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Biomedical subjects

K Kanamasa

Publications and source records attributed to K Kanamasa.

At least 19 recordsLinked to original sources
PubMed1992

ST-segment re-elevation and left ventricular expansion soon after acute anterior myocardial infarction.

The sum of ST-segment elevation (sigma ST on V2-4) was measured to evaluate ST-segment re-elevation during early convalescence in 57 patients with acute myocardial infarction. Following rapid ST-segment elevation resolution during the first 12 h, sigma ST again increased in many patients without signs of reinfarction or pericarditis, reaching a maximum approximately 5 days after onset. The magnitude of this re-elevation (delta sigma ST) was less than 0.3 mV in 30 patients (group A), and 0.3 mV or more in another 27 (group B). Based upon left ventriculography, the global ejection fraction in group B decreased significantly from 51 +/- 10% at the acute phase to 46 +/- 10% at the chronic phase. No such decreases were seen for group A. Regional ejection fraction in the infarcted portion improved significantly from 28 +/- 13% at the acute phase to 35 +/- 14% at the chronic phase in group A, but did not improve in group B. In addition, the non-infarcted portion in group B showed a significantly reduced regional ejection fraction. These results suggest that myocardial expansion of the infarcted portion may contribute to ST-segment re-elevation, an ominous sign of left ventricular dysfunction soon after acute myocardial infarction.

Cineangiography↗
PubMed1992

[A case of cardiac lipoma of the anterior tricuspid leaflet].

A 42-year-old man with cardiac lipoma of the anterior tricuspid leaflet is reported. He had a chief complaint of epigastric discomfort, and a pansystolic murmur was heard at the left sternal border in the 4th intercostal space. Two-dimensional echocardiography disclosed a mobile high density stalkless mass having several areas of low density. Two-dimensional Doppler echocardiogram revealed a moderate degree of tricuspid regurgitation. These findings were more clearly visualized on transesophageal echocardiogram. MRI revealed a high signal intensity on the T1-weighted image and a high radiodensity surrounding the mass using a contrast medium of Gd-DTPA. A 2.0 x 1.3 x 0.8 cm hemispherical, lobulated and sessile yellow mass was excised by means of open heart surgery, and tricuspid valvuloplasty was performed. The mass was adipose tissue and was surrounded by fibrous tissue just under the lamina fibrosa. These findings were compatible with those of the preoperative examinations, although the preoperative diagnosis was not conclusive. This was our first case of cardiac lipoma in which the tricuspid valve was successfully excised.

Adult↗
PubMed1991

The importance of good endocardial reflow immediately after reperfusion for myocardial salvage in dogs.

We studied the importance of reflow after reperfusion for myocardial salvage. In 19 open-chest dogs, the left anterior descending coronary artery was occluded for 3h and then reperfused. Non-radioactive colored microspheres were injected into the left atrium to measure regional myocardial blood flow (RMBF). Immediately after occlusion, RMBF was reduced to 23 +/- 2% (of control) in the inner layer and 32 +/- 2% in the outer layer. Five minutes after reperfusion, RMBF was increased to 170 +/- 20% and 156 +/- 11% of control in the inner and outer layers, respectively. One week later, RMBF in the inner layer was reduced to 63 +/- 4% but it was not reduced (100 +/- 6%) in the outer layer. There was a roughly positive correlation between the inner/outer flow ratio measured 5 min after reperfusion and myocardial creatine kinase activity. Myocardial necrosis determined by triphenyl tetrazolium chloride stain varied inversely with the inner/outer flow ratio. These results indicate that good reflow in the inner layer 5 min after reperfusion is a favorable indicator for myocardial salvage.

Animals↗
PubMed1991

[Clinical characteristics of precordial ST-segment depression in acute inferior myocardial infarction].

Assessments of the significance of precordial ST segment depression in acute inferior myocardial infarction (AIMI) have yielded conflicting results. Among 92 AIMI patients admitted within 6 hrs after the onset, 65 showed ST depression, and the remaining 27 showed no ST depression. These depressions were present in all of V1-4 (right type; 17), V2-5 (middle type; 10), V3-6 (left type; 13) and V1-6 (broad type; 25). The clinical severity was Forrester subset I in the majority (89%) of patients without ST change, while complications were prevalent in patients with ST depression, especially in the right type (44% were Forrester subset II-IV). Peak CK was 2,150 +/- 399 U/L in patients without ST depression, but it was elevated to 3,172 +/- 811 in patients with ST depression, especially in the right type (4,506 +/- 499). Wall motion evaluated by echocardiography and QRS scores on ECG also revealed greater abnormality in patients with ST change. The initial right coronary angiogram on admission revealed complete occlusion in 76% of these patients with ST depression of whom all of the right type had completely occluded artery. Abnormal motion of the anterior wall, which suggests remote ischemia associated with AIMI was proved neither by left ventriculography nor echocardiography. Hospital mortality in patients with ST depression (9.2%) was as twice as high as that in those without ST depression (4.6%). We concluded that ST depression in patients with acute inferior infarction may not be indicative of remote ischemia but manifests as a mirror image of a large infarction with a complicated clinical course.

Adult↗
PubMed1990

Does reperfusion extend necrosis? A study in a single territory of myocardial ischemia--half reperfused and half not reperfused.

The purpose of this study was to confirm or disprove the existence of reperfusion-induced extension of necrosis. To avoid the effect of the variability of collateral circulation when groups of dogs are compared, we compared the effect of reperfusion and nonreperfusion on myocardial necrosis in a single ischemic territory, half of which was reperfused and half of which was not. The left anterior descending coronary artery (LAD) territory between its last diagonal branch and the apex was studied because it was found to have uniform collateral blood flow. In 20 dogs, the LAD was occluded for 90-240 minutes to produce necrosis of different degrees of transmurality. Before release of this occlusion, the LAD was occluded distally halfway to the apex to keep the distal half nonreperfused. After 5 minutes of proximal reperfusion. Monastral blue dye was injected into the left atrium for demarcation of the reperfused region, and the heart was arrested, excised, cut parallel to the LAD, and placed into triphenyl tetrazolium chloride (TTC) solution for delineation of the region of necrosis. The validity of TTC staining under the conditions of this study was confirmed by light and electron microscopy. The transmurality of necrosis, measured within 1 or 0.5 cm on either side of the boundary, ranged from 30% to 88% of wall thickness and was not different in the reperfused compared with the nonreperfused region (paired t test). Reperfusion did not advance the epicardial edge of necrosis compared with the nonreperfused region. In conclusion, at 5 minutes after reperfusion, comparison of necrosis in the reperfused and nonreperfused halves of a single ischemic territory could not demonstrate an extension of necrosis by reperfusion.

Animals↗
PubMed1989

Selective decrease in lysis of old thrombi after rapid administration of tissue-type plasminogen activator.

The safety of thrombolytic therapy of acute myocardial infarction could be improved if a method were developed to dissolve fresh occlusive coronary thrombus without simultaneously dissolving hemostatic thrombi outside the coronary arteries. This study is based on the assumption that, in a patient with evolving acute myocardial infarction, hemostatic thrombi are likely to be older than the thrombus responsible for occlusion of the coronary artery. It explored whether the relative rates of lysis of fresh and old thrombi could be influenced by the rapidity of recombinant tissue-type plasminogen activator (rt-PA) administration. In each of 17 dogs, two 1 h and two 24 h old thrombi were produced by inserting copper coils into both jugular and both femoral veins. After 24 h and 1 h, respectively, the coils with the thrombi were removed, weighed and inserted into the adjacent carotid and femoral arteries. A 1 mg/kg body weight dose of rt-PA was given either over 180 or over 30 min. The coils were removed and weights of the residual thrombi determined at the end of the 180 min infusion (Group I), at the end of the 30 min infusion (Group IIA) and 45 min after the 30 min infusion (Group IIB). The 24 h old thrombi were lysed significantly less than the 1 h old thrombi in all three experimental groups: 53.9 +/- 4.8% (mean +/- SE) versus 86.1 +/- 2.5% in Group I (p less than 0.001), 16.6 +/- 3.5% versus 65.2 +/- 6.0% in Group IIA (p less than 0.001) and 21.6 +/- 5.4% versus 91.7 +/- 1.7% in Group IIB (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[The effects of coronary thrombolysis on the short- and long-term mortality in acute myocardial infarction].

Among 263 patients with acute myocardial infarction, 141 were treated with urokinase (UK group) and 122 received no urokinase (conventional group). Urokinase (UK) was administered intracoronarily in 55 cases; intravenously (mainly 1,920,000 units) in 64 cases; and intravenously and intracoronarily in 22 cases. The mortality rates were ascertained three months after admission and during the mean follow-up periods of 17.5 months for the UK group and 24.5 months for the conventional group. The three month mortality was significantly lower in the UK group (10.6%, 15 cases) than in the conventional group (23.8%, 29 cases) (p less than 0.01). The mortality during the entire follow-up period was also lower in the UK group (14.2%, 20 cases) than in the conventional group (26.2%, 32 cases) (p less than 0.05). Fatalities due to cardiac rupture, ventricular fibrillation, cardiac failure, cardiogenic shock and recurrent infarction were uniformly less in the UK group. It was concluded that coronary thrombolysis is an effective means of reducing mortality in acute myocardial infarction.

Aged↗
PubMed1988

Effects of coronary thrombolysis on left ventricular ejection fraction in patients with acute myocardial infarction.

Left ventriculograms were performed on 65 patients with acute myocardial infarction, once upon admission and again 3 months later. In 29 cases urokinase was injected intravenously and/or intracoronarily. The other 17 were treated without urokinase. In 8 out of 29 patients whose infarct-related coronary arteries remained completely occluded following urokinase therapy, the global ejection fraction was reduced from 54 +/- 3% during the acute stage to 46 +/- 5% during the chronic stage (p less than 0.001). However, for the 21 patients whose coronary arteries were successfully recanalized, the 2 values were the same (52 +/- 2%). The highest global ejection fractions were seen in 19 spontaneously recanalized patients (acute: 54 +/- 2%, chronic: 55 +/- 2%). For the 8 unsuccessful patients, the regional ejection fraction for the infarcted portion was reduced from 20 +/- 5% during the acute stage to 18 +/- 6% during the chronic stage. But for the successful patients there was an improvement from 22 +/- 2% during the acute stage to 27 +/- 2% during the chronic stage. Again, the regional ejection fraction was the highest for the spontaneously recanalized group, being 31 +/- 2% and 36 +/- 3% during the acute and chronic stages, respectively. These results indicate that if the coronary artery remains occluded during the acute stage the reduced left ventricular function continues to deteriorate even more during the chronic stage. Successful coronary thrombolysis, however, might salvage the infarcted myocardium as well as preserve the function of the left ventricle.

Chronic Disease↗
PubMed1988

Effects of mannitol in the prevention of evolving myocardial infarction.

The ability of hyperosmolar mannitol to salvage evolving myocardial infarction was studied in 50 open-chest dogs subjected to 3 hours occlusion of the left anterior descending coronary artery. In 28 dogs, 20% hyperosmolar mannitol was infused into the distal half of the infarcted portion after commencement of reperfusion, leaving the proximal half mannitol free. In the other 22 dogs, physiological saline was infused instead of mannitol. The wall thickness at the distal half of the infarcted portion was increased 2 hours after reperfusion in both the saline and the mannitol groups. After 2 hours reperfusion the chest was closed. Thirteen out of 28 dogs in the mannitol group and 12 out of 22 dogs in the saline group died over one week. Seven days later, myocardial samples were measured for myocardial water content and creatine phosphokinase activity (CPK). Myocardial water content was increased in the infarcted portion in both the saline and the mannitol groups. In the saline group, myocardial CPK was reduced markedly in the proximal half (54.8 +/- 7.8% at the inner layer and 53.1 +/- 4.7% at the outer layer). These depletions were even more marked in the distal half (47.9 +/- 5.8 and 48.3 +/- 3.3%). In the mannitol groups, although the CPK was similarly depressed in the proximal half (44.8 +/- 5.8 and 41.1 +/- 5.4%), the CPK depletion in the distal half was less (48.1 +/- 6.1 and 58.1 +/- 6.7%) than the proximal half, suggesting mannitol preserved CPK depletion in the infarcted portion. It was concluded that intracoronary infusion of mannitol after reperfusion may salvage the infarcted myocardium.

Animals↗
PubMed1988

Reduced early diastolic extension in the infarcted portion in patients with old myocardial infarction.

To study relaxation characteristics of the infarcted myocardium, cyclic changes in the global left ventricular (LV) volume were measured in 20 patients with old myocardial infarction (OMI) and 17 normals (Normal) and those in the regional segment length were measured in 9 patients with anterior old myocardial infarction (anterior OMI) and 11 normals. The LV volume was calculated by using biplane LV cineangiograms. The regional segment length was calculated by measuring the spatial length between the 2 points of the ramifying branches on the left coronary arteries by using biplane coronary cineangiograms. The LV filling volume before atrial contraction (VR) was significantly less in the OMI compared with that in the normals (Normal 38 +/- 6 (mean +/- SD) ml/m2 vs 30 +/- 7 ml/m2: p less than 0.01), while filling volume by atrial contraction (Va) did not significantly differ (Normal 15 +/- 4 ml/m2 vs OMI 17 +/- 5 ml/m2). The lengthening of the segmental wall during diastole before atrial contraction (%LR) in the infarcted portion was 5.0 +/- 2.9% which was also significantly less than that in the non-infarcted portion (9.6 +/- 4.2%). The extent of lengthening by atrial contraction (%La) did not differ between the 2 portions (non-infarcted portion 3.8 +/- 1.1% vs infarcted portion 3.5 +/- 1.2%). Reduction of %LR was speculated to be caused by the incomplete relaxation in the myocardium adjacent to the infarcted portion and stiff myocardium in the infarcted portion. This study suggests that the infarcted myocardium may lead to a reduction of diastolic expansion before atrial contraction.

Angina Pectoris↗
PubMed1988

[Acute myocarditis with localized left ventricular aneurysm: a report of three cases].

Ventricular aneurysms are rarely observed in viral myocarditis. Three cases whose left ventriculograms showed localized left ventricular aneurysms in the chronic phase of myocarditis are reported. The etiology in one case was herpes simplex virus (Case 1). Two cases (Case 2, 3) of myocarditis were admitted to our Coronary Care Unit in the acute phase, when diffuse hypokinesis of the left ventricle was demonstrated by two-dimensional (2-D) echocardiography. Hypokineses progressed to localized left ventricular aneurysm formation, demonstrated by cine angiography. In the acute phase, ST segment elevation was observed in these two cases, but it resolved. Abnormal Q waves also resolved in the chronic phase. Negative T waves were nearly normalized in one of them (Case 3). Abnormal Q waves with ST segment depression were observed in another case (Case 1). Thus, there were no characteristic or consistent findings suggesting a left ventricular aneurysm on electrocardiography. 2-D echocardiography and cine angiography proved useful for diagnosing this uncommon complication. Long-term follow-up of these cases will be important, because viral myocarditis can develop into dilated cardiomyopathy. The mechanism of left ventricular aneurysm following acute viral myocarditis included: (1) direct viral injury of the myocardium, (2) localized injury due to immunological mechanisms, and (3) coronary thrombosis due to increased platelet aggregation by viral infection.

Acute Disease↗
PubMed1987

Paradoxical fall of tachycardia- and hypoxia-induced coronary flow under conditions of severe coronary stenosis in dogs.

It has been stated that the coronary flow paradoxically falls in response to tachycardia if the coronary artery is stenotic and "compliant". To clarify this, we measured coronary vascular resistance by cannulating the left anterior descending coronary artery in open-chest dogs. In constant flow perfusion of 41 +/- 5 ml/min/100 gm, coronary perfusion pressure was decreased by pacing, while at lower flow of 14 +/- 3 ml, it was increased by pacing, indicating that coronary vascular response was reversed. In constant pressure perfusion, coronary vascular resistance was reduced by pacing at high perfusion pressure, while it was paradoxically increased by pacing at low perfusion pressure. In the third experiment at constant flow perfusion, perfusing blood was changed from arterial to venous blood to induce myocardial hypoxia. At high flow, venous blood perfusion reduced coronary vascular resistance, while at low flow it increased coronary vascular resistance. All three experiments indicated that at high perfusion, tachycardia and hypoxia caused a reduction in coronary vascular resistance to meet the increased myocardial oxygen demand; however, at low perfusion, those stimuli increased coronary vascular resistance. The present study showed that the coronary vascular response is reversed at low flow and suggested that those stimuli might reduce flow further in patients with stenotic coronary artery and could be one of the mechanisms causing the development of myocardial infarction in those patients.

Animals↗
PubMed1987

Improved prognosis after coronary thrombolysis with urokinase in acute myocardial infarction.

The effectiveness of coronary thrombolysis with urokinase (UK) on short- and long-term outcome after acute myocardial infarction was studied by comparison of 120 patients treated with UK and 124 with conventional therapy followed up for a period of 20 months. UK was administered to patients within 6 hours of the onset of chest pain, by the intracoronary route (20,000 U/min, at a mean dose of 698,000 U) in 46 patients, intravenously (960,000 to 1,920,000 U in 15 or 30 min, at a mean dose of 1,293,000 U) in 56 patients and by the combined route (at a mean dose of 2,333,000 U) in 18 patients. Complete occlusion or 99% stenosis with severe delay of the contrast medium was found in 72.5% and recanalization by UK was achieved in 68.0%. Cumulative mortality rate was significantly reduced in the UK group (9.2% vs. 29.0%). Cardiac death from recurrent MI was also significantly reduced (2.5% vs. 10.5%). The reduction in mortality rate was demonstrated even in older patients as well as in those cases graded as severe according to the Killip and Forrester classifications. Thus, it is concluded that coronary thrombolysis with UK therapy improves the prognosis of acute myocardial infarction.

Adult↗
PubMed1987

[Time constant of the left ventricular pressure fall, and onset and rate of expansion of the left ventricular segment in hypertrophic cardiomyopathy].

The left ventricular diastolic properties of patients with hypertrophic cardiomyopathy are impaired. Since there is degeneration or disarray of myocardial fibers in patients with hypertrophic cardiomyopathy (HCM), the rate of expansion in diastole may become asynchronous. Biplane coronary cineangiograms were performed in eight normal subjects and nine patients with HCM. The coordinates (x,y,z) of the ramifying points of the left coronary artery were measured, and the distance between any two of the points of the coronary artery was calculated (segment length). Fifteen segment lengths were calculated for each subject. Since the onsets of expansion of these 15 segment lengths were not simultaneous, they expanded at different times and the onsets of expansion occurred within a very short period of time, nearly at end-diastole. The variance (standard deviation) of the timing of expansions of these 15 segments and the rate of expansion within the late 40 msec of the isovolumic relaxation period (% delta L) were calculated. The time constant of the left ventricular pressure fall (T) in normal subjects was 41.3 +/- 7.7 (SD) msec, T in HCM was prolonged to 52.7 +/- 11.1 msec. The variance was 47 +/- 17 msec in normal subjects, but it increased to 99 +/- 26 msec in HCM. The rate of expansion again decreased in HCM (Normal 2.24 +/- 0.60 vs HCM 1.40 +/- 0.96%). The conspicuous diastolic asynchrony in the onset of expansion and the reduced rate of diastolic expansion in HCM may be the mechanism of impairing the diastolic properties of the left ventricle.

Adult↗
PubMed1986

The beneficial effects of 40% and 100% O2 inhalations on acutely-induced myocardial ischemia in dogs.

The effectiveness of O2 inhalation on the acutely-induced ischemic myocardium in dogs was investigated. In 22 open-chest mongrel dogs, the left anterior descending coronary artery was partially occluded to reduce coronary flow. The regional coronary vein accompanying the artery was cannulated to obtain coronary venous blood. Switching of inspiratory gas from room air to 40% O2 produced an elevation of coronary venous O2 saturation from 35.8 +/- 12.7 (S.D.) to 41.1 +/- 11.9% and shifting of myocardial lactate production to utilization (from -0.9 +/- 36.9 to 5.0 +/- 36.7%), indicating that 40% O2 inhalation ameliorated ischemia. Application of 100% O2 inhalation caused even more beneficial effects; coronary venous O2 saturation was elevated to 50.6 +/- 12.6% and myocardial lactate extraction was improved to 7.8 +/- 40.5%. The present study indicated that 40% O2 inhalation was effective and 100% O2 inhalation even more effective in ameliorating acutely-induced myocardial ischemia. Decreases in myocardial contractile force and left ventricular size and suppression of sympathoadrenal activity might be possible mechanisms for these beneficial effects.

Animals↗
PubMed1986

[Effects of nitroglycerin on left ventricular geometry and compliance in man].

The effects of nitroglycerin (NTG) on relaxation characteristics of the infarcted and non-infarcted myocardium were investigated by calculating a segment length on the epicardium of the left ventricle for 16 patients with old myocardial infarction. The spatial segment length was measured between two points which were identified as a junction of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Regional myocardial stiffness was expressed as delta P/delta L, where delta P was an increment of left ventricular (LV) diastolic pressure from the lowest LV diastolic pressure to the pressure at the maximal segment length, and delta L was the difference of two segment lengths corresponding to those pressures. Myocardial stiffness decreased from 0.0402 +/- 0.0293 mmHg/mm to 0.0212 +/- 0.0157 with intracoronary NTG (p less than 0.01) and from 0.0220 +/- 0.0090 to 0.0136 +/- 0.0124 with sublingual NTG (p less than 0.001) in the non-infarcted portions. However, it was unchanged with both intracoronary and sublingual NTG in the infarcted portions. NTG may cause venous pooling and may decrease diastolic wall tension of the left ventricle as its indirect effect on the non-infarcted myocardium. Also, the non-infarcted myocardium may be influenced by dilatation of the epicardial coronary artery. Muscle stiffness of the infarcted myocardium was unchanged, probably due to the rigidity of myocardial fibrosis. It was concluded that in myocardial infarction diastolic distensibility of the non-infarcted portion can be improved by NTG both through indirect and direct effects.

Compliance↗
PubMed1986

[Reduction of myocardial segment shortening during angina-free period in patients with angina pectoris].

In 16 patients with angina pectoris who had no histories of myocardial infarction, myocardial segment shortening was studied during angina-free periods. Myocardial segment length in the anterior wall of the left ventricle was calculated by measuring the spatial length between two points identified as junctions of ramifying branches of the left coronary arteries using biplane coronary cineangiography. Segment shortening was classified according to the severity of coronary arterial stenosis. The patients were categorized according to the severity of coronary arterial stenosis: as 1) the 0% stenosis (normal); 2) the 50% stenosis group; and 3) the 75-90% stenosis group. Total segment shortening in the normal group was the same as that in the 50% stenosis group (10.4 +/- 2.5%). However, in the 75-90% stenosis group, segment shortening was reduced to 7.3 +/- 2.5%. Effective segment shortening during the ejection period was reduced (5.0 +/- 1.8%) in the 75-90% stenosis group, as compared with the normal group (8.4 +/- 2.4%) and the 50% stenosis group (7.2 +/- 3.6%). This study demonstrated that segment shortening was reduced at rest in patients with angina pectoris who had had no previous infarction. A possible mechanism of this reduced segment shortening during angina-free periods may be irreversible myocardial alteration from recurrent ischemic attacks.

Angina Pectoris↗