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Biomedical subjects

K Haze

Publications and source records attributed to K Haze.

At least 19 recordsLinked to original sources
PubMed2005

Intravenous myocardial contrast echocardiography predicts regional and global left ventricular remodelling after acute myocardial infarction: comparison with low dose dobutamine stress echocardiography.

OBJECTIVE: To assess the role of intravenous myocardial contrast echocardiography (MCE) in predicting functional recovery and regional or global left ventricular (LV) remodelling after acute myocardial infarction (AMI) compared with low dose dobutamine stress echocardiography (LDSE). METHODS: 21 patients with anterior AMI and successful primary angioplasty underwent MCE and LDSE during the subacute stage (2-4 weeks after AMI). Myocardial perfusion and contractile reserve were assessed in each segment (12 segment model) with MCE and LDSE. The 118 dyssynergic segments in the subacute stage were classified as recovered, unchanged, or remodelled according to wall motion at six months' follow up. Percentage increase in LV end diastolic volume (%DeltaEDV) was also calculated. RESULTS: The presence of perfusion was less accurate than the presence of contractile reserve in predicting regional recovery (55% v 81%, p < 0.0001). However, the absence of perfusion was more accurate than the absence of contractile reserve in predicting regional remodelling (83% v 48%, p < 0.0001). The number of segments without perfusion was an independent predictor of %DeltaEDV, whereas the number of segments without contractile reserve was not. The area under the receiver operating characteristic curve showed that the number of segments without perfusion predicted substantial LV dilatation (%DeltaEDV > 20%) more accurately than did the number of segments without contractile reserve (0.88 v 0.72). CONCLUSION: In successfully revascularised patients with AMI, myocardial perfusion assessed by MCE is predictive of regional and global LV remodelling rather than of functional recovery, whereas contractile reserve assessed by LDSE is predictive of functional recovery rather than of LV remodelling.

Aged↗
PubMed2001

Elevated levels of oxidized low density lipoprotein show a positive relationship with the severity of acute coronary syndromes.

BACKGROUND: There is accumulating data that acute coronary syndromes relate to recent onset activation of inflammation affecting atherosclerotic plaques. Increased blood levels of oxidized low density lipoprotein (ox-LDL) could play a role in these circumstances. METHODS AND RESULTS: Ox-LDL levels were measured in 135 patients with acute myocardial infarction (AMI; n=45), unstable angina pectoris (UAP; n=45), and stable angina pectoris (SAP; n=45) and in 46 control subjects using a sandwich ELISA method. In addition, 33 atherectomy specimens obtained from a different cohort of patients with SAP (n=10) and UAP (n=23) were studied immunohistochemically for ox-LDL. In AMI patients, ox-LDL levels were significantly higher than in patients with UAP (P<0.0005) or SAP (P<0.0001) or in controls (P<0.0001) (AMI, 1.95+/-1.42 ng/5 microgram LDL protein; UAP, 1.19+/-0.74 ng/5 microgram LDL protein; SAP, 0.89+/-0.48 ng/5 microgram LDL protein; control, 0.58+/-0.23 ng/5 microgram LDL protein). Serum levels of total, HDL, and LDL cholesterol did not differ among these patient groups. In the atherectomy specimens, the surface area containing ox-LDL-positive macrophages was significantly higher in patients with UAP than in those with SAP (P<0.0001). CONCLUSIONS: This study demonstrates that ox-LDL levels show a significant positive correlation with the severity of acute coronary syndromes and that the more severe lesions also contain a significantly higher percentage of ox-LDL-positive macrophages. These observations suggest that increased levels of ox-LDL relate to plaque instability in human coronary atherosclerotic lesions.

Angina Pectoris↗
PubMed2001

Identification of the G13 (cAMP-response-element-binding protein-related protein) gene product related to activating transcription factor 6 as a transcriptional activator of the mammalian unfolded protein response.

Eukaryotic cells control the levels of molecular chaperones and folding enzymes in the endoplasmic reticulum (ER) by a transcriptional induction process termed the unfolded protein response (UPR). The mammalian UPR is mediated by the cis-acting ER stress response element consisting of 19 nt (CCAATN(9)CCACG), the CCACG part of which is considered to provide specificity. We recently identified the basic leucine zipper (bZIP) protein ATF6 as a mammalian UPR-specific transcription factor; ATF6 is activated by ER stress-induced proteolysis and binds directly to CCACG. Here we report that eukaryotic cells express another bZIP protein closely related to ATF6 in both structure and function. This protein encoded by the G13 (cAMP response element binding protein-related protein) gene is constitutively synthesized as a type II transmembrane glycoprotein anchored in the ER membrane and processed into a soluble form upon ER stress as occurs with ATF6. The proteolytic processing of ATF6 and the G13 gene product is accompanied by their relocation from the ER to the nucleus; their basic regions seem to function as a nuclear localization signal. Overexpression of the soluble form of the G13 product constitutively activates the UPR, whereas overexpression of a mutant lacking the activation domain exhibits a strong dominant-negative effect. Furthermore, the soluble forms of ATF6 and the G13 gene product are unable to bind to several point mutants of the cis-acting ER stress response element in vitro that hardly respond to ER stress in vivo. We thus concluded that the two related bZIP proteins are crucial transcriptional regulators of the mammalian UPR, and propose calling the ATF6 gene product ATF6alpha and the G13 gene product ATF6beta.

Activating Transcription Factor 6↗
PubMed2001

Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan.

OBJECTIVES: To determine the clinical features of a novel heart syndrome with transient left ventricular (LV) apical ballooning, but without coronary artery stenosis, that mimics acute myocardial infarction, we performed a multicenter retrospective enrollment study. BACKGROUND: Only several case presentations have been reported with regard to this syndrome. METHODS: We analyzed 88 patients (12 men and 76 women), aged 67 +/- 13 years, who fulfilled the following criteria: 1) transient LV apical ballooning, 2) no significant angiographic stenosis, and 3) no known cardiomyopathies. RESULTS: Thirt-eight (43%) patients had preceding aggravation of underlying disorders (cerebrovascular accident [n = 3], epilepsy [n = 3], exacerbated bronchial asthma [n = 3], acute abdomen [n = 7]) and noncardiac surgery or medical procedure (n = 11) at the onset. Twenty-four (27%) patients had emotional and physical problems (sudden accident [n = 2], death/funeral of a family member [n = 7], inexperience with exercise [n = 6], quarreling or excessive alcohol consumption [n = 5] and vigorous excitation [n = 4]). Chest symptoms (67%), electrocardiographic changes (ST elevation [90%], Q-wave formation [27%] and T-wave inversion [97%]) and elevated creatine kinase (56%) were found. After treatment of pulmonary edema (22%), cardiogenic shock (15%) and ventricular tachycardia/fibrillation (9%), 85 patients had class I New York Heart Association function on discharge. The LV ejection fraction improved from 41 +/- 11% to 64 +/- 10%. Transient intraventricular pressure gradient and provocative vasospasm were documented in 13/72 (18%) and 10/48 (21%) of the patients, respectively. During follow-up for 13 +/- 14 months, two patients showed recurrence, and one died suddenly. CONCLUSIONS: A novel cardiomyopathy with transient apical ballooning was reported. Emotional or physical stress might play a key role in this cardiomyopathy, but the precise etiologic basis still remains unclear.

Adolescent↗
PubMed2001

Endoplasmic reticulum stress-induced formation of transcription factor complex ERSF including NF-Y (CBF) and activating transcription factors 6alpha and 6beta that activates the mammalian unfolded protein response.

The levels of molecular chaperones and folding enzymes in the endoplasmic reticulum (ER) are controlled by a transcriptional induction process termed the unfolded protein response (UPR). The mammalian UPR is mediated by the cis-acting ER stress response element (ERSE), the consensus sequence of which is CCAAT-N(9)-CCACG. We recently proposed that ER stress response factor (ERSF) binding to ERSE is a heterologous protein complex consisting of the constitutive component NF-Y (CBF) binding to CCAAT and an inducible component binding to CCACG and identified the basic leucine zipper-type transcription factors ATF6alpha and ATF6beta as inducible components of ERSF. ATF6alpha and ATF6beta produced by ER stress-induced proteolysis bind to CCACG only when CCAAT is bound to NF-Y, a heterotrimer consisting of NF-YA, NF-YB, and NF-YC. Interestingly, the NF-Y and ATF6 binding sites must be separated by a spacer of 9 bp. We describe here the basis for this strict requirement by demonstrating that both ATF6alpha and ATF6beta physically interact with NF-Y trimer via direct binding to the NF-YC subunit. ATF6alpha and ATF6beta bind to the ERSE as a homo- or heterodimer. Furthermore, we showed that ERSF including NF-Y and ATF6alpha and/or beta and capable of binding to ERSE is indeed formed when the cellular UPR is activated. We concluded that ATF6 homo- or heterodimers recognize and bind directly to both the DNA and adjacent protein NF-Y and that this complex formation process is essential for transcriptional induction of ER chaperones.

Activating Transcription Factor 6↗
PubMed2001

Moyamoya disease and coronary artery disease--case report.

A 26-year-old female with idiopathic moyamoya disease developed chest pain with concomitant ST depression on electrocardiography. Coronary angiography detected no stenotic lesions in the epicardial coronary arteries. The clinical diagnosis was vasospastic angina pectoris. She was medicated with calcium antagonists, which reduced the frequency of chest pain episodes. Angina pectoris is a rare occurrence in young patients with moyamoya disease. Coronary artery disease and moyamoya disease may have common etiological factors.

Adult↗
PubMed2000

ATF6 activated by proteolysis binds in the presence of NF-Y (CBF) directly to the cis-acting element responsible for the mammalian unfolded protein response.

Transcription of genes encoding molecular chaperones and folding enzymes in the endoplasmic reticulum (ER) is induced by accumulation of unfolded proteins in the ER. This intracellular signaling, known as the unfolded protein response (UPR), is mediated by the cis-acting ER stress response element (ERSE) in mammals. In addition to ER chaperones, the mammalian transcription factor CHOP (also called GADD153) is induced by ER stress. We report here that the transcription factor XBP-1 (also called TREB5) is also induced by ER stress and that induction of CHOP and XBP-1 is mediated by ERSE. The ERSE consensus sequence is CCAAT-N(9)-CCACG. As the general transcription factor NF-Y (also known as CBF) binds to CCAAT, CCACG is considered to provide specificity in the mammalian UPR. We recently found that the basic leucine zipper protein ATF6 isolated as a CCACG-binding protein is synthesized as a transmembrane protein in the ER, and ER stress-induced proteolysis produces a soluble form of ATF6 that translocates into the nucleus. We report here that overexpression of soluble ATF6 activates transcription of the CHOP and XBP-1 genes as well as of ER chaperone genes constitutively, whereas overexpression of a dominant negative mutant of ATF6 blocks the induction by ER stress. Furthermore, we demonstrated that soluble ATF6 binds directly to CCACG only when CCAAT exactly 9 bp upstream of CCACG is bound to NF-Y. Based on these and other findings, we concluded that specific and direct interactions between ATF6 and ERSE are critical for transcriptional induction not only of ER chaperones but also of CHOP and XBP-1.

Activating Transcription Factor 6↗
PubMed2000

[Does reperfusion therapy reduce complications in acute inferior myocardial infarction?].

Both right ventricular infarction and complete atrioventricular block were frequently seen in patients with acute inferior myocardial infarction before the introduction of reperfusion therapy (RT). However, the effect of reperfusion therapy on these 2 complications is not well known. To evaluate the effect of reperfusion therapy in them, we retrospectively studied the in-hospital outcome of 103 consecutive patients with acute inferior myocardial infarction within 72 hr after the onset, 23 with right ventricular infarction and 36 with complete atrioventricular block. Patients were divided into 2 groups: RT group (n = 63) in which Thrombolysis in Myocardial Infarction (TIMI) III flow was obtained by reperfusion therapy within 24 hr after the onset, and the non-RT group (n = 40) in which TIMI III flow was not obtained or did not receive reperfusion therapy. Patients with right ventricular infarction in the RT group had a larger proportion of proximal occlusion of the right coronary artery and the absence of preinfarction angina. There were no effects of perfusion on complete atrioventricular block. In 23 patients with right ventricular infarction and 36 patients with complete atrioventricular block, in-hospital stay, duration of using temporary pacing and Swan-Ganz catheter were shorter in the RT group than the non-RT group. Reperfusion therapy does not decrease the incidence of both complications. However, successful reperfusion therapy results in a rapid improvement in hemodynamic instability and atrioventricular conduction injury, and early hospital discharge. Preinfarction angina may be associated with a protective effect against the development of these 2 complications.

Female↗
PubMed1999

Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic reticulum stress.

The unfolded protein response (UPR) controls the levels of molecular chaperones and enzymes involved in protein folding in the endoplasmic reticulum (ER). We recently isolated ATF6 as a candidate for mammalian UPR-specific transcription factor. We report here that ATF6 constitutively expressed as a 90-kDa protein (p90ATF6) is directly converted to a 50-kDa protein (p50ATF6) in ER-stressed cells. Furthermore, we showed that the most important consequence of this conversion was altered subcellular localization; p90ATF6 is embedded in the ER, whereas p50ATF6 is a nuclear protein. p90ATF6 is a type II transmembrane glycoprotein with a hydrophobic stretch in the middle of the molecule. Thus, the N-terminal half containing a basic leucine zipper motif is oriented facing the cytoplasm. Full-length ATF6 as well as its C-terminal deletion mutant carrying the transmembrane domain is localized in the ER when transfected. In contrast, mutant ATF6 representing the cytoplasmic region translocates into the nucleus and activates transcription of the endogenous GRP78/BiP gene. We propose that ER stress-induced proteolysis of membrane-bound p90ATF6 releases soluble p50ATF6, leading to induced transcription in the nucleus. Unlike yeast UPR, mammalian UPR appears to use a system similar to that reported for cholesterol homeostasis.

Activating Transcription Factor 6↗
PubMed1999

Efficacy of percutaneous transluminal coronary angioplasty for patients on hemodialysis. Comparison with those not on dialysis.

Ischemic heart disease has become more important in regard to mortality in hemodialysis (HD) patients. We examined the therapeutic outcome of initial percutaneous transluminal angioplasty (PTCA) in maintenance HD patients with angina pectoris. They consisted of 8 men and 4 women with a mean age of 56.3 +/- 8.6 years and a mean duration of HD of 4.3 +/- 4.0 years. Thirty-six non-HD patients treated with initial PTCA were matched for age, sex and coronary risk factors, and used as a control. Angiographic lesion success was confirmed by angiography in 21 (84%) of the 25 stenotic sites attempted and clinical success was obtained in 9 (75%) of the 12 HD patients, while there were 40 (78%) lesions successfully removed out of the 51 stenotic sites and there were 26 (72%) clinically successful cases out of the 36 non-HD patients, respectively. Angina recurred in 4 (44%) of 9 HD patients, and in 10 (38%) of 26 non-HD patients after successful PTCA, where the follow-up periods were 23 +/- 20 and 28 +/- 25 months, respectively. There was no significant difference in cumulative lesion survival curve between the two groups. In conclusion, PTCA for chronic HD patients is as effective as that for non-HD patients, at least regarding initial PTCA.

Adult↗
PubMed1999

[Clinical significance of improved persistent defect by thallium-201 reinjection imaging in the subacute phase of myocardial infarction].

The clinical significance of new fill-in observed by thallium-201 (201Tl) reinjection in myocardial segments with persistent defect in the subacute phase of myocardial infarction was investigated. Seventy-five patients with subacute phase (mean 20th day) of first myocardial infarction underwent stress-redistribution-reinjection 201Tl single photon emission computed tomography (SPECT) imaging. Percentage 201Tl uptake was calculated and classified as persistent defect without fill-in even after reinjection (PD group, n = 26, 35%), persistent defect with new fill-in after reinjection [REINJ (+) group, n = 19, 25%] and reversible defect [RD (+) group, n = 24, 32%]. The clinical features and angiographic findings were assessed in the same phase in each group. Diameter stenosis of the infarction-related arteries by coronary angiography was 68 +/- 34% in the PD group, 31 +/- 23% in the REINJ (+) group and 83 +/- 27% in the RD (+) group [p < 0.01, REINJ (+) group vs PD group and RD (+) group]. Wall motion of the infarcted myocardial segments significantly improved and the mean left ventricular ejection fraction (EF) was higher in the REINJ (+) group than in the PD group (mean EF 51% vs 43%, p < 0.01). Post infarction angina was more frequent in the RD (+) group than in the REINJ (+) group (38% vs 5%, p < 0.05). Although new fill-in-after 201Tl reinjection has been considered to indicate severe myocardial ischemia in chronic coronary disease, these results indicate that this phenomenon in viable myocardium in patients with subacute phase of myocardial infarction is not always related to residual ischemia in the infarcted myocardial area.

Female↗
PubMed1999

[Prognosis for patients with angina pectoris accompanied by chronic renal failure].

Chronic renal failure (CRF) is one of the risk factors of a worse outcome for patients with coronary artery disease. However, few studies have assessed the outcome in such patients. This study investigated the clinical characteristics, treatment modalities, and prognosis for patients with angina pectoris accompanied by CRF and evaluated the validity of current treatment strategy for these patients. A total of 593 patients (248 with stable angina and 345 with unstable angina) admitted to our institution were studied. Renal failure was defined as serum creatinine of > or = 2.0 mg/dl. Patients were divided into 2 groups, with renal failure (46 patients) and without renal failure (547 patients), and the former group was further divided into 2 groups with hemodialysis (26 patients) and without hemodialysis (20 patients). The mean follow-up period was 2.5 +/- 1.2 years and the follow-up rate was 99%. The prevalences of congestive heart failure (26% vs 3%, p < 0.001), hypertension (72% vs 45%, p < 0.005), and multivessel coronary artery disease (65% vs 33%, p < 0.001) were higher in patients with CRF. The left ventricular end-diastolic volume was greater in patients with CRF than in patients without CRF (114 +/- 36 vs 85 +/- 24 ml/m2, p < 0.001). The calcification score of both coronary arteries and abdominal aorta evaluated by electron-beam computed tomography was higher in patients with CRF (2,187 +/- 2,727 vs 631 +/- 841, p = 0.03; 4,091 +/- 3,068 vs 2,191 +/- 2,249, p = 0.02, respectively). In-hospital cardiac mortality was higher in patients with CRF than in patients without CRF (8.7% vs 0.7%, p < 0.001). The cumulative survival was 88% at 1 year and 65% at 3 years in patients with CRF and 99% and 97% in patients without CRF, respectively (p < 0.001). The incidence of re-hospitalization due to congestive heart failure was higher in patients with CRF (19% vs 1.3%, p < 0.0001). The cumulative survival in CRF was 93% at 1 year, 57% at 3 years in the medical treatment group and 87% and 75% in the invasive therapy group, respectively (p = 0.1). Patients with angina pectoris and CRF had a poor prognosis under the current treatment strategy. Newly developed therapeutic strategies, such as rotational atherectomy, minimally invasive direct coronary artery bypass surgery and combinations, will be necessary to improve the long-term prognosis for these patients.

Aged↗
PubMed1999

[Efficacy of hemostatic puncture closing device for hemostasis and early ambulation after coronary angiography and angioplasty: results of a multicenter trial].

To assess the efficacy and safety of a hemostatic puncture closing device for reducing patient immobilization after cardiac catheterization from a percutaneous femoral artery approach, we conducted a prospective, randomized trial at 4 participating centers. A total of 240 patients (183 men, 57 women, mean age 61 +/- 10 yr; 157 patients underwent diagnostic angiography, 83 patients underwent coronary angioplasty) were randomized to either the device group (n = 120) or the manual compression group (n = 120). There were no statistical differences in age, gender, weight or sheath size between the 2 groups. A 7, 8F sheath was used in 53 patients of the device group and in 43 patients of the manual compression group. One hundred and two patients (85%) in the device group and 96 patients (80%) in the manual compression group received heparin. Protamine was used in one patient of the device group and 23 patients of the manual compression group. Activated clotting time just prior to sheath removal was 206 +/- 64 sec in the device group and 170 +/- 47 sec in the manual compression group (p < 0.01). Successful placement of the device was achieved in 118 of 120 patients (98%). Time to hemostasis was significantly shorter in the device group (0.8 +/- 3.2 vs 12.2 +/- 5.3 min, p < 0.01). Time to ambulation could be reduced in the device group (5.3 +/- 3.7 vs 10.9 +/- 5.1 hr, p < 0.01). The following complication rates occurred in the device group as compared with the manual compression group: hematoma, 16% vs 10%; bleeding, 8% vs 3%; pseudoaneurysm, 0% vs 1%, respectively. None of these differences was statistically significant. These results indicate that early ambulation using a hemostatic puncture closing device is feasible without significantly increasing the risk of peripheral vascular complications.

Adult↗
PubMed1998

Identification of the cis-acting endoplasmic reticulum stress response element responsible for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic leucine zipper transcription factors.

When unfolded proteins accumulate in the endoplasmic reticulum (ER), transcription of glucose-regulated proteins (GRPs) representing ER-resident molecular chaperones is markedly induced via the unfolded protein response (UPR) pathway. In contrast to recent progress in the analysis of yeast UPR, both cis-acting elements and transactivators responsible for mammalian UPR have remained obscure. Here, we analyzed the promoter regions of human GRP78, GRP94, and calreticulin genes and identified a novel element designated the ER stress response element (ERSE). ERSE, with a consensus of CCAATN9CCACG, was shown to be necessary and sufficient for induction of these GRPs. Using yeast one-hybrid screening, we isolated a human cDNA encoding a basic leucine zipper (bZIP) protein, ATF6, as a putative ERSE-binding protein. When overexpressed in HeLa cells, ATF6 enhanced transcription of GRP genes in an ERSE-dependent manner, whereas CREB-RP, another bZIP protein closely related to ATF6, specifically inhibited GRP induction. Endogenous ATF6 constitutively expressed as a 90-kDa protein was converted to a 50-kDa protein in ER-stressed cells, which appeared to be important for the cellular response to ER stress. These results suggest that, as in yeast, bZIP proteins are involved in mammalian UPR, acting through newly defined ERSE.

Amino Acid Sequence↗
PubMed1998

Cardioprotective effect of intravenous nicorandil in patients with successful reperfusion for acute myocardial infarction.

This study was designed to assess the cardioprotective effect of intravenous nicorandil, a potassium channel opener, in preventing reperfusion injury in acute myocardial infarction. Seventy patients were treated with placebo or nicorandil concomitant with reperfusion therapy in a prospective, randomized, double-blind fashion within 6 h after the onset of acute myocardial infarction. Nicorandil was administered before reperfusion as a 2-mg bolus iv injection followed by continuous infusion of 2-6 mg/h for the next 3 h. Thirty-six patients (17 in the placebo group, 19 in the nicorandil group) who demonstrated both complete occlusion of an infarct-related vessel before treatment and successful reperfusion were included in the final analysis. No significant changes in left ventricular ejection fraction were observed between the immediate and chronic phases in each group. In the analysis of regional ventricular function, the placebo group did not show any significant change in regional chord shortening (26.8+/-8.2 vs 24.3+/-7.3%, NS) or hypocontractile perimeter (36.4+/-28.2% vs 28.3+/-24.8%, NS) between immediate and chronic phase left ventriculograms. In contrast, in the nicorandil group, a significant increase in regional chord shortening (21.5+/-11.0% vs 25.8+/-11.3%, p<0.05) and a significant decrease in hypocontractile perimeter (33.3+/-19.6% vs 25.6+/-24.3%, p<0.05) were observed in the chronic phase left ventriculogram. Thus, nicorandil may be a useful adjunctive therapy for preserving myocardial contractile function in patients with acute myocardial infarction undergoing reperfusion therapy.

Acute Disease↗