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Biomedical subjects

J V Perkins

Publications and source records attributed to J V Perkins.

9 recordsLinked to original sources
PubMed1991

Lack of association between keratoconus, mitral valve prolapse, and joint hypermobility.

The authors enrolled 95 patients with keratoconus and 96 matched controls in a cross-sectional study to determine if mitral valve prolapse and hypermobile joints occur with greater frequency in individuals with keratoconus than in individuals without keratoconus. The hypothesis that keratoconus may not be a distinct eye disease, but a nonspecific sign representing a more generalized systemic disorder, possibly a mild collagen tissue abnormality, was considered. M-mode and two dimensional echocardiography and cardiac auscultation detected no statistically significant difference in the prevalence of mitral valve prolapse in patients with keratoconus compared with controls. Formal, systematic examination of five joints also failed to detect a statistically significant difference in the prevalence of hypermobile joints in keratoconus patients and controls. However, as an ancillary finding, a significantly higher proportion of patients with keratoconus was found to have a history of hay fever than was the case with controls.

Adult↗
PubMed1988

Alterations in myocardial thallium-201 distribution in patients with chronic systemic hypertension undergoing single-photon emission computed tomography.

To characterize thallium-201 distribution in single-photon emission computed tomography (SPECT) cardiac images and polar bullseye maps, 100 patients with chronic systemic hypertension due to end-stage renal disease were studied and the results compared with those in 35 normotensive control subjects. Thallium-201 SPECT was performed after exercise in all control subjects and 70 hypertensive patients, and after intravenous dipyridamole in 30 patients. A frequent finding in hypertensive patients was a fixed decrease in the normal lateral-to-septal count density ratio in immediate thallium-201 SPECT images (1.02 +/- 0.10 vs 1.17 +/- 0.08 in control subjects, p less than 0.00001) and in 3-hour delayed images (1.02 +/- 0.11 vs 1.11 +/- 0.08 in control subjects, p less than 0.00001). No significant difference in count density ratio was present in patients undergoing treadmill versus diypridamole intervention. In 35 patients the count density ratio was greater than 2.0 standard deviations below the normal mean, creating the false impression of a fixed lateral defect (i.e., myocardial infarction). In 12 patients, myocardial wall thickness was measured at end-diastole by 2-dimensional echocardiography. Wall thickness was increased (greater than 11 mm) in all patients. The mean lateral-to-septal wall thickness ratio was 1.08 +/- 1.11; in no patient was the ratio less than 0.76 to indicate selective septal hypertrophy. The lateral-to-septal wall thickness and lateral-to-septal thallium-201 count density ratios correlated poorly (r = 0.43).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1978

Sequence of cardiac changes in Duchenne muscular dystrophy.

Boys with Duchenne muscular dystrophy (DMD) rarely have clinical evidence of myocardial dysfunction during life. Nevertheless, congestive heart failure is a frequent terminal event and autopsy invariably shows dystrophic myocardial involvement. Little is known regarding the progression of heart functional abnormalities in boys with DMD from birth to death. Therefore we have examined the hearts of 18 DMD boys aged 4 to 15 years with the following non-invasive methods: cardiovascular physical examination, electrocardiography, chest x-ray, serum enzymes, and echocardiography. Control subjects were 25 normal boys matched to their DMD counterparts by age and by body surface area. The dystrophic patients were divided into early (N = 9) and late (N = 9) DMD according to manual muscle testing of skeletal muscles. In early DMD, six of 23 cardiac indices differed from control boys; in the late stage, an additional five indices became abnormal. Early DMD was characterized by these abnormalities: tachycardia, large ECG R/S ratio in V1, augmented q wave voltages in Leads I, II, and V5 of the ECG, diminished contractile excursion of the left venticular posterior wall (LVPW) and interventricular septum, and decreased rate of relaxation of the LVPW. In late DMD additional cardiac abnormalities appeared: enlarged heart volume by x-ray, reduced cardiac ejection fraction, diminished change in left ventricular diameter from diastole to systole, reduced maximal systolic endocardial velocity, and decreased rate of circumferential fiber shortening as detected in the echocardiogram. Most of the cardiac abnormalities were revealed only by echocardiography, which is thus shown to be a sensitive method for monitoring the progression of cardiac dystrophy during the life span of the DMD child.

Adolescent↗
PubMed1977

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.

Adult↗