Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess whether left ventricular (LV) cavity size relates to functional impairment and syncope in patients with hypertrophic cardiomyopathy (HC). LV diastolic dysfunction influences functional limitation in HC. A reduced LV end-diastolic dimension may underlie impaired diastolic properties and be implicated in hemodynamic syncope. Eighty-two consecutive patients with HC (off drugs, in sinus rhythm) underwent echocardiography to measure LV end-diastolic dimension in the short-axis view (indexed to the body surface area) and radionuclide angiography (n = 50) to calculate peak filling rate (normalized to stroke counts/s). Patients in New York Heart Association functional classes II to IV had smaller LV end-diastolic dimension (23.2 +/- 2.6 vs 25.5 +/- 2.5 mm/M2, p = 0.0001) and lower peak filling rate (4.3 +/- 1.4 vs 5.1 +/- 1.3 stroke counts/s, p = 0.036) than those in New York Heart Association class I. LV end-diastolic diameter was correlated to peak filling rate (r = 0.37; p = 0.008). The most potent predictors of functional limitation were LV end-diastolic dimension (relative risk [RR] 0.63, confidence interval [CI] 0.45 to 0.88; p = 0.008), age (RR 1.09, CI 1.03 to 1.17; p = 0.003), and LV thickness score (RR 1.08, CI 1.02 to 1.13; p = 0.003). LV cavity size was smaller in patients with functional limitation irrespective of obstruction and hypertrophy. Patients with differed from those without a history of syncope for a smaller LV end-diastolic dimension (23.2 +/- 2.5 vs 25.0 +/- 2.7 mm/M2, p = 0.008), which was the only independent predictor of syncope (RR 0.77, CI 0.63 to 0.95; p = 0.013). Thus, a small LV cavity size is associated with functional limitation and history of syncope in HC.
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PMID:Influence of left ventricular cavity size on clinical presentation in hypertrophic cardiomyopathy. 1007 59

Magnetic resonance imaging (MRI) has been shown to be an ideal noninvasive tool for imaging and diagnosing myocardial and pericardial diseases. In dilated and hypertrophic cardiomyopathy, MRI is suitable for the diagnosis and quantification of ventricular volume, stroke volume, and myocardial mass. Recent developments in the area of fast imaging techniques and MR contrast agents rapidly are increasing the utility of MRI for studying and assessing myocardial diseases. MRI may become a helpful technique with which to diagnose myocarditis and myocardial involvement in amyloidosis and sarcoidosis. Contrast-enhanced MRI also can be used for patients who have undergone heart transplantation to assess early signs of transplant rejection by improved contrast between normal and pathologic myocardium. For pericardial diseases, MRI provides an exact evaluation of the pericardial thickness, and it is a very sensitive technique for identifying pericardial effusions. Differentiation between hemorrhagic, serous, or chylous pericardial effusions usually can be made by using the typical signal behavior on T1-weighted and T2-weighted sequences. Due to its greater field of view and its ability to evaluate functionally the regional ventricular and atrial motion abnormalities in the typical tissue pattern, MRI has a significant potential in the evaluation of pericardial inflammation and constrictive pericarditis. J. Magn. Reson. Imaging 1999;10:617-626.
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PMID:Magnetic resonance imaging evaluation of myocardial and pericardial disease. 1054 70

MELAS is a mitochondrial encephalomyopathy characterized clinically by recurrent stroke-like episodes, seizures, sensorineural deafness, dementia, hypertrophic cardiomyopathy, and short stature. The majority of patients are heteroplasmic for a mutation (A3243G) in the tRNAleu(UUR) gene in mitochondrial DNA (mtDNA). In cells cultured in vitro, the mutation produces a severe mitochondrial translation defect only when the proportion of mutant mtDNAs exceeds 95% of total mtDNAs. However, most patients are symptomatic well below this threshold, a paradox that remains unexplained. We studied the relationship between the level of heteroplasmy for the mutant mtDNA and the clinical and biochemical abnormalities in a large pedigree that included 8 individuals carrying the A3243G mutation, 4 of whom were asymptomatic. Unexpectedly, we found that brain lactate, a sensitive indicator of oxidative phosphorylation dysfunction, was linearly related to the proportion of mutant mtDNAs in all individuals carrying the mutation, whether they were symptomatic or not. There was no evidence for threshold expression of the metabolic defect. These results suggest that marked tissue-specific differences may exist in the pathogenic expression of the A3243G mutation and explain why a neurological phenotype can be observed at relatively low levels of heteroplasmy.
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PMID:Oxidative phosphorylation defect in the brains of carriers of the tRNAleu(UUR) A3243G mutation in a MELAS pedigree. 1066 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

In the past decade, maternally inherited disorders have been described manifesting as hypertrophic cardiomyopathy. These are primarily associated with defects in oxidative metabolism due to an alteration in mitochondrial DNA. Although the biochemistry and molecular biology is well-defined, there is little information regarding clinical presentation and course. Reported manifestations can be broad and can include myopathy, encephalopathy, stroke-like episodes, hearing loss, cardiomyopathy, multiorgan dysfunction and sudden death. Predominant or exclusive involvement of the heart is rare. We report the clinical presentations, investigations, pathologic findings, and clinical course in two families with two mitochondrial tRNA defects with exclusive cardiac involvement and demonstrable clinical heterogeneity based on the percentage of mutant tRNA.
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PMID:Maternally inherited hypertrophic cardiomyopathy: a manifestation of mitochondrial DNA mutations--clinical course in two families. 1112 21

Atrial fibrillation (AF) is the most common sustained arrhythmia in patients with hypertrophic cardiomyopathy (HCM), and it bears numerous pathophysiologic consequences that potentially affect patient outcome and symptoms. However, studies regarding the impact of AF on the long-term prognosis of HCM patients have been limited in number, with sometimes conflicting results. Recently, studies on community-based patient populations showed that AF is associated with long-term clinical deterioration, embolic complications, and increased cardiovascular mortality due to heart failure and stroke. The consequences of AF on the long-term prognosis of HCM patients are not uniformly unfavorable, however, and in about one third of patients the arrhythmia is compatible with an uneventful course.
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PMID:Clinical significance of atrial fibrillation in hypertrophic cardiomyopathy. 1117 72

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

Stroke volume (SV), cardiac output (CO) and systolic blood pressure (SBP) were measured during maximal symptom-limited bicycle exercise testing in 13 young patients (age, 11-26 years) with nonobstructive hypertrophic cardiomyopathy (HCM). SV was measured by impedance plethysmocardiography; %SVend, %COend, and %SBPend represent the ratio of the value at termination of the exercise to the respective value at rest. In all patients of HCM-I (the Cardiac Event Group, 3 patients) and 3 of HCM-II (the Non-Cardiac Event Group, 10 patients), the %SVend was less than 100%. The %SVend of HCM-I was significantly lower than the respective values of the HCM-II and Control groups. The %COend values of the HCM-I and HCM-II groups were each significantly lower than that of the Control. The %SBPend values of the HCM-I and HCM-II groups were each significantly lower than that of the Control. Among the HCM patients, the %SVend value was positively correlated with the %SBPend value. The patients who had more severe HCM had poorer exercise-induced increases in SV and SBP. These results suggest that sudden cardiac death in young HCM patients is associated with inhibition of the increase in SV upon exercise.
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PMID:Response of the stroke volume and blood pressure of young patients with nonobstructive hypertrophic cardiomyopathy to exercise. 1131 27

The conversion of atrial fibrillation (AF) to normal sinus rhythm should be attempted in patients who present with this condition, as long as the cure is not worse than the disease itself. In young patients with normal hearts, AF has a small impact on morbidity and mortality. The primary indication for conversion in this population is often symptoms. In contrast, in patients with diseased hearts or who are older than 65 years, maintaining sinus rhythm may have a favorable impact on stroke risk, ventricular function, and symptoms. In the absence of normal sinus rhythm, these patients should receive anticoagulants. Rate control is the preferred first-line strategy for asymptomatic patients and patients presenting with a history of long-standing, persistent AF, making conversion and maintenance of sinus rhythm unlikely. Rate control may be used in patients who develop AF during an acute systemic illness, which will likely terminate with time or therapy. Conversion to sinus rhythm should be considered in patients with a first episode of AF, as unconverted AF tends to perpetuate itself. Conversion can be attempted if the duration of AF is less than 48 hours or if the patient has received anticoagulants when the duration is not known. Other indications for cardioversion are prolonged episodes in patients with otherwise infrequent episodes of paroxysmal AF, and in patients who refuse to take anticoagulants or in whom anticoagulation is contraindicated. After the patient is converted to sinus rhythm, the decision to initiate chronic drug therapy should be based on the presence of other cardiac and medical diseases that increase the risk of recurrence and serious symptoms in case of recurrence (such as hypertrophic cardiomyopathy or mitral stenosis). It is acceptable to manage patients with new-onset AF and normal cardiac function with cardioversion alone and not initiate chronic antiarrhythmic therapy afterwards. However, in patients with abnormal hearts (coronary artery disease, hypertensive or mitral valvular heart disease, and cardiomyopathy) AF is likely to recur, and such patients should be placed on antiarrhythmic medication.
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PMID:Atrial Fibrillation. 1144 57

A growing number of people are involved in recreational physical activity. We examined the clinical and cardiac pathological patterns in 29 persons who died suddenly during a sport activity and were autopsied at the Institute of Forensic Medicine of Paris, 1990-1999. Twenty-seven males ranging in age from 13 to 57 years, mean 30.5, and two females, 8 and 60 years old, died suddenly during a sport activity. The sports included running, 11 cases; cycling, 4; soccer, 3; swimming, 2; basket-ball, 2; rugby, 1, gymnastic exercises, 2; tennis, 1; gockart, 1; skiing, 1; hand-ball, 1 case. The causes of deaths were as follows; coronary artery disease, 9 cases; congenital anatomic anomaly of a coronary artery, 1; hypertrophic cardiomyopathy, 5; right ventricular dysplasia, 3; myocarditis, 2; endomyocardial fibrosis, 1; bridging of the left anterior descending coronary artery, 2; stroke, 2; rupture of aortic aneurysm, 4. Despite severity of lesions, only 4 victims had a known cardiovascular disease. Efforts should be continued to improve sensitivity and specificity of diagnostic tools and screening strategies. Therefore, medico-legal autopsies should be systematically performed for a better knowledge of sport-related mortality.
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PMID:[Sudden death and physical activity and sports]. 1150 65


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