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PubMed1981

Radiation heart disease. Analysis of 16 young (aged 15 to 33 years) necropsy patients who received over 3,500 rads to the heart.

Certain clinical and necropsy findings are described in 16 young (aged 15 to 33 years) patients who received greater than 3,500 rads to the heart five to 144 months before death. All 16 had some radiation-induced damage to the heart: 15 had thickened pericardia (five of whom had evidence of cardiac tamponade); eight had increased interstitial myocardial fibrosis, particularly in the right ventricle; 12 had fibrous thickening of the mural endocardium and 13 of the valvular endocardium. Except for valvular thickening, the changes were more frequent in the right side of the heart than in the left, presumably because of higher radiation doses to the anterior surface of the heart. In six of the 16 study patients and in one of 10 control subjects, one or more major epicardial coronary arteries were narrowed from 76 to 100 percent in cross-sectional area by atherosclerotic plaque; one patient had a healed myocardial infarct at necropsy and one died suddenly. In 10 patients and in the 10 control subjects, the four major epicardial coronary arteries were examined quantitatively: 6 percent of the 469 five millimeter segments of coronary artery from the patients were narrowed from 76 to 100 percent (controls = 0.2 percent, p = 0.06) and 22 percent were narrowed from 51 to 75 percent (controls = 12 percent). The proximal portion of the arteries in the patients had significantly more narrowing than the distal portions. The arterial plaques in the patients were largely composed of fibrous tissue; the media were frequently replaced by fibrous tissue, and the adventitia were often densely thickened by fibrous tissue. In five patients, there was focal thickening (with or without luminal narrowing) of the intramural coronary arteries. Thus, radiation to the heart may produce a wide spectrum of functional and anatomic changes but particularly damage to the pericardia and the underlying epicardial coronary arteries.

Adolescent↗
PubMed1987

Distribution of alpha- and beta-myosin heavy chains in the ventricular fibers of the postnatal developing rat.

Four monoclonal antibodies, two raised against alpha-myosin heavy chain (MHC) and two against beta-MHC, have been used to investigate in situ the fiber distribution of alpha- and beta-MHC in rat cardiac ventricles during postnatal development. Eighteen ventricles from 2-day-old to 1-year-old rats were analyzed. Three fiber populations were determined according to their immunofluorescent labeling: one with only alpha-MHC, one only beta-MHC, and one with mixed alpha- and beta-MHC. Large variations in the proportions of these three fiber populations according to age indicate that: (1) alpha-MHC are expressed in all fibers until the second month; they then disappear in a small endocardial fiber population and in a few apparently conductive fibers around the vessels. (2) beta-MHC are also first expressed in all fibers and then disappear gradually from epicardium to endocardium between the second and fourth weeks, except in the conductive fibers; they reappear during the second month sequentially from endocardium to epicardium; and they are then expressed in almost all fibers, except in a small epicardial fiber population, proportionally larger in the right ventricle than in the left. Immunological characterization of MHC isolated from a 22-day-old-rat ventricle, using anti-beta immunoaffinity chromatography, suggests that MHC of conductive fibers are probably at least partially in an alpha beta heterodimeric form.

Aging↗
PubMed1992

N-cadherin localization in early heart development and polar expression of Na+,K(+)-ATPase, and integrin during pericardial coelom formation and epithelialization of the differentiating myocardium.

N-cadherin, a Ca(2+)-dependent cell adhesion molecule, has been localized previously to the mesoderm during chick gastrulation and to adherens junctions in beating avian hearts. However, a systematic study of the dynamic nature of N-cadherin localization in the critical early stages of heart development is lacking. The presented work defines the changes in the spatial and temporal expression of N-cadherin during early stages of chick heart development, principally between Hamburger and Hamilton stages 5-8, 18-29 hr of development. During gastrulation N-cadherin appears evenly distributed in the heart forming region. As development proceeds to form the pericardial coelom (stages 6, 7, and 8, i.e., between 22 and 26 hr of development) N-cadherin localization becomes restricted to the more central areas of the mesoderm. The localization also shows a periodicity that correlates closely with the distance between foci of cavities that eventually coalesce to form the coelom. This distribution suggests that N-cadherin may have a function in the sorting out of somatic and splanchnic mesoderm cells to form the coelom. This separation of the mesoderm in the embryo for the first time physically delineates the precardiac mesoderm population. Concomitant with cell sorting during coelom formation, the precardiac cells change shape and show a distinct polarity as conveyed by (1) the apical expression of N-cadherin on precardiac cell surfaces lining the pericardial coelom, (2) the primarily lateral expression of Na+,K(+)-ATPase, and (3) an enrichment of integrin (beta 1 subunit) on basal cell surfaces. The somatic mesoderm cells apparently down-regulate N-cadherin expression. N-cadherin is also absent from the precardiac cells close to the endoderm. The latter cells eventually form the endocardium, i.e., the endothelial lining of the heart. By contrast, in the tubular, beating heart N-cadherin is found throughout the myocardium. In summary, immunolocalization patterns of N-cadherin during early cardiogenesis suggest that this cell adhesion molecule has a major role in the dynamics of pericardial coelom formation. Subsequently, its continued expression during cell differentiation of the cardiomyocyte to form the myocardium, but not endocardium, suggests N-cadherin is an essential morphoregulatory molecule in heart organogenesis.

Animals↗
PubMed1985

Distribution of myocardial stress and its influence on coronary blood flow.

The myocardial stress was analyzed by biomechanical modeling in correlation with experimental findings. The pressure-volume relationship follows the stress-strain relationship of muscle fibers. From the knowledge of fiber orientation and the distribution of sarcomere length, the myocardial stress components including fiber, longitudinal, circumferential and radial stresses were expressed as a function of fraction of wall thickness. The coronary blood flow is influenced by the myocardial radial stress. With the use of vascular waterfall theory, it is possible to correlate the theoretically defined stress distribution with experimentally obtained stress distribution. An elevation of radial stress in myocardium causes a reduction of vessel patency. During both systole and diastole, vessel patency remains constant at epicardium. At endocardium, however, vessel patency undergoes rhythmic changes following the systolic and diastolic influences of the radial stress. The physiological implication is that during systole, the endocardium suffers low blood flow and this transient ischemic state requires compensatory replenishment from diastolic perfusion. Such phenomena become less apparent toward the epicardium.

Biomechanical Phenomena↗
PubMed1992

Dependence of local left ventricular wall mechanics on myocardial fiber orientation: a model study.

The dependence of local left ventricular (LV) mechanics on myocardial muscle fiber orientation was investigated using a finite element model. In the model we have considered anisotropy of the active and passive components of myocardial tissue, dependence of active stress on time, strain and strain rate, activation sequence of the LV wall and aortic afterload. Muscle fiber orientation in the LV wall is quantified by the helix fiber angle, defined as the angle between the muscle fiber direction and the local circumferential direction. In a first simulation, a transmural variation of the helix fiber angle from +60 degrees at the endocardium through 0 degrees in the midwall layers to -60 degrees at the epicardium was assumed. In this simulation, at the equatorial level maximum active muscle fiber stress was found to vary from about 110 kPa in the subendocardial layers through about 30 kPa in the midwall layers to about 40 kPa in the subepicardial layers. Next, in a series of simulations, muscle fiber orientation was iteratively adapted until the spatial distribution of active muscle fiber stress was fairly homogeneous. Using a transmural course of the helix fiber angle of +60 degrees at the endocardium, +15 degrees in the midwall layers and -60 degrees at the epicardium, at the equatorial level maximum active muscle fiber stress varied from 52 kPa to 55 kPa, indicating a remarkable reduction of the stress range. Moreover, the change of muscle fiber strain with time was more similar in different parts of the LV wall than in the first simulation. It is concluded that (1) the distribution of active muscle fiber stress and muscle fiber strain across the LV wall is very sensitive to the transmural distribution of the helix fiber angle and (2) a physiological transmural distribution of the helix fiber angle can be found, at which active muscle fiber stress and muscle fiber strain are distributed approximately homogeneously across the LV wall.

Computer Simulation↗
PubMed1994

Mechanical effects of looping in the embryonic chick heart.

During early embryonic development, the heart bends into a curved tube in a vital morphogenetic process called looping. Since looping involves poorly understood biomechanical forces that are difficult to measure, this paper presents a theoretical model for the tubular chick heart, whose development is similar to that of the human heart. Representing the basic morphology of the looped ventricle, the model is a thick-walled, isotropic, pressurized curved tube composed of three layers representing the myocardium, cardiac jelly, and endocardium. The model is analyzed with nonlinear elasticity theory, modified to include residual strain and muscle activation, and material properties are determined by correlating theoretical and experimental pressure-volume relations. The results show that longitudinal curvature significantly influences the biomechanical behavior of the embryonic heart. As the curvature increases, the compliance of the tube increases, especially at end systole. Stress concentrations, which develop in the endocardium during diastole and in the myocardium during systole, also increase with the curvature. The largest wall stress during the cardiac cycle occurs near the beginning of systolic ejection in the myocardial layer at the inner curvature of the tube. Relative to end diastole, the model predicts epicardial strains that are nearly equal in the circumferential and meridional directions, in agreement with experimental measurements. These results provide insight into the interrelation between biomechanical forces and morphogenesis during cardiac looping.

Animals↗
PubMed1991

Distribution of the neural cell adhesion molecule (NCAM) during heart development.

The neural cell adhesion molecule, NCAM, was localized in the embryonic chick heart from Hamburger-Hamilton stage 14 up to hatching and in the adult heart. A monoclonal antibody directed to NCAM was used with the indirect antibody technique to stain frozen sections with immunoperoxidase. The myocardium showed immunoreactivity at stages 15 and 21, with little to no staining of epicardium, endocardium or atrioventricular endocardial cushion tissue. At stage 22, additional immunoreactivity was found in the endocardium of both the atrial septum and the atrial and ventricular surfaces of the atrioventricular cushions. Endocardial-derived mesenchymal cells within the cushions were also immunostained for NCAM. A gradient of NCAM staining was evident in the ventricular wall by stage 16. The staining intensity in the myocardium subjacent to the epicardium was less than found near the ventricular lumen. Biochemical analyses revealed that the embryonic heart expresses polysialylated NCAM. Upon desialylation with the endoneuraminidase Endo-N, the predominant heart NCAM has an apparent molecular weight of 155 to 160 kDa, which is distinct in size from the predominant forms found in embryonic chick nervous system (180, 140 and 120 kDa). NCAM expression is regionally regulated in the heart. The pattern of its expression is consistent with our hypothesis that it is involved in (1) differentiation of the atrial and ventricular walls, (2) fusion of the atrial septum with the endocardial cushions, (3) fusion of the endocardial cushions, and (4) formation and remodeling of ventricular trabeculae.

Animals↗
PubMed1994

Quantitative autoradiographic measurement of cocaine-induced regional myocardial metabolic changes in hypertensive rats.

A rat model of hypertensive cardiomyopathy was studied to evaluate the acute effects of cocaine on the myocardium. Using autoradiographic microimaging techniques, myocardial perfusion (201Tl) and energy substrate utilization (glucose: [14C]2-fluoro-2-deoxy-D-glucose-[14C]2DG and fatty acid (15-[p-iodophenyl])-3-R,S-methyl pentadecanoic acid-[131I]BMIPP) were studied in Dahl strain salt-sensitive normotensive and hypertensive rats with and without intravenous cocaine. The right ventricle, septum, endocardium and epicardium of the left ventricle were analyzed. Increased perfusion (18%) was seen in the myocardium of the hypertensive rats as compared to the normotensive rats. There was higher [14C]2DG (254%) and lower fatty acid (13.2%) uptake in the hypertensive rats, indicative of a shift from aerobic to anaerobic substrate utilization. In cocaine-treated normotensive rats, a generalized decrease in myocardial perfusion (30%) and increased glucose metabolism (89%) was seen. In cocaine-treated hypertensive rats, the increased myocardial perfusion (16%) was heterogeneous and was more pronounced in septum and epicardium. The endocardium and epicardium in the hypertensive rats showed an overall increase (23%) in glucose utilization after cocaine which was not as dramatic as was seen in the normotensive heart and a slight increase in fatty acid utilization. These results are consistent with prior observations that under pressure overload the myocardium responds non-uniformly. It may well be that the hypertensive cardiomyopathic heart is unable to respond to the challenge of cocaine by further increasing glucose utilization. These data obtained in an animal model of hypertension seem to indicate that hypertension may increase the risk of cardiac complications related to cocaine.

Animals↗
PubMed2006

Proximity of coronary arteries to the atrioventricular valve annulus in young patients and implications for ablation procedures.

The distance from the endocardial surface of the atrioventricular valve annulus and adventia of the adjacent coronary artery (CA) has not been delineated and may play an important role in the risk for CA damage during catheter ablation procedures. This distance was measured in 10 normal pediatric heart specimens at 11 locations around the right and left atrioventricular grooves. The endocardium-to-CA distance varied by age and location, with the shortest distances in the region of the os of the coronary sinus and the greatest distances in the right anteroseptal area. Excluding right anteroseptal measurements, in the 5 patients <7 years of age, the endocardium-to-CA distances were <or=4 mm in 76% and <or=5 mm in 96%. Given lesion sizes during ablation procedures, these distances and their potential relation to the risk for CA damage need to be taken into account during catheter ablation procedures in young patients.

Adolescent↗
PubMed2003

heart of glass regulates the concentric growth of the heart in zebrafish.

BACKGROUND: Patterned growth of vertebrate organs is essential for normal physiological function, but the underlying pathways that govern organotypic growth are not clearly understood. Heart function is critically dependent upon the concentric thickening of the ventricular wall generated by the addition of cells to the myocardium along the axis from the endocardium (inside) to the outside of the chamber. In heart of glass mutant embryos, the number of cells in the myocardium is normal, but they are not added in the concentric direction. As a consequence, the chambers are huge and dysfunctional, and the myocardium remains a single layer. RESULTS: To begin to define the factors controlling the concentric growth of cells in the myocardium, we used positional cloning to identify the heart of glass (heg) gene. heg encodes a protein of previously undescribed function, expressed in the endocardial layer of the heart. By alternative splicing, three distinct isoforms are generated, one of which is predicted to be transmembrane and two other secreted. By selective morpholino perturbation, we demonstrate that the transmembrane form is critical for the normal pattern of growth. CONCLUSIONS: heart of glass encodes a previously uncharacterized endocardial signal that is vital for patterning concentric growth of the heart. Growth of the heart requires addition of myocardial cells along the endocardial-to-myocardial axis. This axis of patterning is driven by heg, a novel transmembrane protein expressed in the endocardium.

Amino Acid Sequence↗
PubMed2005

Estimation of right ventricular mass by two-dimensional echocardiography.

BACKGROUND: This report describes two original echocardiographic approaches to measure right ventricular (RV) mass (RVM). METHODS: In the bullet formula (5/24 pi D1 D2 L), where D1 and D2 are short axes and L the log axis, the RVM is obtained by subtracting the cavity volume from the RV total volume and subsequently multiplying the difference by myocardium density. The second method uses 3 endocardium segments measured at: (1) short axis plane of the aortic valve and left atrium (b1); (2) short axis plane at the midpoint between the tricuspid valve annulus and the apex (b2); and (3) 4-chamber view (h). Those segment lengths are applying in the formula A = [(b1 + b2)/2] x h. The result is multiplied by the wall thickness and by myocardium density. RESULTS: Both formulas were primarily tested in 30 mongrel dogs and have shown good correlation with the true mass ( r = 0.869 with the segments formula and r = 0.819 with the bullet formula). The same method was used in 20 human patients before heart transplant with similar results ( r = 0.810 with the segments formula and r = 0.836 with the bullet formula). CONCLUSIONS: The RVM can be satisfactorily estimated by 2-dimensional echocardiography. The linear regression between the calculated mass (using the smoothest and thinner myocardium thickness) and the actual mass may provide the correction factor for the RVM calculation. Two echocardiographic methods were used to measure right ventricular mass. One of them used a bullet formula variant (5/24 pi D1 D2 L). The second method used 3 endocardium segments measured in 3 2-dimensional echocardiographic planes (short axis of aortic valve and left ventricle, and 4-chamber view), and applied in the formula A = [(b1 + b2)/2] x h. Both formulas have shown good correlation with the true mass in 30 mongrel dogs ( r = 0.869 with the segments formula and r = 0.819 with the bullet formula) and in 20 human patients before heart transplant ( r = 0.810 and r = 0.836, respectively).

Animals↗
PubMed2004

Alterations of beta-adrenoceptor responsiveness in postischemic myocardium after 72 h of reperfusion.

To determine the effect of a completely developed reperfused myocardial infarction model on beta-adrenoceptor responsiveness, we induced a 90-min regional ischemia followed by 72 h of reperfusion in dog hearts. Regional myocardial blood flow was determined after 60 min of ischemia using radioactive microspheres. beta-adrenoceptor density was reduced in the ischemic endocardium (95+/-16 fmol/mg) and epicardium (160+/-13 fmol/mg) compared to the nonischemic region (304+/-21 fmol/mg). beta-adrenoceptor density in the ischemic endocardium varied with the degree of collateral blood flow measured (r2=0.79, P<0.05); this relation was the opposite of that in the ischemic epicardium (r2=0.77, P<0.05). Higher levels of tissue catecholamines and G protein-coupled receptor kinase 2 (GRK2) were observed in the ischemic epicardium as compared to nonischemic tissue. Forskolin-induced adenylyl cyclase activities were depressed in both ischemic regions as compared to nonischemic region, correlating with a reduction in regional myocardial blood flow. Using forskolin stimulation as covariate, no difference in isoproterenol-induced adenylyl cyclase activity was identified in the different regions. It is concluded that cAMP production induced by beta-adrenoceptor activation is dependent upon adenylyl cyclase enzyme activity rather than beta-adrenoceptor density in the ischemic myocardium. However, the density of the beta-adrenoceptor in the viable ischemic regions can be modified by the presence of GRK2 and tissue catecholamines, an index of regional sympathetic efferent postganglionic nerve terminal activity.

Adenylyl Cyclases↗
PubMed2005

Age-related intramyocardial patterns in healthy subjects evaluated with Doppler tissue imaging.

BACKGROUND: The aim of this study is to analyse spatial distribution of myocardial velocities (MV) and myocardial velocity gradient (MVG) with color M-mode Doppler tissue imaging (DTI) and to analyse the influence of age in such parameters. METHODS AND RESULTS: A prospective study including 66 healthy volunteers was carried out with color M-mode DTI. Postprocessing of images was performed using proprietary software allowing the division of the myocardial wall into subendocardium, mesocardium and subepicardium. MV corresponding to the three layers and MVG time curves were obtained and systolic, early diastolic and late diastolic peak values were identified. MV were highest in subendocardium in systole, protodiastole and telediastole compared to external layers. Protodiastolic peak MV decreased in all layers with age, but with a higher impact in the subendocardium (r = 0.72, b = 0.136 (IC 95% 0.107-0.164), p = 0.0005). Older age resulted in larger telediastolic peak MV, without significant differences among layers. Linear correlation between protodiastolic peak mitral flow and peak protodiastolic velocity was higher in endocardium than in other layers (r = 0.79, p = 0.0005). CONCLUSIONS: Color M-mode DTI multilayer analysis showed that endocardium is more susceptible to age-related changes involving diastolic function. This dependency on age should be considered when assessing MV in other clinical settings.

Adolescent↗
PubMed2005

The coronary sinus conduit function: anatomical study (relationship to adjacent structures).

BACKGROUND: The mitral valve annulus (MVA) is anchored antero-medially to the aorta. Dilatation of the MVA primarily affects its postero-lateral aspect, which is related to the coronary sinus (CS). The CS and its tributaries have been used for pacing the left ventricle in patients with intractable heart failure. The aim of this study was to determine anatomical relations between the CS and its adjacent structures in 40 adult normal cadaveric heart specimens. METHODS: In 32 specimens, longitudinal sections were made along the free circumference of the MVA in 6 separate regions, 36 degrees between each, with the 0 degree marked by a line joining the centre of the CS ostium and that of the MV. In each section, the relations of the CS to the circumflex artery and the MVA were determined. CS diameter and its distance from the endocardium, just below the MVA, were also measured by a digital calliper. RESULTS: The great cardiac vein (GCV) diameter is 5.6 +/- 1.6 mm. As it leaves the interventricular groove, it curves to the left forming the base of the triangle of "Brocq and Mouchet" with the two branches of the left coronary artery, having a triple relationship with the circumflex artery. It then continues as the CS (diameter 9.3 +/- 5.3 mm) in the inferior atrioventricular groove. The end part of the GCV crosses superficial to the left circumflex artery at the level of the left marginal vein. The shortest distance between the wall of the CS and the endocardium adjacent to the MVA at the level of the anterolateral commissure is 5.2 +/- 1.6 mm, i.e. beyond the Vieussens valve. Thus, together with the CS the great cardiac vein, form a semicircular venous channel at the postero-lateral aspect of the MVA. In 37/40 hearts, this venous channel arches upwards in its middle part to be in direct contact with the left atrium. CONCLUSION: This study demonstrates an intimate proximity between the coronary sinus, at its beginning and end, and the mitral valve annulus. It also highlights the close relationship between the great cardiac vein, the annulus and the left ventricular free wall. Assessing the same relationship using the currently available imaging techniques should aid in the successful cannulation of the coronary sinus for various cardiological interventions.

Adult↗
PubMed2006

Differences in arrhythmogenicity between the canine right ventricular outflow tract and anteroinferior right ventricle in a model of Brugada syndrome.

BACKGROUND: The Brugada syndrome is characterized by ST-segment elevation on the ECG, especially in the right precordial leads sensitive to the right ventricular outflow tract (RVOT). OBJECTIVES: The purpose of this study was to evaluate the hypothesis that right ventricular electrophysiologic heterogeneity caused arrhythmogenicity in the Brugada syndrome. METHODS: Action potentials (APs) were mapped on the epicardium of 14 RVOT preparations and on the transmural surfaces of 15 pairs of RVOT and right ventricular anteroinferior (RVAI) preparations isolated from canine hearts. Brugada ECG and arrhythmias were induced with pilsicainide (2.5-12.5 micromol/L), pinacidil (1.25-12.5 micromol/L), and terfenadine (2.0 micromol/L). RESULTS: Low doses of drugs elevated the J-ST segment and induced APs with both short and long action potential durations (APDs) in contiguous RVOT epicardial regions. In addition, APs in the RVOT had a larger phase 1 notch and longer APD than in RVAI. The longest APDs were in the epicardium in RVOT but in the endocardium in RVAI regions. High doses of drugs eliminated the phase 2 dome of the AP and abbreviated APDs in the epicardium but not in endocardium and reduced the epicardial heterogeneity of APs but increased the transmural gradient of APD in 14 (93%) of the RVOT preparations. In contrast, abbreviations of epicardial APDs occurred in only 4 (27%) of the RVAI preparations. Ventricular tachycardia occurred more frequently in the RVOT (47%) than in paired RVAI preparations (7%). Blocking the transient outward current reduced the heterogeneity of APs and eliminated arrhythmogenicity in all preparations. CONCLUSION: Compared with the RVAI region, the RVOT has greater electrophysiologic heterogeneity that contributes to arrhythmogenicity in this model of Brugada syndrome.

Action Potentials↗
PubMed2004

Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: the importance of low-voltage scars.

OBJECTIVES: The purpose of this study was to evaluate the occurrence, locations, and relationship of ventricular tachycardia (VT) to low-voltage areas in dilated cardiomyopathy (DCM). BACKGROUND: The substrate causing monomorphic VT after infarction is characterized by regions of low-voltage (<1.5 mV) scar on electroanatomic maps. The substrate causing VT associated with DCM is less well defined. METHODS: A total of 28 patients were studied with endocardial (26 patients) and epicardial (8 patients) electroanatomic mapping. The VT circuits were defined by entrainment or pace mapping. RESULTS: Ventricular tachycardia was due to focal VT in 5, bundle-branch re-entry in 2, and myocardial re-entry in 22 patients (both focal and re-entry VTs in 1 patient). All patients with myocardial re-entry had endocardial (20 of 20 patients) and/or epicardial (7 of 7 patients mapped) scar. Most (63%) endocardial scars were adjacent to a valve annulus. Of the 19 VT circuit isthmuses identified, 12 were associated with an endocardial scar and 7 with an epicardial scar. All myocardial re-entrant VTs were abolished in 12 of 22 patients, and inducible VT was modified in 4 patients. During follow-up of 334 +/- 280 days, 54% of patients with myocardial re-entry were free of VT despite frequent episodes before ablation. CONCLUSIONS: The VTs in DCM are most commonly the result of myocardial re-entry associated with scar. Scars are often adjacent to a valve annulus, deep in the endocardium, and can be greater in extent on the epicardium than on the endocardium. The use of epicardial mapping and radiofrequency is likely to improve success.

Adult↗
PubMed2005

Beneficial effect of hydroxyfasudil, a specific Rho-kinase inhibitor, on ischemia/reperfusion injury in canine coronary microcirculation in vivo.

OBJECTIVES: We examined whether hydroxyfasudil, a specific Rho-kinase inhibitor, exerts cardioprotective effect on coronary ischemia/reperfusion (I/R) injury and, if so, whether nitric oxide (NO) is involved. BACKGROUND: Recent studies have demonstrated that Rho-kinase is substantially involved in the pathogenesis of cardiovascular diseases; however, it remains to be examined whether it is also involved in ischemia/reperfusion (I/R) injury. METHODS: Canine subepicardial small arteries (SA, >or=100 microm) and arterioles (A, <100 microm) were observed by a charge-coupled device intravital microscope during I/R. Coronary vascular responses to endothelium-dependent (acetylcholine, intracoronary [IC]) and -independent (papaverine, IC) vasodilators were examined after I/R under the following four conditions: control (n = 7), NO synthase inhibitor alone (N(G)-monomethl-L-arginine [L-NMMA], IC, n = 4), hydroxyfasudil alone (IC, n = 7), and hydroxyfasudil plus L-NMMA (n = 7). RESULTS: Hydroxyfasudil significantly attenuated serotonin (IC)-induced vasoconstriction of SA (-7 +/- 1% vs. 2 +/- 1%, p < 0.01). Coronary I/R significantly impaired coronary vasodilation to acetylcholine after I/R (SA, p < 0.05; and A, p < 0.01 vs. before I/R) and L-NMMA further reduced the vasodilation, whereas hydroxyfasudil completely preserved the responses. The vasoconstriction by L-NMMA after I/R was significantly improved by hydroxyfasudil in both-sized arteries (both p < 0.01). Expression of endothelial nitric oxide synthase (eNOS) protein in the ischemic endocardium of left anterior descending coronary artery area (as determined by Western blotting) significantly decreased (79 +/- 4%) compared with the nonischemic endocardium of LCX area (100 +/- 7%), which was improved by hydroxyfasudil (105 +/- 6%, p < 0.01). Hydroxyfasudil significantly reduced myocardial infarct size, and hydroxyfasudil with L-NMMA also reduced the infarct size compared with L-NMMA alone. CONCLUSIONS: Hydroxyfasudil exerts cardioprotective effects on coronary I/R injury in vivo, in which NO-mediated mechanism may be involved through preservation of eNOS expression.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

Comparison of echocardiographic acoustic quantification system and radionuclide ventriculography for estimating left ventricular ejection fraction: validation in patients without regional wall motion abnormalities.

Echocardiographic automated border detection of blood-endocardium interface is made on the basis of the principle of acoustic quantification. The automated border system is capable of providing on-line left ventricular (LV) cavity area and function. Recently, ABD algorithms have been devised to estimate LV volume on line from a long-axis image, calculated by established area-length method or Simpson's formula. To test the clinical validity of this newly developed echocardiographic method, LV volumes and ejection fraction measured by real-time acoustic quantification were compared with radionuclide ejection fraction in 24 subjects on the same day. Patients were included in the study if > or = 75% of their endocardium was visualized with conventional two-dimensional echocardiography. Sixteen (66%) of 24 patients had a technically adequate conventional echocardiogram with a broad range of ventricular dimensions and systolic function. None of the study patients had regional wall motion abnormalities. Echocardiographic measurements were obtained from the LV apical four-chamber, long-axis view. Ejection fraction, determined by the acoustic quantification and by radionuclide ventriculography, showed a strong linear relation (r = 0.92, standard error of the estimate = 4.4, p < 0.05). However, acoustic quantification overestimated the radionuclide ejection fraction with rather wide limits of agreement (3.8% +/- 16.4%; bias +/- 2 SD). Thus echocardiographic automated border detection technique is a reasonably accurate method for on-line assessment of LV function.

Adult↗