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)

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

Endothelin-1, the most potent endothelium-derived vasoconstrictor peptide identified so far, exerts multiple biologic effects that are potentially relevant for the pathogenesis of coronary atherosclerosis and ischemic heart disease. Since the discovery of the peptide, a good deal of experimental and clinical data have been accumulated to support an important role of endothelin-1 in ischemic heart disease. In experimental animals, exogenous endothelin-1 was found to cause coronary vasoconstriction and, at higher doses, ventricular fibrillation and death. Endothelin receptor subtypes have been demonstrated and pharmacologically characterized in the coronary vascular bed. The plasma levels of immunoreactive endothelin-1 were found to be increased in patients with coronary atherosclerosis, acute myocardial infarction, and angina. Given its growth-promoting and mitogenic action, endothelin-1 has also been suspected to participate in the mechanism of restenosis after PTCA. The purpose of this study was to critically review the experimental and clinical data supporting the involvement of endothelin-1 in ischemic heart disease and the results of more recent studies on the effects of endothelin-1 blockade on experimental myocardial necrosis and restenosis after PTCA.
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PMID:Endothelin-1: a scientist's curiosity, or a real player in ischemic heart disease? 896 76

The purpose of this report is to review the previous and current methods for the detection of a MB and to summarize results of work by other investigators as well as our own recent morphological studies with emphasis on work since 1983. We will discuss the presumable association of MBs with heart disorders, on the basis of significant publications. We describe the importance of both basic and clinical research for the assessment of MB influence in various heart disorders. Aspects covered are: (1) historical background of MBs and the relationship between the MB and CA; (2) general characteristics of MBs; (3) methods for studying MBs; (4) compressive effect of the MB on the CA; (5) clinical symptoms including myocardial ischemia, angina pectoris, myocardial infarction, development of atherosclerosis and thrombosis, ventricular fibrillation and sudden death; (6) treatment of MB-associated heart disorders by resection of MBs and (7) future research trends.
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PMID:Myocardial bridging as a factor in heart disorders: critical review and hypothesis. 922 44

To prevent the atheroembolic complications such as brain infarction due to the manipulation of atherosclerotic ascending aorta during cardiac surgery, the ascending aorta of 55 patients including 6 emergencies (mean age: 67.7 +/- 6.9 years, valvular disease: n = 12, ischemic heart disease only or combined with valvular disease: n = 43) were evaluated with intraoperative echography as a routine, to enable a proper placement of the cannulae, clamp etc. Irregular elevated lesions into the aortic lumen from the intima were identified in 7 patients (13%, mean age: 71.0 +/- 6.9 years) of ischemic heart disease, which included 2 emergent cases. Arch cannulation was employed in 3 patients with wide-spread lesions on the posterior wall and femoral cannulation was done in 1 patient with wide-spread lesions on the anterior wall. Two of these patients received CABG with in situ arterial conduits under ventricular fibrillation, and the other 2 patients received CABG with aortic cross clamping at the lesion-free site during proximal anastomosis of vein grafts (single clamp technique). Two patients with localized lesion were done CABG with partial aortic clamping and one of them had cerebral infarction during the operation. We recognized that manipulation of the ascending aorta has to be done with a meticulous care and well away from the diseased site. In another patient with localized lesion, the arch cannulation and the single clamp technique were used 2 cm away from that lesion. The brain infarcted patient completely recovered without any sequelae and the others also had no atheroembolic complications. Although calcified lesions on CT were correlated with atheromatous lesions on echogram (p = 0.004), these atheromatous plaques were not detected by enhanced CT, except in only one patient. For screening of the atherosclerosis of ascending aorta, the CT examination was not so effective and the intraoperative echography was the most sensitive and could be easily accomplished. In conclusion, in order to prevent the atheroembolism that might occur due to the improper manipulation of the diseased ascending aorta during usual procedures, surgical strategies have to be modified according to the position, extent and quality of the atherosclerotic lesions, diagnosed by intraoperative echoscanning of the aorta.
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PMID:[Modification of the surgical strategy based on intraoperative echographic findings of atherosclerotic ascending aorta]. 945 2

Low rates of coronary heart disease was found in Greenland Eskimos and Japanese who are exposed to a diet rich in fish oil. Suggested mechanisms for this cardio-protective effect focused on the effects of n-3 fatty acids on eicosanoid metabolism, inflammation, beta oxidation, endothelial dysfunction, cytokine growth factors, and gene expression of adhesion molecules; But, none of these mechanisms could adequately explain the beneficial actions of n-3 fatty acids. One attractive suggestion is a direct cardiac effect of n-3 fatty acids on arrhythmogenesis. N-3 fatty acids can modify Na+ channels by directly binding to the channel proteins and thus, prevent ischemia-induced ventricular fibrillation and sudden cardiac death. Though this is an attractive explanation, there could be other actions as well. N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. These cytokines decrease myocardial contractility and induce myocardial damage, enhance the production of free radicals, which can also suppress myocardial function. Further, n-3 fatty acids can increase parasympathetic tone leading to an increase in heart rate variability and thus, protect the myocardium against ventricular arrhythmias. Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1beta, IL-6 and IL-18. Exercise enhances parasympathetic tone, and the production of anti-inflammatory cytokine IL-10 which may explain the beneficial action of exercise in the prevention of cardiovascular diseases and diabetes mellitus. TNFalpha has neurotoxic actions, where as n-3 fatty acids are potent neuroprotectors and brain is rich in these fatty acids. Based on this, it is suggested that the principle mechanism of cardioprotective and neuroprotective action(s) of n-3 fatty acids can be due to the suppression of TNFalpha and IL synthesis and release, modulation of hypothalamic-pituitary-adrenal anti-inflammatory responses, and an increase in acetylcholine release, the vagal neurotransmitter. Thus, there appears to be a close interaction between the central nervous system, endocrine organs, cytokines, exercise, and dietary n-3 fatty acids. This may explain why these fatty acids could be of benefit in the management of conditions such as septicemia and septic shock, Alzheimer's disease, Parkinson's disease, inflammatory bowel diseases, diabetes mellitus, essential hypertension and atherosclerosis.
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PMID:Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how? 1113 72

An autopsied 85-year-old man had suffered from a mild form of diabetes mellitus since the age of 67 and had experienced the first episode of heart failure with arapid ventricular rate of atrial fibrillation at the age of 72. He had remained socially active until he died suddenly of ventricular fibrillation, although he had complications of aortic regurgitation at the age of 76 and later mitral regurgitation at the age of 80. Chest roentgenograms showed gradual increase in the cardiothoratic ratio which reached 68.1% at the final stage. Autopsy revealedmarked left ventricular hypertrophy with a heart weight of 580 g, degeneration ofaortic valves, thickening of mitralvalve cusps and moderate coronary atherosclerosis without ischemic myocardial lesions. There were no specific lesions suggestive of primary cardiomyopathies on microscopic observations and the lesions of both aortic and mitral valves were not significant enough to explain the clinical findings of aortic and mitral regurgitation. Because the pathological examination failed to identify a single disease which was responsible for the marked cardiachypertrophy, we eventually reached the conclusion that the cardiac hypertrophy developed based on a multifactorial heart disease.
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PMID:[An autopsied case of marked cardiac hypertrophy due to multifactorial heart disease in an 85 year-old man who had been socially active]. 1177 30

In selected patients suffering from variant angina, an implantable cardioverter-defibrillator (ICD) and coronary stenting can be helpful to prevent sudden death and treat coronary artery spasm. We report a case of a 47-year-old woman suffering from variant angina, who experienced an episode of ventricular fibrillation promptly cardioverted. After coronary angiography documentation of a mild atherosclerosis, an ICD was implanted and oral nitrates and calcium antagonists were prescribed. The recurrence of chest pain and palpitations prompted us to perform a second coronary angiography that documented a focal coronary artery spasm successfully treated with stent implantation. No other episodes of angina or ventricular arrhythmia were documented during the following 6 months of follow-up.
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PMID:Coronary vasospasm and aborted sudden death treated with an implantable defibrillator and stenting. 1202 77

Free radicals and oxidative stress play a crucial role in the pathophysiology of a broad spectrum of cardiovascular diseases including congestive heart failure, valvular heart disease, cardiomyopathy, hypertrophy, atherosclerosis and ischemic heart disease. We have demonstrated that IH636 grape seed proanthocyanidin extract (GSPE) provides superior antioxidant efficacy as compared to Vitamins C, E and beta-carotene. A series of studies were conducted using GSPE to demonstrate its cardioprotective ability in animals and humans. GSPE supplementation improved cardiac functional assessment including post-ischemic left ventricular function, reduced myocardial infarct size, reduced ventricular fibrillation (VF) and tachycardia, decreased the amount of reactive oxygen species (ROS) as detected by ESR spectroscopy and reduced malondialdehyde (MDA) formation in the heart perfusate. Cardiomyocyte apoptosis detected by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining. In concert, the proapoptotic signals mediated by JNK-l and c-fos proteins were also reduced suggesting that the novel cardioprotective properties of GSPE may be at least partially attributed to its ability to block anti-death signaling mediated through the proapoptotic transcription factors and genes such as JNK-1 and c-JUN. In a separate study, GSPE pretreatment significantly inhibited doxorubicin-induced cardiotoxicity as demonstrated by reduced serum creatine kinase (CK) activity, DNA damage and histopathological changes in the cardiac tissue of mice. Concentration-dependent efficacy of GSPE was also assessed in a hamster atherosclerosis model. Approximately 49 and 63% reduction in foam cells, a biomarker of early stage atherosclerosis, were observed following supplementation of 50 and 100 mg GSPE/kg body weight, respectively. A human clinical trial was conducted on hypercholesterolemic subjects. GSPE supplementation significantly reduced oxidized LDL, a biomarker of cardiovascular diseases. Finally, a cDNA microarray study demonstrated significant inhibition of inducible endothelial CD36 expression, a novel cardioregulatory gene, by GSPE. These results demonstrate that GSPE may serve as a potential therapeutic tool in promoting cardiovascular health via a number of novel mechanisms.
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PMID:Molecular mechanisms of cardioprotection by a novel grape seed proanthocyanidin extract. 1262 6

Coronary calcifications are specific markers for coronary atherosclerosis. The amount of coronary calcium is related to the likelihood of vulnerable plaques. Vulnerable plaques may rupture and may result in sudden coronary thrombus formation, occlusion, ischemia and ventricular fibrillation and finally cardiac death. Therefore, it is reasonable to believe that the risk of cardiac events can be assessed by the quantification of the extent of coronary calcium. However, until now, the predictive value of coronary calcium and the advantage over conventional risk factors has not yet been proven by any prospective cohort study. In practice uncertainty exists in the group of patients with an intermediate risk for cardiac events. In this particular cohort it is likely that the assessment of coronary atherosclerosis may help in the decision to initiate or discard a specific therapy. For this purpose it has been suggested to replace the Framingham age score by a score corrected by the amount of coronary calcium. Follow-up investigations may be helpful in the short term to determine the efficiency of different therapeutical options. To determine a significant progression of the amount of coronary calcium, the absolute mass should be determined in a period of 1 year.
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PMID:Estimation of cardiac event risk by MDCT. 1580 Oct 53

Sudden cardiac death (SCD) is an integral term for several heart diseases among which SCD caused by ischemic heart disease (IHD) designated as sudden coronary death (SCD) ranks first. SCD associated with alcoholic cardiomyopathy ranks second. Risk factors and pathologic manifestations of SCD correspond to those of IHD, atherosclerosis, myocardial infarction. Cardiac arrest takes place because of fibrillation of ventricular myocardium. Factor inducing fibrillation is an advanced irreversable myocardial ischemia complicated with reperfusion. The latter promotes elimination of arrythmogenic substances from the ishemic zone leading to electric unstability of the myocardium and fatal arrythmia. Possibility of idiopathic ventricular fibrillation and its mechanisms is discussed.
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PMID:[Sudden cardiac death: state of the art]. 1607 3


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