1 notch and plateau amplitude decreased compared with normal activation. 4-AP (3 mmol/L) decreased notch size and plateau amplitude during normal activation in epicardium but not endocardium. In contrast, the local anesthetic lidocaine did not change notch size or plateau amplitude in epicardium or endocardium. CONCLUSIONS: These results suggest that the contribution to repolarization of specific potassium channels influences the memory phenomenon and that by blocking Ito and reducing the transmural voltage gradient for repolarization, 4-AP abolishes cardiac memory.

4-Aminopyridine↗
PubMed1994

Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.

BACKGROUND: In hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo. METHODS AND RESULTS: Tagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142 +/- 41 g/m) and normal ejection fraction (mean, 64 +/- 9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall long-axis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29 +/- 6% at the endocardium in hypertensive subjects versus 44 +/- 6% in normal subjects (P = .0001); 20 +/- 6% at the midwall versus 30 +/- 6% (P = .0001); and 13 +/- 5% at the epicardium versus 21 +/- 5% (P = .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10 +/- 9% at the base versus 21 +/- 6% in normal subjects (P = .0001); 14 +/- 8% at the midventricle versus 18 +/- 3% (P = .03); and 14 +/- 8% at the apex versus 18 +/- 4% (P = .04). CONCLUSIONS: In hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.

Female↗
PubMed1995

Sodium pentobarbital versus alpha-chloralose anesthesia. Experimental production of substantially different slopes in the transmural CP/ATP ratios within the left ventricle of the canine myocardium.

BACKGROUND: Transmural analyses of the creatine phosphate (CP)/ATP ratio in various lamina of the canine myocardium have previously revealed significant variations in the CP/ATP ratio, with the subendocardial layer displaying a decreased ratio relative to the subepicardial layer. Without exception, these results were obtained under sodium pentobarbital anesthesia. These findings have been interpreted to imply that the normal endocardium may be operating in the oxygen-limited domain or that there are transmurally varying set points for the regulation of oxidative phosphorylation. METHODS AND RESULTS: In this work, we examine the effect of the anesthetic regimen on the transmural CP/ATP ratio within the left ventricular wall of the canine myocardium using spatially localized 31P-nuclear magnetic resonance (NMR) and an open-chest model. Two anesthetics were compared, alpha-chloralose and sodium pentobarbital. Under sodium pentobarbital, the CP/ATP ratio ranged from 1.92 +/- 0.06 to 2.51 +/- 0.08 from endocardium to epicardium, resulting in a transmural slope in the CP/ATP ratio of 0.149 +/- 0.047 (n = 22). Under alpha-chloralose, CP/ATP ratios ranged from 2.18 +/- 0.05 to 2.32 +/- 0.06, with a transmural slope of 0.035 +/- 0.018 (n = 38). Thus, the transmural slope in CP/ATP ratio was nearly four times greater with sodium pentobarbital than with alpha-chloralose, and the difference in these slopes was statistically significant (P = .029). No difference was observed in average CP/ATP obtained from the entire wall with either anesthetic. CONCLUSIONS: These results demonstrate that the transmural trend in CP/ATP ratio previously reported in the myocardium is likely to be a direct reflection of the sodium pentobarbital anesthetic regimen, not truly reflecting the trend in the normal unanesthetized animal. Moreover, since the transmural variation in CP/ATP ratio was greatly reduced with alpha-chloralose, it appears unlikely that the endocardium in the normal unanesthetized heart is operating in the oxygen-limited domain. These results also point to the importance of the anesthetic regimen in biochemical analysis, indicate the necessity of increased caution in directly translating results obtained under anesthesia, and demonstrate the unique power of in vivo NMR to extract such subtle biochemical information.

Adenosine Triphosphate↗
PubMed1996

Cellular basis for the electrocardiographic J wave.

BACKGROUND: The J wave is a deflection that appears in the ECG as a late delta wave following the QRS or as a small secondary R wave (R'). Also referred to as an Osborn wave, the J wave has been observed in the ECG of animals and humans for more than four decades, yet the mechanism underlying its manifestation is poorly understood. The present study investigates the cellular basis for the J wave using an isolated arterially perfused preparation consisting of a wedge of canine right or left ventricle. METHODS AND RESULTS: A 12-lead ECG was initially recorded in vivo. After isolation and arterial perfusion of the right or left ventricular wedge, transmembrane action potentials were simultaneously recorded from epicardial, M region, and endocardial transmural sites with three floating microelectrodes. A transmural ECG was recorded concurrently. A J wave was observed at the R-ST junction of the ECG in 17 of 20 adult dogs, usually in leads II, III, aVR, and aVF and the mid to lateral precordial leads. The J wave in the transmural ECG recorded across the wedge was closely associated with the presence of a prominent action potential notch in epicardium but not endocardium. The shape and amplitude of the J wave were found to depend on (1) the transmural distribution of the action potential notch amplitude, (2) the relative time course of the early phases of the action potential (width of notch) at different sites within the wall, (3) sequence of activation, and (4) conduction time across the wall. A highly significant correlation was demonstrated between the amplitude of the epicardial action potential notch and the amplitude of the J wave recorded during interventions that alter the appearance of the electrocardiographic J wave, including hypothermia, premature stimulation, and block of the transient outward current by 4-aminopyridine. Ventricular activation from endocardium to epicardium, with epicardium activated last, was also an important prerequisite for the appearance of the J wave. This sequence permits the establishment of a voltage gradient of the early phases of the action potential after activation (ie, the QRS) is complete. CONCLUSIONS: Our results provide the first direct evidence in support of the hypothesis that heterogeneous distribution of a transient outward current-mediated spike-and-dome morphology of the action potential across the ventricular wall underlies the manifestation of the electrocardiographic J wave. The presence of a prominent action potential notch in epicardium but not endocardium is shown to provide a voltage gradient that manifests as a J (Osborn) wave or elevated J-point in the ECG.

Action Potentials↗
PubMed2006

Two distinct pools of mesenchyme contribute to the development of the atrial septum.

Closure of the primary atrial foramen is achieved by fusion of the atrioventricular cushions with the mesenchymal cap on the leading edge of the muscular primary atrial septum. A fourth component involved is the vestibular spine, originally described by His in 1880 as an intra-cardiac continuation of the extra-cardiac mesenchyme of the dorsal mesocardium. The morphogenesis of this area is of great clinical interest, because of the high incidence of atrial and atrioventricular septal defects. Nonetheless, the origin of the participating components is largely unknown. Here we report that the primary atrial foramen is surrounded in its entirety by mesenchyme derived from endocardium. A second population of mesenchyme not derived from endocardium was observed at the caudal margin of the mesenchymal atrial cap, entirely embedded within the mesenchyme derived from endocardium and contiguous with the mesenchyme of the dorsal mesocardium. Our reconstructions show this second population does indeed take the form of a short spine, albeit that it is the right pulmonary ridge, rather than this spine, that protrudes into the atrial lumen. From the stance of morphological description, therefore, there is little thus far to substantiate the existence of an atrial spine.

Embryonic Development↗
PubMed1995

Optical mapping reveals that repolarization spreads anisotropically and is guided by fiber orientation in guinea pig hearts.

Guinea pig hearts were stained with a voltage-sensitive dye and imaged on a photodiode array to record fluorescent action potentials (APs) from 124 sites. Activation and repolarization patterns were recorded from the epicardium during stimulation at different loci and correlated with the underlying fiber architecture. Endocardial APs were recorded by inserting a light guide into the ventricular cavity or by dissecting out the ventricular free wall to expose the endocardium. In hearts paced on the right atrium to simulate sinus rhythm, activation emerged synchronously over a large area of the ventricular epicardium and spread laterally in 5 to 7 ms. The apparent longitudinal and transverse velocities were 2.66 +/- 0.11 and 1.65 +/- 0.09 m/s (n = 12). In contrast, repolarization began near the apex on the endocardium and spread transmurally in 6 +/- 1.3 ms (n = 12) and then anisotropically along the epicardium in 25 to 30 ms with apparent maximum (0.53 +/- 0.11 m/s) and minimum (0.31 +/- 0.10 m/s) repolarization velocities that aligned with the longitudinal and transverse axes of epicardial fibers. When paced on the epicardium, activation of intact hearts (n = 12) and perfused sheets (n = 8) was anisotropic, with longitudinal (0.85 +/- 0.05 m/s) and transverse (0.44 +/- 0.04 m/s) conduction velocities that aligned with the epicardial fiber orientation. When activation was initiated at different sites on the epicardium, repolarization always began near the apex and exhibited patterns similar to those obtained under right atrial pacing, but with slower longitudinal (0.41 +/- 0.09 m/s) and transverse (0.23 +/- 0.07 m/s) repolarization velocities (n = 18). In sheets stretched parallel to the longitudinal axis of surface fibers, AP durations (APDs) increased as a function of fiber length, from the length at zero developed tension to 120% of the length at maximum developed tension (Lmax). Spatial distributions of APDs did not change during stretches along the rising phase of the length-tension curve. In sheets stretched to 50% of Lmax, APDs were shorter and more homogeneous on the endocardium (mean APD, 188 ms; delta APD, 195-186 = 9 ms) than on the epicardium (mean APD, 204 ms; delta APD, 212-186 = 26 ms; n = 8). In guinea pig hearts, activation is rapid; therefore, repolarization depends primarily on intrinsic spatial heterogeneities of APDs. Consequently, repolarization begins at endocardial cells with the shortest APDs and spreads transmurally and then anisotropically on the surface according to the epicardial cell orientation.

Animals↗
PubMed1999

Cell-autonomous and non-autonomous requirements for the zebrafish gene cloche in hematopoiesis.

Vertebrate embryonic hematopoiesis is a complex process that involves a number of cellular interactions, notably those occurring between endothelial and blood cells. The zebrafish cloche mutation affects both the hematopoietic and endothelial lineages from an early stage (Stainier, D. Y. R., Weinstein, B. M., Detrich, H. W. R., Zon, L. I. and Fishman, M. C. (1995) Development 121, 3141-3150). cloche mutants lack endocardium, as well as head and trunk endothelium, and nearly all blood cells. Cell transplantation studies have revealed that the endocardial defect in cloche is cell-autonomous: wild-type cells can form endocardium in mutant hosts, but mutant cells never contribute to the endocardium in wild-type or mutant hosts. In this paper, we analyze the cell-autonomy of the blood defect in cloche. The blood cell deficiency in cloche mutants could be an indirect effect of the endothelial defects. Alternatively, cloche could be required cell-autonomously in the blood cells themselves. To distinguish between these possibilities, we cotransplanted wild-type and mutant cells into a single wild-type host in order to compare their respective hematopoietic capacity. We found that transplanted wild-type cells were much more likely than mutant cells to contribute to circulating blood in a wild-type host. Furthermore, in the few cases where both wild-type and mutant donors contributed to blood in a wild-type host, the number of blood cells derived from the wild-type donor was always much greater than the number of blood cells derived from the mutant donor. These data indicate that cloche is required cell-autonomously in blood cells for their differentiation and/or proliferation. When we assessed early expression of the erythropoietic gene gata-1 in transplant recipients, we found that mutant blastomeres were as likely as wild-type blastomeres to give rise to gata-1-expressing cells in a wild-type host. Together, these two sets of data argue that cloche is not required cell-autonomously for the differentiation of red blood cells, as assayed by gata-1 expression, but rather for their proliferation and/or survival, as assayed by their contribution to circulating blood. In addition, we found that transplanted wild-type cells were less likely to express gata-1 in a mutant environment than in a wild-type one, suggesting that cloche also acts non-autonomously in red blood cell differentiation. This non-autonomous function of cloche in red blood cell differentiation may reflect its cell-autonomous requirement in the endothelial lineage. Thus, cloche appears to be required in erythropoiesis cell non-autonomously at a step prior to gata-1 expression, and cell-autonomously subsequently.

Animals↗
PubMed1999

[Microcirculation in the myocardium].

The coronary artery supplies the arterial blood that contains oxygen and nutrients for the myocardial tissue to produce high-energy phosphates aerobically. The left anterior descending and circumflex coronary arteries run on the epicardial surface of the left ventricle, turn toward the endocardium at a right angle, and nourish the tissues of the subendocardinal layers with the arterial blood. Cessation of coronary blood flow makes the myocardium ischemic. The endocardium is particularly susceptible to ischemia because the arteries that run to the endocardium are pressed due to extravascular compression during every systole. Coronary vasodilators are still used as anti-anginal drugs. However, a potent coronary vasodilator may cause coronary-steal and thereby worsen the ischemia-induced myocardial injury. We will demonstrate changes in the microcirculation of the ischemic myocardium caused by coronary vasodilators and demonstrate that a coronary vasodilator is not always effective on the ischemic myocardium.

Coronary Vessels↗
PubMed1998

Transmural myocardial infarction caused by thromboembolism associated with mitral insufficiency in a dog.

A 10-year-old dog, which had been treated for mitral insufficiency, died suddenly. Transmural myocardial infarction secondary to thromboembolic occlusion of the subsinuosal interventricular branch of the left circumflex artery was noted in the posterior lower half of the left ventricular wall, involving the interventricular septum and a part of right ventricular wall. The mitral valve leaflets were markedly thickened (valvular endocardiosis). These were a patchy area of jet lesion and several mural thrombi on the left-atrial endocardium. The embolus in the subsinuosal interventricular branch was composed of mostly platelets and fibrin, showing the same histologic features as those of the mural thrombi on the left-atrial endocardium. From these findings, it was concluded that dislodgement of part of the mural thrombi on the left-atrial endocardium caused thromboembolism of the subsinuosal interventricular branch.

Animals↗
PubMed1991

Percutaneous fiberoptic cardioscopy of the left ventricle.

The feasibility of percutaneous transluminal cardioscopy of the left ventricle was examined in 35 patients with or without various heart diseases. A guiding balloon catheter (7 or 9 French) was introduced through the right femoral artery into the left ventricle. The balloon was inflated, and a fiberscope (1.6 or 4.3 French) was advanced to the distal tip of the catheter. The balloon was then manipulated against the portion of the ventricle targeted for examination, and heparinized saline (10 U/ml) at body temperature was infused through the catheter at 5 ml/sec for 3 to 6 sec. The images were recorded on videotape and 16 mm cinefilm. In 4 patients without demonstrable heart disease, the endocardial surface of the left ventricle was brown and the trabeculae became prominent during systole. The chordae connected to the mitral leaflets were white. In 3 of 5 patients with dilated cardiomyopathy, the endocardium was light yellow with thin trabeculae which barely contracted during systole. The endocardium was red or reddish-brown in 3 patients with acute myocarditis. In patients with rheumatic mitral stenosis white patches were scattered on the endocardial surface. In 7 of 8 patients the akinetic or dyskinetic segments representing prior infarctions were white. No complications other than transient ventricular arrhythmias were noted. We conclude that percutaneous fiberscopic imaging with a guiding balloon catheter is feasible and safe, and yields highly detailed images of the endocardium.

Acute Disease↗
PubMed2004

Warfarin-intractable, intraatrial thrombogenesis in a 52-year-old woman with mitral stenosis and chronic atrial fibrillation.

Thromboembolic events are serious complications of atrial fibrillation (AF). We histologically investigated intraatrial thrombogenesis in a 52-year-old woman with mitral stenosis and chronic AF who had recurrent attacks of cerebral infarction despite continuous warfarin therapy. She underwent cardiac surgery for mitral valve replacement and maze procedure including left atrial thrombectomy. Macroscopic thrombi were found on the endocardium and their surfaces appeared rough and dark red in most areas. Histological examination showed that a single thrombus mass was composed of several tissue layers or blocks on the endocardium. Immunohistochemistry revealed stratum-like accumulations of small platelet aggregate/fibrin clot complexes in the superficial, fresh thrombus layers and multiple neovessel formation in the basal organized tissue layers. This case study suggests that intraatrial thrombi may develop in a stepwise fashion on the endocardium involving platelet aggregate/fibrin clot complex formation.

Adult↗