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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertrophic cardiomyopathy (HCM) generally shows increased systolic function of the left ventricle at rest, although patients with HCM often have decreased exercise tolerance and develop dyspnea or chest pain. The present study was to investigate of left ventricular (LV) function during exercise in 26 patients with HCM using Tc-99m equilibrium angiocardiography, and to elucidate the mechanism of impaired functional reserve during exercise. Controls consisted of 11 normal volunteers and 12 patients with chest pain syndrome who had no abnormality on coronary arteriography or left ventriculography. In patients with HCM, LV ejection fraction decreased from 65 +/- 8 (mean +/- SD)% at rest to 59 +/- 18% at peak exercise, in contrast to an increase among controls (from 56 +/- 9% to 64 +/- 9%). As compared with resting values, cardiac output increased to 168 +/- 24% at peak exercise in HCM, but the increase was significantly less than that in controls (215 +/- 47%). Stroke volume decreased gradually to 83 +/- 16% during exercise in HCM, while it increased to 114 +/- 10% at an exercise level of half intensity, and it decreased slightly to 106 +/- 16% at peak exercise. LV end-systolic volume decreased among controls to 78 +/- 27% at peak exercise, but remained unchanged in HCM (118 +/- 58%). An increase in peak ejection rate at peak exercise was less in HCM than in controls (143 +/- 26% vs 170 +/- 42%). No significant differences were observed between the two groups concerning changes in indices of LV diastolic function including LV end-diastolic volume, peak filling rate or 1/3 filling rate during exercise. In the analysis of LV function curves, pulmonary arterial diastolic pressure increased to a greater extent in HCM than in controls (19 +/- 6 mmHg vs 11 +/- 6 mmHg); whereas, an increase in the stroke work index was less in HCM (80 +/- 26 g.m/m2/beat vs 121 +/- 21 g.m/m2/beat) at peak exercise. Thus, the LV function curve shifted downward and to the right in patients with HCM. The above findings indicate that LV functional reserve during exercise is impaired, especially as to systolic function in patients with HCM, while deterioration of diastolic function may be partly compromised by elevated filling pressure.
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PMID:[Left ventricular function in hypertrophic cardiomyopathy: a Tc-99m radionuclide angiographic study during exercise]. 372 81

The clinical and haemodynamic significance of the subaortic pressure gradient in patients with muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy) has long been debated. In this report we summarize the evidence which indicates that true obstruction to left ventricular outflow exists in these patients. Rapid left ventricular ejection, through an outflow tract narrowed by ventricular septal hypertrophy, results in Venturi forces causing systolic anterior motion of the anterior (or posterior) mitral leaflets. Mitral leaflet-septal contact results in obstruction to outflow and the accompanying mitral regurgitation. The time of onset of mitral leaflet-septal contact determines the magnitude of the pressure gradient and the severity of the mitral regurgitation, as well as the degree of prolongation of left ventricular ejection time and the percentage of left ventricular stroke volume that is ejected in the presence of an obstructive pressure gradient. Early and prolonged mitral leaflet-septal contact results in a large pressure gradient, significant mitral regurgitation, as well as dramatic prolongation of the ejection time and a large percentage of left ventricular stroke volume being obstructed. Late and short mitral leaflet-septal contact results in little haemodynamic perturbation. Hypertrophic cardiomyopathy patients with obstructive pressure gradients are significantly more symptomatic than those without. Thus the obstructive pressure gradients in hypertrophic cardiomyopathy are of clinical as well as haemodynamic significance. To deny the existence of obstruction to outflow in patients with muscular subaortic stenosis is to deny these patients appropriate medical and surgical therapy.
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PMID:Muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy): the evidence for true obstruction to left ventricular outflow. 377 88

Hypertrophic cardiomyopathy is characterised by hyperkinetic left ventricular function, but the effect of an outflow tract gradient on the haemodynamics of ejection remains controversial. To determine the functional importance of left ventricular gradients in hypertrophic cardiomyopathy technetium-99m gated equilibrium radionuclide angiography was performed in 18 normal subjects and 57 patients, 26 with and 31 without left ventricular gradients. Time activity curves were generated from list mode data, and the proportion of stroke volume ejected during various phases of systole was computed. The proportion of stroke volume ejected during the initial third, the initial 50%, and the initial 80% of systole was greater in patients with hypertrophic cardiomyopathy than in normal subjects but was identical in patients with and without left ventricular gradients. The duration of systole was similar in the three groups. These findings favour the interpretation that a left ventricular gradient does not represent true obstruction and are consistent with previous observations that clinical features and prognostic indicators do not relate to gradients in this disease.
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PMID:Relation between left ventricular gradient and relative stroke volume ejected in early and late systole in hypertrophic cardiomyopathy. Assessment with radionuclide cineangiography. 654 20

Hypertrophic cardiomyopathy (HC) is characterized by impaired diastolic function, and left ventricular (LV) outflow tract obstruction in about one-fourth of patients. Verapamil improves diastolic properties, but may have dangerous adverse effects. This study investigates the effects of diltiazem on hemodynamics and LV function in 16 patients with HC who were studied with cardiac catheterization and simultaneous radionuclide angiography. Studies were performed during atrial pacing (15 beats above spontaneous rhythm) at baseline and during intravenous diltiazem administration (0.25 mg x kg(-1) over 2 minutes, and 0.014 mg x kg(-1) x min(-1). Diltiazem induced a systemic vasodilation (cardiac index: 3.4 +/- 1.0 to 4.0 +/- 1.0 L x min(-1) x m(-2), p = 0.003; aortic systolic pressure: 116 +/- 16 to 107 +/- 19 mm Hg, p = 0.007; systemic resistance index: 676 +/- 235 to 532 +/- 193 dynes x s x cm(-5) x m(-2), p = 0.006), not associated with changes in the LV outflow tract gradient. The end-systolic pressure/volume ratio decreased (30 +/- 42 to 21 +/- 29 mm Hg x ml(-1) x m(-2); p = 0.044). Pulmonary artery wedge pressure (11 +/- 5 to 15 +/- 6 mm Hg, p = 0.006), and peak filling rate increased (4.1 +/- 1.3 to 6.0 +/- 2.4 stroke counts x s(-1), p = 0.004). The time constant of isovolumetric relaxation tau decreased (74 +/- 40 to 59 +/- 38 ms, p = 0.045). The constant of LV chamber stiffness did not change. Thus, active diastolic function is improved by the acute administration of diltiazem by both direct action and changes in hemodynamics and loading conditions. LV outflow tract gradient does not increase despite systemic vasodilation. In some patients, however, a marked increase in obstruction and a potentially harmful elevation in pulmonary artery wedge pressure do occur. Passive diastolic function is not affected.
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PMID:Effects of diltiazem on left ventricular systolic and diastolic function in hypertrophic cardiomyopathy. 875 92

A new method of presenting the in vivo left ventricular pressure-flow data is developed in the present study. This separates left ventricle ejection into unrestricted, progressively restricted and severely restricted cases. This method uses ejection volume and time to define a normalizing 'stroke' pressure, which is successful in collapsing the large variability of in vivo data to a few curves with characteristic shapes, depending on the degree of obstruction. Hypertrophic cardiomyopathy is shown to fall into both unrestricted and progressively restricted categories. Normal hearts form the unrestricted case, while a severe aortic valvular stenosis is characteristic of the severely restricted case.
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PMID:Stroke normalized pressure: a useful parameter for the analysis of left ventricular outflow obstruction. 895 52

Hypertrophic cardiomyopathy is a relatively common genetic disorder with heterogeneity in mutations, forms of presentation, prognosis and treatment strategies. Hypertrophic cardiomyopathy is recognized as the most common cause of sudden cardiac death that occurs in young people, including athletes. The clinical diagnosis is complemented with the ecocardiographic study, in which an abnormal myocardial hypertrophy of the septum can be observed in the absence of a cardiac or systemic disease (arterial systemic hypertension, aortic stenosis). The annual sudden mortality rate is 1% and, in selected populations, it ranges between 3 and 6%. The therapeutic strategies depend on the different subsets of patients according to the morbidity and mortality, sudden cardiac death, obstructive symptoms, heart failure or atrial fibrillation and stroke. High risk patients for sudden death may effectively be treated with the automatic implantable cardioverter-defibrillator.
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PMID:[Hypertrophic cardiomyopathy. Arrhythmia in hypertrophic cardiomyopathy]. 1296 40

Hypertrophic cardiomyopathy is a common genetically transmitted disease, defined clinically by the presence of unexplained left ventricular hypertrophy. The disease has a varied clinical course and outcome; many patients have little or no discernible cardiovascular symptoms, whereas others have profound exercise limitation and recurrent arrhythmias. The overall risk of disease-related complications such as sudden death, endstage heart failure, and fatal stroke is roughly 1-2% per year, but the absolute risk in individuals varies as a function of underlying genetic abnormality, age, myocardial pathology, and other pathophysiological abnormalities such as impaired peripheral vascular responses. Genetic counselling and clinical risk stratification are relevant to all patients, but many therapeutic interventions, including septal alcohol ablation, septal myectomy, and implantable cardioverter defibrillators, are appropriate only in particular patient subsets. We review the management of patients with unexplained myocardial hypertrophy, considering the influence of underlying genetic and pathophysiological substrates on clinical decision-making.
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PMID:Hypertrophic cardiomyopathy. 1518 28

Hypertrophic cardiomyopathy (HCM) is associated with an increased incidence of supraventricular and ventricular arrhythmias. Atrial fibrillation (AF) is the most common arrhythmia in HCM with a prevalence of 20% and an annual incidence of two percent per year. Increased left atrial size and volume along with impaired left atrial function confer an increased likelihood of AF. The onset of AF is often accompanied by a decrease in functional status in conjunction with an increased risk of stroke and overall mortality.
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PMID:Atrial fibrillation in hypertrophic cardiomyopathy: mechanisms, embolic risk and prognosis. 1716 69

Hypertrophic cardiomyopathy (HC) often presents with exercise-induced symptoms, including arrhythmias and sudden death. The investigators prospectively studied whether exercise testing is associated with immediate complications and if stress-induced arrhythmias and echocardiographic variables are associated with long-term adverse outcomes. Exercise echocardiography with 6-channel continuous monitoring for arrhythmias was performed in consecutive patients with HC clinically referred for the test. End points included death, myocardial infarction, revascularization, stroke, atrial fibrillation, ventricular tachycardia, and myectomy. Of 86 patients with HC (mean age 56.6 +/- 16.1 years) who underwent exercise echocardiography, arrhythmias occurred in 39 (45%), including 23 (27%) with premature atrial contractions, 2 (2%) with atrial fibrillation, 28 (33%) with premature ventricular contractions (16 also had atrial arrhythmias), and 1 (1.2%) with nonsustained ventricular tachycardia (hemodynamically stable). During a follow-up of 2.6 +/- 2.8 years, major events occurred in 11 patients (3 deaths, 5 revascularizations, 3 strokes). In addition, 12 patients developed atrial fibrillation, 6 developed nonsustained ventricular tachycardia, and 13 underwent myectomies. Variables associated with major events included hypertension, male gender, and worsening wall motion score index with exercise; increased exercise duration was associated with fewer events. ST-T changes on baseline electrocardiography and premature ventricular contractions were associated with atrial fibrillation risk. In conclusion, in this cohort of patients with HC, exercise testing was safe. Test results were associated with risk for adverse events.
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PMID:Prognostic significance of exercise induced arrhythmias and echocardiographic variables in hypertrophic cardiomyopathy. 1735 Mar 77

Hypertrophic cardiomyopathy is a common genetically transmitted disease, defined clinically by the presence of left ventricular hypertrophy in the absence of loading conditions sufficient to cause the observed degree of hypertrophy. The disease has a heterogeneous clinical course, with many patients having few cardiovascular symptoms and others profound exercise limitation and recurrent arrhythmia. The overall annual rate of disease-related complications such as sudden death, end-stage heart failure and fatal stroke is approximately 1-2%, but risk in individual patients varies as a function of age, disease severity and the underlying cause of the hypertrophy. Genetic counselling and clinical risk stratification are relevant for all patients. Subsets of patients require septal alcohol ablation, septal myectomy and implantable cardioverter defibrillators.
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PMID:Investigation and treatment of hypertrophic cardiomyopathy. 1788 58


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