Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anomalous origin of the right coronary artery from the left sinus of Valsalva is a rare congenital anomaly classified as a "minor" anomaly of no clinical importance. Recently, manifestations of myocardial ischemia (angina pectoris, myocardial infarction, nonfatal ventricular fibrillation, sudden death) have been described in patients with this anomaly in the absence of atherosclerosis or other. Sudden death occurs frequently in symptomatic patients and rarely in asymptomatic patients (sudden unexpected death). In this study we report two cases of juvenile sudden death observed in asymptomatic patients with anomalous origin of the right coronary artery from the left sinus of Valsalva. In both cases the sudden death was exertion-related. In case 1 the coronary anomaly was the cause of death, since it was the only significant anatomic abnormality at necropsy; the microscopic findings revealed ischemic lesions only in the myocardium supplied by the anomalous right coronary artery. In case 2 the coronary anomaly was connected to other cardiac and non cardiac diseases (lymphocytic active myocarditis, chronic portitis, encephalitis, medullary adrenalitis). Since these morphologic lesions were extremely slight and there was no adrenal catecholamine damage in the myocardium, we consider negligible their possible role in determining death, which in this case was induced by the congenital coronary anomaly. The cardiac microscopic findings, also in this case, revealed ischemic lesions in the myocardium supplied by the anomalous right coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anomalous origin of the right coronary from the left sinus of Valsalva. A possible cause of juvenile sudden death]. 817 67

Much progress has been made in defining the mechanisms by which altered systolic and diastolic function of the heart may be produced by components of the immune system activated during allograft rejection and myocarditis and in patients with dilated cardiomyopathy. It is clear that injury of the vascular bed can occur via both humoral and cellular mediators and probably accounts for the acute alterations in ventricular compliance that occur during allograft rejection, as well as the accelerated development of graft atherosclerosis. Altered myocyte function and lysis can be produced by CTL in vitro, but the importance of this injury process in vivo remains uncertain. Other cells present in the inflammatory infiltrate can also affect myocyte function and survival. Neutrophils may cause lysis of myocytes, and cytokines produced by infiltrating macrophages and HtL may reach a sufficient concentration in the interstitial microenvironment to decrease myocyte catecholamine responsiveness and/or directly depress myocyte contractility. Humoral antibodies to myocyte cell surface antigens may cause cell damage by an antibody-dependent cytotoxic cell mechanism or by directly binding to and altering sarcolemmal receptor and/or ion channel function. Further elucidation of the extent of involvement of these different mechanisms in specific clinical settings may provide a basis for improved therapy of immune-mediated cardiac injury and dysfunction.
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PMID:Mechanisms of immune-mediated myocyte injury. 818 Nov 67

Between November 1992 and April 1993, 864 coronary angiographies were performed at our institution. In 14 patients (1.6%), no significant coronary disease (> 50% stenosis) was found despite documented myocardial infarction. Of these, 2 patients (0.2%), aged 46 and 33 years, had perfectly smooth coronary arteries at angiography. The most commonly postulated mechanism of myocardial infarction in such patients is coronary spasm with superimposed thrombosis. The same risk factors as those operative in atherosclerotic coronary artery disease are thought to play a role in this setting. The prognosis is good. In one of the patients with < 50% stenosis of coronary vessels, a history of cocaine abuse could be elicited as the possible causal factor of acute myocardial infarction. Cocaine-induced coronary spasm can lead to arrhythmias, myocardial infarction or accelerated coronary atherosclerosis even in patients with normal coronary arteries. Myocarditis must be considered in the differential diagnosis of acute myocardial infarction in young patients with chest pain, typical electrocardiographic and enzymatic changes but without risk factors.
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PMID:[Myocardial infarct in patients with normal coronary arteries]. 818 2

The term "idiopathic" ventricular fibrillation is used to describe those episodes of unexpected sudden arrhythmic death due to ventricular fibrillation in patients with no demonstrable structural heart disease. Idiopathic ventricular fibrillation has been reported to account for 5-100% of all sudden arrhythmic deaths. Post mortem analysis have shown that about 80% of patients might have some kind of structural anomalies, mainly atherosclerosis, myocarditis, or right ventricular dysplasia. Follow-up of patients with idiopathic ventricular fibrillation has shown a high incidence of recurrent episodes of malignant ventricular arrhythmias. The absence of structural heart disease generally implies an excellent long-term prognosis if ventricular fibrillation can be avoided. Patients with an implantable defibrillator should have a mortality rate similar to the general population. New subsets of patients are being recognized as belonging with those previously classified as idiopathic ventricular fibrillation. More than 60 patients have been identified in different centers around the world with the so-called "right bundle branch block, ST segment elevation, and sudden death syndrome." Recurrence rate of malignant ventricular arrhythmias is very high in these patients, despite antiarrhythmic therapy. An implantable cardioverter-defibrillator seems the treatment of choice. Asymptomatic forms of the syndrome have been described. Follow-up in these asymptomatic patients has shown that some of them might become symptomatic during follow-up. Also, intermittent forms of the syndrome have been described, with transient normalization of the electrocardiogram. Administration of class I drugs in these patients unmasks the typical electrocardiographic pattern. In some of the patients previously classified as having idiopathic ventricular fibrillation, ajmaline or procainamide administration unmasks the electrocardiographic pattern of the syndrome, suggesting that its incidence may be higher than previously suspected.
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PMID:What to do in patients with no structural heart disease and sudden arrhythmic death? 882 Aug 39

One hundred and fifty-four (5.7%) of 2690 patients who had been admitted to a hospital for sarcoidosis of intrathoracic lymph nodes (ITLN) were diagnosed as having various cardiovascular diseases (hypertensive disease, congestive lung, congenital and acquired cardiac diseases, atherosclerosis, aortic aneurysms and myocarditis). Misinterpretation of the X-ray film of the lung root, no lateral X-ray films, inadequate scope of objective studies of the cardiovascular system are the most common errors at prehospital examination. The obligatory making of lateral X-ray films, tomograms, the use of computed tomography, ECG and phonocardiography, and thorough account of objective data are valuable additional methods in the differential diagnosis of ITLN sarcoidosis and cardiovascular diseases accompanied by the appearance of wide truncal large vessels of the root due to pulmonary hypertension.
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PMID:[The differential diagnostic characteristics of sarcoidosis of the intrathoracic lymph nodes and of cardiovascular diseases]. 902 96

Application of molecular genetic tools to inherited cardiovascular disorders has provided important insights into the molecular mechanisms underlying cardiomyopathies, arrhythmias, blood pressure regulation, and atherosclerosis. In addition, alteration of gene expression has been observed under common cardiovascular conditions such as cardiac hypertrophy and heart failure. Recent advances in transgenic and gene-targeting approaches allow a sophisticated manipulation of the mouse genome by gene addition, gene deletion, or gene modifications. These transgenic models enable the dissection of in vivo pathways responsible for these complex disease phenotypes. This review describes tissue-specific promoters suitable for targeting candidate genes to the cardiovascular system as well as a number of valuable transgenic animal models of blood pressure regulation, atherogenesis, defects in the coagulation system, cardiac hypertrophy, myocarditis, cardiomyopathies, and heart failure. Limitations and difficulties associated with these transgenic approaches are discussed. Animal models which may provide a basis for future gene therapy of cardiovascular diseases are introduced. Finally, methods are described to regulate the spatial and temporal expression level of a transgene, to inactivate a target gene in a tissue-specific manner, and to introduce specific mutations into the genome. These recent advances in transgenic technology are expected to have a considerable impact on cardiovascular research in the near future.
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PMID:Transgenic animal models: new avenues in cardiovascular physiology. 908 29

The relation between cocaine use and cardiovascular disease has been well documented including coronary artery vasoconstriction, coronary thrombosis, accelerated atherosclerosis, myocarditis, cardiomyopathies and endocarditis. Cocaine use has reached epidemic proportions. Cocaine is the most commonly abused drug among young patients. We report the case of a 32-year-old male admitted to the emergency department with myocardial infarction secondary to an overdose of cocaine.
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PMID:[Acute myocardial infarction occurring in a young man due to crack use]. 918 11

Sudden cardiac death is the leading cause of death in industrialized countries. It is most frequently due to ventricular tachyarrhythmias occurring in the presence of coronary heart disease, but mechanisms linking sudden death to coronary atherosclerosis are still unclear. In autopsy studies of sudden death patients, the incidence of acute thrombotic coronary occlusions has varied between 4 and 74%. In over 600 consecutive patients with implantable cardioverter-defibrillators, we observed that appropriate shocks for electrogram-verified ventricular tachyarrhythmias was only very rarely followed by signs of acute myocardial infarction (< 3% of cases), not supporting the coronary occlusion theory of fatal arrhythmias. Cellular hypertrophy compensating for cell loss due to ischemia, intraventricular hypertension, cardiomyopathy, and myocarditis might play a role in arrhythmogenesis as evidenced by the fact that experimental induction and regression of hypertrophy are paralleled by changes in the inducibility of ventricular tachyarrhythmias. Atherogenic hyperlipidemias are associated with a systemic inflammatory response manifested by leukocytosis (lymphocytosis) and complex upregulations of proinflammatory-prothrombotic mediators, such as platelet-activating factor, cytokines, and hemostasis factors. The diurnal regulation of these mediators parallels circadian rhythms of coronary morbidity and mortality. Some upregulated mediators have been shown to exert direct arrhythmogenic effects. The potential contribution of hyperlipidemia-associated inflammatory factors to arrhythmogenesis is important, because it opens new molecular targets for antiarrhythmic drug design.
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PMID:Sudden cardiac death: still more questions than answers. 947 68

Histamine H1 receptor expression has been reported to change in disorders such as allergic rhinitis, autoimmune myocarditis, rheumatoid arthritis and atherosclerosis. Here we report the isolation and characterization of genomic clones containing the 5' flanking (regulatory) region of the human histamine H1 receptor gene. An intron of approx. 5.8 kb was identified in the 5' untranslated region, which suggests that an entire subfamily of G-protein-coupled receptors may contain an intron immediately upstream of the start codon. The transcription initiation site was mapped by 5' rapid amplification of cDNA ends to a region 6.2 kb upstream of the start codon. Immediately upstream of the transcription start site a fragment of 1.85 kb was identified that showed promoter activity when placed upstream of a luciferase reporter gene and transiently transfected into cells expressing the histamine H1 receptor. The promoter sequence shares a number of characteristics with the promoter sequences of other G-protein-coupled receptor encoding genes, including binding sites for several transcription factors, and the absence of TATA and CAAT sequences at the appropriate locations. The promoter sequence described here differs from that reported previously [Fukui, Fujimoto, Mizuguchi, Sakamoto, Horio, Takai, Yamada and Ito (1994) Biochem. Biophys. Res. Commun. 201, 894-901] because the reported genomic clone was chimaeric. Furthermore our study provides evidence that the 3' untranslated region of the H1 receptor mRNA is much longer than previously accepted. Together, these findings provide a complete view of the structure of the human histamine H1 receptor gene. Both the coding region of the H1 receptor gene and its promoter region were independently mapped to chromosome 3p25.
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PMID:Structure of the human histamine H1 receptor gene. 979 9

From 1978 to 1993 in the Veneto region, we collected 200 cases of sudden death in the young (</=35 years). Sudden death was cerebral in 15 cases (7.5%), respiratory in 10 (5%), and cardiovascular in 163 (81.5%), whereas it remained unexplained in 12 cases (6%). Among cardiovascular sudden death, obstructive coronary atherosclerosis accounted for 23% of cases, arrhythmogenic right ventricular cardiomyopathy for 12.5%, mitral valve prolapse for 10%, conduction system abnormalities for 10%, congenital coronary artery anomalies for 8.5%, myocarditis for 7.5%, hypertrophic cardiomyopathy for 5.5%, aortic rupture for 5.5%, dilated cardiomyopathy for 5%, nonatherosclerotic-acquired coronary artery disease for 3.5%, postoperative congenital heart disease for 3%, aortic stenosis for 2%, pulmonary embolism for 2%, and other causes for 2%. Cardiac arrest remained unexplained in 6% of the cases. Specific pathology and pathogenetic mechanisms of each disease were investigated and correlated with clinical signs and symptoms in detail. A large spectrum of cardiovascular disorders, both congenital and acquired, may represent the organic substrate of sudden death in the young. The underlying abnormality is frequently concealed and discovered only at postmortem examination. Most of the diseases, although asymptomatic, are potentially detectable during life with proper imaging tests.
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PMID:Cardiovascular causes of sudden death in young individuals including athletes. 1042 63


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