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Biomedical subjects

K Kanamasa

Publications and source records attributed to K Kanamasa.

At least 37 records · Page 2Linked to original sources
PubMed1996

Long-term nitrate treatment increases cardiac events in patients with healed myocardial infarction. Secondary Prevention Group.

BACKGROUND: Nitrates dilate coronary arteries, ameliorate myocardial ischemia, minimize left ventricular remodeling, and reduce mortality in patients with acute myocardial infarction. However, the effects of long-term treatment with nitrates on cardiac events in patients with healed myocardial infarction are not known. METHODS AND RESULTS: A total of 1,002 patients with healed myocardial infarction (789 male and 213 female) were randomly divided into 2 groups: treatment with nitrates or nontreatment. The mean observation period was 18.0 +/- 19.9 months. Primary end points were nonfatal and fatal recurrent myocardial infarction, death from congestive heart failure, and sudden death. Baseline characteristics of the 2 groups were also compared to determine any effects on outcome. Among the 621 cases treated with nitrates, 41 cases (6.6%) experienced cardiac events during the observation period, whereas only 12 of the 381 cases that were not treated with nitrates (3.1%) had cardiac events. This difference was statistically significant (p < 0.05; odds ratio 2.17; 95% confidence interval 1.13-4.19). There were no differences in the incidence of noncardiac death or being lost to follow-up between the 2 groups. Although the precise mechanism of this increase in the occurrence of cardiac events by long-term treatment with nitrates is not clear, nitrate tolerance with possible rebound and neurohormonal effects may be involved. CONCLUSION: Long-term treatment with nitrates increased cardiac events in patients with healed myocardial infarction.

Aged↗
PubMed1996

Recombinant tissue plasminogen activator prevents intimal hyperplasia after balloon angioplasty in hypercholesterolemic rabbits.

The purpose of this study was to clarify whether continuous infusion of recombinant tissue plasminogen activator (rtPA) prevents intimal hyperplasia at the site of arterial injury. Forty-three Kurosawa and Kusanagi hypercholesterolemic (KHC) rabbits which underwent balloon angioplasty of the right common iliac artery were randomly divided into 2 groups; rtPA for 7 days (n = 29) and untreated (n = 14). The former group was subdivided into a high-dose group (n = 15) (2 mg/kg per day continuously for 7 days after 3 mg/kg for 4h) and a low-dose group (n = 14) (0.6 mg/kg per day for 7 days after 0.6 mg/kg for 4 h). Balloon angioplasty was performed with a 2.5-mm balloon (3 x 60-sec, 6-atm inflations at 60-sec intervals) 1 h after the initiation of rtPA infusion via an ear vein. The iliac arteries of the rabbits were histologically studied at 28 days. The cross-sectional areas of the intima, media, and adventitia were calculated at the site of intimal hyperplasia. The intimal cross-sectional area was 0.07 +/- 0.11 (mean +/- SD) mm2 for the high-dose rtPA group and 0.11 +/- 0.07 mm2 for the low-dose rtPA group, and both of these values were significantly less than that for the control group (0.57 +/- 0.21 mm2 p < 0.01). The ratio of the intimal to medial cross-sectional area was significantly (p < 0.01) lower for the rtPA groups than for the control group (high-dose rtPA; 0.10 +/- 0.13, low-dose rtPA; 0.21 +/- 0.19, control; 1.25 +/- 0.55). In conclusion, continuous infusion of rtPA for 7 days prevented intimal hyperplasia after balloon injury.

Angioplasty, Balloon↗
PubMed1996

[Prevention of left ventricular aneurysm formation and left ventricular remodeling caused by percutaneous transluminal coronary angioplasty performed 24-48 hours after onset of acute myocardial infarction].

The prevention of left ventricular aneurysm formation and left ventricular remodeling by percutaneous transluminal coronary angioplasty (PTCA) performed 24 to 48 hours after onset of acute myocardial infarction was investigated. Left ventriculography and coronary angiography were performed in 25 patients within 24 hours of onset of acute myocardial infarction. The patients were divided into two groups; reperfusion group (n = 17) and successful PTCA group (n = 8). The reperfusion group and the PTCA group included patients whose infarct-related coronary arteries were successfully reperfused to 99%, Thrombolysis in Myocardial Infarction (TIMI) grade II or III, immediately after coronary thrombolysis. However, the reperfusion group did not include the patients with spontaneous reperfusion or reperfusion after PTCA. The PTCA group consisted of patients who underwent successful PTCA performed within 24 to 48 hours after onset of infarction (mean 28.4 +/- 6.0 hours). Non-reperfusion in the acute phase was defined as TIMI grade 0-I. The size of the ventricular aneurysm in the PTCA group was significantly reduced compared with the reperfusion group (PTCA group 4.2 +/- 8.7%, reperfusion group 27.2 +/- 6.6%; p < 0.01). The increase of left ventricular end-diastolic volume (delta LVEDVI) from the acute to chronic phases was calculated to estimate left ventricular remodeling. There was a significant difference between the two groups in delta LVEDVI (PTCA group 4 +/- 19 ml/m2, reperfusion group 19 +/- 17 ml/m2; p < 0.05). PTCA performed within 24 to 48 hours after onset in patients with acute myocardial infarction and infarct-related coronary arteries, resulting in reperfusion to 99% TIMI grade II or III immediately after coronary thrombolysis, prevents left ventricular aneurysm formation and remodeling.

Aged↗
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↗