Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six patients with severe combined aortic and mitral valve stenosis underwent double valve balloon dilation as an alternative to surgical valve replacement. Cardiac catheterization in all patients before valve dilation revealed heavily calcified aortic and mitral valves with severe stenosis and minimal regurgitation. Balloon aortic valvuloplasty was performed in each patient with a 20 mm balloon dilation catheter passed retrograde through the aortic valve whereas mitral valvuloplasty was performed transseptally with either a single or double balloon technique. After dilation, the mean aortic and mitral gradients decreased in all patients, with the area of the aortic and the mitral valve increasing from 0.5 +/- 0.3 to 0.9 +/- 0.3 cm2 and from 0.7 +/- 0.1 to 1.5 +/- 0.7 cm2, respectively. The procedures were well tolerated, with no embolic events and no significant increase in valvular regurgitation, and resulted in a reduction in symptoms of dyspnea on exertion and weakness in all patients that has persisted for an average of 5.7 months of follow-up in five of the six patients. It is concluded that combined dilation of stenotic aortic and mitral valves can be accomplished percutaneously and may be considered for patients with combined valvular stenosis who refuse or are deferred from surgical intervention.
J Am Coll Cardiol 1988 Jun
PMID:Combined aortic and mitral balloon valvuloplasty in patients with critical aortic and mitral valve stenosis: results in six cases. 336 95

A 79-year-old woman was admitted to hospital complaining of chest pain, increasing weakness, anorexia, hoarseness, headache and discomfort in the throat and jaws while eating. Physical examination, chest x-rays, serial electrocardiograms and cardiac enzymes were unremarkable. After admission she developed weakness and numbness in the left leg with urinary retention, decreased sensation to touch, weakness, increased tone, absent deep tendon reflexes and a positive Babinski sign on the left. Zeta sedimentation rate was markedly elevated at 0.63. Computerized tomographic head scan, myelography, echocardiography, barium swallow and meal, immunoglobulins, electrophoresis and other laboratory investigations were unremarkable. Repeat sedimentation rate was still markedly elevated three weeks later. A temporal artery biopsy confirmed the diagnosis of temporal or giant cell arteritis. Prednisone, 60 mg daily, was started.
Can J Cardiol 1988 Apr
PMID:Acute chest pain in an elderly woman. 337 98

Emery-Dreifuss muscular dystrophy is an X-linked recessive condition characterized by mild muscular weakness predominantly in a humero-peroneal distribution with variable facial involvement. Onset is in childhood with slow progression of weakness. The disease is often associated with cardiac involvement, mainly with bradyarrhythmias which might be responsible for sudden death. The most striking finding derived from the literature is the high incidence of sudden death; in the 7 large families described, out of the 79 reported patients 32 died suddenly at a young age (between 25 and 56 years). We performed a cardiologic evaluation of 11 subjects of a large italian family with affected males in four generations: 5 affected males (3 adults and 2 boys), 3 carriers and 3 healthy relatives (2 females and 1 male). Supraventricular arrhythmias were documented either in the dystrophic males or in the carriers. There was no correlation between the severity of cardiac rhythm abnormality and the severity of muscular weakness in the affected males, 3 of whom required pacemaker insertion. All the carriers were free of muscular involvement, but showed arrhythmias of variable degree, in one case requiring pacemaker insertion. In conclusion our data indicate an extremely high incidence of bradyarrhythmias, sometimes serious, in patients with Emery-Dreifuss muscular dystrophy. Holter monitoring is therefore mandatory and electrophysiological study is sometime necessary. Because of the high risk of sudden death in adult patients, we recommend permanent pacemaker implantation even in asymptomatic subjects, as soon as bradyarrhythmias are detected.
G Ital Cardiol 1987 Jul
PMID:[Cardiologic evaluation in a family with Emery-Dreifuss muscular dystrophy]. 367 9

We report on a patient with myotonic muscular dystrophy in whom mitral valve prolapse associated with prolonged PR interval and left anterior hemiblock was documented 3 years before any clinical evidence of myotonia, muscle weakness or wasting. One year after diagnosis had been established, he developed atrial flutter with 1:1 atrioventricular conduction, an arrhythmia that in addition to complete heart block and ventricular arrhythmias may account for the occurrence of syncope and sudden death in this group of patients.
Int J Cardiol 1986 Jun
PMID:Unusual cardiac manifestations in a patient with myotonic muscular dystrophy. 372 33

To compare a propranolol-verapamil with a propranolol-nifedipine combination in patients with severe angina of effort, 16 patients (11 men and 5 women, aged 56 +/- 8 years [mean +/- standard deviation]) with more than 5 episodes/week of angina and a positive exercise tolerance test despite propranolol (229 +/- 44 mg/day [range 180 to 360]) were maintained on this dose of propranolol and, in addition, received verapamil (360 mg/day) and nifedipine (60 mg/day) for 3 weeks each in a double-blind, randomized fashion. In comparison with propranolol alone, anginal frequency and nitroglycerin usage were reduced by propranolol-verapamil but not by propranolol-nifedipine. Exercise time (standard Bruce protocol) was similar for the 2 combinations (6.4 +/- 2.0 minutes with propranolol-verapamil, 6.6 +/- 2.1 minutes with propranolol-nifedipine, difference not significant), but the magnitude of ST-segment depression at peak exercise was less (p less than 0.05) during propranolol-verapamil (0.03 +/- 0.06 mV) than during propranolol alone (0.18 +/- 0.07 mV) and propranolol-nifedipine (0.08 +/- 0.07 mV). Left ventricular ejection fraction at rest was higher (p less than 0.05) with propranolol-nifedipine (0.62 +/- 0.10) than with propranolol-verapamil (0.58 +/- 0.10), but neither differed from ejection fraction at rest with propranolol alone (0.59 +/- 0.08). Ejection fraction at peak exercise was similar during all 3 periods. In 2 patients, verapamil caused weakness, lightheadedness, and severe sinus bradycardia (40 to 48 beats/min), and the dosage was reduced (blindly) to 240 mg/day, with the alleviation of bradycardia and associated symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1985 Feb 01
PMID:Propranolol-verapamil versus propranolol-nifedipine in severe angina pectoris of effort: a randomized, double-blind, crossover study. 396 62

A case of pneumonitis and pulmonary fibrosis occurring during long term treatment with amiodarone hydrochloride is described. The patient, a 68 year old woman, presented with severe dyspnoea and weakness 13 months after the institution of amiodarone therapy, 200 mg. bid 6 days/week. Chest x-ray showed patchy infiltrates involving the parahilar and medullary areas of both upper lobes. The clinical symptoms and the pulmonary signs improved only after amiodarone discontinuation and steroid treatment. Radiographic abnormalities gradually cleared over 45 days except for residual lines of fibrosis in the zones of previous alveolar consolidation still present 4 months later.
G Ital Cardiol 1985 May
PMID:Lung disease associated with amiodarone treatment. 405 92

34 patients have been controlled after beta-blocking therapy, for a mean period of 5 years. Symptoms and evolution: syncope disappeared, angoy passed from 47% to 23%, dyspnea from 65% to 47%, dizziness from 70% to 54%, weakness from 30% to 37%. A systolic murmur was present in 75% of the cases. Two patients died by heart failure. Phonocardiogram: the systolic murmur was unchanged, like the carotid pulse. Paradoxical splitting of the 2 degrees sound was more frequent, atrial sound unimodified, isometric contraction shortened (60%) and the Q-1 degree sound interval prolonged (90%). Electrocardiogram: 1 degree A/V block appeared in 24% of the cases, complete A/V block in 9%, atrial fibrillation in 3%. Left atrial enlargement was more frequent; left ventricular hypertrophy unchanged. Heart catheterization (10 cases, after a mean period of 5.5 years): left ventricular pressure gradient passed from 80% to 90%; a low cardiac index from 20% to 30%; telediastolic pressure of left ventricle was unmmodified in 10% of cases, more elevated in 50%, less elevated in 40%. Chest X ray: cardiac size was unchanged in 65% of cases, enlarged in 32%; smaller in 3%. In conclusion, symptoms improved in most of the patients; no case of sudden death was observed. Some data however show that the evolution of the myocardiopathy goes on to congestive heart failure and arise doubts on the real usefullness of beta-blocking drugs in the disease.
G Ital Cardiol 1980
PMID:[beta-Blocking therapy in obstructive hypertrophic cardiomyopathy. Long term results (author's transl)]. 610 83

The clinical, electrocardiographic, pharmacologic, electrophysiologic and Holter monitoring findings are described in four patients with autonomic sinus node dysfunction and one patient with autonomic binodal disease. All showed cerebral symptoms, and had attacks of dizziness, weakness, near-syncope or syncope. After a pharmacologic autonomic blockade with propranolol and atropine, all patients had normal intrinsic heart rates. Electrophysiological studies revealed normal corrected intrinsic node recovery time (less than or equal to 240 msec) a gradual return to the basic cycle length in the secondary postpacing cycles after autonomic blockade, and no intrinsic paroxysmal atrioventricular block. Continuous ECG monitoring (1-3 X 24 hours) revealed severe sinus bradycardia, SA-block, severe sinus arrest, cardiac standstill, atrial fibrillation and in two patients associated AV-block. Autonomic blockade with electrophysiological studies exclude the intrinsic involvement of the sinoatrial and atrioventricular node. Holter monitoring is the best method for assessing the autonomic neurovegetative component of dysrhythmias. Therapy regarding isolated autonomic sinus node dysfunction depended on the pathomechanisms of rhythm disorders: two patients received permanent pacemakers, antiarrhythmic drugs were applied in the case of two patients, and etiological treatment in the case of one. During the follow-up, all patients became symptom-free.
Acta Cardiol 1984
PMID:Autonomic sinus node dysfunction and its treatment. 633 99

Nadolol (N) titrated from 80 to 240 mg or bendroflumethiazide (B) 5 to 10 mg, or the combination (B + N), were randomly assigned double-blind to 365 men with pretreatment diastolic blood pressures (BP) of 95 to 114 mm Hg. After 12 weeks of treatment, a diastolic BP of less than 90 mm Hg was achieved in 49% who received N, 46% who received B and 85% who received B + N. With N, the diastolic BP decreased more in whites than in blacks; with B, this racial trend was reversed. Side effects were infrequent; the most common were impotence, lethargy, weakness and postural dizziness, which occurred more often with B than with N. Addition of hydralazine, 25 to 100 mg twice daily, controlled diastolic BP at a level of less than 90 mm Hg in approximately 60% of those previously uncontrolled. N, and especially B + N, provided an efficacious once-daily treatment for systemic hypertension, and addition of hydralazine was effective in most nonresponders.
Am J Cardiol 1983 Dec 01
PMID:Efficacy of nadolol alone and combined with bendroflumethiazide and hydralazine for systemic hypertension. 635 51

Electrophysiologic studies, echocardiograms, cardiac catheterizations and histologic and biochemical analyses of skeletal muscle biopsies were performed in 10 patients (aged 10 to 37 years, mean 21) who had dysrhythmias as the initial manifestation of cardiomyopathy. Presenting symptoms and signs attributable to dysrhythmias included sudden cardiac arrest in 2 patients, syncope in 3, presyncope in 3 and palpitations in 2. There was no clinical evidence of skeletal muscle weakness in any patient. Multicatheter electrophysiologic evaluation established diagnoses of ventricular tachycardia in 6 patients, primary atrial tachycardia in 2 and third degree infra-Hisian heart block in 1 patient. One patient presenting with palpitations had no inducible arrhythmia or conduction disturbance. Echocardiographic, angiographic and hemodynamic studies demonstrated previously unsuspected dilated cardiomyopathy in 7 patients and restrictive cardiomyopathy in 3. Skeletal muscle histologic characteristics were abnormal in all 10 patients; increases in lipid droplets and endomysial fibrosis were the characteristic findings. Serum free carnitine and short- and long-chain acylcarnitine were normal in 9 patients. However, skeletal muscle long-chain acylcarnitine was reduced in 9 patients. These findings support the concept that in certain patients presenting with dysrhythmias, the dysrhythmia may be a manifestation of cardiac and skeletal (that is, generalized) myopathy.
Am J Cardiol 1984 Mar 01
PMID:Cardiac and skeletal myopathy associated with cardiac dysrhythmias. 670 21


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