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A Heagerty

Publications and source records attributed to A Heagerty.

18 recordsLinked to original sources
PubMed2006

Optimizing hypertension management in clinical practice.

A clear relationship exists between elevated blood pressure (BP) and various manifestations of cardiovascular disease. Despite the availability of numerous treatment guidelines, hypertension remains inadequately controlled, with only a small proportion of patients achieving target BP levels. Many factors, both patient and physician related, contribute to this poor level of hypertension control. Major determinants include the implementation of inappropriate treatment regimens that do not enable patients to achieve goal and poor patient compliance. For example, it is widely acknowledged that most patients require two or more antihypertensive drugs to achieve BP goal; however, physicians may be reluctant to employ such treatment strategies. The aim of this review is to explore factors that contribute to poor hypertension control rates and how to overcome these, including the rationale for selecting combination therapy, with particular reference to angiotensin II receptor blocker combinations.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Contribution of depression and anxiety to impaired health-related quality of life following first myocardial infarction.

BACKGROUND: The extent to which depression impairs health-related quality of life (HRQoL) in the physically ill has not been clearly established. AIMS: To quantify the adverse influence of depression and anxiety, assessed at the time of first myocardial infarction and 6 months later, on the physical aspect of HRQoL 12 months after the infarction. METHOD: In all, 260 in-patients, admitted following first myocardial infarction, completed the Hospital Anxiety and Depression Scale and the Medical Outcomes Study SF-36 assessment before discharge and at 6- and 12-month follow-up. RESULTS: Depression and anxiety 6 months after myocardial infarction predicted subsequent impairment in the physical aspects of HRQoL (attributable adjusted R(2)=9%, P<0.0005). These negative effects of depression and anxiety on outcome were mediated by feelings of fatigue. Depression and anxiety present before myocardial infarction did not predict HRQoL 12 months after myocardial infarction. CONCLUSIONS: Detection and treatment of depression and anxiety following myocardial infarction improve the patient's health-related quality of life.

Age Factors↗
PubMed2004

The risk factors for depression in first myocardial infarction patients.

BACKGROUND: Depression affects outcome following myocardial infarction but the risk factors for such depression have been little studied. This study considered whether the causes of depression occurring before and after myocardial infarction were similar to those of depression in the general population. METHOD: Consecutive patients admitted to hospital following their first myocardial infarction were interviewed with the Schedule for Clinical Assessment in Neuropsychiatry to detect psychiatric disorders and the Life Events and Difficulties Schedule to assess recent stress. Participants completed the Hospital Anxiety and Depression Scale (HADS) at entry to the study and 1 year later and the risk factors associated with a high score at both times were assessed. RESULTS: Of 314 (88% of eligible) patients who were recruited, 199 (63%) were male and 63 (20%) had depressive disorders. Logistic regression identified the following as independently associated with depressive disorder that had been present for at least I month before the myocardial infarction: younger age, female sex, past psychiatric history, social isolation, having marked non-health difficulties and lack of a close confidant. At follow-up 269/298 (90%) responded; of 189 participants not depressed at first assessment, 39 (21%) became depressed by the 1 year follow-up. Logistic regression identified frequent angina as the only significant predictor of raised HADS scores at 12 months. CONCLUSIONS: Depression developing during the year following myocardial infarction does not have the same risk factors as that which precedes myocardial infarction. Further clarification of the mechanisms linking depression to poor outcome may require separation consideration of pre- and post-myocardial infarction depression, and its risk factors.

Age Factors↗
PubMed2004

Lack of a close confidant, but not depression, predicts further cardiac events after myocardial infarction.

OBJECTIVE: To assess the role of depression and lack of social support before myocardial infarction (MI) in determining outcome in a large representative sample of patients admitted after MI in the UK. DESIGN: Prospective cohort design. PATIENTS: 1034 consecutive patients were screened 3-4 days after MI. MAIN OUTCOME MEASURES: Mortality and further cardiac events over one year after an MI. RESULTS: At 12 months' follow up mortality and further cardiac events were assessed in 583 of 654 eligible patients (90% response); 140 of 589 for whom baseline data were collected (23.8%) were depressed before their MI. Patients who were depressed before their MI were not more likely to die (mortality 5.2% v 5.0% of non-depressed patients) or suffer further cardiac events (cardiac events rate 20.7% v 20.3% of non-depressed patients). After controlling for demographic factors and severity of MI, the absence of a close confidant predicted further cardiac events (hazard ratio 0.57, p = 0.022). CONCLUSION: Lack of a close confidant but not depression before MI was associated with adverse outcome after MI in this sample. This association may be mediated by unhealthy behaviours and lack of compliance with medical recommendations, but it is also compatible with difficulties in early life leading to heart disease.

Age Factors↗
PubMed1996

Susceptibility to multiple cutaneous basal cell carcinomas: significant interactions between glutathione S-transferase GSTM1 genotypes, skin type and male gender.

The factors that determine development of single and multiple primary cutaneous basal cell carcinomas (BCCs) are unclear. We describe a case-control study firstly, to examine the influence of allelism at the glutathione S-transferase GSTM1 and GSTT1 and cytochrome P450 CYP2D6 loci on susceptibility to these tumours and, secondly, to identify interactions between genotypes and relevant individual characteristics, such as skin type and gender. Frequency distributions for GSTM1 genotypes in cases and controls were not different, although the frequency of GSTM1 A/B was significantly lower (P = 0.048) in the multiple BCCs than in controls. We found no significant differences in the frequencies of GSTT1 and CYP2D6 genotypes in cases and controls. Interactions between genotypes were studied by comparing multinomial frequency distributions in mutually exclusive groups. These identified no differences between cases and controls for combinations of the putatively high risk GSTM1 null, GSTT1 null, CYP2D6 EM genotypes. Interactions between GSTM1 A/B and the CYP2D6 PM and GSTT1-positive genotypes were also not different. Frequency distributions of GSTM1 A/B with CYP2D6 EM in controls and multiple BCCs were significantly different (P = 0.033). The proportion of males in the multiple BCC group (61.3%) was greater than in controls (47.0%) and single BCC (52.2%), and the frequency of the combination GSTM1 null/male gender was significantly greater in patients with multiple tumours (P = 0.002). Frequency distributions of GSTM1 null/skin type 1 were also significantly different (P = 0.029) and the proportion of subjects who were GSTM1 null with skin type 1 was greater (P = 0.009) in the multiple BCC group. We examined the data for interactions between GSTM1 null/skin type 1/male gender by comparing frequency distributions of these factors in the single and multiple BCC groups. The distributions were almost significantly different (exact P = 0.051). No significant interactions between GSTT1 null or CYP2D6 EM and skin type 1 were identified. Comparisons of frequency distributions of smoking with the GSTM1 null, GSTT1 null and CYP2D6 EM genotypes identified no differences between patients with single and multiple tumours.

Aged↗
PubMed1994

Small arteries and hypertension.

AIM: To review current knowledge on the behaviour of small arteries in hypertension and when the blood pressure is lowered. METHOD: Literature review. CONCLUSIONS: The evidence available at present suggests that despite normalization of blood pressure, the flow reserve in small coronary arteries is not necessarily restored to normal. Therefore the risk of cardiac ischaemia may remain and this may explain the current failure to reduce all cardiac risk associated with hypertension despite effective antihypertensive treatment.

Animals↗
PubMed1993

Regulation of diacylglycerol metabolism by vasoconstrictor hormones in intact small arteries.

The initiation of receptor-mediated small artery contraction is dependent on inositol 1,4,5-trisphosphate-stimulated release of stored calcium. The role of the other product of inositol lipid hydrolysis, 1,2-diacylglycerol, in maintaining contraction remains controversial. Therefore, we have determined the contractile response of rat subcutaneous small arteries (< 300 microns i.d.), when mounted as ring preparations in a myograph, to noradrenaline, angiotensin II, KCl-induced membrane depolarization, and a cell-permeable diglyceride, dioctanoylglycerol. In parallel experiments, the conversion of this diglyceride to dioctanoylphosphatidate was studied in 32P-labeled vessels. Dioctanoylglycerol produced a slow-onset sustained contraction that was dependent on extracellular calcium. This was accompanied by the generation of the lipid dioctanoylphosphatidate. Noradrenaline and KCl induced rapid-onset sustained contractions and increased the production of dioctanoylphosphatidate (75% and 91%, respectively). In addition, dioctanoylglycerol levels were reduced (41%) after noradrenaline stimulation, suggesting activation of diacylglycerol kinase. In contrast, the contractile response to angiotensin II was transient, and this agonist did not significantly affect the conversion of dioctanoylglycerol to phosphatidate. Noradrenaline markedly increased (fourfold) the formation of endogenous phosphatidate, whereas endogenous 1,2-diacylglycerol was increased (47%) with angiotensin II. These results demonstrate that phosphatidate formation is regulated by vasoconstrictor hormones during receptor-mediated contraction, independent of diglyceride mass. Modulation of the levels of lipid second messengers downstream from phospholipid hydrolysis may represent a mechanism by which agonists that act through the same signaling system produce different contractile responses.

Angiotensin II↗
PubMed1992

Familial Conn's syndrome.

We describe the occurrence of primary hyperaldosteronism in two sisters. Although this is only the second published report of familial Conn's syndrome, it does have implications for the relatives of patients with Conn's syndrome and these are discussed.

Adenoma↗
PubMed1991

Lip dermatoses.

Explore the source record for details and available documents.

Adolescent↗
PubMed1990

Agonist-induced production of 1,2-diacylglycerol and phosphatidic acid in intact resistance arteries. Evidence that accumulation of diacylglycerol is not a prerequisite for contraction.

The production of total amounts of 1,2-diacylglycerol as well as those specifically derived from inositol lipid hydrolysis was studied in intact rat resistance arteries stimulated with either noradrenaline, vasopressin, or angiotensin II at 20 s when the onset of contraction would be nearing its maximum, and at 5 min during the sustained phase of contraction. Total amounts of 1,2-diacylglycerol were not altered by any agonist at 20 s, or at 5 min. However, arachidonate-containing species of 1,2-diacylglycerol were differentially influenced being increased at 5 min by noradrenaline, and decreased at 20 s and 5 min by vasopressin. Only angiotensin II produced substantial increases in this class of 1,2-diacylglycerol at both time points. In order to investigate the fate of this second messenger total and inositol lipid derived phosphatidic acids were then measured at both 20 s and 5 min. Noradrenaline induced a rise in both total and arachidonate-containing phosphatidic acid at both times as did vasopressin. Only small increases were induced by angiotensin II at 20 s. These data demonstrate that the accumulation of 1,2-diacylglycerol generated from inositol lipid breakdown is only observed with activation by angiotensin II. Other agonists produced phosphatidic acids with time and the rate of generation of these lipids is agonist-specific. Thus phosphatidic acid may play a more prominent role during the sustained phase of contraction than previously anticipated.

Angiotensin II↗
PubMed1989

Amoxycillin/clavulanic acid (Augmentin)-induced intrahepatic cholestasis.

A 75-year-old man developed a biopsy-proven, drug-induced intrahepatic cholestasis after use of amoxycillin trihydrate combined with the beta-lactam inhibitor potassium clavulanate (Augmentin). Cholestatic liver injury is an uncommonly recognized, probably immunologically based adverse reaction to therapy with penicillin and its derivatives.

Aged↗
PubMed1983

Improvement of renal function during long-term treatment of severe hypertension with minoxidil.

Sixty-nine patients with refractory hypertension were treated with minoxidil and in 66 good control of blood pressure was achieved. Renal function was stabilized in 31 patients in whom the serum creatinine was normal at presentation. Twenty-eight patients with impaired renal function had a substantial fall in serum creatinine (25 per cent) during the first three to six months of treatment and this improvement was maintained. In contrast, renal function in six out of seven patients with primary renal disease continued to deteriorate despite adequate control of blood pressure. Effective control of blood pressure prevents or reverses impairment of renal function in patients with refractory hypertension not associated with primary renal disease.

Blood Pressure↗
PubMed1982

Treatment of refractory hypertension.

126 patients with blood pressure which was unacceptably high despite a conventional stepped-care regimen (diuretic, beta-blocker, and vasodilator) took part in a comparative assessment of different approaches to the treatment of refractory hypertension. One of four regimens was used: oral diazoxide, minoxidil, captopril, or quadruple therapy (diuretic + beta-adrenoceptor blocker + hydralazine + prazosin). Despite the severity of hypertension, blood pressure could be controlled in almost all these patients, and no patient died from cerebrovascular disease while on treatment. 2 patients died of renal failure and 5 patients required long-term haemodialysis. Ischaemic heart disease remained a problem and caused the death of 10 patients. Diazoxide was the most effective treatment but was the most difficult and unpleasant to use. Captopril was the best-tolerated but failed to control blood pressure in 6 of 15 patients. Our experience indicates that there are now sufficient therapeutic alternatives to achieve acceptable blood-pressure control in almost all patients with "refractory" hypertension, although no treatment is ideal.

Adrenergic beta-Antagonists↗