Images in cardiovascular medicine. Percutaneous transcatheter balloon valvuloplasty for bioprosthetic tricuspid valve stenosis.
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
Kazuo Haze
Publications and source records attributed to Kazuo Haze.
Persistent high levels of plasma oxidized low-density lipoprotein after acute myocardial infarction predict stent restenosis.
OBJECTIVE: Recently, elevated levels of plasma oxidized low-density lipoprotein (LDL) have been shown to relate to plaque instability in human atherosclerotic lesions. We investigated prospectively patients admitted with acute myocardial infarction (AMI) who underwent primary coronary stenting to evaluate whether the 6-month outcome could be predicted by measuring plasma oxidized LDL (ox-LDL) levels at the time of hospital discharge. METHODS AND RESULTS: Plasma ox-LDL levels were measured in 102 patients with AMI undergoing primary coronary stenting using a highly sensitive ELISA method. Measurements were taken on admission and at discharge, and the findings related to the clinical outcome. At 6-month follow-up, angiographic stent restenosis occurred in 25 (25%) of the 102 AMI patients. Plasma ox-LDL levels at discharge were significantly (P=0.0074) higher in the restenosis group than those in the no-restenosis group (1.03+/-0.65 versus 0.61+/-0.34 ng/5 microg LDL protein). Multiple regression analysis showed that only plasma ox-LDL levels at discharge were a statistically significant independent predictor for late lumen loss after stenting (beta=0.645; P<0.0001). CONCLUSIONS: This prospective study demonstrates that persistence of an increased level of plasma ox-LDL at discharge is a strong independent predictor of stent restenosis at 6-month follow-up in AMI patients.
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Expression of endothelin-converting enzyme, endothelin-1 and endothelin receptors at the site of percutaneous coronary intervention in humans.
OBJECTIVE: The repair process at the site of injury after percutaneous coronary intervention (PCI) is dominated by neointimal formation composed mainly of smooth muscle cells (SMC). Endothelin-1 (ET-1) is a powerful vasoconstrictor and SMC mitogen. Endothelin-converting enzyme (ECE) is the final key enzyme of endothelin processing. The effects of ET-1 are mediated by binding to endothelin type A (ETA) and endothelin type B (ETB) receptors. The ligand/receptor/ligand-producing system (ET system) could be involved in the pathogenesis of neointimal formation in humans. METHODS: Fifteen post-PCI sites obtained at autopsy and eight atherectomy specimens obtained from restenotic sites were investigated using immunohistochemical single and double staining techniques. Frozen sections were stained with antibodies against ECE, ET-1, ETA and ETB receptors, SMC, macrophages and endothelial cells. RESULTS: At the early stage, less than 3 months after PCI, neointimal SMC were positive for ECE, ET-1, ETA and ETB receptors. The expression of ECE, ET-1, ETA and ETB receptors in these neointimal SMC decreased markedly from 6 months onwards. The ECE, ET-1, ETA and ETB receptor-positive cell areas were significantly (P < 0.005) greater in the first 3 months after PCI compared with 6 months or more after PCI. Atherectomy specimens also showed similar positivity. CONCLUSIONS: These observations strongly suggest that the expression of ECE, ET-1, ETA and ETB receptors is enhanced in neointimal SMC at early stages after PCI injury in human coronary arteries. The increased expression of the ET system may contribute to SMC proliferation/migration and vasoconstriction in human post-PCI coronary lesions.
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Quantitative coronary angiogram analysis: nifedipine retard versus angiotensin-converting enzyme inhibitors (JMIC-B side arm study).
This study was performed to compare the effects of nifedipine retard and angiotensin-converting enzyme (ACE) inhibitors on the progression of coronary atherosclerosis by means of quantitative coronary angiogram. Coronary angiogram was performed before the start of the study and during the 3-year treatment period. This study was conducted on the assumption that possible coronary vasodilation, which may be caused by nifedipine, was excluded by administration of sufficient isosorbide dinitrate. The changes from the baseline in the minimum lumen diameter of the coronary artery in all measured segments were negligible in the nifedipine group (+0.02+/-0.27 mm; P=0.543), whereas they were significantly reduced in the ACE inhibitor group (-0.12+/-0.27 mm; P<0.001), with a significant difference observed between the groups (P=0.002). The number of progressors in the nifedipine group was significantly lower than that in the ACE inhibitor group (P=0.019), and there was also a significant difference between the groups in the number of patients in whom > or =1 lesion developed after treatment (P=0.040). However, the changes of minimum lumen diameter stratified by baseline percent diameter stenosis demonstrated that progression of coronary atherosclerosis was suppressed in the nifedipine group for lesions with a percent diameter stenosis of < or =40 but was suppressed in both groups for those with a percent diameter stenosis of > or =41. This study suggests that nifedipine retard and ACE inhibitors may be effective in suppression of progression of coronary atherosclerosis, and that nifedipine in particular may be effective for mild to moderate stenosis.
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C-Type natriuretic peptide and natriuretic peptide receptors are expressed by smooth muscle cells in the neointima after percutaneous coronary intervention.
Understanding restenosis after percutaneous coronary intervention (PCI) remains a challenge. Neointimal proliferation is the main cause of restenosis. C-Type natriuretic peptide (CNP) plays a role in relaxation and growth inhibition of vascular smooth muscle cells (SMCs); the effects depend on the presence of specific natriuretic peptide receptors (NPRs) consisting of NPR-A, NPR-B, and NPR-C. To test the hypothesis that CNP and NPRs may be involved in restenosis, we immunohistochemically studied the expression of CNP and NPRs during the post-PCI healing process; 10 sites after PCI obtained at autopsy and 14 atherectomy specimens obtained from restenotic sites were investigated. Frozen sections were stained with antibodies against CNP, NPRs, SMCs, macrophages, and endothelial cells. Within 2 months after PCI, most neointimal SMCs expressed CNP and NPR-A. The expression of CNP and NPR-A in these neointimal SMCs decreased from 6 months onward. In contrast, NPR-C was strongly expressed in neointimal SMCs from 1 to 9 months after PCI. In atherectomy specimens, most neointimal SMCs showed weak positivity for CNP and NPR-A, but NPR-C was strongly expressed in the neointimal SMCs. These findings strongly suggest that a paracrine and autocrine system of CNP and NPRs may be important in controlling neointimal growth after PCI in humans.
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A large-scale prospective cohort study on the current status of therapeutic modalities for acute myocardial infarction in Japan: rationale and initial results of the HIJAMI Registry.
BACKGROUND: In Western countries, several multicenter collaborative studies on acute myocardial infarction (AMI) have provided much information about this disease. In Japan, on the other hand, there have been few cohort studies in which a sufficient number of Japanese patients with AMI were registered during a short period. This fact explains the absence of a database from which strategies for treating Japanese patients with AMI could be established. The purpose of this study was to build a comprehensive database on Japanese patients with AMI to elucidate their characteristics. METHODS: Between January 1999 and June 2001, we consecutively registered all patients with AMI who were admitted to 17 participating medical institutions, including The Heart Institute of Japan, Cardiology (HIJC), Tokyo Women's Medical University. A standardized case report form was used to register all the patients. RESULTS: A total of 3,021 consecutive patients was registered (2,136 men, 70.7%; 885 women, 29.3%) with a median age of 69 years [59, 77]. Among the patients, there were 851 elderly individuals (28.2%) > or = 76 years and 1102 patients with diabetes (36.5%). On index electrocardiogram, ST-elevation myocardial infarction was observed in 2,392 patients (79.2%). Within 24 hours after the onset of AMI, coronary angiography was conducted for 2,177 patients (72.1%). Primary percutaneous coronary intervention and coronary thrombolysis were conducted for 1,755 (58.1%) and 491 patients (16.3%), respectively, and percutaneous coronary intervention or coronary artery bypass grafting was additionally carried out in 303 patients. By the time of discharge, coronary angiography and coronary artery bypass grafting were performed in 2,659 (88.0%) and 137 patients (4.5%), respectively. During initial hospitalization, 285 patients died and the overall inhospital mortality rate was 9.4%. During hospitalization, cardiogenic shock and cardiac rupture were observed in 6.1% and 2.8% of the patients, respectively. The inhospital mortality rate is still high in patients with AMI with such mechanical complications and in elderly patients. CONCLUSION: In our prospective cohort, we showed that Japanese patients with AMI could be characterized as (1) having a disease severity comparable with values observed in Western populations and (2) receiving early reperfusion therapy by PCI, which was used widely and safely, but nevertheless (3) exhibiting a high inhospital mortality rate. Our data indicate that further improvements in therapy for AMI in elderly patients and for AMI with mechanical complications are essential in Japan.
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Reperfusion phenomenon is a strong predictor of left ventricular remodeling after acute myocardial infarction.
BACKGROUND: Many clinicians have seen the reperfusion phenomenon, a paradoxical response that includes a transient increase of chest pain, additional ST-segment elevation or ventricular arrhythmias immediately after coronary reperfusion, in patients with acute myocardial infarction (AMI). The aim of the present study was to investigate the impact of this phenomenon during coronary reperfusion on left ventricular (LV) remodeling in patients with AMI. METHODS AND RESULTS: One hundred and thirty-eight consecutive patients with a first anterior-wall AMI, undergoing coronary reperfusion treatment within 24 h of onset were prospectively evaluated for reperfusion phenomenon and followed up with scheduled evaluations of LV function and morphology with left ventriculography for 1 year. Of the 138 enrolled patients, 77 underwent serial left ventriculography at the acute, subacute and 1-year phases. Of these 77 patients, 39 demonstrated the reperfusion phenomenon. The LV end-diastolic volume index significantly increased from the acute to subacute phase and to the 1-year phase, but was unchanged in the 38 patients without reperfusion phenomenon. In multivariate analysis, reperfusion phenomenon was the only determinant of LV dilatation after AMI. CONCLUSIONS: Reperfusion phenomenon was a strong predictor of LV remodeling after reperfusion therapy for AMI.
Acute Disease↗
Immunolocalization of platelet glycoprotein IIb/IIIa and P-selectin, and neutrophil-platelet interaction in human coronary unstable plaques.
Platelet aggregation at the site of plaque rupture or erosion is a dominant feature in the pathophysiology of plaque destabilization. To elucidate the role of glycoprotein (GP) IIb/IIIa in coronary plaque destabilization, we immunohistochemically studied the presence of GP IIb/IIIa in coronary atherectomy specimens obtained from patients with stable angina (SAP) and unstable angina pectoris (UAP). Moreover, we immunohistochemically investigated the presence of P-selectin, which is known to be a marker of platelet activation, in these specimens. All these patients underwent atherectomy at primary atherosclerotic lesions responsible for SAP (n=25) and UAP (n=23). Frozen samples were studied with antibodies against smooth muscle cells, macrophages, neutrophils, endothelial cells, GP IIb/IIIa and P-selectin. Immunoreactive positive areas for GP IIb/IIIa, P-selectin, and macrophages, respectively, were calculated using computer-aided planimetry, and numbers of neutrophils were also counted. In the culprit lesions of UAP patients, 17 of the 23 lesions (74%) contained GP IIb/IIIa positive platelet thrombi, and all these platelet thrombi were positive for P-selectin. In contrast, in the lesions of SAP patients, 3 of the 25 lesions (12%) showed staining positivity for GP IIb/IIIa and P-selectin. Quantitatively, the percentage of GP IIb/IIIa- and P-selectin-positive area was significantly higher (GP IIb/IIIa, P<0.0005; P-selectin, P<0.0001) in patients with UAP than in patients with SAP. The number of neutrophils was significantly higher (P<0.0005) in patients with UAP than in patients with SAP. Moreover, the percentage of GP IIb/IIIa-positive area showed a significant positive correlation with the number of neutrophils (r=0.66, p<0.0001). These findings strongly suggest that platelet activation and aggregation, leading to formation of platelet thrombi, and the interaction between activated platelets and neutrophils play a pivotal role in the pathogenesis of plaque destabilization in human coronary atherosclerotic lesions.
Blood Platelets↗
Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study.
BACKGROUND: Calcification is a common finding in human coronary arteries; however, the relationship between calcification patterns, plaque morphology, and patterns of remodeling of culprit lesions in a comparison of patients with acute coronary syndromes (ACS) and those with stable conditions has not been documented. METHODS AND RESULTS: Preinterventional intravascular ultrasound (IVUS) images of 178 patients were studied, 61 with acute myocardial infarction (AMI), 70 with unstable angina pectoris (UAP), and 47 with stable angina pectoris (SAP). The frequency of calcium deposits within an arc of less than 90 degrees for all calcium deposits was significantly different in culprit lesions of patients with AMI, UAP, and SAP (P<0.0001). Moreover, the average number of calcium deposits within an arc of <90 degrees per patient was significantly higher in AMI than in SAP (P<0.0005; mean+/-SD, AMI 1.4+/-1.3, SAP 0.5+/-0.8). Conversely, calcium deposits were significantly longer in SAP patients (P<0.0001; mean+/-SD, AMI 2.2+/-1.6, UAP 1.9+/-1.8, and SAP 4.3+/-3.2 mm). In AMI patients, the typical pattern was spotty calcification, associated with a fibrofatty plaque and positive remodeling. In ACS patients showing negative remodeling, no calcification was the most frequent observation. Conversely, SAP patients had the highest frequency of extensive calcification. CONCLUSIONS: Our observations show that IVUS allows the identification of vulnerable plaques in coronary arteries, not only by identifying a fibrofatty plaque and positive remodeling, but also by identifying a spotty pattern of calcification.
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Prognostic significance of serum creatinine concentration for in-hospital mortality in patients with acute myocardial infarction who underwent successful primary percutaneous coronary intervention (from the Heart Institute of Japan Acute Myocardial Infarction [HIJAMI] Registry).
This study evaluated the impact of serum creatinine levels on in-hospital mortality in 1,359 consecutive patients with acute myocardial infarction (from a Japanese prospective multicenter registry) who underwent successful primary percutaneous coronary intervention (PCI). Even in the patients who underwent successful primary PCI, the in-hospital mortality of patients with mild (1.2 </= creatinine < 2.0 mg/dl) and severe (creatinine >/=2.0 mg/dl) renal dysfunction was greater (17.1% and 34.5%, respectively) than that of patients without renal dysfunction (3.9%) (relative risk [RR] 1.72, 95% confidence interval [CI] 0.94 to 3.14, p = 0.080; and RR 4.26, 95% CI 1.48 to 12.27, p <0.0001, respectively).
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Effect of fluvastatin therapy on coronary flow reserve in patients with hypercholesterolemia.
Coronary flow reserve was evaluated using transthoracic Doppler echocardiography before and after 3 months of fluvastatin therapy in patients with hypercholesterolemia. Coronary flow reserve increased significantly after lipid-lowering therapy, and coronary microcirculation was improved in patients with hypercholesterolemia.
Coronary Circulation↗
Lesion severity and hypercholesterolemia determine long-term prognosis of vasospastic angina treated with calcium channel antagonists.
Although patients with medically treated vasospastic angina have a good outcome, few data exist regarding the role of underlying lesion severity associated with or without hyperlipidemia in the prognosis. Therefore, the aim of the present study was to assess the relationship between the long-term outcome of vasospastic angina and the factors influencing its prognosis. A total of 256 patients (219 men, 37 women; mean age, 54.1+/-9.2) who had coronary spasm with or without underlying lesions and were being treated with calcium channel antagonists were enrolled and followed for 13.6+/-3.7 years. Cardiac events consisted of cardiac death and ischemic events, which included acute myocardial infarction and unstable angina. Cox analysis selected coronary artery stenosis (CAS, >/=50%) and risk factors such as age, hypertension, diabetes mellitus, low-density lipoprotein-cholesterol (LDL-C), sex and smoking. There were 19 cases of cardiac death (7.4%) and 58 of ischemic events (22.7%) during the follow-up period. The presence of significant CAS was an independent predictor of event-free survival (hazard ratio (HR) =2.84, 95% confidence interval (CI) =1.79-4.52, p<0.0001). In 193 patients without significant CAS, there were 10 cases of cardiac death (5.2%, p<0.05) and 34 of ischemic events (17.6%, p<0.01). In that group, high LDL-C was the independent predictor of event-free survival (HR = 3.89, 95% CI = 1.20-12.6, p=0.02). Kaplan-Meier survival analysis revealed significantly lower event-free survival in patients with than in those without lesions (p<0.0001 by log-rank test). These results demonstrate that the most important factor for long-term prognosis of vasospastic angina treated with calcium channel antagonists is significant CAS. High LDL-C, which might alter the underlying coronary endothelial function and/or accelerate atherosclerotic lesions, could also contribute to the occurrence of cardiac events, particularly in patients without significant CAS.
Angina Pectoris↗
Marked improvement of left ventricular function after parathyroidectomy in a hemodialysis patient with secondary hyperparathyroidism and left ventricular dysfunction.
A 52-year-old woman, a hemodialysis patient, was admitted because of exertional dyspnea. Echocardiography showed left ventricular (LV) dilatation and reduced contraction. Coronary angiography showed no fixed stenosis. She had elevated levels of parathyroid hormone (PTH) as a result of secondary hyperparathyroidism with advanced renal failure. After parathyroidectomy, marked improvement of LV function following immediate decrease of blood levels of PTH was observed. It is suggested that PTH might have a significant role in the pathogenesis of LV dysfunction and that parathyroidectomy might be effective as a therapy for heart failure in some patients with secondary hyperparathyroidism and LV dysfunction.
Electrocardiography↗
[Assessment of coronary artery by four-detector multislice computed tomography: diagnostic accuracy and limitations for coronary artery lesions].
OBJECTIVES: The applicability of four-detector multislice computed tomography (MSCT) was investigated for evaluating coronary arteries. METHODS: MSCT (Somatom Volume Zoom, Siemens) was used to evaluate the coronary arteries in 94 patients. The reconstructed images were analyzed using retrospective electrocardiographic gating to determine the image quality of the coronary arteries. In addition, the ability of MSCT to detect coronary artery lesions of > or = 70% (> or = 50% in the left main trunk) diameter stenoses documented by standard coronary angiography was assessed in 67 patients who underwent coronary angiography within the same period. RESULTS: Good image quality was displayed in 488 (58%) and fair in 184 (22%) of a total of 846 coronary segments, but non-assessable in 174 (21%) due to degraded image quality. MDCT detected 33 stenotic lesions correctly in 494 assessable segments, comparable to coronary angiography. The sensitivity and specificity of MSCT were 0.79 and 0.95, respectively. However, an additional 15 lesions were detected by coronary angiography among the non-assessable segments. In total, 24 lesions were missed by MSCT. Accordingly, coronary segments were completely assessable and correctly detected by MSCT in only 20 patients (30%), or 35 (52%) if the distal coronary segments were excluded from analysis. CONCLUSIONS: Four-detector MSCT for detection of coronary artery lesions was applicable to assessable segments. However, clinical use may presently be limited because of the insufficient overall accuracy. Further technical improvement is expected in the near future.
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[Biventricular pacing dramatically improved critical heart failure in idiopathic dilated cardiomyopathy: two case reports].
Two cases of dilated cardiomyopathy with intraventricular conduction delay, or left bundle-branch block and refractory heart failure, were markedly improved by biventricular pacing. The first patient's condition (Case 1) could not be improved despite administration of intravenous inotropic agents. He required mechanical ventilation and continuous hemodialysis as his condition worsened. Biventricular pacing was performed which was soon followed by increased blood pressure and decreased mitral regurgitation. As a result, mechanical ventilation, continuous hemodialysis and intravenous medication could be withdrawn. The second patient's condition (Case 2) deteriorated because of bradycardia due to advanced atrioventricular block. Unexpectedly, temporary right atrium-right ventricle sequential pacing increased mitral regurgitation and then caused heart failure, requiring a higher dose of inotropic and diuretic agents. Therefore, biventricular pacing was performed which rapidly improved both his symptoms and hemodynamic state, allowing reduction of the medication dose. Biventricular pacing dramatically improves critical conditions in patients in life-threatening states.
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[The type of angina pectoris and the selection of the treatment].
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Angina Pectoris↗
[Percutaneous coronary angioplasty for the treatment of angina pectoris: indication, selection of procedures, and initial and late results].
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Angina Pectoris↗
[Refractory unstable angina].
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Angina, Unstable↗