Left ventricular microaneurysms as a cause of apparently idiopathic ventricular fibrillation.
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Biomedical subjects
Publications and source records attributed to J Auer.
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Abuse of the drugs like amphetamine, cocaine and "Ecstasy" may be complicated by intracerebral, subdural or subarachnoid haemorrhage. Contrary to historical opinion, drug-related intracranial haemorrhage (ICH) is frequently related to an underlying vascular malformation. We report the case of an 18-year-old man with a history of Ecstasy abuse preceding the onset of severe occipital headache. Cerebral computed tomography revealed right-sided subarachnoid haemorrhage and cerebral angiography showed right-sided middle cerebral artery aneurysm of 1 cm diameter. The patient was treated surgically with aneurysm clipping. Three weeks after onset of intracranial haemorrhage, neurological examination demonstrated normal findings. A history of severe headache immediately after using amphetamine, Ecstasy, or cocaine should alert doctors to the possibility of intracerebral haemorrhage. Arteriography should be part of the evaluation of most young patients with stroke or non-traumatic ICH.
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Recanalization of occluded coronary arteries is the aim of percutaneous interventions with acute myocardial infarction. Moreover, chronic coronary occlusion is a common finding during diagnostic coronary angiography and is often a contributing factor in the choice of revascularisation by surgery rather than by percutaneous coronary interventions (PCI). An occluded coronary artery with some degree of collateral supply is functionally comparable to a severe coronary stenosis. Therefore, recanalization of chronic occluded coronary arteries results in less angina and often in improvement of left ventricular function. Success is limited in particular in longer lasting occlusions. Characterization of lesions, where recanalization can performed successfully is warranted. We correlated primary success rates of attempted coronary recanalizations with localisation of lesions and procedural characteristics. We analyzed records of 124 consecutive patients, who underwent attempted coronary recanalization of chronically occluded coronary arteries at our institution in 1998. Revascularisation was successful in 84 (64 male, 20 female) of 124 (92 male, 32 female) patients. Therefore, success rate was 67.7% (69.9% in men, 62.5% in women, p = 0.42). Target vessel was the left anterior descending artery (LAD) in 49 cases. Success rate in the LAD did not differ significantly from that in "non-LAD"-vessels (65.3% versus 69.3%; p = 0.35). Successful recanalizations were performed using only one guide-wire in 77.3%. More than one guide-wires were used during procedures without success in 44.5% and exceeded use in successful interventions (p < 0.05). Procedures, failing to be successful after an attempt with a first guide-wire, could be performed successfully using at least a second wire in 50%. Coronary stenting after recanalization has been performed in 84.4% in the LAD and in 59.7% in non-LAD vessels (p < 0.01). Success rate of attempted recanalizations of chronic occluded coronary arteries in unselected patients is high. Most procedures can be performed successfully using only one guidewire. Additional use of other wires can increase success rates in procedures with primary failure to pass the occlusion. Stenting has been performed in three out of four patients with successful recanalization of chronically occluded coronary arteries.
Restenosis following angioplasty represents a major clinical problem in the field of percutaneous coronary interventions. Intravascular brachytherapy reduces risk of restenosis following percutaneous interventions of native lesions and in-stent restenosis up to 50%-60%. This effect can be shown for at least one to two years. This novel therapeutic strategy is limited by a higher rate of target vessel reinterventions, and late coronary thrombosis, when platelet inhibiting drugs has been withdrawn or after implantation of multiple stents. Currently, intracoronary brachytherapy is mainly considered for treatment of in-stent-restenosis.
Statins significantly reduce cardiovascular-related morbidity and mortality in patients with and without coronary artery disease. The potential of this drug class has yet to be fully explored. Accumulating evidence from basic research and clinical trials indicates that statins have pleiotropic effects that may largely account for the clinical benefits observed. Potential beneficial effects of these agents include enhancement of nitric oxide production in vasculature and the kidney. Statins have been shown to stabilize unstable plaques, improve vascular relaxation, and promote new vessel formation. Clinical trials and animal studies have shown that these agents reduce cardiovascular disease (CVD) risks and events, progression of nephropathy, development of diabetes, and fracture rates; these are benefits that go beyond lipid lowering alone. Potential beneficial effects are due to the positive impact on vascular and glomerular nitric oxide (NO) production and attenuation of vascular inflammation. Effects on bone, including fracture reduction, are thought to be mediated by direct action on bone formation. Moreover, potential reduction in the development of diabetes as observed in the West of Scotland Coronary Prevention Study (WOSCOPS) may relate to the improvement in insulin sensitivity. These actions are mediated, in part, by the effects on small G-proteins, modulation of signaling cascades, transcription, and gene expression. In particular, the inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the direct cellular effects of statins on the vascular wall. The clinical relevance of these effects is beginning to be recognized, and ongoing studies will be able to answer these many questions in the near future. Actions of statins on vascular, glomerular, bone, and insulin-sensitive tissue as well as effects of statins on cognitive function and oncoprotection will be discussed in this review.
BACKGROUND AND AIM: Epidemiological studies have suggested an association between higher body iron stores and coronary artery disease (CAD), but recent trials have reported conflicting data on the role of ferritin in CAD. To assess these findings, we examined the association between serum ferritin and the angiographic extent of coronary atherosclerosis in consecutive patients referred for coronary angiography. METHODS AND RESULTS: We studied 100 consecutive white subjects (41 women and 59 men; mean age 63.7 +/- 11.0 years) who underwent coronary angiography. The data collected at baseline included conventional risk factors for coronary artery disease (CAD), lipid and fasting total homocysteine levels, serum ferritin levels and transferrin saturation, and clinical characteristics. Serum ferritin levels and transferrin saturation (serum iron concentration divided by total iron-binding capacity) were used as measures of the amount of circulating iron available to tissues. Two experienced cardiologists blinded to the clinical and laboratory data reviewed the angiographic cinefilms, and defined the angiographic severity of CAD on the basis of the sum of three vessel scorring systems. The risk of CAD assessed by coronary angiography was not related to ferritin concentrations or transferrin saturation levels. The estimated relative risk of CAD for the fifth vs the first quintile of serum ferritin was 0.83 (95% CI: 0.63-1.24). Forty of the 100 patients had no or minimal CAD (group A; score 0-3), 33 moderate CAD (group B; score 4-8) and 27 severe CAD (group C; score > 8): the serum ferritin levels in the three groups were respectively 165 +/- 126, 167 +/- 121 and 164 +/- 110 ng/ml, and did not represent an independent risk factor for CAD (p = 0.98). Transferrin saturation in the three groups was 22.9 +/- 10%, 21 +/- 9% and 19.9 +/- 10%, with no significant relationship to the severity of CAD (p = 0.23). The presence of angiographic CAD was associated with patient age (p = 0.048), male gender (p < 0.01), high lowdensity lipoprotein cholesterol levels (p = 0.02), low high-density lipoprotein cholesterol levels (p = 0.02), high plasma fibrinogen levels (p < 0.01) and high fasting total homocysteine levels (p = 0.04). CONCLUSION: In patients referred for coronary angiography, higher ferritin concentrations and transferrin saturation levels were not associated with an increased extent of coronary atherosclerosis.
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This article aims to review lessons learned about lipid lowering and statins in the past decade and to consider what developments the future may hold. Results from a series of landmark clinical trials confirm that statins significantly reduce cardiovascular morbidity and mortality in patients with and without previous coronary artery disease. The potential of this drug class has yet to be fully explored. Studies currently under way will answer many of the outstanding questions.
UNLABELLED: CORONARY REVASCULARIZATION: PTCA in patients with refractory unstable angina is associated with a substantial risk of the following complications: death, myocardial infarction, need for emergency surgery, and restenosis. The introduction of intracoronary stents, however, has improved both short-term and long-term outcomes. The newer adjunctive pharmacologic therapies enhance even further the benefits associated with the use of stents. The decision regarding the specific revascularization procedure to be used (e.g., CABG, PTCA, stent placement, or atherectomy) is based on the coronary anatomy, the left ventricular function, the experience of the medical and surgical personnel, the presence or absence of coexisting illnesses, and the preferences of both the patient and the physician. RISK STRATIFICATION: Among patients with unstable angina or non-Q-wave myocardial infarction, there is an increased risk of death within 6 weeks in those with elevated troponin I levels and the risk of death continues to increase as the troponin level increases. Reversible ST segment depression is associated with an increase by a factor of 3-6 in the likelihood of death, myocardial infarction, ischemia at rest, or provocable ischemia during a test to stratify risk. Exercise or pharmacologic stress testing provides important information about a patient's risk. Although the conditions of the majority of patients with unstable angina will stabilize with effective antiischemic medications, approximately 50-60% of such patients will require coronary angiography and revascularization because of the "failure" of medical therapy. High-risk patients are those who have had angina at rest, prolonged angina, or persistent angina with dynamic ST segment changes or hemodynamic instability, and they urgently require simultaneous invasive evaluation and treatment. Medical therapy should be adjusted rapidly to relieve manifestations of ischemia and should include antiplatelet therapy (aspirin, or ticlopidine or clopidogrel if aspirin is contraindicated), antithrombotic therapy (unfractionated heparin or low-molecular-weight heparin), beta-blockers, nitrates, and possibly calcium-channel blockers. Early administration of glycoprotein IIb/IIIa inhibitors may be particularly important, especially in high-risk patients with positive troponin tests or those in whom implantation of coronary stents is anticipated.