Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.1.1.6 (CAD)
4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial perfusion SPECT (MPS) commonly is interpreted qualitatively and not quantitatively. Most of the prognostic literature is based on a semi-quantitative visual analysis (SQA) of MPS. However, data about the comparison between the SQA and coronary angiography (cath) is lacking. We therefore evaluated 167 patients who underwent MPS and subsequent cath. SQA using a 20 segment model was used for MPS interpretation. Patients with a small to moderate amount of ischemia (SDS < or = 4; mean 1.2 +/- 1.5) and with extensive ischemia (SDS > 4; mean 9.6 +/- 4.7) were then compared with respect to clinical and cath variables. Patients with extensive ischemia had more advanced CAD as demonstrated by several cath variables (more often triple vessel and LAD-disease). SQA therefore is a useful tool for MPS interpretation and decision making in patients with (suspected) CAD.
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PMID:[Noninvasive cardiac diagnosis for quantifying scarring, ischemia and pump function within the scope of a study. 20 useful facets in routine cardiology nuclear medicine practice]. 1201 64

Apoptosis is an evolutionarily conserved process critical to tissue development and tissue homeostasis in eukaryotic organisms and, when dysregulated, causes inappropriate cell death. Global ischemia is a neuronal insult that induces delayed cell death with many features of apoptosis. Ischemic preconditioning affords robust protection of CA1 neurons against a subsequent severe ischemic challenge. The molecular mechanisms underlying ischemic tolerance are unclear. Here we show that ischemia induces pronounced caspase-3 activity in naive neurons that die and in preconditioned neurons that survive. Preconditioning intervenes downstream of proteolytic processing and activation of caspase-3 (a protease implicated in the execution of apoptosis) and upstream of the caspase-3 target caspase-activated DNase (CAD, a deoxyribonuclease that catalyzes DNA fragmentation) to arrest neuronal death. We further show that global ischemia promotes expression of the pro-survival inhibitor-of-apoptosis (IAP) family member cIAP, but unleashes Smac/DIABLO (second mitochondria-derived activator of caspases/direct IAP-binding protein with low pI), a factor that neutralizes the protective actions of IAPs and promotes neuronal death. Preconditioning blocks the mitochondrial release of Smac/DIABLO, but not the ischemia-induced upregulation of IAPs. In the absence of Smac/DIABLO, cIAP halts the caspase death cascade and arrests neuronal death. These findings suggest that preconditioning preserves the integrity of the mitochondrial membrane, enabling neurons to survive in the face of caspase activation.
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PMID:Ischemic preconditioning: neuronal survival in the face of caspase-3 activation. 1502 68

Ischemic preconditioning affords the most powerful protection to a heart submitted to a prolonged ischemia-reperfusion. During the past decade, a huge amount of work allowed to better understand the features of this protective effect as well as the molecular mechanisms. Ischemic preconditioning reduces infarct size and improves functional recovery; its effects on arrhythmias remain debated. Triggering of the protection involves cell surface receptors that activate pro-survival pathways including protein kinase C, PI3-kinase, possibly Akt and ERK1/2, whose downstream targets remain to be determined. Much attention has been recently focused on the role of mitochondrial K(+)ATP channels and the permeability transition pore that seem to play a major role in the progression toward irreversible cellular injury. Based on these experimental studies attempts have been made to transfer preconditioning from bench to bedside. Human experimental models of ischemic preconditioning have been set up, including cardiac surgery, coronary angioplasty or treadmill exercise, to perform pathophysiological studies. Yet, protecting the heart of CAD (coronary artery disease) patients requires a pharmacological approach. The IONA trial has been an example of the clinical utility of preconditioning. It helped to demonstrate that chronic administration of nicorandil, a K(+)ATP opener that mimics ischemic preconditioning in experimental preparations, improves the cardiovascular prognosis in CAD patients. Recent experimental studies appear further encouraging. It appears that "postconditioning" the heart (i.e. performing brief episodes of ischemia-reperfusion at the time of reperfusion) is as protective as preconditioning. In other words, a therapeutic intervention performed as late as at the time of reflow can still significantly limit infarct size. Further work is needed to determine whether this may be transferred to the clinical practice.
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PMID:[How to use the paradigm of ischemic preconditioning to protect the heart?]. 1519 Apr 69

The definition of proper patient selection criteria remains a prominent item in constant need of attention. While the concept of gathering evidence in order to determine practice continues to be hopelessly ambiguous, it can never be emphasized too much that these univariate results are just a first foray into analysing predictors of survival; all following results should be regarded and interpreted in this perspective. HEART TRANSPLANT SURVIVAL: The 3-year survival rate for heart transplant recipients under age 16 was 83% versus 72% for adult recipients. Acutely retransplanted adult heart recipients had a 3-year survival rate of 36% compared with 72% for recipients of a first heart allograft. Patients suffering from DCM had the best survival rates at 3 years (74%) compared with patients suffering from CAD (70%) or from another end-stage heart disease (67%). With advancing age of the adult recipient, the mortality risk increased. Patients aged 16-40 had a 3-year survival rate of 77%, compared with 74%, 70% and 61% for transplant recipients aged 41-55, 56-65 and over age 65, respectively. The 3-year survival rates for adult recipients transplanted with an heart allograft from a donor aged under 16 or between 16-44 were 78% and 74%, compared with 66% and 63% for donors aged 45-55 and over 55, respectively. The 3-year survival rates for recipients of hearts with cold ischemic times under 2 hours, 2-3, 3-4, 4-5, 5-6 and more than 6 hours were 74%, 75%, 70%, 65%, 54% and 40%, respectively. Transplanting a female donor heart into a male recipient was associated with the worst prognosis: the 3-year survival rates were 73%, 71%, 66% and 76%, respectively, for the donor/recipient groups male/male, male/female, female/male and female/female, respectively. When the donor-to-recipient body weight ratio was below 0.8, the 3-year survival rate was 64%, compared to 72% for weight-matched pairs and 74% for patients who received a heart from an oversized donor (p=0.004). Better survival rates were obtained for better HLA-matched transplants. The 3-year survival rates were 75%, 89%, 78%, 78%, 69%, 72%, and 71% for HLA-A,-B,-DR zero, 1, 2, 3, 4, 5 and 6 mismatched groups, respectively (p=0.04). Survival was significantly associated with the CMV serologic status of the donor and recipient; the 3-year survival rates were: D+/R+, 71%; D+/R-, 69%; D- R-, 76%; and D-/R+, 76% (p=0.04). Patients in an ICU had a 3-year survival rate of 62%, compared to 72% for patients in a general ward and 74% for outpatients (p<0.0001). Patients that were on a VAD and there-upon transplanted had a 3-year survival rate of 65%, compared to 73% for patients without a VAD (p=0.004). Being on a ventilator was a major risk factor for death after transplantation; patients on ventilator support at the time of the transplant had a 3-year survival rate of 52% compared to 73% for the other patients (p<0.0001). LUNG TRANSPLANT SURVIVAL: The 3-year survival rate for children (73%) appeared to be better than the adult rate (61%; p=0.8). Adult lung transplant survival was significantly worse in the case of a repeat lung transplant; a 3-year retransplant survival rate of 42% was obtained compared with 61% for first transplants (p=0.049). With respect to the underlying end-stage lung disease, no statistically significant difference in long-term survival could be detected in this cohort. The 3-year survival rates were: 62% for COPD/Emphysema, 70% for CF, 58% for IPF, 64% for Alpha-1 ATD and 56% for PPH (p=0.2). Our data demonstrated no effect of the recipient's age on long-term lung transplant survival, except for 2 senior patients in this cohort. At 3-years the survival rates for recipients aged 16-40, 41-55 and 56-65 were 65%, 60% and 62%, respectively (p=0.05). The 3-year survival rates for transplants performed with lungs from donors aged under 16, 16-44, 45-55 and over 55 was 57%, 64%, 55% and 62%, respectively (p=0.1) No association between the duration of cold ischemic time and 3-year survival was observed; under 3 hours, 3-4, 4-5, 5-6 and over 6 hours of ischemia resulted in 3-year survival rates of 53%, 59%, 64%, 68% and 57%, respectively (p=0.2). Early posttransplant outcome tended to be better for gender-matched transplants, while transplanting a female donor lung into a male recipient was associated with the worst prognosis. The 3-year survival rates were 65% for male/male, 63% for male/female, 48% for female/male and 61% for female/female (p=0.009). No effect of donor-to-recipient weight match was observed in this Eurotransplant cohort; when the donor-to-recipient weight ratio was below 0.8, the 3-year survival rate was 57%, compared with 59% for weight-matched pairs and 64% for patients who received a lung from an oversized donor (p=0.5). Long-term survival after lung transplantation was influenced by HLA matching. The 3-year survival rates were 100%, 68%, 70%, 65%, 54% and 55% for the HLA-A,-B,-DR 1, 2, 3, 4, 5 and 6 mismatched groups, respectively (p=0.06). A donor CMV+ and recipient CMV- match was a risk factor for long-term mortality, with 3-year survival rates of 56% for D+/R+, 55% for D+/R-, 71% for D-/R- and 62% for D-/R+ transplants (p=0.046). En-bloc transplantation of both lungs yielded worse early results, but the 3-year survival rates for patients who underwent single (60%), bilateral sequential double lung (63%) and en-bloc double lung transplantation (56%) were not different (p=0.2). Ventilator dependency was associated with a significantly reduced survival at 3 years. Patients on a ventilator support at the time of the transplant had a 3-year survival rate of 48% compared with 63% for other patients (p=0.006).
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PMID:Three-year survival rates for all consecutive heart-only and lung-only transplants performed in Eurotransplant, 1997-1999. 1538

Therapeutic angiogenesis aims at restoring perfusion to chronically ischemic myocardial territories by using growth factors or cells, without intervening on the epicardial coronary arteries. Despite angiogenesis having received considerable scientific attention over the last decade, it has not yet been shown to provide clinical benefit and is still reserved for patients who have failed conventional therapies. Nevertheless, angiogenesis is a very potent physiologic process involved in the growth and development of every animal and human, and it is likely that its use for therapeutic purposes, once its underlying mechanistic basis is better understood, will one day become an important modality for patients with CAD and other types of organ ischemia. This review summarizes current knowledge in therapeutic angiogenesis research.
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PMID:Protein-, gene-, and cell-based therapeutic angiogenesis for the treatment of myocardial ischemia. 1554 41

Presented herein are the data on the condition of central and cerebral hemodynamics in 98 patients with chronic stage III-IV lower limb ischemia and coexistent CAD as dependent, on the severity of painful syndrome as well as on the necessity of preparing patients at a high surgical risk for reconstructions under prolonged epidural anesthesia. The prognostically dangerous changes in central and cerebral hemodynamics were revealed in persons with severe painful syndrome. In 87% of patients, circulation was hypokinetic. Twenty-six patients with unremovable pain and severe coexistent diseases underwent, as preoperative preparation, prolonged epidural anesthesia. It has been proven that prolonged epidural anesthesia allows to reach not only a good analgetic effect but also to refine the indicators of central and cerebral hemodynamics whereby preventing intra- and postoperative ischemic events.
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PMID:[Preoperative preparation of patients with critical lower limb ischemia and pronounced painful syndrome]. 1562 40

North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) reports have shown anti-T cell antibody, OKT3, to be deleterious in pediatric renal transplant recipients treated with mycophenolate mofetil (MMF). Unlike OKT3, basiliximab is a chimeric monoclonal antibody to the alpha subunit of the interleukin-2 receptor on activated T-lymphocytes. We sought to examine the outcome of MMF with or without basiliximab induction therapy in pediatric renal transplantation. Between January 1998, and June 2001, 49 pediatric renal transplants were performed at our center and 41 met the criteria for this study. We retrospectively analyzed the records of 25 patients who received MMF, Prednisone, CSA or TAC, alone (group I) and 16 patients who received MMF, CSA or TAC, and Prednisone in combination with basiliximab (group II). The two groups were similar with respect to recipient or donor age, gender, ethnicity, donor source (LD vs. CAD), cold ischemia time, and primary diagnosis. The basiliximab group had a shorter follow up period because of its more recent addition to our pediatric immunosuppression protocol, 12.9 +/- 5.9 months vs. 35.5 +/- 7.2 months for group I (p < 0.0001). At 6 months, the acute rejection rate was 16% (group I) compared with 25% (group II) (p = 0.689). The patient and graft survival at 6 and 12 months were 100% respectively for both groups. Basiliximab was well tolerated without significant adverse events. At 6 months, there was no significant difference between the groups in the incidence of urinary tract infection or cytomegalovirus infection. These data suggest that in the short-term, MMF with or without basiliximab induction therapy appears to yield excellent and statistically similar outcomes. However, further controlled studies are necessary to verify these findings as well as to define the role of basiliximab in MMF-treated pediatric renal transplant recipients.
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PMID:Mycophenolate mofetil in pediatric renal transplantation: non-induction vs. induction with basiliximab. 1566 17

Cardiovascular disease (CVD) is the major cause of death in patients with type 2 diabetes mellitus. However, the diagnosis of CVD is delayed due to concealment of antecedent symptoms by factors such as autonomic neuropathy. In this study, we aimed to investigate the frequency of silent ischemia by using exercise electrocardiogram (ECG). The present study included 500 Turkish patients with type 2 diabetes (male/female: 222/278), who showed no evidence of CAD and angina pectoris or no sign(s) of ischemic changes in resting ECGs. All patients underwent treadmill exercise test according to Bruce protocol, and 62 cases (12.4%) exhibited abnormal changes. These patients identified by exercise ECG consisted of 28 males (28/222, [12.6%]) and 34 females (34/278, [12.2%]) and were then examined by coronary angiography. CAD was diagnosed in 53 individuals by coronary angiography. The abnormalities of exercise test are associated with the age of the patients or the duration of diabetes (p < 0.05). There is no significant difference in the severity of coronary disease or in the prevalence of silent ischemia between male and female patients. However, among the patients identified by exercise ECG females have higher body mass index than males, suggesting that obesity may represent the risk factor of CAD in women with type 2 diabetes.
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PMID:The prevalence of silent ischemia in Turkish patients with type 2 diabetes mellitus. 1575 Mar 31

The data of modern experimental study of insulin receptors structure characteristics, the hormone effects on receptor and postreceptor molecular-cellular level, the ways hormone signal in cardiomiocites (CMC) as well as intercoupling possibility with other mediators and hormones from the point of view of probable mechanisms of hyperinsulinemia are analysed in the survey. On the basis of personal studies clinical conditions at which hyperinsulinemia manifests in patients with CAD are described. Conception is offered in accordance with which one of the reasons of "insulineresistance" at CAD can be a significant energetic CMC potential decrease as a result of myocardial metabolism remodeling in conditions of prolonged chronic ischemia, which forestalls significantly clinical manifestation of the disease.
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PMID:[Molecular-cellular effects of insulin and possible mechanisms of insulin resistance development in patients with ischemic heart disease (CAD)]. 1590 64

The authors analyzed the efficiency of ECG-gated single-photon emission computed tomography (SPECT) with 99mTc-tetraphosmin in diagnostics of short-term myocardium stunning in CAD patients with transient ischemia. The technique was applied to 16 CAD patients. Combined evaluation of perfusion was based on the analysis of radiotracer uptake level in left ventricle (LV) myocardium. In order to evaluate myocardium function the authors measured LV systolic thickening index, using 20-segment pattern. 8 out of 16 patients (50%) displayed the phenomenon of stress-induced stunning. The volume of stunned myocardium in individual patients was 2 to 7 LV segments. In general, up to 37% (29/78) of reversible perfusion defects are subjected to short-term stunning under the condition of transient ischemia. After surgical treatment, 84% of segments with signs of stunning normalized their functioning both under stress and at rest.
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PMID:[ECG-gated single-photon emission computed tomography with 99mTC-tetraphosmin in diagnostics of short-term myocardium stunning under the condition of stress-induced ischemia in CHD patients with multivascular lesions of coronary vessels]. 1590 35


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