Search PubMed⌕ Search

Biomedical subjects

M Akaishi

Publications and source records attributed to M Akaishi.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effect on short-term prognosis and left ventricular function of angina pectoris prior to first Q-wave anterior wall acute myocardial infarction.

The prognostic significance of angina pectoris before the development of first Q-wave anterior wall acute myocardial infarction (AMI) was assessed in 153 patients. A total of 100 patients in this study had angina before Q-wave AMI, whereas 53 patients had no antecedent symptoms of angina. The presence of angina before AMI was associated with a lower incidence of complications including sustained ventricular tachycardia or fibrillation (7% vs 25%, p = 0.0022), pump failure (24% vs 47%, p = 0.0035), cardiac rupture (1% vs 17%, p = 0.0001), and a lower in-hospital mortality rate (11% vs 28%, p = 0.0067). The peak creatine phosphokinase activity was lower in patients with than without antecedent angina (1,727 +/- 1,238 vs 2,675 +/- 2,569 IU/liter, respectively, p = 0.023). There was no difference in the prevalence of multivessel coronary artery disease or the presence of collateral circulation between the 2 groups. Left ventriculography revealed a higher left ventricular ejection fraction (54 +/- 13% vs 46 +/- 11%, p = 0.034) and smaller left ventricular end-diastolic volumes (75 +/- 15 vs 86 +/- 18 ml/m2, p = 0.017) in patients with than without antecedent angina. These findings suggest that the presence of angina before AMI may be associated with a protective effect on left ventricular function during anterior wall AMI. Although the precise mechanisms underlying the beneficial effects are unknown, they may be related to the development of collateral channels or ischemic preconditioning.

Adult↗
PubMed1993

Clinical evaluation of the use-dependent QRS prolongation and the reverse use-dependent QT prolongation of class I and class III antiarrhythmic agents and their value in predicting efficacy.

We measured the QRS duration during a treadmill exercise test and the QT interval using a 24-hour Holter electrocardiogram at various heart rates to identify use-dependent QRS prolongation and reverse use-dependent QT prolongation of class I and III antiarrhythmic drugs. Use-dependent QRS prolongation was detected in 61%, 53%, and 64% of patients receiving disopyramide, mexiletine, and pilsicainide, respectively. Reverse use-dependent QT prolongation was found in 40% and 70% of patients receiving disopyramide and E4031. Drugs suppressed > or = 75% of the total premature ventricular contractions in all patients who had both use-dependent QRS prolongation and reverse use-dependent QT prolongation, in 79% of patients with use-dependent QRS prolongation alone, in 70% with reverse use-dependent QT prolongation alone, and in 11% with neither use-dependent QRS prolongation nor reverse use-dependent QT prolongation. Use-dependent QRS prolongation and reverse use-dependent QT prolongation were identified noninvasively and were useful in evaluating antiarrhythmic efficacy.

Adult↗
PubMed1993

Acute myocardial infarction without warning: clinical characteristics and significance of preinfarction angina.

We investigated the clinical characteristics of acute myocardial infarction (AMI) not preceded by angina in 256 patients with first AMIs. Complications, including sustained ventricular tachycardia or ventricular fibrillation, pump failure and cardiac rupture, were more frequent in patients with AMI not preceded by angina (group 1, n = 92) than those preceded by angina (group 2, n = 164). The in-hospital mortality rate was higher in group 1 than in group 2. Poor preexisting collateral channels or lack of ischemic preconditioning may be responsible for the poorer outcome in group 1 patients.

Aged↗
PubMed1993

Calcium concentration during anoxic perfusion modifies post-ischemic hypercontraction in the canine heart.

The purpose of this study was to clarify the role of calcium flux in the pathogenesis of transient overshoot in regional myocardial contractile function after brief ischemia (post-ischemic hypercontraction). Six open-chest anesthetized dogs were examined. The left anterior descending coronary artery (LAD) was cannulated with a bypass system from the left carotid artery. Two minutes of total coronary occlusion of the LAD resulted in a post-ischemic hypercontraction 1 minute after reperfusion. Post-ischemic hypercontraction was abolished after reperfusion following 2 minutes of perfusion with anoxic Krebs-Henseleit solution containing 2.5 mM calcium. Post-ischemic hypercontraction occurred after calcium-free anoxic perfusion. The regional myocardial contractile function remained depressed 1 minute after reperfusion following anoxic perfusion with 5.0 mM calcium solution. Thus, post-ischemic hypercontraction was modified by the calcium concentration during anoxia. Alteration in transsarcolemmal calcium influx during reperfusion, which was modified by alterations in the calcium environment during anoxia, could be responsible for this phenomenon.

Animals↗
PubMed1992

Left ventricular ejection performance in mitral stenosis, and effects of successful percutaneous transvenous mitral commissurotomy.

Impaired left ventricular ejection performance was reported in pure mitral stenosis. The speculative mechanisms included insufficient preload, increased wall stress, high right ventricular pressure and unknown myocardial factors, but no definitive mechanism has been established. Fifteen patients with tight mitral stenosis who underwent successful percutaneous transvenous mitral commissurotomy were studied to ascertain whether ejection performance would improve with sufficient blood filling. The indexes of preload (end-diastolic volume) and ejection performance (stroke volume, ejection fraction, and mean systolic and mean normalized ejection rates) were calculated angiographically before and immediately after mitral commissurotomy. Improved blood filling (the result of successful mitral commissurotomy) produced an increase in end-diastolic volume (mean +/- SD 99.0 +/- 30.2 to 112.1 +/- 30.1 ml/m2; p less than 0.05). All 4 indexes of ejection performance also improved. There was good correlation between end-diastolic and stroke volumes before intervention (stroke volume = 0.476 x end-diastolic volume + 16.77; r = 0.76), and the relation between them showed no change even after mitral commissurotomy. It is concluded that both left ventricular preload and ejection performance improved after successful percutaneous transvenous mitral commissurotomy. Insufficient preload could affect ejection performance in patients with tight mitral stenosis.

Adult↗
PubMed1992

Postischaemic hypercontraction is enhanced in ischaemically injured canine myocardium.

OBJECTIVE: The aim was to identify the role of calcium flux in the pathogenesis of transient overshoot of regional myocardial contraction after brief ischaemia, ie, postischaemic hypercontraction. METHODS: Ten anaesthetised mongrel dogs were examined under open chest conditions. The left anterior descending coronary artery was initially occluded for 2 min and reperfused for 10 min. A further period of coronary occlusion of 15 min duration was followed by 15 min reperfusion to produce postischaemic regional dysfunction. A third occlusion of 2 min duration was followed by 10 min reperfusion to induce postischaemic hypercontraction. Coronary blood flow was measured using an ultrasonic transit time flow meter. Segment length was measured by ultrasonic microcrystals. RESULTS: Postischaemic hypercontraction after 2 min coronary occlusion was exaggerated in ischaemically injured myocardium. The 10 dogs were divided into two groups, a control group (n = 5) and a verapamil treated group (n = 5), and were exposed to a final 2 min period of coronary occlusion with or without verapamil in the ischaemically injured myocardium. Postischaemic hypercontraction was attenuated in the verapamil treated group compared with the control group. CONCLUSIONS: Exaggeration of postischaemic hypercontraction in ischaemically injured myocardium may be mediated by a trans-sarcolemmal calcium flux. Changes in calcium flux may play a role in the pathogenesis of this phenomenon in the normal myocardium.

Animals↗
PubMed1992

Mechanisms of transient augmentation of myocardial contraction after a brief coronary occlusion.

The purpose of this study was 1) to clarify whether augmented myocardial contraction after a brief coronary occlusion, i.e. post-ischemic hypercontraction, depends on a transient increase in coronary blood flow or preceding myocardial ischemia, and 2) to identify the role of catecholamines or calcium flux in this phenomenon. Sixteen mongrel dogs were examined in open-chest anesthetized condition. One-minute reperfusion after two-minute total coronary occlusion of the left anterior descending artery resulted in a transient increase in segment shortening. Intracoronary administration of adenosine caused hyperemia without any changes in segment shortening. Two minutes of total coronary occlusion with adenosine caused post-ischemic hypercontraction to the same degree, but without any additional hyperemia. Two minutes of partial occlusion with 75% flow reduction caused less post-ischemic hypercontraction. Post-ischemic hypercontraction did not occur after partial occlusion with 50% flow reduction, irrespective of hyperemia with adenosine during reperfusion. Propranolol or verapamil did not prevent this phenomenon. Thus, post-ischemic hypercontraction is not dependent on the transient increase in coronary blood flow, but is related to the preceding myocardial ischemia. Local release of catecholamines is not likely to be the cause. A calcium antagonist, verapamil, did not modify this phenomenon. The precise mechanism of this phenomenon is still uncertain, although some alterations in cellular hemostasis, such as ionic changes, are likely to be the cause.

Animals↗
PubMed1992

[Conductance catheter for determining left ventricular volume and end-systolic pressure-volume relations: its clinical application].

In this study, the clinical usefulness of the conductance catheter technique was assessed. The end-systolic pressure-volume relations (ESPVR) measured with the increase and decrease in the preload were also compared. Fourteen patients with various heart diseases who underwent diagnostic cardiac catheterization were studied. Using a right atrial pacing catheter, 8 electrical stimuli delivered at a fixed rate of 800 msec were followed by a single early stimulus of 500 msec coupling interval, resulting in premature atrial contraction and post-extrasystolic potentiation (PESP). Left ventricular (LV) volume was measured by 2 methods; namely, the conductance catheter technique and single-plane left ventriculography (LVG). ESPVR was obtained either with the inferior vena cava occlusion induced by balloon inflation, or with the rapid transfusion of saline with electrical resistance identical to the blood volume in the right atrium. The LV volume obtained with the conductance catheter technique (VCON) was correlated with the LV volume as obtained by LVG (VLVG) (end-diastolic volume, VCON = 1.09VLVG - 4.66, r = 0.95; end-systolic volume, VCON = 1.42VLVG - 18.2, r = 0.89). There was correlation of the change in LV volume (delta V) induced by PESP between the 2 methods (end-diastolic volume, delta VCON = 0.52 delta VLVG + 0.94, r = 0.76; end-systolic volume, delta VCON = 0.42 delta VLVG - 4.78, r = 0.72), suggesting that the change in LV volume estimated by the conductance catheter technique was smaller than that estimated by LVG. The LV volume curves were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Left ventricular blood filling in patients with severe mitral stenosis: comparisons before and soon after percutaneous transluminal mitral commissurotomy].

To clarify the effects of mitral obstruction on left ventricular (LV) diastolic blood filling, 15 patients with tight mitral stenosis (each mitral valve area was less than 1.5 cm2) were studied. Each selected patient underwent successful percutaneous transluminal mitral commissurotomy (PTMC), which resulted in a 1.5 fold increase in each mitral valve area. LV pressure, left atrial (LA) pressure and cardiac output were measured before and immediately after PTMC. Left ventriculography was performed before and immediately after PTMC. The ventriculogram was traced frame by frame for one cardiac cycle. The LV volume curve was obtained from the traced image using a computer. The LV end-diastolic and end-systolic volumes (EDVI, ESVI), and ejection fraction in the subsequent cardiac cycle were calculated. The diastolic filling period was divided into 3 equal parts: namely, early, mid-, and late diastole. The blood volume entering the LV during early, mid-, and late diastole, which indicated the filling properties of each part, were calculated. After successful PTMC, both the mitral valve area (1.1 +/- 0.3 cm2 to 1.9 +/- 0.6 cm2, p < 0.01) and the cardiac index (3.2 +/- 0.8 l/min/m2 to 3.6 +/- 1.1 l/min/m2, p < 0.05) increased with the decreases in the mean diastolic pressure gradients between the LA and LV (13.4 +/- 4.5 mmHg to 5.9 +/- 2.6 mmHg, p < 0.01). The blood volume entering the LV during early diastole increased significantly without significant change in the blood volume entering the LV during mid- and late diastole.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Recurrent ischemia after acute myocardial infarction: clinical profile and significance of electrocardiographic ST changes during the attacks].

This study investigated the clinical characteristics of acute myocardial infarction (AMI) complicated by recurrent ischemia, especially relating to the electrocardiographic ST changes during the attacks. Fifty-six patients with AMI were complicated by recurrent ischemia (ischemia group), and 238 were not (non-ischemia group). The ischemia group was preceded by prior episodes of angina or myocardial infarction in 88%, as compared with 65% in the non-ischemia group (p less than 0.05). There were non Q wave infarction in 45% of the ischemia group, and 24% of the non-ischemia group (p less than 0.05). The overall in-hospital mortality rate was similar in the ischemia group (13%) and in the non-ischemia group (17%), although the causes were predominantly pump failure in the former and cardiac rupture in the latter. ST segment elevation occurred in 29 patients and ST depression occurred in 26 patients of the ischemia group during the attacks. Multivessel coronary arterial lesions were more frequently present in the latter subgroup than the former (38% vs 79%, p less than 0.05). The in-hospital cardiac deaths were also more frequently noted in the latter subgroup. Recurrent ischemia after AMI with concomitant electrocardiographic ST depression is a high risk subgroup, and, therefore, aggressive revascularization procedures may be indicated in such cases if suitable.

Coronary Vessels↗
PubMed1991

Diastolic pressure-volume relationship during handgrip exercise in patients with coronary artery disease.

There is some controversy regarding the mechanisms of an upward shift in the left ventricular diastolic pressure-volume curve during ischemia. The effects of handgrip exercise on the pressure-volume curve were examined in 21 patients with coronary artery disease and in 6 control subjects. Pressure-volume curves were constructed from digitized left ventricular pressure and volume derived from biplane left ventriculogram. Diastolic pressure-volume curve shifted upward in 12 patients with coronary artery disease during handgrip exercise (Group 1), but not in the other 9 patients who were similarly afflicted (Group 2). The upward shift did not occur in any control subject. No difference was observed in rate-pressure product gain during exercise. In Group 1, left ventricular end-diastolic pressure increased (p less than 0.01) and ejection fraction was reduced (p less than 0.01), although it did not change in Group 2. In Group 1, the time constant was prolonged (p less than 0.01) with no change in the coefficient for elastic modulus. In Group 2, these parameters remained unchanged. Group 1 was accompanied by more extensive asynergy than Group 2. Thus, isometric handgrip exercise resulted in an upward shift in the diastolic pressure-volume curve in patients with coronary artery disease. Incomplete relaxation and/or the viscoelastic properties of the left ventricle associated with ischemia could be responsible for this phenomenon.

Adult↗
PubMed1991

A case of malignant lymphoma simulating acute myocardial infarction.

A patient with malignant lymphoma suddenly collapsed, and ST segment elevation with complete atrioventricular block was observed on his electrocardiogram during an episode resembling acute myocardial infarction. Cardiac cineangiography revealed posterobasal asynergy of the left ventricle with no significant obstruction in the coronary arterial tree. Autopsy revealed diffuse invasion of the myocardium by lymphoma cells. Left ventricular wall motion was preserved even in the area of massive invasion; there was no true necrosis. Myocardial biopsy may be indicated in patients in whom there is a discrepancy between coronary pathoanatomy and wall motion abnormalities.

Diagnosis, Differential↗
PubMed1991

[Left atrial booster pump function in left ventricular blood filling: clinical and experimental analyses].

Left atrial booster pump function produces variable effects on cardiac output. Generally, cardiac output decreases by only 15-20% when atrial fibrillation occurs, however, in some cases, hemodynamic collapse occurs through loss of left atrial contraction. We evaluated the relative significance of left atrial booster pump function in acute or chronic load and in myocardial ischemia using the left ventricular volume curve. Blood entering into the left ventricle during the left atrial contraction phase (FVLA) represents the left atrial volume work, and the ratio of FVLA to the left ventricular filling volume during one cardiac cycle (%FVLA) represents the relative significance of left atrial booster pump function in cardiac output. In dog experiments, we calculated the change in FVLA and %FVLA by measuring the the left ventricular internal minor axis diameter and using Pombo's method. We also measured the change of the left atrial segment length as a direct indicator of left atrial contraction. In the acute change in preload, FVLA changed with stroke volume, but %FVLA remained unchanged. The change in FVLA correlated with the direct indicator of the left atrial excursion; the extent of the left atrial segment length (LASL). During acute change of left ventricular afterload, both FVLA and %FVLA were unchanged. In regional myocardial ischemia, both FVLA and %FVLA were increased, suggesting an increase in the left atrial booster pump function. In clinical study, we calculated FVLA and %FVLA from the left ventricular diameter using M-mode echocardiography. In chronic volume overloading (aortic regurgitation), FVLA increased while %FVLA was maintained unchanged. The same FVLA-%FVLA relationship was observed in acute volume loading. In cases of left ventricular hypertrophy (LVH) and old myocardial infarction (MI), both FVLA and %FVLA were increased, suggesting the increased left atrial booster pump function. In these cases, the left ventricular rapid filling velocity decreased, suggesting that impairment of rapid filling caused the increase of left atrial preload and hence increased left atrial volume work. The results of this study show that in old MI and in LVH, both left atrial volume work and the relative significance of left atrial booster pump function increase. We concluded that prevention of atrial fibrillation may be very important in these diseases.

Animals↗
PubMed1989

[Prognosis of patients with primary pulmonary hypertension].

Primary pulmonary hypertension is a rare disease entity. Clinical evaluations of such patients were deemed inadequate during a multi-center study in Japan (1976). The prognoses of our patients in Keio Hospital were evaluated, especially in terms of their clinical pictures and hemodynamic backgrounds. The study group consisted of 15 patients, who fulfilled the clinical criteria of primary pulmonary hypertension according to the Research Committee of the Ministry of Health and Welfare in Japan. There were four males and 11 females, whose age ranged from 16 to 72 years and averaged 34.7 years. Follow-up periods from the onsets were from 15 to 152 months, and they averaged 51 months. Nine of the 15 patients were deceased, and autopsies were performed in eight. The periods from onsets to deaths were between 15 and 152 months, and averaged 53 months (4 years and 5 months). Except for four cases followed for less than 2 years, there were seven who survived over three years and four patients who were deceased in this period, but there were no differences between these groups in terms of their clinical pictures, such as age, sex and symptomatology at onset. Survivors included three patients associated with thyroid disease, one with liver cirrhosis, and one with the Sjögren syndrome. Hemodynamically, heart rates and pulmonary artery pressures did not differ among six survivors more than 2 years after the hemodynamic evaluations and five patients who were deceased within this period. In the deceased group, however, cardiac output was low and arterio-venous differences in oxygen content were high.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗