Search PubMed⌕ Search

Biomedical subjects

G M Vincent

Publications and source records attributed to G M Vincent.

66 records · Page 4Linked to original sources
PubMed1987

The financial impact of Medicare diagnosis-related groups. Effect upon hospitals receiving cardiac patients referred for tertiary care.

To evaluate the financial effects of diagnosis-related groups, we compared 128 Medicare and 183 non-Medicare cardiac patients aeromedically evacuated to a major referral center for critical care. A significant difference (p less than 0.05) was found between Medicare patients vs non-Medicare patients for age (71 +/- 7 vs 51 +/- 9 years) and mortality (13 percent vs 6 percent). No significant difference was found for admissions to the intensive care unit (95 percent vs 95 percent), mean length of stay in intensive care (4.7 +/- 5.3 vs 3.9 +/- 5.4 days), mean length of hospitalization (9.6 +/- 7.5 vs 7.9 +/- 7.0 days), mean number of International Classification Diagnoses (ICD-9) surgical operations (0.8 +/- 1.3 vs 0.6 +/- 1.2), and mean number of ICD procedures (3.0 +/- 2.3 vs 3.3 +/- 2.1). The average cost of care ($13,427 +/- $12,700 per patient) for Medicare patients was higher but not statistically different from non-Medicare patients ($10,474 +/- $10,114 per patient). Prior cost-based Medicare payments ($10,594 +/- $9,861 per patient) have been significantly (p less than 0.01) reduced by 24 percent under the Medicare diagnosis-related group (DRG) prospective payment system ($8,024 +/- $4,824). The DRG payments are significantly less than (p less than 0.001) and provide only 60 percent of the true hospital cost required to care for Medicare cardiac patients referred for tertiary care ($13,427 +/- $12,700 per patient). A Medicare DRG system adopted by third-party payers would reduce present hospital revenues from $9,524 +/- $8,422 per patient to $7,968 +/- $4,800 per patient and would provide only 68 percent of the cost required in the care of all cardiac patients referred for tertiary care ($11,690 +/- $11,344). The results of this study indicate that hospitals that receive large numbers of seriously ill cardiac patients, especially Medicare patients, referred for critical care are at a significant financial disadvantage under the Medicare DRG system. Future economic pressures may prohibit critical care treatment centers from accepting large numbers of cardiac patients referred for intensive care and reimbursed under the current Medicare DRG payment policy.

Aged↗
PubMed1986

The heart rate of Romano-Ward syndrome patients.

The Romano-Ward prolonged QT syndrome is associated with an abnormality of ventricular recovery, rendering the patients susceptible to life-threatening ventricular arrhythmias. The pathophysiology has not been clearly defined. It has been proposed that the syndrome involves disparity of right and left cardiac sympathetic activity, with the left side dominant. This could be the result of left-sided overactivity or right underactivity. The right-sided nerves contain the chronotropic fibers, which affect heart rate. A deficiency of the effect of the right-sided nerves might, therefore, be manifest by slower heart rates. To examine this possibility, the resting heart rates of 58 Romano-Ward syndrome patients were compared to those of 255 age-matched normal controls. A significant difference in resting heart rate was observed between the Romano-Ward syndrome patients and the normal controls in newborns and children up through age 3 years. No difference was present in older children or in adults. The data are consistent with right-sided sympathetic deficiency manifest by a slower heart rate at birth and during early years of life, when sympathetic tone is high and contributes to resting heart rate, but not in older children or in adults in whom resting heart rate is principally under parasympathetic control.

Adolescent↗
PubMed1986

Reversible segmental myocardial dysfunction in septic shock.

We report two septic-shock patients who had ECG and echocardiographic changes consistent with myocardial infarction but no evidence of coronary artery disease or myocardial injury at autopsy. The segmental myocardial dysfunction completely resolved in one patient. Because septic shock can cause segmental myocardial dyskinesis, ECG and echocardiographic data may be misleading and should be interpreted cautiously.

Aged↗
PubMed1982

Application of body surface mapping to exercise testing: S-T80 isoarea maps in patients with coronary artery disease.

Body surface electrocardiographic maps were recorded before and after exercise in 25 men with angiographically documented coronary disease. Torso potential distributions at 192 locations were derived from a 32 lead electrode array using methods previously described in our laboratory. The S-T segment was characterized by the spatial distribution of the integral of S-T segment voltage over 80 ms (S-T80). Body surface regions where the S-T80 areas were =8 mV . ms or greater were identified in 18 of 25 patients. The most negative S-T80 site on the map was called the "S-T80 minimum." The S-T80 minima were located 1 or 2 electrode rows away from the standard V4--V6 electrode positions in 6 of 18 patients who developed S-T80 areas of -8 mV . ms or greater. Our data suggest that standard electrocardiographic leads may not be optimal for identifying S-T segment depression in all patients with coronary disease. Furthermore, body surface mapping during exercise provides a more quantitative and qualitative method for characterizing the ischemic response to exercise.

Adult↗
PubMed1979

Clinically practical lead systems for improved electrocardiography: comparison with precordial grids and conventional lead systems.

The use of limited leads for estimating total body surface potential distributions was investigated as a practical solution to the problem associated with extensive electrocardiographic sampling used in surface potential mapping. Two practical, limited lead sets of 32 leads each were derived and contrasted to a set of 30 precordial leads similar to those used in ST-segment and QRS mapping for estimating infarct size, and to a set of nine leads simulating those used in conventional 12-lead examinations. The two arrays, one of which excluded posterior sites for use in recumbent patients, showed little difference in ability to estimate 192 lead measured maps (average rms voltage error of 35 muV and average correlation coefficient of 0.97). The 30- and 9-lead arrays consistently showed twice the voltage (72 muV) and poorer pattern estimation (average correlation coefficient of 0.91) than either of the 32 lead arrays. These findings indicate the need for 20-35 properly located electrodes for accurate total body surface potential estimation. They also show that there is no difference in the abilities of a 30-lead precordial array and conventional leads to estimate maps.

Arrhythmias, Cardiac↗
PubMed1977

Diagnosis of old inferior myocardial infarction by body surface isopotential mapping.

Body surface isopotential maps obtained from 28 patients with old inferior wall myocardial infarction were compared with maps from 120 normal subjects. The 12 lead electrocardiogram of 8 of the 28 patients (29 percent) with inferior wall infarction was normal or showed only nondiagnostic ST-T wave abnormalities at the time the isopotential maps were obtained. In all patients with inferior wall infarction the isopotential map showed a minimum (area of negative potentials) on the inferior or right thoracic surface during the early portions of the QRS complex. This finding was observed in patients with normal or nonspecific abnormalities in the 12 lead electrocardiogram as well as those with QRS abnormalities. By contrast, the minimum during the early QRS complex in normal subjects was located on the right upper back and shoulder region...

Back↗
PubMed1976

The expression of normal ventricular repolarization in the body surface distribution of T potentials.

Isopotential maps from 120 normal subjects were obtained from 192 simultaneously recorded electrocardiographic leads. Maps were plotted at 1 msec intervals during the QRS and 5 msec intervals during the ST-T deflection. Repetition of QRS features was evident during all but the first few msec of the initial half of serial T maps. This suggests similarities of the normal sequence of ventricular excitation and recovery. Such similarities have been demonstrated by direct studies but are not evident from other electrocardiographic examinations. Serial maps during later portions of the T wave showed decreasing intensity of potentials with little change of body surface locations. This also correlates with an established feature of ventricular repolarization, namely that potential difference boundaries with stable locations are widely distributed during part of that process. Findings suggest isopotential maps show features of ventricular recovery not apparent from less extensive examinations.

Action Potentials↗
PubMedDate not supplied

The inherited long QT syndrome: from ion channel to bedside.

The inherited long QT syndrome is caused by mutations of at least 5 ion channel genes. Mutations of the cardiac sodium ion channel gene and 3 potassium channel genes have been identified to this time. A genetic locus on chromosome 4 has been identified, but no gene has been discovered as of yet. More than 120 mutations of the genes have been discovered. The majority of cases are inherited by autosomal dominant transmission. Syncope occurs in approximately two-thirds of gene carriers, with sudden death in 10% to 15% of untreated patients. The primary electrophysiologic disturbance is delayed recovery of the action potential, because of diverse physiologic perturbations dependent upon the specific ion channel and mutation. The delayed recovery predisposes individuals to the development of early afterdepolarizations and initiation of torsade de pointes arrhythmias. The torsade produces the syncope and sudden death. Patients with self-terminating torsade have syncope, whereas those whose torsade degenerates to ventricular fibrillation experience sudden death. The torsade maintenance appears to be because of complex reentry or repetitive triggered beats, both of which have been proposed as capable of explaining the unique and characteristic QRS morphology of torsade. It is proposed that the degree of dispersion of recovery at the time of torsade determines whether the torsade degenerates to ventricular fibrillation or self-terminates. The signs of long QT syndrome are prolongation of the QT interval on the electrocardiogram and abnormalities of T wave morphology. QTc values average 0.49 seconds and vary somewhat by genotype. Approximately 12% of long QT gene carriers have a normal QTc, < or =0. 44 seconds. Thus, a normal QTc interval does not exclude long QT syndrome. T wave morphology is relatively characteristic for each genotype. Diagnosis is likely with a QTc > or =0.48 seconds in females and > or =0.47 seconds in males. Values between 0.41 and 0.46 seconds require additional evaluation, as the disorder can neither be excluded nor made with those QTc intervals. Diagnosis is enhanced by identification of T wave abnormalities consistent with long QT syndrome. The principal treatment is beta-blocker therapy. Appropriate dosing, with ascertainment of efficacy and compliance with administration, are the key elements in therapeutic success. Molecular physiology-based strategies are being considered, including the use of sodium channel blockers in LQT3 and potassium administration in LQT1 patients.

Adrenergic beta-Antagonists↗