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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Frame by frame analysis of left ventriculograms has been performed in 10 normal subjects and 40 patients with heart disease. Left ventricular shape index was derived as 4 pi (cavity area)/(perimeter)2, which has a maximum value of 1 when the outline is circular. In normal subjects systole was always associated with progressive reduction in shape index, indicating that the cavity projection had become less circular. This change was smaller in patients with low ejection fraction and also when inferior or anterior hypokinesia was present, even though ejection fraction was normal. During early diastole shape index rose rapidly due to an increase in minor diameter occurring throughout the period of rapid filling. In some cases this preceded any change in long axis, which was due to upward movement of the aortic root as well as outward movement of the apex. These results have functional implications, suggesting in particular that wall movement during filling may be non-uniform and that assumptions about cavity shape used in the derivation of wall properties from estimates of ventricular volume may require modification.
Br Heart J 1975 Sep
PMID:Continuous assessment of left ventricular shape in man. 123 94

Treatment with intravenous naftidrofuryl may be complicated by ventricular arrhythmias. A case of slow ventricular tachycardia occurring in a 65-year-old man with a dilated cardiomyopathy following an accidental overdose of naftidrofuryl (2 x 200 mg ampules in 250 ml of 5% glucose solution in 2 hours) prescribed for complicated arterial disease of the lower limbs is reported. This sustained ventricular tachycardia converted spontaneously after several hours. This case emphasises the risk of arrhythmogenic effects of this drug and indicates the need for careful monitoring when it is used intravenously in patients with underlying heart disease.
Ann Cardiol Angeiol (Paris) 1992 Sep
PMID:[Slow ventricular tachycardia caused by naftidrofuryl overdose (naftidrofuryl and ventricular tachycardia)]. 128 24

Ray asks the question: 'If A-B does not predict heart disease, why bother with it?' (British Journal of Medical Psychology, 64 (1) 1991). Having worked for several years in prevention of heart attack recurrence, I am inclined to agree with his conclusion that the construct is a trail which should now be abandoned. Grief, hostility and social isolation, fear and work demands have each been implicated in heart disease independently of Type A.
Br J Med Psychol 1992 Sep
PMID:If A-B does not predict heart disease, why bother with it? A clinician's view. 177 80

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.
Jpn Heart J 1992 Sep
PMID:High prevalence of coronary artery spasm in survivors of cardiac arrest with no apparent heart disease. 841 43

Emergency pericardiocentesis, guided by a two-dimensional echocardiography, was performed on twenty patients with symptomatic pericardial effusion of various types and causes. There were fourteen men and six women. The underlying causes were: primary lung cancer (6 cases), metastatic cardiac tumors (3 cases), tuberculosis (4 cases), complicated interventional procedures with cardiac chamber or vessel perforations (2 cases), dissecting aortic aneurysm (1 case), systemic lupus erythematous (1 case), idiopathic pericarditis (1 case), bacterial pericarditis (1 case), and myxedema heart disease (1 case). Seventeen cases were performed through the left xipho-sternal approach and 3 cases through the apical approach. None of the patients died as a result of these procedures. A two-dimensional echocardiogram is useful in diagnosing cardiac tamponade as well as in guiding pericardiocentesis, and obtaines highly positive results (20/20). The positive rate of pericardial fluid cytology for malignant cells was 89% (8/9), however, pericardial fluid cultures or direct smear for tuberculosis were negative (0/4). In cancer patients, the mean survival time following pericardiocentesis was 4.2 months (range, 1-7.8 months). We concluded that neoplastic involvement of the pericardium is the most frequent cause of symptomatic pericardial effusion. Pericardiocentesis assisted by a two-dimensional echocardiogram is safe and easy. In addition, pericarditis caused by TB is still significant and must be considered in every case in our nation.
Zhonghua Yi Xue Za Zhi (Taipei) 1992 Sep
PMID:Pericardiocentesis: a 20 patients study. 133 Feb 47

Rheumatic heart disease contributes to significant cardiac morbidity and mortality in India. The disease predominantly affects the valvular endocardium culminating in crippling valvular deformities, preferentially involving the mitral valve which may be severely affected in children and young adults. This appears to be unique to India and has been termed juvenile mitral stenosis. It is characterized by cardiomegaly, refractory congestive heart failure, and marked by elevated pulmonary vascular pressures and a progressive, fulminant clinical course. Autopsies of patients dying of rheumatic heart disease revealed that the mitral valve was most commonly afflicted either alone or in combination with the aortic and tricuspid valves in 31.6% and 52.8%, respectively. Organic involvement of the tricuspid valve was documented in 38.4% of cases. The extent and severity of the disease process was most marked in the mitral valve, followed by the aortic and tricuspid valves. Mitral valves showed various degrees of calcification, moderate or severe calcification being observed in 36.4%. Chronic inflammatory cell infiltration was observed in both calcified and non-calcified valves. The phenotypic profile of the inflammatory cells by immunohistochemical staining revealed a significant number to be T-helper/inducer lymphocytes. Lungs from cases of mitral stenosis exhibited prominent vascular and parenchymal changes. Pulmonary vessels revealed moderate to marked medial hypertrophy of the medium sized branches of the pulmonary artery. Dilatation lesions were also seen in a few cases. The most striking parenchymal change was the prominent smooth muscle in the bronchoalveolar walls. The extent and severity of the vascular and parenchymal changes were more marked in juvenile patients. The presence of inflammatory cells in cases of chronic heart disease reflects a possible ongoing insult/injury to some persistent antigenic stimulus by beta hemolytic streptococcal antigens that have primed the various target tissues. Further study of surface characteristics of various mesenchymal cells may help in understanding the nature and pathogenesis of this serious cardiac problem.
J Heart Valve Dis 1992 Sep
PMID:Chronic rheumatic heart disease in India: a reappraisal of pathologic changes. 134 Dec 28

Proposed guidelines for the diagnosis of transient ischaemic attack (TIA) involve interpretation of symptoms, so it can be very difficult to distinguish a TIA from other disorders, such as migraine, epilepsy, syncope, or neurosis. Atypical cerebral and visual events may be classified as TIA. To see whether TIA or stroke patients with atypical cerebral or visual symptoms are at high or low risk of cardiac complications, we prospectively followed 572 patients (entered into the Dutch multicentre TIA trial) with a diagnosis of TIA or minor ischaemic stroke, but whose symptoms did not fully accord with internationally accepted criteria. We compared their outcome with that of 2555 other TIA or stroke patients in the trial, who had unequivocal symptoms; all patients were treated with aspirin. During mean follow-up of 2.6 years the risk of a major vascular event did not differ between the groups (14.5% in patients with atypical symptoms vs 15.1% of patients with typical attacks). Patients with atypical attacks had a lower risk of stroke (5.6% vs 9.4%, hazard ratio 0.6, 95% confidence interval 0.4-0.9) and a higher risk of a major cardiac event (8.4% vs 5.9%, 1.4, 1.0-2.0) than did patients with typical attacks. These differences could not be explained by differences in cardiac risk factors, and were independent of minor discrepancies in baseline characteristics between the groups. A heavy or tired feeling in one or two limbs was the only atypical symptom associated with cerebral rather than cardiac events (ratio cardiac/cerebral events 0.8). For all other atypical symptoms cardiac events were about twice as common as cerebral events (range 1.3-2.5). Our findings suggest that TIA or minor stroke patients with atypical symptoms may have symptomatic heart disease, especially cardiac arrhythmia.
Lancet 1992 Sep 12
PMID:Risk of cardiac events in atypical transient ischaemic attack or minor stroke. The Dutch TIA Study Group. 135 13

Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.
Lancet 1992 Sep 26
PMID:Stress failure of pulmonary capillaries: role in lung and heart disease. 809 42

The arrhythmias in competitive athletes may be classified as "benign," "paraphysiological" due to prolonged athletic training, or "pathological" due to hemodynamic effects on the athletic performance-risk-arrhythmogenic substratum. Pathological arrhythmias include life-threatening forms that are severe enough to produce symptoms (presyncope, syncope, cardiac arrest) during athletic activity. These forms are in particular rapid VT, VF, torsades de pointes, preexcited atrial fibrillation, sinus atrial and AV block. Our study population includes 766 competitive athletes, mean age 21.1 years (74 top international level), investigated with a cardioarrhythmological work-up for symptoms and for arrhythmias from 1974 to June 30, 1991. Three leading categories, represented by 16 aborted sudden death, 8 sudden death, and 7 induced VF (by EES or TAP) athletes, are described. All athletes with life-threatening arrhythmias, previously as asymptomatic or with minor symptoms had an arrhythmogenic substratum due to underlying silent cardiopathy or primary arrhythmic disorders. Athletic activity can be regarded as a trigger of electrical destabilization.
Pacing Clin Electrophysiol 1992 Sep
PMID:Life-threatening tachyarrhythmias in athletes. 138 4

Systolic blood pressure and heart rate measured at rest and during a standardized exercise test were analyzed in the cohort of middle-aged male employees followed-up an average of 17 years in the Paris Prospective Study I. The population sample selected for the analysis included 4,907 men who completed at least 5 minutes of bicycle ergometry, who had no heart disease at entry, and whose resting blood pressure was less than or equal to 180/105 mm Hg. Exercise-induced increase in systolic blood pressure was positively correlated with resting systolic blood pressure (r = 0.104, p less than 0.0001), whereas the correlation of exercise-induced heart rate increase with resting heart rate was negative (r = -0.169, p less than 0.001). Using Cox regression analysis with the inclusion of resting systolic blood pressure and heart rate; exercise-induced elevations of systolic blood pressure and heart rate; and controlling for age, smoking, total cholesterol, body mass index, electrical left ventricular hypertrophy, and sports activities, cardiovascular mortality was found to be associated with the systolic blood pressure increase (p less than 0.05), whereas no association with resting systolic blood pressure was found. Total mortality was predicted by resting systolic blood pressure and its elevation (p less than 0.01 for both) and by resting heart rate (p less than 0.0001). The heart rate increase did not contribute to death prediction. In conclusion, the magnitude of the exercise-induced increase of systolic blood pressure, but not of heart rate, may represent a risk factor for death from cardiovascular as well as noncardiovascular causes, independently of resting blood pressure and heart rate.
Hypertension 1992 Sep
PMID:Prognostic significance of exercise blood pressure and heart rate in middle-aged men. 138 30


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