Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transmyocardial laser revascularization is a promising surgical technique that relieves angina and improves subendocardial perfusion in patients with chronic ischemic heart disease refractory to medical management and not amenable to conventional revascularization techniques. We detail our laboratory experience at the Brigham and Women's Hospital with transmyocardial laser revascularization and discuss the potential clinical applications of this work.
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PMID:Combination TMR and gene therapy. 993 Jul 10

A variety of experimental studies have confirmed that preconditioning the myocardium by brief periods of ischemia represents a powerful cardioprotective effect resulting in a reduction of infarct size. After 15 years of research in the experimental laboratory, some evidence shows the existence of preconditioning in human patients with coronary artery disease: repeated balloon inflations before coronary angioplasty induce preconditioning-like effects; moreover, some studies demonstrate better clinical outcome in patients with angina before acute myocardial infarction, resembling a preconditioning effect. So far, a few drugs have been identified as potential mediators of preconditioning, e.g., adenosine, adenosine receptor agonists, and adenosine triphosphate-sensitive potassium channel openers. Before coronary angioplasty and heart surgery, these preconditioning mimetics might be used to protect myocardial tissue by means of preconditioning. Further research is required before preconditioning mimetics could be used for therapy in patients with chronic myocardial ischemia. Possible antipreconditioning effects of several drugs, e.g., sulfonylurea drugs have to be considered in the treatment of patients with coronary artery disease.
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PMID:Clinical effects of ischemic preconditioning. 1044 15

Mortality rates are considerably higher in chronic ischemic heart disease (IHD) patients with non-insulin-dependent diabetes mellitus (NIDDM) than in those who are nondiabetics. The relationship between different types of antihyperglycemic pharmacological therapy and mortality rate in this NIDDM population is uncertain. We aimed to examine the survival in NIDDM patients with IHD using various types of oral antidiabetic treatments over a 5-year follow-up period. The study sample comprised 11,440 patients with a previous myocardial infarction and/or stable anginal syndrome, aged 45-74 years, who were screened, but not included in the Bezafibrate Infarction Prevention study. Among them, 9,045 were nondiabetics and 2,395 diabetics. The diabetic patients were divided into four groups on the basis of their therapeutic regimen at screening: diet alone (n = 990), sulfonylureas (n = 1,041), metformin (n = 78) and a combination of a sulfonylurea and metformin (n = 266). All NIDDM groups were similar with regard to age, gender, hypertension, smoking, heart failure, angina and prior myocardial infarction. Crude mortality rate was lower in the nondiabetic group (11.21 vs. 21.8%; p < 0.001). In the diabetic group, mortality was 18.5% for patients on diet alone, 22.5% for those on sulfonylureas, 25.6% for patients on metformin, and 31.6% for the combined sulfonylurea/metformin group (p < 0.01). When analyzing age-adjusted mortality rate and actuarial survival curves, the lowest mortality was found in patients on diet alone and the highest in patients on metformin (alone or in combination with sulfonylureas). After adjustment for variables connected with long-term prognosis, the use of metformin was associated with increased relative risk (RR) for all-cause mortality of 1.42 (95% CI 1.10-1.85), whereas the use of sulfonylureas alone was not [RR 1.11 (95% CI 0.90-1.36)]. NIDDM patients with IHD using metformin, alone or in combination with sulfonylureas, exhibited a significantly increased mortality. Until the results of problem-oriented prospective studies on oral control of NIDDM will be available, alternative therapeutic approaches should be investigated in these patients.
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PMID:Antihyperglycemic treatment in diabetics with coronary disease: increased metformin-associated mortality over a 5-year follow-up. 1051 15

Myocardial stunning and hibernation are both clinically important causes of myocardial dysfunction and are caused by episodes of myocardial ischaemia. Stunning tends to occur acutely and may produce transient but clinically important reductions in left ventricular function in the setting of myocardial infarction, post coronary artery bypass grafting and even following episodes of effort induced angina. Hibernation refers to a chronic down-regulation of myocardial function in response to chronic myocardial ischaemia. Hibernating myocardium may be present in up to 50% of patients with significantly impaired left ventricular function and evidence of heart failure. Importantly, both these entities can be either prevented or ameliorated by preventing or lessening ischaemic burden. There is also evidence that there may be an overlap between these two entities and that hibernating myocardium may result from repeated episodes of myocardial ischaemia causing chronic stunning.
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PMID:Myocardial stunning and hibernation in clinical practice. 1122 Dec 79

St Elizabeth's Medical Center of Boston is developing VEGF gene therapy for the potential treatment of angina and diabetic neuropathy. The center is studying three isoforms of VEGF, although the expression of phVEGF165 has yielded the most positive results [312563]. VEGF-2 gene therapy augments perfusion of ischemic myocardium that contributes to improved clinical outcomes in patients with chronic myocardial ischemia as assessed by NOGA electromechanical mapping [390786]. Phase I trials demonstrated that gene transfer directly into the heart of the patient facilitates blood flow to the primary muscles of the heart, providing relief of angina [348564]. Reduced angina was reported by 28 out of 30 patients and tolerance of exercise increased from 240 to 410 s up to 180 days post-therapy [348632].
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PMID:VEGF-2 (St Elizabeth's Medical Center). 1157 59

Ranolazine is a novel drug that has shown promise in the treatment of cardiovascular disease. Ranolazine exerts its effect by shifting myocardial energy metabolism away from free fatty acids and toward glucose as the substrate for production of adenosine triphosphate. Preclinical data have confirmed that ranolazine reduces myocardial ischaemic injury in various animal models. Researchers are continuing to gather clinical data but findings to date support the conclusion that ranolazine has anti-ischaemic effects without inducing the typical reduction in blood pressure and heart rate associated with the use of traditional anti-ischaemic agents. Given the absence of haemodynamic effects associated with ranolazine, it has great promise as a drug that could be added to existing therapy without concern for hypotensive or bradycardic side effects. Ranolazine has been shown to improve exercise-induced myocardial ischaemia and to lessen the severity of angina in the setting of chronic ischaemic heart disease. Early preclinical observations also suggest positive effects of ranolazine in the management of congestive heart failure; however, trials in this area are ongoing. Several recently completed Phase III clinical studies in patients with chronic ischaemic heart disease have confirmed the findings of smaller trials and should satisfy regulatory concerns necessary to place ranolazine on the commercial market in the US. The maker of ranolazine, CV Therapeutics (Palo Alto, California), will file a New Drug Application (NDA) with the US FDA for the approval of ranolazine as an anti-anginal in the near future.
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PMID:The use of ranolazine in cardiovascular disease. 1177 26

Research in animal models of ischemia has shown that administration of angiogenic growth factors, either as a recombinant protein or by gene transfer, can augment nutrient perfusion through neovascularization to promote the development of supplemental collateral blood vessels that will constitute endogenous bypass conduits around occluded native arteries; a strategy termed "therapeutic angiogenesis." In animal models and clinical trials, the best studied cytokines with angiogenic activity are vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF). Clinical trials of therapeutic angiogenesis in patients with critical limb ischemia demonstrated resolution of rest pain and/or improved limb integrity, increased pain-free walking time and ankle-brachial index, newly visible collateral vessels by digital subtraction angiography, and qualitative evidence of improved distal flow by magnetic resonance imaging. Initial clinical trials in patients with end-stage coronary artery disease using direct myocardial injection via thoracotomy resulted in large increases in exercise time and marked reductions in anginal symptoms, as well as objective evidence of improved perfusion and left ventricular function. Larger scale placebo-controlled trials have been limited to intracoronary and intravenous administration of recombinant protein, and have not shown significant improvement in exercise time or angina compared to placebo. Larger scale placebo-controlled studies of gene transfer using catheter-based endocardial delivery are in progress. Future clinical studies are required to determine the optimal dose, formulation, route of administration, and combinations of growth factors, as well as the requirement for endothelial progenitor cell or stem cell supplementation, to provide effective and safe therapeutic angiogenesis for patients with critical limb ischemia and chronic myocardial ischemia who are not candidates for conventional revascularization procedures.
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PMID:Therapeutic angiogenesis in critical limb and myocardial ischemia. 1205 43

Therapeutic angiogenesis, in the form of growth factor protein administration or gene therapy, has emerged as a new method of treatment for patients with severe, inoperable coronary artery disease. Improved myocardial perfusion and function after administration of angiogenic growth factors has been demonstrated in animal models of chronic myocardial ischemia. Recently, preliminary clinical trials using growth factor proteins or genes encoding these angiogenic factors have demonstrated clinical and other objective evidence of relevant angiogenesis. A recent study reported beneficial long-term effects of therapeutic angiogenesis using fibroblast growth factor (FGF)-2 protein in terms of freedom from angina and perfusion on single-photon emission computed tomographic imaging. Thus, therapeutic angiogenesis has the potential to extend treatment options to patients who are not optimal candidates for conventional methods of myocardial revascularization. However, endogenous antiangiogenic influences, intrinsic lack of response of patients with severe endothelial dysfunction, and other limitations will need to be overcome before angiogenesis becomes a standard therapy for the treatment of patients with severe coronary disease.
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PMID:Vascular growth factors and angiogenesis in cardiac surgery. 1260 13

Norman J. Holter attention drew to the possibility to use ambulatory ECG monitoring not only for the diagnosis of arrhythmias but also myocardial ischaemia by already in 1961. It was found that patients with chronic stable angina pectoris have multiple episodes of myocardial ischaemia characterized by transient depressions of the ST segment, very frequently without a clinical correlate. Electrocardiography thus was the first objective method to draw attention to the fact that angina pectoris is associated with approximately one fifth of ischemic episodes of the myocardium in patients with chronic ischaemic heart disease. This was later expressed objectively by further methods which with a different sensitivity and specificity can diagnose current myocardial ischaemia. It was found that developing myocardial ischaemia is gradually manifested within several to tens of seconds by detectable metabolic changes (PET, sampling from the coronary sinus), changes at the level of the microcirculation with impaired perfusion (thalium scan, contrast echocardiography, PET, contrast angiography), impaired diastolic function of the left ventricle (direct assessment of pressures, Doppler echocardiography), regional disorders of left ventricular kinetics (contrast ventriculography, echocardiography, isotope ventriculography). Only after that electrocardiographic signs of myocardial ischaemia develop, in some patients associated with angina pectoris. It is obvious that the diagnosis of myocardial ischaemia by electrocardiographic signs and subjective manifestations is late and not very sensitive.
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PMID:[Role of electrocardiography in the diagnosis of silent myocardial ischemia]. 1274 19

Therapeutic angiogenesis, in the form of growth factor protein administration or gene therapy, has emerged as a new method of treatment for patients with severe, inoperable coronary artery disease. Improved myocardial perfusion and function after the administration of angiogenic growth factors has been demonstrated in animal models of chronic myocardial ischemia. A recent clinical study reported beneficial long-term effects of therapeutic angiogenesis using FGF-2 protein in terms of freedom from angina and myocardial perfusion on nuclear imaging and suggested that protein angiogenic therapy has the potential to extend treatment options to patients who are not optimal candidates for conventional methods of myocardial revascularization. The ultimate role that angiogenesis will play in the treatment of ischemic heart disease will, however, be determined from adequately powered, randomized, double-blind, placebo-controlled trials. It is likely that endogenous antiangiogenic influences, intrinsic lack of response of patients with severe endothelial dysfunction, and other limitations will have to be overcome before angiogenesis becomes standard therapy for the treatment of coronary artery disease.
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PMID:Angiogenic protein therapy. 1297


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