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Biomedical subjects

D O Nutter

Publications and source records attributed to D O Nutter.

At least 37 records · Page 2Linked to original sources

Neurogenic skeletal myopathy in patients with primary cardiomyopathy.

Eleven patients with hypertrophic obstructive cardiomyopathy and eight patients with idiopathic congestive cardiomyopathy underwent extensive neuromuscular studies to determine if a skeletal myopathy is associated with uncomplicated primary cardiomyopathy. The clinical examination revealed peripheral neuropathies in six patients, but no evidence of muscle weakness or atrophy. Nerve conduction studies demonstrated a neuropathy in five of these six and in one other patient: three were in the hypertrophic group and three in the congestive group. Seven patients had abnormal electromyography, but none had characteristic myopathic changes. Of these seven patients, muscle biopsies showed denervation in two patients in the congestive group and type II atrophy in two patients in the hypertrophic group. We found no evidence of primary skeletal muscle involvement; however, neuropathic features and biopsy changes of denervation were present in both groups.

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Reversible severe congestive cardiomyopathy in three cases of hypophosphatemia.

Three patients presented with severe congestive cardiomyopathy of unknown cause. All three had a profound depression of serum phosphorus levels resulting from the chronic ingestion of large quantities of a phosphorus-binding antacid. Results of physical examination and echocardiograms were consistent with cardiomegaly and severe myocardial dysfunction, and chest films showed enlargement of the cardiac silhouette with interstitial pulmonary edema. Serum phosphorus was restored to normal levels, and within 2 to 5 weeks the results of physical examination and echocardiogram of each patient returned to normal. We conclude that these patients had reversible hypophosphatemic cardiomyopathy and show the importance of inorganic phosphorus in myocardial metabolism and function. Serum phosphorus measurements should be a part of the routine evaluation of patients with congestive cardiomyopathy because, at least in some patients, hypophosphatemia appears to be a reversible cause of this disorder.

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Echocardiographic study of cardiac dimensions and function in the endurance-trained athlete.

Adaptive cardiac responses to isotonic training were studied with echocardiographic measurement of cardiac dimensions and function in 20 endurance runners whose maximal aerobic capacity on the treadmill was 4.88 +/- 0.13 (mean standard error of mean) liters of oxygen/min. They were compared with 26 young sedentary control subjects whose capacity was 3.34 +/- 0.11 liters of oxygen/min (P less than 0.001). A modest degree of right and left ventricular chamber enlargement and left ventricular hypertrophy was observed in endurance runners (left ventricular mass index 140 +/- 6 g/m2 compared with 107 +/- 4 g/m2 in sedentary control subjects, (P less than 0.001). Resting heart rate was slower in endurance runners (51 +/- 2 versus 62 +/- 2 beats/min, P less than 0.001) and resting left ventricular function as evaluated with ejection fraction and maximal posterior wall shortening velocity and mean circumferential shortening velocity (VCF) was comparable or slightly depressed in endurance runners (0.98 +/- 0.03 versus 1.02 +/- 0.05 circumferences/sec [difference not significant]). This study suggests that isotonic training results in adaptive changes in ventricular volume and mass, slower heart rates that may be associated with more efficient pumping function (that is, increasing stroke volume) and insignificant alterations in resting ejection phase indexes of left ventricular function.

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Cardiac features of an unusual X-linked humeroperoneal neuromuscular disease.

To characterize an unusual, sex-linked recessive neuromuscular disease, we studied two families with 37 males who had involvement of distal leg and proximal arm muscle groups. Electromyography and muscle biopsy in five subjects showed features of both neuropathy and myopathy. Bradycardia and syncope in 15 involved subjects were associated with early death (before the age of 50 years). Electrocardiograms in 15 others showed a spectrum of atrial abnormalities that ranged from abnormal P waves to permanent atrial paralysis and from first-degree atrioventricular block to complete heart block. No patient exhibited clinical muscle disease without electrocardiographic atrial disease. Dilated, hypertrophied left ventricles with normal indexes of function were found in three cases with permanent atrial paralysis and chronic junctional bradycardia. Cardiomegaly and cardiac failure were not present in the other cases. We conclude that permanent ventricular pacing (instituted four patients) is indicated in many of these patients to prevent serious sequelae.

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The pathophysiology of idiopathic mitral valve prolapse.

Left ventricular structure, function, and the coronary circulation were studied in a subset of patients with mitral valve leaflet prolapse. This group of 26 patients (21 females, five males, with mean age of 46 years), had the syndrome identified as idiopathic mitral valve prolapse (IMVP), which was characterized by a systolic click-murmur, clinical symptoms that were highly variable in duration and intensity, angiographically-documented mitral prolapse, and no obvious associated systemic or cardiovascular disease. Mitral regurgitation was of moderate degree in four, mild in 14, and absent in eight. The left ventricular (LV) end-diastolic volume index was elevated in ten of 25 (40%), the LV mass index was elevated in six of 17 (35%), but the LV anterior wall thickness was increase in only one of 17. Three major patterns of ventricular contraction were identified: 1) normal in seven; 2) abnormal, usually an inferior deformity and/or anterior asynergy, in eight; and 3) hyperkinetic in 11. Normal resting left ventricular function, assessed as an ejection fraction greater than 55%, was present in 17 of 25 (68%). Selective coronary arteriography was essentially normal in all 25 patients studied. An ischemic ECG response was detected during only one of 12 maximal treadmill exercise tests and in none of ten atrial pacing stress tests (AP). Myocardial lactate extraction did not change significantly during AP in six patients. We conclude that cardiomyopathy does not appear to be a primary cause or an important associated component of the IMVP syndrome. Abnormalities of the coronary circulation or of myocardial metabolism were not demonstrated by available methods. A proposed pathophysiological mechanism to explain the clinical and angiographic findings in IMVP is discussed.

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