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Biomedical subjects

D P Dutka

Publications and source records attributed to D P Dutka.

17 recordsLinked to original sources
PubMed2000

Prolonged left ventricular dysfunction occurs in patients with coronary artery disease after both dobutamine and exercise induced myocardial ischaemia.

OBJECTIVE: To determine whether pharmacological stress leads to prolonged but reversible left ventricular dysfunction in patients with coronary artery disease, similar to that seen after exercise. DESIGN: A randomised crossover study of recovery time of systolic and diastolic left ventricular function after exercise and dobutamine induced ischaemia. SUBJECTS: 10 patients with stable angina, angiographically proven coronary artery disease, and normal left ventricular function. INTERVENTIONS: Treadmill exercise and dobutamine stress were performed on different days. Quantitative assessment of systolic and diastolic left ventricular function was performed using transthoracic echocardiography at baseline and at regular intervals after each test. RESULTS: Both forms of stress led to prolonged but reversible systolic and diastolic dysfunction. There was no difference in the maximum double product (p = 0.53) or ST depression (p = 0.63) with either form of stress. After exercise, ejection fraction was reduced at 15 and 30 minutes compared with baseline (mean (SEM), -5.6 (1.5)%, p < 0.05; and -6.1 (2.2)%, p < 0. 01), and at 30 and 45 minutes after dobutamine (-10.8 (1.8)% and -5. 5 (1.8)%, both p < 0.01). Regional analysis showed a reduction in the worst affected segment 15 and 30 minutes after exercise (-27.9 (7.2)% and -28.6 (5.7)%, both p < 0.01), and at 30 minutes after dobutamine (-32 (5.3)%, p < 0.01). The isovolumic relaxation period was prolonged 45 minutes after each form of stress (p < 0.05). CONCLUSIONS: In patients with coronary artery disease, dobutamine induced ischaemia results in prolonged reversible left ventricular dysfunction, presumed to be myocardial stunning, similar to that seen after exercise. Dobutamine induced ischaemia could therefore be used to study the pathophysiology of this phenomenon further in patients with coronary artery disease.

Aged↗
PubMed1999

Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction.

BACKGROUND: Impaired alveolar-capillary membrane conductance is the major cause for the reduction in pulmonary diffusing capacity for carbon monoxide (DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmonary microvascular damage, or is variable is unknown. The aim of this study was to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects of volume loading on airflow rates. METHODS AND RESULTS: Ten patients with left ventricular dysfunction (LVD) and 8 healthy volunteers were studied. DM and Vc were determined by the Roughton and Forster method. The forced expiratory volume in 1 second (FEV1), vital capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL. kg-1 body wt of 0.9% saline acutely reduced DM (12.0+/-3.3 versus 10.4+/-3.5 mmol. min-1. kPa-1, P<0.005), FEV1 (2.3+/-0.4 versus 2.1+/-0.4 L, P<0.0005), and PEFR (446+/-55 versus 414+/-56 L. min-1, P<0.005). All pulmonary function tests had returned to baseline values 24 hours later. In normal subjects, saline infusion had no measurable effect on lung function. CONCLUSIONS: Acute intravascular volume expansion impairs alveolar-capillary membrane function and increases airflow obstruction in patients with LVD but not in normal subjects. Thus, the abnormalities of pulmonary diffusion in heart failure, which were believed to be fixed, also have a variable component that could be amenable to therapeutic intervention.

Aged↗
PubMed1999

Marked variation in the cardiomyopathy associated with Friedreich's ataxia.

OBJECTIVE: To document the cardiac phenotype associated with Friedreich's ataxia, a recessively inherited disorder characterised by spinocerebellar degeneration. SETTING: Individuals with Friedreich's ataxia who accepted the invitation to participate in the study. HYPOTHESIS: The cardiomyopathy associated with Friedreich's ataxia may offer a human model for the study of factors modulating cardiac hypertrophy. METHODS: 55 patients (mean (SD) age 30 (9) years) with a clinical diagnosis of Friedreich's ataxia were studied by clinical examination, electrocardiography, cross sectional and Doppler echocardiography, and analysis of the GAA repeat in the first intron of the frataxin gene. RESULTS: A wide variety of cardiac morphology was documented. Subjects with normal frataxin alleles had no evidence of cardiomyopathy. In homozygous subjects, a relation was found between the thickness of the interventricular septum (r = 0.53, p < 0.005), left ventricular mass (r = 0.48, p < 0.01), and the number of GAA repeats on the smaller allele of the frataxin gene. No relation was shown between the presence of electrocardiographic abnormalities (mainly repolarisation changes) and either the pattern of ventricular hypertrophy (if present) and degree of neurological disability or the length of time since diagnosis. No tendency to ventricular thinning or dilatation with age was found. Although ventricular systolic function appeared impaired in some cases, Doppler studies of ventricular filling were within the normal range for age. CONCLUSIONS: The cardiomyopathy associated with Friedreich's ataxia shows a variable phenotype which is not concordant with the presence of ECG abnormalities or the neurological features of the condition. As the genetic basis for Friedreich's ataxia has been established, further studies will help to clarify the molecular mechanisms of the cardiac hypertrophy.

Adolescent↗
PubMed1997

Differences in myocardial velocity gradient measured throughout the cardiac cycle in patients with hypertrophic cardiomyopathy, athletes and patients with left ventricular hypertrophy due to hypertension.

OBJECTIVES: We sought to compare the myocardial velocity gradient (MVG) measured across the left ventricular (LV) posterior wall during the cardiac cycle between patients with hypertrophic cardiomyopathy (HCM), athletes and patients with LV hypertrophy due to systemic hypertension and to determine whether it might be used to discriminate these groups. BACKGROUND: The MVG is a new ultrasound variable, based on the color Doppler technique, that quantifies the spatial distribution of transmyocardial velocities. METHODS: A cohort of 158 subjects was subdivided by age into two groups: Group I (mean [+/-SD] 30 +/- 7 years) and Group II (58 +/- 8 years). Within each group there were three categories of subjects: Group Ia consisted of patients with HCM (n = 25), Group Ib consisted of athletes (n = 21), and Group Ic consisted of normal subjects; Group IIa consisted of patients with HCM (n = 19), Group IIb consisted of hypertensive patients (n = 27), and Group IIc consisted of normal subjects (n = 33). RESULTS: The MVG (mean [+/-SD] s-1) measured in systole was lower (p < 0.01) in patients with HCM (Group Ia 3.2 +/- 1.1; Group IIa 2.9 +/- 1.2) compared with athletes (Group Ib 4.6 +/- 1.1), hypertensive patients (Group IIb 4.2 +/- 1.8) and normal subjects (Group Ic 4.4 +/- 0.8; Group IIc 4.8 +/- 0.8). In early diastole, the MVG was lower (p < 0.05) in patients with HCM (Group Ia 3.7 +/- 1.5; Group IIa 2.6 +/- 0.9) than in athletes (Group Ib 9.9 +/- 1.9) and normal subjects (Group Ic 9.2 +/- 2.0; Group IIc 3.6 +/- 1.5), but not hypertensive patients (Group IIb 3.3 +/- 1.3). In late diastole, the MVG in patients with HCM (Group Ia 1.3 +/- 0.8; Group IIa 1.4 +/- 0.8) was lower (p < 0.01) than that in hypertensive patients (Group IIb 4.3 +/- 1.7) and normal subjects (Group IIc 3.8 +/- 0.9). An MVG < or = 7 s-1, as a single diagnostic approach, differentiated accurately (0.96 positive and 0.94 negative predictive value) between patients with HCM and athletes when the measurements were taken during early diastole. CONCLUSIONS: In both age groups, the MVG was lower in both systole and diastole in patients with HCM than in athletes, hypertensive patients or normal subjects. The MVG measured in early diastole in a group of subjects 18 to 45 years old would appear to be an accurate variable used to discriminate between HCM and hypertrophy in athletes.

Adult↗
PubMed1996

Effects of aging on neuroendocrine activation in subjects and patients in the presence and absence of heart failure with left ventricular systolic dysfunction.

The neuroendocrine profile and echocardiographic features of 40 patients (81 +/- 1 years, means +/- standard error) with heart failure and impaired left ventricular systolic function were compared with those of an age-matched group of healthy subjects, 20 younger patients with heart failure (aged 58 +/- 1 years) and 15 younger healthy subjects. Normal elderly subjects had a neuroendocrine profile similar to that of healthy younger subjects apart from elevated plasma norepinephrine (958 +/- 84 vs 302 +/- 118 pg/ml; p< 0.001) and atrial natriuretic peptide ( 40 +/- 6 vs 28 +/- 5 pg/ml; p<0.05). Despite a similar severity of heart failure, elderly patients had smaller ventricular dimensions (left ventricular internal dimension in diastole 51 +/- 2 vs 69 +/- 3 mm;p<0.0001 and greater impairment of ventricular compliance using Doppler indexes. Plasma norepinephrine was higher (1,191 +/- 80 vs 620 +/- 67 ppg/ml; p<0.01), and plasma atrial natriuretic peptide, plasma active renin, and angiotensin II were lower in elderly patients than in the younger patients with heart failure. As functional capacity declines with age, elderly patients may have less severe cardiac dysfunction for any given level of functional impairment, and this may account for most of the differences in neuroendocrine activity with age. Age appears to be an important determinant of plasma norepinephrine and may be a confounding factor in interpreting the prognostic significance of this hormone.

Aged↗
PubMed1995

Reduced alveolar-capillary membrane diffusing capacity in chronic heart failure. Its pathophysiological relevance and relationship to exercise performance.

BACKGROUND: The pulmonary diffusing capacity for carbon monoxide (DLCO) is reduced in chronic heart failure (CHF) and is an independent predictor of peak exercise oxygen uptake. The pathophysiological basis for this remains unknown. The aim of this study was to partition DLCO into its membrane conductance (DM) and capillary blood volume components (Vc) and to assess if alveolar-capillary membrane function correlated with functional status, exercise capacity, and pulmonary vascular resistance. METHODS AND RESULTS: The classic Roughton and Forster method of measuring single-breath DLCO at varying alveolar oxygen concentrations was used to determine DM and Vc in 15 normal subjects and 50 patients with CHF. All performed symptom-limited maximal bicycle exercise tests with respiratory gas analysis; 15 CHF patients underwent right heart catheterization. DLCO was significantly reduced in CHF patients compared with normal subjects, predominantly because of a reduction in DM (7.0 +/- 2.6 versus 12.9 +/- 3.8 versus 20.0 +/- 6.1 mmol.min-1.kPa-1 in New York Heart Association class III, class II, and normal subjects, respectively, P < .0001), even when the reduction in lung volumes was accounted for by the division of DM by the effective alveolar volume. The Vc component of DLCO was not impaired. DM significantly correlated with maximal exercise oxygen uptake (r = .72, P < .0001) and inversely correlated with pulmonary vascular resistance (r = .65, P < .01) in CHF. CONCLUSIONS: Reduced alveolar-capillary membrane diffusing capacity is the major component of impaired pulmonary gas transfer in CHF, correlating with maximal exercise capacity and functional status. DM may be a useful marker for the alveolar-capillary barrier damage induced by raised pulmonary capillary pressure.

Blood-Air Barrier↗
PubMed1995

Plasma neuro-endocrine activity in very elderly subjects and patients with and without heart failure.

Marked neuro-endocrine activation in patients with heart failure indicates a worse prognosis and a greater prognostic benefit from the use of ACE inhibitors. However, although the incidence of heart failure rises rapidly with age, relatively little is known about activation of the renin-angiotensin and sympathetic nervous system in patients with heart failure over the age of 75 years. This study was undertaken to investigate plasma concentrations of neurohormonal variables in elderly patients referred to the cardiac clinic with a presumptive, but unconfirmed, diagnosis of heart failure, and to compare these values to plasma concentrations found in age-matched normal subjects. Fifty patients referred with a diagnosis of heart failure were studied. All were receiving a diuretic but not an ACE inhibitor. Patients with renal, haematological and valve disease were excluded. Routine biochemistry and neurohormonal measurements were performed at their first visit, together with an electrocardiogram, chest X-ray and a full clinical examination by an experienced cardiologist. An echocardiogram and Doppler study was also performed and the diagnosis of heart failure either confirmed or refuted. Plasma concentrations of neuro-endocrine variables in healthy elderly subjects were similar to our normal laboratory range in younger subjects with the exception of atrial natriuretic peptide (ANP) (40 +/- 6 pg.ml-1, normal range < 40) and noradrenaline (5.7 +/- 0.7 nmol.l-1, normal range < 2.8). Impairment of left ventricular systolic function was confirmed in 38 of the 50 symptomatic patients (76%) and was associated with increases in plasma concentrations of active renin (58 +/- 8 IU.mol-1, P < 0.001 compared to healthy elderly subjects), angiotensin II (23 +/- 5 pg.ml-1, P < 0.008), noradrenaline (7.7 +/- 1.2 nmol.l-1, P < 0.01) and atrial natriuretic peptide (121 +/- 18 pg.ml-1, P < 0.002). Plasma concentrations were similar in normal subjects and those receiving treatment for heart failure but in whom the diagnosis was not confirmed. A weak relationship between plasma atrial natriuretic peptide (ANP) and left ventricular fractional shortening was demonstrated (r = -0.5, P < 0.001). Using an upper limit of ANP in the healthy elderly subjects of 62 pmol.ml-1 (mean + SD), plasma concentrations of ANP in the population with suspected heart failure had a sensitivity of 74% and specificity of 66% for the diagnosis of heart failure among elderly patients in the community or where access to echocardiography is limited. Left ventricular diastolic filling (assessed by Doppler) was abnormal in healthy elderly subjects and patients with heart failure, and appeared of limited value in the diagnosis of heart failure secondary to diastolic dysfunction. This study confirms that the renin-angiotensin system is activated in elderly patients with heart failure treated with diuretics. ANP may be helpful in diagnosing heart failure where it appears to have a complimentary role to echocardiography.

Aged↗
PubMed1995

Effect of arterial cannulation and contrast agents on blood coagulation.

RATIONALE AND OBJECTIVES: Nonionic contrast media have been considered by some to have thrombogenic properties. We prospectively assessed the effect of femoral artery catheterization and both nonionic and ionic contrast media on the coagulation parameters--fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FpA)--during clinical angiography. METHODS: Seventeen patients undergoing aortography were included. Blood samples were obtained before and after arterial puncture and before and up to 30 min after contrast administration. RESULTS: An increase in FpA was observed after arterial puncture (range = 8.4 +/- 1.9 to 13.6 +/- 2.3 ng/ml, p < .004; data are written as mean +/- standard error of the mean). There was an observed increase in F1 + 2 after arterial puncture that was not statistically significant (2.0 +/- 0.4 to 2.3 +/- 0.4 nmol/l). No further increase was observed in either FpA or F1 + 2 levels after nonionic or ionic contrast media administration. CONCLUSION: The increased activity of the coagulation system during angiography is related to the arterial puncture, and nonionic and ionic contrast media have no thrombogenic potential in vivo.

Adolescent↗
PubMed1994

Optimising heart failure pharmacotherapy: the ideal combination.

Good management of all patients with heart failure is complex. Fortunately most patients fall into only one or two categories, making management less daunting. Most patients with heart failure need treatment with loop diuretics and ACE inhibitors and for many these drugs, possibly combined with antithrombotic measures, are all that is needed for optimal treatment, but optimal treatment can only follow adequate diagnosis. This needs a partnership between the specialist and the family doctor, with ease of access to non-invasive investigations such as echocardiography.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Streptokinase neutralisation titres up to 866 days after intravenous streptokinase for acute myocardial infarction.

OBJECTIVE: To follow the change in streptokinase neutralisation titres in a group of patients after treatment with streptokinase for acute myocardial infarction. DESIGN: Venous blood samples suitable for analysis were obtained up to 866 days after treatment with 1.5 million units of streptokinase in 189 patients. The ability of the patient's plasma to inhibit lysis of a thrombin clot by streptokinase was assessed. SETTING: A coronary care unit in a district general hospital. PATIENTS: A retrospective review of coronary care records and the district health authority computer showed that 329 patients who had received streptokinase were alive. All were invited for venepuncture and 220 (67%) attended. Satisfactory samples were obtained from 189 patients. RESULTS: Raised titres of antibody sufficient to neutralise a standard dose of 1.5 million units of streptokinase were found in 90% of patients. There was a fall in streptokinase neutralisation titre with increasing time after administration of streptokinase (r = -0.35, P < 0.0001) and though there was considerable variation among the group the neutralisation titre was higher than in the general population in all patients, even those who had received streptokinase at least two years previously. CONCLUSION: The ability of streptokinase to lyse a thrombin clot was appreciably inhibited in vitro by the plasma from patients who had received 1.5 million units of streptokinase. High streptokinase neutralisation titres persisted for a long time after the use of streptokinase as thrombolytic treatment for acute myocardial infarction. Readministration of streptokinase may not be efficacious for considerably longer than the one year currently advocated. Until the in vivo effects of streptokinase readministration are known a non-antigenic thrombolytic agent should be used instead.

Antibodies↗
PubMed1993

Tumour necrosis factor alpha in severe congestive cardiac failure.

OBJECTIVE: To examine the concentration of circulating tumour necrosis factor alpha (TNF alpha) in patients with severe congestive heart failure (New York Heart Association class IV) during one year and to correlate changes in this cytokine with changes in plasma noradrenaline, plasma renin activity, and weight. DESIGN: A prospective study of the role of TNF alpha in severe chronic heart failure. Blood samples were collected at intervals of three months. SETTING: Medical research centre of a teaching hospital. PATIENTS: 16 patients with chronic stable severe heart failure. INTERVENTIONS: Vasodilator treatment with captopril or flosequinan. MAIN OUTCOME MEASURES: Changes in TNF alpha and the correlation with changes in plasma noradrenaline, plasma renin activity, and weight during optimal medical treatment for one year. RESULTS: The mean concentration of TNF alpha was greater than the upper 95% confidence interval for healthy controls throughout the year of the study but there was considerable between and within patient variation. No correlation was seen between TNF alpha and plasma noradrenaline, plasma renin activity, or weight. CONCLUSIONS: The stimulus resulting in enhanced plasma concentrations of TNF alpha in congestive heart failure remains unclear and concentrations at any particular time were not prognostic.

Body Weight↗
PubMed1991

Lymphatic abnormalities in Alagille's syndrome.

Chylous pleural effusions developed in a patient with Alagille's syndrome who had dysplasia of the lymphatic system. Lymphatic abnormalities are not a recognised feature of Alagille's syndrome.

Adult↗
PubMed1990

Intracardiac thrombus formation in association with hydatid disease.

Cardiac hydatid disease is rare, but life threatening. A pedunculated hydatid cyst which mimicked a left atrial myxoma was diagnosed on two-dimensional echocardiography. The degree of cardiac involvement at necropsy was much greater than indicated by either echocardiography or limited cardiac catheterization. The suggestion that only echocardiography be performed before surgery is undertaken may be inappropriate in many cases.

Aged↗
PubMedDate not supplied

Flosequinan: a new vasodilator for the treatment of heart failure.

The incidence and prevalence of congestive heart failure is increasing despite improvements in the management of myocardial infarction and hypertension. This trend is likely to continue as the proportion of elderly in the community increases. A new vasodilator, flosequinan, is currently under investigation and may improve prognosis.

Heart Failure↗