Biomedical subjects
Publications and source records attributed to H Nonogi.
A 25-year-old Japanese woman was admitted due to acute inferior myocardial infarction. Coronary angiography showed complete occlusion of the proximal right coronary artery and vague calcification distal to the complete occlusion. Using ultrafast computed tomography, two coronary artery aneurysms in the right coronary artery that could not be detected by coronary angiography were visualized.
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We have performed lipid analyses by using a table-top ultracentrifuge based on the Hatch and Lees' method in 77 subjects (60 men, 17 women: mean age, 63 years) to clarify lipoprotein disorders in coronary artery disease. Sixty-four subjects had coronary artery disease and 13 normal subjects were controls. They were divided into the groups with stable angina pectoris and with unstable angina pectoris or acute myocardial infarction (acute coronary syndromes). In patients with coronary artery disease, there were no significant differences from control in age, body mass index, total cholesterol, however, HDL cholesterol was significantly lower than those in the controls. LDL cholesterol:LDL apoB ratio, which is thought to reflect the size of LDL in coronary artery disease, was significantly smaller than that in the controls; mean values were 1.2 in coronary artery disease and 1.4 in controls. There were no significant differences in those lipoprotein disorders between the patients with stable angina and those with acute coronary syndromes. Though these lipoprotein abnormalities would not play a trigger role in acute coronary syndrome, they are characteristic of the lipid profile of patients with coronary artery disease.
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A 64-year-old patient with silent myocardial ischemia after anterior myocardial infarction was treated with directional coronary atherectomy, balloon angioplasty, and placement of Palmaz-Schatz stent. An unexpanded Palmaz-Schatz stent was retained in the left main coronary artery and was treated successfully with a nitinol goose-neck snare. After this procedure, another Palmaz-Schatz stent was successfully implanted without any complications.
To evaluate the effect of intracoronary diltiazem on myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA), 38 patients were randomly assigned to receive inactive placebo (n = 19; group C) or a low dose (1 mg, n = 10; group D1), or a high dose (2 or 3 mg, n = 9; group D2) of diltiazem in a double-blind manner. The agent was administered directly into the coronary artery via a balloon catheter following a control balloon inflation. Chest pain score (maximum, 10) and the magnitude of ischemic ST elevation on standard and intracoronary electrocardiograms (ECGs) during a balloon inflation were assessed in the control and posttreatment periods. After the administration of diltiazem, the chest pain score was significantly decreased in group D1 (control: 5.1 +/- 3.6, posttreatment: 3.8 +/- 3.1, P < 0.01) and group D2 (3.4 +/- 2.5 vs 2.5 +/- 2.0, P < 0.01), but not in group C (4.1 +/- 3.1 vs 3.7 +/- 3.3, difference not significant). The magnitude of ST elevation relative to the control on standard and intracoronary ECGs was significantly smaller in groups D1 and D2 than in group C (standard ECG; D1: 51.8 +/- 10.6% of control, D2: 41.6 +/- 28.7% vs C: 93.3 +/- 15.6% and intracoronary ECG; D1: 47.1 +/- 11.7% of control, D2: 27.5 +/- 26.9% vs C: 94.6 +/- 29.3%, all P < 0.01). Although systolic blood pressure decreased slightly in groups D1 and D2, there was no significant correlation between the change in ST elevation and the change in the rate-pressure product. Pretreatment with a small dose of intracoronary diltiazem attenuated myocardial ischemia during PTCA and this pretreatment may enable us to perform balloon inflation for a longer period.
The purpose of this study was to elucidate the effect of repeated brief coronary occlusions on reactive hyperemia during percutaneous transluminal coronary angioplasty (PTCA) in patients with or without ischemic tolerance. Seventeen patients undergoing PTCA for chronic stable angina were studied. Patients with well developed collateral vessels were excluded. After successful predilatation, coronary flow velocity was recorded with the use of a Doppler flow guide wire, and reactive hyperemia was assessed immediately after each of two 2-min coronary occlusions followed by 2 mins of reperfusion. The intracoronary electrocardiogram (icECG) was recorded via the flow guide wire placed in the center of the ischemic zone. Patients were divided into two groups: those who showed a reduction of ST elevation in the icECG recorded at the time of the second coronary occlusion (group I), and those who showed no difference in ST elevation between the two occlusions (group II). There were no significant differences in blood pressure, heart rate, or baseline coronary flow velocity between the two groups before the first occlusion, but the ST elevation at the time of the first coronary occlusion was greater in group I than in group II (8.9 +/- 6.2 versus 1.1 +/- 2.0 mm, P < 0.01). Reactive hyperemia was significantly greater after the second coronary occlusion than after the first in group I (22.1 +/- 15.8 versus 30.4 +/- 21.0 cm/s, P < 0.05), but it did not change in group II (25.6 +/- 13.0 versus 23.5 +/- 11.2 cm/s NS). Reactive hyperemia was enhanced in patients with ischemic tolerance who showed a reduction in St elevation in the icECG. These results suggest that observed reactive hyperemia does not necessarily reflect the severity of ischemia.
The myocardial uptake of F-18 fluorodeoxyglucose (FDG) has been shown to indicate ischemia. To elucidate whether this is applicable to reperfused myocardium in patients with acute myocardial infarction (AMI), Tl-201 SPECT and F-18 FDG PET were performed in 10 patients with successfully recanalized AMI (male myocardial perfusion on the infarct-related area was classified, on the basis of Tl-201 images, into 2 groups (normal and defect) during the sub-acute phase, and into 3 grades (normal, redistribution (RD), and persistent defect) during the chronic phase (1 and 3 months after onset). Regional FDG uptake was calculated as FDG uptake in the region of interest normalized relative to that in a normal area. During the chronic phase, FDG accumulated only in the region of RD, indicating ischemia, but during the sub-acute phase, FDG accumulated mainly in the peri-infarct area. To elucidate whether the reperfused myocardium itself shows signs of accelerated glucose uptake, an experimental study was performed in rats. Glucose uptake in the isolated heart was measured by deoxyglucose and 31P-NMR spectroscopy, and was significantly increased after reperfusion compared with the pre-ischemic level. In conclusion, the enhancement of FDG uptake during the sub-acute phase was observed in successfully reperfused myocardium of patients with acute myocardial infarction. Such augmentation disappeared during the chronic phase. An experimental study in rats indicated that ischemia and reperfusion themselves augment glucose uptake. This mechanism may be responsible for the increase in FDG uptake of reperfused myocardium observed clinically.
We compared the post-hospital prognosis after an acute coronary event (acute myocardial infarction and unstable angina) in 106 patients in Japan vs. 789 patients in North America who were prospectively enrolled in the Multicenter Study of Myocardial Ischemia and were followed-up for an average of 26 months per patients. Risk factors more frequent in Japan were older age, males and smoking at enrollment, but the rest of many risk factors were similar. After adjusting for differences in clinical and medication variables, Cox analyses indicated patients in North America had a significantly greater risk of experiencing a primary end-point (cardiac death, non-fatal myocardial infarction or unstable angina) than patients in Japan (hazard ratio [North America:Japan] = 3.1, P = 0.003). There was a non-significant trend in the restricted end-points (cardiac death or non-fatal myocardial infarction) with North America having more frequent events than Japan (hazard ratio = 2.2, P = 0.12). The long-term outcome after recovery from an acute coronary event is more favorable in Japan than in North America, mostly due to a reduction in subsequent hospitalization for unstable angina. The reason for these findings cannot be explained by differences in the measured risk factors or medications.
To elucidate the clinical features of acute myocardial infarction (AMI) and post-MI silent myocardial ischemia (SMI) in the elderly, and efficacy of therapy in an era of coronary intervention, a total of 10,607 patients with AMI who were enrolled in a multicenter survey between 1982 and 1992 were examined. The elderly had a higher ratio of females, noncardiac illness, atypical symptoms at the onset of AMI, severe pump failure at admission, cardiac rupture and multivessel disease. Hospital mortality was markedly higher in patients > or = 75 years, and it was 4-fold compared with patients < 65 years. In the last 5 years, the rate of application of coronary angiography and primary PTCA significantly increased even in the very elderly. In contrast, use of thrombolysis highly diminished. Hospital mortality declined (14.6 vs 11.9%, p < 0.001) in every age group compared with the first 5 years, although it was higher in the elderly even in the last 5 years. Investigation of 642 survivors after AMI admitted to one hospital showed that the elderly had a higher incidence of SMI and post-MI angina compared with the non-elderly. Clinical features of SMI were similar in both groups. However, medical treatment was more prevalent and recurrence of MI and cardiac death during follow-up (average 27 months) were more frequent in the elderly. In this retrospective study, characteristics of AMI and SMI, and effectiveness and limitation of therapy in the elderly were clearly demonstrated. It was evident that hospital mortality of the elderly had improved, although it was still higher than the non-elderly.
Recently, percutaneous cardiopulmonary support (PCPS) combined with femoro-femoral bypass without reservoir has become valued because of its quick and easy application. We developed a fully preconnected compact integrated cardiopulmonary bypass (CPB) unit (priming volume of 250 ml) with a blind pore membrane oxygenator (Kuraray Menox) for PCPS. From 1990 to 1995, PCPS was performed in 49 patients of whom 26 were weaned from support. In most cases, we applied this CICU in patients with no active bleeding (22 patients); in patients with active bleeding (n = 13), we used Medtronic's heparin-bonded close chest support pack (CCSP). Of these, PCPS was performed uneventfully for 2 h (median) in 8 elective cases; all of these patients were weaned or were switched to a left ventricular assist system (LVAS). In 8 urgent cases, such as those with low cardiac output syndrome, PCPS was performed for 4 days (median), 1 was weaned, and 2 CICU were cases switched to other procedures. In 32 cases of shock, 5 CICU patients were weaned, and 3 of them survived. Eight patients including 5 CICU patients and 1 CCSP patient were switched to operation or LVAS, and 2 CICU patients remain alive. From these data, PCPS has been shown to support the patient's circulation in the acute phase and earn time to switch to operation or LVAS; the quick and easy set-up of the CICU can improve the clinical results. The use of the Medtronic device broadened the indication for PCPS. The CCSP enlarged the indication of PCPS but could not improve the results. To improve the results, a heparin-bonded surface is desired.
Women appear to be protected, until the menopause, from the development of coronary artery disease. The incidence of acute myocardial infarction in young women is very low, so there is little information on the etiology, clinical features, and prognosis for such patients. We studied 24 young female patients with acute myocardial infarction (< 50 years) among 2,457 consecutive patients with acute myocardial infarction admitted to the coronary care unit of the National Cardiovascular Center from December 1977 through August 1994. Their clinical features and in-hospital mortality were compared with 100 consecutive young male patients (< 50 years) with acute myocardial infarction. The fraction of patients of age younger than 50 years among all age groups was lower in female than in male acute myocardial infarction patients (5% vs 13%, p < 0.01). The increase of the coronary risk factors, hypercholesterolemia (25% vs 55%, p < 0.05) and cigarette smoking (17% vs 96%, p < 0.05) were less common in women. In female patients, the serum total cholesterol level was lower (195 +/- 50 vs 216 +/- 48 mg/dl, p = 0.06), and the serum high-density lipoprotein cholesterol level was higher (50 +/- 12 vs 39 +/- 12 mg/dl, p < 0.05) than in male patients. Other risk factors did not differ significantly between the two groups. Angiography 1 month after myocardial infarction showed fewer diseased coronary arteries (> 75% stenosis) in female than male patients (0.8 +/- 0.9 vs 1.8 +/- 1.0, p < 0.01), and normal coronary arteries were seen in 35% of female patients (male 6%, p < 0.05). Ten female patients (42%) had obviously non-atherosclerotic causes of acute myocardial infarction: Takayasu aortitis in three patients, coronary embolism in two, acute dissection of the aorta in two, and idiopathic coronary artery dissection, Kawasaki disease, and systemic lupus erythematosus in one each. In contrast, among male patients, only one had coronary embolism (1%). In-hospital mortality was higher in women (17%) than in men (2%, p < 0.05). Young female patients (< 50 years) with acute myocardial infarction have a low incidence of hyperlipidemia and normal coronary arteries or involvement of the left main trunk are more common compared with male patients (< 50 years). Although 42% of female patients had obvious non-atherosclerotic etiology of acute myocardial infarction, the causes varied widely.
To investigate the clinical application of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI) in the management of acute myocardial infarction (AMI), we examined 44 patients with AMI within 1 month after onset. Enhanced images were classified into 4 types: nontransmural (type 1), transmural and homogeneous (type 2), transmural and marginal (type 3), and no enhancement (type 4). Each enhancement pattern was correlated with angiographic and thallium-201 imaging results. The redistribution images of thallium were graded on a 4-point scale from 0 (normal) to 3 (markedly reduced or absent activity). The percentage of the perimeter affected by asynergy was obtained from the left ventriculogram. Peak creatine kinase and the percentage of asynergic perimeter were significantly higher in type 3 than in other type patients. End-diastolic volume index was significantly higher in type 3 than in type 2 patients. Left ventricular ejection fraction was lowest, and end-systolic volume index, thallium-201 score, and incidence of wall thinning on MRI were highest in type 3 patients. Therefore, the transmural and marginal enhancement pattern (type 3) was compatible with extensive myocardial infarction with infarct expansion and less viable myocardium. In the other types, the infarction was small to moderate in size and left ventricular function was well preserved. Thus, Gd-DTPA-enhanced MRI may be useful in the evaluation of left ventricular function and myocardial viability of the infarct region after AMI.
BACKGROUND: Coronary angiography has been used to assess the anatomy of coronary artery and intraluminal pathological changes. However, it has several limitations in its diagnostic quality and sensitivity in the detection of intraluminal details. Angioscopy has enabled coronary artery lumens to be visualized directly and fine intraluminal morphological changes to be detected. The information obtained by angioscopy is expected to provide new insights into the mechanisms and pathophysiology of transluminal coronary angioplasty. METHODS AND RESULTS: Forty-seven patients (39 men and 8 women) with stable angina were enrolled in the present study. Angioscopy was performed before and after angioplasty with a 0.68-mm angioscope with a double-guiding catheter system. The patients who were successfully evaluated by angioscopy were divided into two groups according to the color of the lesion: group 1, mainly yellow; and group 2, white. Angiographic, angioscopic, and clinical parameters in the two groups were compared. Detailed angioscopic findings were obtained in 36 of the 47 patients (77%) before percutaneous transluminal coronary angioplasty (PTCA) and in 24 of the 47 (51%) after PTCA. Yellow plaque were found in 13 of 36 (36%). Age, sex, presence of coronary risk factors, serum cholesterol level, and duration of angina showed no correlation with plaque color. The incidence rates of dissection and thrombi after angioplasty also were not different. Successful dilatation was achieved in 13 of 13 patients (100%) in group 1 and in 21 of 23 (91%) in group 2. The restenosis rate of group 1 was significantly lower than that in group 2 (16.7% versus 57.9%, P < .05). Cox proportional hazards model revealed that plaque color was the independent variable associated with restenosis after PTCA (P = .03). CONCLUSIONS: The restenosis rate after successful balloon angioplasty differs, with the color of the target lesion being significantly higher in patients with solely white plaque. Therefore, angioscopic findings are highly predictive of restenosis.
Serum troponin T, a myocardial contractile protein, has been reported to be a sensitive marker for the diagnosis of acute myocardial infarction. However, there have been few reports on its ability to detect coronary reperfusion and to predict left ventricular function in the chronic stage. Twenty two patients (20 males and 2 females, 61 +/- 10 y.o.) with acute myocardial infarction were enrolled in this study. They were divided into 2 groups, one with successful reperfusion (group A: n = 13) and one without reperfusion (Group B: n = 9) and the serial changes of their serum troponin T levels were evaluated. Serum myosin light chain was measured in another group of patients with acute myocardial infarction without history of old myocardial infarction (group C: n = 8). The slope of the logarithm of serum troponin T on a time-value curve was calculated from the time of admission to the first peak within 24 hours of the onset of acute myocardial infarction. The correlation coefficient between the late peak of serum troponin T and the left ventricular ejection fraction in 11 patients with first Q wave acute myocardial infarction was compared with that between the serum myosin light chain peak and the left ventricular ejection fraction in group C. 1) The slope of the logarithm of serum troponin T on the time-value curve in group A was greater than that in group B (0.57 +/- 0.45 vs. 0.22 +/- 0.16) (p < 0.05). 2) There was a good correlation between the late peak level of serum troponin T (78 +/- 10 hours after the onset) and the left ventricular ejection fraction in 11 patients with first Q wave acute myocardial infarction (r = -0.84, p < 0.01), which was similar to that of the serum myosin light chain peak and the left ventricular ejection fraction (r = -0.72, p < 0.05). On the other hand, there was no correlation between the peak level of serum creatine phosphokinase and the left ventricular ejection fraction (r = -0.55, NS). The serum troponin T levels 24, 36, 48 and 60 hours after the onset also correlated well with the left ventricular ejection fraction (r = -0.65, -0.7, -0.65 and -0.89, respectively). We conclude that the serial measurement of serum troponin T in patients with acute myocardial infarction is useful in the evaluation of left ventricular function in the chronic stage and that it is a potential non-invasive predictor of coronary reperfusion.
Therapeutic efficacy of intermittent and continuous injection of isosorbide dinitrate (ISDN) was compared in 22 patients (mean age 64 +/- 10, 18 males and 4 females) with unstable angina at rest. They were randomized into 2 groups that received either continuous (10 mg/h, group A) or intermittent (10 mg/10 min every 2 hours, group B) injection of ISDN for 3 days (phase 1). Each injection protocol was switched (phase 2) and subsequently switched back to the initial protocol (phase 3) in a cross-over fashion. The serum concentrations of ISDN, 2-isosorbide mononitrate (2-ISMN) and 5-ISMN were measured serially during both intermittent and continuous injection protocols. In addition, the incidence and duration of angina and changes in systolic blood pressure were analyzed. There were 3 treatment-failure cases during the intermittent injection period and 1 during the continuous injection period. Three of these treatment-failure cases developed small acute myocardial infarcts despite emergent coronary arteriography followed by intra-coronary thrombolysis and percutaneous balloon angioplasty. There was no difference in therapeutic efficacy between continuous and intermittent ISDN in terms of the incidence, duration of angina attacks and the number of patients whose angina was suppressed. After bolus injection of ISDN (10 mg/10 min), the serum concentration of ISDN increased rapidly and returned to the control level at 60 minutes after the injection. The serum 5-ISMN and 2-ISMN concentrations also increased immediately after injection and then decreased gradually reaching statistically insignificant level to the control values at 60 minutes after injection. With continuous injection, ISDN and its metabolites increased gradually and reached similar but slightly lower serum concentrations to the peak levels during intermittent injection. We conclude that the therapeutic efficacy of intermittent and continuous injection of ISDN is similar in patients with unstable angina.
To characterize regional cardiac sympathetic dysfunction due to myocardial ischemia, we examined 123I-metaiodobenzylguanidine (MIBG) myocardial distribution of initial 15-min and 4-hr delayed SPECT images in 14 patients with recent myocardial infarction (MI), 25 patients with vasospastic angina which was angiographically proven with elgonovine maleate (Gp VSAP) and 16 patients with chest pain syndrome and normal CAG findings (GpCP). In those with MI, the study was serially done at 2 weeks after (Gp MI-1) and at 3 months after the onset of MI (Gp MI-2). We estimated regional tracer uptake in 20 segments of tomographic images by using a 4-point scoring system (0 = normal, 1 = mild, 2 = moderate, 3 = severe reduction) and calculated the total defect score (IDS). In all patients with MI, the area of reduced MIBG uptake was more extensive than the 201Tl perfusion defect in the acute stage (Gp MI-1) indicating the presence of viable but denervated myocardial tissue. Also, the MIBG defect was persistently observed from initial (TDS: 24 +/- 13) to delayed imaging (TDS: 26 +/- 12). However, in the chronic stage (Gp MI-2), the initial MIBG uptake improved (TDS: 18 +/- 9) but the delayed uptake remained almost the same (TDS: 22 +/- 10) indicating high washout of MIBG from the ischemic myocardium. Fourteen in Gp VSAP and 14 in Gp CP showed the regional MIBG defect in the delayed image more extensively than in the initial image indicating high washout of MIBG in the involved myocardial regions. These results suggest that neuronal uptake of MIBG is impaired in the acute stage of MI although neuronal retention of MIBG is predominantly impaired in the chronic stage of MI or in Gps VSAP and CP.
Visual interpretation of 123I-BMIPP (BMIPP) myocardial images has difficulties in detecting mild reduction in tracer uptake. We studied the significance of the objective assessment of myocardial BMIPP maldistributions at rest by using a Bull's-eye map and its normal data file for detecting ischemic heart disease. Twenty nine patients, 15 with prior myocardial infarction and 14 with effort angina were studied. The initial 15-min BMIPP image was evaluated by visual analysis and by generating the extent Bull's-eye map which exhibits regions with reduced % uptake under mean-2SD of 10 normal controls. The sensitivity for determining coronary lesions in non-infarcted myocardial regions with the extent map was superior to that with visual analysis (67% vs. 33%). In the regions supplied by the stenotic coronary artery, those which showed visually negative but positive in the map and which showed positive in both had higher incidence of wall motion abnormalities and severe coronary stenosis than those with normal findings in both. These results suggest that the objective assessment based on the normal data file in a Bull's-eye polar map is clinically important for improving the limitation of the visual interpretation in 123I-BMIPP imaging.