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Biomedical subjects

C M Oakley

Publications and source records attributed to C M Oakley.

At least 55 records · Page 3Linked to original sources
PubMed1994

Enhanced basal nitric oxide production in heart failure: another failed counter-regulatory vasodilator mechanism?

Endothelial dysfunction in heart failure could impair nitric oxide production and lead to increased vascular resistance. If endogenous production of nitric oxide is reduced, NG-monomethyl-L-arginine (L-NMMA), an inhibitor of such production, should have a diminished vasoconstrictor effect. We administered L-NMMA to 12 patients being investigated for heart failure. L-NMMA increased median pulmonary and systemic vascular resistances by 61 (range -3 to 240) and 430 (63 to 1609) dynes s cm-5, respectively (p < 0.03 and p < 0.005). Arterial pressures also increased. Median cardiac output fell by 0.6 (0 to -2.3) L per min (p < 0.005). These data suggest that vascular nitric oxide may be another example of a failed counter-regulatory vasodilator system in heart failure.

Aged↗
PubMed1994

Relationship between hemostatic abnormalities and neuroendocrine activity in heart failure.

Thromboembolism is an important complication of heart failure. To test the hypothesis that heart failure may be associated with hemostatic dysfunction, we studied hemostatic function in 21 patients with stable chronic heart failure and related these measures to the severity of heart failure as assessed by clinical evaluation, neuroendocrine activation, radionuclide ventriculography, and cardiopulmonary exercise testing. Plasma and blood viscosity were elevated; all patients showed evidence of platelet activation, and many had elevated plasma concentrations of fibrinopeptide A, D-dimer, and von Willebrand factor. The plasma concentrations of these variables were poorly interrelated and related poorly to the severity of heart failure. Plasma concentrations of angiotensin II and endothelin were correlated, and the latter was also correlated with the plasma concentration of von Willebrand factor. Patients with chronic heart failure have hemostatic abnormalities that may predispose them to thromboembolic events and may be in part due to neuroendocrine activation.

Adult↗
PubMed1994

Carcinoid heart disease: early failure of an allograft valve replacement.

A woman who had carcinoid syndrome and carcinoid heart disease underwent tricuspid and pulmonary valve replacements with a xenograft and a cryopreserved allograft, respectively. Within 3 months of the operation severe pulmonary regurgitation and pulmonary hypertension refractory to medical therapy developed. Autopsy found the biomechanical tricuspid valve to be free of disease but the allograft in the pulmonary position was involved by carcinoid heart disease in a fashion similar to the excised native pulmonary valve.

Carcinoid Heart Disease↗
PubMed1994

Influence of haemodynamics and myocardial ischaemia on Doppler transmitral flow in patients undergoing dobutamine echocardiography.

To examine whether pulsed Doppler left ventricular filling indices can reliably detect myocardial ischaemia in patients with coronary artery disease undergoing dobutamine stress echocardiography we studied three groups matched for age and global indices of left ventricular function. Group I patients (n = 10) had normal coronary arteries whereas those in Groups 2 (n = 12) and 3 (n = 15) had significant coronary disease (> or = 70% diameter stenosis) at angiography. After stopping cardioactive treatment, patients underwent incremental dobutamine stress (5, 10, 15 and 20 micrograms.kg-1.min-1) during pulsed Doppler interrogation of diastolic filling with simultaneous heart rate and blood pressure measurements. Only Group 3 patients developed myocardial ischaemia using electrocardiographic and cross sectional echocardiographic criteria; subset 3A (n = 4) comprised those with inducible mitral regurgitation on colour Doppler. Electrocardiographic R-R interval decreased (-311 +/- 123 ms, P < 0.001) and mean blood pressure altered (5 +/- 17 mmHg, P = ns) uniformly across groups. The respective changes in peak early velocity, peak atrial velocity and their ratio for Groups 1 (0.08 +/- 0.09 m.s-1, 0.26 +/- 0.18 m.s-1 and -0.32 +/- 0.36), 2 (0.07 +/- 0.07 m.s-1, 0.18 +/- 0.15 m.s-1 and -0.13 +/- 0.21) and 3 (0.09 +/- 0.12 m.s-1, 0.20 +/- 0.13 m.s-1 and -0.17 +/- 0.21) were similar (all P = ns between groups). Corresponding data for subset 3A (0.23 +/- 0.04 m.s-1, 0.20 +/- 0.10 m.s-1 and 0.00 +/- 0.16) revealed a significantly greater increase in peak early velocity and normalized velocity ratio in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1994

Elevated plasma endothelin concentrations in heart failure; an effect of angiotensin II?

Endothelin is a powerful vasoconstrictor that may be partly responsible for the increases in venous and arterial tone characteristic of heart failure. The release of endothelin from endothelial cells in culture is stimulated by angiotensin II. We investigated the relationship between plasma concentrations of immuno reactive endothelin-1 and angiotensin II in 25 patients with heart failure and eight with ischaemic heart disease but normal left ventricular function. Plasma concentrations of endothelin and angiotensin II were correlated (Spearman rank correlation coefficient of 0.72; P < 0.0001) in patients with heart disease. Plasma concentrations of angiotensin II and endothelin were higher in those patients with heart failure. Angiotensin II was infused over a 3 h period in eight healthy volunteers. Infusion of angiotensin II increased plasma concentrations of angiotensin II to levels greater than those usually found in patients with severe heart failure but induced only a modest rise in plasma concentrations of immunoreactive endothelin-1 (0.77 +/- 0.16 to 1.03 +/- 0.03 pmol.l-1, P < 0.02). Increased plasma concentrations of angiotensin II and endothelin-1 both appear to reflect the presence and severity of heart failure. Although a significant correlation exists between plasma concentrations of angiotensin II and endothelin in patients with heart failure, the relationship may not be causal.

Adult↗
PubMed1994

Massive pulmonary embolism in pregnancy treated with streptokinase and percutaneous catheter fragmentation.

Despite heightened awareness, pulmonary embolism remains a major cause of maternal mortality in the antenatal period and one which has not decreased in incidence over the four triennia since 1976. We report a patient who suffered massive pulmonary embolism with circulatory collapse in the second trimester and who was treated with intravenous streptokinase followed by percutaneous mechanical dispersion of thrombus using a catheter and guide wire. She made an excellent recovery despite complicating antepartum haemorrhage. In life-threatening circumstances pharmacological thrombolysis is mandatory particularly for hospitals without a cardiac catheterization laboratory on site.

Adult↗
PubMed1994

Outcome of pregnancy in women with valve prostheses.

OBJECTIVE: To study the outcome of pregnancy in women with artificial heart valves treated in major European centres, and to compare the safety and efficacy of different anticoagulant regimens and of mechanical and bioprosthetic valves. DESIGN: Retrospective study. METHOD: The information was obtained by questionnaire sent to all major cardiac centres in Europe sending one cardiologist from each centre a covering letter suggesting that the questionnaire be handed on where appropriate to the most relevant colleague. RESULTS: 214 pregnancies were reported in 182 women; 151 pregnancies in 133 women with mechanical valves, and 63 pregnancies in 45 women with bioprostheses. Most women were in New York Heart Association class I or II and in sinus rhythm. 150 women with mechanical valves and 11 (17%) with bioprostheses received anticoagulants during pregnancy. One patient with an aortic valve prosthesis refused to take anticoagulants. Including the spontaneous abortions reported as well as the therapeutic abortions 83% of the pregnancies in women with bioprostheses and 73% in those with mechanical valves resulted in a healthy baby, full term or premature, who did well (NS). The incidence of stillbirths (3% and 6%) and of reported spontaneous abortions are excluded (because they are unlikely to have been fully reported), the success rate was 91% for women with bioprosthetic valves and 84% for women with mechanical valves (NS). 114 (53%) of the women had taken warfarin for some part of the pregnancy (46 (40%) of these during the first trimester) but there were no embryopathies. There were 13 valve thromboses (four fatal), eight embolic events (two fatal), and seven bleeds in women with mechanical valves. Most of these complications occurred with heparin but fatal aortic valve thrombosis occurred in the one woman who refused anticoagulant treatment out of the 151 women with mechanical valves. There were no maternal deaths in the bioprosthesis group but in 17/49 (35%) of these valves functional deterioration led to urgent replacement during pregnancy (two) or soon after. CONCLUSIONS: The outcome of pregnancy was similar for women with mechanical valves or bioprostheses. Warfarin treatment was safe and effective and was not associated with embryopathy. Heparin treatment was associated with more thromboembolic complications and more bleeding complications. Bioprostheses deteriorate rapidly during pregnancy.

Abortion, Spontaneous↗
PubMed1994

Natural history of secundum atrial septal defect in adults after medical or surgical treatment: a historical prospective study.

OBJECTIVE: To compare outcome in patients with medically treated secundum atrial septal defect (ASD) first diagnosed after the age of 25 with the long-term outcome in a similar group of patients after surgical closure. DESIGN: A historical, prospective, unrandomised study. SETTING: A tertiary referral centre. PATIENTS: All patients with ASD followed up since 1955 who fulfilled the entry criteria and had reached a current age of over 45 years--that is, 34 medical and 48 surgical patients with a mean follow up of 25 years. MAIN OUTCOME MEASURES: Survival, symptoms, and complications. RESULTS: There was no difference in survival or symptoms between the two groups and no difference in the incidence of new arrhythmias, stroke or other embolic phenomena, or cardiac failure. No patient in either group developed progressive pulmonary vascular disease. CONCLUSION: Outcome in adults with ASD was not improved by surgical closure. Because progressive pulmonary vascular disease did not develop in any of these patients its prevention is not a reason for advising closure of ASD in adults.

Adult↗
PubMed1994

Increased alveolar/capillary membrane resistance to gas transfer in patients with chronic heart failure.

OBJECTIVE: To investigate pulmonary diffusive resistance to gas exchange in patients with heart failure and healthy volunteers, assessing the relative contributions of the alveolar/capillary membrane and pulmonary capillary blood. SETTING: Hospital outpatient department and pulmonary function laboratory. PATIENTS: 38 patients (mean age 60) receiving treatment with loop diuretics and angiotensin converting enzyme inhibitors for stable symptomatic heart failure of > 6 months duration (New York Heart Association (NYHA) classes II and III). Results were compared with those of 17 healthy volunteers (mean age 52). METHODS: The alveolar/capillary membrane diffusive resistance and the pulmonary capillary blood volume available for physiological gas exchange were determined by the Roughton and Forster method, which measures the single breath pulmonary diffusing capacity for carbon monoxide at varying alveolar oxygen concentrations. RESULTS: Total pulmonary diffusive resistance was higher in patients than controls. Alveolar/capillary membrane resistance formed the main component of this increase, accounting for a mean (SD) of 63% (20%) and 86% (8%) of total pulmonary diffusive resistance in patients in NYHA II and III classes respectively, compared with 53% (10%) in controls. The pulmonary capillary blood volume was not significantly different between controls and patients in NYHA class II (66 (18) ml v 61 (18) ml), but was increased in those in NYHA class III (95(46) ml, P < 0.05). CONCLUSION: This study confirmed impairment of pulmonary diffusion at rest in patients with chronic heart failure and identified impaired alveolar/capillary membrane function as the main factor responsible.

Adult↗
PubMed1994

Effect of intense angiotensin II suppression on the diuretic response to furosemide during chronic ACE inhibition.

BACKGROUND: Contrary to expectation, most studies have demonstrated that initiation of an angiotensin-converting enzyme (ACE) inhibitor in conventional doses in patients with heart failure reduces the diuretic efficacy of furosemide. Recently, it has been suggested that single low doses (1 mg) but not high doses (25 mg) of captopril enhance furosemide-induced diuresis. It is not known whether the interaction between diuretics and ACE inhibitors are altered during long-term dosing. METHODS AND RESULTS: Eight patients with heart failure treated with diuretics and ACE inhibitors for at least 3 months were studied. All patients were established on captopril 12.5 mg three times daily for 2 weeks before the study. Sodium intake was fixed before the study, and usual medication was withheld on study days. Intravenous furosemide was given on each of 2 study days to maintain a moderate, constant diuresis. Renal plasma flow and glomerular filtration rate (GFR) were determined using clearance techniques, and urine was collected hourly over 4 hours. Captopril 12.5 mg or placebo was given in a randomized, single-blind fashion at the end of the first hour. Compared with placebo, captopril reduced plasma concentrations of angiotensin II (23 +/- 18 versus 4 +/- 3 pg/ml 1 hour after dosing, P < .02) and systolic (131 +/- 31 versus 122 +/- 29 mm Hg, P < .01) and diastolic (74 +/- 15 versus 67 +/- 13 mm Hg, P < .05) blood pressures. GFR fell (55 +/- 24 versus 51 +/- 22 mL/min, P < .02) and effective renal plasma flow rose during the first (198 +/- 76 versus 231 +/- 49 mL/min) and second hours after dosing (185 +/- 69 versus 247 +/- 74 mL/min, P < .02). Similarly, urine volumes, in response to furosemide, increased after captopril (238 +/- 90 versus 283 +/- 111 mL, P < .05, and 245 +/- 78 versus 311 +/- 92 mL, P < .01, 1 and 2 hours after dosing). Urinary electrolyte concentrations fell, but total urinary sodium (22 +/- 7 versus 28 +/- 12 mmol/hr, P < .01) and chloride (20 +/- 6 versus 25 +/- 11 mmol/hr, P < .05) excretion increased in the 2 hours after dosing, as did fractional excretion of sodium (urinary sodium/urinary creatinine) (61 +/- 27 versus 75 +/- 36 mmol/mumol, P < .01). CONCLUSIONS: Intense although transient ACE inhibition with captopril enhances the diuretic effects of furosemide during long-term ACE inhibition.

Aged↗