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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The application of molecular biology to human genetics has led to the development of a new field, human molecular genetics. This field has already had a dramatic impact on our understanding of cardiovascular disease and has helped improve diagnosis and treatment of these disorders. We have learned a great deal during the past decade about the long QT syndrome, familial hypertrophic cardiomyopathy, Duchenne muscular dystrophy, hypertension, and supravalvular aortic stenosis. In the coming decade, the pace of discovery will accelerate, offering new opportunities for the prediction and prevention of cardiovascular disease.
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PMID:Genetics of the long QT syndrome. 818 85

Nineteen consecutive patients with Turner's syndrome and different karyotypes underwent full cardiological evaluation (physical examination, electrocardiogram, chest X-ray and echocardiogram). Congenital heart disease was found in 26%. Other cardiovascular pathologies (long QT syndrome or systemic hypertension) were found in two patients. When compared with the general population, a higher incidence was present for all types of congenital heart diseases observed. Among cardiac anomalies in Turner's patients, aortic malformations (aortic coarctation and bicuspid aorta) were the most frequent, followed by patent ductus arterious and pulmonary valve stenosis. We have observed that the most severe malformations were preferably found with the 45,X karyotype. Pulmonary valve stenosis was found in a mosaicism 45,X/46,XX case. No anomaly was found in patients with X isochromosome. The ring pattern was not found in our series.
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PMID:[The Turner syndrome and cardiovascular changes]. 883 May 99

The management of unexplained syncope begins with the patient's history and physical examination, which are oriented to help separate benign from serious causes. Malignant etiologies are more likely to occur with exertional syncope. Cardiac causes should be considered, particularly cardiomyopathy, postoperative congenital heart disease, right ventricular dysplasia, anomalous coronary artery, pulmonary artery hypertension, myocarditis, long QT syndrome, and Wolff-Parkinson-White syndrome. Neurological and metabolic disorders may underlie a syncope episode. After malignant causes of syncope have been excluded and the diagnosis of neurocardiac syncope has been established, treatment strategies include behavior modification, salt and increased fluids, and pharmacological agents. Efficacious agents include beta-blockers, dysopyramide, fludrocortisones, and alpha agents. Yet, behavior modification alone may be as effective as salt or pharmacological therapy. Because the natural history of neurocardiac syncope in children is spontaneous resolution, it is appropriate to try the simple measures before introducing drug therapy.
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PMID:Unexplained syncope: clinical management. 927 5

This review introduces recent progress in molecular genetics of cardiovascular diseases. Many genes and their mutations causing familial cardiovascular diseases have been discovered, including familial hypertrophic cardiomyopathy which is caused by mutated cardiac beta myosin heavy chain, light chains, troponin T, troponin I, or alpha-tropomyosin, and long QT syndrome by KvLQT1, HERG, minK or cardiac voltage-dependent Na channel mutation. The mutations in causative genes can affect clinical courses of diseases; amino acid substitutions of cardiac beta myosin heavy chain with charge changes seem to cause poorer prognosis of hypertrophic cardiomyopathy. Besides monogenic diseases, there are many cardiovascular diseases affected with genetic polymorphisms, such as hypertension, ischemic heart disease and atherosclerosis. Specific amino acid mutations or polymorphisms in the promoter region of the genes are known to become a risk factor of these diseases. Polymorphisms of genes encoding apolipoprotein E, angiotensin converting enzyme, angiotensinogen and endothelial NO synthase (ecNOS) have been well characterized as an important risk factor of cardiovascular diseases. We recently found a novel gene which seems to affect human aging phenotype and vascular endothelial function. It is important as a future study to clarify the regulatory mechanisms of the klotho gene in the cardiovascular system and the clinical significance of klotho gene polymorphisms.
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PMID:[Molecular genetics of cardiovascular diseases]. 956 64

We have long known that there are diseases which are inherited from the parents, but it has not been until this last decade, with the introduction of the techniques of molecular biology, that we have been able to study them. These techniques have enable us to localize and detect the gene that causes a disease in the members of a family. The identification of a disease-causing gene does not lead only to the diagnosis and possible treatment of a very select patient population (the one with the familial disease), but also to a better understanding of the molecular basis and pathogenesis of the non-familial forms of the disease. Cardiology, despite having received these techniques more slowly, is now completely. Involved in the study of the molecular basis of cardiac diseases. The first gene to be mapped was that of hypertrophic cardiomyopathy in 1989. Since then, advances have been achieved at all levels in familial cardiac diseases. Hypertension, atherosclerosis, congenital heart diseases, and arrhythmias have all benefitted from the new techniques. Spectacular progress has been achieved in understanding familial heart rhythm disturbances, like long QT syndrome, both as congenital and acquired diseases. In the last five years 4 loci and 3 genes have been identified. The first studies of genetic based therapy have shown that in the near future patients with receive medication depending on the affected gene. Other familial arrhythmias are presently under study. Loci have been detected in some, such as bundle branch block and familial atrial fibrillation. At the speed that the techniques are evolving, and with the impressive advances of the Human Genome Project, we can expect to find the rest of the genes causing familial diseases in the next few years. These results are encouraging and clearly indicate the need for genetic diagnosis in all patients with these diseases. The diagnostic and therapeutic implications of all these discoveries could be of paramount importance.
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PMID:[Genetic bases of arrhythmias]. 960 99

QT interval has been determined in 103 monozygotic (MZ) and 198 dizygotic (DZ) female twins. Mean values of corrected QT (QTc) were almost identical for both groups at 413 ms (MZ) and 412 ms (DZ). There was a significant age and environmental effect on QT interval. Heritability explained about 25% of the variation in QT. Further research will show whether any of the genes known to cause Long QT syndrome have any effect on QT interval at the sub-clinical level. Journal of Human Hypertension (2000) 14, 389-390
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PMID:QT interval in twins. 1087 1

QT dispersion reflects in homogenecity of ventricular repolarization. It is calculated using 12-leads standard synchronized ECG or 24-hours Holter monitoring. The most common used indicators are: QT dispersion (QTd), based on Bazett's formula corrected for heart rate QT dispersion (QTcd) and QT dispersion ratio (QTdR). QT apex and QTd corrected for total number of leads ECG in which QT interval was counted are rare used. Increased QT dispersion is observed among others: following myocardial infarction (MI), coronary heart disease (CAD), hypertension, chronic heart failure (CHF), long QT syndrome, as well as diabetes. Following mentioned diseases increased QT dispersion has prognostic value for sustained ventricular tachycardia. Dispersion of repolarization > or = 80 ms after MI is a risk factor for sudden cardiac death. Following acute MI decrease of QT dispersion after successful thrombolytic therapy is observed and its value > or = 100 ms is regarded as a marker of reperfusion insufficiency. QT dispersion in patients with CAD correlates with extent of ischemia and decreases after coronary angioplasty (PTCA). In recent years beneficial effect of angiotensin-converting enzyme inhibitors and beta-adrenolytic therapy on QT dispersion was described. Actually the improvement of computerised methods in assessment of QT dispersion is observed, but it require further investigations.
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PMID:[Measurement dispersion of the QT interval and its significance in different diseases]. 1157 33

In the United States alone 300,000-400,000 people die of sudden cardiac death every year. Much of this mortality is assumed to be caused by ventricular tachyarrhythmias. Prolonged QTc reflect cardiac repolarization prolongation and/or increased repolarization inhomogenity known to be associated with increased risk of arrhythmias. The paper gives a review of the possibilities to assess the risk of ventricular arrhythmia and/or cardiac death from QTc. Prolonged QTc may hold independent prognostic importance for mortality in common diseases as ischemic heart disease and diabetes mellitus where as the prognostic importance in heart failure and arterial hypertension is more uncertain. In more rare diseases as the inborn long QT syndrome the QT interval gives not only important hint to the diagnosis but the magnitude also provides information on prognosis. QTc has probably no independent prognostic importance in hypertrophic cardiomyopathy or in the arrhythmogenic right ventricular disease. The degree of QTc prolonging during treatment with QTc prolonging drugs is prognostic for the risk of ventricular arrhythmia in form of torsade de pointes and QTc prolonging drugs should probably not be prescribed for patients with a QTc greater than 460 ms and withdrawn if QTc exceeds 500 ms during treatment. Data from the DIAMOND study suggest that QTc can be used to point out those heart failure patients who will benefit from antiarrhythmic therapy.
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PMID:QTc interval in the assessment of cardiac risk. 1211 54

A 60-year-old woman who had been successfully treated with atenolol and cardiac pacing for hypertension and long QT syndrome developed recurrent episodes of palpitations and syncope. Several days prior to these episodes, indapamide 2.5 mg/day was taken for better control of hypertension. The episodes were associated with prolongation of QT interval and mild hypokalemia (3.1 MEQ/L). Indapamide was immediately stopped, but the QT remained prolonged 2 days later, although the potassium level was normalized. This case suggests that indapamide can cause potassium independent prolongation of the QT interval, resulting in arrhythmia induced syncope.
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PMID:Indapamide induced syncope in a patient with long QT syndrome. 1238 Jul 80

Multiple studies have identified resting heart rate as a risk factor for cardiovascular disease independent of other cardiovascular disease risk factors (such as dyslipidemia and hypertension). Previous studies have examined heart rate in hypertensive individuals, but little is known about the genetic determination of resting heart rate in a normal population. Therefore, our objective was to perform a genome screen on a population containing normotensive and hypertensive individuals. We performed variance decomposition linkage analysis using maximum likelihood methods at approximately 10 cM intervals in 2209 individuals of predominantly North European ancestry. We estimated the heritability of resting heart rate to be 26% and obtained significant evidence of linkage (logarithm of the odds [LOD]=3.9) for resting heart rate on chromosome 4q. This signal is in the same region as a quantitative trait locus (QTL) for long QT syndrome 4 and a QTL for heart rate in rats. Within the 1-LOD unit support interval, there are 2 strong candidates: ankyrin-B and myozenin 2.
Hypertension 2004 May
PMID:Major quantitative trait locus for resting heart rate maps to a region on chromosome 4. 1499 99


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