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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52-year-old man, having been treated for 4 months with chlorpropamide for diabetes mellitus type II, developed severe cholestatic hepatitis following a short course of erythromycin ethylsuccinate. Despite prompt withdrawal of both drugs, the cholestatic picture worsened and was associated with morphological evidence of disappearing interlobular bile ducts. After a 2-year course of profound cholestasis complicated by steatorrhea and striking hyperlipidemia, the patient died of ischemic cardiomyopathy. It is believed that this is the first published case of irreversible cholestasis with disappearance of ducts potentially related to a metabolic interaction between erythromycin ethylsuccinate and chlorpropamide.
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PMID:Prolonged cholestasis and disappearance of interlobular bile ducts following chlorpropamide and erythromycin ethylsuccinate. Case of drug interaction? 326 70

From November 1985 to July 1993, 29 out of 241 patients (12%) who underwent heart transplantation (HTx) at our institution had one or more "classical" contraindications to HTx: age > or = 60 years (20 patients); insulin-dependent diabetes mellitus (5 patients); irreversible renal failure requiring combined heart-kidney transplantation (2 patients); previous surgery for malignancy (1 patient); familial hypercholesterolemia (1 patient) and active systemic infection (1 patient). The main indication for HTx was ischemic cardiomyopathy (21 patients, 61%). Immunosuppression regimen consisted of Cyclosporine and Azathioprine, oral prednisone being subsequently added in 6 patients because of persistent rejection. There were 2 perioperative deaths and one late death. Follow-up ranged from 1 to 88 months (mean, 28 +/- 20) with an actuarial survival at 5 years of 85 +/- 8%. Annual cardiac catheterization demonstrated normal graft function and coronary arteries in all. No significant differences in survival, incidence of rejection and infection, renal function and duration of hospitalization were found when these patients were compared with those with no contraindications to HTx. In conclusion, HTx can be performed with good early clinical results in selected patients with "classical" contraindications to HTx; longer follow-up, however, is needed to confirm whether extension of the recipient selection criteria justified.
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PMID:Results of heart transplantation by extending recipient selection criteria. 799 27

We retrospectively analyzed 275 consecutive transplanted patients, dividing them into group A (128 patients) affected by ischemic cardiomyopathy and group B (147 patients) affected by dilated cardiomyopathy. The difference in demographic, clinical and hemodynamic preoperative and postoperative data between the groups was studied; group A patients presented at transplantation with a less compromised hemodynamic picture, requiring inotrope infusion and mechanical assistance less frequently. The influence of etiology on early postoperative complications was also analyzed: group A patients needed postoperative mechanical assistance, inotrope, infusion and prolonged mechanical ventilation more often, therefore requiring a longer stay in the intensive care unit (ICU). Hospital mortality was twice as high in group A. The older age of group A patients per se did not influence these results significantly. The long-term follow-up was then studied with particular attention to parenchymal functions, hemodynamics, coronary artery disease, metabolic and surgical complications, and survival. The complication rate was higher in group A, with more severe hypertension and higher cholesterol levels at 1 year, a higher prevalence of accelerated coronary artery disease (CAD) and a more frequent onset of insulin-dependent diabetes. Surgical and vascular complications were also more frequent. The final result was a better 5-year actuarial survival rate for group B patients. Donor and recipient ages at the time of transplant did not influence this result. We conclude that ischemic patients, even if they are transplanted in better condition and operated more electively, have a more critical early and long-term postoperative course and a worse survival rate. These findings are not explained by advanced age, but could be due to the impact of atherosclerosis and metabolic impairments associated with ischemic disease.
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PMID:Different results of cardiac transplantation in patients with ischemic and dilated cardiomyopathy. 875 Dec 54

AIM OF THE STUDY: Heart failure is the final clinical presentation of a variety of cardiovascular diseases, such as coronary artery disease, hypertensive, toxic, and inflammatory heart disease. However, the cellular mechanisms responsible for the progressive deterioration of myocardial function observed in heart failure remain unclear and may result from cell death (programmed or not) and from an increase in number of nuclei and in the degree of their ploidy. METHODS: We examined thirty-eight explanted hearts obtained during transplantation for DNA content in the myocytic population. All thirty-eight patients had severe chronic heart failure: 23 had idiopathic dilated cardiomyopathy, and 15 had ischemic cardiomyopathy. Ten hearts of people whose death was not due to primary heart disease or as a consequence of major risk factors of coronary artery disease, including hypertension, diabetes, obesity, or severe atherosclerosis, were used as controls. DNA content in the myocytic population was evaluated using Image Cytometry. RESULTS: The DNA content per nucleus and per myocyte in cardiomyopathic hearts are characterized by: a) a decrease of the diploid DNA content of myocytic nuclei; b) an increase of DNA ploidies higher than 4c; c) a decrease in mononucleated myocytes; d) an increase in binucleated and multinucleated myocytes. The changes are more prominent in dilated cardiomyopathy. e) The total ploidy index, used to calculate the total DNA content, is related to heart weight and ventricular weight. CONCLUSIONS: Ischemic and dilated cardiomyopathies result in reduction of ventricular mass-to-chamber volume ratio and in discrete foci of myocyte cell death, leading to an elevation in systolic and diastolic stress on the remaining viable cells. Therefore mechanical stimuli generated by global and local loading abnormalities associated with end-stage failure may contribute to activate genes implicated in cell proliferation. Observations in this investigation are consistent with recent results documenting that in the presence of overload conditions the myocytes may retain their capacity to proliferate throughout life and this growth reserve mechanism may become operative in response to severe myocardial dysfuntion and overt failure. Polyploidization and multinucleation are prominent phenomena in the end-stage of ischemic and dilated cardiomyopathy in humans.
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PMID:DNA Content in End-Stage Heart Failure. 1035 69

The diagnosis coronary artery disease is classically based on patient's symptoms and morphology, as analyzed by angiography. The importance of risk factors for the development of coronary atherosclerosis and disturbance of coronary vasomotion is clearly established. However, microembolization of the coronary circulation has also to be taken into account. Microembolization may occur as a single or as multiple, repetitive events, and it may induce inflammatory responses. Spontaneous microembolization may occur, when the fibrous cap of an atheroma or fibroatheroma (Stary i.v. and Va) ruptures and the lipid pool with or without additional thrombus formation is washed out of the atheroma into the microcirculation. Such events with progressive thrombus formation are known as cyclic flow variations. Plaque rupture occurs more frequently than previously assumed, i.e. in 9% of patients without known heart disease suffering a traffic accident and in 22% of patients with hypertension and diabetes. Also, in patients dying from sudden death microembolization is frequently found. Patients with stable and unstable angina show not only signs of coronary plaque rupture and thrombus formation, but also microemboli and microinfarcts, the only difference between those with stable and unstable angina being the number of events. Appreciation of microembolization may help to better understand the pathogenesis of ischemic cardiomyopathy, diabetic cardiomyopathy and acute coronary syndromes, in particular in patients with normal coronary angiograms, but plaque rupture detected by intravascular ultrasound. Also, the benefit from glycoprotein IIb/IIIa receptor antagonist is better understood, when not only the prevention of thrombus formation in the epicardial atherosclerotic plaque, but also that of microemboli is taken into account. Microembolization also occurs during PTCA, inducing elevations of troponin T and I and elevations of the ST segment in the EKG. Elevated baseline coronary blood flow velocity, as a potential consequence of reactive hyperemia in myocardium surrounding areas of microembolization, is more frequent in patients with high frequency rotablation than in patients with stenting and in patients with PTCA. The hypothesis of iafrogenic microembolization during coronary interventions is now supported by the use of aspiration and filtration devices, where particles with a size of up to 700 microns have been retrieved. In the experiment, microembolization is characterized by perfusion-contraction mismatch, as the proportionate reduction of flow and function seen with an epicardial stenosis is lost and replaced by contractile dysfunction in the absence of reduced flow. The analysis of the coronary microcirculation, in addition to that of the morphology and function of epicardial coronary arteries, and in particular appreciation of the concept of microembolization will further improve the understanding of the pathophysiology and clinical symptoms of coronary artery disease.
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PMID:Coronary microembolization--its role in acute coronary syndromes and interventions. 1060 63

The most common causes of the heart failure syndrome are coronary heart disease, dilated cardiomyopathy, secondary decompensated hypertension and cardiac defects. Apart from the establishment of the diagnosis, essential diagnostic aims are the clarification of the etiology, the identification of reversible causes, the clarification of specific therapeutic options, assessment of severity and evaluation of the prognosis. A standardized diagnostic work-up based on current consensus recommendations, makes good sense. Symptoms and clinical findings have limited sensitivity and specificity. The leading diagnostic procedure is (Doppler) echocardiography. In the case of ischemic cardiomyopathy, the angiographic coronary status and myocardial vitality evaluation are necessary to clarify the revascularisation option. Further diagnostic examinations (invasive hemodynamics, myocardial biopsy, CT/MRI, ergospirometry, markers of neurohormonal activation) should be carried out as dictated by the individual situation. In patients with an increased risk of developing heart failure (e.g. post-myocardial infarction status, essential hypertension, diabetes mellitus) the aim should be the early detection of an asymptomatic ventricular dysfunction by means of echocardiography.
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PMID:[Diagnostic procedures in chronic heart failure. What is necessary, significant, contraindicated?]. 1253 41

Our aim is to summarize and discuss the recent literature linking diabetes mellitus with heart failure, and to address the issue of the optimal treatment for diabetic patients with heart failure. THE STUDIES LINKING DIABETES MELLITUS (DM) WITH HEART FAILURE (HF) : The prevalence of diabetes mellitus in heart failure populations is close to 20% compared with 4 to 6% in control populations. Epidemiological studies have demonstrated an increased risk of heart failure in diabetics; moreover, in diabetic populations, poor glycemic control has been associated with an increased risk of heart failure. Various mechanisms may link diabetes mellitus to heart failure: firstly, associated comorbidities such as hypertension may play a role; secondly, diabetes accelerates the development of coronary atherosclerosis; thirdly, experimental and clinical studies support the existence of a specific diabetic cardiomyopathy related to microangiopathy, metabolic factors or myocardial fibrosis. Subgroup analyses of randomized trials demonstrate that diabetes is also an important prognostic factor in heart failure. In addition, it has been suggested that the deleterious impact of diabetes may be especially marked in patients with ischemic cardiomyopathy. TREATMENT OF HEART FAILURE IN DIABETIC PATIENTS : The knowledge of the diabetic status may help to define the optimal therapeutic strategy for heart failure patients. Cornerstone treatments such as ACE inhibitors or beta-blockers appear to be uniformly beneficial in diabetic and non diabetic populations. However, in ischemic cardiomyopathy, the choice of the revascularization technique may differ according to diabetic status. Finally, clinical studies are needed to determine whether improved metabolic control might favorably influence the outcome of diabetic heart failure patients.
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PMID:Influence of diabetes mellitus on heart failure risk and outcome. 1255 46

Cardiovascular (CV) disease in uremic patients is a major concern to the nephrologist because it represents the main cause of morbidity and mortality in chronic renal failure patients, both predialysis and while on dialysis therapy. CV mortality is 3 to 20 times higher in dialysis patients than in the general population at similar age. Of note, a high prevalence of CV comorbidity is already present at start of maintenance dialysis, and is predictive of subsequent mortality on dialysis. CV disease progresses over years prior to the onset of ESRD, because risk factors develop from the early stage of chronic renal insufficiency. However, CV disease may be prevented or attenuated in patients who benefit from early, regular care of CV risk factors. Mechanisms of uremic cardiopathy, the major cause of mortality in uremic patients, are multifactorial and their effects are cumulative. Risk factors for left ventricular hypertrophy are hypertension, anemia, fluid overload and arteriosclosis, all of which are amendable by therapy. Risk factors for accelerated atherosclerosis, responsible for ischemic cardiopathy and myocardial infarction, are both common factors (e.g., hypertension, tobacco smoking and diabetes) and factors more specific for the uremic state (e.g., dyslipidemia, hyperhomocysteinemia and oxidative stress), all of which also are amendable by proper therapy. As a result, mixed hypertensive and ischemic cardiomyopathy develops, ultimately leading to cardiac failure, together with accidents resulting from valvular and arterial calcifications (favored by calcium-phosphate disorders), and from occlusion of coronary, cerebral and peripheral arteries. Cardioprotective therapy thus has become a cornerstone in the management of chronic renal failure patients, in conjunction with renoprotective therapy. Cardioprotective strategy involves optimal treatment of hypertension, anemia, fluid overload, dyslipidemia, hyperhomocysteinemia and calcium-phosphate disorders, and smoking cessation. To achieve a maximal efficacy, such treatment has to be initiated as early as possible in the course of renal failure. Because of its complexity, the integrated combined nephrotective and cardioprotective therapy requires early and sustained guidance by a nephrologist throughout the whole predialysis period.
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PMID:[Cardioprotection: an essential component for predialysis chronic renal failure treatment]. 1272 13

Diabetes is a risk factor for coronary atherosclerosis, myocardial infarction, and ischemic cardiomyopathy. Insulin resistance is associated with left ventricular (LV) hypertrophy and hypertensive cardiomyopathy. Even in the absence of coronary artery disease or hypertension, "diabetic cardiomyopathy" can develop because of myocardial autonomic dysfunction or impaired coronary flow reserve. The relationship between insulin resistance and cardiomyopathy is bidirectional. Systemic and myocardial glucose uptake is compromised in heart failure independent of etiology. These abnormalities are associated with cellular deficits of insulin signaling. Insulin resistance in heart failure can be detrimental, because transcriptional shifts in metabolic gene expression favor glucose over fat as a substrate for high-energy phosphate production. Although preexisting diabetes accelerates this process of "metabolic death," insulin resistance can also develop secondary to cardiomyopathy-associated overabundance of neurohormones and cytokines. Insulin resistance and fatty acid excess are potential therapeutic targets in heart failure, striving for efficient myocardial substrate utilization. Peroxisome proliferator activator receptor gamma (PPARgamma) agonists are antidiabetic agents with antilipemic and insulin-sensitizing activity. Experimental studies suggest salutary effects in limiting infarct size, attenuating myocardial reperfusion injury, inhibiting hypertrophic signaling and vascular antiinflammatory actions through cytokine inhibition. However, clinical applicability in diabetic patients experiencing heart failure has been hampered because of increased edema and even fewer reports of exacerbation associated with these compounds. Evidence to date argues for peripheral mechanisms of edema unrelated to central hemodynamics. Nevertheless, they are currently contraindicated in New York Heart Association (NYHA) III-IV patients, particularly in combination with insulin. Investigations are underway to decipher mechanisms, risks, and benefits of PPARgamma agonists, as well as the role of the structurally related PPARalpha receptor on cardiovascular metabolism and function.
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PMID:Peroxisome proliferator activator receptors (PPAR), insulin resistance, and cardiomyopathy: friends or foes for the diabetic patient with heart failure? 1507 85

Atrial fibrillation, the most frequent arrhythmia, has a growing incidence with increasing age and the most important complication of the disease is thromboembolic events that may be prevented by antivitamin K. They are the most efficient therapeutic class for the prevention of these events but they are associated with an increased haemorrhagic risk leading to a reduced prescription in general practice. Optimisation of the management should be based on an individual evaluation of the thromboembolic and haemorrhagic risks, taking into account age, the presence of an associated heart disease, hypertension, diabetes, history of cerebrovascular event, history of previous haemorrhagic event and the ability to achieve a stable target INR. The challenge in ventricular arrhythmias lies in identifying a high risk of sudden death, mainly related to ventricular fibrillation. In patients with structural heart disease, left ventricular dysfunction is the strongest predictor of sudden death. Non invasive markers such as non sustained ventricular tachycardia, late ventricular potentials, decreased heart rate variability and baroreflex sensitivity, and repolarization altemans are further elements to assess risk. However, most of these markers have a poor positive predictive value and a low specificity. In patients with normal hearts, genetic predisposition may in the future identify high risk patients. The electrophysiologic study with programmed ventricular stimulation remains a costly and invasive method and only has a strong positive predictive value in ischemic cardiomyopathy. More precise algorithms for risk stratification are thus needed that may help the strategy of therapy with prophylactic implantable cardioverter defibrillator in the future.
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PMID:[Risk stratification in atrial and ventricular arrhythmias]. 1679 27


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