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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

The electrophysiologic effects of intravenously administered propranolol (0.1 mg/kg) on three parameters of sinus node function were examined in ten symptomatic patients with sinus node dysfunction. The patients ranged in age from 26 to 79 years. Symptoms ranged from fatigue to frank syncope. Sinoatrial (SA) block and sinus pauses were observed in one patient; sinus pauses alone were observed in three patients. Five (5/10) patients had intraatrial block; three (3/10) patients had atrioventricular block; four (4/10) patients had an intraventricular conduction disturbance. At the time of electrophysiologic study, two patients had a control spontaneous sinus cycle length that exceeded 1000 msec. Following propranolol, the mean spontaneous cycle length increased by 17.4% (924 to 1085 msec, P less than 0.005) and spontaneous second degree SA block reappeared in the one patient. The maximum escape cycle ranged from 116% to 229% of the prepacing spontaneous cycle length and was considered to be prolonged in two of ten patients. Propranolol had no significant effect on the maximum escape cycle/prepacing cycle length X 100 (%). The estimated sinoatrial conduction time (SACT) was determined in seven patients and ranged in value from 120 to 238 mes. Propranolol increased the mean value of the estimated SACT from 179 to 213 msec, P less than 0.025. Propranolol may cause marked bradyarrhythmias in some patients with sinus node dysfunction, and should be used with caution in these patients.
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PMID:Electrophysiologic effects of propranolol on sinus node function in patients with sinus node dysfunction. 94 74

Twenty-two patients with congenital valvular aortic stenosis were surgically treated between 1967 and July 1975. Five (23%) were under 1 year of age (group I) and 17 (77%) were between 2 and 24 years (group II). All infants exhibited severe congestive heart failure and electrocardiographi (ECG) evidence of left ventricular hypertrophy (LVH) with strain pattern. In group II, angina was present in three cases, syncope and fatigue in two; the ECG indicated LVH in 10 cases (59%) with strain pattern in five (29%). A bicuspid aortic valve was present in 77% (17/22) of the cases; 32% had other cardiac anomalies. Aortic valvotomy was performed on cardiopulmonary bypass in 20 cases, and with deep hypothermia and circulatory arrest in two. Three infants under 1 month of age with associated anomalies died (hospital mortality 14%). Intraoperative average peak left ventricular-aortic systolic pressure gradient decreased from 86 to 21 mmHg (P less than 0.001). Late clinical (in all cases) and haemodynamic (26%) follow-up showed severe restenosis in two patients of group II; one of them had a second operation, the other one died three and a half years postoperatively. Results assessed on the basis of symptoms, ECG changes, aortic valve function, and/or haemodynamic findings were fair in the two surviving infants. Results in group II were excellent in three, satisfactory in seven, fair in four, and poor in two cases. In infants, aortic valvotomy is a palliative procedure which carries a high risk. In the older age group, early and late results are more gratifying.
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PMID:Surgical treatment of congenital valvular aortic stenosis. 96 96

This report details our total experience with documented chronic His bundle block in 24 patients. Ten patients had second-degree block (eight with 2:1 block and two with type-1 block), and 14 patients had complete heart block. There were 16 women (67 percent) and eight men (33 percent) with ages ranging from 17 to 87 years. Diagnoses were as follows: hypertensive cardiovascular disease, nine patients (38 percent); arteriosclerotic heart disease, six patients (25 percent); aortic valvular disease, three patients (13 percent); primary conduction disease, two patients (8 percent); primary myocardial disease, two patients (8 percent); congenital heart block, one patient (4 percent); and traumatic heart block, one patient (4 percent). Pacing was instituted in 20 patients because of the following; congestive heart failure, seven patients; syncope, seven patients; fatigue, four patients; and recurrent dizziness, two patients. Permanent pacing was indicated within ten days of initial diagnosis in 13 patients, from 20 to 80 days in four patients, and later than 100 days in three patients. An additional two asymptomatic patients were treated with prophylactic pacing.
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PMID:The clinical spectrum of chronic His bundle block. 100 Oct 51

From 1960 through 1972, 236 cases of amyloidosis with histologic proof were found. The amyloidosis was primary (without evidence of preceding or coexisting disease) in 132 cases (group 1) and associated with multiple myeloma in 61 (group 2). Secondary amyloidosis appeared in 19 cases (associated with rheumatoid arthritis or osteomyelitis in two-thirds of them). There were 22 patients with amyloid localized to a single organ (bladder, lung, skin, or larynx in more than half of them). Two patients had familial amyloidosis. In group 1 and group 2, the most common presenting symptoms were fatigue, weight loss, edema, dyspnea, light-headedness or syncope, and paresthesias. Symptoms of the carpal-tunnel syndrome were frequent. The liver was palpable in almost 50% of the series, but splenomegaly was an initial finding in less than 10%. Macroglossia was recorded in 26% of group 2 and in 12% of group 1. Enlargement of submandibular structures was noted in about 10% of cases; and purpura, particularly around the eyes, was a significant feature. Substantial numbers of the patients had carpal-tunnel syndrome, nephrotic syndrome, congestive heart failure, sprue, peripheral neuropathy, or orthostatic hypotension. Approximately 50% of patients had renal insufficiency at the time of diagnosis. Proteinuria was found in more than 90%. A monoclonal protein was found in the serum of 49% of group 1 and in 74% of group 2. Monoclonal proteins were found in the urine of 35% and 81%, respectively. Only 12% of patients in group 1 had no monoclonal protein when both serum and urine were analyzed, and all patients of group 2 had a monoclonal protein in the serum or urine when both were analyzed. Lambda light chains were more common than kappa. None of the patients in group 1 had more than 15% plasma cells in the marrow, whereas more than half of group 2 had more than 15% plasma cells. Roentgenograms showed no evidence of skeletal disease in 94% of group 1, but 50% of group 2 had skeletal abnormalities. Rectal biopsy was positive for amyloid in 84% of cases. Kidney, liver, and carpal-tunnel biopsies were positive in 90% or more. Follow-up of all 193 patients in groups 1 and 2 revealed that 80% of group 1 and 97% of group 2 had died. The median survival was 14.7 months in group 1 and 4 months in group 2. Cardiac failure was the most common cause of death, accounting for 30% of the fatalities. We also reclassified all cases by the method of Isobe and Osserman (105), which is based on clinical patterns: pattern I--principal involvement of tongue, heart, gastrointestinal tract, muscle, nerves, skin, and carpal ligaments; pattern II--principal involvement of liver, spleen, kidneys, and adrenals; and mixed pattern I and II. This analysis failed to reveal predictive value in the clinical pattern classification, and did not discern the survival differences between primary amyloidosis (group 1) and amyloidosis with myeloma (group 2). Consequently, for the present we prefer the classification used in this study.
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PMID:Amyloidosis: review of 236 cases. 115 71

In a 14-month period mitral leaflet prolapse was diagnosed in 85 patients by echocardiography or cineangiography. Chest pain alone was the presenting complaint in 30 patients and linked with palpitation, dyspnoea, or syncope in 9. Eleven presented with major neurological disturbances (9 had transient ischaemic attacks), 10 with palpitation, 4 with undue and persistent fatigue, 2 with dyspnoea, and 2 with dizziness. Seventeen were referred not because of symptoms but because of clicks and murmurs. Overall, chest pain affected 61 patients and unless associated with coronary artery disease was not anginal. Palpitation was admitted by 42 patients; dizziness, lightheadedness, or paraesthesiae by 15, and syncope by 12. Systolic auscultatory abnormalities were noted in 69: 25 had single clicks, 3 had multiple clicks, 19 had both click(s) and murmur, and 22 had a murmur alone. Electrocardiography revealed ST segments flat for greater than 0-10 s in 21, prolonged QTc in 18, and T wave flattening or inversion in inferior limb and lateral chest leads in 14. The exercise stress test was abnormal in 13 of 27 patients. Mitral valve echograms showed definite mitral leaflet prolapse in 61, 'possible' prolapse in 14, and were normal in 8 patients with angiographic proof of mitral leaflet prolapse. Cardiac catheterization with left ventriculography showed prolapse of posterior mitral leaflet in 36, of both leaflets in 2, and left ventricular wall motion abnormalities in 16 cases. Selective coronary arteriography in 31 cases showed major vessel narrowing of larger than or equal to 80 per cent lumen diameter in 4, all with angina. This consecutive series indicates that the physical event of mitral leaflet prolapse is more common than hitherto appreciated, is priminently associated with non-anginal chest pain, palpitation, and neurological disturbances, and in 90 per cent of cases could be shown echocardiographically.
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PMID:Clinical features and investigative findings in presence of mitral leaflet prolapse. Study of 85 consecutive patients. 125 39

Based on our experience and the experience of others, the following classification of patients with mitral valve prolapse has been proposed. Mitral valve prolapse - Anatomic includes patients with a wide spectrum of mitral valve abnormalities from mild to severe. Symptoms, physical findings and laboratory abnormalities in these patients are directly related to mitral valve dysfunction and progressive mitral regurgitation. Complications related to abnormal mitral valve include infective endocarditis, thromboembolic events, cardiac arrhythmias, progressive mitral regurgitation, rupture of chordae tendineae and congestive heart failure. Individuals with thick mitral leaflets and mitral systolic murmur are at higher risk of developing complications. The term mitral valve prolapse syndrome refers to the occurrence of symptoms such as palpitation, chest pain, fatigue, poor exercise tolerance, dyspnea, orthostatic phenomena and syncope or presyncope in patients with mitral valve prolapse which cannot be explained on the basis of mitral valve abnormality alone. The pathogenesis of these symptoms in patients with mitral valve prolapse syndrome appears to be related to metabolic neuroendocrine abnormalities. Preventing infective endocarditis is a major consideration in patients with mitral valve prolapse. Significant mitral regurgitation with the development of congestive heart failure often requires mitral valve surgery. The most important therapeutic approach in patients with mitral valve prolapse syndrome is to explain the mechanisms of symptoms and to reassure the patient.
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PMID:Mitral valve prolapse: etiology, clinical presentation and neuroendocrine function. 134 25

A total of 1,431 patients (mean age 63.4 +/- 14.1) with pacemakers (96.2% VVI) primoimplanted between 1967 and 1985 were followed for a mean duration of 78.2 +/- 40 pacing months, with 0.6% loss to follow-up. Cumulative survival for 1, 3, and 10 years was 0.9427, 0.9136, and 0.7536, respectively. There was no significant difference in survival between atrioventricular block (AVB) and sick sinus syndrome (SSS) patients. In addition to age and gender, factors existent prior to implantation that independently affected prognosis included manifest coronary heart disease (CHD), congenital/acquired heart lesions, heart failure, noncardiac internal disease, syncope, and generalized fatigue. After implantation, the most important factor was generalized fatigue, then age, stroke, myocardial infarct (MI), gender (male), heart failure, and syncope. Patients with no underlying disease showed an extremely high cumulative survival (0.9173 at 10 years). Compared to the general population of Yugoslavia, the pacemaker patients showed a similar yearly mortality rate until 1981. After that, elderly males (70+) had a significantly lower yearly mortality than the matched population. Thus, in this large series of pacemaker patients followed into the most recent period with an extremely low loss to follow-up, short- and long-term survival was very high. Pacemaker patients of any age who are otherwise in good health have an excellent prognosis.
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PMID:Survival in 1,431 pacemaker patients: prognostic factors and comparison with the general population. 137 12

In a 16 weeks open label therapeutic trial, studies were performed on isradipine (Lomir) to evaluate its haematological and biochemical safety and hypotensive capacity in the management of adult black hypertensive patients. The mean sitting diastolic blood pressure decreased from 105.5 +/- 9.66 mm hg at the end of the washout period to 92.1 +/- 7.59 mm hg at the end of the study, p less than 0.0001; while the mean standing diastolic blood pressure was 108.0 +/- 7.10 mm hg and 93.9 +/- 8.4 mm hg at the end of the washout phase and at the completion of the therapy respectively, p less than 0.0001. The corresponding mean sitting systolic blood pressures were 155.4 +/- 9.91 mm hg and 140.6 +/- 9.47 mm hg, p less than 0.001 while the corresponding mean standing systolic blood pressures were 156.6 +/- 12.50 mm hg and 142.6 +/- 9.15 mm hg, p less than 0.001. There were negligible changes in the mean heart rate; from 79.5 +/- 9.23 beats per minute (bpm) at the end of the placebo phase to 78.2 +/- 9.15 bpm at the end of the study in the sitting position, p greater than 0.1. The corresponding mean standing values of heart rate were 82.5 +/- 11.33 and 78.6 +/- 8.76, p greater than 0.5. The haematological, biochemical and electrocardiographic parameters remained within normal limits during the study. Side effects were mild, transitory, improved with therapy and consisted of dizziness, palpitations, headache, nocturia, tiredness and fainting attacks. The study achieved 96% good-to-excellent results with respect to both efficacy and tolerability. Isradipine (Lomir) is therefore an efficacious and safe antihypertensive agent in the management of black adult patients with mild to moderate primary arterial hypertension when administered in the dose of upto 2.5 mg twice daily alone or in combination with a beta-blocker.
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PMID:Clinical studies on isradipine in the management of adult hypertensive patients at Moi University Teaching Hospital, Eldoret, Kenya. 138 77

In seven patients who presented with lightheadedness, fatigue, "weakness," and sometimes syncope, blood pressure was found not to fall after standing for 3 to 4 minutes but to fall severely, frequently with syncope or presyncopal symptoms, after 13 to 30 minutes when measured every minute with an automatic device. This delayed orthostatic hypotension could be corrected with inflation of a pressure suit to 45 mm Hg. Its mechanism was further investigated with measurements of plasma catecholamines, plasma cortisol and aldosterone responses to corticotropin, and the effects of norepinephrine infusions on blood pressure and venous contractility. There was normal or excessive orthostatic norepinephrine release in all patients, evidence of impaired venous innervation in the legs in some, and various disorders in the other patients. Since therapeutic improvement in the orthostatic hypotension greatly reduced the symptoms, we concluded that orthostatic hypotension occurring after more than 10 minutes of standing is a potentially debilitating and often correctable disorder.
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PMID:Delayed orthostatic intolerance. 158 Jul 14


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