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Tadanori Aizawa

Publications and source records attributed to Tadanori Aizawa.

At least 19 recordsLinked to original sources

What are arrhythmogenic substrates in diabetic rat atria?

INTRODUCTION: Diabetes mellitus is one of the significant independent risk factors for the development of atrial fibrillation (AF). However, the pathophysiological mechanisms of the relationship have not been fully elucidated. METHODS AND RESULTS: The genetic type II diabetes (GK) rats and their original (Wistar) ones were subjected to electrophysiological (n = 8 per group) and histological (n = 7 per group) studies. At 40 weeks old, when GK rats had significantly (P < 0.01) more increased plasma glucose and HbA(1c) values than Wistar rats, atrial electrical stimuli in the isolated-perfused hearts induced significantly greater number of repetitive atrial responses in GK rats than in Wistar rats (47.9 +/- 17.5 vs 3.1 +/- 1.3 beats, respectively, P < 0.01). GK rats showed significantly longer intra-atrial activation time than Wistar rats (18.3 +/- 0.4 ms vs 15.9 +/- 0.5 ms, P < 0.01) without any significant difference in the atrial refractoriness. The histological examination revealed significantly increased diffuse fibrotic deposition in GK rats atria compared with Wistar ones (P < 0.01). CONCLUSION: The present diabetic GK rat showed increased atrial arrhythmogenicity with intra-atrial conduction disturbance, and thus indicated that the structural remodeling of atrium characterized by diffuse interstitial fibrosis would be a major substrate for diabetes-related AF.

Animals↗

Critical level of cerebral oxygenation during exercise in patients with left ventricular dysfunction.

BACKGROUND: In a recent study the indexes of cerebral oxygenation decreased during maximal exercise in nearly half of all patients with left ventricular dysfunction. Whether these levels decrease severely enough to influence mental status or level of consciousness was evaluated in the present study. METHODS AND RESULTS: Forty-two patients with idiopathic dilated cardiomyopathy (IDC) and 29 healthy subjects underwent a symptom-limited maximal exercise test. The cerebral oxyhemoglobin (O(2)Hb) and tissue oxygenation index (TOI) were continuously monitored using near-infrared spectroscopy. The changes in O(2)Hb and TOI were also measured in 7 subjects: 2 who experienced episodes of reduced consciousness caused by sudden decreases in blood pressure during exercise recovery and 5 who exhibited sustained ventricular tachycardia during an electrophysiological study. The change in cerebral O(2)Hb during exercise in patients with IDC averaged 0.38+/-3.39 micromol/L, significantly lower than in the normal subjects (4.30+/-4.47 micromol/L, p<0.0001). The cerebral O(2)Hb decreased during exercise in 18 of 42 patients with IDC. The change in cerebral TOI in the IDC patients during exercise was significantly less than that in the normal subjects (-2.0+/-4.7 vs 2.1+/-5.8%, p=0.002). The mean decreases in cerebral O(2)Hb and TOI were -5.34 micromol/L and -9.7%, respectively, in the patients with reduced consciousness during exercise recovery, and -2.52 micromol/L and -16.5%, respectively, in those with ventricular tachycardia. CONCLUSION: The indexes of cerebral oxygenation may drop severely enough during maximal exercise in some patients with severe IDC that consciousness is affected.

Aged↗

Coronary artery spasm and the polymorphisms of the endothelial nitric oxide synthase gene.

BACKGROUND: Coronary artery spasm plays an important role in the pathogenesis of vasospastic angina, and contributes to the development of several acute coronary syndromes. Endothelial nitric oxide synthase (ecNOS) catalyzes the synthesis of nitric oxide, which regulates vascular tone, and may be related to coronary vasospasm. The present study investigated whether coronary spasm is related to particular polymorphisms of the ecNOS gene. METHODS AND RESULTS: Spasm provocation by serial infusions of acetylcholine was performed on 165 patients who were clinically suspected of having angina. In both study patients and healthy controls (n=400), genomic polymorphisms of the ecNOS gene were determined by using polymerase chain reaction. Quantitative luminal diameter measurements of the 3 major coronary arteries were initially obtained before and after acetylcholine injection, and then after isosorbide dinitrate injection, by using a computer-assisted analysis system. Logistic multiple regression analysis identified the a/a or a/b genotype in intron 4 of ecNOS (NOS4a: p=0.0431, odds ratio (OR) 2.43) and diabetes mellitus (p=0.0060, OR 4.88) as significant predictors of coronary spasm. In the patients with NOS4a, both the induced and spontaneous contractions were augmented. CONCLUSION: The present study results indicated that NOS4a could be a good marker for coronary artery spasm.

Acetylcholine↗

Molecular and electrophysiological differences in the L-type Ca2+ channel of the atrium and ventricle of rat hearts.

BACKGROUND: Many pathological conditions induce electrical remodeling, possibly through intracellular Ca2+ overload, but the currently available L-type Ca2+ channel blockers may be detrimental because of their global negative inotropic effects. METHODS AND RESULTS: To determine whether the L-type Ca2+ channel is identical throughout the heart, the distribution of the mRNAs and proteins comprising the L-type Ca2+ channel and its electrophysiological properties were analyzed in rat atria and ventricles. The mRNA of alpha2delta-2 (Cacna2d2) was more abundantly expressed in the atrium (approximately 5-fold) than in the ventricle. In contrast, alpha1C (Cacna1c) (Cav1.2) mRNA was significantly less abundant in the atrium. The level of the alpha1C (Cacna1c) (Cav1.2) protein was decreased (approximately 0.5-fold) and that of alpha2 delta-1 (Cacna2d1) was increased (approximately 2-fold) in the atrium compared with the ventricle. Although the peak ICa,L density showed no significant differences, voltage dependence of inactivation and activation of the current showed a more depolarized shift in the atrium than in the ventricle. CONCLUSION: These results indicate that in the rat heart the L-type Ca2+ channel differs between the atrium and ventricle with regard to gene expression and electrophysiological properties.

Animals↗

Premature atrial complex with P'R prolongation indicates multiple atrioventricular nodal pathways.

BACKGROUND: The goal of the present study was to test if ambulatory Holter recordings can predict the electrophysiologic study (EPS) findings in patients with supraventricular tachycardia (SVT). METHODS AND RESULTS: The study involved 110 patients with SVT who underwent Holter recording, and then EPS. The hypotheses were that (1) a P'R interval of premature atrial complexes (PACs) between 280 and 400 ms in the Holter recordings predicted dual atrioventricular nodal (AVN) pathways, (2) P'R interval >400 ms predicted triple or more AVN pathways, and (3) SVT initiated by a single PAC suggested easy SVT induction during the EPS. The EPS revealed dual AVN pathways in 14 (93%) of 15 patients with P'R intervals between 280 and 400 ms on the Holter recordings, and triple or more AVN pathways in 18 (90%) of 20 patients with P'R intervals >400 ms. In addition, a single extrastimulus easily induced SVT during the EPS in 11 (85%) of 13 patients in whom SVT was initiated by a single PAC during Holter recording. CONCLUSION: The ambulatory Holter recording criteria specifically predicted the EPS findings, thereby providing useful advance information.

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Preload-adjusted 2 wave-intensity peaks reflect simultaneous assessment of left ventricular contractility and relaxation.

BACKGROUND: The magnitudes of the first (WI1) and the second wave-intensity peak (WI2) during the ejection period can be used as indices of left ventricular (LV) contractility and relaxation, respectively. However, use of WI to characterize LV dp/dt and the end-diastolic volume (V ed) relationship may be more problematic, as WI may be affected by changes in preload. METHODS AND RESULTS: The LV pressure-volume data sets, consisting of 23 recordings obtained by the conductance method from 12 heart disease patients, were studied. End-systolic elastance (E es) and volume-axis-intercept (V0) were calculated with varying preload. Time constant of LV relaxation (tau), V ed, and WI were calculated from steady-state averaged data. The E es showed a weak correlation with WI1 (r = 0.46, p < 0.05) but a better correlation with preload-adjusted WI1 [WI1/V ed; r=0.86, WI1/V(ed)2; r = 0.92, WI1/(V ed - V0)2; r = 0.89, all p < 0.01]. Similarly, tau did not correlate with WI2 but did correlate with preload-adjusted WI2 [WI2/V ed; r = -0.73, WI2/V(ed) 2; r = -0.63, WI2/(V ed - V0)2; r = -0.78, all p < 0.01]. CONCLUSIONS: These data demonstrate the importance of preload-adjustment when using the WI index for simultaneous assessment of LV contractility and relaxation.

Diastole↗

Pilsicainide-induced coronary vasospasm in a patient with Brugada-type electrocardiogram.

A 65-year-old man with Brugada-type electrocardiogram (ECG) was admitted to our hospital for chest pain, palpitation and faintness. In the cardiac electrophysiological study, no ventricular tachyarrthymia was induced either at baseline or after pilsicainide (50 mg) infusion. Intravenous administration of pilsicainide exaggerated ST-segment elevation in V(1-4) and converted it to the coved type in V(1), accompanied by severe chest pain. Coronary angiography revealed the vasospasm of the right coronary artery was induced by pilsicainide, not by ergonovine. This is the first case report of coronary vasospasm induced by a pure sodium channel blocker in a patient with Brugada-type ECG.

Aged↗

Cibenzoline attenuates upregulation of Kv1.5 channel gene expression by experimental paroxysmal atrial fibrillation.

Antiarrhythmic drugs exert their effects by inhibiting the ion channels of cardiomyocytes. However, these effects could also modify the ionic environment around them, and thereby affect the expression of ion channels, leading to biochemical enhancement or attenuation of the antiarrhythmic effects. To test this hypothesis, the physiological and biochemical effects of cibenzoline were evaluated in a rapid atrial pacing model in rats. In rats with rapid atrial pacing, pretreatment with cibenzoline significantly inhibited the increases in Kv1.5 mRNA at 2 hours and immunoreactive protein at 4 hours by 35 +/- 15% and 30 +/- 10%, respectively. These effects were observed only in the rapid atrial pacing group, not in the sham-operated group. With cibenzoline pretreatment, 4-hour rapid atrial pacing resulted in significant prolongation of the atrial refractory period compared to the untreated group even after removal of cibenzoline. In contrast, the sham and rapid atrial pacing model with and without cibenzoline pretreatment showed similar acute physiological responses to cibenzoline. In conclusion, in addition to the acute physiological effects, pretreatment with cibenzoline exerted pleiotropic effects of inhibition of Kv1.5 channel upregulation by rapid pacing, implying differences in the cibenzoline effects when administered before and after onset of paroxysmal atrial fibrillation.

Animals↗

High diastolic blood pressure during exercise is associated with hypercholesterolemia in patients with coronary artery disease.

Evaluating blood pressure response during exercise rather than during rest might better detect a subtle impairment in relaxation of the resistance vessel in hypercholesterolemia. We examined the relation between serum cholesterol and blood pressure response during exercise in patients with coronary artery disease. One hundred and forty-eight consecutive patients with coronary artery disease were monitored during symptom-limited incremental exercise testing with a cycle ergometer. Cuff blood pressure was measured every minute during exercise testing with an automatic indirect manometer. Although there were no significant differences in systolic or diastolic blood pressure at rest between the patients with hypercholesterolemia (total cholesterol > or = 220 mg/dL, n = 39) and those without it (n = 109), the former reached a higher diastolic blood pressure at peak exercise (94.8+/-16.0 versus 87.8+/-12.9 mmHg, P = 0.007). The increase in diastolic blood pressure at peak exercise versus the resting value in the patients with hypercholesterolemia was 20.6+/-11.3 mmHg, and this was significantly higher than the increase in patients without hypercholesterolemia (14.8+/-11.8 mmHg, P = 0.009). However, there were no differences in the peak exercise systolic blood pressure and the magnitude of the increase in systolic blood pressure between the two groups. Among the patients with coronary artery disease in our study, we found that those with hypercholesterolemia had significantly higher diastolic blood pressure during exercise than those without hypercholesterolemia, strongly suggesting that patients with hyperlipidemia are at a higher risk of developing hypertensive complications.

Aged↗

Cerebral oxygenation during exercise and exercise recovery in patients with idiopathic dilated cardiomyopathy.

We compared cerebral oxygenation during exercise and during exercise recovery between 22 healthy subjects and 35 patients with idiopathic dilated cardiomyopathy (IDC). Although cerebral oxyhemoglobin increased during exercise in most of the healthy subjects, oxyhemoglobin decreased during exercise in 15 of 35 patients with IDC. Cerebral oxygenation during exercise and exercise recovery was related to left ventricular function in the patients with IDC.

Cardiomyopathy, Dilated↗

Frequency and time course of reocclusion and restenosis in coronary artery occlusions after balloon angioplasty versus Wiktor stent implantation: results from the Mayo-Japan Investigation for Chronic Total Occlusion (MAJIC) trial.

BACKGROUND: Compared with balloon angioplasty, stent implantation has been shown to reduce restenosis and reocclusion after treatment of chronic total coronary artery occlusions (CTOs). However, little is known about the time course of restenosis and reocclusion after the 2 procedures. The purpose of this study was to examine the frequency and time course of restenosis and reocclusion after treatment of CTOs with balloon angioplasty and Wiktor stent implantation. METHODS AND RESULTS: A total of 221 patients with successfully recanalized CTOs were randomly assigned to either treatment with a coil stent implantation (Wiktor stent, n = 110) or standard balloon angioplasty (n = 111). Repeat angiography was performed the day after treatment and at 6 months. Patients undergoing balloon angioplasty showed 29.8% restenosis and 1.1% reocclusion the following day versus 2% restenosis and no reocclusion in stent patients the following day. The cumulative reocclusion rate was significantly lower in the stent group than in the balloon group at 6 months (2.1% versus 9.3%, P <.05). As a result of the more frequent need of target vessel revascularization (49.5% in the balloon group and 30.6% in the stent group, P <.005) and earlier final follow-up angiography in the balloon group, the frequency of angiographic restenosis at 6 months was similar in both groups (57.3% in the stent group and 54.5% in the balloon group). CONCLUSIONS: The frequency and time course of reocclusion and restenosis after balloon angioplasty and stent placement differ within 24 hours of the procedure and remain different on angiography at 6 months.

Aged↗

A serum amyloid A and LDL complex as a new prognostic marker in stable coronary artery disease.

BACKGROUND: Although some reports have indicated that acute phase proteins such as C-reactive protein (CRP) and serum amyloid A (SAA) can predict the prognosis in patients with acute coronary syndrome, the value of these markers in patients with stable coronary artery disease (CAD) still remains obscure. Therefore, our aim was to determine the prognostic value of inflammatory markers in patients with stable coronary artery disease. METHODS AND RESULTS: We conducted a prospective cohort study in 140 consecutive patients with stable coronary artery disease who had at least one coronary stenosis more than 50% in diameter seen on diagnostic coronary angiography (CAG). We determined serum levels of the SAA/LDL complex as a new marker in addition to CRP and SAA. Serum levels of the SAA/LDL complex were measured by a sandwich enzyme-linked immunosorbent assay (ELISA). End-points were defined as cardiac death, myocardial infarction, cerebral infarction, and coronary revascularization. End-point events occurred in 21 patients (2 death from myocardial infarction, 2 cerebral infarction, and 17 revascularization). Age (year) (OR = 1.14, CI: 1.05-1.25), diabetes mellitus (OR = 3.50, CI: 1.08-11.40), triglyceride (10mg/dl) (OR = 1.12, CI: 1.01-1.23) and SAA/LDL complex (10 microg/ml) (OR = 2.32, CI: 1.05-4.70) were independently related to the events. A reconstitution experiment suggested that the SAA/LDL complex is derived by oxidative interaction between SAA and lipoproteins. CONCLUSIONS: The SAA/LDL complex reflects intravascular inflammation directly and can be a new marker more sensitive than CRP or SAA for prediction of prognosis in patients with stable coronary artery disease.

Aged↗

Soft plaque detected on intravascular ultrasound is the strongest predictor of in-stent restenosis: an intravascular ultrasound study.

AIMS: Although various predictors of in-stent restenosis (ISR) have been reported, the subject of parameters relating to ISR on intravascular ultrasound (IVUS) still leaves room for discussion. The aim of this study was to clarify the strongest predictors of ISR using IVUS. METHODS AND RESULTS: Ninety-two native coronary lesions undergoing single bare-metallic stent implantation were investigated retrospectively. We classified them into the ISR (n=46) and non-ISR (n=46) groups using quantitative coronary angiography. On serial IVUS studies, plaque morphology, and areas and volumes of each component in vessel were evaluated. Among all parameters, diabetes mellitus and soft plaque appearing hypoechoic on IVUS were associated with ISR. By multivariate analysis, soft plaque was the only independent predictor of ISR (p=0.0057). Compared with non-soft plaque, soft plaque had a larger plaque reduction rate (-7.1% vs. -1.6%, p=0.0613) and smaller percent plaque volume (53.0% vs. 55.5%, p=0.0273) after stenting. Conversely, soft plaque had a larger neointimal area (4.39 vs. 3.33 mm2, p=0.0437) and percent plaque area (80.5% vs. 75.1%, p=0.0503) at follow-up. CONCLUSION: Soft plaque detected on IVUS was the strongest predictor of ISR. Soft plaque was compressed more easily by stenting, however, causing more proliferation of neointima subsequently and resulted in a worse prognosis.

Aged↗

Early aerobic training increases end-tidal CO2 pressure during exercise in patients after acute myocardial infarction.

BACKGROUND: End-tidal CO2 partial pressure (PETCO2) has been suggested as a noninvasive index reflecting cardiac output under constant ventilation. The aim of this study was to examine whether PETCO2 does reflect cardiac output, even during exercise, in patients with acute myocardial infarction (AMI) undergoing exercise training early after onset. Method and Results Patients aged 47-73 years were randomly assigned to either a training group (n=18) or a control group (n=18) 1 week after the onset of AMI. Those in the training group performed exercise training under supervision at the anaerobic threshold level for 2 weeks, while patients in the control group followed a conventional walking regimen. In the training group, but not in the control group, PETCO2 at the respiratory compensation point increased significantly from 39.1+/-3.5 to 41.1+/-3.7 mmHg (p<0.01). Similarly, the cardiac index at peak exercise increased only in the training group (from 6.04+/-0.98 to 7.31+/-0.97 L/min per m2, p<0.01). These 2 measurements correlated well both before and after the study period. Peak oxygen uptake and anaerobic threshold were increased only in the training group. Conclusions Aerobic exercise training early after the onset of AMI significantly increased PETCO2 during exercise, which may reflect an improvement in cardiac output during exercise in response to physical training via a decreased ventilation-perfusion mismatch.

Adult↗

Cerebral oxygenation during exercise in cardiac patients.

BACKGROUND: Until recently, compensatory mechanisms have been believed to regulate adequately cerebral blood flow in humans. However, this has been called into question by a series of new investigations suggesting that patients with left ventricular dysfunction suffer from cerebral hypoperfusion. We compared cerebral oxygenation during incremental exercise between patients with valvular heart disease and normal subjects. METHODS: Thirty-three patients with valvular disease and 33 normal subjects performed a symptom-limited incremental exercise test using a cycle ergometer. Oxyhemoglobin at the forehead was continuously monitored during exercise using near-infrared spectroscopy. Respiratory gas measurements were performed on a breath-by-breath basis. RESULTS: The increase in oxyhemoglobin during exercise was significantly lower in the patients with valvular disease than in normal subjects. The change in oxyhemoglobin during exercise (DeltaO(2)Hb) at the forehead was negatively correlated with the slope of the increase in minute ventilation to the increase in carbon dioxide output (DeltaE/DeltaCO(2)), and positively correlated with the peak oxygen uptake (O(2)), gas exchange threshold (GET), and slope of the increase in O(2) to the increase in the work rate (DeltaO(2)/DeltaWR). Among the patients with valvular disease, 15 patients showed a decrease in oxyhemoglobin at the forehead during exercise. When compared with the patients with increased oxyhemoglobin, those with decreased levels exhibited a higher DeltaE/DeltaCO(2) and a lower peak O(2), GET, and DeltaO(2)/DeltaWR. CONCLUSIONS: The present findings strongly suggest that cerebral oxygenation during exercise is dependent on the cardiovascular and pulmonary systems. The study also indicated the presence of cerebral hypoperfusion during exercise in cardiac patients whose cardiac output fails to increase normally.

Adult↗

[Development of blood examination method of serum amyloid A and LDL complex, and clinical application to prediction of cardiovascular event].

In recent years, it has been reported that the acute-phase proteins C-reactive protein(CRP) and serum amyloid A(SAA), the sera levels of which are elevated in inflammation, are also elevated in coronary artery disease such as acute myocardial infarction. Also, high-sensitivity CRP assay is thought to be useful in predicting the prognosis of coronary heart disease. While investigating complexes of acute-phase proteins and low-density lipoprotein(LDL), we found a complex of LDL and SAA(SAA/LDL complex). The SAA/LDL complex in blood are formed from LDL and HDL by an oxidation reaction. Therefore, we developed an ELISA using anti-human SAA antibody and anti-human apoB, and determined a new method for measuring SAA/LDL complex in sera. We evaluated SAA/LDL complex as a new marker for prediction of prognosis in addition to the ordinary markers in consecutive 140 patients with stable coronary heart disease who had at least 1 coronary artery stenosis more than 50% in diameter at the diagnostic coronary angiography. Of these 140 patients, 2 developed fatal myocardial infarction, 2 cerebral infarction, and 17 angina pectoris requiring coronary revascularization therapy during 1 year and 6 months after blood examinations. The SAA/LDL complex value in this EVENT group of 21 patients was significantly higher than that in the control group of 119 individuals. High-sensitivity CRP (hs-CRP) assay and SAA measurement showed no significant difference between the 2 groups. The SAA/LDL complex reflects intravascular inflammation directly and can be a new marker more sensitive than hs-CRP or SAA for prediction of prognosis in patients with stable coronary artery disease.

Acute-Phase Proteins↗

[Sex differences in coronary atherosclerosis: coronary angiography and intravascular ultrasonography].

OBJECTIVES: Women have higher mortality and frequency of complications compared with men after coronary intervention. Possible differences in coronary atherosclerosis between men and women were investigated. METHODS: The left anterior descending arteries of 214 patients (164 men, mean age 62.3 +/- 9.10 years; 50 women, mean age 67.8 +/- 7.76 years) were examined. Lesion length, reference diameter, percentage diameter stenosis and minimal lumen diameter were measured by quantitative coronary angiography. Vessel area, lumen area, percentage area stenosis, and remodeling index were measured by intravascular ultrasonography, and presence of calcification in the lesion was classified. These parameters were compared between men and women. RESULTS: There were no significant differences in quantitative coronary angiography, but intravascular ultrasonography showed calcification was more severe in women, vessel area was significantly smaller in women (13.25 +/- 4.21 vs 15.91 +/- 4.35 mm2, p = 0.004), and remodeling index was significantly lower in women (0.95 +/- 0.13 vs 1.04 +/- 0.18, p = 0.015). CONCLUSIONS: Vessel area measured by intravascular ultrasonography was significantly smaller in women, and calcification was more severe in women. Such factors may be involved in the higher mortality in women.

Aged↗

Arterial remodeling patterns before intervention predict diffuse in-stent restenosis: an intravascular ultrasound study.

OBJECTIVES: The aim of this retrospective study was to determine the predictors of diffuse in-stent restenosis (ISR) among the lesions causing the first ISR by intravascular ultrasound (IVUS) studies. BACKGROUND: Although some predictors of diffuse ISR have been reported, parameters on IVUS relating to diffuse ISR are not well characterized. METHODS: We classified 52 ISR lesions that had undergone successful stent implantation and led to restenosis into two types--focal and diffuse ISR--using quantitative coronary angiography. Restenosis was defined as > or =50% diameter stenosis, and diffuse ISR as lesion length > or =10 mm at follow-up. The remodeling index (RI) was defined as the vessel area at the target lesion divided by that of averaged reference segments. RESULTS: There were no significant differences in patient, angiographic, and procedural characteristics between the focal (n = 25) and diffuse (n = 27) ISR groups. Baseline RI was significantly greater in the diffuse ISR group (1.03 +/- 0.18 vs. 0.88 +/- 0.24, p = 0.0159). Negative remodeling, defined as RI <0.9, was detected in 60% of the focal ISR group and in only 26% of the diffuse ISR group. By logistic regression analysis, baseline RI was the only independent predictor of diffuse ISR (p = 0.0341). Moreover, volumetric analyses revealed that lesions developing into diffuse ISR had less capacity to compensate for further plaque growth. CONCLUSIONS: Among the first ISR lesions, baseline positive remodeling was the most powerful predictor of diffuse ISR. Measuring pre-interventional arterial remodeling patterns by IVUS may be helpful to stratify lesions at higher risk.

Aged↗