PubMed Health⌕ Search

Biomedical subjects

J J Ross

Publications and source records attributed to J J Ross.

At least 19 recordsLinked to original sources
PubMed1992

Single-plane transesophageal echocardiography for assessing function of mechanical or bioprosthetic valves in the aortic valve position.

To assess the value and limitations of single-plane transesophageal echocardiography in the evaluation of prosthetic aortic valve function, 89 patients (69 mechanical and 20 bioprosthetic aortic valves) were studied by combined transthoracic and transesophageal 2-dimensional and color flow Doppler echocardiography. In the assessment of aortic regurgitation, the transthoracic and transesophageal echocardiographic findings were concordant in 71 of 89 patients (80%). In 8 patients, the degree of aortic regurgitation was underestimated by the transthoracic approach; in each case the quality of the transthoracic echocardiogram was poor. In 10 patients, transesophageal echocardiography failed to detect trivial aortic regurgitation due to acoustic shadowing of the left ventricular outflow tract from a mechanical valve in the mitral valve position. Transesophageal echocardiography was superior to transthoracic echocardiography in diagnosing perivalvular abscess, subaortic perforation, valvular dehiscence, torn or thickened bioprosthetic aortic valve cusps, and in clearly distinguishing perivalvular from valvular aortic regurgitation. Transesophageal echocardiography correctly diagnosed bioprosthetic valve obstruction in 1 patient, but failed to diagnose mechanical valve obstruction in another. In conclusion, transesophageal echocardiography offers no advantage over the transthoracic approach in the detection and quantification of prosthetic aortic regurgitation unless the transthoracic image quality is poor. Transesophageal echocardiography is limited in detecting mechanical valve obstruction and in detecting aortic regurgitation in the presence of a mechanical prosthesis in the mitral valve position. However, it is superior to transthoracic echocardiography in identifying perivalvular pathology, differentiating perivalvular from valvular regurgitation and in defining the anatomic abnormality responsible for the prosthetic valve dysfunction. Combined transthoracic and transesophageal examination provides complete anatomic and hemodynamic assessment of prosthetic aortic valve function.

Adolescent↗
PubMed1992

Closure of eyelid defects.

BACKGROUND: Repair of eyelid defects can be achieved by an array of procedures. OBJECTIVE: To provide a basic approach to repairing eyelid defects. METHODS: Defects are categorized by size. The method of repair for each defect is described. CONCLUSION: By selecting the proper method of closure, with due consideration of the size, location, and configuration of the defect, the cutaneous surgeon can repair eyelid defects whilst maintaining the best possible function and cosmetic appearance.

Eyelid Diseases↗
PubMed1992

Transesophageal echocardiographic recognition of subaortic complications in aortic valve endocarditis. Clinical and surgical implications.

BACKGROUND: Secondary involvement of the mitral-aortic intervalvular fibrosa and the anterior mitral leaflet (subaortic structures) can occur in patients with aortic valve endocarditis. The secondary involvement of these structures occurs as a result of direct extension of the infection from the aortic valve or as a result of an infected aortic regurgitant jet striking the ventricular surfaces of the mitral-aortic intervalvular fibrosa and the anterior mitral leaflet. The abscess of mitral-aortic intervalvular fibrosa can expand to form an aneurysm. Subsequently, this mitral-aortic intervalvular fibrosa aneurysm can develop a perforation and communicate with the left atrium, resulting in the systolic regurgitation of blood from the left ventricular outflow tract into the left atrium. Secondary infection can also occur on the ventricular surface of the anterior mitral leaflet and result in the formation of an aneurysm or perforation of anterior mitral leaflet. METHODS AND RESULTS: This study examines the utility of transesophageal echocardiography in the detection of these subaortic complications in 55 consecutive patients with aortic valve endocarditis. A total of 24 patients (44%) had involvement of subaortic structures, including four with an abscess in the mitral-aortic intervalvular fibrosa, four with mitral-aortic intervalvular fibrosa aneurysm, seven with perforation of the mitral-aortic intervalvular fibrosa with communication into the left atrium, two with an aneurysm of the anterior mitral leaflet, and seven with perforation of the anterior mitral leaflet. The transesophageal echocardiographic findings were confirmed at surgery in 20 patients and at necropsy in two. By comparison, transthoracic echocardiography visualized these lesions in five of 24 patients (21%), including none of four with mitral-aortic intervalvular fibrosa abscesses, two of four with mitral-aortic intervalvular fibrosa aneurysms, one of seven with mitral-aortic intervalvular fibrosa perforations, one of two with anterior mitral leaflet aneurysms, and one of seven anterior mitral leaflet perforations. Eccentric mitral regurgitation-type systolic jets were noted in eight additional patients by transthoracic color flow imaging, and this finding suggested the possibility of these unusual subaortic complications. If these patients are included, then transthoracic echocardiography suggested the presence of these subaortic complications in 13 of 24 patients (54%). CONCLUSIONS: The results indicate that 1) involvement of the subaortic structures in patients with aortic valve endocarditis may be more common than previously recognized, 2) patients with aortic valve endocarditis and eccentric jets of mitral regurgitation on transthoracic echocardiography should undergo further evaluation by transesophageal echocardiography to exclude these unusual complications, 3) precise recognition of these complications is of value in the optimal medical and surgical management of these patients, and 4) these complications may be responsible for unexplained congestive heart failure and hemodynamic deterioration in some patients with aortic valve endocarditis.

Abscess↗
PubMed1992

Diagnosis of superior vena caval obstruction by transesophageal echocardiography.

Superior vena caval (SVC) syndrome may be caused by extravascular compression or intravascular obstruction. Knowing the mechanism of SVC syndrome enables the physician to choose appropriate treatment. Transesophageal echocardiography (TEE) is a safe bedside procedure that is excellent for evaluating the SVC and its surrounding structures. We report the valuable role of TEE in demonstrating the mechanism of SVC syndrome.

Aged↗
PubMed1991

Recognition and embolic potential of intraaortic atherosclerotic debris.

Atherosclerotic disease of the thoracic aorta is common in the elderly and patients with clinical coronary artery disease. Although embolization can occur from atherosclerotic debris within the thoracic aorta, it is not commonly considered in the differential diagnosis of the source of a systemic embolism. In the current study, the prevalence, clinical significance and embolic potential of intraaortic atherosclerotic debris as detected by transesophageal echocardiography was determined. Intraaortic atherosclerotic debris was identified in 38 (7%) of 556 patients undergoing transesophageal echocardiography. An embolic event occurred among 11 (31%) of the 36 study patients with intraaortic atherosclerotic debris. The incidence of an embolic event was higher when the debris was pedunculated and highly mobile (8 [73%] of 11 patients) than when it was layered and immobile (3 [12%] of 25 patients) (p less than 0.002). Among 15 patients undergoing an invasive procedure of the aorta, the incidence of embolism was 27%. In conclusion, in a patient with an embolic event, the thoracic aorta should be considered as a potential source. Transesophageal echocardiography can reliably detect intraaortic atherosclerotic debris, and when it is identified, an invasive aortic procedure should be avoided if possible.

Aged↗
PubMed1990

Transthoracic high frequency (7.5 MHz) echocardiographic assessment of coronary vascular reserve and its relation to left ventricular mass.

Transthoracic high frequency (7.5 MHz) ultrasonography can visualize the distal left anterior descending coronary artery. Thirty-seven patients were studied before and after administration of 0.4 mg sublingual nitroglycerin to determine whether this technique could quantitatively record changes in coronary artery diameter after intervention. Left anterior descending coronary artery diameter increased from 2.2 to 2.8 mm (p less than 0.05). The vasodilator response of this artery was compared with left ventricular mass index in normal subjects, patients with congestive cardiomyopathy and those with end-stage renal disease and left ventricular hypertrophy. Left anterior descending artery diameter increased 55% in normal subjects, 27% in patients with dilated cardiomyopathy and 10% in those with end-stage renal disease with left ventricular hypertrophy. These results demonstrate that high frequency ultrasound can detect nitroglycerin-induced changes in left anterior descending artery diameter. The percent increase is related to the diameter before nitroglycerin administration, which is related to the underlying diagnosis and left ventricular mass index.

Adult↗
PubMed1990

Transthoracic two-dimensional high frequency (7.5 MHz) ultrasonic visualization of the distal left anterior descending coronary artery.

High frequency (7.5 MHz) two-dimensional ultrasound in combination with modified acoustic windows allowed visualization of the distal left anterior descending artery in 61 (85%) of 72 patients studied. Visualization was confirmed in one patient who underwent simultaneous high frequency ultrasound recording and selective dye injection into the left coronary artery. In addition, calcific coronary atherosclerosis was identified in one patient. The saphenous vein bypass graft along with its distal site of anastomosis was clearly seen in 3 patients and coronary artery flow was detected in 24 (33%).

Adult↗
PubMed1988

A critical period for formation of secondary myotubes defined by prenatal undernourishment in rats.

Rats fed a restricted diet during gestation and lactation gave birth to pups with about 60% the normal birthweight. Maintaining the undernutrition after birth reduced the rate of growth of the pups so that their body weights were only 40% of control at PN7. Soleus and lumbrical muscles in these animals had reduced numbers of muscle fibres, and quantitative examination of embryonic muscles revealed that this was due solely to a decreased formation of secondary myotubes; the number of primary myotubes remained normal. Undernutrition did not affect the number of motoneurones surviving normal developmental death. Restoration of normal dietary intake on E21, one day before birth, did not correct the deficit in muscle fibre numbers in soleus muscles examined when the animals reached one month of age. Development of the lumbrical muscle lags behind the soleus and unrestricted feeding from E21 onwards allowed a normal number of fibres to develop from this time on, although the initial deficit was never restored. These experiments define a critical period in muscle development during which the potential maximum number of secondary myotubes is determined.

Animals↗
PubMed1987

Embryonic somatic nerve destruction with beta-bungarotoxin.

The effects and time course of a single injection of beta-bungarotoxin into E14 rat embryos were examined with an electron-microscopic study of development of the internal intercostal somatic nerve. Within 24 h of injection, axons in this nerve became swollen and fused at points along their length. By 48 h after injection no component of the nerve remained in distal segments of ribcage; complete loss of axons and components of the nerve sheath from proximal regions took slightly longer. At later times, no trace of peripheral nerve axons, Schwann cells or elements of the nerve sheath remained. beta-Bungarotoxin applied on E17 destroyed developing axons in a similar manner, but the perineurium remained in place, and axons regenerated within the original nerve trunk. The study confirms that sensory and motor neurons are much less able to survive axon degeneration on E14 than after the major period of normal cell death (which is nearly over by E18), and that the maintenance and continued development of the perineurium during E14-E16 depends on the presence of peripheral nerve axons.

Animals↗
PubMed1987

Formation of primary and secondary myotubes in rat lumbrical muscles.

Numbers of myoblasts, primary myotubes and secondary myotubes in developing rat embryo hindlimb IVth lumbrical muscles were counted at daily intervals up until the time of birth, using electron microscopy. Motoneurone death at the spinal cord level supplying the lumbricals was assessed by counting axons in the 4th lumbar ventral root. Death of the motoneurones that supply the intrinsic muscles of the hindfoot was monitored by comparing the timecourse of development of total muscle choline acetyltransferase activity in control embryos with that in embryos where motoneurone death was inhibited by chronic paralysis with TTX, and by counting axons in the mixed nerve trunks at the level of the ankle at daily intervals. Condensations of undifferentiated cells marking the site of formation of the muscle were seen on embryonic day 15 (E15). Primary myotubes began to appear on E16 and reached a stable number (102 +/- 4) by E17. Secondary myotubes first appeared two days later, on E19, and numbered 280 at the time of birth (E22). The adult total of about 1000 muscle fibres, derived from both primary and secondary myotubes, was reached at postnatal day 7 (PN7) so considerable generation of secondary myotubes occurred after birth. There was a linear correlation between the number of undifferentiated mononucleate cells in a muscle and the rate of formation of secondary myotubes. The major period of motoneurone death in lumbar spinal cord was during E16-E17, when axon numbers in the L4 ventral root fell from 12,000 to 4000, but a discontinuity in the curve of muscle ChAT activity versus time indicated that death in the lumbrical motor pool occurred during E17-E19, after all primary myotubes had formed and before generation of secondary myotubes began. We suggest that motoneurone death, by regulating the final size of the motoneurone pool, regulates the ratio of secondary to primary myotube numbers in a muscle.

Animals↗
PubMed1987

Neural determination of muscle fibre numbers in embryonic rat lumbrical muscles.

The generation and development of muscle cells in the IVth hindlimb lumbrical muscle of the rat was studied following total or partial denervation. Denervation was carried out by injection of beta-bungarotoxin (beta-BTX), a neurotoxin which binds to and destroys peripheral nerves. Primary myotubes were generated in denervated muscles and reached their normal stable number on embryonic day 17 (E17). This number was not maintained and denervated muscles examined on E19 or E21 contained many degenerating primary myotubes. Embryos injected with beta-bungarotoxin (beta-BTX) on E12 or E13 suffered a partial loss of motoneurones, resulting in a reduced number of axons in the L4 ventral root (the IVth lumbrical muscle is supplied by axons in L4, L5 and L6 ventral roots) and reduced numbers of nerve terminals in the intrinsic muscles of the hindfoot. Twitch tension measurements showed that all myotubes in partly innervated muscles examined on E21 contracted in response to nerve stimulation. Primary myotubes were formed and maintained at normal numbers in muscles with innervation reduced throughout development, but a diminished number of secondary myotubes formed by E21. The latter was correlated with a reduction in number of mononucleate cells within the muscles. If beta-BTX was injected on E18 to denervate muscles after primary myotube formation was complete, E21 embryo muscles contained degenerating primary myotubes. After injection to denervate muscles on E19, the day secondary myotubes begin to form, E21 muscles possessed normal numbers of primary myotubes. In both cases, secondary myotube formation had stopped about 1 day after the injection and the number of mononucleate cells was greatly reduced, indicating that cessation of secondary myotube generation was most probably due to exhaustion of the supply of competent myoblasts. We conclude that nerve terminals regulate the number of secondary myotubes by stimulating mitosis in a nerve-dependent population of myoblasts and that activation of these myoblasts requires the physical presence of nerve terminals as well as activation of contraction in primary myotubes.

Animals↗
PubMed1986

Transfer of differentiated synaptic terminals from primary myotubes to new-formed muscle cells during embryonic development in the rat.

Most fibres in adult muscles are derived from secondary myotubes which form around an earlier developing population of primary myotubes. We examined embryonic rat IVth lumbrical muscles at a stage when most secondary myotubes were less than 24 h old, in order to study their acquisition of synaptic terminals. Single nerve terminals were frequently seen to synapse simultaneously with a well-developed primary myotube and a new-formed secondary myotube. Reconstructions of serial section electron micrographs revealed that most of these shared terminals had synaptic specializations opposed to the primary myotube, but others appeared to transmit mainly to the secondary myotube. Primary myotubes are contacted by multiple nerve terminals before secondary myotube formation has begun, and we suggest that synaptic terminals are progressively transferred from primaries to secondaries, the observed shared terminals representing intermediate stages in this transfer.

Animals↗