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S Koyanagi

Publications and source records attributed to S Koyanagi.

88 records · Page 5Linked to original sources
PubMed1983

Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs.

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Abnormalities in the coronary circulation that occur as a consequence of cardiac hypertrophy.

Myocardial ischemia is frequently observed in patients with cardiac hypertrophy even when the conduit coronary arteries are normal. Recent studies indicate that impaired coronary reserve in hypertrophied hearts probably occurs because growth of the coronary bed does not keep pace with increases in cardiac mass. The imbalance between vascular proliferation and muscle growth is probably most severe when cardiac hypertrophy is produced by pressure overload. Experimental studies also suggest that abnormalities intrinsic to pressure-hypertrophied heart muscle (decreased capillary density; decreased coronary reserve; electrophysiologic abnormalities) adversely affect the response of the enlarged heart to sudden coronary occlusion. When animals with hypertension and left ventricular hypertrophy are subjected to sudden coronary occlusion, the incidence of sudden cardiac death is increased severalfold and infarct size is substantially augmented. These observations suggest that abnormalities in the coronary microcirculation that accompany cardiac hypertrophy play a significant role in the pathogenesis of the complications associated with cardiac hypertrophy.

Animals↗
PubMed1983

Effect of ischemia, hypertrophy, hypoxia, acidosis, and alkalosis on canine defibrillation.

Our purpose was to assess the effect of myocardial ischemia, left ventricular hypertrophy, and systemic hypoxia and acid-base abnormalities on the energy requirements for defibrillation. We determined the defibrillation threshold (DFT), the minimum energy required to defibrillate. DFT was not significantly elevated after left anterior descending coronary occlusion, nor was there a relationship between the size of the occluded coronary distribution area (coronary risk area) and the change in DFT in individual animals. Renal hypertension and left ventricular hypertrophy were induced by unilateral nephrectomy and contralateral renal artery stenosis. DFT in left ventricular hypertrophy dogs was not significantly higher than in dogs without hypertrophy. Finally, we induced systemic hypoxia and acid-base abnormalities. Neither respiratory nor metabolic acid-base disturbances affected DFT, but during systemic hypoxia (O2 tension 45 +/- 2) DFT fell from 83 +/- 49 to 58 +/- 28 J (P less than 0.01). Thus in dogs, myocardial ischemia, left ventricular hypertrophy, and acid-base abnormalities do not elevate defibrillation energy requirements, whereas hypoxia reduces the energy needed to defibrillate.

Acidosis↗
PubMed1983

Detection of acute myocardial infarction in closed-chest dogs by analysis of regional two-dimensional echocardiographic gray-level distributions.

We hypothesized that acute myocardial infarction could be detected in standard two-dimensional echocardiograms of closed-chest dogs by evaluating regional echo amplitude distributions using computerized image analysis. We tested this hypothesis by performing standard, 2.4 MHz two-dimensional echoes before and 2 days after circumflex coronary occlusion in seven closed-chest dogs. Control and infarcted regions of interest were studied in digitized stop-frame images. Average gray level was calculated for each region of interest, and the shape of the gray-level distribution was analyzed by calculation of skewness and kurtosis and by qualitative features of shape. Average gray level increased significantly from the pre- to postocclusion images in the infarcted regions (16.7 +/- 4.2 vs. 32.4 +/- 4.4 units, P less than 0.01), but not in the control regions (17.4 +/- 4 vs. 22.3 +/- 5.5., P = NS). Average gray level could not distinguish between infarcted and normal regions within the postocclusion images (36 +/- 5.2 vs. 33.6 +/- 5.8, P = NS). Three independent observers qualitatively evaluated histogram shape and correctly identified 7/7 MI regions (100% sensitivity) and 14/20 normal regions (70% specificity). Quantitatively, infarct regions exhibited a significant decrease in kurtosis from pre- to postocclusion images (7.1 +/- 4.0 vs. 5.2 +/- 2.9, P = NS). Within postocclusion images, infarcted regions displayed a significantly lower kurtosis than did normal regions (0.27 +/- .47 vs. 2.5 +/- 1.0, P less than .01). We conclude that acute myocardial infarction may be detected in closed-chest dogs by analyzing regional echo amplitude data from standard two-dimensional echocardiograms.

Animals↗
PubMed1982

Transmural variation in the relationship between myocardial infarct size and risk area.

To test the hypothesis that the relationship between infarct area (IA) and area at risk (AR) varies in different layers of the left ventricle (LV), we occluded the circumflex coronary artery for 48 h in 20 conscious dogs. AR was determined by postmortem coronary stereoarteriography, and infarct area by pathological examination. Both AR and IA were divided into four layers: posterior papillary muscle (PPM), subendocardium (Endo), midwall, and subepicardium (Epi) and quantified with planimetry. Hemodynamics and regional myocardial flow with tracer microspheres (7-10 micrometers diam) were measured before and after coronary occlusion. IA was closely correlated with AR for PPM (r = 0.96), Endo (r = 0.97), and Epi (r = 0.92). However, the slope of IA/AR for Endo (1.30 +/- 0.08) was significantly steeper (P less than 0.05) than that for Epi (0.89 +/- 0.11); furthermore, the intercepts at zero infarction for PPM (0.5 +/- 0.1% of LV), Endo (4.2 +/- 0.4%), and Epi (0.1 +/- 0.7%) were significantly different from each other. Regional blood flow measurements indicate that the differences in IA/AR in various layers reflected earlier and greater total collateral flow to the noninfarcted AR in the epicardium. Thus IA/AR for the entire LV is a composite representing separate IA/AR specific to various transmural layers of the LV. In addition, this study demonstrates that the lateral border zone between the IA and the AR is minimal (less than 3-5 mm) in the subendocardium and midwall layers of the left ventricle.

Animals↗
PubMed1982

Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs.

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.

Animals↗
PubMed1981

Effects of dilazep on regional myocardial blood flow during selective coronary hypotension.

Effects of 1,4-bis-[3-(3,4,5-trimethoxybenzoyloxy)-propyl]-perhydro-1,4-diazepine (dilazep), a powerful coronary dilator via adenosine potentiation, on regional blood flow during acute selective coronary hypotension were studied in the canine heart under anesthesia and thoracotomy. The proximal left circumflex coronary artery (LCX) was partially obstructed and mean LCX pressure distal to obstruction was reduced to 40-45 mmHg and two different doses of dilazep were given i.v. The left ventricular free wall and interventricular septum were divided into normally perfused, borderline ischemic, moderately ischemic and severely ischemic area according to the level of regional myocardial blood flow measured by tracer microspheres. 50 microgram dilazep/kg b.w. increased myocardial flow in the normally perfused and borderline ischemic areas without a significant alteration of blood flow to the moderately and severely ischemic areas. The fall of aortic pressure was more striking in dogs receiving 100 microgram dilazep/kg b.w. than in animals with 50 microgram dilazep. 100 microgram dilazep increased flow in the normally perfused area, but increased the number of segments in the moderately and severely ischemic area. These results indicate that an appropriate dose of dilazep causing a slight reduction of aortic pressure increased flow to the borderline ischemic as well as normally perfused myocardium in selective coronary hypotension.

Animals↗
PubMed1980

The change in the left atrial dimension during diastole. Echocardiographic assessment of mitral stenosis.

The change in the left atrial dimension during diastole was examined in patients with mitral stenosis using echocardiography. The left atrial emptying fraction (LAEF), defined as the ratio of enddiastolic dimension to endsystolic dimension of the left atrium, was 0.65 +/- 0.03 (mean +/- SE) for normal subjects, 0.86 +/- 0.01 for low grade mitral stenosis, and 0.92 +/- 0.01 for high grade stenosis. The LAEF correlated well with mitral valve area index (r = -0.70), but the correlation between E-F slope of the anterior mitral leaflet and mitral valve area index was less significant (r = 0.48). In patients who received mitral valve replacement the LAEF and the left atrial dimension significantly improved. The left atrial emptying fraction is an easily obtainable and reliable index to estimate the severity of mitral stenosis, even in patients who have undergone mitral valvular surgery.

Adult↗
PubMed1979

Early closure of the tricuspid valve in a case of Ebstein's anomaly with type B Wolff-Parkinson-White Syndrome.

Echocardiographic studies of a 19-year-old female with Ebstein's anomaly and type B Wolff-Parkinson-White syndrome showed an earlier closure of the anterior tricuspid leaflet (ATL) than of the anterior mitral leaflet (AML), contrary to the previous reports. The interval between the closure of the ATL and the AML was 20 msec and 30 msec, respectively, before and after administration of edrophonium chloride. However, closure of the AML preceded that of the ATL after administration of atropine sulfate and during supraventricular tachycardia by 10 msec and 60 msec, respectively, concomitant with the shortening of the duration of the QRS complex. We conclude that early closure of the ATL may depend on preexcitation of the right ventricle.

Adult↗