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

Since the mid-1980s resistance training has become an accepted part of the exercise rehabilitation process for patients eligible for traditional cardiac rehabilitation programs. A growing number of studies have demonstrated the safety of resistance training in Phase III/IV programs (Phase III--community based, beginning 6-12 wk posthospital discharge; a typical patient would be clinically stable with a functional capacity of > or = 5 METs; Phase IV--long-term maintenance) and more recently in Phase II (beginning within 3 wk posthospital discharge and lasting up to 3 months). Evidence is consistent that this form of training provokes fewer signs and symptoms of myocardial ischemia than aerobic testing and training, perhaps because of a lower heart rate (HR) and higher diastolic pressure combining to produce improved coronary artery filling. The major role of resistance training in heart disease patients is to promote increased dynamic muscle strength. Increases in muscular strength have been associated with increased peak exercise performance, improved submaximal endurance, and reduced ratings of perceived leg effort. Two studies show that resistance training may result in improved self-efficacy for strength and exercise tasks and improved quality of life parameters such as total mood disturbance, depression/dejection, fatigue/inertia, and emotional health domain scores. The data on risk factor modification are somewhat equivocal. Studies on blood lipid profiles have mostly been contaminated by confounders, and the effects on blood pressure (BP) are inconsistent. There are encouraging reports that resistance training may increase glucose tolerance and insulin sensitivity, independent of changes in body fat or aerobic capacity. Future studies are needed in patients with congestive heart failure and orthotopic heart transplantation; muscle weakness is common in these groups and makes them excellent candidates to benefit from this form of exercise.
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PMID:Role of resistance training in heart disease. 978 66

Paroxysmal supraventricular tachycardia (SVT) may have numerous electro-physiologic mechanisms. The most common type of SVT is AV-nodal reentry tachycardia (60%) followed by the bypass tract-mediated SVT (preexcitation. 30%) and a smaller group (10%) comprising paroxysmal atrial flutter or fibrillation and atrial ectopic tachycardia. In persons with otherwise normal hearts symptoms are usually mild and include palpitations or an uneasy feeling in the chest. But some describe precordial pain. Weakness, dizziness, nausea, vomiting, and even syncope. Whenever possible a 12-lead-ECG during an episode of SVT should be obtained. If not possible the use of several Holter-ECG or of an event-recorder may be helpful. Conversion of a SVT can be accomplished by vagal maneuvers or intravenous adenosine (6-18 mg bolus injection). Further diagnostic procedures should prove or rule out a significant structural heart disease. Therapeutic options (expectative, pharmacological prophylaxis, invasive electrophysiologic testing and catheter-mediated modification or ablation) are chosen according to the objective threat (e.g. ventricular fibrillation due to 1:1 conducted atrial fibrillation in a preexcitation syndrome) and the subjective complaints. Definitive healing of the AV-nodal reentry tachycardia and the bypass tract-mediated SVT can be achieved by use of catheter-mediated modification or ablation in 95 to nearly 100%.
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PMID:[Modern therapy of paroxysmal supraventricular tachycardia]. 1009 47

A 35-year-old obese man presented with a chief complaint of hand dryness of 5 years' duration. He was a store manager and denied exposure to chemicals, repetitive trauma, chronic irritation, and hard manual labor. However, he did admit to frequent hand washing. He had no itching or swelling in his hands, but on occasion he had tenderness in the dry areas. He had no personal or family history of diabetes, heart disease, or renal disease, and he stated that at his annual physical examination 6 months earlier, routine blood work was normal. He reported polyuria (every 2 hours), nocturia (five times per night), and polydipsia but no weakness, weight loss, visual changes, or neurosensory changes. Examination revealed xerosis of his hands and "pebbles" on the dorsal aspect of his fingers. The papules were most dense over the knuckles and interphalangeal joints (figures 1 through 3). He also had dozens of acrochordons (i.e., cutaneous papillomas, or skin tags) 1 to 4 mm in diameter on his neck, axilla, and groin. No other cutaneous lesions were noted. Specifically, there was no scleredema adultorum, necrobiosis lipoidica diabeticorum, acanthosis nigricans, bullae, or patchy pretibial pigmentation, although he did have several brown macules 1 to 5 mm in diameter on the sides of his lower legs. The macules had been present for years. Levels of hemoglobin A1c and glycated hemoglobin were 7.5% and 9.5%, respectively (normal, 4.4% to 5.9% and 5.0% to 7.3%). The patient was referred to his family physician, and his diabetes has been well controlled with insulin.
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PMID:Finger 'pebbles'. A dermatologic sign of diabetes mellitus. 1072 45

Emery-Dreifuss muscular dystrophy (EDMD) was delineated as a separate form of muscular dystrophy nearly 40 years ago, based on the distinctive clinical features of early contractures and humero-peroneal weakness, and cardiac conduction defects. The gene, STA at Xq28, for the commoner X-linked EDMD encodes a 34 kD nuclear membrane protein designated 'emerin', and in almost all cases on immunostaining is absent in muscle, skin fibroblasts, leucocytes and even exfoliative buccal cells, and a mosaic pattern in female carriers. The gene, LMNA at 1q21, for the autosomal dominant Emery-Dreifuss muscular dystrophy encodes other nuclear membrane proteins, lamins A/C. The diagnosis (at present) depends on mutation analysis rather than protein immunohistochemistry. It is still not at all clear how defects in these nuclear membrane proteins are related to the phenotype, even less clear that LMNA mutations can also be associated with familial dilated cardiomyopathy with no weakness, and even familial partial lipodystrophy with diabetes mellitus and coronary heart disease! What began as clinical studies in a relatively rare form of dystrophy has progressed to detailed research into the functions of nuclear membrane proteins particularly in regard to various forms of heart disease.
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PMID:Emery-Dreifuss muscular dystrophy - a 40 year retrospective. 1083 46

Pure motor stroke is the commonest lacunar syndrome, but it may be associated with nonlacunar mechanisms of infarction. Pure motor brachiofacial weakness has been considered as a partial syndrome depending on a lacunar mechanism. We studied the correlations between stroke type, topography of infarction and etiology in 22 patients with pure motor brachiofacial weakness who were consecutively admitted to our stroke unit during a 10-year period. Seventeen patients had a small deep infarct, 4 had a cortical infarct in the superficial MCA territory and 1 had no specific lesion. The part of the cardiovascular risk factors was about 36% for smoking, 13% for diabetes mellitus, 60% for dyslipidemia and 40% for heart disease. Hypertension was present in 75% of our cases. None of the patients had a large artery stenosis on Doppler ultrasonography. We concluded that brachiofacial pure motor stroke is not always correlated to lacunar infarcts and may be due to a cortical infarct. MRI should be performed when brain CT is normal because of the implications it may have in management and therapy.
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PMID:Brachiofacial pure motor stroke. 1143 77

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

Continuous chronic drug infusion with PGE1 via a portable pump and neuromuscular electrical stimulation (NMES) help to improve the quality of life in patients with severe chronic heart failure waiting for a donor heart, as both treatments can be performed at home. We report a 56-year-old woman suffering from severe chronic heart failure, who was referred for a cardiac rehabilitation program because of progressive muscle weakness and weight loss. Due to her underlying heart disease she was unable to perform voluntary exercise. NMES of both knee extensor muscles was started. Under simultaneous chronic drug infusion with PGE1 via a portable pump the patient developed clinical signs of hypertrophic osteoarthropathy, which prevented her from continuing the rehabilitation program. X-ray examinations and bone scans concurred with the diagnosis of secondary hypertrophic osteoarthropathy. After the PGE1 dose had been reduced, the clinical signs of the osteoarthropathy resolved and the patient was able to continue the rehabilitation program with no difficulty. This case report underlines the importance of being aware of the potential side effects of modern cardiac drugs in the complex treatment of patients waiting for a donor heart.
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PMID:Hypertrophic osteoarthropathy caused by PGE1 in a patient with congestive heart failure during cardiac rehabilitation. 1206 Sep 68

Aging is associated with a number of physiologic and functional declines that can contribute to increased disability, frailty, and falls. Contributing factors are the loss of muscle mass and strength as age increases, a phenomenon called sarcopenia. Sarcopenia can result or be exacerbated by certain chronic conditions, and can also increase the burden of chronic disease. Current research has demonstrated that strength-training exercises have the ability to combat weakness and frailty and their debilitating consequences. Done regularly (e.g., 2 to 3 days per week), these exercises build muscle strength and muscle mass and preserve bone density, independence, and vitality with age. In addition, strength training also has the ability to reduce the risk of osteoporosis and the signs and symptoms of numerous chronic diseases such as heart disease, arthritis, and type 2 diabetes, while also improving sleep and reducing depression. This paper reviews the current research on strength training and older adults, evaluating exercise protocols in a variety of populations. It is clear that a variety of strength-training prescriptions from highly controlled laboratory-based to minimally supervised home-based programs have the ability to elicit meaningful health benefits in older adults. The key challenges as this field of exercise science moves forward are to best identify the most appropriate strength-training recommendations for older adults and to greatly increase the access to safe and effective programs in a variety of settings.
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PMID:The benefits of strength training for older adults. 1455 38

Falls are a common and serious cause of disability and death amongst the growing older population. As most falls are multifactorial, effective fall prevention strategies require a package of measures to be addressed in parallel (medication review and modification; detection and treatment of postural hypotension and heart disease; strength and balance exercise training for muscle weakness and instability; home hazard modification). The last decade has seen the emergence of a wealth of research evidence on effective fall prevention, but unfortunately, real world clinical practice is lagging far behind the evidence base. Much of the expertise and skills for effective fall prevention already exists within the primary care team. Responsibility for injury prevention extends beyond general practice, but the primary care team must be prepared to play its part.
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PMID:Falls, bones and the primary care team. 1461 Oct 8

In myotonic dystrophy type 2 (DM2/PROMM), cardiac muscle involvement is usually more benign than in DM1, but clinically severe cardiomyopathy has been reported in some patients. Using a novel method of magnetic resonance spectroscopy (MRS), we examined the left ventricular myocardium and the left gastrocnemius muscle in 11 unselected DM2/PROMM patients without overt cardiac disease. Data on cardiac morphology and function were obtained by gradient echo two-dimensional cine magnetic resonance imaging (MRI); no significant differences were found between DM2 patients and healthy controls, but using a median split approach older patients showed mildly increased left ventricular (LV) volumes, i.e., 59% increase of end-systolic volume index (ESVI) and 35% increase of end-diastolic volume index (EDVI), and an increase of LV mass (26%). On cardiac MRS, DM2/PROMM patients showed a reduction of phosphocreatine (PCr) and adenosine triphosphate (ATP) by 25 and 20% compared to matched healthy controls. No significant differences were found between younger and older patients. In skeletal muscle of the DM2 patients, no significant decrease of PCr and ATP concentrations was found. However, in older patients, who commonly show overt hip flexor muscle weakness, we observed reduced values for PCr and ATP. Our MRS and MRI findings reveal evidence for subclinical cardiomyopathy in DM2/PROMM patients without overt heart disease. Future prospective studies are needed to clarify the risk of developing overt cardiac disease in DM2 and to define prognostic factors.
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PMID:Cardiac and skeletal muscle involvement in myotonic dystrophy type 2 (DM2): a quantitative 31P-MRS and MRI study. 1545 41


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