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Biomedical subjects

F G Dunn

Publications and source records attributed to F G Dunn.

At least 37 records · Page 2Linked to original sources
PubMed1996

Left ventricular hypertrophy as a risk factor in hypertension.

Hypertension is established as one of the major risk factors for congestive heart failure, renal failure, cerebrovascular accident and coronary artery disease. Left ventricular hypertrophy (LVH) is an adaptive response to the increased afterload in hypertension, and therefore serves to normalize wall stress. However, LVH has been established as an independent risk factor for adverse cardiovascular events and death in hypertension. For this reason, considerable attention has been directed towards a better understanding of LVH as a risk factor. As recognition of the risk associated with LVH has grown, investigators have increasingly focused attention on improving methods for the detection of LVH, assessing its effects on cardiac function, defining its relationship with myocardial ischaemia and sudden death, evaluating the role of antihypertensive treatment in the regression of LVH and assessing whether such regression is beneficial in the long term.

Death, Sudden, Cardiac↗
PubMed1995

Effects of warfarin therapy on plasma fibrinogen, von Willebrand factor, and fibrin D-dimer in left ventricular dysfunction secondary to coronary artery disease with and without aneurysms.

Cardiac impairment in patients is associated with intracardiac thrombus formation and thromboembolism. A high prothrombotic state may exist in such patients, and abnormalities in plasma markers of thrombogenesis may be indicative of such a state. The aim of this study was to determine the associations of left ventricular (LV) aneurysm formation and dysfunction with plasma fibrinogen, von Willebrand factor, and fibrin D-dimer, which are markers associated with thrombus formation (thrombogenesis) and to investigate the effects of warfarin given to patients with LV aneurysms on fibrinogen and D-dimer levels. A cross-sectional study of 112 patients with coronary artery disease was initially performed: 34 patients had normal LV function (group 1); 30 had LV dysfunction without aneurysm formation (group 2); 29 had LV aneurysms without anticoagulation (group 3a); and 19 patients had LV aneurysms with warfarin therapy (group 3b). Results were compared with 158 population controls from a random population sample. A longitudinal study of 10 patients given warfarin was also performed. In group 1, plasma fibrinogen (median difference 0.36 g/L; p = 0.0009) and von Willebrand factor (median difference 17 IU/dl; p = 0.04) were elevated, whereas plasma D-dimer levels (median difference 23.0 ng/ml; p = 0.001) were lower than those in population control subjects. There were no significant differences in plasma fibrinogen, von Willebrand factor, or D-dimer levels between groups 1 and 2. In group 3a, plasma fibrinogen was elevated when compared with group 1 (median difference 0.6 g/L; p = 0.0001), with a trend toward high von Willebrand factor levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Is diastolic dysfunction associated with thrombogenesis? A study of circulating markers of a prothrombotic state in patients with coronary artery disease.

Clinical data on the contributory role of heart failure to thromboembolic risk does not differentiate between systolic and diastolic left ventricular dysfunction. We therefore conducted a population-controlled cross-sectional study to determine levels of plasma fibrinogen (associated with thromboembolism), fibrin D-dimer (a marker of fibrin turnover) and von Willebrand factor (a marker of endothelial dysfunction) in patients with ischaemic heart disease (a common cause of diastolic dysfunction) in whom left ventricular diastolic function was defined by echocardiography. We studied 106 patients: those with normal left ventricular function (n = 42, Group 1); those with left ventricular dysfunction but without aneurysms (n = 34, Group 2); and those with left ventricular aneurysm formation (n = 30, Group 3). Each of these groups was subdivided into those with (a) and without (b) diastolic dysfunction. Diastolic dysfunction was present in over 60% of patients, irrespective of left ventricular systolic impairment. There were no significant differences in median levels of plasma fibrinogen, fibrin D-dimer or von Willebrand factor in each group of patients with ischaemic heart disease, whether or not left ventricular diastolic dysfunction was present (Mann-Whitney test; P = N.S.). Systolic (rather than diastolic) dysfunction was the main correlate of these (analysis of variance, general linear model--ANOVA-GLM--P < 0.05) and the greatest abnormalities of fibrinogen, endothelial dysfunction and intravascular fibrin turnover were seen in patients with left ventricular aneurysms whether or not diastolic dysfunction was present. This study demonstrates that there is no evidence of a significant additional contribution to thrombotic risk (as assessed by plasma fibrinogen, von Willebrand factor and fibrin D-dimer) for patients with left ventricular diastolic dysfunction. A relationship is noted between some prothrombotic factors and Doppler indices of flow, which suggests a possible association between cardiac haemodynamics and thrombogenesis.

Analysis of Variance↗
PubMed1995

Plasma fibrinogen and fibrin D-dimer in patients with atrial fibrillation: effects of cardioversion to sinus rhythm.

Cardioversion of atrial fibrillation carries a serious risk of major thromboembolism and stroke. To determine whether or not the procedure alters plasma levels of fibrin D-dimer (a marker of intravascular fibrin turnover and thrombus formation) and plasma fibrinogen (associated with stroke and thromboembolism), we performed a prospective study in 19 patients with atrial fibrillation in whom cardioversion was attempted: seven patients without prior oral anticoagulant therapy (but with intravenous heparin for 24 h) (Group I), and 12 patients with full oral anticoagulation pre- and post-cardioversion (Group II). Plasma fibrinogen and fibrin D-dimer were measured pre-cardioversion, and at Days 3, 7 and 14 post-cardioversion. In Group I, there was a significant reduction in median plasma fibrin D-dimer levels by 14 days following cardioversion (200 vs. 52 ng/ml; paired Wilcoxon test, P = 0.02). In Group II, there was no change in median plasma fibrin D-dimer levels over the 14 days following cardioversion. There were no significant changes in plasma fibrinogen with cardioversion in either group of patients. The reduction of plasma fibrin D-dimer in Group I suggests a beneficial reduction of intravascular fibrin turnover and thrombogenesis by the cardioversion of patients with atrial fibrillation to sinus rhythm. Furthermore, it strongly suggests that it is atrial fibrillation itself which is the major risk of thromboembolism and that the risk continues for up to 14 days post-cardioversion. In Group II, the low pre-cardioversion fibrin D-dimer levels and lack of change with cardioversion is consistent with the prophylactic effect of warfarin therapy against thromboembolism during the cardioversion of atrial fibrillation.

Adult↗
PubMed1995

The interface of hypertension and ischemic heart disease.

Myocardial infarction remains the single most common cause of death in patients with essential hypertension. This becomes particularly evident when the hypertension is associated with left ventricular hypertrophy. To combat the continuing high mortality from myocardial infarction in hypertensive heart disease, however, all aspects of the relationship must be studied. Thus, addressing the interface from an epidemiological standpoint as well as from a pathological point is critical and progress in these areas as well as in areas of management are ultimately likely to lead to a fall in morbidity and mortality from ischemic heart disease in patients with hypertension.

Coronary Disease↗
PubMed1995

Increased markers of thrombogenesis in chronic atrial fibrillation: effects of warfarin treatment.

OBJECTIVE: To determine whether chronic atrial fibrillation is associated with abnormalities in plasma fibrinogen, von Willebrand factor (vWF) (a marker of endothelial disturbance), or fibrin D- dimer (a measure of fibrin turnover); and if so, whether such levels are related to haemodynamic disturbance (enlarged left atrium, poor left ventricular function) or existing treatment with warfarin or aspirin. To investigate the effects of introducing warfarin in patients with atrial fibrillation on fibrinogen and D- dimer levels. DESIGN: Cross sectional population sample controlled study and longitudinal study of patients undergoing anticoagulation. SETTING: District general hospital. SUBJECTS: 87 patients (44 men and 43 women of mean (SEM) age 63.0 (1.0)) with chronic atrial fibrillation. At the time of the study, 37 were taking no antithrombotic medication (group 1), 31 were taking warfarin (including two on warfarin and aspirin) (group 2) and 19 were taking aspirin alone (group 3). They were compared with 158 population controls from a random population sample (the second Glasgow monitoring trends and determinants in cardiovascular disease study). As part of clinical treatment warfarin was introduced in 20 patients with chronic atrial fibrillation (14 men and six women of mean (SEM) (range) age 63.9 (2.35 (32-74) years). RESULTS: Plasma fibrinogen remained significantly increased in patients of group 1 (no antithrombotic medication) compared with that of the population controls (median difference 1.23 g/l; 95% confidence interval (CI) 0.88 to 1.62, P < 0.0001). There was also a significant increase in plasma D-dimer levels (median difference 77 ng/ml; 95% CI 38 to 122, P < 0.01) and vWF (median difference 63 IU/dl; 95% CI 38 to 89, P < 0.0001). There was no significant difference in plasma fibrinogen (median difference 0.14 g/l; 95% CI -0.44 to 0.77, P = 0.65) or vWF (median difference 3.5 IU/dl; 95% CI - 41 to 41, P = not significant in patients of group 2 (warfarin treatment) compared with that of patients in group 1. Levels of D-dimer were significantly lower in group 2 (median difference 90 ng/ml, 95% CI 39 to 150, P < 0.0001) than in group 1. There were no significant differences in plasma fibrinogen (median difference 0.08 g/l; 95% CI - 0.52 to 0.77, P = 0.73), D-dimer (median difference - 34 ng/ml; 95% CI - 114 to 21.0, P = 0.25), or vWF (median difference 2%; 95% CI - 35 to 41, P = not significant) levels between patients of groups 1 and 3. There were no significant correlations between the coagulation indices and left atrial volume or ventricular function. There was a significant positive correlation between plasma fibrin D-dimer and vWF levels in patients of groups 1 and 3 (r = 0.52, P < 0.001). There was a significant reduction in median plasma fibrin D-dimer levels at 2 months after the introduction of warfarin (181 ng/ml v 80 ng/ml, P < 0.001), but no effect on plasma fibrinogen. CONCLUSIONS: Increased median plasma fibrinogen and vWF levels were found in patients with chronic atrial fibrillation. Plasma D-dimer levels were also increased in patients with chronic atrial fibrillation not receiving warfarin, suggesting increased intravascular thrombogenesis in such patients. Introduction of warfarin normalised circulating fibrin D- dimer levels, suggesting that warfarin treatment was effective in preventing excessive fibrin turnover, consistent with the antithrombotic effects of warfarin. These results suggest three possible thrombotic markers to assess patients with atrial fibrillation who are at high risk of thrombogenesis; D-dimer also merits assessment as a measure of reduction in thrombotic risk in patients receiving warfarin.

Adult↗
PubMed1995

Cardiac hypertrophy and hypertension.

The epidemiology of left ventricular hypertrophy (LVH) in hypertension has been extensively studied and its importance as a cardiovascular risk factor is established. Significant advances in recent years have also occurred in pathophysiology, detection of LVH, and in management including regression of hypertrophy. Advances in pathophysiology have demonstrated that a number of trophic factors such as stretch, angiotensin II and stimulation of the sympathetic nervous system contribute towards the hypertrophy of the myocyte. In addition, it is important to emphasise factors such as aldosterone and angiotensin which contribute towards the proliferation of fibroblasts. The mechanisms involved in the increased mortality in patients with left ventricular hypertrophy remain to be determined, but myocardial ischaemia, left ventricular dysfunction and a propensity to ventricular arrhythmias have all been studied in detail. Echocardiography is a more reliable method for detecting LVH than ECG, but these investigations should be regarded as complementary rather than one being performed to the exclusion of the other. It remains unclear as to whether regression of LVH specifically contributes to a reduction in overall cardiovascular risk, but the key point seems to be optimal control of blood pressure, and only with further clinical trials will the exact impact of regression of LVH on morbidity and mortality be known.

Humans↗
PubMed1994

The role of nuclear cardiology in hypertension.

In view of the increased risk of cardiac events in systemic hypertension, particularly in patients with left ventricular hypertrophy, it is important to have reliable methods of assessing cardiac structure and function and myocardial perfusion in these patients. While echocardiography is the noninvasive method of choice for measuring the severity of left ventricular hypertrophy there is no alternative at present to invasive coronary angiography to define accurately coronary artery anatomy. Nuclear cardiological investigations are extremely useful in the assessment of systolic and diastolic function at rest and during exercise. Furthermore, myocardial perfusion imaging is of value in identifying myocardial ischaemia and assessing the functional importance of coronary artery lesions. Recent studies have also suggested that nuclear cardiology investigations may be the best way to identify nonfunctioning but viable areas of the myocardium which may benefit from revascularization.

Coronary Disease↗
PubMed1994

Treatment of atrial fibrillation in a district general hospital.

OBJECTIVE: To assess current strategies used to investigate and manage acute atrial fibrillation in hospital. DESIGN: Prospective survey of all acute admissions over 6 months. SETTING: District general hospital serving a population of 230,000 in north east Glasgow. SUBJECTS: 2686 patients admitted as emergency cases over 6 months. RESULTS: Of the 2686 patients, 170 (age range 38-95, mean (SD) 73.5 (10.6) years; 70 men (41%) and 100 women (59%)) were admitted with atrial fibrillation. The principal underlying medical conditions were ischaemic heart disease in 79 (46.5%), rheumatic heart disease in 26 (15.3%), and thyroid disease in six (3.5%). Cardiac failure was present on admission in 61 (36%), cerebrovascular events in 23 (14%), and myocardial infarction in 17 (10%). Of those with a history of atrial fibrillation (102 (60%) including 10 with paroxysmal atrial fibrillation) treatment on admission included digoxin in 71 (70%), warfarin in 20 (20%), and aspirin in 17 (17%); the aspirin was predominantly given for concomitant vascular disease. The mean (SD) inpatient stay was 16 days (19.7) (range 1-154) largely due to the patients with stroke. Thyroid function tests were performed in only 63% and echocardiography in 33%. Overall, the rate of introduction of anticoagulation (seven patients) and attempted cardioversion (21 patient: 19 pharmacological and two electrical) was surprisingly low. Only 49 patients (34% of those not on warfarin) had contraindications to anticoagulation: these included peptic ulcer or gastrointestinal bleeding in 18 (12%), dementia in eight (6%), chronic renal failure or dialysis in eight (6%), and alcohol excess in four (3%). CONCLUSION: Standard investigations were inadequately used in patients with atrial fibrillation and there was a reluctance to perform cardioversion or to start anticoagulant treatment.

Adult↗
PubMed1994

Pre-dosing antibody levels and efficacy of thrombolytic drugs containing streptokinase.

OBJECTIVE: To evaluate the influence of pretreatment streptokinase resistance titre and the concentration of IgG antibodies to streptokinase on the efficacy of thrombolytic drugs containing streptokinase in restoring coronary patency in acute myocardial infarction. DESIGN: Comparative observational study. SETTING: City general hospital. PATIENTS: One hundred and twenty four previously unexposed patients presenting within six hours of onset of acute myocardial infarction. INTERVENTIONS: Streptokinase, 1.5 MIU as intravenous infusion over 60 minutes (60 patients), or anistreplase, 30 units as intravenous injection over five minutes (64 patients). MAIN OUTCOME MEASURES: Pretreatment streptokinase resistance titre and concentration of IgG antibodies to streptokinase were measured in 96 and 124 patients respectively and coronary patency assessed angiographically at 90 minutes and 24 hours. RESULTS: Pretreatment streptokinase resistance titre and concentrations of IgG antibodies to streptokinase were low and skewed towards higher values. Those patients with coronary occlusion at 24 hours had a significantly higher median streptokinase resistance titre (100 v 50 streptokinase IU ml-1, P = 0.02). There were trends towards a higher streptokinase resistance titre in those patients with coronary occlusion at 90 minutes (50 v 20 streptokinase IU ml-1, P = 0.06) and higher concentrations of IgG antibodies to streptokinase in those with coronary occlusion at both 90 minutes and 24 hours (1.53 v 0.925, P = 0.03; 1.65 v 1.04 micrograms streptokinase binding ml-1, P = 0.06). Coronary patency rates were similar in the two treatment groups. CONCLUSIONS: In the range measured in previously unexposed patients the streptokinase resistance titre has a small, but significant, negative influence on the efficacy of streptokinase and anistreplase. This effect should be considered if retreatment with streptokinase or anistreplase is proposed.

Adult↗
PubMed1993

Unilateral pulmonary artery agenesis: a rare cause of haemoptysis and pleuritic chest pain.

Haemoptysis and pleuritic chest pain are common presentations of cardiopulmonary disease. While a number of common disorders may explain these symptoms, occasionally unusual causes may emerge which should be considered in the differential diagnosis especially if pulmonary embolism is unlikely; so that inappropriate anticoagulation or thrombolytic therapy is avoided. We present a case of unilateral pulmonary artery agenesis, who presented with pleuritic chest pain and haemoptysis, and was initially treated as a case of pulmonary thromboembolism.

Chest Pain↗
PubMed1993

An audit of emergency echocardiography in a district general hospital.

Eighty patients (43 M, 37 F), aged 23-89 years who were referred for emergency echocardiography over a 12-month period were prospectively studied in order to determine the reasons for emergency echocardiography and the influence of its results on patient management. The most frequent emergency request was to clarify whether the basis for cardiomegaly in a haemodynamically unstable patient was pericardial effusion or left ventricular dilatation. Other reasons for requests were for assessment for source of systemic emboli, acute complications of myocardial infarction, endocarditis, valve dysfunction and cardiac trauma. As a consequence of the emergency echocardiography, management was immediately influenced in 19 patients. This study has provided information on the specific settings in which emergency echocardiography can be justified.

Adult↗
PubMed1993

The incidence and mechanism of hypotension following thrombolytic therapy for acute myocardial infarction with streptokinase-containing agents--lack of relationship to pretreatment streptokinase resistance.

The incidence, amplitude, mechanism and relationship to prior exposure to streptococcal antigen of blood pressure changes to streptokinase-containing thrombolytic agents were investigated in 125 patients treated with either 1.5 x 10(6) IU streptokinase over 60 min or 30 U anistreplase over 5 min, within 6 h of onset of acute myocardial infarction. Twenty-one of 52 patients with anterior and 34 of 73 with inferior myocardial infarction had a hypotensive response. There were no significant differences in the incidence, duration or amplitude of hypotension between the two treatment groups. The maximum mean fall in systolic blood pressure was 16.9 mmHg (95% confidence limits, CL 12.2 to 24.5 mmHg), and the maximum mean fall in diastolic blood pressure was 13.7 mmHg (CL 10.3 to 17.1 mmHg), starting 4 min after start of therapy and resolving within 34 min. Blood pressure changes were well tolerated. Hypotension was not related to pretreatment streptokinase resistance titre, or anti-SK IgG concentration, to changes in plasma fibrinogen, B-beta 15-42 peptide, D-dimer--as indices of thrombin activation and fibrin (-ogen) breakdown--to plasma viscosity. The blood pressure changes following treatment with streptokinase-containing thrombolytic agents in acute myocardial infarction are frequent but well tolerated. The mechanism of hypotension remains unclear, but is not related to prior exposure to streptococcal antigen.

Anistreplase↗
PubMed1993

Sudden cardiac death, ventricular arrhythmias and hypertensive left ventricular hypertrophy.

OBJECTIVE: To evaluate the relationship between sudden cardiac death, ventricular arrhythmias and left ventricular hypertrophy in patients with hypertension. DATA IDENTIFICATION: Epidemiological studies assessing the importance of left ventricular hypertrophy as a risk factor for sudden cardiac death, studies assessing the prevalence of arrhythmias in left ventricular hypertrophy and studies assessing whether there is an electrophysiological substrate in the hypertrophied myocardium for ventricular dysrhythmias. RESULTS OF DATA ANALYSIS: Current evidence indicates that left ventricular hypertrophy is a risk factor for sudden cardiac death and that ventricular arrhythmias are more prevalent in hypertensive patients with than in those without left ventricular hypertrophy. However, there is a lack of evidence that these dysrhythmias are important as an underlying mechanism for sudden cardiac death, and there is no clear evidence that the hypertrophied myocardium is, itself, an arrhythmogenic substrate for malignant ventricular dysrhythmias. One possible mechanism for sudden cardiac death is myocardial ischaemia, either as a consequence of associated coronary disease or due to left ventricular hypertrophy, but this remains unproved. CONCLUSIONS: There is currently no evidence that the ventricular ectopic activity seen in patients with hypertensive left ventricular hypertrophy is a marker for sudden cardiac death. Clarification of the mechanisms involved in sudden cardiac death will help in selecting appropriate preventive and therapeutic strategies for these patients.

Animals↗
PubMed1993

Assessment by general practitioners of suitability of thrombolysis in patients with suspected acute myocardial infarction.

OBJECTIVE: To assess the clinical ability of general practitioners to decide to give thrombolytic therapy to patients with suspected myocardial infarction and to assess the contribution of the electrocardiograph (ECG) to this decision-making process. SETTING: 7 practices on the North side of Glasgow and the coronary care unit of Stobhill General Hospital. SUBJECTS: 137 patients presenting with chest pain who required direct admission to the coronary care unit. MAIN OUTCOME MEASURES: Agreement between the general practitioner's clinical decision to give thrombolytic therapy with or without reference to the ECG and the prescription of thrombolytic therapy in the coronary care unit. RESULTS: The predictive accuracy of the general practitioner's assessment of the necessity for thrombolytic therapy was 71.5%. The ECG had no impact on the accuracy of this decision and there were problems with the recording and interpretation of the ECG. Clinical decision making was altered in six cases by the ECG: wrongly in four. CONCLUSION: The diagnostic accuracy among general practitioners would result in some patients who did not have acute myocardial infarction being given thrombolytic therapy. In this study the ECG did not contribute towards diagnostic accuracy. Substantial improvement in both the recording and interpretation of ECGs is needed before thrombolytic agents can be routinely prescribed at home.

Clinical Competence↗