Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fear, anger, and grief may precipitate myocardial ischemia and infarction. The prognosis of patients with inducible ischemia during mental stress is worse than in those without inducible ischemia. The sympathetic nervous system plays an important role in stress-associated changes in cardiovascular regulation and contributes to cardiovascular morbidity and mortality by inducing vasoconstriction and tachycardia, as well as arrhythmia. Hostility--previously termed type A personality--is often associated with sympathetic hyperreactivity to mental stress and carries an increased risk for atherosclerotic vascular disease. As endothelial dysfunction is an early manifestation of atherosclerosis, the impact of mental stress on endothelial function is also important. Acute mental stress induces prolonged endothelial dysfunction in healthy volunteers, which is prevented by selective endothelin A receptor antagonism. This represents an important link between mental stress and atherosclerotic vascular disease. In addition, patients with depression show hypercortisolemia, and changes in platelet function leading to a prothrombotic state. These findings help to explain the increased cardiovascular risk in patients with depression.
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PMID:[Pathophysiologic cardiovascular changes in stress and depression]. 1466 4

Diabetes mellitus is a common disease and contributes to a high degree of morbidity and mortality. Cardiovascular complications, including diabetic cardiomyopathy are major causes of morbidity and mortality in diabetic patients. Diabetic cardiomyopathy is a condition that affects the myocardium, primarily. It is not necessarily associated with ischemic heart disease, high blood pressure, valvular or congenital anomalies. The pathology of diabetic cardiomyopathy includes interstitial fibrosis, apoptosis of cardiomyocytes, abnormal energy utilization, small vessel disease and cardiac neuropathy. These pathologies are induced by hyperglycemia and oxidative stress. Biochemical as well as electrolyte changes, especially reduced calcium availability also occurs in the myocardium of diabetic patients. The abnormal structure and biochemistry of the myocardium result in functional problems such as diastolic and systolic dysfunctions, which may cause symptoms of dyspnea and inability to tolerate exercise. No single specific therapeutic agent can treat diabetic cardiomyopathy because once the disease is overt, the management may require a variety of approaches such as risk factors and lifestyle modification, glucose control (insulin, alpha glucosidase inhibitors, sulfonylureas, biguanides, meglitinides, thiazolidinediones and dipeptidyl peptidase 4 (DPP-4) inhibitors); hormones (IGF-1); ACE inhibitors (captopril, enalapril); angiotensin II receptor antagonists (losartan, olmesartan); beta adrenoreceptor antagonists (acebutolol, carvedilol); peptides (adrenomedullin); endothelin-1 receptor antagonists (bosentan, tezosentan); calcium channel blockers (amlodipine, verapamil); antioxidants (methalothionein, alpha tocopherol, alpha lipoic acid) and antihyperlipidemic drugs (simvastatin, fenofibrate, ezetimibe) to effectively treat patients with diabetic cardiomyopathy.
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PMID:Medicinal chemistry of drugs used in diabetic cardiomyopathy. 2001 35

Sudden cardiac death constitutes a major health-related problem. In the majority of cases, sudden cardiac death is due to ventricular tachyarrhythmias secondary to acute myocardial infarction. The pathophysiologic chain of events leading to ventricular tachyarrhythmias after acute coronary occlusion is complex and incompletely understood. Experimental and clinical studies have indicated that endothelin-1 production rises markedly very early in the course of myocardial infarction. Endothelin-1 exerts significant electrophysiologic actions on ventricular cardiomyocytes and participates in the genesis of ischemic ventricular tachyarrhythmias. Endothelin-1, acting via two G-protein-coupled receptors (ETA and ETB), prolongs the action potential duration and increases the occurrence of spontaneous calcium transients, resulting in early afterdepolarizations and ventricular tachyarrhythmias via triggered activity. Moreover, endothelin-1 enhances sympathetic stimulation, a well established contributor to ventricular arrhythmogenesis during acute myocardial infarction. Despite these considerations, the therapeutic potential of endothelin receptor antagonists as antiarrhythmic drugs during myocardial ischemia/infarction is still under investigation. To date, a number of endothelin-1 receptor antagonists are available, presenting different degrees of selectivity for ETA and ETB receptors. The arrhythmogenic effects of endothelin-1 are exerted mainly via stimulation of the ETA receptors, but the role of ETB receptors remains controversial, as previous studies have produced conflicting results. This review summarizes the current state-of-the-art on the role of endothelin-1 in the genesis of ventricular arrhythmias during acute myocardial infarction and raises some hypotheses that could be explored in future studies.
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PMID:Do endothelin receptor antagonists have an antiarrhythmic potential during acute myocardial infarction? Evidence from experimental studies. 2053 2