Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, regional diastolic patterns and their relations with transmitral Doppler inflow were investigated in hypertrophic cardiomyopathy (HC) by pulsed Doppler tissue imaging (DTI). Doppler echocardiography and DTI of basal septum and lateral wall (apical 4-chamber view) were performed in 20 patients (15 men and 5 women) with HC and in 10 healthy subjects (7 men and 3 women). Diabetes, hypertension, coronary artery and valvular disease, mitral regurgitation, New York Heart Association functional classes III to IV, sinus tachycardia, atrial fibrillation, and inadequate echocardiograms were exclusion criteria. Peak velocity and time-velocity integral of early and late waves and their ratios, and deceleration and isovolumic relaxation times were determined by standard Doppler and by DTI at the septal and lateral wall levels. The 2 groups were comparable for age, heart rate, blood pressure, and ejection fraction. Transmitral peak velocity and time-velocity integral E/A ratios were reduced (both p <0.05) and deceleration and isovolumic relaxation times prolonged (both p <0.00001) in HC. Septal DTI showed lower peak velocity and time-velocity integral e/a ratios (p <0.00001 and p <0.001, respectively) and lengthened regional deceleration (p <0.01) and isovolumic (p <0.001) relaxation times. DTI of the lateral wall showed a prolongation of deceleration and isovolumic relaxation times (both p <0.01). By dividing HC according to transmitral E/A, 8 patients with E/A <1 had lower DTI septal e/a ratio (p <0.01) and prolonged septal deceleration and isovolumic relaxation times (both p <0.01) but no changes in DTI pattern of lateral wall than 12 patients with E/A > 1. In conclusion, DTI is useful and complementary to standard Doppler imaging to characterize diastolic properties in HC, reflecting a typical pattern of intramyocardial impaired relaxation at the level of hypertrophied septum and also providing information about the degree of this regional impairment. The lateral wall presents minor changes in diastolic times, which indicate how diastolic asynchrony is not confined to the hypertrophied segment in HC.
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PMID:Use of pulsed Doppler tissue imaging to assess regional left ventricular diastolic dysfunction in hypertrophic cardiomyopathy. 1172 73

The prevalence of coronary artery disease (CAD) and the incidence of new coronary events are similar in older men and women. Independent risk factors for new coronary events in older women include age, prior CAD, cigarette smoking, hypertension, diabetes mellitus, high serum total cholesterol and triglycerides, and low serum high-density lipoprotein cholesterol. Older women have a higher prevalence of hypertension than older men. In older women with hypertension, echocardiographic left ventricular hypertrophy is a powerful independent predictor of new coronary events, atherothrombotic brain infarction, and congestive heart failure (CHF). Older women have a higher prevalence of rheumatic mitral stenosis and of mitral annular calcium than older men. Older women and men have a similar prevalence of valvular aortic stenosis, aortic regurgitation, mitral regurgitation, hypertrophic cardiomyopathy, and idiopathic dilated cardiomyopathy. The prevalence and incidence of CHF increase with age. The prevalence of normal left ventricular ejection fraction associated with CHF increases with age and is higher in older women than in older men. The prevalence of chronic atrial fibrillation increases with age and is similar in older men and women. Atrial fibrillation is an independent predictor of new coronary events and thromboembolic stroke in older women. Older women with unexplained syncope should have 24-hour ambulatory electrocardiograms to determine whether pauses > 3 seconds are present, requiring permanent pacemaker implantation.
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PMID:Prevalence of heart disease in older women in a nursing home. 986 88

Cardiac involvement and its clinical course in a diabetic patient with a mitochondrial tRNA(Leu)(UUR) mutation at position 3243 is reported in a 54-year-old man with no history of hypertension. At age 46, an electrocardiogram showed just T wave abnormalities. At age 49, it fulfilled SV1 + RV5 or 6>35 mm with strain pattern. At age 52, echocardiography revealed definite left ventricular (LV) hypertrophy, and abnormally increased mitochondria were shown in biopsied endomyocardial specimens. He was diagnosed as having developed hypertrophic cardiomyopathy associated with the mutation. However, at age 54, SV1 and RV5,6 voltages were decreased, and echocardiography showed diffuse decreased LV wall motion and LV dilatation. Because he had mitochondrial diabetes, the patient's heart rapidly developed hypertrophic cardiomyopathy, and then it seemed to be changing to a dilated LV with systolic dysfunction. Rapid progression of cardiomyopathy can occur in mitochondrial diabetes.
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PMID:Rapid progression of cardiomyopathy in mitochondrial diabetes. 1008 76

The increased incidence of hypertrophic cardiomyopathy in children of diabetic mothers has already been demonstrated, but its prenatal diagnosis has not yet been extensively studied. The purpose of this prospective study was to evaluate the frequency, severity, and echocardiographic features of fetal hypertrophic cardiomyopathy in a population with several indications for prenatal echocardiography. From March 1987 to April 1991, 283 fetuses were submitted to comprehensive prenatal echocardiography, including M-mode measurements, cross-sectional imaging, Doppler studies, and color flow mapping. One hundred seventy-six were pregnancies complicated by previous or gestational diabetes. The diagnosis of disproportionate septal hypertrophy was made in 39 fetuses (mean septal thickness 7.12 +/- 1.6 mm), at a mean gestational age of 32 weeks. Diabetes mellitus was present in 36 of these pregnancies (92.3%). In four cases, nonimmune hydrops was detected. A systolic anterior motion of the mitral valve was present in three fetuses, but only one showed a gradient across the left ventricular outflow tract. Postnatal echocardiographic examination in 27 babies did not show false positivity. In ten cases, spontaneous regression of the septal hypertrophy was shown. There were three neonatal deaths, unrelated to the myocardial disease. We concluded that transient hypertrophic cardiomyopathy is a frequent entity, especially when associated with diabetes during gestation, being a potential cause for nonimmune hydrops. Fetal echocardiography is the method of choice for its prenatal diagnosis and should always be indicated in diabetic mothers.
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PMID:Role of prenatal echocardiography in the study of hypertrophic cardiomyopathy in the fetus. 1014 77

Postnatal exposure to steroids has been associated with hypertrophic cardiomyopathy (HCM) in the newborn. Such an effect has not been described in infants born to mothers who received antenatal steroids. We report three newborns whose mothers were treated with betamethasone prenatally in different doses, duration of time, and who developed various degrees of HCM diagnosed by echocardiography. There was no maternal evidence of diabetes except for one infant whose mother had a normal fasting and post-prandial blood glucose prior to steroid therapy, but an abnormal one hour postprandial glucose after 8 weeks of betamethasone therapy, with a normal HbA1 C level. There was no family history of HCM, no history of maternal intake of other relevant medications, and no hypertension in all three newborns. Follow-up echocardiography revealed complete resolution of the HCM changes in all infants. We suggest that repeated antenatal maternal steroid intake may cause changes of HCM in the newborn. These changes appear to be dose- and duration-related and are mostly reversible. Further prospective controlled studies to evaluate these observations and to investigate potential mechanisms are warranted.
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PMID:Transient hypertrophic cardiomyopathy in the newborn following multiple doses of antenatal corticosteroids. 1036 77

CAD is the most common cause of death in older men and was present in 44% of 664 men, mean age 80 years. Independent risk factors for new coronary events in older men include increasing age, prior CAD, cigarette smoking, hypertension, diabetes mellitus, high serum total cholesterol, and low serum HDL cholesterol. In older men with hypertension, echocardiographic LVH is a powerful independent predictor of new coronary events, atherothrombotic brain infarction, and CHF. In 554 older men with a mean age of 80 years, two-dimensional and Doppler echocardiography demonstrated that the prevalence of aortic stenosis was 14%, 1 + aortic regurgitation or greater was 31%, rheumatic mitral stenosis was 0.4, 1 mitral regurgitation or greater was 32%, mitral annular calcium was 35%, hypertrophic cardiomyopathy was 3%, idiopathic dilated cardiomyopathy was 1%, left atrial enlargement was 29%, LVH was 41%, and abnormal LVEF was 29%. The prevalence and incidence of CHF increase with age in older persons. The prevalence of a normal LVEF associated with CHF as a result of prior myocardial infarction or hypertension was 22% in men aged 60 to 69 years, 33% in men aged 70 to 79 years, 41% in men aged 80 to 89 years, and 47% in men aged 90 years or older.
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PMID:The older man's heart and heart disease. 1050 66

Diabetic fetopathy is still a common clinical problem correlated with a high morbidity of the neonate. These children are often macrosome, suffer from respiratory distress syndrome due to delayed lung maturity, acidosis, hypoglycaemia, electrolyte-imbalances and polycythaemia. We describe a male neonate with diabetic fetopathy as a result of gestational diabetes of the mother. In addition to the symptoms described above, our patient clinically presented with severe hypertrophy of the right ventricle associated with intrauterine heart failure. The boy was born with serious prenatal asphyxia which made initial neonatal intensive care treatment necessary. The hypertrophic cardiomyopathy normalized within 6 weeks after birth without further treatment. Different causes of a hypertrophic cardiomyopathy (infections, metabolic disorders, neurologic affections, syndromes) could be ruled out, so that the diabetic fetopathy was the most probable cause for the condition. If we are looking at the heart only, this case-report suggests a good prognosis of septumhypertrophy as well as right ventricular hypertrophy in patients with diabetic fetopathy. The case also elucidates that not only the diabetes type I can entail serious fetal damage but also gestational diabetes can. Therefore, in suspect mothers screening for gestational diabetes should be expanded to oral glucose tolerance testing.
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PMID:[Heart failure caused by myocardial hypertrophy in diabetic fetopathy]. 1059 17

We describe an 8-day-old baby girl presenting a fatal infantile form of hypertrophic obstructive cardiomyopathy, associated with an A8296G mutation in the mitochondrial tRNA(Lys) gene. She was born from a healthy unrelated couple, and was the first infant of dizygotic twins. Soon after birth, she was noted to have tachypnea and generalized hypotonia. She had high levels of lactate and pyruvate, and was diagnosed as having hypertrophic cardiomyopathy using echocardiography. She died by cardiac failure. Mitochondrial DNA analysis was performed by sequencing after PCR-subcloning methods, and the percentage of mutation was measured using PCR-RFLP methods. In various tissues obtained at autopsy, analysis showed a heteroplasmic population of A8296G mutation in the mitochondrial tRNA(Lys) gene in all the tissues examined. Maternal inheritance was demonstrated in the family members. Our data demonstrated that an A8296G mutation in the mitochondrial tRNA(Lys) gene showed clinical heterogeneity from a milder form previously reported as mitochondrial diabetes mellitus, to a more severe form as hypertrophic obstructive cardiomyopathy, according to the spatial distribution of this mutation. Hum Mutat 15:382, 2000.
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PMID:Fatal hypertrophic cardiomyopathy associated with an A8296G mutation in the mitochondrial tRNA(Lys) gene. 1073 88

Atrial fibrillation is a major clinical problem that is predicted to be encountered more frequently as the population ages. The clinical management of atrial fibrillation has become increasingly complex as new therapies and strategies have become available for ventricular rate control, conversion to sinus rhythm, maintenance of sinus rhythm, and prevention of thromboembolism. Clinical and transthoracic echocardiographic features are important in determining etiology and directing therapy for atrial fibrillation. Left atrial size, left ventricular wall thickness, and left ventricular function have independent predictive value for determining the risk of developing atrial fibrillation. Left atrial size may have predictive value in determining the success of cardioversion and maintaining sinus rhythm in selected clinical settings but has less value in the most frequently encountered group, patients with nonvalvular atrial fibrillation, in whom the duration of atrial fibrillation is the most important feature. When selecting pharmacological agents to control ventricular rate, convert to sinus rhythm, and maintain normal sinus rhythm, transthoracic echocardiography (TTE) allows noninvasive evaluation of left ventricular function and hence guides management. The combination of clinical and transthoracic echocardiographic features also allows risk stratification for thromboembolism and hemorrhagic complications in atrial fibrillation. High-risk clinical features for thromboembolism supported by epidemiological observations, results of randomized clinical trials, and meta-analyses include rheumatic valvular heart disease, prior thromboembolism, congestive heart failure, hypertension, older (> 75 years old) women, and diabetes. Small series of cases also suggest those with hyperthyroidism and hypertrophic cardiomyopathy are at high risk. TTE plays a unique role in confirming or discovering high-risk features such as rheumatic valvular disease, hypertrophic cardiomyopathy, and decreased left ventricular function. Validation of the risk stratification scheme used in the Stroke Prevention in Atrial Fibrillation-III trial is welcomed by clinicians who are faced daily with balancing the benefit and risks of anticoagulation to prevent thromboembolism in patients with atrial fibrillation.
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PMID:Role of transthoracic echocardiography in atrial fibrillation. 1097 8

Mitral annulus calcification (MAC) is a chronic, non-inflammatory, degenerative process of the fibrous support structure of the mitral valve. It occurs more often in women and the elderly. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known that patient with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80s present a theory that MAC is a form of atherosclerosis. In order to test this theory we conducted during the last years a few clinical studies to examine the association of MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC and atheroma thickness. We also found in MAC patients higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of beta2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels. The purpose of this review is to summarize the data concerning MAC and atherosclerotic processes, emphasizing that MAC in itself may be an atherosclerotic process.
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PMID:Mitral annulus calcification--a window to diffuse atherosclerosis of the vascular system. 1122 20


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