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P Hanly

Publications and source records attributed to P Hanly.

17 recordsLinked to original sources
PubMed2001

The importance of age and obesity on the relation between diabetes and left ventricular mass.

OBJECTIVES: The study investigated the relation of age with diabetes, obesity and hypertension on left ventricular mass (LVM). BACKGROUND: Epidemiological studies demonstrate a general rise of LVM with aging, but whether this phenomenon is independent or a function of coexisting diseases that accompany the aging process is unclear. Although obesity, hypertension and diabetes often coexist and increase in prevalence with age, studies of LVM in diabetics have been reported in mostly nonobese populations, and with little regard to the age-hypertension-obesity interactions and effects on LVM. METHODS: We prospectively measured LVM in 875 consecutive, mostly obese individuals (673 men, 202 women). Clinical data were obtained by chart review and clinical history. Echocardiographic measurements of LVM (American Society of Echocardiography criteria) were calculated using the Devereux formula and corrected for height2.7 (LVM/Ht). RESULTS: Mean age was 49.3+/-12.3 years, body mass index 33.3+/-8.0 kg/m2, and LVM/Ht2.7 41.7+/-13.4 g/m2.7. Of the total cohort, 673 patients were men, 519 obese, 228 hypertensive, and 52 diabetic. Of the 519 obese, 183 were hypertensive and 44 were diabetic (22 of those were hypertensive). Of the 228 hypertensives, 183 were obese and 26 were diabetic. On multivariate analysis, obesity (p = 0.0001), age (p = 0.0001), hypertension (p = 0.0003) and diabetes (p = 0.62) were all independently associated with LVM/Ht2.7. Obesity was the most potent independent predictor of LVM/Ht2.7, associated with an increase of 8.1 g/m2.7 in LVM/Ht2.7. In diabetics, obesity had a synergistic effect on LVM/Ht2.7 (p = 0.006), which was further amplified by age (p = 0.03). CONCLUSIONS: Age, obesity, hypertension and diabetes are all independent determinants of LVM. The magnitude of the effect of diabetes on LVM is mainly consequent to a significant interaction of diabetes with obesity and age.

Age Factors↗
PubMed1995

Snoring and arousals: a retrospective analysis.

The purpose of this retrospective analysis was to search for possible associations between snoring and arousals. We searched our data base containing more than 2,000 records and selected only patients who 1) had objective measurements of snoring, 2) were not taking sedating medication, 3) did not have sleep apnea (apnea/ hypopnea index < 10) and 4) did not have periodic leg movements (myoclonus index < 5). This procedure left 367 patients available for analysis. We hypothesized that arousals observed in these patients were associated with snoring, and we performed univariate and multivariate regression analysis with arousals as the dependent variable, and age, body mass index, snoring, maximum nocturnal sound intensity and nocturnal oxygen saturation as the independent variables. The results showed that only snoring and mean nocturnal oxygen saturation were significant (p < 0.05) but weak determinants of arousals, accounting for only 7% of their variance. To examine whether snorers have more arousals than non-snorers, we compared a control group of non-snorers (< 50 snores/hour of sleep), with a group of heavy snorers (> 400 snores/hour of sleep). We found that the arousal index was significantly but weakly higher in snorers than non-snorers [mean +/- standard deviation (SD) = 14 +/- 8 vs. 10 +/- 6, p < 0.002]. Conversely, patients within the highest arousal quartile snored significantly more than those within the lowest quartile (snoring index 293 +/- 292 vs. 179 +/- 282, p < 0.008, respectively). We conclude that despite the limitations of this retrospective analysis, there appears to be an association between snoring and arousals, warranting further, properly designed prospective studies.

Adolescent↗
PubMed1995

Daytime sleepiness in patients with congestive heart failure and Cheyne-Stokes respiration.

STUDY OBJECTIVE: To determine whether patients with congestive heart failure who develop Cheyne-Stokes respiration (CSR) during sleep experience excessive daytime sleepiness. This was addressed by comparing sleep quality and daytime sleepiness in three groups: patients with CHF and CSR during sleep (CSR group), patients with CHF without CSR (CHF group), and healthy control subjects (control group). DESIGN: Single-blind, cross-sectional study. SETTING: Patients referred by cardiologists and control subjects recruited from the general community. PATIENTS: Twenty-three men: 7 in the CSR group, 7 in the CHF group, and 9 in the control group. MEASUREMENTS: Each subject had an overnight sleep study and an assessment of sleepiness the following day. RESULTS: The three groups were a similar age: CSR, 68 +/- 5 years; CHF, 62 +/- 4 years; and control, 65 +/- 4 years; and left ventricular ejection fraction was the same in patients with CSR (20 +/- 1.5%) and CHF (23 +/- 5%). Sleep latency was significantly shorter in patients with CSR (4 +/- 1.1 min) than patients with CHF (11.3 +/- 4.8 min) and healthy controls (12.4 +/- 1.9 min) and was within the diagnostic range of severe sleepiness. Patients with CSR had significantly more stage 1 and 2 non-rapid eye movement (NREM) sleep (CSR, 83 +/- 7; CHF, 64 +/- 9; control, 63 +/- 9% total sleep time), less REM sleep (CSR, 10 +/- 3; CHF, 22 +/- 8; control, 22 +/- 7% total sleep time), and a higher frequency of arousals from sleep (CSR, 30 +/- 16; CHF, 18 +/- 15; control, 10 +/- 2/h of sleep); 66% of arousals were associated with CSR. Regression analysis revealed that sleep latency was inversely related to the amount of stage 1 and 2 NREM sleep (r = -0.67), arousal frequency (r = -0.46), and the apnea-hypopnea index (r = -0.63) and was positively correlated with the amount of slow-wave sleep (r = 0.45) and REM sleep (r = 0.56) and the mean oxygen saturation during sleep (r = 0.50). CONCLUSIONS: Patients with CHF who develop CSR experience excessive daytime sleepiness due to sleep disruption. This should be considered the clinical evaluation of these patients' daytime complaints.

Age Factors↗
PubMed1993

ST-segment depression during sleep in obstructive sleep apnea.

It was hypothesized that obstructive sleep apnea may precipitate myocardial ischemia, reflected by ST-segment depression, in some patients during sleep. Overnight sleep studies and simultaneous 3-channel Holter monitoring were performed on 23 consecutive patients with obstructive sleep apnea without a history of coronary artery disease. Each patient was randomly assigned to nasal continuous positive airway pressure for the first half of the night. An episode of significant ST depression was defined as > 1 mm from baseline for > 1 minute. The total duration (minutes) of ST depression was indexed to the total sleep time (minutes per hour of sleep). Seven patients (30%) had ST depression during sleep. In all 7 patients the duration of ST depression decreased during nasal continuous positive airway pressure (30 +/- 18 vs 11 +/- 13 minutes per hour of sleep) in association with a reduction in the apnea-hypopnea index (65 +/- 35 vs 7 +/- 6/hour), arousal index (49 +/- 14 vs 6 +/- 4/hour) and the duration that oxygen saturation was < 90% (44 +/- 27 vs 12 +/- 23% total sleep time). When patients were not on nasal continuous positive airway pressure, the apnea-hypopnea and arousal indexes were higher during periods of ST depression than when ST segments were isoelectric, whereas oxygen saturation was not different. These 7 patients underwent exercise testing, which was positive for inducible myocardial ischemia in 1 patient. It is concluded that ST depression is relatively common in patients with obstructive apnea during sleep and that the duration of ST depression is significantly reduced by nasal continuous positive airway pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Pathogenesis of Cheyne-Stokes respiration in patients with congestive heart failure. Relationship to arterial PCO2.

In order to determine which patients with congestive heart failure (CHF) develop Cheyne-Stokes respiration (CSR) during sleep, we compared the cardiorespiratory profiles of CHF patients with CSR to those of CHF patients without CSR. Overnight polysomnography and continuous transcutaneous PCO2 (tc PCO2) monitoring, estimation of left ventricular ejection fraction (LVEF), pulmonary function tests, and chest radiograph were performed on 16 consecutive patients with chronic, stable CHF. The tc PCO2 monitor (Kontron 7640) was calibrated so that measurements reflected arterial PCO2 values. A mean value was calculated for wakefulness (W) and total sleep time (TST). Circulation time (CT) from the lung to the carotid body was estimated from the end of an apnea or voluntary breath-hold to the nadir of oxygen desaturation recorded on an ear oximeter. The duration of CSR was expressed as a percent of TST. Nine patients developed CSR during sleep (52.5 +/- 31.6 percent TST) (group 1) and 7 did not (group 2). All patients were male and both groups were a similar age (64 +/- 8 vs 63 +/- 4 years) and weight (body mass index, 28.1 +/- 3.5 vs 25.4 +/- 3.4 kg/m2). There were no significant intergroup differences between LVEF (22 +/- 5.2 vs 24.1 +/- 5.2 percent), CT (19.1 +/- 3.6 vs 15.9 +/- 6.7 s), SaO2 (W) (94 +/- 1.2 vs 92.4 +/- 2.1 percent), and SaO2 (TST) (90.8 +/- 2.7 vs 92.4 +/- 2.1 percent). The tc PCO2 (W) was lower in group 1 (34.4 +/- 3.5 vs 38.1 +/- 1.9 mm Hg), increased during sleep by a similar amount in both groups (1.6 +/- 1.5 vs 2.1 +/- 2.2 mm Hg), and was significantly lower during sleep in group 1 (36.1 +/- 3.4 vs 40.2 +/- 2.2 mm Hg). We conclude that CHF patients with CSR hyperventilate during sleep and wakefulness and that CHF patients with awake hypocapnia are more likely to develop CSR during sleep. These findings indicate that arterial PCO2 is important in determining which CHF patients develop CSR.

Blood Gas Monitoring, Transcutaneous↗
PubMed1993

Hypnotics should never be used in patients with sleep apnea.

Although benzodiazepine medication is generally considered to be inappropriate for patients with obstructive sleep apnea, further investigation is required to evaluate this. Non-benzodiazepine hypnotics may improve sleep quality without causing respiratory depression. In central sleep apnea, hypnotics not only improve sleep but also decrease apnea frequency probably by reducing arousals and elevating arterial PCO2. Consequently, I submit that the statement 'hypnotics should not be used in patients with sleep apnea' should be changed to 'hypnotics may sometimes be used in patients with sleep apnea'.

Benzodiazepines↗
PubMed1992

Short technical note: quantification of periodic breathing: preliminary studies.

Although the apnea/hypopnea index is the most widely used measure of breathing pattern abnormality during sleep, this index gives no information about the strength of the oscillation in the breathing pattern, its periodicity or its regularity. Such information may be required in research studies involving breathing patterns and how they are affected by interventions. We are exploring spectral analytic methods to determine two normalized indices, the periodicity index and the modified modulation index, to examine periodic breathing for all-night sleep studies. These methods are automatic and require no user interaction. Data were obtained from 11 heart failure patients who slept for a total of 21 nights in the sleep laboratory. Because individual patients had a marked regularity of their Cheyne-Stokes respiration during sleep, one would expect an extremely high correlation between the traditional measures of breathing pattern abnormality and these spectral analytic techniques. Indeed we found that there was an extremely high correlation between the periodicity index and the modulation index and the traditional measures of apnea/hypopnea index and the proportion of the night with periodic breathing (p less than 0.02 in all cases). When the breathing pattern was irregular but still with many apneas there was a discrepancy between the apnea index and the indices of periodicity. These techniques are still preliminary and future studies will determine their limitations in other patient populations and where the pattern is unstable.

Adult↗
PubMed1992

Ventricular function in snorers and patients with obstructive sleep apnea.

We hypothesized that intermittent hypoxemia and increased ventricular afterload due to obstructive apnea during sleep (OSA) would cause chronic left ventricular dysfunction. Overnight polysomnography, M-mode and two-dimensional echo-Doppler studies while awake were performed on 51 consecutive snorers, 30 with OSA and 21 without apnea. Patients with previous myocardial infarction, awake hypoxemia or hypercapnia, or other causes of nocturnal hypoxemia were excluded. Echo-Doppler measurements included end-diastolic right and left ventricular dimensions and wall thickness, indices of left ventricular systolic performance (fractional shortening, ejection fraction and ejection time and diastolic performance, (isovolumic relaxation time, ratio of peak early [E] to late [A] diastolic transmitral flow and mitral pressure half-time). Both OSA patients and nonapneic snorers were of similar age. Although OSA patients were heavier, had a greater apnea-hypopnea index, and significant nocturnal hypoxemia, their echo-Doppler measurements were within normal limits and were not significantly different from nonapneic snorers. It is concluded that isolated obstructive sleep apnea does not cause chronic left ventricular dysfunction.

Adult↗
PubMed1992

Periodic leg movements during sleep before and after heart transplantation.

We report the association between periodic leg movements (PLM) during sleep and congestive heart failure (CHF) in a patient who had a successful heart transplant. Pretransplant, the patient had chronic insomnia and CHF. Overnight polysomnography revealed severe PLM disorder and sleep disruption. Three months following transplantation his insomnia had resolved associated with a dramatic reduction in PLM.

Carbon Dioxide↗
PubMed1989

Plasma volume expansion and PEEP in a canine model of acute Pseudomonas pneumonia.

Four groups of anesthetized, ventilated dogs (n = 6 in each group) inoculated endotracheally with Pseudomonas aeruginosa were studied over 5 h as bilateral, hemorrhagic pneumonia developed. Groups I and II were ventilated with zero end-expiratory pressure (ZEEP) and groups III and IV with positive end-expiratory pressure (PEEP) (8 cmH2O). Hetastarch (6%) in saline was infused intravenously to maintain similar transmural pulmonary wedge pressures (Pwtm) in groups I and III (approximately 5 mmHg) and groups II and IV (approximately 10 mmHg) throughout the experiment. The effects of plasma volume expansion were analyzed by comparing groups I and III with groups II and IV and of PEEP by comparing groups I and II with groups III and IV. The number of lobes with gross consolidation was greater in groups II (4.8 +/- 1.2) and IV (5 +/- 0.9) than in groups I (2 +/- 1.1) and III (3.3 +/- 1). The mean lung wet weight/body weight ratio was greater in groups II (40 +/- 11 g/kg) and IV (48 +/- 12 g/kg) than in groups I (19 +/- 3 g/kg) and III (32 +/- 6 g/kg) and in groups III and IV than in groups I and II. Plasma volume expansion, in the absence of PEEP (group II vs. group I), dramatically increased intrapulmonary shunt (Qs/Qt 5 h after inoculation: group II, 62 +/- 13%; group I, 25 +/- 12%). However, overall gas exchange 5 h after inoculation was not significantly different between PEEP-treated groups and ZEEP-treated groups despite more extensive disease in the former. Despite maintenance of Pwtm, cardiac output fell significantly over the 5 h study period in groups III (4.3 +/- 0.7 to 3.3 +/- 1.0 L/min) and IV (7.2 +/- 1.7 to 3.8 +/- 2.4 L/min) compared to groups I (3.8 +/- 1.0 to 3.5 +/- 1.2 L/min) and II (6.9 +/- 3.2 to 7.3 +/- 2.6 L/min). We conclude that plasma volume expansion, within the normal physiological range of Pwtm, increases the extent of pneumonia. Positive end-expiratory pressure with maintenance of Pwtm also independently increases pneumonia size, possibly by increasing pulmonary capillary hydrostatic pressure, but masks this effect by maintaining arterial oxygenation through recruitment of additional lung units for gas exchange. The data also suggest that PEEP adversely affects cardiac performance in this model of acute pneumonia.

Acute Disease↗
PubMed1987

Lung mechanics, gas exchange, pulmonary perfusion, and hemodynamics in a canine model of acute Pseudomonas pneumonia.

Acute bilateral hemorrhagic pneumonia was induced in 6 dogs (pneumonia group) by endotracheal inoculation with Pseudomonas aeruginosa. Measurements of lung mechanics, gas exchange, distribution of pulmonary blood flow, and hemodynamics were made prior to inoculation and 5 hr later when pneumonia was established. These findings were compared to the same measurements in 6 other dogs inoculated with a sterile broth (control group). While there were no significant changes in lung mechanics in the control group, pneumonia caused a significant and proportional reduction (42%) in total lung capacity (TLC) and functional residual capacity (FRC). Although tidal lung compliance was reduced in the pneumonia group, neither the specific compliance nor the deflation pressure-volume curve, with lung volume expressed as a percentage of observed TLC, changed significantly. Pneumonia caused marked hypoxemia with a mean increase in shunt and venous admixture of 35% and 52%, respectively, while the control group developed only minimal abnormalities in gas exchange. Perfusion of the consolidated lung region, determined by radioactive microspheres and expressed as a percentage of total pulmonary blood flow, showed a small but significant decrease from baseline (53 +/- 13%) to established pneumonia (44 +/- 14%), while no change in lobar perfusion was seen in the control group. Only the infected animals showed significant changes in hemodynamics with a rise in cardiac output and fall in mean systemic arterial pressure and vascular resistance. We conclude that acute experimental Pseudomonas pneumonia causes reduction of FRC by filling of alveoli with inflammatory exudate and further reduction of TLC by preventing these alveoli from inflating at higher lung volumes without evidence for a change in the elastic properties of the remaining inflated lung; marked hypoxemia caused by maintenance of perfusion of consolidated lung with reduced or absent ventilation; and a hyperdynamic septic hemodynamic state similar to that seen in humans.

Animals↗
PubMed1987

Effect of cyclooxygenase blockade on gas exchange and hemodynamics in Pseudomonas pneumonia.

Acute bilateral Pseudomonas aeruginosa pneumonia was induced in 10 anesthetized dogs, after which five dogs received intravenous indomethacin (2 mg/kg) (indomethacin group), whereas five others were infused with saline (2 ml/kg) (control group). Plasma levels of 6-ketoprostaglandin F1 alpha(6-keto-PGF1 alpha) and thromboxane B2 (TxB2), stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), respectively, were measured by radioimmunoassay. Although TxB2 levels were not different before and after inoculation in either group, 6-keto-PGF1 alpha levels increased from their base-line value in each animal as pneumonia developed (indomethacin group: less than 100 to 330 +/- 90 pg/ml; control group: less than 100 to 630 +/- 300 pg/ml). Both prostaglandins fell to less than 100 pg/ml in each dog after indomethacin infusion, whereas they remained elevated in the control group after infusion of normal saline. Perfusion of consolidated lung regions (Qp/QT), measured with radioactive microspheres and expressed as a percent of total pulmonary blood flow, was dramatically reduced after indomethacin (35 +/- 3 to 16 +/- 1%) with consequent improvement in pulmonary shunt (Qs/QT: 30 +/- 8 to 18 +/- 6%) and arterial O2 tension (PaO2: 123 +/- 25 to 274 +/- 77 Torr). These parameters remained unchanged or deteriorated further in the control group after infusion of saline. Three additional dogs with Pseudomonas pneumonia were studied in which the indomethacin-induced reduction in Qp/QT was substantially but not completely reversed by intravenous infusion of PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1984

HLA-A, -B and -DR antigens in IgA nephropathy.

Fifty-six Irish patients with IgA Nephropathy were typed for HLA-A and -B antigens. Forty-six were typed for HLA-DR antigens. The frequencies of these antigens did not differ significantly from the frequency in the general population. The influence of genetic factors in the pathogenesis of this disease remains uncertain.

HLA Antigens↗
PubMed1983

Aetiology of chronic constrictive pericarditis.

In a consecutive series of 32 cases of chronic constrictive pericarditis treated by pericardiectomy during the past 25 years, four were attributable to rheumatoid disease, two to trauma, one to sarcoidosis, and four, at a maximum, to tuberculosis. In the remaining 21 cases of undetermined aetiology there was no evidence of tuberculosis. It appears, therefore, that tuberculosis was not a common cause of chronic constrictive pericarditis during the period under review, which included the 1950s and early 1960s when tuberculosis was widespread.

Adolescent↗